How Men And Women Cope Differently With Stress Traced To Genetic Differences

A research conducted by Hebrew University of Jerusalem is looking into how men and women reaction when stress come into their life. Genetic code plays a prominent role in different responses to stress. Cortisol is the stress hormone that responsible to manage stress. Small increase of cortisol has some positive effects such as quick burst of energy, improve memory functions, increase immunity, and maintain homeostasis in body. However high level of cortisol for long period tends to kill brain cells, decrease the memory function and reduces leaning abilities.
In the test, mouthwash sample were taken to test brain-derived neurotrophic factor (BDNF) gene which involve in supporting the growth and differentiation of brain cells. BDNF gene characterizes by a variant that code for either valine (Val) or methionine (Met) amino acids. Subjects carrying Val/Val were compared in their cortisol response to those carrying Val/Met. Val/Met men and women carriers had nearly equal cortisol levels. Val/Val men can produce higher cortisol than Val/Met men. For women, surprisingly, Val/Val women can produce lower cortisol than Val/Met women. In the other word, Val/Val women own better ability to regulate stress than others. But the reason why Val/Val women produce lower cortisol level than Val/Val men is still an enigma.


Reference:
http://www.psychologicalharassment.com/stress_and_stress_management.htm
http://www.sciencedaily.com/releases/2009/04/090405185031.htm
http://stress.about.com/od/stresshealth/a/cortisol.htm


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Extra gene at chromosome 21 is a key to fight cancer.

People with Dawn’s Syndrome have a third copy of chromosome 21. This extra copy gives them extra versions of 231 different genes. Researchers from Harvard University found out that people with Dawn's Syndrome rarely get many kind of cancer except leukemia. Their hypothesis is that the third copy of chromosome 21 has copies of gene that help to regulate cancer growth. They carried out a study on more than 18000 patients with Dawn’s Syndrome and it showed only 10% of then is expected rate of cancer.

The experiment had been done by using induced Pluripotent Stem cell (iPS cell) from a volunteer with Dawn’s Syndrome and genetically engineered (GE) mice. The iPS cells are made from skin cells but have ability to perform like a stem cell. As results, the researchers succeeded to locate one gene that responsible to protect the GE mice against tumor. The gene is Dawn’s Syndrome Candidate Region-1 (DSCR1 or as known as RCAN1). This gene codes for a gene that suppresses vascular endothelial growth factor (VEGF). This protein is a necessary compound for angiogenesis of tumor cells. The transcription of VEGF is inhibiting by DSCR1 and hence no angiogenesis process occur. Down’s Syndrome patients have extra copy of DSCR1 gene in their genome. In the experiment, GE mice that are resistant to tumor also carry this extra gene. It is believe that there are other useful genes in this extra chromosome 21 and researchers are looking forward to explore more.

Glossary

iPS cell - A differentiated cell that has been modified so that it regains its ability to develop into other types of cell.

Angiogenesis - blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor.

reference:

www.reuters.com/article/healthNews/idUSTRE54J5IN20090520

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature08062.html

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student ID 42101747

Hibtat loss "hitting shellfish"

Habitat loss 'hitting shellfish'

Effective conservation measures can help oyster reefs cover, the study says

Marine habitat loss is causing a decline in shellfish populations, which is having an adverse knock-on effect on sensitive ecosystems, a study suggests.

Described as the first global assessment of its kind, it warns that 85% of the world's oyster reefs have already been lost.

The findings, published by The Nature Conservancy (TNC), adds that many other reefs are now "functionally extinct".

It blames poor fishing practices and coastal developments for the declines.

Lead author Mike Beck said the report showed that oyster reefs were the most severely impacted marine habitats on the planet.

"We're seeing an unprecedented and alarming decline in the condition of oyster reefs, a critically important habitat in the world's bays and estuaries," he said.

Shell shocked

The study, written by scientists based in five continents, found reefs that were "functionally extinct" in a number of regions, including North America, Europe and Australia.

"However, realistic and cost effective solutions within conservation and coastal restoration programmes, along with policy and reef management programmes provide hope for the survival of shellfish," Dr Beck added.

Oysters provide a number of key services within their ecosystems, such as filtering water, and provide food for other organisms, such as fish, crabs and birds.

The assessment identified a number of "driving forces" behind the reefs' decline, including "destructive fishing practices, coastal overdevelopment, poorly managed agriculture and poor water quality".

Although these problems have been around for decades, the report said there were two main barriers that were impeding oyster recovery efforts.

The first was a lack of awareness that shellfish habitats were in trouble, and the second was an assumption that non-native shellfish can be introduced in areas where native species are declining.

"We want to raise awareness that the world's remnant oyster reefs and populations are important, since they represent some of the last examples of reef habitats produced by a particular species of oyster," explained co-author Dr Christine Crawford, from the University of Tasmania.

"We have an opportunity to conserve such reefs in Australia and elsewhere with the results of this assessment," she added.

Among the report's recommendations were to elevate native, wild oysters as a priority species for conservation, and ensuring existing protection policies were extended to include the vulnerable reefs.

Hibtat loss "hitting shellfish"

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41769887

Chromosome 21 and a possible cure for cancer

Research has confirmed, the long suspected theory, arisen from the low prevalence of cancer in Down syndrome patients, that the genes on chromosome 21 could be beneficial in treating cancer. Cancer research Sandra Ryeom and her collegues have shown that an extra copy of the Dscr1 gene, located on the 21^st chromosome and therefore affected by trisomy, is significant enough to suppress tumour growth in mice, and angiogenesis (blood vessel formation) in humans.

Ryeome found that the protein expressed by this gene, DSCR1, elevated in the tissues of Down syndrome patients due to the extra gene, suppresses signals from the vascular endothelial growth factor (VAGF) which promotes angiogenesis. VAGF is a protein, secreted by cancerous cells, which attaches to specific receptors on nearby blood vessels, encouraging new blood vessels to form. Studies conducted on mice showed that endothelial cells showed a decreased growth response to VEGF when they had an extra copy of Dscr1. It was also found that DSCR1 suppresses VEGF signalling via the calcineurin pathway, a specific signalling pathway contained within the cells which make blood vessel walls.

By working with induced pluriptent stem cells (iPS cells), which are known to induce tumours when inserted into mice, Ryeome validated that the tumours with reduced number of blood vessels found in mice with an extra chromosome 21 is viable to work in humans. But it is highly likely that more than one gene located on chromosome 21 is responsible for angiogenesis, so more study needs to be done.

Original article : Why Do People with Down Syndrome have less Cancer ? Research in Mice and Human Stem Cells suggests New therapeutic targets.
http://www.sciencedaily.com/releases/2009/05/090520140359.htm

"Micro Switch" Influences Expression of Nicotine Addiction Gene

"Micro Switch" Influences Expression of Nicotine Addiction Gene

For several years, scientists have tried to find genetic links to nicotine dependence. Although studies have found many genes to be associated with tobacco smoking, only small handful are actually considered causative, and these genes are difficult to identify. As denoted by the central dogma of biology, DNA encodes RNA, and RNA codes for proteins; however, it is now widely know that some types of RNA have alternate roles. One type of non-protein-coding RNA is microRNA. Named for their relatively small size, microRNA influence the extent to which genes are expressed, which in biological terms, is the rate of conversion of specific DNA to RNA.

To date, microRNA has not been shown to play a significant role in psychiatric disorders; however, a recent study published in Biological Psychiatry has made the discovery that variations in the expression of the dopamine D1 receptor gene may have a causal link to the likelihood of nicotine addiction. In a previous study, researchers at the University of Virginia, Huang and Li showed the dopamine D1 receptor gene is causatively linked with nicotine dependence (the dopamine D1 receptor is one of the major receptors in the brain that mediate the action of dopamine neurotransmitters). Huang and Li found that the two alleles of the dopamine D1 receptor gene can be expressed to different degrees. Their current study demonstrates that the variations in expression are regulated by microRNA miR-504, thus it can be said that microRNA directly influences the expression of genetic variations that predispose an individual to developing an addiction to nicotine. This finding is of interest to the scientific community because it shows how certain genes can vary their degree of expression by using a “micro switch”, that is, microRNA.

Original Article: http://www.sciencedaily.com/releases/2009/04/090423082758.htm

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