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

GM Rice and Allergies

Allergies affect a large percentage of the population and by the genetic modification of rice; a solution to this common problem may develop in the very near future. A research team from Japan’s National Institute for Agrobiological Sciences led by researcher, Fumio Takaiwa, have designed rice for people allergic to Japanese cedar pollen, blocking symptoms of runny noses and sneezing. This rice has been genetically modified to contain seven proteins of cedar pollen which provoke allergic reactions. Upon regular ingestion of these proteins, patients develop an “oral tolerance” to them and allergic responses are dampened down because the immune system learns not to overreact to harmless foreign material.

The proteins have been engineered in rice such that they are produced the endoplasmic reticulum, a part of plant rice cells that does not digest in the stomach. This strategy allows the proteins to have their effect, which is soon to be proven by the clinical trials on people. This follows the assessment conducted on macques that has affirmed the safety of these different proteins. If successful, this genetic modification of rice strategy would expand to other allergies like house mites, and thus further eliminating the need for antihistamines products like nasal sprays and eye drops.

http://www.newscientist.com/article/dn17413-gm-rice-makes-allergies-easy-to-stomach.html
Linh Esmail 42067357

Lose the Y chromosome, gain a new species?

Photo by Biophoto/Photo Researchers

The human X and Y chromosomes were originally differentiated from a pair of autosomal (non-sex) chromosomes which could readily share DNA. Once these two separate chromosomes emerged, they each had an additional region of DNA for the expression of sex; after the initial divergence, some X-degenerate genes were retained on the Y chromosome, even though these genes were probably unnecessary. As the chromosomes evolved, it became evident that the Y chromosome had a much faster evolutionary rate than the X chromosome. This may have facilitated the development of mutations within the Y chromosome, causing the somewhat rapid deletion of genes from non-recombining regions; there are now under 200 working genes left on the chromosome. The X chromosome, however, retained the majority of its genes through a slower evolutionary rate similar to that of the original autosomal pair, and functions with approximately 1100 working genes.

It is speculated that most genes were lost from the Y chromosome because they were deemed unnecessary for the survival of the species, though in a study done on the evolution and survival of sex chromosomes, it was found that many of the genes on the Y chromosome have functions that are completely unique to the function of genes on the X chromosome. This suggests that certain genes carried only on the Y chromosome are important and should be retained, which is why degeneration of the male chromosome is providing interesting theories as to what will happen if the chromosome disappears completely.

One such theory is that an entirely new species will evolve with the demise of the Y chromosome, though if this actually eventuated, it is speculated that it would take from 6 - 15 million years. This is not to say that the male population will become extinct; the missing genes that are vital for making humans male that are usually found on the Y chromosome could be expressed on the X chromosome instead. It is thought that non-sex chromosomes would start functioning as sex chromosomes for males, though this could potentially give rise to DNA mutations resulting in a variety of structural, physiological or behavioural changes that could significantly alter the way in which the theoretical new species functions.

The possibility of a new species seems far-fetched, though there is no way to correctly predict what would happen to the human race given the loss of one sex chromosome. It is thought that the male species would have to develop in some way to deal with the loss, the consequences of which will be unknown until the need for such evolution arises, if indeed it ever does.

Amy Pammenter (42002198)

Journal:

Wilson, A.M., Makova, K.D. (2009) Evolution and Survival on Eutherian Sex Chromosomes. PLoS Genetics. 5:1 - 11

(Picture from http://www.popsci.com/files/imagecache/article_image_large/files/articles/sci0206Ychrom_485.jpg)

One of the most prevalent problems existing in the fight against bacterial infections is their ability to develop a resistance to antibiotics. For long term patients, this means multiple changes to new antibiotics each time the bacteria develop a resistance. The main issue with this is when the point is reached that there are no new antibiotics. Researchers are dedicated to continually finding new medications for fighting infections, but a discovery has been made that may make the need for this redundant. Scientists at New York University have examined the effect of antibiotics on bacteria and discovered that antibiotics compel bacteria produce charged particles which damage their DNA and lead to their eventual death. Unfortunately, the bacteria are also able to produce nitric oxide which protects them from the particles and leads to the resistance to antibiotics.

The possibility of reducing the resistance to antibiotics comes from the exploration of compounds to act as inhibitors to the enzymes involved in the production of nitric oxide. Due to the fact that bacteria use nitric oxide to protect themselves against a range of antibiotics, the discovery of effective nitric oxide synthase inhibitors would be extremely beneficial to society. Hindering the resistance of bacteria could save the many thousands of lives which could possibly be lost to drug-resistant bacteria.

Article Source : Steenhuysen, Julie 2009, 'Study exposes how bacteria resist antibiotics', News Daily, Article, Sep 10, Science Daily, [Online], Available: http://www.newsdaily.com/stories/tre5895rz-us-bacteria-antibiotics/#

Image Source: http://www.offthemarkcartoons.com/cartoons/2000-08-24.gif

The Gene That Causes Premature Skin Aging

When someone says one looks younger than one’s real age and there is no wrinkles on the face, it makes that person so happy, and that is what every person is trying to achieve. External beauty now given so much of importance to life and it does not only involve the female gender but the male ones too. Dr. Reversade and his international research team had found out that mutations in PYCR1 gene cause the rare genetic condition that causes the premature skin aging or wrinkly skin syndrome. Dr.Reversade had identified the PYCR1 gene on chromosome 17 is defective and found specific mutations in the gene that led to the conditions in the elderly people such as loose skin, cataract and many others. The two tissues which have high levels of PYCR1 proteins are skin and bones. By developing therapies that increases the activity of the PYCR1 protein has the high chances to reverse the process aging in individuals who suffer from this genetic condition and slow the in the normal people.

They also had found out that the PYCR1 protein is located in mitochondria. They observed changes in mitochondrial morphology and cell death in tissues with individuals with PYCR1 mutations. When PYCR1 is mutated, the mitochondrial is not working properly which results in increased occurrence of cell death. this shows the significance of mitochondrial function in aging process. Dr.Reversade and his research team also highlighted that metabolism is important as PYCR1 is important in synthesis of proline, a common amino acid involved in metabolism. Age-defying and anti-wrinkling treatments for ageing also can benefit from proline metabolism. Basically, this PYCR1 gene plays an important part on our skin condition, if its mutated it can cause the genetic condition. If the scientists in future could increase the activity of the PYCR1 protein in the mitochondrial, we could be looking at youthful and healthy looking skin.

Mohana E. Ragu
42129693

Sources:
Website: http://www.sciencedaily.com/releases/2009/08/090831213214.htm
Journal Reference: Reversade et al. Mutations in PYCR1 cause cutis laxa with progeroid features. Nature Genetics, 2009; DOI: 10.1038/ng.413
Adapted from materials provided by Agency for Science, Technology and Research (A*STAR), Singapore, via EurekAlert!, a service of AAAS.

Fighting Cane Toads with Genetics

Large double stranded DNA viruses were one of the first to be constructed into recombinant viruses. One of tese large double stranded DNA Iridoviridae, a genre of virus which infects invertebrates and cold blooded vertebrate, has yet to be used to construct recombinant viruses.
The researchers found and isoltaed a non-essential gene, the viral homologue of eukaryotic initiation factor eIf 2alpha, in Bohle iridovirus. A recombinant Bohle iridovirus was then created with the neomycin resistance gene and the Cane Toad adult globin gene. This was all inserted into the eIF 2alpha region mentioned earlier.
Adult globin expressed by the virus was detected on western blot which shows that the recombinant iridovirus can express the foreign genes. This shows evidence that stains of recombinant iridovirus could be used as a means of controlling Cane Toad populations.

Refernece: Pallister J. Goldie S. Coupar B. Shiell B.
Michalski W., 'Siddon N. Hyatt A. Bohle iridovirus as a vector for heterologous gene expression', Journal of Virological Methods vol. 146 (2007) pp. 419–423, viewed 7 September, 2009.

Image From: http://images.the-scientist.com/supplementary/flash/54509/images/IMG_7582.jpg

Summarised by Luke Carpenter 41776791

Body Clock Linked to Weight Gain?

Could that midnight trip to the fridge be doing more damage to your body than you think?
Most people know that it is poor dietary standards if you eat anything right before you go to bed. According to a study published in the Journal of Obesity It was found that the body’s natural circadian rhythm and related rest cycles might also play a roll in weight gain than once previously thought.
Almost One-third of the people living in the US are considered Obese. "How or why a person gains weight is very complicated, it is clearly not just a matter of calories in and calories out," Fred Turek, a professor at Northwestern University's Weinberg College. Researches at Northwestern University were interested in conducting a study that involved late-night shift workers. This was simple due to the fact that their schedules force them to eat at times that conflict with their natural body rhythms". Placing them as the best candidates for this experiment. This is one piece of evidence that got scientist thinking – eating at the wrong time if the day might be contributing to weight gain. So they started an investigation with this experiment.
To compare these results another experiment was conducted using mice. The mice were divided into two groups Active period eaters and rest-period eaters. The mice that were given unlimited access to high-fat food only during their normal rest periods increased in heft by 48 percent, whereas those given unlimited access to fatty food during their normal activity periods put on about 20 percent of bulk over their baseline.
In 2007 researches located Nocturnin, a gene that works in both circadian clock and in controlling weight gain in fatty diets. As can be seen a simple thing such as shifting snack time could in fact help some people trim down "Better timing of meals, which would require a change in behavior, could be a critical element in slowing the ever-increasing incidence of obesity," Turek said.

Bridgette-Rose Taylor 41724345
Reference :http://www.scientificamerican.com/blog/60-second-science/post.cfm?id=body-clock-linked-to-weight-gain-2009-09-03

Monoclonal Antibodies Based on Genotype

Monoclonal Antibodies Based on Genotype
s41743001

For those of us studying pharmacy, recent advances in genetics are having an increasing impact on our careers. As mapping the human genome becomes more accessible and less expensive, we may find ourselves tailoring pharmaceutical treatments to our patients’ individual genetic information. There are many benefits to this. In current practise, patients are initially prescribed the medication which has proved most effective and cheapest to produce, in the majority of individual cases. If they react poorly to the first drug, health professionals can attempt alternate therapies, until the best option is found. However, if we could predict how patients would react to medication based on genetic information, we could immediately give the medication most likely to work for them, without wasting money and time on trial treatments.

Already, advances in genetics enable treatments to be chosen based on genotype. Monoclonal antibody therapy can be used to treat autoimmune diseases and cancer, and is undergoing clinical trials for many other conditions. This treatment has an advantage over many others, because it targets very specific pathogens and induces an immune response. It can be very successful in some patients, but has no effect on others due to natural variations in the shape of a receptor protein on the surface of immune cells.

The company PIKAMAB has produced a test which determines whether patients are expected to respond well to therapy or not. The test divides patients into 9 groups based on their immune cell receptor types. The company’s CEO suggests that different antibodies should be produced, one to suit each patient type, to maximise effectiveness of monoclonal antibody treatment. If the drug can be optimised, cancer patients may be able to use the treatment without combining it with radiation or other cytotoxic therapies, reducing side effects and increasing quality of life.

Refer to http://www.technologyreview.com/biomedicine/22795/page1/ for further detail.