By Icon Health Publications
This can be a 3-in-1 reference ebook. It offers an entire clinical dictionary masking 1000s of phrases and expressions with regards to ataxia. It additionally supplies broad lists of bibliographic citations. eventually, it offers info to clients on how one can replace their wisdom utilizing numerous net assets. The ebook is designed for physicians, clinical scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to get to grips with examine devoted to ataxia. in case your time is effective, this publication is for you. First, you won't waste time looking the net whereas lacking loads of suitable info. moment, the ebook additionally saves you time indexing and defining entries. ultimately, you won't waste money and time printing thousands of websites.
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Additional resources for Ataxia - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
We will map the phosphorylation site, test for the kinase involved and assess the changes in complex size in response to multiple stimuli. Identification of new proteins and elucidation of FA pathway mechanisms promise to shed light on a novel area of cancer biology with the potential to provide direct clinical applicability. ; Professor; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2002; Project Start 01-JAN-1998; Project End 31-MAR-2003 Summary: Ataxia Telangiectasia (A-T) is an autosomal recessive, pleiotrophic human disorder characterized by progressive neurodegenerative cerebellar ataxia, radiosensitivity, immunodeficiencies, telangiectases of eyes and skin, a greatly enhanced predisposition for lymphomas and premature death.
We cannot predict a priori how the SCA8 CTG expansion may affect the KLHL1/KLHL1AS gene system. Both of these genes, however, are specifically expressed in the cerebellum, and so these transcripts are likely candidates for mediating the pathogenic effect of this expansion either directly or through altered antisense interactions. We will perform multiple, iterative modifications of a BAC clone encoding the human KLHLAS gene and the first two exons of KLHL1 in E. coli using homologous recombination.
Experiments outlined in this grant will identify the molecular lesion in the Aif gene in Hq mutant mice. In addition, the effect of the Hq mutation on mitochondrial function and oxidative stress will be analyzed. Lastly, to test whether the ectopic expression of sonic hedgehog is sufficient to cause cell cycle re-entry and subsequent apoptosis, transgenic mice will be generated that abnormally express this molecule in terminally differentiated granule cells. The results of these experiments will allow validation of Hq mutant mice as a model for elucidation of the molecular interplay between oxidative stress, mitogen activation and cell cycle re-entry, and neuronal death in the adult nervous system.