According to new research by scientists at the University of Glasgow published in the January issue in the Proceedings of the National Academy of Sciences USA, a good indicator of an individual's life expectancy can be obtained from early in life using the length of specialized pieces of DNA called telomeres, which occur at the ends of the chromosomes that contain our genetic code. Telomeres work similar to plastic caps at the end of shoelaces. They mark the end of the chromosome, and protect them from various processes that gradually cause the ends to be worn away. This DNA protection method is equal to that in most animals and plants, as well as humans. The eventual loss of the telomere cap has been proven to cause malfunction in cells. The study, funded by the European Research Council, with additional support from the UK Natural Environment Research Council, the Wellcome Trust and the US National Science Foundation, is the first study in which researchers have measured the length of telomere in the same individuals from early life onwards, and repeatedly during the rest of their natural lives.
In the images of fruit flies, clusters of neurons are all lit up, forming a brightly glowing network of highways within the brain. It's exactly what University at Buffalo researcher Shermali Gunawardena was hoping to see: It meant that ORMOSIL, a novel class of nanoparticles, had successfully penetrated the insects' brains. And even after long-term exposure, the cells and the flies themselves remained unharmed. The particles, which are tagged with fluorescent proteins, hold promise as a potential vehicle for drug delivery. Each particle is a vessel, containing cavities that scientists could potentially fill with helpful chemical compounds or gene therapies to send to different parts of the human body. Gunawardena is particularly interested in using ORMOSIL - organically modified silica - to target problems within neurons that may be related to neurodegenerative disorders including Alzheimer's disease.
The investigational drug ganetespib, a synthetic second-generation Hsp90 inhibitor, slowed the growth of cancer cells taken from non-small cell lung cancer tumors with a mutation in the KRAS gene. The drug was even more active when combined with traditional lung cancer treatments and other investigational targeted therapies, according to preclinical study data. David A. Proia, Ph.D., and Jaime Acquaviva, Ph.D., scientists at Synta Pharmaceuticals Corp., presented the data at the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer: Biology, Therapy and Personalized Medicine, held Jan. 8-11, 2012. Currently, patients with non-small cell lung cancer (NSCLC) with KRAS mutations have no effective treatment strategy. A phase 2 trial showed tumor shrinkage in more than 60 percent of patients with KRAS-mutant NSCLC at eight weeks after treatment with ganetespib administered once weekly as a monotherapy, indicating the drug's potential effectiveness, according to Proia.
As an embryo develops, different genes are turned on in different cells, to form muscles, neurons and other bodily parts. Inside each cell's nucleus, genetic sequences known as enhancers act like remote controls, switching genes on and off. Scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, can now see - and predict - exactly when each remote control is itself activated, in a real embryo. Their work is published in Nature Genetics. Stefan Bonn, Robert Zinzen and Charles Girardot, all in Eileen Furlong's lab at EMBL, found that specific combinations of chromatin modifications - chemical tags that promote or hinder gene expression - are placed at and removed from enhancers at precise times during development, switching those remote controls on or off.
The discovery of a gene that causes a form of hereditary spastic paraplegia (HSP) may provide scientists with an important insight into what causes axons, the stems of our nerve cells, to degenerate in conditions such as multiple sclerosis. In the Journal of Clinical Investigation, an international team of scientists led by Dr Evan Reid at the University of Cambridge, and Dr Stephan Zuchner from the University of Miami, report that mutations in the gene known as 'reticulon 2' on chromosome 19 cause a form of HSP, a condition characterised by progressive stiffness and contraction (spasticity) of the legs, caused by selective and specific degeneration of axons The team identified three mutations in the reticulon 2 gene as causing a type of HSP - in one case, this mutation included an entire deletion of the gene.