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


By,
41876598

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

by,

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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i cannont for some reason publish my post. i will speak to you when i get into the lab.
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

Posted by 42014007

Could Addiction Be Genetic?

Addiction experts at the University of Virginia Health System and the University of Michigan have found that several genes are linked with multiple addictions. Ming Li, Ph.D., professor of psychiatry and neurobehavioral sciences at the UVA School of Medicine said, "We're narrowing the scope to specific genetic targets. Once researchers can pinpoint exact genetic variants and molecular mechanisms, then we can create much more effective, even personalized, treatments for individuals addicted to a variety of substances."

This discovery could have huge ramifications for those suffering from addiction. It could also be used to identify those who would be more susceptible to addictions in the future.

The study showed "a summary of specific genomic locations on 11 chromosomes where addictions to alcohol, cannabis, cocaine, heroin, nicotine and opoids are clustered together." This means that right now we do not know which genes encode for which addiction however we know that someone with addictive behavior is most likely to have many addictive genes for many different substances. By using this information we can greatly improve our understanding of addiction and find new and better ways to treat those suffering from it.

Original article: http://www.sciencedaily.com/releases/2009/03/090310142912.htm
Picture: A summary of chromosomal locations of peaks or intervals for addictions to alcohol, cannabis, cocaine, heroin, nicotine and opoids. (Image courtesy of University of Virginia Health System)

By Joel Pettersson, 42066752

Scientific research links genes to depression in older men

Research at the Western Australia Centre for Health and Ageing has demonstrated an increased risk of depression in people who a genetic polymorphism of the C-Reactive Protein (CRP) gene. CRP is a protein “found in the blood in response to inflammation”. Already knowing depression is prevalent among older Australians, researchers used the electorol role to randomly select 12,000 men aged 65, or older, living in Perth. 3,700 men consented to blood tests for genetic analysis, which, along with other health and lifestyle factors, contributed to this finding.

Professor Osvaldo Almeida, Centre Research Director, stated “The results of our study suggest that these genetic variations lead to a relative deficiency in an individual’s ability to address the physiological changes that occur as a result of acute stressful events. The consequence of such a deficit is that the body takes much longer to be restored to full health, and depression may ensue because of the ongoing high circulating levels of chemicals known as cytokines.”.

The consequent challenge to such studies as this is to find the practical application for improved management and treatment strategies, but as Professor Almeida commented: “A lot of work has to go into that.”.

Article: http://www.sciencealert.com.au/news/20091905-19141-2.html

Original Source: http://www.news.uwa.edu.au/200905181199/media-statements/scientific-breakthrough-links-gene-controls-immune-response-depression

Original Study: Edition not yet published, Current Issue:(Volume 38 Issue 2 April 2009)

Tasmanian Devils saved by genes?

Australia’s Tasmanian Devil population has been in freefall due to a virulently infectious cancer; and it is predicted that this unique species may be wiped out within three years. The disease, which appears as facial lesions, is spread by biting during mating and is one of only three communicable cancers which exist in the world.
Scientific research into major histocompatibility complex (MHC) – which activates an immune response in vertebrates – has shown that the devils have little genetic diversity which means that their immune systems do not treat the tumour cells as a threat. However, scientists are focusing on the more isolated devils from the west of Tasmania (as opposed to the common eastern variety), which appear to have a different MHC type. Researchers have only uncovered one devil that resists the disease, and tests showed he had a different MHC type from the eastern devils. When injected with dead tumour cells the devil’s immune system began to fight the tumour. The devil was then injected with live tumour cells and, at the present, is still healthy. Now, 6 devils are being injected with live tumour cells in an attempt to find resistant animals that can be bred. The tumour is unlike any other disease of its kind, but it seems natural that resistant devils ought to exist (scientists pin their hopes on the tumour obeying this ‘rule’). If the 6 devils prove resistant scientists plan to breed them back into the wild and into captive populations, improving the species’ immunological fitness.
As the genetic detective work continues into this disease, and the Tasmanian devils’ potential to genetically resist the tumour is uncovered, devils are being ‘stockpiled’ in zoos and wildlife parks in order to implement a massive breeding program when the secrets to the disease are uncovered. Meanwhile, other avenues to solve the disease are being explored. For example a number of scientists are seeking financial support to sequence to devil genome, and some ecologists suggest a scheme to fence off areas in Tasmania to establish new devil colonies or even create devil populations on mainland Australia. However, if the 6 devils achieve resistance, these measures may not be required.

(Source: TIME Magazine, May 19, 2008, pg 44)

Major Leap made towards Discovery of Gene that causes Kidney Failure in Children

This article was taken from Science Daily (May 21, 2009)

Researchers from the American Society of Nephrology are getting closer to locating the gene which causes susceptibility to Primary Vesicoureteral Reflux (pVUR). This condition occurs where a defective valve in the bladder permits urine to pass back into the kidneys and is one of the major causes of pediatric kidney failure. It affects about one percent of children and is genetically inherited through families.

A study involving 12 families was conducted, where 72 affected individuals underwent a genome wide linkage scan. It was found that the pVUR susceptibility gene was located on chromosome 12p11-q13. This locus is less than one percent of the human genome. Contrary to what was previously thought it was found that this gene could be inherited in an autosomal dominant fashion. This means that there may be several possible forms of inheritance for VUR.

While the exact location of the gene has not yet been identified, this is a major leap forward. Hopefully this will be provide better understanding if the kidney disease and, in the future, help to improve diagnostic tests and treatment.

By Emily Impey, 21 May 2009

For more information:
Journal of the American Society of Nephrology
http://jasn.asnjournals.org/cgi/content/abstract/ASN.2008111199v1
Vesicoureteral Reflux
http://www.keepkidshealthy.com/welcome/conditions/vesicoureteral_reflux.html

Pediatric Nephrology - A genome search for primary vesicoureteral reflux shows further evidence for genetic heterogeneity
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2259258

Article from:
American Society of Nephrology. "Important Clue Found To Help Identify Common Cause Of Kidney Failure In Children." ScienceDaily 21 May 2009. 21 May 2009

Picture from:
Kure it! Kidney Cancer Research Fund, 21 May 2009,

XX Chromosome found in Male Mice

(Sutton, 2007)

This article was taken of the ABC News website and was posted Tuesday august 21 2007.

A south Australian research team looking at the effect the Sox3 gene has one mouse has stumbled across a peculiar discovery: male mice with two X chromosomes. Characteristically, a mouse will have a single X chromosome and then either a single Y chromosome indicating it is a male, or an additional X chromosome indicating it is a female.  But now South Australian researchers have discovered a way of changing a single gene to create male mice without a Y-chromosome. The so-called "pseudo-male" mice look and act like other males, but they have two X-chromosomes, which is previously described as the normal female pattern. The litter of mice doctor Edwina Sutton, from the University of Adelaide, was working on were 80% male. However many of these had two X chromosomes, yet could not be told apart from those with a Y chromosome.

"What we know is that some of them are XX with extra copies of the brain gene, so they are the sex-reversed animals, and there are some that are actually XY," Dr Sutton said. She began experimenting with the mice to examine a brain gene known as Sox3. Differing levels of that gene in humans has been known to cause mental retardation. "We created a mouse that has increased amounts of this particular brain gene to try and then look really closely at the brain and work out what's occurring differently during their development," she said. "So they were chromosomally female, but they had extra amounts of this brain gene which had caused them to switch from being female to male." These mice however were unable to reproduce, which is a common outcome of abnormal breeding.  Dr Sutton believes she may have uncovered a link between the brain gene and the gene that determines whether an animal is male or female.

 What is believed to have been found is the original version of the maleness gene on the y chromosome.  This research may be able to help assist in the research into why 1 in 500 Australians are born with a genital defect.  An aspect that Dr Sutton has yet to pursue is whether the brain of the XX males is ‘hardwired’ to be male or female.

 

 

Sutton, D. E. (2007, August). Chromosome study reveals new insight into sexual genetics. ABC News , 2.

 

 

 

 

Mice, Stem Cells & the Future of Human Blood

Sickle-cell anaemia is an autosomal recessive disorder that causes the sufferer’s red blood cells to change from its regular oblong shape into a sickled form. Sickle-cell anaemia is caused by a mutation in the haemoglobin gene. As a result of this mutation, the abnormality of the shape of the cells obstructs blood flow and oxygen flow into a tissue or organ, which can result in a shorter life-expectancy in affected individuals.

A gene therapy experiment carried out on mice by the Massachusetts Institute of Technology attempted to replace the sickle-cell encoding mutation with an anti-sickling gene using stem cells.

Red blood cells are formed from the stem cells in bone marrow. Therefore the treatment had to be delivered through that pathway. Firstly, the bone marrow of the mice was killed will irradiation, before the treatment was applied.

The way in which this was carried out was by delivering the anti-sickling gene into the blood forming stem cells of the affected mice. This new genetic matter is then taken up by the stem cells in the bone marrow which in turn give rise to new red blood cells. These newly formed red blood cells now have been genetically modified to exhibit normal red blood cell structure.

Prolonged monitoring of the treated mice found that the instances of sickle-cell anaemia had dropped. Some tests proved that it had been eradicated or completely eliminated.

Whilst the treatment proved effective on the mice in eradicating the instances of sickle cell, further research will continue to be carried out to develop a safe method for administering this gene therapy in humans. Based on the evidence, this cure is not too far away.

By Kimberley Martinz s4201269

Original Article:
http://www.sciencemag.org/cgi/content/full/sci;294/5550/2368?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=sickle+cell+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

For Blood Stem Cells, The Force Is Stong

This article talks about a research that focuses on how blood flow, nitric oxide boost production of stem cells. Researchers from the independent groups at Children's Hospital Boston, tested the ability of blood flow to turn cells into blood stem cells, also known as hematopoietic stem cells. In the research led by George Daley, mouse embryonic stem cells were placed in a centrifuge-like device that is similar to shear stress, which is the frictional force blood creates when it flows over cells in a mouse's aorta. Embryonic stem cells that are exposed to the same shear stress as found in the mouse aorta, produced blood stem cells, but cells that were exposed to different level of shear stress did not. The researchers then gave a drug called the nitric oxide blocker to the pregnant mice, and found out that the embryos had problems making blood stem cells. Similar experiments was done on mutant zebrafish embryos with nitric oxide, and found out that the mutant embryos, which do not have a heartbeat because of a defect in a heart muscle protein that prevents the making of hematopoietic stem cells in their tails, produced blood stem cells.

Although it is unclear on how the cells sense shear stress, researchers are trying to unravel the myth behind all this in order to manipulate the process of making blood stem cells for bone marrow transplants.


Picture from:
http://repairstemcell.files.wordpress.com/2009/02/red-blood-cells1.jpg

Article from:
http://www.sciencenews.org/view/generic/id/43761/title/For_blood_stem_cells%2C_the_force_is_strong

LIN28B Gene gets the hands ticking for women's biological clocks

It is common knowledge that some women hit puberty before others; researchers have now uncovered the first genetic evidence to explain differences in length of women’s fertility.
Women go through their first menstruation cycle between the ages of 9 and 16, and the variations in the LIN28B gene can be held accountable for a portion of these differences. For instance, one study found that Icelandic girls with two genetic letter Ts at a spot near LIN28B experience menarche 2.4 months earlier, on average, than girls with two Cs at that site.
In humans, LIN28B seems to be involved in variations in adult height, as well. This helps explain why women who go through menarche later are taller than women who have their first cycle at a younger age.
Genes also play a role in menopause, and two research teams have identified several gene variants associated with advancing or delaying menopause by as much as two years. However these genes influence over only a small portion of the possible age range of menopause (which is 40 – 60 years)


Original Article
http://www.newscientist.com/article/dn17141-puberty-gene-sets-our-sexual-clocks.html

Luke Vasanthakumar (41718483)

“Genetically Engineered Mice Don’t Get Obese, But Do Develop Gall Stones”

This article discusses the results of an experiment involving a group of genetically engineered mice, which are on high fat diets. The findings were that these mice do not become obese – or overweight for that matter – but the researchers concluded that they are more susceptible to developing gallstones.

Gallstones are deposits of cholesterol or calcium salts that form in the bile (from the liver) or the gallbladder and are the result of high concentrations of these substances in the body. Normally, people who are obese or have diabetes tend to develop gallstones. The researchers involved in the experiment hypothesized that because these mice do not become obese, they are protected against gallstones. However, the results show that these mice were actually more susceptible to the problem.

The experiment went as follows:

Two groups of mice ate a high fat diet for two weeks. One group consisted of normal mice, the other were genetically engineered mice. The normal mice had a particular protein in their bodies called, “Liver Fatty Acid Binding Protein” (L-Fab protein). The genetically engineered mice lacked this protein. After two weeks the normal mice became obese and developed gallstones and the genetically engineered mice maintained their normal weight but still developed gallstones. The researchers concluded that not having the L - Fab protein would make an individual more susceptible to gallstones. Hang on, didn’t the normal mice develop gallstones as well?
What the scientists should have also tested were the two types of mice on a healthy diet. If the genetically engineered mice weren’t on a high fat diet, would they develop gallstones? It is very likely that neither groups of mice would develop gallstones or even become obese. Therefore, I don’t think that lacking the L-Fab protein is a factor causing gallstones. The real problem is the diet. Whether you are obese or not, if you consume excessive amounts of fat and “bad” cholesterol, then you will develop gallstones. It’s as simple as that.

The article did not mention what the L-Fab protein actually does to the body, so it’s difficult to make any judgment on how this protein has anything to do with gallstones or whether lacking this protein is the cause for not being obese. It could be interpreted that because it’s a fat binding protein, the high cholesterol and fat consumed are “bound” by these proteins to produce actual fat deposits in the body. Thus, having the L-fab protein could be a possible factor aiding in the cause for an individual’s obesity. This premise is supported by the fact that, on a high fat diet, the mice with this protein became obese but the mice lacking this protein maintained a normal weight.

The researchers insist that studying this protein in the mouse genome would offer clues to the genetic factors related to gallstones in humans. I think this offers a bigger clue into the genetics involved in obesity in humans. Do humans have the L-Fab protein? If we do have this protein (and if the premise that an individual was not obese due to lacking the L-Fab protein were true), wouldn’t it be beneficial if we removed this protein from our genome? If doing this were possible, the obesity rates would certainly go down. However the problem here lies in “personal discipline” (ethical problems are involved as well – but everybody’s aware of that already).

Knowing that you cannot become obese, could typically result in a person choosing not to eat healthy foods – after all, without the L –Fab protein, you can’t get fat after spending the day at McDonald’s. So if this were the case, then yes, individuals without the protein (who have poor diets) would still be susceptible to gallstones. We would be better off to leave our genome alone!
So if everyone just lived a healthy lifestyle it wouldn’t necessary to alter our DNA and we wouldn’t be obese or have gallstones either.

Reference:
Washington University School of Medicine (2009, May 13). Genetically Engineered Mice Don’t Get Obese, But Do Develop Gallstones. Science Daily. Retrieved May 20, 2009 from http://www.sciencedaily.com/releases/2009/05/090507094216.htm

Environmental Exposure to Particulates May damage DNA in as Few as Three Days

A new study indicates that the inhalation of certain particulates can actually cause some genes to become reprogrammed. The effects of the particulate matter have now opened new hypotheses about how air pollutants modify human health. Researchers from the University of Milan tested 63 healthy subjects who worked at a foundry in Italy. Blood DNA samples were taken from all the participants on their first day of work, and again three days later. When they compared the samples they found that significant changes had occurred in four of the genes associated with tumour suppression.
Changes in the genes were due to a chemical transformation called methylation which has been found in the blood of lung cancer patients. Dr Baccarelli (M.D., Ph.D., assistant professor of applied biotechnology) discovered that after only three days, these changes were easily detectable of exposure to the particulate matter. This indicates that environmental factors need little time to cause gene reprogramming, which could potentially be associated with causing certain types of disease. However these changes in the DNA methylation are reversible and are currently being used for targets of cancer drugs.

http://www.sciencedaily.com/releases/2009/05/090517143218.htm

Human Nose too Cold for Bird Flu

A recent study conducted by the Imperial College of London found that the avian flu would need to undergo several mutations before it was a threat to humans. As it cannot function in the human nose environment because it is too cold.

The virus is suited to the warmer environment of the gut of birds, which is at 40 degrees, opposed to the 32 degrees of the human nose. The avian influenza viruses and a human virus where both able to grow normally at 37 degrees, the temperature inside the human lung. However it was found that only the human viruses was able to grow at 32 degrees. The low temperature made the avian virus unable to replicate and grow.

The researchers also tried to simulate a mutation of the human flu with the avian strain, by adding a protein from the surface of the avian flu to the human flu. However when cultured the new mutated virus did not grow at 32 degrees.

The study leader Professor Wendy Barclay suggested that the avian influenza virus would have to undergo a number of mutations, and possibly mix with the human strain, before it could become a threat to humans. She goes on to explain how viruses which are transmitted between animals at low temperatures are more likely to cause pandemics. Swine flu appears to be an example of a virus which has adapted to the cooler environment of the human nose.

Professor Ian Jones, a virologist at the University of Reading, has said that this study has shown that the proteins on the outside of the virus are likely to determine how well a virus will function at different temperatures.

Reference:
14/05/09, Human Nose too Cold for Bird Flu, BBC, [Online], 18/5/09, http://news.bbc.co.uk/2/hi/health/8050523.stm

Future of Personalized Cancer Treatment: New System Delivers RNA Into Cells

RNAi has been discovered to have unbelievable potential to manage and treat cancer, by silencing genes through short interfering, double-stranded RNA fragments called siRNAs. This has led to the development of a technology that allows for siRNA drug delivery into the entire population of cells, both primary and tumor-causing, without being toxic to the cells. However, the size and negative electrical charge of the siRNA, prohibits them from readily entering the cell. This problem was overcome by utilizing a small section of protein called a peptide transduction domain (PTD), which has the ability to permeate cell membranes, as a delivery mechanism. However, simply adding the siRNAs to a PTD didn't work due to siRNAs having a highly negative charge and PTDs having a positive charge, which results in aggregation with no cellular delivery. This issue was overcome by making a PTD fusion protein with a double-stranded RNA-binding domain, termed PTD-DRBD, which masks the siRNA's negative charge. This allows the resultant fusion protein to enter the cell and deliver the siRNA into the cytoplasm where it specifically targets mRNAs from cancer-promoting genes and silences them.

It was found that the entire cellular population undergoes a maximum RNAi response. Also, no toxicity to the cells or innate immune responses, and a minimal number of transcriptional off-target changes occur. These RNAi methods can be continually tweaked to combat new mutations – a way to overcome a major problem associated with current cancer therapies.

Posted by: 42034377
Reference: Science daily (2009). Future of Personalized Cancer Treatment: New System Delivers RNA into Cells. Viewed: May 20, 2009, at http://www.sciencedaily.com/releases/2009/05/090517081157.htm

More than a single species: Aetobatus Narinari

Results from a recent study suggests that one vulnerable species, Aetobatus narinari, may in fact constitute a species complex (a monophyletic group of similar species that do not differ enough from others in the genus to warrant separation at the the genus or subgenus level).





The Spotted Eagle Ray is a is a large, coral-reef dwelling batoid which is currently causing conservation concern. As a species, it has relatively low recruitment and is subject to intense and unregulated inshore fisheries. It is therefore considered highly vulnerable to sustained harvest. Currently, it is classified as a single, circumglobally distributed species. However, results from this study reveal that A. narinari is composed of at least 3 distinct lineages, with no genetic exchange among individuals from the Central Atlantic, Eastern Pacific, and Western/Central Pacific regions. These findings support the recognition of at least 2 distinct species within "A. narinari" and 2 lineages that should arguably be provided subspecies status.

The experiment obtained tissue samples from 36 A. narinari individuals from globally distributed regions. Aetobatus flagellum obtained from Ariake Bay, Japan, was used as an outgroup for intraspecifit phylogenetic analysis. The genomic DNA from the samples was amplified and sequenced using the Polymerase Chain Reaction and DNA Sequencing, and the data was analysed using computer software. Evolutionary relationships between the individuals were then estimated by constructing unrooted statistical parsimony networks for each locus using the Templetion et all. method as implemented in the software package TCS version 1.13 (more computer software). Phylogenetic analyses were conducted on concatenated mitochondrial and nuclear sequence data sets to further explore the evolutionary relationships among the A. narinari sequences. To assess the genetic divergence thresholds that might be informative for species delineation, divergence between the 3 major A. narinari phylogeographic lineages obtained (Western/Central Pacific, Eastern Pacific, and Central Atlantic) were compared with that between other taxonomically uncontested batoid and shark congener pairs. A likelihood ratio test was also performed to test for the existence of a molecular clock on the A. narinari data sets.

The study utilised a combination of genealogical concordance and genetic distance criteria to delineate the globally distributed species of A. narinari into at least 2 distinct species. One species was found to range through the Western and Central Pacific, while the other was found to range the Central Atlantic and the Eastern Pacific. The latter species was further divided into 2 subspecies separated by the Isthmus of Panama. These findings not only providing taxonomic clarification and insight into evolutionary history, but they also have direct management implications. The reduced population sizes and ranges of the delineated species reinforce concerns about the already threatened and vulnerable status of the Spotted Eagle Ray.

Submitted by 41714805.

Source: Richards, VP, Henning, M, Witzell, W, Shivji, MS 2009, 'Species delineation and evolutionary history of the globally distributed Spotted Eagle Ray (Aetobatus narinari)',
Journal of Heredity, vol. 100, no. 3, pp. 273-283, viewed 20 May 2009,

All pictures from Wikipedia (http://en.wikipedia.org).

Genetic Advances to Provide Worldwide Longevity

Researchers at the Case Western Reserve University, Ohio, have developed groundbreaking genetic modification techniques, which could significantly extend the modern human’s life expectancy.

Utilizing advanced genetic technology, the scientists conducted innovative experiments to create 500 “bio-mice”. The mice were modified on the gene level to possess outstanding abilities, including being able to run at speeds and distances far greater than their natural counterparts, as well as living and breeding for considerably longer periods of time. The researchers were able to pinpoint and alter a single metabolism gene in the mice, which gave rise to the animals’ astonishing new capabilities.

Incidentally, this particular gene found in the mice is shared with humans and could be a pivotal step towards acquiring the ever-sought-after remedy for aging. Whilst the researchers hope to one-day transform these revolutionary techniques for use on humans, they admit that, at present, insufficient research has been undertaken into the matter. Within just three decades however, living well beyond 100 years of age may become a reality.

Posted by Jennifer Garlick (s4205381)

Original Article:
http://www.infowars.net/articles/november2007/021107Genetic.htm

Algae used for Computer Chips

Biologists and engineers work with a unicellular algae, known as the diatom, for computer chip nanofabrication.
April, 2008
Engineer: a person who uses scientific knowledge to solve practical problems.
Biologist: a specialist in the science of life and of living organisms, including their structure, function, growth, origin, evolution and distribution.
Professor Franco Cerrina explains the electrical aspects of diatom research.
These two fields of study form a natural pairing for Michael Sussman, professor of biochemistry at UW-Madison, and Franco Cerrina, professor of electrical engineering at UW-Madison. “You can’t get much more interdisciplinary than what we’ve been doing,” Sussman says.
“We do something together that we couldn’t do alone,” Sussman says. As engineers, the importance of teamwork is regularly stressed; however, Sussman was referencing something slightly different. He has been working with Cerrina to discover industrial applications for a unique biological organism—the diatom.
Diatoms are unicellular algae encased in cell walls made of silicate, a form of silicon. In engineering, silicon is used in the nanofabrication of computer chips. Sussman understands the chemistry and mechanisms behind researching the diatom’s structure, while Cerinna is an expert in the nanofabrication process. By combining both of their concentrated scientific backgrounds, they were able to recognize the potential use of diatoms in computer chip manufacturing.
“The chips are getting smaller and smaller and higher and higher density,” Cerrina says. However, engineering technology has already reached its smallest possible chip. The speed cannot be further increased unless a new method of production is designed.
“You can do it yourself and that is what we are doing today. You develop the techniques yourself and make things smaller and smaller… Or you can take something that already knows how to make small things and use it as a tool,” Cerrina says.
“Synthetic biology. Let’s assume that we know system biology. Can we use that to build new things?” Cerrina says of how the idea was initiated. These diatoms are able to “make little machines—little structures in dimensions that engineers have trouble with,” Sussman says. “We are hoping that we can discover how they do that.”
“No one has been able to genetically modify [the diatoms], to manipulate them and use them,” Sussman says. When a team at the University of Washington was able to sequence the diatoms, Sussman knew he was part of an amazing research project. “This group of organisms is so far out there,” Sussman says. “In this case, prior information is useless.” The diatom is the first silicate-requiring organism that has ever been studied.
How exactly did this discovery take place? Cerrina, Sussman and their teams built a microarray synthesizer to make DNA chips. Then they decided to starve the organisms of silicate to see which genes get turned on and which get turned off. It is “an easy way to figure out which genes are involved in the [nanofabrication] process,” Sussman says.
The organisms were similarly starved of nitrogen, carbon and other important components that have been previously studied on known systems. “Out of the 10,000 genes, 2,000 genes were affected by one of those conditions,” Sussman says. “Out of the 2,000 genes, we identified 75 genes that were specifically impacted by silicate starvation... 67 of them have no sequence seen before.” Since this is the first researched organism that requires silicate, they think an entire world of silicate chemistry is yet to be discovered.
A second investigation performed at UW-Madison was to find out where in the cell the genes specific to the silicate process exist. It is hypothesized that they are in the cell wall since this is the silicate’s location. In order to test the theory, the diatom protein was modified by fusing half with a glowing jellyfish protein.
“It glows in the cell wall,” Sussman says. “We are going in the right direction.” Next on the agenda is to mutate the genes, create imperfect cell walls and overexpress the organisms to see how they react, a process known as “reverse genetics.”
What about these possible computer chips that may be formed by “reprogramming” the diatoms? In what kind of computer will they be used? “It is not going to be a computer in the way that we know a computer,” Cerrina says. “[The diatoms] will be nanofabricators… The plan is to teach these diatoms to fabricate the shape that we want, not the shape that they want.” The process is analogous to taking a machine that is designed to make sunglasses and reprogramming it to create reading glasses.
Located in the NanoTech Lab, the microarray
synthesizer is an essential instrumentation
device for researching the specific genes of diatoms.
“We are trying to make biological systems to mimic engineering systems,” Cerrina says. “We are trying to find the set of instructions to make the diatom work.”
Finally, the scientists will want to modify the diatom’s set of instructions for purposes of computer chip production.
“It’s a new time that requires collaboration.” Natural science needs people who are comfortable in thinking outside of their own area. “Engineers are very good at this,” Sussman says.

http://www.engr.wisc.edu/wiscengr/cgi-bin/archivearticle.php?article=apr08breakthrough
Wisconsin Engineering Magazine – 2008
Written by Sally Green

Antiviral activity of the TRIM5 gene

In recent studies of the TRIM5 gene scientists have observed antiretroviral properties. This ability to restrict viruses has sparked significant interest in the international science community as the TRIM5 in some primates is effective against HIV, giving hope to virologists and those working to eradicate HIV (Welkin & Sawyer, 2009).
Already the TRIM5 of a Rhesus monkey (rhTRIM5) has been used to prevent the infection of human cell lines from HIV-1. The genetic structure of the TRIM5 gene in most primates differs to humans, most notably in the ability of some monkeys to restrict HIV-1 preventing the spread of infection (something which humans are unable to achieve). South American Owl monkeys were among the primates with a resistance to HIV-1. This restriction ability was experimented with and it was determined that Owl monkeys possess coding for cyclophilin A (CypA) in the TRIM5 locus. The ability of CypA to bind to the capsid protein of HIV-1 (thereby identifying the virus) combined with the antiviral capabilities of the TRIM5 provides the Owl monkey with a defence mechanism against HIV-1 and other lentiviruses. Research is already underway using the TRIM5 gene in monkeys to enhance the ability of human cells to recognise the HIV-1 virus. So far scientists have been experimenting with altering amino acids in the Human TRIM5 protein in accordance with the structure of the Rhesus protein to increase the recognition of HIV. This small change has had positive results with improved restriction of HIV-1 (Welkin & Sawyer, 2009).
TRIM5 is always competing with viruses for supremacy and as such its evolutionary process is significantly different from other genes. Instead of a long history of purifying selection with rare instances of genetic innovation, the TRIM5 gene has evolved almost entirely by positive selection with variations in the DNA occurring as the result of various evolutionary changes from insertions and deletions to convergence and exon capture (Welkin & Sawyer, 2009).
It is hoped that the study of TRIM5 and its restriction loci will be invaluable in discovery of new antiviral factors, the identification of other gene functions and maybe even the prevention of HIV (Welkin & Sawyer, 2009).

REFERENCES
Welkin, J., & Sawyer, S. (2009). Molecular evolution of the antiretroviral TRIM5 gene. Immunogenetics , 163-176.

The Genetics of Addiction

Drug addictions are becoming more and more common in media and in the general society today. The physical, psychological, societal and economic costs of drug addictions can be extremely detrimental. A recent article in Nature has published that recently conducted studies show certain genetic factors to operate in susceptibility of substance addiction, including vulnerability, initiation of substance addiction, and dependency on a substance. Interestingly, it has been determined that in women, genetic factors have a larger role in the initiation of addiction than in persistence, whereas studies of men have shown the opposite. The studies have shown several genes and regions of genes that can exhibit addiction to various substances including alcohol, tobacco and other drugs. Rare mutations in these genes have also been associated schizophrenia and autism showing the importance of these genes in psychiatric disorders.

In recent years, studies have been able to identify numerous genes of susceptibility for addictions. However, few studies currently exist in the examination of genetics on illicit drug addiction and for multiple substance addiction. It has been determined that the heritability of drug addictions is affected by factors such as sex, age, education, socioeconomic status and cultural background. Currently, scientists are trying to determine the role of genetic and environmental factors on substance addiction whilst attempting to isolate these findings in individuals.

References:

http://www.nature.com/nrg/journal/v10/n4/full/nrg2536.html

Image:

http://www.markhoustonrecovery.com/images/upload/addiction.jpg

Approaches for unravelling the joint genetic determinants of schizophrenia and bipolar disorder

This article looks at the different methods that can and have been used to find genetic links to the liability of bipolar and the possibility that the same genes that can cause schizophrenia may also cause Bipolar do to both these disorders displaying some of the same symptoms and possible co-morbidity. There is evidence of an overlap in both these disorders especially in psychotic and depressive symptoms such as hallucination, delusions, disorganised thought and catatonic behaviour.

The paper goes through a few methods of research that have been explored and suggests that further exploration should be carried out on these. I identifying shared risk genes using recombination frequencies to infer distances between genetic markers and target risk loci by using association studies on genetic polymorphism, using more single nucleotide polymorphisms for this.

Endophenotyes are also suggested as a point of study. This is a psychiatric concept of a bio marker divided into behavioural symptoms. These a different types of neurological components and cognitive components of assertions. One of these smaller phenotypes is classified as a deficiency of smooth pursuit of eye movement caused by a number of genes tied into schizophrenia and dopamine. This paper also outlines different research results done on the gene marks of both these disorders including twin and family studies as well as dopamine.

web link

http://apps.isiknowledge.com/full_record.do?product=BIOSIS&search_mode=GeneralSearch&qid=5&SID=2D7LeaHb7b6C8HLa5I@&page=1&doc=6