Modern Genetics

Sugar fuels growth of insulin-making cells

2011-05-18T06:05:00.000-07:00

A spoonful of sugar may be a remedy for diabetes. The more glucose that insulin-producing cells in the pancreas use, the faster those cells reproduce, a new study in mice shows. Giving animals more food to eat or bathing cells with glucose — the type of sugar that cells burn for energy — can increase the amount of insulin-producing pancreatic cells known as beta cells. But exactly how the sugar increases the number of beta cells has not been clear.

In the new study, researchers led by Yuval Dor and Benjamin Glaser of the Hebrew University of Jerusalem used genetic techniques to wipe out about 80 percent of the beta cells in the pancreases of mice. The mice became unable to produce enough insulin and thus diabetic, but between a month and six weeks later, the mice’s blood sugar levels dropped to normal. The researchers discovered that some of the beta cells had grown back.

He and his colleagues wanted to know whether that slow growth was fueled by the mice’s high blood sugar or by other factors. To find out, the researchers again killed about 80 percent of beta cells in another group of mice, but this time transplanted insulin-producing cells elsewhere in the mice to keep their blood sugar at normal levels. That meant the surviving beta cells in the pancreas didn’t have to work as hard. The cells’ regeneration rate dropped along with their work load, the team found. The result convinced researchers that glucose really was involved in the cells’ regrowth.

To confirm the finding the team removed an enzyme called glucokinase from the mice’s beta cells. Glucokinase is a key enzyme in the conversion of glucose to energy. Without glucokinase “the beta cell replication dropped nearly to zero.
The result also suggested that drugs that boost activity of glucokinase might increase beta cell growth. Such drugs might boost beta cell growth while still lowering circulating blood sugar levels.
People with mutations that increase glucokinase activity also have more beta cells in their pancreases.

Source:http://www.sciencenews.org/view/generic/id/72225/title/Sugar_fuels_growth_of_insulin-making_cells

Shih-Wei Kuo - 42621209

How Long Will You Live?

2011-05-17T05:16:00.000-07:00

In the past, guessing how long that you will live for has been a task left to mystics rather than scientists. New breakthroughs in genetics following the mapping of the human genome have made the development of a blood test that makes the prediction the life span of an individual possible. The test measures the length of a person’s telomeres, which are the vital pieces of DNA at the end of chromosomes. As cells continue to divide with age, telomeres become shorter and are believed to correspond with a kind of ‘biological age’ which is often different from chronological age. The recent breakthroughs have been in the accuracy of such tests, which can now detect very small differences in length in a fast, simple and affordable technique. It is more important to determine the length of the shortest telomere, which can be responsible for causing cells to stop growing, rather than the average telomere length. Scientists do not believe that the test can narrow a person’s life to a specific number of months and years but can provide an insight into the speed of their aging. Research has shown that people with shorter telomeres on average die younger than others with longer telomeres. The importance and revolutionary nature of new research into telomeres is evidenced by the recent awarding of a Nobel Prize in medicine to three American geneticists studying the DNA segments.

The test, which is said to be available later this year at a cost of around $700 Australian dollars, is not short of controversy. Such tests would be of great interest to insurance companies offering life insurance policies and the results could affect premiums. Some scientists also doubt the tests usefulness as it evaluates only part of the genetic basis of aging and neglects other genetic and environmental factors. Although the test could provide a very interesting snapshot into a person’s general health, it does nothing to change the need for people to live a healthy lifestyle by eating well and regularly exercising to extend their lifespan.
References:
Connor, S. (2011) The 400 pound test that tells you how long you’ll live. The United Kingdom: The Independent, Available from: http://www.independent.co.uk/news/science/the-163400-test-that-tells-you-how-long-youll-live-2284639.html, Accessed 17 May 2011.
Carollo,K. (2011) Can a blood test determine how long people will live. Place Unknown: ABC News, Available from: http://abcnews.go.com/Health/blood-test-determine-quickly-body-aging/story?id=13613344 , Accessed 17 May 2011.

Genetic Mutation and Schizophrenia

2011-05-16T09:39:00.000-07:00

Schizophrenia is a brain disorder that caused by environmental and genetic factors. Approximately 1% of population suffers from schizophrenia and 10% of people with this illness commit suicide. People with schizophrenia have gene mutation 4 times more frequently than normal people. From previous study in the last three years, researchers have discovered that these mutations consist of copy-number variation, the CNVs, which is a type of genetic variation that delete or insert a base pair from the normal DNA sequence and changes the entire DNA sequence from the mutated point and causing mRNA changes during the transcription and produces new amino acids.

A new research was published in Nature this year in February by Professor Aiden Corvin of the Psychosis Research Group. They not only confirmed the CNVs identified in earlier studies, but they also found that duplications at the tip of chromosome 7q are 14 times higher in people with schizophrenia than in healthy people. These CNVs (the duplications) impact a gene called VIPR2, formally known as the Vasoactive Intestinal Peptide Receptor 2 which is expressed in nervous system and is important for brain development. It also helps to regulate the formation and activity of neurons in the brain. In mice, VIPR2 is also responsible for behavioral processes like learning and daily activities. Researchers also found that individuals with mutations had a greater expression of VIPR2 and they believed that these mutations increase signaling in the VIP pathway. In conclusion, there are more duplications occur in chromosome in people with schizophrenia than normal people. This mutation makes the VIPR2 gene more active and this mutated VIPR2 gene caused schizophrenia.

Original Article:
http://www.sciencedaily.com/releases/2011/02/110202132334.htm

Jenny(42632447)

Apoptosis and its role in chemotherapy

2011-04-11T17:26:00.000-07:00

The apoptosis is physiological cell death program which could take control the number of normal cells. This is also the way that cancer drugs kill tumor cells.

The apoptosis pathways are controlled by caspases. These inactive substances could be stimulated to active state. There are two main pathways lead to the activation. One is initiated by the ligation of transmembrane death receptors. This could be regulated by c-FLIP through affecting the activator and effector of capases. The other way needs the mitochondrial protein released through the disruption of mitochondria membrane. Capases-9 is activated and thus starts the apoptotic process.

Chemotherapy was used for cancer therapy for more than half a century. But why does it fail sometimes? There are two main reasons: the defects in apoptosis and the drug resistance.

Chemotherapy is expected to only target on the cancer cells by cytotoxic effects. However, sometimes the actual effect is not notable as expected. Also, the normal fast-replicating cells (e.g. bone cells) could be affected.

The tumors cells proliferate much faster than normal cells and this is how they are detected. So, the drugs are used to interfere the DNA replication. Chemotherapeutic agents induce cellular response (e.g. apoptosis) which affects the cell proliferation.

However, thorough the mutation, the gene coding the apoptosis could be changed and thus the tumor cells could get advantages in cell survive and drug resistance. These two factors develop the formation of tumors and affect the effectiveness of chemotherapy.

How does drug action mechanisms work? There are classical drug resistance proteins inside the body which will inhibit the primary drug effect. Depends on its extent, the induced damage would bring in the cells death.But the mutation takes place during this process will develop the multidrug resistance and affect the outcome of chemotherapy.

Jianchao Ge (Student Number: 42572691)

Source: http://www.labcim.unipam.edu.br/download/link%20entre%20apoptose%20quimioterapia%20e%20cancer.pdf

Image source: http://www.sciencedaily.com/releases/2008/12/081201105847.htm

Designer Babies

2010-10-02T18:41:00.000-07:00

Thanks to our knowledge in genetics and medical technology’s always improving, doctors are now able to screen the in-vitro patients, soon to be children for genetic defects and diseases. The women can now choose specific traits for their children such as blood type, athleticism and capability to fight of diseases. This is all possible because of our understanding and ability to do genetic mapping. The main screening process used is preimplantation genetic diagnosis (PGD), and this detects genetic and natural diseases just by looking at a few of the embryo’s cells. These trouble spots in the DNA sequence are then suppressed or interrupted or fixed to stop any genetical defects or diseased occurring

There are many positives about this and also some negatives. It is positive because of all the diseases that will be stopped before they can start in the children prolonging their lives and making them healthier. The more negative side to this science is that people are screening and choosing specific phenotypes and traits and making “designer babies”. This has caused a lot of ethical problems with this developing research.

http://ezinearticles.com/?Designer-Babies---Playing-With-Genetics&id=3501268

Genes important to sleep discovered

2010-06-02T07:00:00.000-07:00

Sleep is a behaviour that is common in all animals but the reason to how lack of sleep can affect the animal’s condition requires further investigation. A study was done to look more closely at this behaviour from sleep and activity patterns of 40 different lines of 3,500 of wild Drosophila melanogaster (fruit flies) at the genetic level as it may contribute to the understanding of human sleep. Fruit flies normally sleep 12 hours a day. The researchers found out that the fruit flies were homozygous but the lines were different and each one of these flies were placed in a small glass tube which were connected to a machine that monitored the activity of the flies every minute using infrared sensors. The study found that in male flies, the duration of sleep was longer than female flies on average. Also, males slept more during the day and were more active when awake than females. Almost 1700 genes were identified in the study and some were not known to have an effect on the variability of sleep in fruit flies before this study was conducted. Some genes that were thought to have an effect on sleep duration were verified by separate mutations in those important genes and effects on sleep duration were observed. They also found mutants that survived on little to no sleep - one to two hours a day or none at all. The sleepless flies had a mutation of a particular gene and they have named Sleepless. “They believe the Sleepless gene encodes a protein that affects whether potassium ion channels in the brain stay open or closed. When the channels are open, the brain is connected and working – the fly is awake. When closed, the channel shuts down and the fly sleeps. The insomniac fruit flies had less of the Sleepless-produced protein.” Groups of genes that affect sleep were identified in the study and now there is a greater understanding of how genes relate to sleep.
Sleep is regulated by two processes known as circadian and homeostatic. Circadian regulation affects the timing of sleep, and the homeostatic mechanism affects the need for sleep. The Sleepless gene affects the homeostatic mechanism.
Sleep is not just for humans ,it has been observed in everything from flies to dogs to people, indicating that it's essential to life. Insufficient and poor-quality sleep is an increasing problem in industrialized nations. In the U.S. alone, about 70 million people suffer from chronic sleep problems, which reduce workplace productivity, affect quality of life and can even be lethal. Therefore, we should do further investigation to have a better understanding of how genes relate to sleep.
By 42282570
http://www.sciencedaily.com/releases/2009/02/090222142149.htm http://www.sciencedaily.com/releases/2008/07/080729160819.htm

Evolution: the Raw Power of Jumping Genes

2010-06-01T23:06:00.000-07:00

Researchers at the University of Pennsylvania School of Medicine have discovered that a kind of gene labelled "jumping genes" within a genome has extensive variations in different individuals, as found through gene mapping of these jumping gene locations. From this finding, the researchers have postulated that these jumping genes may be a driving factor in our genetic diversity. This is highlighted by the results of the study, which showed that out of the 1139 genome sites observed, approximately 285 sites would be different for any two individuals. The reason for these variations were found to be due to the jumping genes, which are essentially DNA sequences that may "jump" from one location in a cell's genome and "land" in another location within the same cell's genome.

While previously the significance of these genes influence on genetic diversity was underestimated, this study proves these genes result in large variation in genome sites and that jumping genes could thus be described as the raw force behind genetic evolution.

Also known as transposons, jumping genes can influence an organism in many ways, as even subtle changes in an organisms genome can result in distinctly different phenotypes. Every individual would have these jumping genes, which may jump and insert genetic material into new locations. This could thus result in negative effects on cell structure (like genetic diseases and cancer), creation of new genes, or decreasing the expression of genes near the jumping genes' landing site. All factors would increase the diversity of an organisms' genome.

DNA Sequence Itself Influences Mutation Rate

2010-05-25T08:30:00.000-07:00

In a report published online in Genome Research, researchers have identified intrinsic properties of DNA that influence mutation rate, shedding light on mechanisms involved in genome maintenance and potentially disease.

Some DNA mutations are subject to natural selection, either conferring a biological advantage that is selected for, or a negative effect that is selected against. Mutations not under selection are said to be neutral, and the rate at which neutral mutations accumulate is reflective of the true DNA mutation rate.

Interestingly, the neutral mutation rate can vary significantly between different regions of chromosomes. Sequence high in pairs of the bases C and G (CpGs) where the C's are chemically modified, have been positively correlated with mutation rate.

Walser and Furano compared the CpG content and DNA changes in inactive L1 retrotransposons shared by humans and chimpanzees.
The researchers had previously noted that the older L1s have a lower CpG content than the younger sequences as expected, but here they observed two particularly striking features: "The overall mutation rate in the older fossil sequences dropped dramatically," said Furano, indicating a certain CpG content threshold is required to affect the non-CpG mutation rate. "And most provocatively, the types of mutations changed significantly."

This means that CpGs are not only promoting mutations, but they are also influencing how the non-CpG sequences around them are being mutated, an extension of what the authors call the "CpG effect." These findings strongly support the hypothesis that the co-variation of CpG content and non-CpG mutation rate is a property of the DNA sequence itself, and not a result of the chromosomal location.

"Intriguingly, the CpG effect revealed by our studies mimics the altered mutational state that has been demonstrated for certain cancers," Furano noted.

Weblink:
http://www.sciencedaily.com/releases/2010/05/100524092348.htm

Raymond Ng (42161040)

Closing on to the answer to the cause and cure of Huntington's

2010-05-23T01:12:00.000-07:00

The use of fruit flies are helping scientists and doctors to slowly uncover the secrets revolving around huntington's disease (the cure and cause of it). They have been testing fruit fly genes too see whether there were any formation of plaque-like protein aggregates within their cells. They have discovered a small group of genes (more than 70% same for humans) which play a role in regulating the formation of these aggregates. Also they discovered that these aggregates formed in different tissues, such as those in the brain and cells. These were similar to those formed in humans.

Thus, fruit flies have allowed for scientists to find the genes which control the formation of plaque-like protein aggregates. Thus this is allowing scientists to move closer towards finding the answer to how the formations are regulated which will lead to the formation of a drug to prevent and treat these diseases. Overall proving that the fly genome is a significant factor in current and possible future discoveries, such as those of medicine for brain disease

Weblink:
http://esciencenews.com/articles/2010/05/21/scientists.make.important.step.toward.stopping.plaque.formations.huntingtons.disease

Paul Kim (42344281)

Gene From Algae Could Help Crops Cope With Climate Change

2008-05-26T20:08:00.000-07:00

Researchers at the ANU in Canberra have isolated genes in algae which could be integrated into cereal plants within the next 10 years. These genes, according to Professor Murray Badger, would help the plants conserve water and deal with higher levels of atmospheric carbon dioxide. They do this by impoving the efficiency of photosynthesis in high temperature and CO2 environments.

The research has provoked some interest, particularly in rice dependant countries. The International Rice Reasearch Institute in the Phillipines is interested in the technology, in the context of integrating maize genes into rice, but for the present, this scale of genetic engineering remains unfeasable.
http://www.abc.net.au/news/stories/2008/05/15/2245515.htm

Skin Cancer and Marijuana

2008-05-26T08:17:00.000-07:00

University of Minnesota researchers looking to answer the question ‘why does ultraviolet light induce skin cancer?’ believe they have found how sun-induced skin cancer starts. They found the cancer starts in receptor molecules or molecular “hooks” on the outer surface of cells that also pull cannabinoid compounds found in marijuana out of the bloodstream.
These receptor molecules are protein structures that are components of a cell’s outer membrane. They act like receiving docks and catch specific compounds from the blood and enable the cells to engulf or interact with the compounds.
The researchers found that two receptors for cannabinoids also responded to UV light. They made the discovery during a search for the initial interaction between UV light and human skin cells.
If cannabinoid receptors are important in the initiation of skin cancer by UV light, then animals that lack the receptors should be relatively protected from the ravages of the light
Working with mouse embryos, the researchers removed the genes for the cannabinoid receptors. They found that the skin of the resulting adult mice, which lacked the receptors, was resistant to the development of UV-induced inflammation and skin tumors called papillomas.
The next question is why evolution should have produced receptors that respond to both UV light and cannabinoids?

Chandan Mangar
41726312

Corn Powered Cars

2008-05-26T06:31:00.000-07:00

Scientists from Michigan State University have discovered that an enzyme produced by microbes living in the stomachs of cows is the key to efficiently turning corn plants into biofuels. This enzyme is essential to the digestion of grasses by cows. It can also be utilized to turn other plant fibers into simple sugars. These simple sugars can then be used to produce ethanol to fuel trucks and cars.

Michigan State University scientists have conveniently grown corn plants that contain this enzyme by inserting the particular gene from a bacterium that live in cows' stomachs. This effectively converts the un-usable sugars, such as cellulose, which are locked up in the plant’s stalks and leaves into usable sugar without the aid of costly synthetic chemicals and processes.

Originally only the kernels of corn plants could be utilized to make ethanol, but this innovative discovery will allow the whole corn plant to be used. Consequently, more fuel can be produced at a smaller cost.

The main target for the enzyme produced in the corn plants is the vacuole as it is a safe and convenient place for the enzyme to be stored until harvest. The enzyme will accumulate in the vacuole with other cellular and metabolic waste products and will only become active when it is being used for biofuels. Since it is located only in the vacuole, the enzyme is only to be produced in the leaves and stalks of the plant where it is required and not in the seeds, roots or the pollen.

This revolutionary idea promises an effective carbon neutral and renewable energy source.

For more information visit: http://www.sciencedaily.com/releases/2008/04/080408085453.htm

41777163

Genetic code linked to obesity

2008-05-26T05:37:00.000-07:00

Scientists found that there is a section of genetic code which has been linked to obesity and they hope the findings can assist the treating of obesity. People who are suffering from expanding waist lines, gaining excessive weight and having diabetes should pay attention to this passage.

It is very common in people with Indian Asian rather than European ancestry. The DNA sequence is combined with gaining two kilogram in weight, two centimetre expansion of waist circumference and the tendency to become resistant to insulins, which cannot convert glucose in to glycogen, resulting in a Type 2 diabetes. It is one of the explanation why they expect 40% of the population of Indian Asians will have global heart disease by 2020.

It actually calls Melanocortin 4 receptor, short term MC4R. It is a human gene. It regulates energy levels in the body by influencing how much energy we use and conserve. The researchers believe that the DNA sequence plays the role to control the MC4R gene.

New Meaning for the Term ‘Computer Bug’

2008-05-26T04:38:00.000-07:00

Researchers in the US have created ‘living computers’ by using genetically altered bacteria. The findings of this research demonstrate that computing in living cells is feasible. It also opens the doors to a number of potential applications including data storage and as a tool in manipulating genes for genetic engineering.

The research team was from the biology and mathematics departments of Davidson College, North Carolina and Missouri Western State University, Missouri, USA. They achieved execution of DNA-based computation in living cells by engineering Escherichia coli to address a classic mathematical puzzle called the Burnt Pancake Problem (BPP).

The BPP is solved by sorting a stack of distinct objects (pancakes) into proper order and orientation using the minimum number of manipulations. The pancakes are of different sizes, each of which has a golden and a burnt side. The largest pancake must be on the bottom and all pancakes golden side up. Each manipulation reverses the order and orientation of one or more adjacent objects in the stack.

A system was designed that uses site-specific DNA recombination to mediate inversions of genetic elements that represent pancakes within plasmid DNA. Inversions (or “flips”) of the DNA fragment pancakes were driven by genes added from the Salmonella typhimurium Hin/hix DNA recombinase system. The system used sorts DNA segments by inversions to produce different permutations of a promoter and a tetracycline resistance coding region; E. coli cells become antibiotic resistant when the segments are properly sorted. The time required to reach the mathematical solution reflects the minimum number of flips needed to solve the burnt pancake problem.

It is believed the system has the potential to be scaled up to larger and more complex problems and by exploiting the infinitesimally tiny scale of DNA and bacteria, ‘living computers’ could carry out complex parallel processing problems that would otherwise utilise very large and expensive electronic computing systems. Since bacteria multiply naturally and have their own repair mechanisms, ‘living computers’ could be less expensive and require less space compared with conventional devices. Additionally, ‘living computers’ could evolve through DNA mutations to solve new problems.

For further reading:
http://www.jbioleng.org/content/pdf/1754-1611-2-8.pdf
http://www.sciencedaily.com/releases/2008/05/080520090551.htm
http://www.itnews.com.au/News/NewsStory.aspx?story=76534

Malcolm Keth (41751819)

New clues: gene variations may contribute to MS risk.

2008-05-01T00:58:00.000-07:00

MS (muscular dystrophy) is a type of disease that depletes the fatty sheaths that protect nerve fibres, causing a loss of muscle control. In the 1970s, scientists found that a specific version of a gene conferred a fourfold increase in the risk of MS. This gene encoded for an immune system protein called human leukocyte antigen DRB1.

Recently, studies in the USA and Sweden have now indicated that people with MS are 20-30% more likely than non-sufferers to have a variation of other immunity-linked genes. These genes encode the protein interleukin-2 receptor alpha, and also the receptor for the immune system messenger protein, interleukin-7.

The interleukin-7 receptor is attached to the membrane of cells, most typically immune system T-cells. When the interleukine7 binds to it, the receptor signals the cell to take part in immune response reactions.

The variant of the interleukin-7 receptor gene slightly favours production of a free-floating version of the receptor. The membrane-bound receptors compete with free-floating receptors for interleukin-7, therefore an excess of these free-floating receptors affects the fine-tuning of immune responses.

Previously, MS was believed to have a hereditary component, however the recent discovery of more MS-conducive gene variations may also indicate that MS is an autoimmune disease. This is because interleukine-2-receptor-alpha (a protein produced by one of the gene-variants) has been linked to Graves’ disease and type1 diabetes, which have autoimmune traits.

Interested? Find more information at

http://findarticles.com/p/articles/mi_m1200/is_5_172/ai_n19479152
http://www.nationalmssociety.org/about-multiple-sclerosis/index.aspx
http://www.labtestsonline.org/understanding/conditions/autoimmune.html

Ethanol; a blue green fuel alternative

2008-04-30T22:13:00.000-07:00

The impending peak oil crisis is a hot topic at the moment in the news along with it are the so called “designer” fuels; fuels that are environmentally and economically viable. One such possibility has arisen from the ecologically significant cyanobacteria. This little organism is opening possibilities for a clean, green source of fuel.

It has long been known that the molecule cellulose is a potential bio-fuel source as it is comprised mainly of sugars which can be fermented to ethanol. However in most plants the cellulose is a structural molecule; this means that it is tightly packaged along with many ligands. The refinement of this cellulose to sugars is an expensive process as it requires many enzyme assisted steps.

Professor R. Malcolm Brown Jr. and Dr. David Nobles Jr. are the scientists who developed this particular cyanobacteria. It has been genetically modified to produces cellulose in a gel like form. Not only this but the bacteria excretes sucrose and glucose which can also be used to me ethanol. This ability was sourced from genetic material from a non-photosynthetic ‘vinegar’ bacterium.

This bacteria is suggested to be one of the most sustainable bio-fuel production methods around as it is photosynthetic, nitrogen fixing and can be gown in second grade water not suitable or humans or corps. Another bonus is that the bacteria secretes the cellulose as waste so it can be harvested without damaging the bacteria making it a renewable source. All in all, the cyanobacteria provides a realistic and viable blue green fuel source thanks to a little genetic engineering.

Photo (bellow) of the cyanobacteria with
chlorophyll (pink/red) producing cellulose (blue)

http://www.sciencedaily.com/releases/2008/04/080423115917.htm

Sigrid Hillier 41772887

Scientist identify human proteins that help HIV

2008-04-30T19:53:00.000-07:00

HIV Virus article

In an article that appeared on Basesciences.com in January this year, it showed there was new progress in understanding the new treatments for the deadly virus, HIV.
US scientists identified close to 300 human proteins that help the Human Immunodeficiency Virus to reproduce. This provides us with hope that there is a way to fight the condition.
Researchers from the Harvard Medical School have identified the new proteins through a process called ‘RNA interference’.

The team of researchers found 273 particular proteins that could provide a way to help cure people with HIV, as the virus develops resistance to existing anti-viral drugs.

Stephen Elledge of the department of genetics of the School says that ‘the anti-viral drugs that already exist are doing a good job of keeping people alive but all therapeutics are suffering from the same problem’. That is, as it continues to mutate, people develop resistance. So the team has decided to take a different approach by focussing on the human proteins exploited by the virus.

He continues by saying that the virus will not be able to mutate further to overcome the drugs that interact with these proteins. It will work on a hypothetical basis, where scientists will be able to predict why HIV needs a particular protein and then test their hypotheses.

He added that the immune cells targeted by HIV contain high concentrations of many of the 273 proteins.

He finishes saying: ‘We’re closing in on a system-level understanding of HIV, which opens new therapeutic avenues’.

Reference : http://www.basesciences.com/article.asp?articleid=25060&Scientists-identify-human-proteins-that-help-HIV , 30/04/08.

Deciphering The Protein Editing Code

2008-04-30T17:42:00.000-07:00

By Dannielle Brown

Minor errors in protein production could be a thing of the past now with the aid of recent data collected by members of the Scripps Research Institute.
___________________________________________

Research conducted under the ever watchful eye of Professor Paul Schimmel of the Scripps Research Institute, could in the future hold the key to identifying underlying causes of certain diseases and possibly in time play a part in their demise.
This process of protein manufacturing is a somewhat complicated and vitally crucial process and one minute mistake can result in catastrophic effects. Many phases and components are involved in this method, such as the messenger RNA which acts as an instruction manual for protein synthesis, or the tRNA carrying amino acids. The majority of these tRNA only carry a singular amino acid at a time and are joined using an enzyme known as synthetase. These tRNA then unite together and form the specified protein.
Sometimes during protein synthesis the tRNA can accidentally combine with the incorrect amino acid. When this occurs and the problem is not rectified serious health consequences can result. After mind boggling amounts of investigating by scientists it is now understood that the segments of the synthetases that are responsible for the adhesion and recognition of tRNA and the correct amino acids are that precise that little to no editing is mandatory. But whatever little editing required was thought to have taken place at only one place.
But this new study tends to provide evidence that falsifies this claim. After studying Alanine (an amino acid found in everything from humans to birds) it was revealed that a second checkpoint was present. This other checkpoints function was to identify any mistranslations and the removal of any foreign amino acid (not Alanine) that attempted to bind with the Alanine tRNA.Surprisingly this second station of the enzyme synthetase also focuses on the same pair of nucleotides as the first station.
Many experiments were conducted on this second editing station. Including the separation of the enzyme from the rest, resulting in the observation that the enzyme still had the ability to removed incorrect amino acids from the Alanine TRNA.
The astonishing research that was conducted also lead to another discovery. That freestanding domains (genome-encoded fragments that have not yet been proven to have a particular function) have a very similar genetic sequence to the second editing location found in the Alanine enzyme synthetase. These freestanding domains were also experimented upon and were shown to independently eliminate the incorrect amino acids.
This result provokes the thought that these fragments could act as a third checkpoint, used to once again observe whether the protein synthesis was a success.
Further research is now being conducted with the assistance of other scholars from many prestigious institutions to see if this new knowledge can be put into use in the medical world, either by complete irradiation of some diseases caused by mutations or just assist in the comprehension of conditions that are not yet understood.

Reference - http://www.sciencedaily.com/releases/2008/01/080103090655.htm

Cloned sniffer dogs

2008-04-30T16:58:00.000-07:00

The Korea Customs Service reported that seven cloned puppies named Toppy ("Tomorrow's puppy") were born in late 2007 to three surrogate mothers under a state-funded project. Lee Byung-Chun who managed to clone the Toppies played a key role in cloning a three year old Afghan Hound. The cost of cloning the Toppies was approximately 301,205 dollar. Lee Byung-Chun used the nuclei of somatic cells from a sniffer Golden Retriever, Chase, to clone the puppies. The project manager Lim Jae-Yong said that it would be easier to train sniffer cloned dogs than ordinary canines. The Toppies have passed the first round of tests for behavourial patterns and genetic qualities, and they will report for duty in June this year after completing a second round of tests.

Indeed, successful cloning of dogs show that the use of genetics in technology is essential. However, with regards to the issue of cloning humans and other organisms, ethical issues are always involved.

Reference: http://news.yahoo.com/s/afp/20080421/hl_afp/healthskoreacloningdogs_080421171230

“Researchers have identified location of genes responsible for osteoporosis and osteoporotic fractures”

2008-04-30T15:49:00.000-07:00

Osteoporosis is a highly heritable bone disease which results in a decrease in the amount of bone mineral density, hence a very high chance of osteoporotic fractures. This study was conducted to identify the genetic loci that influence bone mineral density.

This study revealed that there is an association between bone mineral density and two single nucleotide polymorphism (SNPs). One SNP located on chromosome 8, which increases the risk of osteoporosis by 20%, and the other SNP on chromosome 11, which increases the risk by 30%. These variants increase the risk of osteoporosis by reducing bone mineral density.

These findings would enable medical practitioners to identify osteoporosis early, before the age at which fractures are likely to occur and take preventative measures. Also by using a panel of genetic markers it would be possible to identify patients who are at a higher risk of osteoporotic fractures. The research team suggested that people with this variant will respond the best to the medications which increase bone marrow density.

The findings of this study provide the genetic basis of osteoporosis, enabling scientists to investigate the mechanism in which osteoporosis proceeds.

J. B. Richards, et al., 2008, “Bone mineral density, osteoporosis, and osteoporotic features: a genome-wide association study”, Published online April 29, 2008 DOI:10.1016/S0140-6736(08)60599-1

Gene Therapy: The Attraction is Magnetic

2008-04-30T04:37:00.000-07:00

Gene therapy is considered by medical researchers around the world to be a greatly promising potential treatment for many diseases, including cancers. Thanks to a researcher at the University of Sheffield, UK, this potential may have come a step closer to realisation.

Gene therapy involves delivering new modified genetic material to diseased cells, in the hope that the action of these new genes will correct the disease in each cell. While the process has repeatedly been shown to work in principle, there are practical difficulties which have prevented gene therapy from becoming widely utilised thus far. Foremost of these difficulties has been ensuring that sufficient numbers of genes arrive at the relevant area of tissue.

Claire Lewis may have found a solution, using magnets to make sure the modified genes reach their targets. Working on tumours in mice, she began the gene therapy process as normal, inserting the modified gene into myocyte white blood cells. But before injecting these monocytes, Lewis’ team added magnetic nanoparticles to the cells. When injected into the bloodstream, cells containing these nanoparticles could be guided to their target tissue by a magnetic field. Simply placing a magnet over the mice’s tumours was enough to ensure that the cells congregated there. It is believed that by utilising precisely variable magnetic fields like those of MRI machines, this process could also be used to reach deep-seated tumours.

Lewis' group are now investigating the capabilities of their technique in more detail. It could eventually make gene therapy the next big thing in tumour treatment.

Michael Horn

References:
http://www.nature.com/gt/journal/vaop/ncurrent/full/gt200857a.html
http://www.genengnews.com/news/bnitem.aspx?name=33901120
http://technology.newscientist.com/channel/tech/mg19826535.600-magnetic-killer-cells-zero-in-on-cancers.html

Culling the Cane Toads

2008-04-30T04:27:00.000-07:00

Throw them in the freezer, hit them with them with a golf club or even poison them, we can't effectively control the Australian Cane Toad population, or can we?

The University of Queensland's molecular bioscience researcher, Professor Peter Koopman, is innovating a strain of “daughterless” cane toads. Wthe females will only give birth to males of the species. And the males thtat are produced via this method will only be able to produce male offspring, and so on. As the generations go on, the effective breeding capacity of the cane toad population will decrease, hopefully till it is all males.

Proffesor Koopman says, “The simplest way of explaining it is that we hope to transplant a ‘gene’ into toads that will cause any female tadpoles they produce to change course and become males.” “We have a clear idea from our research at what molecular point in development you can change sex, and we will apply that knowledge to cane toads to create a ‘switch’ that flicks females back to males.”

Proffesor Koopman is lokking at the Cane Toad equivilant of SRY (Sex-determining Region Y), a sex-determining gene on the Y chromosome in humans and other primates. This intronless gene encodes a transcription factor that is a member of the high mobility group (HMG)-box family of DNA-binding proteins. This protein is the testis-determining factor (TDF), which initiates male sex determination.

Being such a green and humane solution to the problem faced, this method has recieved great support, and shows promise in eliminating the Cane Toads of Australia.

Luke Carpenter

Re-creating the Big Bang

2008-04-30T03:43:00.000-07:00

Deep beneath the Swiss-French border near Geneva, thousands of physicists are building the world's largest and most expensive science experiment — a particle collider that they hope will bring them one step closer toward unlocking some of the universe’s oldest secrets.

The Large Hadron Collider (LHC) is a $4 billion instrument that scientists at the European Center of Nuclear Research, or CERN, hope to use to re-create the big bang by crashing protons together at high speed. The big bang theory is just one of the ideas believed by some, which created what we know as the universe.

A 27-kilometer circular tunnel several hundred feet beneath Switzerland and France, the LHC will operate at -271 degrees Celsius, and collisions will occur 800 million times a second.

When they switch on the LHC in November, the magnet and several others will help to drive two streams of protons in opposite directions around the ring at close to the speed of light. Upon collision, the beams are expected to create many new particles and possibly a reconstruction of the universe in its very first moments. If the experiment is successful, all that work could explain the origins of mass.

Particle physicists believe the Big Bang was a huge explosion of energy that took place roughly 13 billion years ago, generating the matter that makes up humans, animals, plants, stars, galaxies — in short, the universe as we know it. But they still have niggling questions, including the deceptively simple riddle of why matter actually has mass. “Cosmologists can’t understand or measure the size of the universe,” says Grey. “It’s the missing mass problem.”

For more information visit the following web address:

http://www.umich.edu/~gs265/bigbang.htm and

http://www.msnbc.msn.com/id/17399245/

Blog by Greg Barker 41750081

Glow In The Dark Cats

2008-04-30T02:48:00.000-07:00

South Korean scientists have cloned cats that glow red under ultraviolet light, as part of research aimed at developing treatments for human genetic diseases. A team of scientists led by Professor Kong Il-keun, a cloning expert at Gyeongsang National University in Jinju, produced three glowing Turkish Angoras cats. According to the Korea Times, the scientists added red fluorescence protein (RFP) genes to the skin cells of the mother cat. They then inserted the skin cells into ova to produce cloned cats genetically modified to contain the RFP gene.

The ability to produce cloned cats with the manipulated genes is significant as it could be used for developing treatments for genetic diseases and for reproducing model [cloned] animals suffering from the same diseases as humans. Cats have similar genes to those of humans and because of this it is possible to make genetically modified cats that can be used to develop new cures for genetic diseases.

Full stories at: http://www.abc.net.au/science/articles/2007/12/13/2118028.htm?site=science&topic=latest and: http://www.huffingtonpost.com/huff-wires/20071214/skorea-glowing-cats/

Genes load cancer dice against black people

2008-04-29T23:52:00.001-07:00

When I first saw this article inside NewScientist magazine my first thoughts were ‘genes being racist?’ However it turned out to be an interesting piece of information. Did you know that prostate and breast cancers are more deadly for African Americans than say white people? In the US around 60 percent of black men are more likely to develop prostate cancer, and twice as likely to die from it. The differences in the activity of key genes may be partly to blame. Until now, social and economic factors such as access to healthcare have been blamed. However at the annual meeting for Cancer Research of the American Association in San Diego, California, on April 15, Tiffany Wallace of the US National Cancer Institute in Bethesda, Maryland, implicated biological differences between the tumours of blacks and whites. 160 genes differing in activity between blacks and whites were found in screened prostate tumours removed from 33 African American and 36 white patients by Wallace and her colleagues.
The differences could indicate that tumours are more inflamed in black people. However some genes that were identified govern production of interferons, which defend against viruses. Therefore it’s possible the extra cases of prostate cancer in African Americans could be due to a higher rate of infection with an unknown cancer-causing virus. This is now undergoing investigation and whether if it is the case.
Meanwhile, African American women are slightly less likely to develop breast cancer than whites – however it often strikes them at a younger age and is more lethal. Lori Field of the Windber Research Institute in Pennsylvania compared breast tumours taken from 26 black and white women, matched for age and the stage of their cancer, who were either members of the US military, or were the dependant of a serving member. The researchers found 65 genes with significantly different levels of activity between tumours from the black and white patients. This time however there was no clear link with the immune system, and few of the genes discovered had previously been linked to cancer, so the cause of the differences is unclear. This is also to undergo further investigation. Field says the long-term goal is to identify new targets for drugs which could improve survival prospects for African Americans.

For further reference: Original article by Peter Aldhous, San Diego, NewScientist magazine.

2008-04-29T23:35:00.000-07:00

Genetically modified, or simply GM foods are foods that have been produced from genetically modified organisms, and are achieved through genetic engineering. Despite their surge in popularity after the turn of the century, many controversies have arisen from the synthesising of these foods. These controversies are varied, but are mainly concerned with the health and safety oh human ingestion of these foods.

The modern process involved in creating GM foods is quite simple. A genetic engineer will simply take out the required DNA from one organism, and transfer it to the organism aimed at producing a new genotype and/or phenotype. There are a number of other ways to achieve a new GMO without having to transfer genes across, such as silencing or omitting certain aspects of the gene sequence.

The first GM food readily available for consumption was a tomato dubbed the ‘FlavrSavr’ tomato (Deakin university, 2006). Nowadays, food items such as corn, rice, soybeans and sugarcane are on the market, ready to buy by the consumer.

There are quite a few benefits involved in the creation and consumption of genetic foods. These include a higher nutritional yield, greater shelf life, lower costs and less need for crop spraying. However the synthesising of these foods can lead to a few negative effects. One such effect is the transferring of one particular allergen of a food to another. A prime example is that of brazil nut allergies to GM soybean allergies, as the allergen has been passed on in the production of the GMO. It can also have a major effect on the biodiversity of a given area, as animals may react adversely to the change from natural food to GM food.

Although the production of GM foods can be controversial and at times even disadvantageous to consumers, their production is important as they provide an inexpensive and highly nutritious alternative to naturally grown foods. The fact they are so readily available for consumers to buy is an indicator of our progression in biotechnology.

Some useful Links:
Genetically Modified Foods - Harmful or helpful?
Genetically Modified Foods - Better health Channel

Identification Of Genes For Common Heart Condition

2008-04-29T05:33:00.000-07:00

New studies has identified that a gene that causes the heart to become enlarged could be the major factor of heart attacks and heart failures. A journal published in Nature Genetics reveals a gene called osteoglycin, which previously not been linked to heart function, now plays a key role in regulating heart growth. The cause of the enlarged heart is due to this gene acting abnormally in some people.

Scientists believe that enlarged hearts are caused by a combination of genetic factors and external stimuli such as high blood pressure and obesity. However, the role played by genes has remained largely unknown.

The researchers found that higher than normal levels of osteoglycin were associated with the heart becoming enlarged in rats and mice and in humans.

Researchers hope that their findings will provide new avenues for treating people who either have an enlarged heart or are at risk of developing one. At present enlarged hearts can only be treated by lowering blood pressure.

Further information: http://www.medicalnewstoday.com/articles/105682.php

New Vector Carries Big Genes

2008-04-29T05:26:00.000-07:00

Newly developed vector derived from AAV has been used to successfully carry large genes into cells and improve eye function in a mouse model of an inherited disease causing progressive loss of sight.

In gene therapy, the curative gene is packages in an agent known as vector, which carries the gene into cells where it is required. The most common vector is derived from adeno-associated virus (AAV) has linear single-stranded DNA genome of approximately 4.7-kilobases. From the data generated by Alberto Auricchio and colleagues reveals that the new vectors derived from AAV known as AAV5 can now accommodate large gene, and AAV5 could be used to induce cells to successfully convert the information in the large genes into protein properly. AVV5 has a linear single stranded DNA genome of 5kb and the new AAV5 opens possibility of developing better gene delivery vehicles, in the case of most gene therapy targets on retinal cells can be transfected by AAV5 as well it is the most divergent of the group of primate AAV.
In the study on mouse, When AAV5 containing the mouse gene Abca4, which is the mouse correlate of the gene mutated in individuals with recessive Stargardt disease (an autosomal recessive genetic form of juvenile macular degeneration that causes progressive vision loss), was injected into the eye of mice lacking Abca4, improvement in the function of the eye was observed. Therefore the vectors of AAV5 concluded could be useful for treating individuals with recessive Stargardt disease. Based on many studies of the behavior of AAV vector serotypes in the retina, including cell specificity, efficiency, stability and immunogenicity (Auricchio, 2003), AAV vectors are clearly a promising tool for retinal gene delivery in a wide variety of disease contexts and have been used to deliver therapeutic genes to correct disorders in animal models of various human retinal diseases

Further information:
1. Journal reference: Serotype-dependent packaging of large genes in adeno-associated viral vectors results in effective gene delivery in mice.
http://www.sciencedaily.com/releases/2008/04/080415185025.htm
2. Auricchio, 2003 A. Auricchio, Pseudotyped AAV vectors for constitutive and regulated gene expression in the eye, Vision Research 43 (2003), pp. 913–918. Article PDF (205 K) View Record in Scopus Cited By in Scopus (13)

Blog by: Samantha Yau Yin Chang 41380714

Spot the Benefits!

2008-04-29T05:12:00.000-07:00

"Acne's a trial, but is it a disease? One scientist argues that, in evolutionary terms, it's good for us." (Daniel Williams, Time Magazine)
It is a theory that has rapidly gained increasing support. It is scientist Dale Bloom's belief that acne is 'misdiagnosed' and 'misunderstood'. That acne is not a disease but that it began as an evolutionary adaptation that discourages sex among still-developing youths who were not yet fit to be parents. In other words, acne serves to scare away potential sexual partners until both mates are equipped mentally, physically and emotionally to raise children.
Evidence to support her theory are summarised in the following points: that acne is universal in adolescents and triggered by the hormones released in puberty; that it is generally unattractive and tends to repulse potential 'mates' (for lack of a better word); and typically only sticks around until one is mature enough to cope with all that 'reproducing' involves.
So why didn't natural selection just delay the capacity to reproduce rather than create acne?Bloome argues that it is because "pubescent hormones are needed for brain development." And, why would evolution select for something that inhibits breeding when reproduction is the fundamental drive of all species? To this Bloome says, "The disadvantage of fewer births is outweighed by higher rates of survival."
It is an interesting theory but even Bloome admits that acne, as an evolutionary adaptation, has probably "largely outlived its usefulness" thanks to the commercial and pharmaceutical powers that be. However, if considered an adaptation of sorts, it can't also be considered a disease - as it is often referred to as, even by medical practitioners themselves - and therefore one might find solace in the idea that spots are part of growing up, not just for individuals but for the human species.

Maggie Eden
41186943

Further information:
www.ncbi.nlm.nih.gov/pubmed/14975524

Jurassic Genes... and angry raptors.

2008-04-29T04:03:00.000-07:00

Using modern molecular analysis, additional evidence has been collected showing the close phylogenetic relationship between a T. Rex and modern day birds. Soft tissue preservation was amazingly discovered within a 68 million year old fossilised thigh bone from the infamous Tyrannosaurus.

Despite being unable to extract DNA from the bone, it was possible obtain six precious peptides, 89 amino acids in total, which was enough to further establish the relationship between the dinosaurs, birds, and alligators; as predicted from skeletal anatomy. This provides the first molecular evidence for the evolutionary relationships of non-avian dinosaurs. Similar analysis was also achieved with collagen protein sequences derived from a fossilised mastodon bone, showing the close relationship between the extinct beast and a modern day elephant.

Furthermore, using the relationship between genome size and cell size, scientists have also catalogued the specific phylogenetic links between two major lineages of dinosaurs and modern day species. Carnivores such as T. Rex and Velociraptor had very small genomes similar to those of modern day birds, while Ornithischians, including Stegosaurus and Triceratops had moderately sized genomes closer to that of modern day crocodilians and lizards. This brings to light the sincerity of my suggestion when a friend commented that the raptors in Jurassic Park looked so angry, and I replied: "you'd be mad too if you were resurrected in the future only to discover your entire gene pool had amounted to no more than a chicken."

Due to the taxonomic links between modern day species and dinosaurs, it has even been suggested that the possibility of modern dinosaurs remains without access to preserved dinosaur DNA. By taking some bird DNA, essentially dinosaur DNA that has undergone millions of years of evolution, and somehow allowing evolution to proceed in reverse (perhaps 'anti-evolution') for the right amount of time, a blueprint for dinosaur DNA could be the result.

Posted by Alexander Bunt.
Further reading:
http://www.sciencedaily.com/releases/2008/04/080424140418.htm
http://www.sciencedaily.com/releases/2007/03/070307153009.htm
http://www.newscientist.com/article/mg17123004.600-monsters-in-our-midst.html
http://www.sciencedaily.com/videos/2006/0607-jurassic_docs.htm (interesting medical advances in disease evolution)

Parasite Resistance in Sheep

2008-04-28T18:01:00.000-07:00

A research team in New Zealand has recently discovered a DNA marker for parasite resistance in sheep. The ‘wormSTAR’ test was developed by taking measurements from over 100,000 sheep, all major breeds were included and samples were taken from all over the country. It was determined that some animals had higher parasite resistance, shed less eggs, and had higher fleece weights, weaning weights and carcass yields.

Parasites can have a detrimental effect on sheep. Some of the symptoms of parasite infection include: weakness, poor growth and reproduction, scouring, anaemia and in sever cases death. Drenches are becoming less effective, as parasites are building up resistance. The wormSTAR test will allow farmers to select animals that have a natural ability to fight parasites, this natural ability used in conjunction with drenching will allow for more comprehensive parasite protection.

Parasite resistance is not the only benefit associated with the wormSTAR test. Animals that have the gene responsible for parasite resistance were also found to have increased productivity. So animals with this gene have greater parasite resistance, higher wool and meat yields, and shed fewer eggs lowering the chance of infecting other animals in the flock.

This gene is an important discovery for the agricultural industry. It provides a genetic solution that draws on an animal’s natural ability and is environmentally maintainable. It is hoped that in the near future similar test will be developed for use on cattle.

For more information see:
www.catapultsystems.co.nz/products/55_wormstar.cfm

2008-04-28T17:00:00.000-07:00

Smokers’ genetic ‘double whammy’

http://www.baltimoresun.com/news/health/bal-te.cancer03apr03,0,7169921.story

As if the social and psychological factors of quitting smoking didn’t offer smokers a large enough challenge, studies indicate that some people have a genetic variation that makes them smoke more, makes quitting harder and makes them more susceptible to lung cancer. An article printed in the Baltimore Sun on April 3rd reports studies can also provide answers to the question of why some long term smokers get lung cancer and others do not. The study found a genetic variation on chromosome 15 to be linked with lung cancer. Also the carriers of the genetic variation were more likely to smoke more and to have difficulty in quitting. Three recent studies on 35 000 people have indicated such similar findings with this genetic variation. One group of researchers found that being a carrier of this genetic variation does not make a person take up smoking however once they do, they are more likely to smoke more cigarettes than a smoker without this genetic variation, making it tougher for them to quit. A smoker with this genetic variation from both parents is reported to be 80% more likely to get lung cancer than a smoker who doesn’t have this genetic variation. It is also reported that 50% of Caucasians of European descent have this genetic variation. So how does this genetic discovery help advance biomedical science? Researchers and scientists can now look at ways in which they can combat this gene variation and use these genetic differences to create more effective and suitable quitting programs for smokers.

Posted by Allegra Boccabella

Read full article
http://www.baltimoresun.com/news/health/bal-te.cancer03apr03,0,7169921.story

Gene discovery opens door to tackling disease

2008-04-28T16:26:00.000-07:00

A group of “Western Australian researchers [led by Professor Peter Leedman] have discovered a new gene that could lead to breakthroughs in breast and prostate cancer, as well as diabetes.” The gene they discoverd was called SLIRP and Professor Leedman states that it “…has the potential to shut down oestrogen in breast cancer cells and testosterone in prostate cancer cells. Most of those cancers depend on the hormones to stay alive, so if we can use SLIRP to block the hormones we may be able to help stop those diseases in their tracks."

An outcome of this discovery may be the development of new cancer treatments. If researchers can discover how this SLIRP gene functions, they may be able to develop ‘smart’ drugs with less side-effects, which will effectively target only cancer cells. It may also mean that a simple blood test can diagnose a breast cancer and this type of detection can happen early on in the cancers development, giving rise to an improved survival rate.

The discovery of this gene was a surprise as in the past this gene was not “characterised during the mapping of the human genome.” This gene discovery may also help treat diabetes and weight problems as the hormone SLIRP has the “…ability to turn off one of the key regulators of energy metabolism…”

This gene discovery could help countless people battling cancer or diabetes. Each year around 2500 men and women die from prostate and breast cancer, and breast cancer is the most common of all cancers in Australian women.

http://www.eurekalert.org/pub_releases/2006-06/ra-gdo060706.php

Seeing into the dark.

2008-04-28T06:13:00.000-07:00

Scientists in The UK successfully treated a teenage patient with a rare inherited blindness called Leber’s congenital Amaurosis (LCA). The 18 year old showed significant improved night vision after a breakthrough operation, whereas he had the ability to navigate through a simulation of a night time street with few errors. This was the worlds first landmark clinical trial to test the new gene therapy.

The trial began in early 2007 involving young patients with LCA, which is cause be a fauly gene known as RPE65 which stops the light sensitive cells in the retina from working properly. The project had two goals, first to test whether gene therapy would be safe patients with retinal disease, and secondly to test whether it could improve vision in young adults with an advanced retinal disease. In the trial, healthy copies of the faulty RPE65 into the cells of the retina of three young adults using a harmless virus to carry the gene. The vector was engineered by the US company targeted Genetics.

Daniel Barham
http://news.theage.com.au/scientists-use-genes-to-restore-vision/2008

Seeing into the dark.

2008-04-28T06:10:00.001-07:00

Scientists in The UK successfully treated a teenage patient with a rare inherited blindness called Leber’s congenital Amaurosis (LCA). The 18 year old showed significant improved night vision after a breakthrough operation, whereas he had the ability to navigate through a simulation of a night time street with few errors. This was the worlds first landmark clinical trial to test the new gene therapy. The trial began in early 2007 involving young patients with LCA, which is cause be a fauly gene known as RPE65 which stops the light sensitive cells in the retina from working properly. The project had two goals, first to test whether gene therapy would be safe patients with retinal disease, and secondly to test whether it could improve vision in young adults with an advanced retinal disease. In the trial, healthy copies of the faulty RPE65 into the cells of the retina of three young adults using a harmless virus to carry the gene. The vector was engineered by the US company targeted Genetics.

Yeast, worms and people may age together?

2008-04-28T05:49:00.000-07:00

All organisms experience aging, however, there were a study published recently provides pathways and evolutionary conservation of the genes regarding aging since experimental evidence strongly suggests that aging is modulated by genetic factors.

Researchers conducted a genome-wide analysis of the yeast and nematode, to identify genes that may related to aging in humans and therefore, explained that Nematodes and humans have a similar evolutionary scale and by doing comparing a particular gene modulates aging in both yeast and nematodes. The compiled a set of genes that were known to modulate aging and scanned the yeast's genes with highly similar sequences which then individually analyzed for a potential role in longevity by measuring the life span of yeast cells lacking each gene.

In a result, 15 out of 25 yeast genes are highly similar to human genes and this work is readily applicable to human aging research. More importantly, they reckon that there is a significant overlap between nematode and yeast aging genes especially those in nutrient-response pathways. At the end, it gives a basic knowledge and evidence for larger reserch on determining how each of these genes modulate aging at the moleculr lever, and to examine whether modulates aging in a mammalian model. So, to be a useful therapeutic target fir treating age-associated diseases.
Wai Ning (Wilson) Ng
41597240
Reference:
http://hum-molgen.org/NewsGen/03-2008/000015.html

Breakthrough in Gene Therapy Helps Reverse Blindness

2008-04-28T02:49:00.000-07:00

Scientists have for the first time successfully used gene therapy to partially restore the sight of patients with a rare form of blindness known as Leber’s congenital amaurosis. Some of the patients who were only able to detect hand motions were in a matter of weeks able read a couple lines on an eye chart. This blindness is caused by a mutation in the gene that is responsible for making the protein that is in turn needed by the retina. This protein is in charge of sensing light and sending images to the brain and people without this working gene gradually lose their sight until it is completely gone around early adulthood.

Gene therapy is basically the process of removing a faulty gene and replacing it with a normal one and over the years has had limited success. This study, however is a major breakthrough for gene therapy, as stated by some scientists “I think it’s a really big shot in the arm for gene therapy and for medicine in general,” said Dr Ronald Crystal, who is head of genetic medicine at Weill Cornell Medical College in New York. They achieved this breakthrough by injecting millions of copies of the healthy working gene behind the retina. And although not a huge improvement was seen in all, this is just the beginning and over time hopefully we will be able to perfect this technique to completely reverse blindness.

by Adam McNicol 41202544

References:

http://news.theage.com.au/scientists-use-genes-to-restore-vision/20080428-28zd.html

http://www.lowvision.com/wp-content/uploads/binoic-eye.jpg

Muscly Cows....yeah...

2008-04-28T00:31:00.002-07:00

Belgian Blues are among the most heavily bred cattle in the world. Known; not only for their bountiful lean meat, but also their jaw dropping muscular physique.

This substantial muscle growth is caused by a natural mutation to the Belgian Blues pair of myostatin genes which causes the effect scientists have termed as, double muscling. Myostatin is a protein which limits skeletal muscle growth. The mutation of the Belgian Blues myostatin genes, render the growth factor defective, allowing them to grow significantly larger muscles. In Belgium, this characteristic is reinforced through selective breeding to produce even larger Belgian Blues. For over 100 years, only the highest muscle mass cows and bulls are allowed to mate. To ensure that the effective gene is passed on, scientists collect the semen produced by the bulls and hand pick (not really) the most active sperm to pass on the gene. The cows are then artificially inseminated.

However, Belgian Blues are not the only species that possess this mutation. Although very rarely, naturally defective myostatin genes are also known to be held in the Piedmontese cattle, dogs and also humans; as found in two young boys from Germany and the United States. Scientists have also been able to produce a strain of mice carrying the mutation.

All species with a deficiency of myostatin exhibit a significant increase in muscle mass and strength.

Scientists believe the discovery of the advantages mysotatin deficiency holds, could eventually lead to a treatment for people with muscular dystrophy and other muscle eradicating diseases.

S4175108

Cool pictures and a video clip:
http://www.who-sucks.com/people/monstrous-myostatin-misfortunes-a-collection-of-myostatin-deficiency-pictures
http://video.msn.com/video.aspx?mkt=en-us&vid=740e8f1b-0c90-4b1b-b8c8-0ea69baa9e7b

Vitamin gene 'may fight breast cancer'

2008-04-28T00:04:00.000-07:00

About 10% of women in the West will develop breast cancer at some stage of their lives. But there is a gene which helps the body benefit from vitamin D may protect against breast cancer. It is believed that vitamin D protects against breast cancer and in some forms may even be used to shrink existing tumours. Vitamin D is essential for building strong bones because it helps the body to take up calcium from food, but it may also help protect against breast cancer because it has a role in cell growth and death. Researchers have discovered that some women have a different version of a gene involved with vitamin D called the vitamin D receptor (VDR) and may be less able to benefit from this protective effect.
Now scientists have identified this version of the gene, so it is possible to find out which women are at increased risk from breast cancer and tailor treatment to reduce this risk. Researcher Dr Kay Colston said: "Vitamin D normally binds to the VDR like a key fits into a lock. There is now evidence that vitamin D may protect against some cancers but this only works if vitamin D 'fits' the VDR." There has been a great deal of research into vitamin D and its effects on cancer, and some potential new cancer treatments are based on vitamin D. This is very important because it may help the doctors to identify more women who are at risk from breast cancer and gives them more clues on how to treat them."

Siau Yee Ho
41495355

Resources:
http://news.bbc.co.uk/2/hi/health/1579025.stm
http://news.bbc.co.uk/2/hi/science/nature/1600887.stm

Gene therapy targets cholesterol

2008-04-27T22:12:00.000-07:00

The latest technology termed microRNA (miRNA) promises to regulate gene expression to cut cholesterol levels. This technique has also been used to stop hepatitis C infecting cells.

This cutting edge technology is related to earlier forms of RNA interference, unlike its counterparts it works by inhibiting the increases in the amount of protein that is produced by intercepting the molecules. In essence it acts as a ‘brake’ on the mRNA translation.

MicroRNA’s are thought to control up to 30 percent of all gene activity, directing and expressing a whole network of genes rather than just single genes. These therapies have failed thus far as it is difficult to get the therapeutic molecule into the target cell. Work conducted at Santaris Pharma in Hørsholm, Denmark, however has lead to the absorption of the miRNA through an inhibiting drug. This eliminates the need for a “delivery vehicle”. The company has been targeting a miRNA called miR-122, which is thought to regulate up to 450 genes, around 100 of which are involved in cholesterol and lipid metabolism. It is only expressed in liver cells.
This miRNA inhibitor, or antimiR, was readily taken up by liver cells (in mice) and lowered cholesterol by up to 35 per cent. The more antimiR that was given, the greater the cholesterol-lowering affect it had on the mice. Inhibiting miR-122 also seems to protect the liver against hepatitis C infection; this is suggested by the culture tests. Without miRNA-122 viral replication is no longer supported and therefore antimiR-122 has the potential for hepatitis C and cholesterol reduction.
miRNA find it easier to cross cell membranes as they are single stranded and shorter than other RNA therapies. The nucleotide structure of antimiR has also been modified to make it more stable. It now last longer in the body and ensures stronger bonding to miRNA. This makes the treatment much more effective.
Although some researches question the wisdom of developing miRNA inhibitors before understanding the miRNA regulatory system, most agree that the results do seem promising. "People have been trying to knock down miRNA since it was first discovered," says Graham Brock, director of target and drug discovery at Ordway Research Institute in Albany, New York. "It has been done in cell lines and animal models, but I think this is the first time it has been done therapeutically."
Speculation has also been made in the use of miRNA to down-regulate cancer. Further screening of molecules is now in the process.

References:
http://www.newscientist.com/channel/life/genetics/mg19426044.000-new-gene-therapy-targets-cholesterol.html

Amy Beugelsdyk

41442621

Gene that prolong life after heart failure

2008-04-27T19:07:00.000-07:00

About 5 million people in the United States have heart failure, and it results in about 300, 000 deaths each year.
About 40% of African Americans have a genetic variant that can protect them after heart failure and prolong their lives by years, according to research conducted at Washington University School of Medicine in St. Louis and collaborating institutions. This race specific variant has an effect that resembles that of beta blockers, drugs widely prescribed for heart failure.
Adrenaline is a hormone released from the adrenal glands that prompts the fight-or-flight response- it increases cardiac output to give a sudden burst of energy. In heart failure patients decreased blood flow from the struggling heart ramps up, the body’s secretion of adrenaline to compensate for a lower blood flow. Overproduction of the hormone makes the weakened heart pump harder, but eventually worsens the heart failure.
The gene variant present in 40% of African Americans codes for an enzyme called GRK- Lev 41 which depresses the heart’s response to adrenaline in the same way beta blockers do; by blocking adrenaline at its receptor in heart and blood vessels.
Beta blockers prolong life to the same degree as the protective GRK 5 variant, but did not further increase the already improved survival of those with the variant. So, people with this variant can survive without beta blocker therapy as they have nature working for them already.
This discovery adds to the accumulating evidence that genetic differences contribute to the way people respond to medications. In addition it’s also a step toward individualized therapy.

To view the complete article follow the link below.
http://www.medicalnewstoday.com/articles/104746.php

Detailed gene map will lift lid on diseases

2008-04-27T16:40:00.000-07:00

In this article it tells the tale of why different people are susceptible to different diseases than other people. All of this could be proven why just by looking at one person's set of genes by the mapping tool of life. British and American scientists have come together to figure out the reasons behind diseases, obesity, diabetes, heart disease and cancer and how do they come about obtaining them.

The scientists know that 99% of all people are identical by their genes but its the other one percent that the scientists want to have a look at. In this one percent they will know why and how different people are susceptible to the conditions in which are killing humanity off. With a couple of experiments the scientists are able to map out the whether the patients have an ancestry from Europe, Africa, Japan, China, India and Mexico. Also with this knowledge they can allow scientists to pinpoint the genetic causes of common disorders swiftly and help tailor medical treatments to individual patients.

Reference:

1. http://www.guardian.co.uk/science/2008/jan/23/stemcells.genetics

2. picture is from http://current.com/items/88821737_ever_feel_like_your_genes_are_a_bit_misguided_a_gene_map_is_on_it_s_way

Anceint Bacteria feed on Uranium

2008-04-27T10:49:00.000-07:00

Recently, a major discovery was made of self-sustaining communities of Uranium-dependent bacteria living independently of the outer Biosphere shell. It is generally known that in order for life to exist, sunlight is the key for producing the energy needed for reproduction and growth. However, the recent discovery of Uranium-dependent bacteria found in the gold mines of South Africa, Johannesburg has proved that it is indeed possible for communities of life to exist deep within the Earth’s crust.

It was found in this deep, isolated environment that the radiation of the uranium rocks in the underground water supply facilitated the formation of hydrogen gas from water and sulfates from sulfur minerals. The Uranium-dependent bacteria harvest the energy created by these reactions, allowing other microbes to feed on the waste of these bacteria. In this way, the uranium-dependent bacteria perform the same vital role that photosynthetic organisms do on the surface of the Earth, where they are the primary producers responsible for harnessing the energy required for all other life.

DNA analysis of this new species of bacteria also showed that they were related to the hydrothermal vent bacteria, known as Firmicutes, which also feed on sulfate and hydrogen. It is thought that these new Firmicutes were separated from their relatives anywhere between 3 million and 25 million years ago, however it remains a mystery as to how these Firmicutes could have populated these areas deep within the Earths Crust.

Since the discovery of these Firmicute related life forms, there has been renewed interest in the possibility that life may well exist in the groundwater beneath the permafrost on Mars. After all, if bacteria isolated in the deep substrates of Earth can survive, who’s to say that there couldn’t be some other form of super-hardy bacteria living on Mars?

Cited from http://www.sciencedaily.com/releases/2006/10/061019192814.htm
Image obtained from http://posthumanblues.blogspot.com/2006_10_01_archive.html

Inherited Hyperactivity?

2008-04-27T07:45:00.000-07:00

It has been discovered that Attention Deficient Hyperactivity Disorder is inherited. ADHD affects 3 to 6% of all children and many adults, who continue to fidget.

Research has been carried out using identical twins, non- identical twins, adopted children and their adopted brothers and sisters, as well as their parents. It has been discovered that there is a 72-83% chance of the identical twins both having ADHD and only a 21-45% for the non-identical. Parents and siblings of ADHD children are 5 times more likely to have the disorder than others. This is evidence of a heritable connection.

Researchers now believe that there are several genes which influence the development of ADHD. These genes influence the production of the particular neurotransmitters called dopamine and noradrenalin in the brain which influences the way one learns. This occurs by how effective glucose can be used in the brain. It has been discovered that those with ADHD since childhood only efficiently use glucose in some parts of their brains, whilst the others have a lower amount being used. This creates an imbalance and thus, ADHD symptoms.

56 families who had a sufferer of ADHD were studied and a consistency in the presence of these genes were found. This however, only opens more doors for research. It is possible that there is a specific combination of these genes and other genes which influence development of this disorder.

Ed Cook, the associate professor of psychiatry and of pediatrics at the University of Chicago says: “If we can establish a link between abnormal forms of this gene and ADHD, it could provide us with a powerful new tool for precise diagnosis and early identification of children at risk, and a signpost toward designing better drug treatment,"

The genes now thought to affect ADHD have also been found to influence the development of schizophrenia.

Danni Burgess, 41756609, P2

For more information, see:

http://premium.netdoktor.com/uk/adhd/childhood/behaviour/article.jsp?articleIdent=uk.adhd.childhood.behaviour.uk_adhd_xmlarticle_004622
http://www.schizophreniaforum.org/new/detail.asp?id=500
http://www.uchospitals.edu/news/1995/19950000-adhd-gene.html
http://www.rps.psu.edu/sep96/hyper.html

Unlocking their origins - the new key to fighting diseases

2008-04-27T04:43:00.000-07:00

Unlocking their origins -
the new key to fighting diseases

A mathematically derived algorithm is helping researchers to isolate the genetic causes of certain diseases by detecting the geographical origin of certain recurrent disease genes. The impact will be on identifying inherited genes which cause diseases in people of mixed races - what researchers refer to as population admixture.

A team of researchers from Washington University in St Louis and the Israeli Institute of Technology (Technion) in Haifa has developed this technique to detect the ancestry of disease genes in hybrid (mixed) human populations. Using the new algorithm, the technique, called EMI (expected mutual information), determines how a set of DNA markers is likely to discover the ancestral origin of locations on each chromosome.

For instance, it has been found that African Americans are much more likely than Europeans to die rapidly of end stage, progressive kidney failure. Because, due to ethnic mixing, many African Americans also have genes that originated in Europe, the technique will help to isolate the genetic causes of disease by finding from which continent the recurrent disease genes originated. It is hoped that through gene therapy or, perhaps drugs, the disease can be prevented or treated and, also, the technique and algorithm will be able to be applied to many other diseases.

So far the research has analysed DNA from 575 cases of African Americans with end-stage, progressive renal failure and compared them to controls, which did not have the disease, resulting in a panel of about 2,000 genetic markers. To find the origins of disease-causing genes, researchers routinely use a technique called MALD (mapping by admixture linkage disequilibrium), to identify regions of the genome which have genes associated a disease. This identifies differences in disease presence between populations to seek variation patterns which could be over-represented in groups with high susceptibility to a certain disease.

“It Don’t Matter if Your Black or White”

2008-04-27T02:55:00.000-07:00

In 2006 a British couple gave birth to a pair of twin sisters, one black and one white. Both the mother and father were of mixed race with both their mothers’ being white and both their fathers’ black. This phenomenon shocked many people worldwide, as the odds of a mixed couple having twins of different skin colour are quite rare.

The skin colour is believed to be determined by up to seven different genes working together. A woman of mixed race contains a mixture of genes coding for both black and white while a man of mixed race will have a variety of genes. When these genes come together they normally produce a baby of mixed race but sometimes an egg or sperm might contain genes coding for only one skin colour.

Researchers believe that if both the egg and sperm contain white genes then the baby will be white and if both contain the black gene the baby will be black. If in any given circumstance the sperm containing all-white genes fuses with a similar egg and sperm coding for a purely black gene, then two babies of different colour will be born. However the chance of this happening is about a million to one.

For more information go to:

http://www.news.com.au/couriermail/story/0,23739,20620127-3102,00.html

http://www.hoax-slayer.com/black-white-twins.html

http://www.dailymail.co.uk/pages/live/articles/news/news.html?in_article_id=377839&in_page_id=1770&in_a_source=&ct=5

Alcoholism: ‘Rums’ in the Family

2008-04-27T02:48:00.000-07:00

With binge drinking on the rise, alcoholism is a disorder that has recently gained significant media attention. Alcohol dependence affects millions of people worldwide with significant impacts on the individual’s health and social relationships. Current research has found that genes play an important role in the likelihood of alcohol dependence.

Recent studies conducted by the Washington University School of Medicine and the Psychiatry Institute of St Louis have convincingly demonstrated that there is a relationship between genes and the abuse of alcohol. The studies of twins, families and adoption all showed evidence of this relationship with estimates of heritability in both men and women found to be between 50 and 60 percent.

Researchers are now looking to uncover specific genes associated with alcohol susceptibility. One of the genes thought to increase the risk of developing alcoholism is the gene related to a receptor which enables movement of the inhibitory chemical Gamma-amino butyric acid (GABA) between nerve cells. GABA is a chemical found mainly in the central nervous system and is thought to be involved in the actions of individuals under the influence of alcohol.

The challenge for future researchers lies in discovering how specific genes influence the risk of developing alcoholism. This discovery would lead to insights into the control of genetic susceptibility. Despite all the evidence connecting genetic inheritance and alcohol dependency, environmental influences still appear to be the determining factor in developing alcohol dependence problems.
Posted By:

Katherine Radnedge 41733927

References:
http://www.medicalnewstoday.com/articles/105174.php
http://alcoholism.about.com/cs/genetics/a/bluwa040114.htm

http://bjp.rcpsych.org/cgi/content/full/185/6/449

The FAT gene

2008-04-24T21:18:00.001-07:00

Gene Causes Double Trouble For Smokers

2008-04-24T18:53:00.000-07:00

It is common knowledge that tobacco is a danger to our health. However recent studies done by three teams at the M.D. Anderson Cancer Centre in Houston Texas have uncovered a genetic mutation that dramatically increases a smokers already high odds of getting lung cancer.

The variant, which is found in a region of DNA that encodes parts of the nicotine receptors, is thought to increase smoker’s chance of contracting lung cancer by 30% if they inherit one copy of the variant and by 80% if two copies of the variant are inherited. According to Paul Brennan, a geneticist at the International Agency for Research on Cancer in Lyon, this means that a smoker with 2 copies of the variant has a 1 in 4 chance of developing lung cancer.

The variant which is carried by about half of people with European ancestry may not only sensitise a person’s cells to nicotine but make it harder for them to quit. Furthermore it if you start smoking and you have the variant you will smoke a lot more than the rest of the population on average. According to Kari Stefansson, CEO of deCode Genetics in Reykjavik, Iceland, the variant is also a causal force behind peripheral arterial disease, another common disease among smokers.

Despite the startling evidence, not everyone involved is decided on what underlies the link. Brennan himself believes that addiction alone cannot explain the increasing odds of cancer. Doug Easton at the University of Cambridge adds that perhaps studying people who have the variant but have never smoked might hold the answer. Either way, researchers are now keen to use the newly discovered link to help fight lung cancer and potentially combat tumours.

For futher information see:
http://www.newscientist.com/channel/life/genetics/mg19826504.000-doublewhammy-gene-keeps-smokers-hooked.html

http://www.theaustralian.news.com.au/story/0,25197,23476551-12377,00.html

Picture from: http://www.abc.net.au/news/stories/2008/01/09/2134636.htm

Published by: Isaac Halloran 41767155

(Ethical) Food for Thought

2008-04-21T20:12:00.000-07:00

People for Ethical Treatment of Animals has recently announced that it is putting up a US$1,000,000 prize for the person or organisation that can develop a way to grow In Vitro meat, as in test tube meat, ham in a can anyone?

"The reward would go to the participant who got a test-tube chicken into commercial production by 2012 and sold it in at least 10 US states at a competitive price.

A team of 10 PETA jurors would taste the entries to make sure they matched the texture and flavour of chicken, and they must score at least 80 out of 100 points to win the prize."

The idea is to use genetically altered stem cells that will only grow muscle tissue and no other bodily tissues, to be placed in a medium that can promote the growth of the muscle tissue, that can then be mass produced, sold and consumed in the manner that meat is today.

source: "Chicken - from test tube to table"
http://www.news.com.au/story/0,23599,23578965-23109,00.html

41761452

Cancer cure through the canine?

2008-04-16T16:11:00.000-07:00

Cancer Cure through the canine?

Have we finally found a link between the human and the dog that can possibly help us determine a cure for cancer?
From a recent article in ‘Science News’ from March the 2^nd of this year talks about a Genetic Link between humans and dogs that has recently been discovered. Researchers from the University of Minnesota and North Carolina State University unearthed that humans and dogs share the same genetic basis for some types of cancer. Professor Breen says that ‘forms of human cancer are associated with specific alterations to the number or structure of chromosomes and the genes they contain’. From this they have also found that the same structures occur in some canine cancers. The only types of cancers that they have tested in both the human and the canine are the blood and bone marrow, including chronic myelogenous leukaemia, Burkitt’s lymphoma, and chronic lymphocytic. It was found that these same genetic structures are near same of that of the humans with the same cancers. To some degree it is believed that the cancer is inevitable to humans and dogs with the way that our genomes have developed since the separation of the common ancestor.

Not concrete as of yet, the researchers believe that they can study these forms of cancer through the genomes and chromosomes in dogs and hopefully apply these studies to humans as well and create a better understanding of the risks and diagnosis’ applied in humans. Even though the number of chromosomes is almost double in that of the human amount, researchers found that the same translocation that occurs from the duplication process of cells was found for three blood and bone marrow cancers that they had tested.

Therefore, this has been a key factor in the research for cancer and can be the start of the process of research to continuous observations of the changes in the genomes of dogs that can also be found in humans and have the same consequences as in humans and dogs and is yet to be tested on various other dog breeds and with different forms of cancer.

So future studies and further research maybe it is possible that anything may happen. If researchers have found this much who knows what else they will be able to unearth, and inevitably, maybe a cure.

For further information you can go to the article:

http://www.sciencedaily.com/releases/2008/02/080228112011.htm

Genomes in Medicine

2008-04-16T06:35:00.000-07:00

The once considered far fetched idea of using gene sequencing for personalised medical treatment in routine clinical care has recently become a realistic possibility. Contemporary scientific research in gene sequencing has uncovered the possibility to search the genomes of large numbers of individuals for statistical associations between genetic variation, single nucleotide polymorphisms and the occurrence of disease. Currently, the technology to sequence and interpret human DNA requires a lot of time and is at a high cost. However, it is seen as a plausible and scientifically possible way to understand, diagnose and treat various genetic diseases. There is has been a significant interest in this developing technology as it would allow for potential inherited diseases to be distinguished early on in a persons life. This information would allow for lifestyle adjustments and early detection or treatment of disease which would vastly increase curing probabilities.
The focus of such technology currently lies on its use to identify and help prevent chronic disorders including diabetes, heart disease, Crohn disease, following the discovery of such illnesses there is a potential for drug development and enhanced tests, diagnosis and prognosis. Although there seems to be numerous advantages to such technology there is also many obstacles that need to be overcome before it is a reality. Such obstacles include it’s the current high cost and possibility of genetic discrimination. Although the technology is not advanced enough for gene sequencing for personalized medical treatment it is evident that this is a promising technique that will be gratefully accepted into the medical industry in future years.
By
Celeste White
41727757
References:
Feero, Gregory, Francis S. Collins, and Alan E. Guttmarch. "The Genome Gets Personal—Almost." JAMA 299 (2008). 16 Apr. 2008 .

Other interesting websites:
http://www.labtechnologist.com/news/ng.asp?id=84047-applied-biosystems-dna-sequencing
http://www.bmj.com/cgi/content/full/317/7172/1568
http://www.mja.com.au/public/issues/179_04_180803/mat10736_fm.htm

New Drug Targets Leukaemia Trio

2008-04-16T05:36:00.000-07:00

by Erin Crighton

In 2005, a genetic mutation that causes three types of leukaemia was discovered. Now only 3 years later, a new drug has been developed that inhibits the gene mutation, and is already being moved into clinical trials.

The mutated gene, JAK2, is the cause for most cases of the three types of leukaemia; polycythemia vera, essential thrombocytosis, and primary myelofibrosis. These diseases cause the body to overproduce white and red blood cells, and platelets, which result many complications such as blood clotting. The JAK2 gene produces a specific enzyme (from the ‘tyrosine kinases’ enzyme family) that causes any extra blood cells to be transferred into the bone marrow. In the mutated version of this gene, the enzyme gets stuck in a certain position, which causes blood proliferation to run out of control because it is no longer regulated, therefore causing the overproduction of the white and red blood cells, and platelets.

The most promising drug, a compound called TG101348, specifically inhibits JAK2, but leaves the related enzymes unaffected. It is soluble in tissue which also allows it to be distributed throughout the body, and can simply be taken as a pill rather than an injection. Along with these benefits, this drug has a long half-life, meaning it will stay in the body for a sufficient amount of time, and doesn’t show non-specific toxicity.

The compound was first tested on mice, which proved the compound to be very affective, resulting in all mice induced with polycythemia vera that were given high doses of TG101348 survived. It actually reversed the symptoms, making the blood cell count return to normal, and proving the mice healthy. The results showed the drug eliminates clinical manifestation of the three types of leukaemia, without any toxicity.

Human clinical trials for the drug were approved based on the results of the studies performed on mice and more preclinical data, and began in March this year. Small doses will first be given to leukaemia patient to make sure no toxicities appear.

Research news article can be found at: http://www.hhmi.org/news/gilliland20080407.html

Postmenopausal women keeping abreast of tipsy genes!

2008-04-16T04:49:00.000-07:00

First it was diet coke, now it seems that alcohol could possibly increase the chances of breast cancer in women. This was recently determined via a study by Dr Peter Shields, professor of medicine and oncology based at Georgetown University's Lombardi Comprehensive Cancer Center in Washington DC, and Dr Jo Freudenheim, chair of social and preventive medicine at the State University of New York in Buffalo. It was found that two genes that code for enzymes that breakdown alcohol, ADH1B and ADH1C, are possibly linked to increased risk of breast cancer in postmenopausal women who favour a drink or two. Lead author of the study, Dr Catalin Marian stated the obvious, saying: "The higher their alcohol consumption, the higher their risk."(Medical news today, 2008).
The study showed that the variations in the DNA sequences of the two genes caused significant susceptibility towards the risk of breast cancer. In the case of the ADH1B gene, women who consumed alcohol whilst possessing the gene variant were twice as susceptible to breast cancer compared to the women who abstained from drinking alcohol. Alternatively, the ADH1C gene actually protected the subjects from breast cancer, but as alcohol consumption increased, the effectiveness of this protection decreased, thus causing a contrasting, but nevertheless significant increase in the risk of breast cancer.
“The results showed that increased breast cancer risk in postmenopausal women was linked to variations in DNA sequences in two genes: ADH1B (sequence rs1042026) and ADH1C (sequence rs1614972).Among postmenopausal women with the ADH1B (sequence rs1042026) gene variant, the risk of breast cancer for the alcohol drinkers was nearly double that of the abstainers.Among women with the ADH1C (sequence rs1614972) gene variant, there was a protective effect against breast cancer risk that varied inversely with the amount of alcohol: the more alcohol a woman with this gene variant consumed, the less protection offered, and the higher the risk of breast cancer. (Conversely, this could be viewed as the protection conferred by the gene appeared to get stronger as alcohol consumption dropped).” (Medical news today, 2008).
In light of this obviously depressing news, there maybe some cause for celebration, in that the aforementioned Dr Catalin Marian implied that more research was needed to validate the findings and show that the genes are more than just ‘linked’ to the risk of breast cancer, and have yet to be proven to be a potential cause of breast cancer. "We have to keep in mind that the gene sequence variations we observed are not located directly in coding regions, but they may be associated and inherited together with other variations that have this effect on the enzyme function." Says Marian

Nathan Crouch (41453627)
References:
http://www.medicalnewstoday.com/articles/103911.php
http://www.cbsnews.com/stories/2008/04/14/health/webmd/main4014147.shtml http://imagecache2.allposters.com/images/pic/153/817586~Blood-Alcohol-Posters.jpg

Postmenopausal women keeping abreast of tipsy genes!

2008-04-16T04:30:00.000-07:00

First it was diet coke, now it seems that alcohol could possibly increase the chances of breast cancer in women. This was determined by Dr Peter Shields, professor of medicine and oncology based at Georgetown University's Lombardi Comprehensive Cancer Center in Washington DC, and Dr Jo Freudenheim, chair of social and preventive medicine at the State University of New York in Buffalo. It was found that two genes that code for enzymes that breakdown alcohol, ADH1B and ADH1C, are possibly linked to increased risk of breast cancer in postmenopausal women who favour a drink or two. Lead author of the study, Dr Catalin Marian stated the obvious, saying: "The higher their alcohol consumption, the higher their risk."(Medical news today, 2008).
The study showed that the variations in the DNA sequences of the two genes caused significant increases in the susceptibility towards breast cancer. In the case of the ADH1B gene, women possessing the gene variant who consumed alcohol were twice as susceptible to breast cancer compared to the women who abstained from drinking alcohol. Alternatively, the ADH1C gene actually provides some protection against breast cancer; but as alcohol consumption increases, the effectiveness of this protection decreases, thus causing a contrasting, but nevertheless significant increase in the risk of breast cancer.
“The results showed that increased breast cancer risk in postmenopausal women was linked to variations in DNA sequences in two genes: ADH1B (sequence rs1042026) and ADH1C (sequence rs1614972).Among postmenopausal women with the ADH1B (sequence rs1042026) gene variant, the risk of breast cancer for the alcohol drinkers was nearly double that of the abstainers.Among women with the ADH1C (sequence rs1614972) gene variant, there was a protective effect against breast cancer risk that varied inversely with the amount of alcohol: the more alcohol a woman with this gene variant consumed, the less protection offered, and the higher the risk of breast cancer. (Conversely, this could be viewed as the protection conferred by the gene appeared to get stronger as alcohol consumption dropped).” (Medical news today, 2008).
In light of this obviously depressing news, there maybe some cause for celebration, in that the aforementioned Dr Catalin Marian implied that more research was needed to validate the findings and show that the genes are more than just ‘linked’ to the risk of breast cancer, and have yet to be proven to be a potential cause of breast cancer. "We have to keep in mind that the gene sequence variations we observed are not located directly in coding regions, but they may be associated and inherited together with other variations that have this effect on the enzyme function." Says Marian

Nathan Crouch (41453627)
References:
http://www.medicalnewstoday.com/articles/103911.php
http://www.cbsnews.com/stories/2008/04/14/health/webmd/main4014147.shtml
http://imagecache2.allposters.com/images/pic/153/817586~Blood-Alcohol-Posters.jpg

Healing faster

2008-04-16T03:34:00.000-07:00

Have you ever wished a cut or burn would heal faster and leave no scars? Research from the University of Bristol suggests that this can happen in the future by simply applying a gel. When a cut or burn occurs, blood vessels constrict to decrease the amount of blood loss. After a blood clot is formed by the platelets, in response to the completion of the clot the blood vessel enlarges to allow white blood cells to fight off the foreign invaders In addition the white blood cells bring collagen to help heal the skin, which also produces the scar. One of the genes responsible for scars is the osteopontin (OPN). Therefore by creating a gel that suppresses this gene, it could accelerate healing and leave no scar.

Reference:
University of Bristol (2008, January 24). Skin Care: Scar-free Healing Shown With Gene Suppression. ScienceDaily. Retrieved April 16, 2008, from
http://www.sciencedaily.com¬ /releases/2008/01/080121080355.htm

http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Skin_cuts_and_abrasions?Open

Hung Le
41724288

Errors in Mitochondrial DNA the source of cancer spreading

2008-04-16T03:14:00.000-07:00

The way in which a cancer spreads is through the process of metastasis, wherein primary cancer cells breaks away from the main tumour, travels through the lymph system or in the bloodstream, settles in a new area and begins to form a new tumour. It is this process which differentiates the less dangerous benign tumours from the deadly malignant kind and preventing it would result in a tumour being easily excisable once identified. A recent study has shown that mutations in Mitochondrial DNA may be responsible for metastasis, and that curing cancer may be as easy as treating a patient with antioxidants.

Mitochondria are organelles within eukaryotic cells that produce energy molecules to fuel cellular processes. They also have their own DNA, referred to as mtDNA, found within the mitochondria itself, rather than the nucleus where most of the cell’s genetic material is stored. This allows the mitochondrion to replicate themselves (with some assistance from the nucleus) depending on the energy needs of the cell, though replication is still controlled by genes within the nucleus. Unfortunately, the protein packaging and self-repair abilities of mtDNA are not as effective as that of nuclear genetic material and so are more susceptible to mutations. It is these mutations that have been suspected of being closely related to metastasis in cancer cells. An earlier study on cancer cells showed that the mitochondria of these cells possessed many more mutations than that of healthy cells, though whether this was a result of the cancer or the cancer was a result of the mutations was unknown.

Researchers at the University of Tsukuba in Japan have recently performed a study on whether mtDNA mutations were responsible for metastasis. The experiment involved swapping the mtDNA of a tumour cell that tends to metastasize with one that does not and injecting the cells into mice. What their results showed was that when these cells were injected into mice the rarely metastasising tumour cells, now containing mtDNA from metastasising tumours, did in fact metastasise, while the originally metastasising tumour cells containing mtDNA from non-metastasising cells did little. This would imply that the basis for tumours metastasising is mtDNA.

Further study showed that the mutations in the mtDNA caused the Mitochondria to produce an excess of reactive oxygen species molecules, which are damaging to DNA. Since mtDNA appears to be the root of metastasis in tumour cells it can be inferred that it is these oxygen species molecules that damage the nuclear genetic material of healthy cells, creating cancer cells. Perhaps most interesting is that these oxygen species molecules can be neutralised with antioxidants and that when mice that had been injected with metastatic tumour cells were treated with these antioxidants, they showed little to no new tumour growth. As a result, antioxidant treatment of malignant cancer has warranted further study.

Original article:

http://sciencenow.sciencemag.org/cgi/content/full/2008/403/1

Image source:

http://www.a3243g.com/image_mitochondria.asp

Kiel Headrick, 4176059

Weather NOT too hot to handle for "superplants"

2008-04-15T15:05:00.000-07:00

A new study by the University of Toronto is planning to find how plants "breathe" so that can help us breed plants that would better survive the hot summers.
This study shows the first example of a gene that controls how leaves close their surface pores. "It's very exciting," says university's botany professor and senior author Malcolm Campbell. "This is a gene that helps regulate carbon dioxide uptake. If plants are the Earth's lungs, we've just discovered a key piece of information about how the Earth breathes."
The pores on the surface of plant leaves, called stomata, function like little mouths that open and close in response to cues such as light, temperature, and water availability. Using mouse-ear cress, a relative of mustard, cabbage and radish plants, Campbell and co-authors from the university,together with the University of Lancaster, then compared the cooling rates of plants with normal, high and low levels of gene activity. From their data, they were able to link the gene to plant exhalation.
This discovery is another step in understanding how plants might respond to their environment. In hot temperatures, plants keep their mouths "shut" longer than usual, to avoid losing gases and water through evaporation. However, they must open their stomata at some point, both to pick up carbon dioxide needed for photosynthesis and to release oxygen back into the atmosphere. This information will be important to plant breeders looking to improve crop resistance to drought, as well as to those seeking to understand plants' evolutionary responses to climate.
"These genes are of high importance. They allow plants to adapt to changes in light, carbon and water availability. Ultimately, they shape the flux of carbon and water throughout entire ecosystems and affect the carbon cycle on a global-scale." says Campbell.
The study was supported by the University of Toronto, the Natural Sciences and Engineering Research Council of Canada and the Biotechnology and Biological Sciences Research Council of the U.K.

links : http://www.sciencedaily.com/releases/2005/07/050718214711.htm

by,
Zulaikha Razali ( 41600720 )

Gene Splicing: The key human success?

2008-04-15T06:10:00.000-07:00

It has now been proven that chimpanzees are the closest living relatives to humans on this planet with genomes that are almost 99% identical to our own. But if we really are that closely related on paper, what are the causes of the vastly different structural, behavioural, and mental variations that occur between the two species? With the help of innovative new research from the University of Toronto's Centre for Cellular and Biomolecular Research, potential new explanations to this conundrum have finally been uncovered. In performing several comparisons between the heart and brain tissue extracted from humans and chimpanzees, University of Toronto Professor Benjamin Blencowe and his team, including graduate student researcher John Calarco, have discovered considerable differences in the way mRNA is spliced during protein production (ScienceDaily, 2007).

"It's clear that humans are very different from chimpanzees on several levels, but we wanted to find out if it could be the splicing process that accounts for some of these fundamental differences," says Blencowe, a professor with the Banting and Best Department of Medical Research and Department of Molecular Genetics (ScienceDaily, 2007).

"The surprising thing we found was that six to eight per cent of the alternative splicing events we looked at were showing differences, which is quite significant. And those genes that showed differences in splicing are associated with a range of important processes, including susceptibility to certain diseases" (ScienceDaily, 2007).

mRNA splicing is the process of protein production that occurs following the transcription phase of protein production in which the primary RNA transcript is modified before leaving the nucleus to be translated by a ribosome. This process of modification involves the attachment of a splicesome, formed from several ribozymes and protein molecules, to the pre-mRNA molecule which then removes the non-coding portions of RNA called introns and splices together the two adjacent exons. The variation that comes about from this process is determined by a function called alternative RNA splicing, in which different sections of the genetic code are treated as exons during RNA splicing, thus allowing many different proteins to be created from the same gene. The new findings have confirmed that this rocess of exon recognition differs significantly between humans and chimpanzees, thus creating some of the major differences between the two species.

The study, which has now made its appearance in the Journal of Genes and Development, is likely to have positive implications for the future study of disease in chimpanzees and humans. This study is one of the essential steps in identifying and understanding why different diseases will have large effects one species and not the other.

To learn more about this interesting topic please consult the following websites:

http://www.sciencedaily.com/releases/2007/11/071114151513.htm

http://www.mukto-mona.com/Articles/jaffor/evolution080306.htm

http://www.genesdev.org/cgi/content/full/21/22/2963?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Blencowe&searchid=1&FIRSTINDEX=0&volume=21&issue=22&resourcetype=HWCIT

Reference:

University of Toronto (2007, November 15). Humans And Chimps Differ At Level Of Gene Splicing. ScienceDaily. Retrieved April 15, 2008, from http://www.sciencedaily.com /releases/2007/11/071114151513.htm

By: Thomas Bennett, 41761902

Gene Splicing: The key human success?

2008-04-15T06:03:00.000-07:00

To learn more about this interesting topic please consult the following websites:

http://www.sciencedaily.com/releases/2007/11/071114151513.htm

http://www.mukto-mona.com/Articles/jaffor/evolution080306.htm

http://www.genesdev.org/cgi/content/full/21/22/2963?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Blencowe&searchid=1&FIRSTINDEX=0&volume=21&issue=22&resourcetype=HWCIT

Reference:

By: Thomas Bennett, 41761902

INJECTION OF HOPE - Alzheimer’s Vaccine

2008-04-15T03:58:00.000-07:00

A revolutionary drug that stops Alzheimer’s disease could be available within a few years.

It could prevent people from reaching the devastating final stages of the illness in which sufferers lose the ability to work, talk or even swallow, and end up totally dependent on others.

Alzheimer's, the most common cause of dementia, affects about 200,000 Australians. Possibly thousands of others are undiagnosed or in the very early stages of the disease.

Existing drugs can delay the progress of the symptoms, but their effect wears off relatively quickly, allowing the disease to take its devastating course. In contrast, the new vaccine may be able to hold the disease at bay indefinitely, known as CAD106, showed it is highly effective at breaking up the sticky protein that clogs the brain in Alzheimer’s destroying vital connections between brain cells.

The vaccine uses a tiny section of the amyloid protein attached to an empty virus shell to trick the immune system into attaching and breaking up deposits of protein clogging the brain.

The development of tests capable of detecting the disease in its earliest stages would allow the jab to be given as early as possible and also used to keep the disease at bay in those with a strong family history of the illness.

But while the jab may stop the disease in its tracks, it is not expected to repair dear tissue, so will not be a cure.

HOW IT WORKS:

Step 1) Amyloid plaque builds up on the brain. Connections between brain cells are destroyed, causing memory loss.
Step 2) A series of vaccine injections are give to patient. Vaccine produces antibodies which trigger break-up of the plaque.
Step 3) Levels of antibodies are kept high by booster injections and the disease is halted.

Original post: Courier Mail 23/06/07 Saturday.

By Chiung-Yin Tu #4138534

Deus ex machina.

2008-04-14T09:15:00.000-07:00

Deus ex machina.

Two Californian scientists recently had an article published in PLos Biology detailing an experiment in which they created a machine that shows a very literal representation of the somewhat abstract concept of evolution. Abstract in the sense that it is difficult to perceive the progression of a reality that you exist in yourself. Thus Brian Paegel and Gerald Joyce of the Scripps Resacrh Institute developed a computer that can drive the evolution of improved RNA enzymes without human interference. This has allowed the modern consciousness lead by these scientists a vessel by which to step outside ones understanding of evolution and observe it occurring right in front of them.
Molecules of different nature have been evolved in laboratories around the world since the 1990’s, but this work is special as for the first time this process has been made automatic without any human input except for switching the machine on and the initial necessary ingredients. Using this computer Paegel and Joyce have managed to r-create the criteria necessary for evolution to occur.
As we all know evolution occurs when there is a variation in a population, and some of the characteristics of these variants provide the host with certain survival or reproductive advantages and where the basis for this advantage can be inherited. In addition there must be a selection pressure, in other words, a reason that not all organisms can survive or reproduce.
Paegel and Joyce’s system fulfilled all of these criteria and created an existence for animals to grow and reproduce and die and live, to evolve. After the experiment was concluded they found that the final enzyme at the end of the experiment had 11 mutations. These mutations made it 90 times more efficient at using the starting ingredients and thus the “evolution machine” portrays quite eloquently the beautiful symmetry of evolution.

Original article: http://www.sciencedaily.com/releases/2008/04/080408085508.htm

Journal reference: Paegel BM, Joyce GF (2008) Darwinian evolution on a chip. PLoS Biol 6(4): e85. doi:10.1371/journal.pbio.0060085
Adapted from materials provided by PLoS Biology, via EurekAlert!, a service of AAAS.

Free will or Determinism?

2008-04-14T05:38:00.000-07:00

The current understanding of genetics is undergoing a paradigm shift and looking away from DNA as the sole determinant of heredity. After examining complex relationships among genes, environment, disease and phenotype scientists have realised how restrictive the ‘DNA as destiny’ paradigm is and is moving towards the newly emerged field of epigenetics. The epigenome can turn genes on and off and is like the body’s chemical switchboard. The epigenome is highly susceptible to its environment. The food, the air, the water you drink and the stress or happiness you feel can change your genetic make- up, not by changing the DNA sequence but by changing what genes are expressed through the epigenome. Many cancers are not hereditary in origin but are epigenetic. It has become apparent that epigenetic changes are just as significant as genetic mutations in the formations of cancers. Epigenetic changes like genetic changes can be passed down through generations. A gene can’t be un-mutated but it is potentially possible to reverse an epigenetic effect. According to this research free will can have as much sway over health and actions as genetic determinism can.

For more information see:
http://www.philly.com/inquirer/opinion/20080413_A_paradigm_shift_in_genetics.html

AlligatorMan – reptile blood may be the answer to antibiotic resistant infections

2008-04-14T02:36:00.000-07:00

Alligators, those big reptiles with the power in their jaws to rip to shred almost anything, are now being investigated by scientists as potential lifesavers in treating infectious diseases. These predators, portrayed in movies as deadly human killers may ironically be the ones to save our lives one day. Powerful proteins with the ability to fight off multiple infections such as the methicillin-resistant bacteria, Staphylococcus Aureus have been detected in their blood. Other infections related with diabetic ulcers, severe burns and “superbugs” resistant to current antibiotics are also seem to be targeted by the newly found alligator protein. Mark Merchant, Ph.D., a biochemist at McNeese State University in Lake Charles, La, claims that the newly protein might be called “alligacin” and suggests that we might one day be treated with an alligator blood product.

Alligators have been shown to have an unusually strong immune system, they are able to fight bacteria and other microorganisms without previous encounter. Alligators’ evolutionary adaptations are believed promote fast wound healing due to severe injuries alligators obtain during various battles.

The famous proteins were extracted from alligator leukocytes by researchers from the Lousiana State Univeristy, Kermit Murray and Lancia Darville, Merchant and colleagues.

When tested in laboratories, these proteins were shown to be deadly to a wide range of bacteria including MRSA (methicillin-resistant Staphylococcus Aureus), potent bacteria that have arisen in health care setting which are now spreading into communities. These type of bacteria are known to be resistant to multiple antibiotics and are growing out of control in any environment.

The proteins were also tested against strains of the yeast Candida Albicans and were shown to eradicate six out of eight strains. There is also hope that the blood proteins might help in fighting HIV and various infections contracted when affected by this virus.

Scientists believe that the proteins will in the future be turned into antibacterial and antifungal drugs, in pill sand ointment form.

Research is now being carried out in hope to find these proteins in other related animals such as crocodiles. With funding from the state of Louisiana and the National Science Foundation, Merchant is planning to study extensive samples to explore these animals’ disease fighting potential.

Frogs and other amphibians have been identified with other unique types of proteins that are yet to be analysed thoroughly but Daniel Brown, University of Florida, College of Veterinary Medicine in Gainesville, says that these animals are in major decline due to diseases.

By Cedric Ng Liet Hing 41760419

References:

Ehrenberg, R. (2008) "Antibiotic Alligator: Promising proteins lurk in reptile blood" Science News Online, vol. 175, no. 15, p. 228. URL:http://www.sciencenews.org/articles/20080412/fob2.asp

Marsh, C., Bernstein, M. (2008) "Alligator blood may put the bite on antibiotic-resistant infections" URL: http://www.eurekalert.org/pub_releases/2008-04/acs-abm031108.php - size 9.3K

The food you eat can change your ‘genetic expression’

2008-04-13T23:45:00.000-07:00

Have you ever thought how beneficial your diet is? Not just in terms of loosing kilos, but to what extent it can cause behavioural changes and or diseases to your body. Scientific researchers believe that what you eat influences your genetic expression that in turn regulates all your body processes.

As Professor Ian Johnson sated at the Institution of Food Research “It's quite a strong possibility that nutrients might cause DNA changes. We think diet may have a role to play as a regulator in genes.”

There are around 1000 to several hundred thousand genes in an organism, but not all of them are active. Studies in various mammals show that nutrients can alter genetic information of animals by switching on or off certain genes. As suggested by in the article by New Scientist, there is a good chance that food can do same in humans. While mutations to DNA may be responsible for many human disorders, however some disorders such as cancer occurs when specific genes are turned on or off.

Moshe Szyf from McGill University in Canada carried out an animal experiment that proves diet is important in controlling gene activity. When specific amino acids of L-methionine were injected in adult rats their normal behaviour was observed to change. They were less confident when exposed to new surroundings and increased levels of stress hormones. Through the addition of a methyl group, the L-methionine amino acid had changed the gene for glucocorticoid that helps reduce an animal’s response to stress.

Scientists are now researching to convert such negative impacts into positive behavioural variation by using richostatin A (TSA) which is reverse to L-methionine, it removes the methyl groups.
Furthermore it is suggested that due to change in mother’s level of DNA methylation can have a great impact on the offspring’s genes.

Jhonson’s team are further studying healthy individuals before initiation of colon cancer in order to investigate whether it is activated by diets through DNA methylation. Although more research is required it is believed that shortage in folate levels can lead to development of breast and colon cancer in most adults.

As he advised “one would want to choose diets that would give you the most beneficial pattern of DNA methylation in the gut.”

References:

http://news.bbc.co.uk/2/hi/health/4441564.stm
http://www.answers.com/topic/nutrient-regulation-of-gene-expression

Images:
http://pro.corbis.com/search/searchFrame.aspx
http://commons.wikimedia.org/wiki/Image:Arcimboldo_Vegetables.jpg

www.factorfiveleidensupport.org/history.html

Human-Cow embryo created, new hope for stem cell research.

2008-04-13T22:32:00.000-07:00

British researches, from Newcastle University have successfully created a human – cow embryo. It has been strongly opposed by the Catholic Church, but for researchers this is one step closer to providing a limitless supply of stem cells for developing therapies for diseases such as Alzheimer’s, Parkinson’s and spinal cord injuries.

Permission to create the embryos, was given to Lyle Armstrong, the lead researcher for this project, in January from the Human Fertilisation and Embryology Authority. The embryos also known as cytoplasmic hybrids are 99.9% human and 0.1% animal. These embryos were crated by taking a skin cell from a human and inserting the DNA into a cow egg. The cows’ egg had all it genetic material removed before the human DNA was inserted. An electric shock then induced the hybrid embryo to grow. The embryo grew for three days, until it had 32 cells.

Eventually the researchers hope to grow the embryos for six days and then extract stem cells from them. The cells grown using the animal eggs cannot be used to treat patients on safety grounds, but they will help researches to understand diseases better by working with those cells. If researchers can produce cells which will survive it culture, it will lead to a better understanding of disease processes without having to use human eggs.

Relevant links:
http://www.guardian.co.uk/science/2008/apr/02/medicalresearch.ethicsofscience?gusrc=rss&feed=networkfront
www.news.com.au/story/0,23599,23476268-38200,00.html?from=public_rss

Kristin Heath 41419315

The food you eat can change your ‘genetic expression’

2008-04-13T06:27:00.000-07:00

As Professor Ian Johnson sated at the Institution of Food Research “It's quite a strong possibility that nutrients might cause DNA changes. We think diet may have a role to play as a regulator in genes.”

There are around 1000 to several hundred thousand genes in an organism, but not all of them are active. Studies in various mammals show that nutrients can alter genetic information of animals by switching on or off certain genes. As suggested by in the article by New Scientist, there is a good chance that food can do same in humans. While mutations to DNA may be responsible for many human disorders, however some disorders such as cancer occurs when specific genes are turned on or off.

Jhonson’s team are further studying healthy individuals before initiation of colon cancer in order to investigate whether it is activated by diets through DNA methylation. Although more research is required it is believed that shortage in folate levels can lead to development of breast and colon cancer in most adults.

As he advised “one would want to choose diets that would give you the most beneficial pattern of DNA methylation in the gut.”

References:
http://news.bbc.co.uk/2/hi/health/4441564.stm
http://www.answers.com/topic/nutrient-regulation-of-gene-expression
Images:
http://pro.corbis.com/search/searchFrame.aspx
http://commons.wikimedia.org/wiki/Image:Arcimboldo_Vegetables.jpg

http://www.factorfiveleidensupport.org/dna.jpg

Zohal Azami, 41732032

New hope for Osteoarthritis

2008-04-13T05:29:00.000-07:00

2008-04-13T05:23:00.000-07:00

Longevity Genes: Long Life Just a Mutation Away

2008-04-13T04:42:00.000-07:00

As time goes on, we grow old. While many of us would like to deny it, our bodies are aging from day one, and inevitably our cells maintenance and repair mechanisms begin to deteriorate. But what if there was a way to postpone our fate, not with anti-ageing creams but with our genes? Unlocking the secrets to longevity may now well rest on the understanding of our bodies on a cellular level.

While it has been observed before many times in worms and mice, a mutation in a certain set of genes has now been found in humans. A study conducted on the Ashkenazi Jews has led to an intriguing discovery in some of its most long-lived individuals. Those who have lived past the age of 95 have been discovered to be much more likely to carry one of two mutations in the gene for insulinlike growth factor 1 receptor (IGF1R).

This mutation appears to make cells less responsive to the insulinlike growth factor 1 (IGF1) which is a key growth hormone secreted by the liver, and it is these mutations that may well be linked to longevity. Previous studies have shown that IGF1 disruption in mice led to a life up to 40% longer, while delaying the onset of age related diseases.

A group of 348 Ashkenazi Jewish seniors with a history of longevity (aged 95 – 105) were asked to participate in a study along with a control group of 312 living and dead individuals. The groups could not be compared directly as the control group died nearly 30 years ago, but the solution was to examine both groups’ offspring, searching for clues in their genetic makeup.

It was found that the female offspring of the centenarians were on average up to 2.5 centimetres shorter than their control counterparts (a sign that the IGF1R may be less responsive), and upon examination of their genes 2 IGF1R mutations were found in 9 of the centenarians, but only one of the controls. The centenarians also possessed up to 35% more IGF1 in their blood, a possible reaction to the less responsive IGF1 receptors. Males however, could be unaffected by the mutation as they have many other hormones that make them sensitive to IGF1.

This leaves us with a tantalising insight into the correlation between certain genes and long life, but it is likely it requires more than one lucky gene. Until we discover the perfect gene cocktail for longevity, we may have to wait before we can enjoy a shorter, yet longer life.

For the full article see: http://www.sciam.com/article.cfm?id=methuselah-mutation-linked-to-long-life

Viruses to be used in food and health testing?

2008-04-13T03:34:00.000-07:00

How often do you really think about what kinds of bacterium are living in the food you’ve just ordered at your local restaurant, or even in the pus secreting wound you got while trying to imitate the guys from jackass? Now scientists have developed a sensor that can detect bacterium in minutes, not hours or days, and are even able to determine bacterium down to specific species, all using viruses known as Bacteriophages.

Bacteriophage literally means ‘eater of bacteria’. These Bacteriophages are currently underway to be used in the identification of bacterium in the health industry as well as the food industry.

Food safety as well as public health is a very important aspect of society. Food Poisoning can have devastating effects on individual’s health as well as a business’s success. Scientists of the University of Toronto, Canada, have built a sensor that uses the Bacteriophages to detect bacteria. Viruses cannot reproduce on their own, like eukaryotic cells or in this case bacteria cells, a virus must ‘hijack’ a cells replication process in order for more of the virus to be made. Bacteriophages attack bacterium by hijacking the cells replication process to make virus replicas. The cell replicates the virus until so many viruses are made that the cell bursts, thus releasing more viruses and ultimately killing the cell.

What the scientists at the University of Toronto have done is created a ‘bacteria sensor’. This sensor uses the bacteriophages in the following way:

This mechanism is used to identify one particular bacterium. The sensors are only a square millimetre in size, meaning that hundreds of different bacterial sensors may be added to a sensor. Each sensor would contain a well full of bacteriophages that are specific to certain species of bacterium. Conventional methods to identify the bacterium in foods or infections involves either culturing the bacterium or until there are enough to look at under a microscope, both methods of which may take up hours even days, as apposed to the sensors that take only a few minutes. Current developments on the sensor have been able to determine

Bacteriophages attacking bacterium

Some Video Links of Bacteriophages:

http://www.youtube.com/watch?v=Dh4C-qmfuro&NR=1

http://www.youtube.com/watch?v=41aqxcxsX2w&feature=related

http://www.cellsalive.com/qtmovs/phage_mov.htm

References:

http://technology.newscientist.com/channel/tech/mg19726435.800-picky-phages-put-to-work-in-bacteria-sensor.html

Deelan Govind-Vanmali - 41743823

Salmonella Flagella Beats Radiation Waves

2008-04-13T02:56:00.000-07:00

A drug developed from flagella of a benign strain of Salmonella bacteria has been found inhibit the devastating effects of radiation on mice and monkeys. This implication means it may be possible to develop less toxic treatments of cancer and also help shield against the radiation exposure of rescuers entering a radioactive area.

Radiation initiates a programmed cell death known as apoptosis when they are exposed to its waves. This causes death when radiation destroys the cells lining the gut and also those within the bone marrow that create blood cells, vital to our body.

In order to prevent this cell death, Andrei Gudkov and his colleagues at the Roswell Park Cancer Institute ideated that turning off apoptosis for short periods of time would effectively protect cells from the harmful effects of radiation. It was then found that the flagella of benign Salmonella living within the intestine were capable of doing so, a defence which protected the gut cells they huddled against.

The active parts of the Salmonella flagellum protein were put together in a carrier molecule in order to be applied as a radiation resistant medication. This molecule, codenamed CBLB502, was then injected into mice approximately an hour before receiving an immense 13 Grays of radiation. This amount of radiation has the capacity to be fatal in humans. The result showed that 90% of the mice survived the radiation.

One setback of the Salmonella drug however, is that the application of this drug is not very effective once radiation poisoning has already occurred. In tests, the drug could only save mice when injected within an hour of receiving 9 Grays of radiation. The innovation of this drug although still has the capacity to save many lives.

For more information, see

http://www.newscientist.com/article/dn13652

http://uk.reuters.com/article/healthNewsMolt/idUKN1030291520080411?pageNumber=1

Guy Pfaff - 41764846 - P2

THE GENE THAT COULD CODE THE FUTURE FOR SMOKERS

2008-04-13T01:59:00.000-07:00

Could a gene be responsible for increasing a smoker's addiction to nicotine and even lung cancer? According to genetist Christopher Amos, the discovery of a gene variant on the region of DNA known to encode parts of the nicotine receptor could indicate exactly that. Amos and his team at the M.D. Anderson Cancer Centre in Houston, discovered this gene after previous theories as to the link between smoking and genetics.

The variant, possessed by about half of people with European ancestry, may not only sensitise cells to nicotene but also make it harder for smokers to give up the habit. Scientists theorise that the gene variant may directly increase a person's risk of cancer by influencing a cell's response to nicotine or its metabolites. The metabolite of nicotine is thought to stimulate cell division via this particular receptor.

New statistics suggest that smokers possessing one copy of the variant are 30 per cent more likely to develop lung cancer and what's worse, an inheritance of two copies boosts the rick by 80 per cent.

Further studies are to be undertaken as to the effect of the gene variant on people who do not smoke. Whether or not they are subject to lung cancer could determine the usefullness of this mutation in combating cancerous symptoms. If related to lung cancer directly, drugs targeting the nicotine-sensing proteins may be effective against tumours. Similary, if the gene is involved in cigarette addiction, genetic counselling could be a method used to dissuade people from taking up smoking in the first place.

For more information visit www.newscientist.com [April edition, 2008]

Phoebe Watt (41416622) - P1

Perfect Baby: all in the genes

2008-04-13T00:42:00.000-07:00

Conceiving a child is no longer what it once was. With the latest technology and scientific advances couples are now opting to use preimplantation genetic diagnosis (PGD) to select only the healthy embryos for implantation. A British couple’s aim for this choice of conceiving was to ultimately eradicate breast cancer, which they have an extensive family history of, from their family lines once and for all.

Although this procedure is quite common for screening for serious genetic disorders and diseases, a troubling fact is that depending on certain circumstances, an embryo carrying such genes could go to live on for 40 or 50 years before developing the disease or, it might never develop at all.

However, while the technology can go on to improve the health quality of the child there are fears that the science may head off in the wrong direction as the technology improves. Such uses of genetics would include parents being able to choose their children’s traits as seen in the movie “Gattaca”. There are many ethical and religious arguments on such a topic but it is quite plausible for what started out as making the world free of disease to warp into eugenic obsession for perfection.

Genomic science is racing toward a future in which foreseeable improvements include reduced susceptibility to a host of diseases, increased life span, better cognitive functioning. Hopefully, when technology advances to better stages, the science doesn’t lose sight of the original goal.

For more information, see:

http://www.washingtonpost.com/wp-dyn/content/article/2008/04/11/AR2008041103330.html?hpid=opinionsbox1

Linda Lee - 41770641

Altered skin cells improve Parkinson's symptoms in rats

2008-04-10T14:27:00.001-07:00

Studies in a number of research institutes have discovered that reprogrammed skin cells which function similarly to stem cells derived from human embryos can be useful in easing the symptoms of Parkinson’s disease. The created cells were transplanted into the brains of rats which had been altered to resemble the neurodegenerative Parkinson’s disease, with positive results. The discovery avoids the controversial issue of using embryonic stem cells for cell transplants, because the human embryos they are sourced from are normally destroyed.

The reprogrammed skin cells, referred to as induced pluripotent stem cells or IPSCs, are synthesized by the transfection of the genes OCT4, SOX2, NANOG and LIN28 into human somatic cells, essentially transforming them into the highly malleable stem cells. The created cells have similar morphological and biochemical properties to naturally created embryonic stem cells. These cells are then integrated into the neural system of rats to replace the brain cells that produce dopamine, a chemical which carries neural messages. The preliminary results of these tests are positive, with 100% of the test subjects showing marked improvement after treatment with the IPSCs.

However there will need to be further studies and improvements on the technique before it can be tested on humans. Currently the required genes are transported into somatic cells using retroviruses, which have the potential to cause cancer. Also, the synthesized IPSCs can differentiate into tissues other than those under study. This setback has been combated though, with the use of fluorescent proteins to mark the brain cells which produce dopamine.

References

Fox, M 2008, ‘Stem cells from skin treat brain disease in rats’, Web Article, viewed 8 April 2008, http://www.reuters.com/article/topNews/idUSN0719560620080407?feedType=RSS&feedName=topNews.

Baker, M 2007, ‘Adult cells reprogrammed to pluripotency, without tumours’, Web Article, viewed 8 April 2008, http://www.nature.com/stemcells/2007/0712/071206/full/stemcells.2007.124.html

By Julia Sullivan

Student Number: 41723731

Transplant Rejection: A Light At Last?

2008-04-10T08:36:00.000-07:00

Throughout the ages, mankind had endeavoured in medical research, striving to discover cures for the many disorders that had plagued our species. One of the most significant advancements in this area is, no doubt, the technique of organ transplantation. Since this procedure became viable, countless lives had been saved from organ failures that will otherwise be fatal. Yet despite the best efforts of researchers, organ transplantation has yet to be perfected.

One of the main problems is rejection: when the patient’s immune system attacks the foreign, transplanted organ. Currently, the only way to combat this complication is through the use of immunosuppressants, drugs designed to suppress the immune system: but use of these drugs has numerous undesirable side effects. Obviously, immunosupressants is not the answer to rejection. For decades researchers had strived to discover an alternative, but had been unsuccessful: until when a teenage girl named Demi-Lee Brennan underwent a remarkable change.

Demi-Lee Brennan was only nine years old when her liver failed. Luckily, she received a transplant in time to save her life: but it seemed to be a life that was fated to be forever dependent on the notorious immunosuppressants. It turned out, however, that was not what life had in store for her. A few years after her transplant, doctors were flabbergasted when Demi-Lee’s body actually conformed to the tissue of the donor liver: her blood type was converted from O-negative to the donor’s O-positive, and stem cells from the donor had entered her bone marrow, effectively a bone marrow transplant; allowing her to continue to produce blood of the donor liver’s type.

What does this all mean, you may ask? Well, all this basically means that Demi-Lee no longer had to rely on immunosuppressants: her body will not reject her liver anymore. How did it happen? What triggered it? Can this unique phenomenon be replicated in other transplant recipients? Researchers don’t know yet, but they’re eager to find out. If Demi-Lee’s miracle could be isolated and reproduced medically, it could mean the near-perfection of organ transplantation technology: and bring us that much closer to the age old vision of defeating all the disorders that inflict themselves upon our bodies.

References:

http://www.news.com.au/entertainment/story/0,26278,23106284-5007185,00.html

http://abc.com.au/news/stories/2008/01/24/2146032.htm

By Albert Chen, #41806241

Genes to Blame for Positive Steroid Testing?

2008-04-09T21:57:00.000-07:00

It’s always disappointing when an inspiring, encouraging and not to mention rippling athlete is tested positive for ‘stimulants’. But at this year’s controversial Beijing Olympics, athletes may just have a viable excuse for that embarrassing urine test.
A study just published in the JOURNAL OF CLINICAL ENDOCRINOLOGY & amp by Jenny Jakobsson Schulze suggests that the genetic makeup of an athlete could allow the guilty to escape detection or even convict the innocent. The standard doping test for testosterone abuse relies on measuring the ratio of two chemicals found in the urine: testosterone glucuronide (TG) and epitestosterone glucuronide (EG). Any ratio above 4TG:1EG is considered suspicious.
However, the production of TG is controlled by an enzyme that is encoded by a gene called UGT2B17 which can come in two varieties: working or not-working. An individual can therefore either have none, one or two working copies of this gene (inherits one copy from each parent). Dr Schulze hypothesized that these genetic variations would affect the results when testing a group of healthy male volunteers that had their DNA investigated and then injected with a single 360mg shot of testosterone.
The results were as she had expected. Nearly half of the men who carried no functional copies of UGT2B17 would have gone undetected in the standard doping test. By contrast, 14% of those with two functional copies of the gene were over the detection threshold before they had even received the injection.
From these results it is estimated that this would give a false-positive testing rate of 9% in a random population of young men. So, maybe at this year’s Olympics when the suspiciously hairy track runner flatly denies testosterone abuse after a positive doping test they may just be telling the truth.

Web link: http://www.economist.com/science/displaystory.cfm

Human-Cow Embryos - A New Creation?

2008-04-09T19:12:00.000-07:00

Have it ever crossed your mind that we are able to create a new type of embryos, just by using the stem cells of human cells and the egg cells of cows? Well the BRITISH researchers said they have!

I don't know what most of you guys think about this, but for one thing for sure, this is surely weird! The experts of Newcastle University have inserted human DNA into the egg cells of the cattle, which they have hollowed out in order to create a growing embryo. Thus, they try to get the embryonic stem cells by taken it apart.

So what's the point of doing this? Well the other experts believed this is just the first step of understanding the biology of embryonic stem cells. John Burn, the Head of the Institute of Human Genetics at Newcastle University said "If the team can produce cells which will survive in culture it will open the door to a better understanding of disease processes without having to use precious human eggs."

So therefore, in order to have excess number of stem cells, without using human eggs, the researchers are trying to figure a new placement for the human eggs to continue their further research of stem cells, which their original aim is to find a regenerative medicine, which doctors hope for eventual treatments for spinal cord injuries, and diseases such as diabetes and even cancer.

However, there is always ethical issues in regards to using stem cells, like the destruction of human embryos and which the embryos must be treated with dignity, "This is one of the most controversial ethical issues in all of cloning and stem cell research," said Arthur Caplan, director of the Centre for Bioethics at the University of Pennsylvania.

This type of research is not the first, for example, in 2004, the Chinese researchers have said that they had created embryos by putting human DNA into a rabbit cell.

However, therefore, experts are trying their best by going into various approaches in order to understand the biology of embryonic stem cells.

But like I have said, its too weird to create human-animal embryos in the first place!

REFERENCES:
Article;
http://www.news.com.au/story/0,23599,23476502-5011761,00.html
Image;
http://www.worth1000.com/entries/168500/168545dIkH_w.jpg

By David Truong 41180893

"Double Trouble with Insecticide-Resistant Mosquitoes."

2008-04-09T18:42:00.000-07:00

Mosquitoes harbouring two insecticide-resistance genes have been found to survive unexpectedly well in an insecticide-free environment where carrying such genes would normally be expected to be a burden. As outlined in research published by the open access journal BMC Evolutionary Biology, this results from the genes interacting with one another to the advantage of the host Culex quinquefasciatus mosquitoes and to the detriment of pest management strategies affecting human health.

The research team, led by Dr Vincent Corbel and colleagues from the Université Montpellier II, Genetics and Evolution of Infectious Diseases and The Research Institute for Development (IRD) in France compared the survival rates or evolutionary fitness of one strain of the mosquito that carried two resistance genes (ace-1R and KdrR) for two different insecticides to mosquitoes that only had one insecticide-resistance gene, a French research team discovered that the survival cost of having both genes was far lower than the cost of having just ace-1R.

"We know from evolutionary theory that mutations such as these are likely to be costly to their owners in environments where they have not been selected for" explained Dr Corbel. "We've found that in C. quinquefasciatus the cost of having the ace-1R mutation in the absence of insecticides is counterbalanced when the mosquito also has the KdrR mutation. Mosquitoes with both mutations will also be harder to control as they are resistant to two different types of insecticide."

The authors also found evidence that resistance alleles interact with one another in the presence of insecticides. For instance, synergism (that is, a more than an additive effect) in toxicity was observed when a pyrethroid insecticide and a carbamate insecticide were applied simultaneously to the strain sharing both mutations (the insecticide had a greater activity and more of the mosquitoes died), whereas antagonism (that is, a less than an additive effect) was noted with Culex mosquitoes carrying only ace-1R.

Resistance to so-called xenobiotics (antibiotics, insecticides and herbicides) is a problem affecting the control of organisms of medical or economic importance. In C. quinquefasciatus insecticide resistance mutations interacted to positively and negatively influence the mosquitoes' fitness. Costs were associated with both resistance genes in an insecticide-free environment. The KdrR form of the gene, or allele, however, compensated for the costs associated with the ace-1R allele, suggesting that mosquitoes with both genes in the wild could be more prevalent. Females with both alleles were more likely to mature than those with just the ace-1R mutation."

"It is important to identify genetic interactions such as this and how they influence the fitness of multiply resistant organisms in order to better structure management strategies" says Dr Corbel. "We have found in this case that resistance genes do interact and even compensate. We will have to be very careful in how we use insecticides in future as our results have major implications for pest and health management."\

Webber, Charlotte. "Double Trouble with Insecticide-Resistant Mosquitoes." Medical News Daily 9 Apr. 2008. 10 Apr. 2008 .

Module Map Links Embryonic Stem Cells And Cancer Stem Cells

2008-04-09T18:27:00.000-07:00

A new study suggests that a genetic fingerprint associated with normal embryonic stem cells may be important for the development and function of cancer stem cells. The research, published by Cell Press in the April 10th issue of Cell Stem Cell, demonstrates that embryonic stem cells and multiple types of human cancer cells share a genetic expression pattern that is repressed in normal differentiated cells, a finding that may have significant clinical implications for cancer therapeutics."Self-renewal is a hallmark of stem cells and cancer, but existence of a shared stemness program remains controversial," explains study co-author, Dr. Howard Y. Chang from Stanford University. Dr. Chang, Dr. Eran Segal from the Weizmann Institute in Israel and their colleagues constructed a gene module map to systematically relate transcriptional programs in embryonic stem cells (ESCs), adult tissue stem cells and human cancers.
The researchers identified two predominant gene modules that distinguish ESCs and adult tissue stem cells. "Importantly, the ESC-like transcriptional program was activated in diverse human epithelial cancers and strongly predicted metastasis and death," says Dr. Segal. Conversely, the adult tissue stem gene module had an opposite pattern, activated in normal tissues relative to cancer and repressed in various human cancers when compared to normal tissues.
The researchers went on to demonstrate that c-Myc, but not other oncogenes, was sufficient to reactivate the ESC-like program in normal and cancer cells. In primary cells transformed by tumor-inducing genes Ras and I B, c-Myc increased the number of tumor-initiating cells that exhibited key properties associated with cancer stem cells and dramatically increased the frequency of tumor formation in mice.
These findings suggest that activation of an ESC-like transcriptional program in differentiated adult cells may induce pathologic self-renewal characteristics of cancer stem cells. Further, the map of gene modules may prove to be a valuable tool for establishing improved standards for classifying and defining stem cells by using the expression signature modules as "fingerprints" rather than reliance on just a few molecular markers.
http://www.sciencedaily.com/releases/2008/04/080409130711.htm

presence of original cells nervous in the human spinal-cord

2008-04-09T17:24:00.000-07:00

The original cells nervous, compensating the losses of neurones, are present in the adult human spinal-cord, according to an official statement of the french institute of Inserm medical. Their work was published in March 2008 in the journal of neuroscience research.

These adult original cells could potentially contribute to repair the spinal-cord of people having undergone a traumatic lesion.

They could also find a therapeutic use in neurodegeneratve diseases such as amyotrophic sclerosis causing paralysis.

The spinal-cord is located in the prolongation of the brain inside the spinal column. It ensures the good performance of a network of driving neurons essential to the movements but also with the transmission of the sensitive signals (of which the pain) and controls other functions (sphincters and génito-sexual). Currently the lesions affecting this wiring of neurons are irreversible.

http://www.jneurosci.org/

The Future Vaccination ---- Tattoos

2008-04-09T06:09:00.000-07:00

Tattoo is always seen as a mere fashion icon. However, one would never expect the painful process of tattooing has a great potential value in the medical field – DNA vaccination by tattooing.

First, what is DNA vaccination? It is a process whereby a DNA vaccine is administered into the body, and the body will convert the information in the DNA vaccine into a protein which activates an immune response. This was initially done via simple injection of DNA but it is considered to be one of the less effective methods of DNA vaccination as it often failed to produce the expected immune response. A study done by Dana Pokorna, Ivonne Rubio and Martin Müller shows that tattooing is a more effective way of delivering DNA vaccines than intramuscular injection.

A coat protein from the human papillomavirus (HPV, the cause of cervical cancer) was used as a model DNA vaccine antigen in their research. 3 ways of DNA vaccination were examined and compared, which are tattooing, standard intramuscular injection with adjuvants, and injection without molecular adjuvants (adjuvants function to boost immune response).

Tattooing gave a stronger humoral (antibody) response and cellular response than intramuscular injection, even with adjuvants in the latter. The study shows that 3 doses of DNA vaccine administered by tattooing produced at least 16 times higher antibody levels than 3 intramuscular injections with adjuvant included.

Tattooing is done with a solid vibrating needle, causing a wound and inflammation to stimulate immune system. In the study, the skin surface area of the mouse of approximately 2cm² was tattooed by 30 times repeated two-second-lasting treatments with the tattoo needle vibrating at 145 punctures per second. Results show that DNA-tattooing induces higher levels of specific antibodies cellular immune responses compared to intramuscular injection.

Tattooing involves much larger area of the skin than intramuscular injection, thus DNA vaccine can enter more cells, accounting for a stronger immune response. Tattooing hurts tremendously but Müller explained that: "This is probably what makes it work better than normal injections because the tissue is damaged and this affects the immune cells, which then look out for antigens."

The advantages of tattoo vaccination are the low price of the tattoo device and a standardized method for the application. On the other hand, not only that tattooing includes pain on animals, but it is also a cumbersome procedure. Nevertheless, it seems to be the method of choice if faster and stronger immune responses need to be achieved, such as in the case to treat cancer. Potential applications might be vaccination of life stock for prophylaxis or for human therapeutic purposes.

Reference list

Pokorna, D, Rubio, I, Müller, M, 2008, ‘DNA-vaccination via tattooing induces stronger humoral and cellular immune responses than intramuscular delivery supported by molecular adjuvants’, Genetic Vaccines and Therapy, vol.6, no.2.

http://www.gvt-journal.com/content/6/1/4

Tattoos: Vaccinations of the Future?, viewed 7 February 2008.

http://www.redorbit.com/news/health/1245900/tattoos_vaccinations_of_the_future/

McGrath, M, 2008, ‘Tattoos may help deliver vaccine’, BBC News, 7 February 2008.

http://www.news.bbc.co.uk/2/hi/science/nature/7231913.stm

Posted by Yoon E Kok

Student Number: 41498936

New genetic discoveries linking to Macular Degeneration

2008-04-09T05:10:00.000-07:00

Macular degeneration also known as MD or AMD affects one in seven people over the age of fifty with case numbers increasing as age increase (Macular Degeneration Foundation, n.d). MD is the leading cause of vision impairment in the elderly population. This disease causes a progressive painless loss of the central vision. This is a disease of the retina in the eye. The retina connects what we see, to our brains. There are both wet and dry forms of MD. Both forms start by the retinal Pigment Epithelium which passes oxygen, sugar and other essential products into the retina which in turn disposes of waste produces. However the retina of people with MD can not dispose of this waste. The waste builds up which can be seen as yellow spots. This waste causes pressure build up on the eye which in turn causes the macular cells to die off. As this disease affects so many people The University of Columbia began looking into whether genetics plays a role in who is diagnosed with the disease. The University has discovered this disease is linked to three in four cases to the genetic codes in our bodies. Scientists have discovered what they call as Factor H and Factor B. These factors code for specific proteins. It is when these the Factor H proteins mutate that people have a greater increased chance of having MD. This is because people with the mutant Factor H “are less able to control inflammation caused by infectious triggers” (Streich.E, 2005). Meanwhile the Factor B is an activator of the immune response. Thus Factor B people are at lower risk of developing MD. This only holds true to three in four cases. It is yet to be discovered why the other 25% of people get MD.

References
Craig Leoult, Columbia University, University of Iowa, n.d, ‘Variation In Gene That Regulates Immune Response Causes Age-Related Macular Degeneration When Triggered, Study Shows’, 8-04-2008,
http://www.cumc.columbia.edu/news/press_releases/AMD-Allikmets.html.

Elizabeth Streich, 5th March 2005, ‘New genetic discovery explains 74 percent cases of age-related macular degeneration’, 8-04-2008, http://www.eurekalert.org/pub_releases/2006-03/cumc-ngd022406.php.

Macular Degeneration Foundation, n.d, ‘What is Macular Degeneration?’, 8-04-2008,
http://www.mdfoundation.com.au/page122150.aspx.
Alexandra Henderson 41724626

Artificial Letters Added to Life's Alphabet

2008-04-09T04:01:00.000-07:00

US researchers have created two artificial DNA bases, or 'letters', that can actually be accurately and efficiently replicated by a natural enzyme. Eventually, the researchers say, they may be able to add these two artificial building blocks to the four natural genetic bases that comprise DNA, opening up doors to widely different kinds of genetic engineering.

This unnatural but functioning new base pair is the result of nearly a decade of researcher by chemical biologist Floyd Romesberg, from the Scripps Reseach Institue, California, US.

Romesberg borrowed some tricks from drug development companies and, with the help of graduate student Aaron Leconte, used these to synthesis 3600 potential candidates for the artificial bases to see if they would be treated normally by a polymerase enzyme.Two different methods of screening both turned up the same pair of molecules, called dSICS and dMM02. A minor chemical alteration was made on the dSICS, due to its greater readiness to pair with itself rather than its intended partner, finally making an unnatural base pair, d5SICS and dMM02, that efficiently replicated without the need of an unnatural polymerase.

The molecular pair that worked surprised Romesberg. "We got it and said, 'Wow!' It would have been very difficult to have designed that pair rationally."

In the near future it is expected that these bases will be used to synthesize DNA with new and unnatural properties. These could include highly specific primers for DNA amplification; tags for materials, such as explosives, that could be detected without the risk of contamination from natural DNA; and building novel DNA-based nanomaterials.

Further Readings:
-http://www.newscientist.com/channel/life/genetics/dn13252-artificial-letters-added-to-lifes-alphabet.html

Blog post by Bethany Reid (41807444)

Combating antibiotic resistant 'superbugs'

2008-04-08T07:59:00.000-07:00

41522279

In recent lectures it was mentioned that since the discovery of penicillin we have been unintentionally causing many bacteria to develop into antibiotic resistant 'super bugs'. This is not breaking news but i thought i might try and locate some articles relating to recent discoveries that are helping in the fight against these 'super bugs'.

In recent years, a group of Australian researchers stumbled across a chemical known as AGG01 that is able to kill bacteria 100 times more effectively than some of the most potent forms of penicillin. The discovery was made when researchers pondered over what it was that prevented infections in baby wallabies when they are less than 100 days old and have not yet developed immune systems (netdoctor, 2006). They found that the wallabies milk contained the aforementioned chemical AGG01 that was the 'antibiotic' wallabies used 'naturally' to combat all kinds of infections.

Another recent report questioned weather doctors should be using probiotics, harmless bacteria found in yoghurt's, rather than antiseptic soaps to slow the spread of hospital bugs (netdoctor, 2006). They noticed that when bacteria is grown in a lab, it is well known that they generally do not grow on top of one another, rather, they spread out across the surface. With this principle in mind, Professor Mark Spigelman of University College London, suggested that after doctors wash their hands in antiseptic soap, they should then proceed to cover their hands in a harmless bacteria to prevent any room for the pathogenic bacteria to find room to settle (netdoctor, 2006). This kind of precaution could effectively help reduce the spread of 'super bugs', and for that matter any other kind of pathogenic bug, not so much by 'killing' the bacteria but by preventing their reproduction.

For more information on the referred articles and any other related research, please follow the links below.

The Crisis in Antibiotic Resistance

http://www.sciencemag.org/cgi/content/abstract/257/5073/1064

Wallaby milk 'could treat super bugs'

http://www2.netdoctor.co.uk/news/index.asp?id=122630&D=20&M=4&Y=2006

Doctors should use yoghurt to fight super bugs

http://www2.netdoctor.co.uk/news/index.asp?y=2005&m=11&d=1&id=120860

Picture source

http://www.dkimages.com/discover/Home/Animals/Mammals/Marsupials/Families/Wallabies-and-Kangaroos/Unidentified-Kangaroo-and-Wa.../Unidentified-Kangaroo-a-11.html

MRSA, is there a cure?

2008-04-08T03:53:00.000-07:00

MRSA; simply state those four lettters to anyone associated with the health system and no doubt, a cold wave of shudders shall come your way in return. Methicillin-resistant Staphpylococcus aureus, or MRSA for short, is a strain of the common Staphpylococcus aureus bacterium . Yet what seperates this strain from the others is its ability to remain immune against treatments ranging from penicillin and methicillin, to cephalosporins and beta-lactam antibiotics, thus making it a considerably difficult disease to treat.

Although first discovered in 1961, the "superbug" as it is termed, was refrained only to limited areas in the UK. Yet through eventual progression throughout the world it has become one of the most serious diseases known today. Only last year was a study done by the CDC that revealed, as of Oct 07, that MRSA was responsibe for more deaths in the US than AIDS.
Although the propsed drug of use at the moment is vanomycin, there have already been reports of a vanomycin resistant MRSA. So what is the cure for this potentially lethal disease?

It seems that as recently as this month, according to the UPI, scientists in the New Orleans found aligators may hold the potential antidote within thier very blood. Thier reason to test this theory relies on the unusually resistant immune system, that aligators possess against variety of viruses, bacteruim and fungi. Steve would be so proud!

Yet this is not the only curious method of treatment that has been proposed. Scientists have also suggested the use of basic clay, which they believe possesses three minerals capable of inhibiting MRSA progress. Of course these are simply proposals that are still in considerable development, and cannot provide a definate identification or method by which MRSA can be treated.

Thus the only possible reliant possibility, at present, lies with prevention. Through the use of sterilizing alcohol, strict rules of sanitation, regulated hygiene practices hospitals, various places around the world have been able to slowly decrease the affect that MRSA has on the population has it large. Of course even this method is one with considerable holes, yet until our scientists can conjour some magic clay or miraculous blood potion, it is this method that we must abide by and hence attempt to stop the "unstoppable" superbug.

By: Sarah Chaudhry

Student ID: 41726107
web links:
http://www.dogflu.ca/04072008/12/clay_shows_ability_to_treat_mrsa_staph_infections
http://www.upi.com/NewsTrack/Science/2008/04/08/alligator_blood_may_beat_mrsa/6665/
http://en.wikipedia.org/wiki/MRSA

Alligator Blood – A Source of New Antibiotics

2008-04-08T01:44:00.000-07:00

Despite their reputation for deadly attacks on humans and pets, alligators are wiggling their way toward a new role as potential lifesavers in medicine, biochemists in Louisiana reported. They described how proteins in gator blood may provide a source of powerful new antibiotics to help fight infections associated with diabetic ulcers, severe burns, and “superbugs” that are resistant to conventional medication.
Their study, described as the first to explore the antimicrobial activity of alligator blood in detail, found a range of other promising uses for the gator’s antibiotic proteins. Other uses include combating Candida albicans yeast infections, which are a serious problem in AIDS patients and transplant recipients, who have weakened immune systems, the scientists say.
“We’re very excited about the potential of these alligator blood proteins as both antibacterial and antifungal agents,” says study co-author Mark Merchant, Ph.D., a biochemist at McNeese State University in Lake Charles, La. “There’s a real possibility that you could be treated with an alligator blood product one day.”
Previous studies showed that alligators have an unusually strong immune system that is very different from that of humans. Unlike people, alligators can fight microorganisms such as fungi, viruses, and bacteria without having prior exposure to them. Scientists believe that this is an evolutionary adaptation to encourage quick wound healing, as alligators are often injured during severe defensive battles.
Blood samples were collected from American alligators from which, disease fighting white blood cells (leucocytes) were secluded and the active proteins from those cells were extracted. In laboratory tests, tiny amounts of these protein extracts killed a wide range of bacteria, including MRSA (methicillin-resistant Staphylococcus aureus), the deadly bacteria that are moving out of health care settings and into the community. These “superbugs” are increasingly resistant to multiple antibiotics and cause thousands of deaths each year. The proteins also killed six out of eight different strains of Candida albicans, the researchers say. Their previous research also suggests that blood proteins may help fight HIV, the virus that causes AIDS.
The scientists are working to identify the exact chemical structures of the antimicrobial proteins and determine which proteins are most effective at killing different microbes. The gator blood extract may contain at least four capable substances, they estimate.
With the chemical structures in hand, scientists can begin developing them into antibacterial or antifungal drugs, including pills and creams, for fighting infections. These drugs show particular guarantee as topical ointments, Merchant says. Gator-blood creams could possibly be rubbed onto the foot ulcers of patients with diabetes to help prevent the type of uncontrolled infections that lead to amputations, he says. The creams could also be applied to burns to keep infections at bay until damaged skin can heal, the researcher adds.
Merchant suggests that the proteins might be called “alligacin.” If studies continue to show positive results, the drugs could land on pharmacy shelves in another seven to ten years, he estimates. Raw, unprocessed alligator blood could make you sick or even kill you if injected so it should not be tried by your own home treatments.
Similar antimicrobial substances might also be found in related animals such as crocodiles, Merchant notes. In the future, he plans to study blood samples from alligators and crocodile species throughout the world to test their disease-fighting potential.
Reference: http://www.biologynews.net

Altered skin cells improve Parkinson's symptoms in rats

2008-04-08T01:16:00.000-07:00

References
Fox, M 2008, ‘Stem cells from skin treat brain disease in rats’, Web Article, viewed 8 April 2008, http://www.reuters.com/article/topNews/idUSN0719560620080407?feedType=RSS&feedName=topNews.

Baker, M 2007, ‘Adult cells reprogrammed to pluripotency, without tumours’, Web Article, viewed 8 April 2008, http://www.nature.com/stemcells/2007/0712/071206/full/stemcells.2007.124.html

Reshaping DNA could reshape your life

2008-04-08T01:07:00.000-07:00

According to recent findings at the University of Illinois, Chicago, reshaping of the DNA scaffolding that supports and controls the expression of genes in the brain may play a major role in the alcohol withdrawal symptoms, particularly anxiety, that make it so difficult for alcoholics to stop using alcohol.

"This is the first time anyone has looked for epigenetic changes related to chromatin remodelling in the brain during alcohol addiction," said Dr. Subhash C. Pandey, professor and director of neuroscience alcoholism research at the UIC College of Medicine and the Jesse Brown VA Medical Centre in Chicago, the lead author of the study.

These ‘epigenetic’ changes are minor chemical modifications of chromatin and have been previously found to alter anxiety and alcohol-drinking behaviour in animal models. Chemical modification of histones, which are proteins contained in the chromatin, can change the way DNA and histones are wound up together. Histone acetyltransferases (HATs) are enzymes that add acetyl groups to histones and loosen the packing, promoting gene expression. On the other hand, histone deacetylases (HDACs) remove acetyl groups from histones, causing them to wrap with DNA more tightly, decreasing gene expression.

In this new study, the conductors looked at the HDAC activity, acetylation of histones, and expression of the genes for NPY in the amygdala and the anxiety-like behaviours associated with withdrawal from chronic alcohol use. They found that acute exposure to alcohol decreases HDAC activity; increases the acetylation histones; increases levels of NPY – and subsequently reduced anxiety in the animals. On the other hand, anxiety-like behaviours during withdrawal in animals with chronic alcohol exposure were associated with an increase in HDAC activity and decrease in histones acetylation and NPY levels. Most importantly, it was found that the development of anxiety-like behaviours during alcohol withdrawal could be prevented by blocking the observed increase in HDAC activity using an HDAC inhibitor and causing histone acetylation and NPY expression levels in the amygdala to increase also.

"Our findings suggest that HDAC inhibitors may have potential as therapeutic agents in treating alcoholism," Pandey said. "We need new strategies to treat alcoholism that are directed toward the prevention of withdrawal symptoms. Anxiety associated with withdrawal from alcohol abuse is a key factor in the maintenance of alcohol addiction."

Do genes decide if we're vertically challenged?

2008-04-07T22:38:00.000-07:00

Recently a team of scientific researchers identified a common gene that determines human height. Early this year the same researchers identified a sum of twenty regions of our genome that code for our height. This scientific discovery may lead to the advancement of other scientific investigations and could possibly even help in the battle against disease.

Last year DNA samples from 30,000 people across the world gave evidence to suggest that there are common variations of which influence adult height. Not only do the recent discoveries in this field create exciting new avenues in genetics concerning human growth, it also may contribute to other areas such as disease; particularly osteoarthritis and cancer.

"Our research implicates genes that could shed light on a whole range of biological processes. By identifying which genes affect normal growth, we can begin to understand the process that lead to abnormal growth not just height disorders but also tumour growth, for example", says Dr Frayling a devoted genetic researcher.

It was thought that a person's height was dependent on an even mix of genetic and environmental factors, similar to the chance of suffering from obesity. The recent discoveries have disproved this theory and research currently shows that approximately 90 percent of our normal variation in height is due to our genetics rather then environmental factors like our diet.

"There may be more than a hundred genes which affect our height, many of which will work in surprising and unpredictable ways", says Dr Mike Weedon. "The challenge for us now is to understand how they influence growth in the body. This could open up new avenues for treating a range of diseases."

Genes are vital for the development and function of the human body. Genetics is always making leaps and bounds with their breakthroughs and the wealth of knowledge yet to be discovered is astronomical. The discovery of genes that encode for our height discourages the idea of environmental influence and in doing so, pushes 'nature' in the limelight and 'nurture' into the shadows.

Written by Rohan Crothers (41751501)

For further information:
http://www.bio-medicine.org/biology-news-1/A-tall-story-3A-New-research-adds-to-growing-body-of-knowledge-of-genetics-of-height-2771-1/

Gene Linked to Addiction, Cancer!

2008-04-07T19:49:00.000-07:00

Gene Linked to Addiction, Cancer April 3rd 2008

Scientists have pinpointed three closely connected genes that a) makes people more prone to tobacco addiction AND
b) more likely to develop lung cancer (as a result of smoking more cigarettes in a day than those without the genes)

'The genetic variations which encode nicotine receptors in cells could eventually help explain some of the mysteries of chain smoking, nicotine addiction and lung cancer’

This discovery, made by three teams of scientists funded by governments in the US and in Europe could just mean that a predisposition to smoking is hereditary!

‘A smoker who inherits the genetic variations from both parents has an 80% greater chance of lung cancer than a smoker without the variants’.

The team also found that smokers with the genes are more likely to ‘light up’ on average two more cigarettes a day than those who do not have the genes. Not only do they smoke more but they find it harder to quit!

This discovery opens the possibility for better ‘tailor made’ treatments . And by putting this information out there it might better awareness campaigns (which haven’t been doing so well lately!) urging smokers to quit whilst discouraging the younger population from taking up smoking.

If informed of this new information children with parents that smoke may be more inclined to avoid smoking.

For more information the journals Nature and Nature Genetics contain the published results.

Or read the article in full:
HERE
Posted by Sarah McNeill

Genetic Link to Smoking Addiction

2008-04-07T15:16:00.000-07:00

Scientists have recently identified genetic variations, on chromosome 15, which evidently raise the risk of attaining lung cancer for smokers and people with a history of smoking. These variants are apparently common in the general population and only raise lung cancer risk for those who smoke, or have smoked before.

The three research teams, that investigated this genetic link to smoking addiction, have made conclusions that may someday in the near future give rise to screening tests and customised treatments for smokers trying to quit.

One of the interesting things they've uncovered includes the fact that people that are smoking now, or have smoked in the past, who have two copies of the variants (one from each parent) have a 70%-80% greater risk of getting cancer.

This research is still ongoing and some questions such as how exactly the key variants influence lung cancer risk, and whether or not the key set of variants affect just one gene or three closely placed genes, are still trying to be answered.

by Biyanka Komandur

To read the main articles featuring this research visit either ( or both) of the following links:

http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/7325971

http://www.foxnew.com/wires/2008Apr03/0,4670,SmokersGenes,00.html

2008-04-07T09:04:00.000-07:00

Have you ever wondered wether your child will be tall or short?
As weird as it sounds perhaps Sonic the hedgehog may have the answer.
In the endless search through our genome, scientists have uncovered a cluster of key genes that control height, and some of the DNA sequences make genes that control the bizzarly named proteins, sonic hedgehog, Indian hedgehog and desert hedgehog.
The British study, published yesterday in the journal, Nature Genetics, involved through samples from over 30,000 Europeans to in search of common variations in the genetic code that may determine height.
The scientists found 20 new regions, or loci, when combined these 20 loci alone can change height in an individual by up to 6 cm.

Unlike obesity, which is driven by genetic and environmental factors, height is almost entirely a genetic affair.
Ninety per cent of normal variation in human height can be attributed to one's DNA heritage rather than nutrition.
The 20 loci account for roughly 3 per cent of this 90 per cent.
Last September, the same team found a genetic variant that accounted for another 0.3 per cent.
Some of the 20 genes spotted in the new probe are well known and their function has been intensively explored.
They include genes, such as the hedgehogs, that are essential for cell division, a finding that may be useful for cancer research. Some genes act as switches, which turn other genes on and off. And others play a role in cell-to-cell signalling.
But roughly half the genes are a completely unknown quantity.

Solomon Osei-Amo

41741388

http://news.bbc.co.uk/2/hi/health/6975865.stm

http://www.newton.dep.anl.gov/askasci/mole00/mole00125.htm

http://www.ingentaconnect.com/content/bsc/ahg/1998/00000062/00000004/art00005

Stress Linked to Ancestry

2008-04-07T06:27:00.000-07:00

Stress Linked to Heritage

According to a recent study conducted by researchers at the National Institute on Alcohol Abuse and Alcoholism, coping standards of individuals can be explained by inheritance variations of the molecule neuropeptide Y (NPY) [2].

It has long been known that NPY regulates anxiety responses in the brain, however, this experiment sort to determine if ‘genetic variants’ [2] encoding the protein contributed to the effectiveness of anxiety responses. “NPY is induced by stress and its release reduces anxiety” said David Goldman, chief of NIAA Laboratory of Neurogenetics, “we sought to determine if genetic variants of NPY might contribute to maladaptive stress responses” [2].

The research team found that genetic variations did in fact alter levels of NPY in the brain and stimulated different emotion responses. Via functional brain imaging, it was found that those who had low levels of NPY reacted higher to threatening images and muscular pain than those with high levels of NPY. This demonstrated the “close tie between emotionality and resilience to pain and other negative stimuli” [2]. It was also found that a low level NPY gene variant was more common among individuals with anxiety disorders.

These results could stimulate new research involving some of the consequences of inherited variation on other neuropeptide Y functions such as circadian rhythms, sexual function, vascular resistance and feeding behaviour [1].

References

[1] Bowen, R 16/03/1997 Neuropeptide Y http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/bodyweight/npy.html Colorado State University, Colorado date viewed 05/04/2008

[2] Medical News Today 03/04/2008 Discovery of Genetic Factor In Stress Response Variability http://www.medicalnewstoday.com/printerfriendlynews.php?newsid=103704 MediLexicon International Ltd, United Kingdom date viewed 05/04/2008

Picture

~gotmyphilosophy, 01/04/2005 Stress http://gotmyphilosophy.deviantart.com/art/Stress-16766785 date viewed 05/04/2008

Alligators, Potential Lifesavers?

2008-04-07T05:22:00.000-07:00

Now I know this sounds weird, an alligator, the close relative of the Aussie Crocidile, saving lives but it could be a possibilty! No the alligators aren't going to save you from drowning, rather they would more likly prefer to take a bit out of you. According to Louisiana biochemists, proteins in gator blood may provide a source from which potent antibiotics and antifungal medications can be derived from.

According to Mark Merchant, Kermit Murray and Lancia Darville, the chemical stuctures in the the proteins from alligator blood could be used to treat many different afflictions such as "diabetic ulcers, severe burns, and “superbugs” that are resistant to conventional medication" and "six out of eight different strains of Candida albicans" which is a problem that faces people who have weak immune systems such as AIDS suffers and transplant recipients.

Previous studies have shown that gators have a much stronger immune system then human, thought to be due to the fact that gators fighting so much and recieving injurys that they have evolved to handle fungi, viruses, and bacteria without having prior exposure to them. This led to the examination of their white blood cells and the extraction of the key proteins.

At present Merchant and his colleagues are trying to isolate the chemical structures from the proteins that are the key to the fighting the microbes. So in the next 7 to 10 years you may be seeing Alligator blood medications hit the market. In the mean time I would reconmend that no one out there decides to be smart and inject themselves with gator blood as it would most likly make you very sick if not kill you. Also I am sure that the alligator who's blood you have taken would not appreciate it very much.

References
http://www.biologynews.net/archives/2008/04/06/alligator_blood_may_put_the_bite_on_antibioticresistant_infections.html Picture
http://www.marathonbooks.com/images/Alligator2.jpg
By Anthony Rawkins (Student No. 41751136)

The Obesity crisis

2008-04-06T23:56:00.000-07:00

Obesity may be thought of as Australia’s biggest current health crisis. Recently, much research and analysation has gone into understanding how adenovirus-36 functions and how it is thought to be responsible for some cases of obesity, due to the fact it causes fat cells to grow.
Dr. Nikhil V. Dhurandhar, a university professor at Louisiana State University at Baton Rogue published details about the adipogenic effect of the human adenovirus-36 on laboratory animals, and also its association with human obesity. He coined this term infectobesity. He was able to show that a single viral gene triggers this process and put forward that in the future it may be possible to treat ‘viral obesity’, simply by altering the action of this particular gene.
Along with his highly qualified team, he engineered stem cells taken from human fat to express a single gene, adenovirus-36, named called E4 ORF-1. Through results it was seen that these cells were more likely to differentiate into fat cells, in comparison to those cells that did not express the gene. When blocking the E4 ORF-1 expression in cells infected by adenovirus-36, the cells failed to differentiate into fat cells. From these results it was thought that this gene is both necessary and sufficient for fat cell differentiation. Therefore through blocking the E4 ORF-1 expression in humans would prevent adenovirus-36 induced obesity. Along with this, the gene seems to become more responsive to insulin, suggesting that drugs that copy this part of the gene’s action may be used to treat sufferers of type 2 diabetes.

From issue 2650 of New Scientist magazine, 04 April 2008, page 15

Posted by Ashta Murugesan

A virus: Help to those with Huntington’s.

2008-04-06T04:44:00.000-07:00

IMAGINE a disease so severe, that even though there's a blood test that can tell if you have the disease no one wants to be told they have it.

Huntington’s disease (“HD”) is a genetic disorder commonly confused with the effects of Alzheimer’s, Parkinson’s and Schizophrenia, that causes the loss of neurons in a specific part of the brain, the basal ganglia (responsible for performing an important role in motor and intellectual functions of the human body).

HD develops when a certain part of the gene’s DNA sequence is repeated an abnormal number of times and is caused by having 40 or more copies of C-A-G codons simultaneously in a region of the DNA that comprises the Huntington gene. The gene repetition disrupts the function of the Huntingtin protein normally produced by the Huntington’s gene, resulting in the neuron loss, creating death of nerve cells and structural problems with the basal ganglia.

Occurring in approximately 1 in 10,000 people HD kills brain cells, depriving its victims of their abilities to speak, eat, think, and walk over a period of years. The first symptoms of HD usually appear between the ages of 30 and 45 and the disease progresses slowly and eventually results in complete immobility, ending in death 15 to 20 years after diagnosis.

Gene therapy research for HD is aimed at finding viruses that can reach the diseased nerve tissues with the least immune response, thus letting the virus enter the body undisturbed. Currently, viruses are used to carry the replacement DNA into these cells. These viruses have had their harmful properties removed. It is evident that Gene therapy could give HD victims the answers to a cure; however problems can arise if the body distinguishes the viruses as foreign and mounts an immune response causing the therapeutic DNA to erase any beneficial effects.

Whilst there is no cure for Huntington’s disease at present; there are some positive developments on the horizon. We can only hope that gene therapy will result in a breakthrough treatment that will curtail the onset of the disease.

Posted by Ella Hilton

Sources:
-Australian Huntington Disease Association:
http://www.ahda.asn.au/

- BBC News - Health
http://news.bbc.co.uk/1/hi/health/2843419.stm

-Medicine Plus
http://www.nlm.nih.gov/medlineplus/huntingtonsdisease.html

-National Institute of Neurological Disorders and Stroke:
http://www.ninds.nih.gov/disorders/huntington/huntington.htm

Student number: 41759477

Harvesting Chlorophyll d

2008-04-06T03:26:00.000-07:00

Researchers from Arizona state University and Washington University have reported that they have sequenced the genome of the cyanobacteria Acaryochloris marina, which produces chlorophyll d enabling it to absorb near infrared long wavelength light (light invisible to the naked eye). The genome of Acaryochloris marine is 8.3 million base pairs long and is the largest of the 55 cynobacteria strains in the world. It is also the first chlorophyll d organism to be sequenced.

The researchers said that now the genome has been sequenced the immediate goal is to find the enzyme that causes a chemical structure change in chlorophyll d that differentiates it from other forms of chlorophyll. The synthesis of chlorophyll by an organism is a complex process that involves 17 steps. To make chlorophyll d an enzyme needs to transform a vinyl group to a formyl group near the end of the process. The researchers already have some candidate genes that they will test by inserting them into an organism that only makes chlorophyll a. If that organism is able to then synthesis chlorophyll d the gene responsible will have be isolated.

Once the responsible gene is found the scientific advance has applications in plant research. If the gene that causes the chemical transformation is inserted successfully into other plants or organisms it could mean an extra 5% increase in available light for the organism to use. Scientists also believe that harvesting solar power from genetically altered plant or organisms is not out of the question.

SOURCE: http://www.biologynews.com

posted by Rachel

Next Genome Project:Giant Panda

2008-04-06T00:32:00.000-07:00

Cardiff University will team up with international colleagues in the first genome project of an endangered species, the giant panda. "Giant Panda Genome Project" will map out the genes of the 'living fossil' and help to understand giant panda's unique adaptations, including its dietary specialization of eating the bamboo shoots. Giant panda has 20 00-30 000 genes which is almost similar to the size of human genome. This maybe can help researchers to investigate more on diseases affecting humans and its link to genome size. The giant pandas are known to be related to ancestors existed 8 million years ago in China. Doing a genome project on panda can be a helping hand to prevent the extinction of giant pandas.

Obesity Epidemic Not So Unfounded

2008-04-05T22:55:00.000-07:00

A research team at the Louisiana State University has found that a virus may be to blame for the increasingly high incidences of obesity in the western world.

When undifferentiated cells were infected with Adenovirus-36 (also known as AD-36) they more readily became fat cells, whereas in precursor cells that had not been infected the prevalence of fat cells was not apparent.

Adenovirus-36 is just one of 51 known adenoviruses that can infect humans, most of which cause respiratory infections (i.e. the common cold) and have also been associated with the formation of some tumours. Adenovirus-36 has been found in approximately 30% of people suffering from obesity and only 11% of people who are not.

The team lead by Dr Nikhil Dhurandhar manipulated stem cells separated from human adipose tissue to express only one gene from the virus, E4 ORF-1. The expression of this viral gene in the undifferentiated cells triggered them to become fat cells, whereas stem cells that were not expressing E4 ORF-1 differentiated into a variety of cells.

The discovery that the expression of a single viral gene in undifferentiated cells triggers fat cells to be formed may one day lead to a treatment for a certain percentage of obesity cases around the world.

Created by Laura - 41753774

Adapted from NewScientist, Issue 2650, April 04, page 15.