43 research outputs found

    A review of the association between congestive heart failure and cognitive impairment.

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    Heart failure is a growing epidemic with an estimated 5 million Americans suffering from this condition. Several clinical trials have demonstrated a high correlation between congestive heart failure (CHF) and cognitive impairment. The severity of cognitive impairment correlates positively with the degree of CHF. The underlying mechanism for cognitive impairment remains unclear but appears to be related to cerebral hypoperfusion and impaired cerebral reactivity with selective impairment of verbal memory and attention domains. Furthermore, cognitive dysfunction represents one aspect of frailty, a novel concept that encompasses a range of clinical conditions that results in functional impairment in patients with heart failure. In addition, frailty independently predicts mortality in CHF patients. Cognitive impairment is a common and predictable effect of CHF that contributes with social and behavioral problems to decreased compliance to prescribed therapy and increased hospital readmissions. A multidisciplinary approach is necessary to deal with the complexity of this clinical syndrome

    Cyclosporin A does not Inhibit ILā€lĪ±ā€Induced Epithelial Cell ILā€6 Secretion

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    Trauma and infection activated a murine mucosal ILā€6 response in different ways: the ILā€6 response to bacteria was sensitive to Cyclosporin A (CsA); the ILā€6 response to trauma was not. The aim of the present study was to identify possible activators of the CsAā€insensitive ILā€6 secretion at the epithelial cell level. Two human epithelial cell lines from the kidney (A498) and bladder (J82) were exposed to Escherichia coli Hu734, interleukinā€lĪ± (ILā€lĪ±) and tumour necrosis factor a (TNFā€Ī±). The E. coli strain had been used for the in vivo experiments which led to this study, and ILā€lĪ± and TNFā€Ī± were likely to be released during infections and trauma. The secretion of ILā€6 into the supernatants was compared between cells stimulated in the presence or absence of CsA. E. coli Hu734, ILā€lĪ± and TNFā€Ī± stimulated an ILā€6 response in the two epithelial cell lines. The ILā€lĪ±ā€induced ILā€6 response was rapid, and the secreted ILā€6 levels were significantly higher than those induced by E. coli Hu734 or TNFā€Ī±. The ILā€6 response to ILā€ lĪ± was insensitive to CsA. By contrast, the ILā€6 response to E. coli Hu734 and TNFā€Ī± was inhibited by CsA. These results demonstrated that the inhibitory effect of CsA depends on the stimulus triggering the ILā€6 response. ILā€lĪ± may play a role in the induction of traumaā€associated CsAā€insensitive ILā€6 secretion
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