Hepatitis C Holy Grail

Researchers at the Duke University Medical Center have discovered a biomarker which has been compared to finding a “Holy Grail” (by David Goldstein of Duke’s Institute for Genome Sciences & Policy).

The biomarker is an innovation in Hepatitis C treatment which can be used to presage how different patients will react to treatment and also can be used to explain why different racial and ethnic groups fluctuate so much in their response to treatment.

The discovery of the marker, the result of a single letter change (C to T), has given patients and doctors valuable information in terms of deciding the best treatment for each individual. This information is so important as "The side effects of hepatitis treatment can be brutal, and about half the time, the treatment fails to eradicate the virus.” said Goldstein.

Review by Rachael Lee, 18.08.2009

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Rearrangements of Multifunctional Genes Cause Cancer

A thesis presented by the University of Gothenburg, Sweden, shows that several genes lie in the tumor diseases are involved in fundamental processes in the cell, this may be the cause that tumors arise early in life affect children and young people. The “FET” genes have been the main problem. They are in the form known as “fusion genes” in these tumors; they changed form into unusual fusion proteins which transform normal cells to cancer cells.

Human body has many specialized cells such as fat cells and nerve cells. Cancer arises when something is wrong in the process when those stem cells formed, and mature along different development paths. Scientists believe that the activity of FET fall as the cells grow, therefore those genes have an important impact on the early stages of cell maturation. When these genes contain FET arise, the maturation paths become blocked, thus a cancer cell can multiply in an uncontrolled behavior. Normally, it requires damage to different genes before cancer cells build up, however, FET genes are involved in normal cells processes, and scientists believe that in rearranged form, they can affect many control systems preventing a normal cell becoming a cancer cell. This gives rise to development of cancer and is the reason that tumors with FET fusion genes are often found in children and young people.

Thomas Chou(42054151)

Original article can be found at: http://www.sciencedaily.com/releases/2009/03/090310120355.htm

How Much Sleep Do We Really Need?

Recently published research has located a gene on the human genome which is implicated in regulating the length of sleep the human being requires. Through extensive research, a gene mutation was discovered and is believed to be a result of repressed transcription of certain other genes andnimplicated in the regulation of circadian rhythms. Sleep still remains a biological phenomenon: though it is known that it is regulated largely by circadian rhythms and homeostasis.



This rare gene mutation was discovered in two members of a small extended family, with both mother and daughter having shorter long term sleeping requirements than the previous standard of eight hours sleep a night. Genetically engineered mice and flies which expressed the mutated human gene were studied, with results similar to the observations made in affected humans. The mice with the mutated human gene slept less over a 24 hour period as compared to the normal mice, and also needed less compensation after a sleep deprivation period.

This new research will lead to a further understanding of sleep and the human genome, and in the near future pathologies relating to sleep disturbance may be extinct. It will also lead to further mapping of other genes and mutations present in human beings in order to understand ourselves further.

Caitlin O'Hare
s41431782

Viral Evolution? Not a problem

The infamous swine flu virus is teetering on the edge of a world wide pandemic, with signs of resistance to the Governments stockpile of Tamiflu. It’s a relief to note the work being done in genetics to develop a new generation of antiviral drugs. Michael Goldblatt from the biotech company, Functional Genetics, is one of a group of researchers that believe they have found the key to viral evolution or at least preventing infection from slight mutations, which render conventional antiviral useless in treating the new strains. At present the antiviral blocks replication by binding to the viral protein, which relies on drug specificity for each individual strain of viral infection? The discoveries by Goldblatt rely on the basis that viruses are dependant on their hosts. They hijack normal host cells processes to facilitate viral propagation and deceive the host into making copies of the virus. Some of these host proteins that are in fact essential for the replication of the virus are not required by the cell for its normal functioning and survival. The proposal is to disable these proteins in order to block viral replication. Many viral strains are found to use the TSG101 protein, as it is involved in mediating intracellular transport and when hijacked plays a role in viral budding and release of the virus. By using this form of transport however is leaves a ‘fingerprint’ of human protein, one by which multiple viruses use as their mechanism for attack, and therefore is not specific mechanism to each virus. It has been found that there are many viral families that rely on this one mechanism for viral propagation, and as a result you have a therapeutic that can identify and block every virus that uses this mechanism.

Philip Thorpe, a pharmacologist at the University of Texas Medical Centre, has developed an antibody that is able to bind to these ‘fingerprinted’ infected cells, and destroys it to prevent further replication. The antiviral drugs on the market today do not take into consideration the ease in which the virus can mutate when the drug is interacting with the viral protein. It is not clear however, how a virus can mutate to such a great degree to change the mechanism by which they infect cells, which appears to be a far sure and more effective angle to approach to take when trying to prevent the spread of viral infection. There is the probability that a virus will eventually overcome this, but how far away that time is, is uncertain, and definitely not obvious.

By Dion Zunker (42063519)

Original Article: New scientist; Bob Holmes (10 August 2009); Magazine issue 2720; http://www.newscientist.com/article/mg20327200.100-how-to-cure-diseases-before-they-have-even-evolved.html

Perfect pearls for women!

Looking into your jewelry box, you might find that some pearl earrings or necklaces are not entirely perfect and shiny. If they do, it might have cost you a fortune to obtain such high quality pearls. But most women know it is worth to have them! Of all the jewels and precious stones that are dug out from the Earth, pearls are an exception. They are formed biologically inside a living organism, amazingly the oyster. If you are a pearl lover, you might find this good news to you!

Recent research at Townsville's James Cook University in north Queensland discovered a list of all the genes in the oyster which are responsible of producing a pearl. Project leader Dr Dean Jerry is taking the next step to identify the five or six fundamental genes out of about one million gene bases found in South Pacific pearl oysters. By working out the perfect gene combination and breed the genetically-modified pearl oysters, he hoped to grow high-quality pearls with the best characteristics like round, shiny and pure gold colour.

Dr Jerry said there was a small yield of high quality natural pearls; only 5 per cent to 10 per cent of oysters create the best products. He emphasized that they could manipulate the oyster’s genes combinations with the aid of the latest genetic engineering techniques and thus boost the production outcome of these perfect round pearls. Consequently, he stated that there would be substantial profits in the pearl industry.

According to Dr Jerry, culturing oysters to get high quality pearls can be very complicated and costly. It is a long process before a pearl farmer can obtain a few cultured pearls of substantially high quality out of many unsuccessful ones. However, by selective breeding, he hoped to yield a higher frequency of gem quality, high value pearls.


Related articles can be found at:

http://www.abc.net.au/news/stories/2009/08/05/2646298.htm
http://www.sciencealert.com.au/news/20090708-19528.html

By 41911622

A GENE FOR A SHORT NIGHT'S SLEEP

Regardless to differences in age, gender or background, one thing that all humans have in common is the desire for a good night’s sleep. However for some people this is a truly challenging task, every night a new battle. Common sleeping disorders, such as insomnia and night terrors, have been clinically diagnosed as being caused by anxiety, chronic pain or sudden changes in lifestyle, but who would have thought genetics could be to blame? A new study has identified a particular gene that controls the amount of sleep required by people each night. Outcomes of the research have shown that people with a rare genetic variation of the gene, DEC2, will naturally sleep less during the night. Although scientists knew that the variation in people’s sleeping patterns could be genetically explained, this research is the first of its kind to actually identify and locate the gene.

The research involved two controlled experiments, the first conducted on humans, the second on mice and fruit flies. To collaborate information, scientists examined the genes of several people who naturally slept less than average. Eventually the DEC2 gene was located in two sleep-deprived women, a gene that was absent in the rest of their family members who slept normal hours. To confirm the accuracy of their findings, the scientists ran a second experiment, this time using recombinant DNA technology to insert the ‘short-sleep’ gene into mice and fruit flies. Results show that the mice and flies with the DEC2 gene slept less than those with the standard version of the gene. Although it is still unsure whether people with this gene require more sleep to lead healthy functioning lives, this research is definitely a breakthrough in understanding the complexities of sleep and how genetics account for more than we’ll ever know.

By Omotola Oladapo

Related article:
http://www.sciencenews.org/view/generic/id/46390/title/A_gene_for_a_short_night’s_sleep

Advances for Infertility

Dramatic advances in the research of male fertility were recently made when scientists developed human sperm from embryonic stem cells. Researchers at the Newcastle University and North East England Stem Cell Institute have developed the method which involves cultivating male stem cells into germ line stem cells which are then prompted to undergo meiosis and form mature sperm, namely, “In Vitro Derived sperm”. The procedure was also attempted with female stem cells however after forming into early stage spermatagonia the process ceased, signifying to researches that the Y chromosome is necessary for meiosis and sperm maturation.

As the topic of stem cell research is still under debate, researchers have stated that the sperm will not be used in fertility treatment as it is prohibited in the UK and also holds no value to their study. Researchers are hoping that by gaining a comprehensive understanding of the formation of sperm they can provide new alternatives for couples suffering infertility problems, including helping them have a child that is genetically their own. It will also allow scientists to study how these cells are affected by toxins, possibly helping young boys who have become infertile due to medications they have had administered. Researchers believe that studying the formation of sperm could also lead to a better understanding of how genetic diseases are passed on. This research could ultimately bring relief to the frustrations of thousands of couples who struggle with infertility.

Newcastle University (2009, July 8). Human Sperm Created From Embryonic Stem Cells. ScienceDaily. Retrieved August 18, 2009, from http://www.sciencedaily.com­ /releases/2009/07/090708073843.htm

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