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奥氮平和利培酮对精神分裂症小鼠模型的作用 总被引:1,自引:0,他引:1
利用精神分裂症小鼠模型比较临床上使用的非典型抗精神分裂症药物利培酮(Risperidone)和奥氮平(Olanzapine)的作用.试验结果:①利培酮和奥氮平都能有效地抑制小鼠的快速移动行为,高剂量的利培酮和奥氮平都能有效地抑制小鼠的刻板性行为;②利培酮的半最大效应浓度比奥氮平的半最大效应浓度小,表明其治疗效果更明显;③从共济失调副反应的半最大效应浓度与快速移动效应的半最大效应浓度的比值来看,利培酮的疗效也优于奥氮平. 相似文献
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Comparison of the growing number of disorders known to be associated with triplet repeat expansions reveals both common features
and a diversity of molecular pathways. Despite significant progress towards the characterization of proteins coded by the
mutant genes, the complex nature of these disorders requires identification of all molecular components of the triplet repeat
pathways. In this brief review we will discuss recent progress in determining the molecular mechanisms of disorders with unstable
trinucleotide mutations.
Received 13 January 1999; received after revision 8 March 1999; accepted 9 March 1999 相似文献
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Green PH Alaedini A Sander HW Brannagan TH Latov N Chin RL 《Cellular and molecular life sciences : CMLS》2005,62(7-8):791-799
The extra-intestinal manifestations of celiac disease (CD), including ataxia and peripheral neuropathy, are increasingly being recognized as the presenting symptoms of this autoimmune disease. Although there is a greater understanding of the pathogenesis of the intestinal lesions in CD the mechanisms behind the neurologic manifestations of CD have not been elucidated. In this article, the authors review the cellular and molecular mechanisms behind the histopathologic changes in the intestine, discuss the presentation and characteristics of neurologic manifestations of CD, review the data on the mechanisms behind these manifestations, and discuss the diagnosis and treatment of CD. Molecular mimicry and intermolecular help may play a role in the development of neurologic complications.Received 11 March 2004; received after revision 29 October 2004; accepted 12 November 2004 相似文献
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Kingsbury MA Yung YC Peterson SE Westra JW Chun J 《Cellular and molecular life sciences : CMLS》2006,63(22):2626-2641
The brain is remarkable for its complex organization and functions, which have been historically assumed to arise from cells
with identical genomes. However, recent studies have shown that the brain is in fact a complex genetic mosaic of aneuploid
and euploid cells. The precise function of neural aneuploidy and mosaicism are currently being examined on multiple fronts
that include contributions to cellular diversity, cellular signaling and diseases of the central nervous system (CNS). Constitutive
aneuploidy in genetic diseases has proven roles in brain dysfunction, as observed in Down syndrome (trisomy 21) and mosaic
variegated aneuploidy. The existence of aneuploid cells within normal individuals raises the possibility that these cells
might have distinct functions in the normal and diseased brain, the latter contributing to sporadic CNS disorders including
cancer. Here we review what is known about neural aneuploidy, and offer speculations on its role in diseases of the brain.
Received 13 April 2006; received after revision 2 June 2006; accepted 13 July 2006 相似文献
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Ramírez CL Cadiñanos J Varela I Freije JM López-Otín C 《Cellular and molecular life sciences : CMLS》2007,64(2):155-170
Disorders in which individuals exhibit certain features of aging early in life are referred to as segmental progeroid syndromes.
With the progress that has been made in understanding the etiologies of these conditions in the past decade, potential therapeutic
options have begun to move from the realm of improbability to initial stages of testing. Among these syndromes, relevant advances
have recently been made in Werner syndrome, one of several progeroid syndromes characterized by defective DNA helicases, and
Hutchinson-Gilford progeria syndrome, which is characterized by aberrant processing of the nuclear envelope protein lamin
A. Although best known for their causative roles in these illnesses, Werner protein and lamin A have also recently emerged
as key players vulnerable to epigenetic changes that contribute to tumorigenesis and aging. These advances further demonstrate
that understanding progeroid syndromes and introducing adequate treatments will not only prove beneficial to patients suffering
from these dramatic diseases, but will also provide new mechanistic insights into cancer and normal aging processes.
Received 28 July 2006; received after revision 5 September 2006; accepted 13 October 2006 相似文献
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