24 September 2009
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
23 September 2009
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
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.htmlLinh Esmail 42067357
22 September 2009
Lose the Y chromosome, gain a new species?
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)
15 September 2009
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
10 September 2009
The Gene That Causes Premature Skin Aging
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
09 September 2009
Body Clock Linked to Weight Gain?
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
08 September 2009
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.
07 September 2009
Is a three-parent family the way to go?
In the UK, a research group have been experimenting to try and create an embryo which is linked to three individuals, biologically. Surprisingly, this is not the first time that researchers have tried to create three parent embryos. In the 90s, a genetically modified human was created from adding a section of a woman’s egg into another. This was initially done help prevent infertility, but was quickly banned by the US Food and Drug Administration.
To this day, researchers are certain that by replacing the faulty mitochondria in the eggs of women with the healthy ones of another female it can help prevent future children from inheriting diseases, such as diabetes, heart disease and deafness. As a consequence, the resulting children would have nuclear genes from the couple and mitochondria DNA from the other ‘mother’. The reason another female’s mitochondria is used is due to the fact that mitochondria’s can only be transferred through the mother. Males do contain many mitochondria in their sperm, but they are destroyed once it enters the egg.
Mitochondria do not only affect common and rare diseases, but it can also affect one’s sporting ability, longevity, intelligence and so forth. This means that we can also have the power of creating designer babies with traits stereotyped by the public. Not only will it be a highly debated topic, but it can so have a big consequence in other traits. This is evident in Japan, when the mitochondrial group measured the highest intelligence, but they were extremely likely to have a heart disease. However, researchers believe that they can minimise these consequences by choosing females who have a high mitochondria compatibility with the nucleus of the female whom has a faulty mitochondria. By choosing compatible mitochondria, it would decrease possible inherited dangers through this method.
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Reference: Lane, N. (2008). Genetically modified humans: Here and more coming soon. Available: http://www.newscientist.com.ezproxy.library.uq.edu.au/article/mg19826591.700-genetically-modified-humans-here-and-more-coming-soon.html. Last accessed 6 September 2009.
IMAGE: http://www.smh.com.au/ffximage/2008/02/05/embryo_wideweb__470x338,0.jpg
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Kylie Poon (42043593)
Cultivating Sperm Cells
Many people regard childbirth as one of the most extraordinary, memorable and life changing experience in their lives. Unfortunately, for reasons not yet known to scientists, childbirth is physically impossible for people suffering from infertility.
It is known that from a human embryonic stem cell, develops a type of primordial germ cell called germline stem cells which are set aside during development of the embryo. When the baby is born, these germline stem cells form gonocytes, and then adult male sperm stem cells which have the ability to produce sperm cells.
Their research also showed that while male embryonic stem cells, carrying XY chromosomes, were able to perform meiosis and mature into adult sperm cells, they were unable to do so with female embryonic stem cells, concluding that the genes in the Y chromosome may play an integral part in allowing for successful cell division and subsequent development into functional adult sperm cells.
UK scientists have announced that they have developed a way to mimic the conditions in which this development from human embryonic stem cell to male sperm stem cells occurs. They are hoping that their research will allow for better understanding of the cause of infertility and possibly new forms of treatment.
http://www.medicalnewstoday.com/articles/156730.php
Shu-Ying Chang 41798261
Tutor: PW