1,134 research outputs found

    INDEX, NULLITY AND FLUX OF n-NOIDS

    Full text link

    Clinical Determinants of Dementia Related to Stroke

    Get PDF
    Among 251 patients examined 3 months after the onset of acute ischemic stroke, we diagnosed dementia in 66(26.3%) by using modified DSM-III-R criteria based on neuropsychological, neurological, functional, and psychiatric examinations. We uses a logistic regression model to derive odds rations(ORs) for clinical factors independently related to dementia in this cross-sectional sample. Dementia was significantly associated with age, education, and race. A history of prior stroke (OR= 2.7) and diabetes mellitus (OR=2.6) was also independently related to dementia, but hypertension and cardiac disease were not. Stroke fearures associated with dementia included lacunar infarction compared with all other subtypes combined (OR=2.7) was also independently related to dementia, but hypertension and cardiac disease were not. Stroke features associated with dementia included lacunar infarction compared with all other subtypes combined (OR= 2.7) and hemisphetic laterality in relarion to brainstem or cerebellar location. There was a predominance of dementia in patients with left-sided lesions(Or-4.7), an effect not explained by aphasis. Dementia was especially common with infarctions in the left posterior cerebral and anterior cerebral artery territories. A major dominant hemispheral syndrome (reflecting size and laterality) was also independently associated with dementia (OR=3.9). We suggest that dementia after ischemic stroke is a result of multiple independent factors, including both small subcrtical and large cortical infarcts especially involving the left medial frontal and temporal regions, with additional contributions by demographic and vascular risk factors

    Low-voltage, high-gain, and high-mobility organic complementary inverters based on N,N'-ditridecyl-3,4,9,10-perylenetetracarboxylic diimide and pentacene

    Get PDF
    This is the pre-peer reviewed version of the following article: PHYSICA STATUS SOLIDI-RAPID RESEARCH LETTERS 2(2): 47-49, 2008 FULL CITE, which has been published in final form at http://www3.interscience.wiley.com/journal/117862140/abstract.ArticlePHYSICA STATUS SOLIDI-RAPID RESEARCH LETTERS. 2(2): 47-49 (2008)journal articl

    Cerebral Hypoxia and Ischemia in the Pathogenesis of Dementia after Stroke

    Get PDF
    While it has been reported that ischemic stroke significantly increases the risk of delayed dementia,1,2 the underlying mechanisms are not well understood. Hypoxic and ischemic (HI) injury resulting from cerebral hypoperfusion due to systemic illness has been proposed as a pathogenic mechanism in certain subgroups of patients.1,3 Thus, the aim of this study was to investigate whether cerebral HI injury resulting from certain systemic illnesses (e.g., cardiac arrhythmias, cardiac failure, pneumonia, seizures, sepsis) would be an independent risk factor for the development of incident dementia after ischemic stroke

    Expression of RAE-1, a ligand of the NKG2D Receptor, in Mice Adipocytes

    Get PDF
    Although epidemiological evidence has confirmed the role of heavy alcohol consumption as an established risk factor for esophageal, liver, and breast cancers, the molecular mechanisms underlying this effect are not fully understood, particularly with regard to breast cancer. In this study, expression of the retinoic acid early inducible-1 (RAE-1) gene was determined in mice adipocytes. RAE-1 is a ligand of the natural-killer group 2 member D (NKG2D) receptor, which plays a crucial role in tumor immunity. RT-PCR and Western blotting analysis demonstrated that TNF-α treatment induced RAE-1 mRNA and RAE-1 protein expression in adipocytes obtained from differentiated 3T3-F442A cells. Real-time RT-PCR analysis showed that 300 mM ethanol enhanced RAE-1 mRNA expression, which peaked 6 h after administration. In addition, RAE-1 mRNA was detected in visceral adipose tissue obtained from mice. These observations indicate that RAE-1mRNA is expressed in adipocytes and that its expression is enhanced by TNF-α, which has been shown to be induced in adipose tissue by long-term alcohol consumption. Furthermore, ethanol directly enhanced RAE-1 mRNA expression, suggesting that alcohol consumption enhances RAE-1 expression in adipose tissue and might modify tumor immunity. This finding might provide novel insight into the mechanism of alcohol-associated carcinogenesis
    corecore