يعرض 1 - 8 نتائج من 8 نتيجة بحث عن '"Zhang, Shu-Xing"', وقت الاستعلام: 0.94s تنقيح النتائج
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    دورية أكاديمية
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    دورية أكاديمية
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    دورية أكاديمية
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    دورية أكاديمية

    المصدر: genesis ; volume 35, issue 4, page 220-226 ; ISSN 1526-954X 1526-968X

    الوصف: Summary: Mouse Nkx2‐5 gene is essential for early heart development and it is regulated by a complex array of regulatory modules. In order to establish an efficient in vivo system for mapping the Nkx2‐5 genomic locus for regulatory regions, we developed improved homologous recombination technology for use in Escherichia coli and then knocked an IRES‐hrGFP reporter gene into Nkx2‐5 gene in a 120 kb Nkx2‐5 bacterial artificial chromosome (BAC) clone. We employed the recombination genes redα and redβ under the pBAD promoter, which was specifically induced by the addition of L‐arabinose. Recombination was selected for by our universal targeting cassette which conferred kanamycin resistance in bacterial cells and neomycin resistance in mammalian cells. Transgenic mouse lines generated from this modified BAC clone closely resembled the endogenous Nkx2‐5 expression in the heart, pylorus sphincter, and spleen, but expression was not detected in the tongue. Nkx2‐5 BAC‐GFP expression was copy number‐dependent and locus site‐independent. BAC transgenics using the GFP reporter offers an efficient model system to study gene expression and regulation. genesis 35:220–226, 2003. © 2003 Wiley‐Liss, Inc.

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    دورية أكاديمية

    المصدر: Alcoholism: Clinical and Experimental Research ; volume 21, issue 3, page 434-443 ; ISSN 0145-6008 1530-0277

    الوصف: The relative etiologic roles of ethanol and thiamine deficiency in the cortical atrophy and loss of cerebral white matter in chronic alcoholics are uncertain. The present study examined the distribution of degenerating axons within cortical and subcortical tracts 1 week after recovery from early to late symptomatic stages of thiamine deficiency in the absence of ethanol in Sprague‐Dawley rats. The brains of rats exposed to an early symptomatic stage of pyrithiamine‐induced thiamine deficiency, 12–13 days of treatment, contained degenerating axons in corpus callosum, anterior commissure, external and internal capsules, optic and olfactory tracts, and fomix and mammillothalamic tracts. A dense pattern of degenerating axons was evident in layers Ill‐IV of frontal and parietal cortex. Less intense and more evenly distributed degenerating axons were present in layers IV‐VI of frontal, parietal, cingulate, temporal, retrosplenial, occipital, and granular insular cortex. Neuronal counts in mamrnillary body nuclei and areal measurements of the mammillary body were unchanged from controls and the thalamus was relatively undamaged. In animals reversed at later and more advanced symptomatic stages of thiamine deficiency, 14–15 days of treatment, degenerating axons were found in other cortical regions and hippocampus and there was extensive neuronal loss and gliosis within mammillary body and medial thalamus. These results demonstrate that a single episode of thiamine deficiency can selectively damage cortical white matter tracts while sparing the thalamus and mammillary body and may be a critical factor responsible for the pathological and behavioral changes observed in alcoholics without Wernicke's encephalopathy.

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    دورية أكاديمية
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    دورية أكاديمية

    المصدر: Journal of Neurochemistry ; volume 61, issue 6, page 2175-2182 ; ISSN 0022-3042 1471-4159

    الوصف: The current study measured extracellular fluid (ECF) levels of excitatory amino acids before and during the onset of thiamine deficiency‐induced pathologic lesions. Male Sprague‐Dawley rats were treated with daily pyrithiamine (0.25 mg/kg i.p.) and a thiamine‐deficient diet (PTD). Microdialysates were simultaneously collected from probes inserted acutely via guide cannulae into right paracentral and ventrolateral nuclei of thalamus and left hippocampus of PTD and pair‐fed controls. Hourly samples were collected from unanesthetized and freely moving animals. Basal levels obtained at a prelesion stage (day 12 of PTD treatment) were unchanged from levels in pairfed controls. In samples collected 4–5 h after onset of seizures (day 14 of PTD), the levels of glutamate were elevated an average 640% of basal levels in medial thalamus and 200% in hippocampus. Glutamine levels declined, taurine and glycine were elevated, and aspartate, GABA, and alanine were unchanged during this period. Within 7 h after seizure onset glutamine was undetectable in both areas, whereas glutamate had declined to ∼200% in thalamus and 70% in hippocampus. No significant change in glutamate, aspartate, or other amino acids was observed in dialysates collected from probes located in undamaged dorsal‐lateral regions of thalamus. Number of neurons within ventrolateral nucleus of thalamus was significantly greater in PTD animals in which the probe was dialyzed compared with nondialyzed, suggesting that removal of excitatory amino acids was protective. No significant pathologic damage was evident in hippocampus. Pretreatment with MK‐801 completely blocked the rise of ECF glutamate and significantly reduced the pathologic damage within thalamus of PTD rats and produced a significant decrease in ECF glutamate in control rats.