Stress CAN reverse the aging process!

Every organism has to deal with exposure to stresses and this applies to cells as well. Despite the popular belief that stress can cause cell death and hasten the aging process, a research conducted by biologist Sandy Westerheide and her group from Northwestern University found results that suggest otherwise. In actuality, stress can prolong life, provided that the stress is mild and sub-lethal. The research discovered a new regulated mechanism that cells use to prevent protein damage from stress.

The study focused on an enzyme Sirtuin 1 (SIRT1), a protein that is activated by the chemical resveratrol, which is found in red wine. Already known for its link to aging, the role of SIRT1 is to deacetylate proteins, which contribute to cellular regulation, allowing it to stay on the DNA and to keep producing special protein repair molecules (which work to prevent cell death and extent the life of the cell). Controversially, newfound evidence was discovered by the scientists who suggested that SIRT1 also regulated heat shock response (the damage-limiting of cells and organisms to protect against other stresses) in human cell lines. Variables of mild stress were experimented and results showed that when under mild stress, heat-shock response increased, as well as the level of SIRT1. Westerheide explained that this mechanism was due to the removal of the acetyl groups which allowed more protein repair molecules to be produced. The researchers concluded that the cell is protected against damage when more of SIRT1 is activated under mild stress conditions.

Although the study only tested on human cell lines, the scientists hope that with a greater understanding and further discovery of the heat shock factor 1, SIRT 1 and of the two functioning together they may be able to introduce a mechanism that may be able to protect the cells of whole organism as well. If this is successful, we may be able to alter and manipulate lifespan.

Read more at:

http://esciencenews.com/articles/2009/02/19/anti.aging.pathway.enhances.cell.stress.response

http://www.sciencenews.org/view/generic/id/41044/title/Antiaging__A_little_stress_may_keep_cells_youthful

Second Genetic Link To Obesity Identified

Obesity is simply the body mass index that is greater than 30Kg/meter square with more than 30% of Americans being obese and obesity also constitutes 5-7% of National Health spending (Walley, Blakemore & Froguel, 2006).The number of obese children has also tripled in the last thirty years. A new genetic variation that affects individual’s fat mass, abosolute weight and disposition to obesity was recently found. A mutation in MC4R gene usually results in familiar obesity which makes children of obese more at risk than other children whose parents are not obese (MRC, 2008). The study established that individuals possessing copies of MC4R genetic variant gain an average weight of 1.5 kg compared to those who do not have the variation. Similarly, the FTO gene has also been held culprit and individuals who carry two copies of the FTO variant also have higher weight of about 2-3 kg on the average compared to persons with no copies of the variation (MRC, 2008).
Individuals who have both the FTO variant and the recently discovered MC4R together were 3.8kg heavier on average. The third identified gene in causation of obesity is the NeXN3 (Neurexin gene 3), the same gene that has been linked to addiction and alcohol dependence as well as substance abuse. Identifying genes responsible for obesity may help to produce drugs that can target the molecular pathways via which obesity genes carry out their effect (Scientist Live).
The fourth gene that has also been implicated in a study, in the causation of obesity is the ENPPI gene which contributes to obesity in children and also simultaneously increases diabetes risk. The study revealed that obesity is majorly inherited from grandparents and parents to the children. The conclusion was reached when researchers found similar patterns in the risk of obesity in children parent and grandparent. (Biomedicine, 2008).
Fat cell biology reveals that obese children have more fat cells and this is regarded as hyperplasic obesity which is also genetically determined..Genetics influences close to 70% of obesity. Sixty percent of children with single parent obese come down with obesity while the percentage increases to eighty percent when both parents are obese. Finally, a protein called leptin is produced by the OB gene (obese gene) and this leptin circulates in the human blood (Q&A, 2009) The lepton also acts on the brain and signal satiety leading to reduction in appetite and food intake (Q&A, 2009).The DB gene found in diabetes patient also stimulates the OB protein receptor leading to production of leptin, hence the link between diabetes and obesity.
In conclusion, obesity is really a genetic problem involving a lot of genetic diversity which makes its moral solution almost impossible. Article based on http://www.mrc.ac.uk/Newspublications/News/MRC004564

By SeoRin Park 41365654

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Genetically Mapping the Acne Bug

Acne, is a skin condition which many of us have faced at sometime. The appearance and development of acne is greatly assisted by Propinonibacterium, a bacteria which live in our hair follicles. Although, they are generally harmless when the hair follicles become overfilled with sebum, an oily secretion they aggravate the skin and aid the development of acne. As acne is a prevalent and quite psychologically harmful for many people, scientists have been constantly studying the disease in the last couple of years. German microbiologist Dr Holger Brueggemann and his research team recently mapped the genetic code of the Propinonibacterium. Interestingly, they found that it contains a plasmid which contains 2 333 genes which enable highly destructive properties which are aimed in breaking down the skin. They actually found that the Propinonibacterium has genes which encode for enzymes which are very similar to those in “flesh eating bacteria”. It even had genes which code for substances which destroy competitors.
Most current treatments and medication used to treat acne are based on killing Propinonibacterium or preventing blockage of the hair follicles. Unfortunately, like most antibiotic treatments, the bacteria has rapidly developed resistance to the antibiotic. So what this German research team is hoping to do from mapping genome of the Propinonibacterium is to gain a better and more in depth understanding of the organism to find a more effective cure for acne. As scientists have mapped the genome of the Propinonibacterium, there is not much let to discover about this organism and hence, should not be long till they find a better treatment for acne.

Articlebased on:
http://www.articlesbase.com/acne-articles/scientists-discover-genetic-makeup-of-acne-bacterium-1332831.html#

Other suggested readings-
http://archderm.ama-assn.org/cgi/content/extract/137/9/1250
http://www.highbeam.com/doc/1G1-107524610.html

Puppy Genes: A Guide to Human Behaviour

Have you ever wondered why you behave a certain way? A team of scientists from the University of Tokyo have used guide dogs to determine how much of our behaviour is based on our genes.
The area of human behavioural genetics has exploded in recent years. Increased studies are being performed on the links between universal behavioural patterns such as violence and passiveness and heritable genes. However due to ever increasing technological advancements especially in the areas of media, it has become increasingly hard for scientists to identify meaningful relationships between our behaviour and our genes. For this reason the researchers from Tokyo University choose to study guide dogs due to their decreased cognitive complexity and the ability for them to raised in a fairly consistent environments.
The study revealed that polymorphisms within T471C in the SLC1A2 gene and G216A within the COMT gene were both significantly related to the relative activity levels of the dogs. These same genes in humans are associated with common behavioural disorders such as schizophrenia, bipolar disorder, OCD and ADHD. Thus these genes are believed to be involved in both aggressiveness and arousal. Overall the researchers concluded that further studies into these genes and other genes associated with behavioural attributes could assist in the selection of the most suitable dogs for vision impairment. Furthermore further studies into these genes could assist in the identification of heritable factors which cause debilitating behavioural and physiological conditions in humans.

Aimee Davidson 41885527

Article found at:
http://www3.interscience.wiley.com.ezproxy.library.uq.edu.au/cgi-bin/fulltext/121645332/PDFSTART
Picture found at:
http://www.famu.edu/TeachingGym/UserFiles/Image/Guide%20Dog2.jpg

no EYE-dea? well, have a look here.

Beauties such as the cascading hues of flowers in spring and the majestic colours of a rainbow after the rain are definitely worth to gaze upon. With this, it can be said that a world without sight truly is a dull one. However, one does not need to fear now as the family of genes which are responsible for the regeneration of the optic nerve have been recognized. This hence brings light upon the treatments for diseases such as optic nerve stroke, spinal cord injuries as well as neurodegenerative diseases of the spinal chord and brain.

It is the axons of retinal ganglion cells (RGCs) from the optic nerve which allow one to see as they aid in transmitting electrical impulses from the retina to the brain. Hence when one’s vision is impaired or lost, it is these RGCs which are damaged. Widely known, neurons have the potential to grow as usual during development and they can then switch off their growth ability when they are unable to reconnect efficiently as a result of diseases or injuries.

Nevertheless, with the discovery of a transcriptional repressor gene related to axon growth in RCGs and other central nervous system neurons namely the Kruppel-like- factor-4 (KLF4), regeneration of RCGs in the optic nerve is now made possible. Other than the KLF4 there is as well the KLF6, and these cluster of KLF genes have a regenerative purpose in several classes of the central nervous system. All in all with the discovery of these new wonders, researchers anticipate to further develop their studies in search of more beneficial uses for these genes.

the eyes are an ocean where dreams are reflected

xuyen lim [41349935]

http://www.medicalnewstoday.com/articles/167067.php

Don't want to on diet?

The number of people who has diabetes and over-weight problem are increasing in the developed country include Australia. However the scientists from University of Michigan made a new discover that may be able to help these sufferers.

The scientists found that if one of the genes in mice is missing, mice will “turn a high-fat diet into heat instead of body fat.” This gene called I kappa B kinase epsilon or IKKε, it “helps regulate inflammation also stops fat cells from wasting energy.” The study shows that when IKKε is missing in mice, on a high-fat diet they gain 8 grams less than the normal mice on average in three months. Even the mice still gain weight but it clear shows there is a link between the gene missing and mice’s energy balance.

Now days drug only help control diabetes or over-weight problem, people still need to change their diet and have to exercise to help with their conditions. If the “gene works the same way in humans as in mice,” this will be a great news also a new target for antiobesity drug.

4180639

http://www.sciencenews.org/view/generic/id/46990/title/Mice_with_mutation_feel_the_burn

Can Genes Replace Drugs?

With heart disease becoming an increasing problem in the developed world, there may be a new ray of hope out there for sufferers. The current treatment for heart disease is to take a cocktail of drugs to sustain the failing organ. Now, scientists from the University of Michigan and the University of Minnesota have teamed up and developed a new concept of treating the heart with genes.

The scientists modified a virus to carry a gene that would produce a protein that expressed a fast molecular motor, enabling heart cells to contract normally. They treated diseased hearts of rabbits and humans, containing slow molecular motor, with this modified virus and the diseased heart cells were again able to express this fast molecular motor, showing that the heart is healing itself.

Current drug treatments only provide a temporary solution to the problem, by depleting current sources of calcium to activate the contractions, and create problems of its own. Gene therapy goes to the crux of problem and aims to heal the heart. Dr Herron, from the University of Michigan hopes that this will open a new door for ‘closed heart surgery’.

42031518

http://www.sciencedaily.com/releases/2009/10/091005102649.htm

http://www.fasebj.org/cgi/content/abstract/fj.09-140566v1

11 genes responsible for Type 2 Diabetes identified thanks to...mathematicians

While it may seem an odd realm for mathematicians to be involved in, a team of mathematicians from Michigan Technological University have recently tried their hands at genetics. The team has built a series of programs which allow for the determination of specific gene combinations involved in severe and hard to treat diseases, particularly Type 2 Diabetes. Quiying Sha, an assistant professor at MTU, explains, “With chronic, complex diseases like Parkinson's, diabetes and ALS [Lou Gehrig's disease], multiple genes are involved [and] you need a powerful test.”

Previous attempts at determining the genes responsible for diseases such as Type 2 Diabetes have been an overwhelming task due to the sheer number of calculations required for possible gene combinations of the roughly 500 000 genes in the human genome. As such the team of mathematicians has developed not one but two powerful programs to handle these calculations, known as the Ensemble Learning Approach (ELA). The first program is designed to trace possible genes responsible for Type 2 Diabetes back through generations, much further back than previous analysis, allowing for the majority of genes to be ignored, thus greatly narrowing the number of possible combinations responsible for the disease.

With the field of possibilities now suitably thinned the genes are fed into the second program, this one a purely statistical system calculating possible combinations. After using the ELA to test genes from 1000 people, half without Type 2 Diabetes and the remaining half sufferers of Type 2 Diabetes, the ELA returned to the team 11 variations, known as single nucleotide polymorphisms (SNPs), within human genes that, separately or in various combinations, have a high probability of causing Type 2 Diabetes.

While the discovery of these 11 SNPs is a large achievement it is overshadowed by the future prospects for the Ensemble Learning Approach. With the programs now operational analysis is “relatively simple” according to Sha, and with the necessary data sets any genetic disease may be analysed for the genes responsible.

Jared Miles (42024211)

Article: http://www.sciencedaily.com/releases/2009/10/091006121115.htm

Picture: http://repairstemcell.files.wordpress.com/2009/02/diabetes_0

Blame that extra flab on your genes!

Are you a size 12 when you want to be a size 10? Don’t blame it on that piece of chocolate cake you just had, blame your genes! Genes that affect our appetite and energy have been associated with excess weight, according to papers published in the journal Nature Genetics in January this year. Scientists have made a genetic discovery that has linked obesity to how the brain functions, instead of how our food intake is digested.

The genomes of over 120000 people were studied by deCODE genetics in Iceland and it was found that the brain is the location of where most of these genes are triggered, focusing mainly in the hypothalamus. It was also discovered that age affected the genes and that at different ages, your weight is influenced by different mechanisms. At a young age, children were heavier when three of the genes were examined but when the other three genes were studied, there was no effect observed.

Of course these genes only affect a person’s weight in a small way, but more studies and experiments on this topic will further our knowledge and allow us to find possibly treatments for obesity.

For more information or to see the original article, visit http://www.ama-assn.org/amednews/2009/01/05/hlsf0106.htm#.




Alexandra Bongaarts
42015004

Genetic Screening & IVF

What if you could stop babies being born with genetic defects? According to research conducted in America, scientists have estimated that one in every 200 babies born will suffer from a single-gene disorder. This results in babies being born with genetically-inherited disorders due to one or two carrier parents. The scientists at the Genetics and In Vitro Fertilisation Institute in Fairfax, Virginia have developed numerous genetic innovations including that of creating embryos free from genetically inherited diseases. The way this is done is through tracking an inherited DNA segment from the parents to an embryo. Scientists are then able to conclude if the embryo of interest is affected with one of several genetic diseases.

This very same institute that has revolutionised IVF is currently working on a test called 24 Chromosome testing that can detect 18000 diseases prior to implanting embryos. Once available, this will revolutionise and change the face of IVF forever as it will greatly reduce the number of babies born with inherited diseases and yield healthy babies with little risk of carrier parents passing on defects. All this would not be called genetic engineering, rather genetic screening as scientists are in no way modifying embryos but selecting the healthiest embryos. For families with histories of inherited diseases, this scientific breakthrough could be the answer they’ve been waiting for and improve the quality life for all.

Josephine Fong (42054786)

Original article: http://www.cbsnews.com/stories/2009/10/01/earlyshow/health/main5355659.shtml

Turning off cancer

Cancer is a disease of the genes responsible for cell differentiation have been damaged or changed, causing an uncontrolled differentiation of those cells, which can eventually form a tumour and cause many other complications. One of our body’s means of stopping cancers is by the production of tumour-suppressor proteins, that bind to and stop cancerous cells from spreading.

However, researchers at Yale School of Medicine and Sichuan University in Chengdu, China, have found that these tumour-suppressor proteins are deactivated by a RNA molecule from a non-coding area of the genome. They found that in mice, the tumour could be stopped by removing this non-coding RNA which enables the body’s tumour-suppressor proteins to function properly. Researchers are continuing with this study in order to find a way to regulate or even eliminate this RNA from our cells, turning off the cancer's defence against tumour-supressor proteins.

Ben Lew (42005863)
Original article: http://www.sciencedaily.com/releases/2009/09/090923143341.htm

Mice can eat 'junk' and not get fat!

Researchers from the University of Michigan have discovered a gene that has the ability to act as a switch and avoid obesity in
mice. In mice, a gene called IKKE, which when deleted, stops the mice from gaining any weight. This gene in humans on the other hand can lead to type 2 diabetes which is related to obesity. Deletion of this gene in mice also protected them from chronic inflammation, a fatty liver and insulin resistance.

An enzyme in the gene, protein kinase, turn proteins on and off, in this case look for proteins which control the genes that regulate the metabolism in mice. When a normal mouse is fed a diet of high fat, its metabolism slows down as the protein kinase levels rise and the animals puts on some weight. However, when a mouse with a deleted IKKE gene is fed a fatty diet, the mouse's metabolism speeds up and more calories are burnt and are not stored as fat.

The team are now finding small molecules that might assist in blocking the IKKE protein kinase activity which can act as methods of drug development in association with obesity and diabetes.

By: Sara Sarkhoh (41870019)

Source: http://www.sciencedaily.com/releases/2009/09/090903163719.htm

Light controlled mouse cells

Scientiests have genetically encoded mouse cells to respond to light, creating cells that can be trained to follow a light beam or stop on command like microscopic robots.

We can generlly see this action in plant cells, how the plant cells will response to the sunlight to preform general metabolism. Now! Animal cells can do it as well.
This is the first time researchers have been able to import a light controlled "on-off switch" from plants into a mammalian cell to instantly control a variety of cell functions

This research is led by Klaus Hahn, Ph.D., and his colleagues at the University of North Carolina, Chapel Hill. In Sep. 13 advanced publicant presented this research.

The findings could have various therapeutic applications down the road, such as the ability to guide nerve cells to reconnect across a broken spinal pathway in a spinal cord injury. it offers both a powerful new tool in cancer and cardiovascular research, as well as the potential to ultimately control complex processes such as nerve growth.

This new reseach would be a great hope in order to use nutral resource to treat human diseases.

Reference: http://www.sciencedaily.com/releases/2009/09/090914111001.htm

Ran Luo 42005694

Gene Therapy for Life in Full Colour

A recent breakthrough in genetic therapy is promising a viable cure to red-green colour blindness in humans; one of the most common single locus genetic disorders in society.
The dichromatic vision associated with red-green colour blindness arises from a faulty or lacking L-opsin gene which creates visual photo pigments, which are sensitive to long and middle wavelengths used to detect red and green light. The idea behind this new gene therapy is to establish this gene within the eye of a patient, initiating the production of L-opsin and in turn enabling full trichromatic, or normal, vision.

Two monkeys, colour blind from birth, at the University of Washington were able to experience ‘normal’ vision for the first time with the use of this therapy. In order to do this a harmless recombinant virus containing the human L-opsin gene was inserted into the photoreceptor layer of the retina, where red and green cones are normally found. Once in the retina it was established that the pigment production of some of the blue-yellow cones were restricted, allowing the processing of red-green light at these sites while still maintaining blue-yellow vision.
After twenty weeks of daily testing, the monkeys began to respond to visual colour tests for both green and red colours, with their results eventually matching those of a control monkey known to have trichromatic vision.

One of the most interesting and promising aspects of this new technology is the fact that the monkeys who received trichromatic vision successfully were ‘middle-aged’. At first researchers believed that due to a lack of trichromatic neural pathways which are normally established during birth and development, that the monkeys would not be able to process the input of the red green light. Much to their surprise the middle aged monkeys were able to have full colour vision implying that in regards to colour blindness there is no need for evolutionary changes, just a third set of photo pigment cones. This is especially relevant for the possible treatment of adult human’s that have suffered colour blindness since birth, with the option of having colour vision restored at almost any age.
Although experimentation on this new gene therapy is in the early stages, the astounding results are promising a more colourful future for that suffer colour blindness.

By Elizabeth McCourt, 41777882
Original article: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature08401.html