World First: Chinese Scientists Create Pluripotent Stem Cells from Pigs

A scientist named Dr Xiao and colleagues have managed to induce cells from pigs to transform into pluripotent stem cells (cells that, like embryonic stem cells, are capable of developing into any type of cell in the body). It is the first time in the world that this has been achieved using somatic cells (cells that are not sperm or egg cells) from any animal with hooves (known as ungulates).

Dr Xiao succeeded in generating induced pluripotent stem cells by using transcription factors to reprogram cells taken from a pig's ear and bone marrow. After the combination of reprogramming factors had been introduced into the cells through a virus, the cells changed and developed in the laboratory into colonies of embryonic-like stem cells. Further tests confirmed that they were, in fact, stem cells capable of differentiating into the cell types that make up the three layers in an embryo – endoderm, mesoderm and ectoderm – a quality that all embryonic stem cells have. The information gained from successfully inducing pluripotent stem cells means that it will be much easier for researchers to go on to develop embryonic stem cells that originate from pig or other ungulate embryos. Dr Lei Xiao, who led the research, said: “it is entirely new, very important and has a number of applications for both human and animal health."

Pig pluripotent stem cells would be useful in a number of ways, such as precisely engineering transgenic animals for organ transplantation therapies. They could also be used to create models for human genetic diseases. However, Dr Xiao warned that it could take several years before some of the potential medical applications of his research could be used in the clinic.

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

Why Can We Talk? 'Humanized' Mice Speak Volumes About Evolutionary Past

Mice found with a gene, similar to the human gene that is believed to influence speech, tho unable to speak show a huge link to humans evolutionary past. This is because human and mice’s genes are essentially the same and they work similarly. This study gives us a first glimpse that mice can be used to study not disease but also the history of human evolution. It is only in the last decade or so that scientist have discovered how similar mice and human genes are.

Wolfgang Enard of the Max-Planck Institute for Evolutionary Anthropology said that his team studies the genomic differences between humans and other primates. And important difference between humans and chimpanzees that has been studies by the team is two amino acids substitutions in FOXP2, these changes became fixed once human’s lineage had split for chimpanzees. Many changes in FOXP2 have occurred over the course of human evolution and this is the most likely candidate for the genetic changes that allow human speech. The study to determine this cannot be done on humans for obvious reasons. This lead researcher to introduce the substitutions into the mice’s FOXP2 gene, they identified that the mice’s gene is identical to that of chimpanzee’s so this is a reasonable model for ancestral human version.

Mice with the human FOXP2 show changes in brain circuits that have previously been linked to human speech. Intriguingly enough, the genetically altered mouse pups also have qualitative differences in ultrasonic vocalizations they use when placed outside the comfort of their mothers' nests. However Enard stated that not enough is known about mouse communication at this time to read to much into what this means. 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.

The study of FOXP2 has shown that people with one nonfictional allele have show impairments in the timing and sequencing of orofacial movements, one possibility is that the amino acid substitutions in FOXP2 contributed to an increased fine-tuning of motor control necessary for articulation. Through the further studies of human mice and other primates the reason for speech will be discovered.

Original article: http://www.sciencedaily.com/releases/2009/05/090528120643.htm

Adam Gauger -42014016

Drug hope for advanced melanoma

Skin cancer, which is caused by excessive exposure to ultraviolet radiation, generally from the sun, is the most commonly diagnosed form of cancer. The most deadly form of this cancer, melanoma, claims many lives around the world every year. Currently melanoma is very difficult to treat when it is at an advanced stage, with less than 5% of those diagnosed with malignant melanoma which has spread around the body, live for more than two years. However UK scientists believe that they have discovered a drug that can treat the melanoma skin cancer in its most advanced incurable stages.

Two UK scientists, Roche and Plexxikon, have discovered that an experimental drug, PLX4032 (R7204) has the potential to help many patients with the incurable disease live longer and keep the disease in check. They presented their findings at a recent renowned US cancer meeting.

60% of malignant melanomas are implicated with a mutation called the BRAF mutation. The PLX4032 drug works by seeking out and destroying tumour cells which carry this mutation. This can help to not only shrink the size of the skin cancer, but also delay its spread. The early findings of their study involving 16 patients, with BRAF positive melanoma and treated with PLX4032, saw that over half of the patients saw the extent of their cancer reduce by at least 30%. These patients also lived for a median of six months without their disease getting worse. This included patients where the cancer had spread to the liver, lung and bone.

Current treatments for advanced melanoma, such as chemotherapy, can lead to an improvement in symptoms and quality of life but does not greatly extend life as this drug has the potential to do. The results are very exciting especially in areas such as Queensland which holds claim to the title “skin cancer capital of the world”, however there is still a long way to go. Dr Jodie Moffat of Cancer Research UK said: “While these results are interesting, they need to be followed up in much larger studies before we know if this is a new treatment for people with advanced melanoma.”

By Hannah Brodie - 41770436

Link :

http://news.bbc.co.uk/2/hi/health/8076743.stm

Possible cause of Alzheimer’s disease caused by hyperphosphorylation of tau proteins may have a genetic link.

A recent discovery by researchers at McGill University and Lady Davis Research Institute for Medical Research at Montreal's Jewish General Hospital promises to help in the diagnosis and curing of Alzheimer’s disease. They found that in patients will AD, there was a hyperphosphorylation (extra phosphate added) to one of the amino acids on a tau protein in the CNS. The 6 isoforms of Tau proteins are involved in the stabilisation of microtubules by their reaction with tubulin. When they are hyperphosphorylated, it causes a protein cascade with interaction between tau proteins resulting in neurofibrillary tangles that cause the neuron transport system to fail. This causes incorrect signals to be sent, and eventually neuron death. These tangles often occur in older individuals, but not on nearly as large a scale as in a patient with AD. A protein called beta-amyloid that builds up in neurons is also associated with AD, and thought to help cause cell death by interrupting cell homeostasis, causing apoptosis. By investigating the cause of this hyperphosphorylation, and build up of beta-amyloids, researchers hope to eventually find a cure for AD, as they believe that this hyperphosphorylation may be genetically linked. APOE is a gene that is present in 50% of late-onset Alzheimer’s disease cases. Genetic interpretation of this gene could help to find a cure, and genetic modification of this gene in embryos could also help to cure it.

This discovery is very important, as Alzheimer’s disease is a very prominent disease in society’s elderly, and can have disastrous effects, such as initially short-term memory loss, then as the disease progresses, resulting in greater cognitive degeneration, confusion, irritability, mood swings, language breakdown and long-term memory loss. This draws on many of the concepts covered in the course, such as protein interactions, protein cascades, genetic modification and interpretation.

Andrew Buchan - s4202068

http://www.genengnews.com/genCasts.aspx

http://www.ncbi.nlm.nih.gov/pubmed/11801334

Transgenic monkeys pass on glow in the dark gene to offspring

A team of Japanese scientists have genetically modified monkeys whose hair, skin and blood glow when exposed to UV light and who have passed on this gene to their offspring, making them the first transgenic animals to do so.

The discovery was made by a team of scientists led by Erika Sasaki from the Central Institute of Experimental Animals and Professor Hideyuki Okano of the Keio University School of Medicine.

The team used viral DNA to integrate a fluorescent jellyfish gene for green fluorescent protein (GFP) into the common marmoset causing them to glow green. The researchers hope that the transgenic marmosets can one day be breed to study infectious human diseases, immunology and neurological diseases such as Parkinson’s disease.

Dr Kathie Raphael, a lecturer in Genetics at the University of Sydney explains how it could work saying, “If you want to study motor-neurone disease or Parkinson's disease, and you have a candidate gene that you believe causes the disease, then you introduce that gene into the monkey and…observe the effect that it has… if it causes the types of symptoms that it does in humans… then you've got a model to study the disease and try treatments."

link:

http://livenews.com.au/rss-link/breakthrough-as-glowing-monkeys-have-glowinthedark-babies/2009/5/28/208010


original research published in science journal Nature




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