Wednesday, May 18, 2011

Sugar fuels growth of insulin-making cells

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

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

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

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


Shih-Wei Kuo - 42621209

Tuesday, May 17, 2011

How Long Will You Live?

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

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

Monday, May 16, 2011

Genetic Mutation and Schizophrenia

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

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

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Monday, April 11, 2011

Apoptosis and its role in chemotherapy

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

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

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

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

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

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

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

Jianchao Ge (Student Number: 42572691)


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