Hundreds Of Cell-surface Proteins Can Be Simultaneously Studied With New Technique

So far, complex tissue cancer can only be diagnosed by using the antibodies method which will binds to the specific protein on the cancer cell’s surface. However, researches in Institute for Molecular Systems Biology at ETH Zurich and Julian Watts from the Institute of Systems Biology in Seattle (USA) had come out with the new method to develop better antibodies know as “Cell Surface-Capturing” (CSC).

According to the researcher’s leader, Bernd Wollscheid, this technique can identify a large number of proteins on the cell’s surface at certain time. The successful behind this method is, the researches use the fact that the protein’s surface is all glycoprotein in which then will broken into fragments by using an enzyme. Next, the protein’s fragments that attached to the sugar residue will then extracted by matching counterpart to the adaptor. Thus, these extracted fragments can be analysis for the mass and composition through the comparison with the protein databanks.

In short, through this new technology, different cell types or cancer forms and stages can be distinguished by looking at the differences in the quantity and type of the proteins on the cell’s surface.

By: 42111278

Reference:
http://www.sciencedaily.com/releases/2009/06/090606194216.htm

Intelligence Gene Identified

Researchers at The Zucker Hillside Hospital campus have discovered that the dysbindin-1 gene (DTNBP1) might have an influence on intelligence which is also linked to schizophrenia. "We looked at several DNA sequence variations within the dysbindin gene and found one of them to be significantly associated with lower general cognitive ability in carriers of the risk variant compared with non-carriers in two independent groups," said Katherine Burdick, leading researcher.

The experiment was carried out by measuring the cognitive performance of 213 patients with schizophrenia and 126 healthy volunteers. Researchers then analysed 6 specific variations of the participants’ SNP (single nucleotide polymorphisms) in the dysbindin-1 gene and discovered a correlation between one particular pattern, known as the haplotype, and general cognitive ability. Their data showed that there was a significant impairment in cognition in schizophrenia patient and carriers of this risk variant in the dysbindin-1 gene.

However this only accounts for about 3% of intelligence influence on humans while multiple genetic and environmental influences are the main factors. From previous understanding, the main function of dysdindin, however still debated, enables communication between brain cells whilst maintaining their survival in regions of learning, problem solving, judgment, memory and comprehension. If, however, an alteration has occurred in the dysbindin gene, this could reduce its effectiveness in maintaining the life span of brain cells and results in an increase in interruption between cell communications. Such discoveries as these could be the stepping stone in defining the origin of intelligences or assist in the further development in intelligence in humans.

http://www.sciencedaily.com/releases/2006/04/060427161424.htm

GM MONKEY WITH JELLYFISH GENE

Eight years back ANDi, the first genetically modified monkey carried green fluorescent protein (GFP) gene which being transferred from its parents. However, this is a faulty gene since ANDi cannot glow green as expected.

Now in present scientist is inserting this green fluorescent protein (GFP) gene into marmoset which is another monkey species. This is a very important research since if this genetic modification is a success, scientist will use GM monkey to study human disease since GM primates provide better model than GM mice.

For this research, viral vectors method was used to introduce green fluorescent protein (GFP) gene from jelly fish into the host cell (marmoset).The modified virus that carried the gene of interest is injected into the monkey embryos. Then, these embryos being inserted into seven surrogate mothers which four gave birth, producing 1 male and 4 female marmosets that carried the green fluorescent protein (GFP) gene.

Later, when the male baby was sexually mature, he successfully fathered a single offspring which also glowed green, showing that it had inherited the GFP gene. One of the females also produced IVF embryos carrying the gene thus shows that this research is success.

References:

http://www.newscientist.com/article/dn17194

http://www.newscientist.com/article/dn319-monkey-business.html

By: Siti Nur Hasanah Binti Mohd Yusuf

42102052

Genetic Link Found for Allergies and Asthma

There are many of us that suffer from allergies, from asthma to cat allergies. The good news is that research is beginning to show why these allergies occur and eventually new medications can treat allergies and other related issues. The Journal of Leukocyte Biology published a paper about newly discovered cellular on and off switch for allergies and asthma. The scientists who published this paper have determined that there is a gene which turns the immune system on and off. And that a miss function of this gene is what causes allergies and asthma.
Bone marrow cells are responsible for producing mast cells and cytokines; the cytokines essentially turn the immune system on. The bone marrow also uses the cytokines as an off switch to stop the production of mast cells. By experimenting with mice showed researchers that the “off switch” did not work correctly in those mice which were prone to allergies.
Therefore this research has concluded that allergies may be caused by genes which prevent the “off switch” from working properly. This research may lead to new treatments for allergies which will fix the problem which causes allergies instead of the allergies themselves.
Federation of American Societies for Experimental Biology (2009, May 4). Cellular On And Off Switch For Allergies And Asthma Discovered. ScienceDaily. Retrieved June 2, 2009, from http://www.sciencedaily.com¬ /releases/2009/04/090430101451.htm

First Testicular Cancer Risk Genes Found

A study conducted by the Institute of Cancer Research has found the first genes linked to testicular cancer. The genes of 730 men, who had at some time developed testicular cancer, were compared with those of healthy men. Most of the men who suffered from testicular cancer shared common DNA variants on chromosomes 5, 6 and 12, that weren’t present in the other men.

It has been known for some time that there was an hereditary aspect of the gene, but this is the first time that a gene has been pinpointed. The study found that men possessing these genes can be at a significantly higher risk of developing testicular cancer than men who don’t. Men who inherit the strongest of the three genes can be up to 3 times as likely to fall victim to testicular cancer. Men who have inherited all three of the DNA variants can be up to four times more likely to develop testicular cancer.

Researchers believe there are still more genetic risk factors related to testicular cancer. With the knowledge gained from this study, scientists are one step closer to being able to identify men of high risk factors, possibly leading to early detection or prevention.

Full article available from:
http://www.medicalnewstoday.com/articles/152190.php

By Melanie Johnston- 42001436

Discovery of a genetic link to reoccurring hair loss

A recent investigation undertaken by the National Institute of Genetics in Tokyo has identified a gene associated with hair loss (1). The findings of this study indicate that by blocking the activity of the Sox21 gene in mice, cyclic alopecia (or re-occurring hair loss) can be induced.

Previously linked to the formation of nerve cells, the Sox21 gene encodes for proteins which are capable of binding to DNA and are believed to assist in controlling the expression of specific genes. Kiso and co-researchers (2009) genetically engineered mice which were Sox21 gene deficient, and found that the hair of the mice fell out soon after birth, resulting in a completely hairless phenotype by the time the mice were 25 days old. Following this baldness, the mice hair took extended periods of time to grow back, only to fall out again.

When examining the expression of genes in the skin cells of the mice lacking Sox21 compared to normal mice, 5 genes were more active and 114 were less active. The less active genes are those which produce structural proteins and proteins which allow cells to adhere to one another. Examples of such cells are the keratin proteins, which are formed in hair cuticle cells. From this information, it can therefore be concluded, that a lack of the Sox21 gene causes a lower expression of the interlocking protein structures which anchor the hair shaft in the hair follicle, resulting in reoccurring hair loss.

It is thought that this gene functions in a similar way in humans as it does in the mice model. If, with further research, this suggestion remains true then investigation into the expression of Sox21 may lead to novel strategies for treating patients with hair loss disorders. The gene may also prove to be a useful indicator for people who are predisposed to hair loss. It is important however, that, as this gene is linked to the development of nerve cells, precautions are taken when influencing its expression in human.

Reference:
(1) Kiso, M, Tanaka, S, Saba, R, Matsuda, S, Shimizu, A, Ohyama, M, Okano, H, Shiroishi, T, Okano, H & Saga, Y, 2009, ‘The disruption of Sox21-mediated hair shaft cuticle differentiation causes cyclic alopecia in mice’, Proceedings of the National Academy of Sciences of the United States of America, Available: http://www.pnas.org/content/early/2009/05/25/0808324106.abstract

Original Article:
NHS Choices, 2009, Scientist ‘find hair loss gene’, 27 May, Accessed: 1/06/09 Available: http://www.nhs.uk/news/2009/05May/Pages/HairLossGeneBaldnessCure.aspx

Emma Davis (42065885)

World First: Chinese Scientists Create Pluripotent Stem Cells From Pigs

Scientists have managed to induce cells from pigs to transform into pluripotent stem cells. It is the first time in the world that this has been achieved using somatic cells from any animal with hooves.

Dr Xiao, leader of the research, and his colleagues succeeded in generating induced pluripotent stem cells by using transcription factors to reprogram cells taken from a pig's ear and bone marrow. A virus introduced the reprogramming factors into the cells and they changed and developed in the laboratory into colonies of embryonic-like stem cells. Further tests confirmed that they were pluripotent stem cells.

Pig pluripotent stem cells are useful in a number of ways, such as precisely engineering transgenic animals for organ transplantation therapies and creating models for human genetic diseases. To combat the swine flu, for instance, a precise, gene-modified pig could be made to improve the animal's resistance to the disease.

This could be done by first finding a gene that has anti-swine flu activity, or inhibits the proliferation of the swine flu virus and then introducing this gene to the pig via pluripotent stem cells. Alternatively, the swine flu virus receptor can be knocked out from the pig via gene targeting in the pluripotent stem cells so that the virus cannot proliferate and infect the pig.

The next stage of his research is to use the pig iPS cells to generate gene-modified pigs that could provide organs for patients, improve the pig species or be used for disease resistance.


Posted by:
42095743

Original Link:
http://www.sciencedaily.com/releases/2009/06/090602192557.htm

Journal reference:
Wu et al. Generation of pig induced pluripotent stem cells with a drug-inducible system. Journal of Molecular Cell Biology, DOI: 10.1093/jmcb/jmp003

Genetics Can Mediate Vulnerability To Alcohol’s Effects During Pregnancy

Teratogenesis is a condition that affects embryos causing defects in their development. A likely cause of teratogenesis is the consumption of alcohol while pregnant. This condition results in Foetal Alcohol Spectrum Disorders (FASD), which refers to a wide-array of effects due to alcohol-exposure. It occurs in approximately one percent of live births in the United States. However not every woman who consumes alcohol while pregnant gives birth to children that have
observable deficits.

A study done on mice has presented that alcohol-related susceptibility and resistance may be attributed to genetics.

To do the study, the researchers, led by Chris Downing, a research associate at the University of Colorado, used mice so they could control a variety of variables that impact teratogenesis and FASD. To control the differences in genetics the researchers bred five inbred strains of mice. They did this because every individual in an inbred strain is “virtually genetically identical, greater than 99.9 percent”.

The researchers gave the pregnant mice 5.8g/kg of alcohol (or malto-dextrin) on the ninth day of pregnancy which is approximately equivalent to day’s 28-31 of the human gestation period. On the eighteenth day of pregnancy the mice were put down and the foetuses were examined to identify any ‘gross morphological malfunctions’.

It was revealed that one strain of mice had foetal weight deficits. This strain also had malformations of the digits, kidney, brain, ventricle and vertebrae. Another strain, however, showed no obvious evidence of teratogenesis. The three remaining strains all showed varying degrees of teratogenesis.

These results emphasise that genetics does play a role in teratogenesis as the different genetic strains of mice are affected in different ways.

There is the possibility that these results could be extrapolated to human teratogenesis as mice and humans have an astonishingly similar genome, so it is reasonable to suggest that genetics could play a role in human teratogenesis as well.

Article Link:

http://www.sciencedaily.com/releases/2009/04/090422175142.htm

By Lachlan Hooper (42065607)

Stem cells without defects

It may now be possible to create stem cells from a patients own body which contain their own DNA except for the the target mutation. Scientists have recently reprogrammed tissue cells, from patients with anaemia, into stem cells which include the patients DNA sans the mutations responsible for their condition. These resulting cells are then grown into blood precurser cells which are the type that are usually transplanted into patients with this type of anaemia. In this case however, they contain the patients DNA rather than the donors.

Since these cells contain the patients own DNA, they can be introduced into their body without the risk of them being rejected by the body's immune system. In other words, the cells were identical to the patients original cells except that they didn't contain the genetic mutation responsible for the disease. Even though there still need to be a few more modifications to this process, it is a proof of concept, as well as being a significant breakthrough in the treatment of patients with genetic conditions.

42023915

Original article: http://www.timesonline.co.uk/tol/news/uk/science/article6402006.ece

Image: http://www.usask.ca/alumni/alumnisite/publications/green_white/issues/spring2006/cover_story.php

'Humanized' Mice Speak Volumes About Evolutionary Past

New research shows that mice carrying a "humanized version" of a gene believed to influence speech and language reveals important new insights into our evolutionary past.

Researchers says that changes in FOXP2 occurred over the course of human evolution and are the best candidates for genetic changes that might explain why we can speak.

FOXP2 is a gene that is implicated in the development of language skills, including grammatical competence.

The new research indicates that Mice with the human FOXP2 show changes in brain circuits that have previously been linked to human speech, and the genetically altered mouse pups also have qualitative differences in ultrasonic vocalizations they use when placed outside the comfort of their mothers' nests.

Although FOXP2 is active in many other tissues of the body, the altered version did not appear to have other effects on the mice, which appeared to be generally healthy.

Those differences offer a window into the evolution of speech and language capacity in the human brain and it will now be important to further explore the mechanistic basis of the gene's effects.

Reference

Cell Press (2009, May 31). Why Can We Talk? 'Humanized' Mice Speak Volumes About Evolutionary Past. ScienceDaily. Retrieved June 4, 2009, from http://www.sciencedaily.com­ /releases/2009/05/090528120643.htm

Variations in gene copy number and disease risk

Various studies conducted in Britain and America resulted in the groundbreaking discovery that variations between humans are predominantly due to differences in the copy number of key genes that make up the human genome (Connor, 2006). In fact, current research suggests that approximately 10% of the human genome is made up of multiple gene copies, and that human variability is determined to a greater extent by variations in the gene copy number than single-base variations that occur in the genetic code (Medical News Today, 2007).

According to researchers, this discovery may be utilised to explain why some individuals are more prone to certain diseases (Connor, 2006). It is believed that additional copies of genes may lead to an overproduction of the gene’s protein which may affect traits such as cancer risk (Medical News Today, 2007). In fact, scientists at the University of Washington and Nimblegen Systems Inc. have successfully developed a technique for identifying disease risk based on the method of identifying variations in the number of copies of particular genes (Medical News Today, 2007).

It is becoming increasingly apparent that many diseases and characteristic appear to be influenced by the number of copies of certain genes (Connor, 2006). For instance, Parkinson’s disease is associated with variations in the copy number of particular genes (Connor, 2006). Furthermore, direct relationships have been observed with disease severity and the number of copies of certain genes, as observed in a study which identified a relationship between the number of SMN2 gene copies and the severity of spinal muscular atrophy in children (Arkblad, Tulinius, Kroksmark, Henricsson, & Darin, 2009). Ultimately, greater research on variations in gene copy number will result in advancements in the understanding, medical treatment, and diagnostic tests for diseases such as cancer (Connor, 2006).

41807800

References
Arkblad, E., Tulinius, M., Kroksmark, A. K., Henricsson, M., & Darin, N. (2009). A population-based study of genotypic and phenotypic variability in children with spinal muscular atrophy. Acta Paediatrica, 98, 865-872.
Connor, S. (2006). Genetic breakthrough that reveals the differences between humans. Retrieved May 26, 2009, from http://www.independent.co.uk/news/science/genetic-breakthrough-that-reveals-the-differences-between-humans-425432.html
Medical News Today. (2007). Effects assessment of multiple copies of genes on disease risk. Retrieved May 26, 2009, from http://www.medicalnewstoday.com/articles/61987.php
Photo: http://www.latimes.com/media/photo/2008-04/37760560.jpg

Discovery Of Shared Genetic Link Between The Dental Disease Periodontitis And Heart Attack

A recent discovery of a gene has confirmed the link between Coronary heart disease and a dental disease known as periodontitis. For a long time it was believed that the two diseases were linked in some form but a genetic relationship between the two conditions has now been discovered.

The researchers discovered a genetic variant situated on chromosome 9 which was shared between the two diseases. a genetic locus on chromosome 9p21.3 that had previously been identified to be associated with myocardial infarction, in a group of 151 patients suffering from the most aggressive, early-onset forms of periodontitis and a group of 1097 CHD patients who had already had a heart attack were studied. The genetic variation associated with the clinical pictures of both diseases was identical according to the results. The scientists went on to verify the association in further groups of 1100 CHD patients and 180 periodontitis patients.They found that the genetic risk variant is located in a genetic region that codes for an antisense DNA called ANRIL and it is identical for both diseases.

Both CHD and periodontitis are propagated by the same risk factors, most importantly smoking, diabetes and obesity, there is also a gender relationship, with men possibly more liable to these diseases than women. Researchers have also shown similarities in the bacteria found in the oral cavity and in coronary plaques, and both diseases are characterised by an imbalanced immune reaction and chronic inflammation.

This discovery is significant as it can act as an alarm, if evidence of one of the diseases is showing then tests can be done to investigate susceptibility to the other disease and take appropriate preventative action.

http://www.medicalnewstoday.com/articles/151392.php
Source:
Mary Rice
European Society of Human Genetics
Article Date: 26 May 2009 - 4:00 PDT

By: Sebastian Egan 42041405

MicroRNA Protects Beta Cells

27th May 2009.

It has been recently discovered that short, noncoding RNAs are able to used to regulate important processes in the human body. For example, miRNA-375, which is present in the pancreas. Without this molecule, the beta cells in the pancreas degenerate, resulting in Diabetes.

MicroRNA was only discovered 10 years ago and research into the subject has revealed many new biological mechanisms. These RNA sequences can regulate as many as 100 genes at a time. They are found in specific cells and tissues - this fact has caused various pharmaceutical industries to conduct research using these RNA strands in the treatment of metabolic diseases and cancer.

miRNA-375 is highly concentrated in the beta cells of the pancreas. Beta cells play an important role in the regulation and control of glucose levels in the blood, as they produce the hormone insulin. Without insulin, the blood glucose levels rise and, if left untreated, the person becomes severely unwell. Without miRNA-375, the beta cells cannot grow and divide and therefore die. This leads to an overall decrease in the number of beta cells, which reduces or even completely stops the production of insulin, leading to Diabetes.

Because of their ability to regulate genes, if it were possible to influence the action of microRNA it could be possible to manipulate cells and organs to modify the development of certain conditions and diseases. The short RNA strands can be inactivated in a specific way, by a product called an Antagomir. These antagomirs can be produced synthetically and bind perfectly to the corresponding microRNA, destroying them in an efficient manner.

It is expected that this new information and the related scientific methods will be used to prevent or treat many types of medical conditions and diseases in the future.

link: http://www.sciencedaily.com/releases/2009/04/090425203534.htm

Gene Discovery Sheds Light on Childhood Cancer

Pleuropulmonary blastoma (PPB) is a rare and aggressive form of childhood lung cancer, affecting only 50 to 60 children globally a year. If identified early, it has a 90 percent cure rate however; doctors rarely expect to find lung cancer in newborns or young children. If not treated correctly, children diagnosed with PPB only have a 40 percent chance of survival.

Researchers have found that children diagnosed with PPB are born with a mutation in DICER1, a master controller gene that helps regulate other genes. In addition to this, children have normal looking cells in their lungs that appear to cause neighbouring cells to turn cancerous.

About 40 percent of cases of PPB are found in children whose families have a history of some kind of cancer, suggesting an inherited genetic cause. Researchers were surprised to discover the mutation in DICER1, which is named for its function of chopping up large molecules into smaller molecules called microRNAs that help regulate other genes.

The children with the DICER1 mutations had the defect in every cell of their body. The fact that the cell induces cancer in neighbouring cells has never been seen by scientists before. The next step for researchers is to attempt to develop a test for the DICER1 mutation that can be used to identify whether children born to high-risk families carry it and are at high risk themselves.

Researchers say that the discovery of this unexpected genetic mutation represents a whole new mechanism for the development of cancer. They also believe that the finding may shed light on adult cancers.

Published by 4209763
27^th May 2009

Reference:

Fox, Maggie (2009). Gene discovery sheds light on childhood cancer. Reuters.