共找到 20 条结果
Journal Article Journal of Neuropathology and Experimental Neurology Get access Journal of Neuropathology & Experimental Neurology, Volume 42, Issue 1, January 1983, Page 111, https://doi.org/10.1097/00005072-198301000-00016 Published: 01 January 1983
Journal of Experimental Neurology is an international publication primarily dedicated to publish original research and novel findings in the neuroscience field. This journal offers a great opportunity to the neuroscientists to discuss and exchange their ideas and major advances in clinical and experimental neurology.
暂无摘要(点击查看原文获取完整内容)
The results of a histological study of the changes produced by high intensity ultrasound on tissue of the central nervous system are presented. The study was restricted to the nontemperature effects of the sound since these are of particular significance for neurology. The results obtained show that nerve cell bodies are particularly sensitive to the action of the ultrasound, while blood vessels and nerve fibers are much more resistant. The use of a focused beam of ultrasound to produce discrete lesions deep in the brain without disturbance of the vascular system or through-going nerve tracts in the region of the lesion is demonstrated by a study on the bulboreticular inhibitor formation of the cat medulla. Physical factors which require consideration are discussed in terms of the histological work.
A recent discussion expanded the debate about the experimental research on Gelsemium in anxiety. Herbal medicine is widely used in anxiety and mood disorders, often with contradictory evidence, although some authors are yet prompted to promote their full introduction in pharmacology as a promising therapy. Complementary and alternative medicine (CAM) in anxiety is particularly appreciated by individual healthcare, but deserves further investigation, as many critical issues have been recently raised. Comments about the ability of negligible doses of Gelsemium hydroalcoholic extracts to affect gene expression were recently reported.
raised titres for both haemagglutinating and complement- fixing techniques.In addition they found raised protein- bound iodine as well as butanol extractable iodine (B.E.I.) levels to be characteristic, though not pathognomonic.The authors consider that it is quite possible that damage to the thyroid gland, perhaps a virus infection, may initiate escape of thyroid antigens from the gland, so allowing an auto-immune process to become established.They consider the diagnosis to be of considerable importance in that, on the one hand, the condition is not unlikely to go on to complete destruction of the gland, and on the other, that treatment with dried thyroid extract for at least two years is an effective therapeutic regime.This review is undoubtedly authoritative and its conclusions sound.Its reading is made unnecessarily difficult by a rather oblique style of writing, by tables that are difficult to understand because of inadequate caption- ing, and by occasional unnecessary mistakes.On page
暂无摘要(点击查看原文获取完整内容)
暂无摘要(点击查看原文获取完整内容)
暂无摘要(点击查看原文获取完整内容)
暂无摘要(点击查看原文获取完整内容)
Basic relevant information on methodologies used in neurological disease models can be extremely hard to find. Originally published in 2006, this important reference work contains 30 chapters from over 60 internationally recognized scientists and covers every major methodology and disease model used in neuroscience research. Divided into two major sections, the first deals with general methodologies in neuroscience research covering topics from animal welfare and ethical issues to surgical procedures, post-operative care and behavioral testing. Section two covers every major disease model including traumatic brain injury, ischemia and stroke, to Parkinson's, motor neurone disease, epilepsy and sleep disorders. Delivering critical methodological information and describing small animal models for almost all major neurological diseases, this book forms an essential reference for anyone working in neuroscience, from beginning students to experienced researchers and medical professionals.
暂无摘要(点击查看原文获取完整内容)
暂无摘要(点击查看原文获取完整内容)
暂无摘要(点击查看原文获取完整内容)
暂无摘要(点击查看原文获取完整内容)
The purpose of this study was to investigate the induction of inducible nitric oxide synthase (iNOS) mRNA in the brain tissue of rats and mice under the following experimental conditions: in rats infected with borna disease virus and rabies virus, in mice infected with herpes simplex virus, and in rats after the induction of experimental allergic encephalitis. The results showed that iNOS mRNA, normally nondetectable in the brain, was present in animals after viral infection or after induction of experimental allergic encephalitis. The induction of iNOS mRNA coincided with the severity of clinical signs and in some cases with the presence of inflammatory cells in the brain. The results indicate that nitric oxide produced by cells induced by iNOS may be the toxic factor accounting for cell damage and this may open the door to approaches to the study of the pathogenesis of neurological diseases.
Pharmacologic inhibition of excitatory amino acid (EAA) neurotransmission attenuates cell death in models of global and focal ischemia and hypoglycemia and improves neurologic outcome after experimental traumatic spinal cord injury. The present study examined the effects of the noncompetitive N-methyl-D-aspartate (NMDA) receptor blocker MK-801 on cardiovascular and neurologic function after experimental fluid-percussion (FP) brain injury in the rat. Animals received either an intravenous bolus of MK-801 (1 mg/kg) or saline (equal volume) 15 min prior to FP brain injury or 15 min following FP brain injury. MK-801 pretreatment significantly improved postinjury cardiovascular variables and attenuated postinjury neurologic dysfunction. Postinjury treatment with MK-801 also significantly improved cardiovascular variables, but had little effect on postinjury neurologic scores. These results suggest that EAA neurotransmitters may be involved in the pathophysiological sequelae of traumatic brain injury and that noncompetitive blockade of the NMDA receptor prior to brain injury may reduce EAA-induced damage and limit neurologic dysfunction.