A team of scientists (lead by Kevin Eggan) from the Harvard Stem Cell Institute (HSCI) and Columbia University have produced human stem cell lines from the cells of two elderly men suffering from Amyotrophic Lateral Sclerosis (ALS), commonly known as Lou Gehrig’s disease.
The team turned skin cells collected from elderly patients with ALS into induced pluripotent stem (iPS) cells. Pluripotent cells are cells that can develop into many different cells and tissues in the body. Induced Pluripotent stem cells are artificially derived from non-pluripotent cells by inducing ‘forced’ expression of certain genes. They then directed the iPS cells to differentiate into the nerve cells that are killed by the disease. Using this method allows limitless supplies of the cells to be grown.
To produce iPS cells, four DNA transcript factors (Klf4, Sox2, Oct3/4 and c-Myc) were integrated into adult cell genome. This process eliminates the need for embryo’s.
This breakthrough gives hope that one day it may be possible to treat patients with chronic diseases through stem cell derived from their own cells. Currently the newly created cells cannot be tested in human subjects as one of the four transcript factors (c-Myc) is cancer causing.
To view original article; http://www.huliq.com/65502/neurons-created-skin-cells-elderly-als-patients
Wednesday, April 22, 2009
Nine New X Chromosome Genes Linked to Learning Disabilities in Males
An international team of 70 researchers have now determined nine new genes on the X chromosome which lead to learning disabilities if knocked out. The team studied nearly all X chromosome genes in as many as 208 families with these disabilities, in what was the largest screen of this sort ever reported. 720 out of the approximately 800 known genes on the X chromosome were sequenced. It is estimated that the prevalence of learning disability is 2 to 3 per cent and is much more common in males than females. This is obviously because it is more likely for a gene mutation to occur on the X chromosome of males, as they only have one X chromosome compared to females, who have two.
As well as these new gene discoveries, there was another significant finding which stunned researchers. This was that approximately one to two per cent of X chromosome protein coding genes have no effect on an individual in any respect, when knocked out. Geneticists have already said that further research is needed in this area due to the effect this finding will have on following studies. From now onwards researchers must be wary of the fact that just because a knocked out gene in an individual with a particular disease is present, does not mean that this gene is the causal factor of the disease.
The next step now is to implement this improved knowledge of the complex of genes in clinical practise. Genetic counselling is already offered to families with learning disabilities. However, these new findings will improve the provision of diagnostics to families and allow for more comprehensive genetic counselling, which will allow family members to make more efficient decisions. Although improved treatments in this area are waiting to be developed, information this research can bring will provide support to effected families. Families will also be able to make better informed reproductive choices.
Reference:
Wellcome Trust Sanger Institute (2009, April 20). Learning Disabilities In Males: Nine New X Chromosome Genes Linked To Learning Disabilities. ScienceDaily. Retrieved April 22, 2009, from http://www.sciencedaily.com /releases/2009/04/090419133841.htm
Advances in genetics and molecular biology allow better understanding of Cystic fibrosis.
Cystic Fibrosis (CF) is a hereditary disease that specifically targets the lungs and the digestive system. This disorder causes sickness by disrupting cells that make up sweat glands and the lining of passageways inside the liver, pancreas, lungs and the digestive and reproductive systems. These cells are otherwise known as epithelial cells. Patients suffering from CF inherit a trait that forces the epithelial cells to produce a faulty form of protein called Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). The faulty protein results in a lack of regulation of chloride through the cell membrane. Consequently, essential balances between salt and water (two vital ingredients in maintaining the mucous and liquid) are disrupted which causes a thickening of the mucous inside lungs, allowing germs to congregate and infect the sufferer of the disorder (refer to image on right). Cystic fibrosis affecting the pancreas involves a mucous blockage and results in a lack of digestive enzyme secretion. Sufferers of CF inside the pancreas generally have difficulties gaining weight even with a normal appetite and a healthy diet.
Until of late, knowledge of the biochemistry of CF has been severely lacking. Advances in molecular genetics have allowed geneticists to discover that the CF’s loci is coded on chromosome 7. On top of that, a protein known as the CF antigen is coded on chromosome 1. In non sufferers of CF, the products of the two genes interact with each other in a balanced matter to enable normal catabolism. Other discoveries also suggest that the structure of CF antigen possibly regulates ion transport. Another discovery that clarifies the difficulty in examining fetuses at risk of CF is that restriction fragment length polymorphism markers (structures on the chromosome that prevent prediction of gene expression in babies) are closely linked to the CF gene.
Until of late, knowledge of the biochemistry of CF has been severely lacking. Advances in molecular genetics have allowed geneticists to discover that the CF’s loci is coded on chromosome 7. On top of that, a protein known as the CF antigen is coded on chromosome 1. In non sufferers of CF, the products of the two genes interact with each other in a balanced matter to enable normal catabolism. Other discoveries also suggest that the structure of CF antigen possibly regulates ion transport. Another discovery that clarifies the difficulty in examining fetuses at risk of CF is that restriction fragment length polymorphism markers (structures on the chromosome that prevent prediction of gene expression in babies) are closely linked to the CF gene.
Sources:
http://www.annclinlabsci.org/cgi/content/abstract/18/4/289
http://ghr.nlm.nih.gov/condition=cysticfibrosis
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Do aliens share our genetic code?
Do aliens share our genetic code?
All terrestrial life forms are somewhat alike and share the same 20 amino acids. Biochemists at McMaster University in Hamilton, Ontario, Canada, conducted experiments which simulated various lifeless pre-biotic environments and managed to synthesize 10 of these amino acids.
Image 1: Jabba the Hutt (aka alien)
Two of the biochemists from the University, Paul Higgs and Ralph Pudritz, pointed out that each of the experiments produced the same group of 10 amino acids. They then calculated that these 10amino acids require the least amount of energy to form. They then suggest that from these results if alien life did exist it would have the same 10 amino acids at its core.
“Do aliens share our genetic code?” New Scientist, Retrieved April 22, 2009 from http://www.newscientist.com/article/dn16930-do-aliens-share-our-genetic-code.html
Blog by: Jarrad Oxley 41728576
All terrestrial life forms are somewhat alike and share the same 20 amino acids. Biochemists at McMaster University in Hamilton, Ontario, Canada, conducted experiments which simulated various lifeless pre-biotic environments and managed to synthesize 10 of these amino acids.
Image 1: Jabba the Hutt (aka alien)
Two of the biochemists from the University, Paul Higgs and Ralph Pudritz, pointed out that each of the experiments produced the same group of 10 amino acids. They then calculated that these 10amino acids require the least amount of energy to form. They then suggest that from these results if alien life did exist it would have the same 10 amino acids at its core.
“Do aliens share our genetic code?” New Scientist, Retrieved April 22, 2009 from http://www.newscientist.com/article/dn16930-do-aliens-share-our-genetic-code.html
Blog by: Jarrad Oxley 41728576
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