China Becoming Worlds Powerhouse in Science

China becomes a physics powerhouse Saturday, 02 August 2008 Judged by the astonishing increase in journal papers written by scientists in China, there can be little doubt that China is finding its place as one of the world’s scientific power houses. Michael Banks, Physics World's News Editor, quantifies this surge in scientific output from China and asks whether quality matches quantity in Augusts’ Physics World. Nanoscience, quantum computing and high-temperature superconductivity are three of the cutting-edge areas of physics that have seen particularly large increases. Published journal articles in nanoscience, for example, with at least one co-author based in China, have seen a 10-fold increase since the beginning of the millennium, rising to more than 10,500 in 2007. China has already overtaken the UK and Germany in the number of physics papers published and is beginning to nip at the heels of the United States. If China's output continues to increase at its current pace, the country will be publishing more articles in physics - and indeed all of science - than the US by 2012. Quantity alone however is not enough. The number of times a journal paper is cited by other academics in their own journal papers is often used as a guide to journal papers' quality. Unfortunately for China, they are currently a long way from the national citation top spot, ranked in 65th for physics, just ahead of Kuwait, with an average of 4.12 citations for each of the papers published. As China has only just started to publish large volumes of work, it is not a fair reflection. Werner Marx, an information scientist from the Max Planck Institute for Solid State Research in Stuttgart, Germany, who carried out a bibliometric study for the Physics World article, said: "The figure is still quite impressive, and I estimate this will rise substantially in the next few years." All indications suggest that China's propensity for world-leading research is growing. In March this year scientists in Japan first reported a new class of iron-based superconducting material that can conduct electricity without resistance when cooled to below 26 Kelvin (K). Researchers in China quickly picked up the baton and, within a month of the initial Japanese discovery, had boosted the transition temperature at which the material loses all its electrical resistance to 52 K. "China has become a notable factor in the scientific landscape. Usually scientific development in nations does not show such a strong acceleration as we have seen in China, so it will be interesting to see how it responds and develops in the future," Werner Marx said. A similar trend can be seen in the medical and biomedical field, although no official analysis yet has been made. ......... ZenMaster

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Cannabis Receptor Is a Tumour Suppressor

Researchers find CB1 suppresses colorectal tumour growth Saturday, 02 August 2008 New preclinical research shows that cannabinoid cell surface receptor CB1 plays a tumour-suppressing role in human colorectal cancer, scientists report in the Aug. 1 edition of the journal Cancer Research. CB1 is well-established for relieving pain and nausea, elevating mood and stimulating appetite by serving as a docking station for the cannabinoid group of signalling molecules. It now may serve as a new path for cancer prevention or treatment. "We've found that CB1 expression is lost in most colorectal cancers, and when that happens a cancer-promoting protein is free to inhibit cell death," said senior author Raymond DuBois, M.D., Ph.D., provost and executive vice president of The University of Texas M. D. Anderson Cancer Center. DuBois and collaborators from Vanderbilt-Ingram Cancer Center also show that CB1 expression can be restored with an existing drug, decitabine. They found that mice prone to developing intestinal tumours that also have functioning CB1 receptors develop fewer and smaller tumours when treated with a drug that mimics a cannabinoid receptor ligand. Ligands are molecules that function by binding to specific receptors. Agonists are synthetic molecules that mimic the action of a natural molecule. "Potential application of cannabinoids as anti-tumour drugs is an exciting prospect, because cannabinoid agonists are being evaluated now to treat the side-effects of chemotherapy and radiation therapy," DuBois said. "Turning CB1 back on and then treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention." Cannabinoids are a group of ligands that serve a variety of cell-signalling roles. Some are produced by the body internally (endocannabinoids). External cannabinoids include manmade versions and those present in plants, most famously the active ingredient in marijuana (THC). Receptor shutdown by methylation Endocannabinoid signalling is important to the normal functioning of the digestive system and has been shown to protect the colon against inflammation. Since chronic inflammation is a known risk factor for colorectal cancer, the researchers decided to look into the role of cannabinoid receptors in a mouse model of colon cancer. "People have looked at cannabinoids in cancer earlier, mainly in cell culture experiments," DuBois said. "The molecular mechanisms for loss of the receptor and its effect on cancer have not been previously shown." First, the team found that CB1 was largely absent in 18 of 19 human tumour specimens and in 9 of 10 colorectal cancer cell lines. Further experimentation showed that the gene that encodes the CB1 protein was not damaged, but shut down chemically by the attachment of methyl groups - a carbon atom surrounded by three hydrogen atoms - to the gene encoding CB1. Treating cell lines with decitabine, a demethylating agent approved for some types of leukaemia, removed the methyl groups, restoring gene expression in 7 of 8 cell lines and full expression of CB1 protein in three lines. Next, the group found that deletion of the CB1 gene in a strain of mice that spontaneously develops precancerous polyps resulted in a 2.5-to-3.8-fold increase in the number of polyps and a 10-fold increase in the number of large growths, those most likely to develop into cancer. Treating mice that had the CB1 receptor with an endocannabinoid agonist resulted in a decline in polyps ranging from 16.7 percent to 50 percent. The reduction was greater for larger polyps. CB1 thwarts survivin, a protein that protects cancer Cannabinoids previously had been shown to kill cancer cells in lab experiments by inducing apoptosis - programmed cell death. The team confirmed the role of CB1 in apoptosis, showing that tumour cells with high CB1 expression were sensitive to apoptosis when treated by a cannabinoid agonist. Cell lines with silenced CB1 resisted cell death. A series of experiments showed that CB1 increases cancer cell death by stifling a protein called survivin. Survivin is over-expressed in nearly every human tumour but is barely detectable in normal tissue, DuBois noted. Over-expression of survivin is associated with poor outcome and reduced apoptosis in colorectal cancer patients. The researchers pinpointed a cell signalling pathway by which activated CB1 cuts down survivin. "Just increasing the levels of cannabinoids to treat colorectal cancer won't work if the CB1 receptor is not present," DuBois said. This suggests that treating first with a demethylating agent, such as decitabine, to reactivate CB1 in the tumour and following up with a cannabinoid might be an effective attack on colorectal cancer. Scarcity of CB1 also is associated with Huntington's disease, Alzheimer's disease and multiple sclerosis. Further investigation, the researchers note, is needed to define its role in those diseases and other types of cancer. The team also analyzed the other main cannabinoid receptor, CB2, and found no role for it in colorectal cancer. They also treated the mice with a CB1 antagonist, a compound that binds to the receptor but does not activate it. Mice with CB1 blocked in this manner also showed an increase in the number and size of polyps. A CB1 antagonist called rimonabant is currently marketed overseas for weight loss. The researchers note that a patient's risk for colorectal cancer should be assessed when use of such drugs is being considered. ......... ZenMaster

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ALS iPS Cells Created from Skin Cells of Human Lou Gehrig Sufferer

Research team creates human ALS motor neurons Thursday, 31 July 2008 A team of researchers from the Harvard Stem Cell Institute (HSCI) and Columbia University, in a collaboration catalyzed by the Project ALS/Jenifer Estess Laboratory for Stem Cell Research, has demonstrated that pluripotent stem cells generated from a patient with ALS (amyotrophic lateral sclerosis) can be directed to differentiate into motor neurons — the very brain cells destroyed by ALS. The results of the team's study appear in today's online issue of Science. This is the first published report to show that disease-specific stem cells may be derived from an individual patient. In the study, led by Kevin Eggan, of the Harvard Stem Cell Institute, skin cells taken from a patient with a familial form of ALS were induced to become pluripotent stem cells. Scientists then differentiated the pluripotent cells into motor neurons and glia (support cells in the brain) that featured an ALS genotype. "This is a seminal discovery," said Valerie Estess, director of research for Project ALS "The ability to derive ALS motor neurons through a simple skin biopsy opens the doors to improved drug discovery. For the first time, researchers will be able to look at ALS cells under a microscope and see why they die. If we can figure out how a person's motor neurons die, we will figure out how to save motor neurons." Starting in 1999, Project ALS recruited leading scientists and clinicians to define the potential role of stem cells in understanding and treating ALS, the fatal neurodegenerative disease, also known as Lou Gehrig's disease. Project ALS-funded scientists began by transplanting stem cells directly into mice with ALS, with limited success. More recent experiments have shown that stem cells may be more valuable as tools to understand the disease process and create mini-representations of disease — or assays — for the purpose of drug screening.

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Patient specific motor neurons created in the Eggan laboratory. Image courtesy of John Dimos/Eggan Lab at HSCI.

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"For the first time, we have the opportunity to examine cellular and molecular defects in motor neurons and glial cells derived from patients with ALS. And we can now begin drug screens on disease-specific classes of human motor neurons," said Thomas Jessell, a Howard Hughes Investigator at Columbia University, and Project ALS advisor. "Through the work of the Jenifer Estess Laboratory for Stem Cell Research we now can glimpse the new age of ALS research, an age of progress and promise." Co-author on the paper, Christopher Henderson, who is co-director of the Columbia University Center for Motor Neuron Biology and Disease, and senior scientific advisor to the Project ALS Laboratory, said: "It has been a privilege to collaborate with Kevin Eggan and his team and to contribute to this critical step forward. We will continue to work hand-in-hand with Harvard researchers and Project ALS to exploit the potential of these cells for drug screening". Three years ago, Project ALS asked Dr. Eggan, a stem cell expert, and Chris Henderson, Hynek Wichterle, as authorities on motor neuron biology and drug screening at Columbia University, to work together to understand ALS, one of our most complicated and devastating neurological disorders. Today's publication marks the first major breakthrough of this collaboration. About Project ALS: Project ALS is a non-profit 501©3 whose mission is to understand, treat, and cure ALS, also known as Lou Gehrig's disease. The hallmark of the company's approach is collaboration between researchers and clinicians, many of whom have not focused on ALS specifically, or worked together before. In ten years, Project ALS has raised over $37 million for research worldwide. Located in New York, the Project ALS/Jenifer Estess Laboratory for Stem Cell is the world's only privately funded laboratory to focus exclusively on stem cell and ALS. The laboratory was named for Project ALS founder Jenifer Estess, who died from ALS in 2003. See also: Neurons created from skin cells of elderly patients with ALS HSCI – July 31, 2008 Harvard-Columbia team creates neurons from ALS patient's skin cells Eurekalert! – July 31, 2008 NY Stem Cell Foundation plays critical funding role in major new ALS research announced today Eurekalert! – July 31, 2008 Induced Pluripotent Stem Cells Generated from Patients with ALS Can Be Differentiated into Motor Neurons John T. Dimos, Kit T. Rodolfa, Kathy K. Niakan, Laurin M. Weisenthal, Hiroshi Mitsumoto, Wendy Chung, Gist F. Croft, Genevieve Saphier, Rudy Leibel, Robin Goland, Hynek Wichterle, Christopher E. Henderson, Kevin Eggan Science July 31, 2008, DOI: 10.1126/science.1158799 ......... ZenMaster

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