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
Monday, May 26, 2008
Skin Cancer and Marijuana
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
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
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
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.
Further reading:
By Dennis Yeung (41596953)
New Meaning for the Term ‘Computer Bug’
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)
Thursday, May 1, 2008
New clues: gene variations may contribute to MS risk.
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
Wednesday, April 30, 2008
Ethanol; a blue green fuel alternative
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.
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)
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
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.
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
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
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
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.
“Researchers have identified location of genes responsible for osteoporosis and osteoporotic fractures”
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
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
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
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
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
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:
Blog by Greg Barker 41750081
Glow In The Dark Cats
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.
Tuesday, April 29, 2008
Genes load cancer dice against black people
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.
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
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.
Further information: http://www.medicalnewstoday.com/articles/105682.php
New Vector Carries Big Genes
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
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!
"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
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.
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)
Monday, April 28, 2008
Parasite Resistance in Sheep
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.
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.
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
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
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.
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
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.
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?
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
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
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:
Muscly Cows....yeah...
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
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'
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."
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
Sunday, April 27, 2008
Gene therapy targets cholesterol
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.
41442621
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.
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.
Amy Beugelsdyk
41442621
Gene that prolong life after heart failure
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
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:
Anceint Bacteria feed on Uranium
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
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.
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?
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.
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
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.
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”
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.
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:
Alcoholism: ‘Rums’ in the Family
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.
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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
Thursday, April 24, 2008
Gene Causes Double Trouble For Smokers
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
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