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by Simon Hadlington
Researchers in the Czech Republic have shown that an unusual class of boron-containing compound can inhibit HIV protease, a key enzyme involved in replicating the virus that causes Aids. The finding is potentially signficant because the compounds - metallacarboranes - attack the enzyme in a different way to most existing drugs and could help overcome problems of resistance.
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- Parent Category: Chemistry
- Category: Medicinal
Together with a surgical team at University of Oxford we are developing novel tissue expanders for use in reconstructive surgery, with the ability to expand in only one direction. Tissue expanders are essential in providing extra soft tissue for a wide range of reconstructive techniques. However they have a number of disadvantages. Inflatable silicone balloons are bulky and unsuitable for small delicate areas. They must be regularly inflated by means of a filling port, which is both time demanding and painful for the patient and there is a risk that the device may leak. Self-inflating hydrogel expanders have heralded a significant advance. However they expand isotropically at an uncontrolled rate and have limited expansion limits. Therefore their use in specific applications such as cleft palate surgery, syndactyly (fused digit) release and facial reconstruction has been limited.
Read more: Novel Tissue Expanders for Maxillo-Facial Reconstruction
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New research shows that a protein often accused of sparking autoimmune disease can actually tamp down inflammation and suppress the onset of inflammatory bowel disease. Experiments by Howard Hughes Medical Institute researchers at Yale University reveal that the immune protein interleukin 17A, or IL-17A, can take on the characteristics of Dr. Jekyll or Mr. Hyde – depending on the time and place.
Read more: Protein May Have a Good Side in Preventing Inflammation
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by Clive Svendsen
Results of unregulated stem cell transplant were predictable and avoidable
(This commentary provides an expert perspective to an article published in PLoS Medicine, which has been reported in Nature and Nature Reports Stem Cells.)
The study by Amariglio et al. describes a stem cell transplant attempt in a child with ataxia telangiectasia, a rare genetic disease that leads to poor coordination and dilation of blood vessels1. These patients also have weakened immune systems and are more prone to cancer.
Read more: Stem Cell Clinical Trials Must be Closely Monitored
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by Monya Baker
An analysis of when and where pluripotency factors bind indicate that c-Myc shuts down specialization and the remaining three turn on pluripotency
Scientists are still shocked that only a handful of introduced genes can turn a specialized cell's clock back so far that it behaves like an embryonic stem cell. Even with current established techniques, such reprogramming is a rare event, and researchers around the world are trying to figure out exactly how reprogramming can be triggered by genes for the pluripotency factors, which encode the transcription factors Oct4, Sox2, Klf4 and c-Myc. Publishing in Cell, researchers led by Kathrin Plath of the University of California, Los Angeles, show which genes are bound by the transcription factors in mouse embryonic stem cells, fully reprogrammed cells (induced pluripotent stem cells) and partially reprogrammed cells. The results, she believes, will help researchers find small molecules to replace the viral vectors currently used in the reprogramming process, which could result in more homogenous cells that are better suited for clinical applications.
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by Monya Baker
G9a silences gene expression two ways
As embryonic stem cells differentiate, the pluripotency gene known as Oct4 goes on lockdown. In fact, the gates to gene expression are doublelocked: the gene-encoding DNA strands are wound up into a structure called heterochromatin, in which the DNA is complexed with histones and other proteins in such a way that it is inaccessible to the transcriptional machinery. Furthermore, gene-expression machinery is kept at bay by chemical modifications to the DNA that signals the start of a gene. New work published in Nature Structural and Molecular Biology1 shows not only that both of these modifications are regulated by a single master protein, the histone methyltransferase G9a, but that this enzyme apparently brings about the inactivation of many early embryonic genes.