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Brain Attack Coalition Adopts New Message For National Stroke Awareness Month
In recognition of Stroke Awareness Month in May, a national stroke coalition announced that its member organizations have adopted a new public education message: "Stroke strikes fast. You should too. Call 9-1-1." The Brain Attack Coalition (BAC), chaired by the National Institute of Neurological Disorders and Stroke (NINDS) and composed of leading organizations committed to stroke prevention and treatment, recognized the need for a new actionable message that all member organizations can use with their current stroke awareness efforts. The NINDS is part of the National Institutes of Health.
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Johns Hopkins School Of Medicine To Offer New Degree Program In Informatics
A new, intensive, one-year master"s degree program designed to prepare graduates for informatics leadership positions in clinical, public health and scientific settings will be offered beginning in September by the Johns Hopkins University School of Medicine. The Maryland Higher Education Commission (MHEC) approved the new program in June.
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Family Physician Survey In Mainz: Patients With Depression Frequently Suffer From Medically Unexplained Pain
Pain symptoms that cannot be attributed, or at least not fully attributed, to an organic origin are more frequently and more severely experienced by patients with depression than by those without. "It is the case that women are much more frequently affected by depression and also by so-called somatoform pain disorder than men," explains Dirk Frieser, psychologist at the Institute of Psychology at Johannes Gutenberg University Mainz. For the purposes of his doctoral dissertation, Frieser and fellow psychologist Stephanie Kç¶rber questioned 308 patients attending two practices of general practitioners in Mainz. Patients were asked about their state of health and their pain symptoms, but also about their anxieties with regard to illness, how they react when ill, what social support they receive, and what psychological stress they experience, together with many other aspects. Subsequently, the pain symptoms reported by the patients were evaluated by their doctors.
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Generation Of A Severe Memory-Deficit Mutant Mouse By Exclusively Eliminating The Kinase Activity Of CaMKIIalpha

Ca2+/calmodulin-dependent protein kinase II alpha (CaMKII alpha) is an enzyme that adds phosphates to a variety of protein substrates to modify their functions. CaMKII alpha is enriched in the hippocampus, the memory center of the brain, and is believed to be an essential mediator of activity-dependent synaptic plasticity and memory functions. However, the causative role of the enzymatic activity of CaMKII alpha in such processes has not been demonstrated yet, because this enzyme has multiple protein functions other than the kinase activity. A Japanese research group, led by Dr Yoko Yamagata of the National Institute for Physiological Sciences, Japan, has successfully generated a novel kinase-dead mutant mouse of the CaMKII alpha gene that completely and exclusively lacks its kinase activity. They examined hippocampal synaptic plasticity and behavioral learning of the mouse, and found a severe deficit in both processes. They reported their findings in the Journal of Neuroscience, published on June 10, 2009. The research group successfully generated a novel CaMKII alpha (K42R) knock-in mouse that completely lacks the kinase activity of CaMKII alpha, and examined the effects on structural, functional, and behavioral expression of synaptic memory. In the K42R brain, tetanus-induced long-term potentiation (LTP), a proposed cellular mechanism of memory, and sustained postsynaptic spine enlargement, a structural basis for LTP, were both impaired, whereas dynamic postsynaptic movement of CaMKII alpha protein was preserved. In addition, the K42R mouse showed a severe deficit in inhibitory avoidance learning, a form of memory dependent on the hippocampus. The research group concluded that the mutant mouse could not form memories and did not remember the events that had just happened. "We demonstrated that the mutant mouse has a severe memory deficit because of the lack of the kinase activity of CaMKII alpha. This finding supports the idea that the kinase activity of CaMKII alpha is essential to memory functions. Such a memory-deficit mutant mouse could serve as an animal model to study the molecular mechanisms of memory, and be a useful tool for the development and screening of therapeutic reagents for memory-deficit disorders. It may also help open a new therapeutic approach to memory dysfunctions in patients.", said Dr Yamagata. This research was carried out in collaboration with Profs. Shigeo Okabe, Toshiya Manabe, Yuchio Yanagawa, Keiji Imoto, Kunihiko Obata and others. Dr Yoko Yamagata and Prof Yuchio Yanagawa have applied for a patent on this technology through Japan Science and Technology Agency (JST). Dr. Yoko Yamagata National Institute for Physiological Sciences


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