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  • Human herpesvirus-6 and -7 after lung and heart-lung transplantation. 17234516

    BACKGROUND: The impact of herpesvirus-6 and -7 (HHV-6, HHV-7) activation in lung transplant recipients is still poorly understood. We report the appearance of HHV-6 and HHV-7 antigenemia after lung transplantation and evaluate the efficacy of anti-viral drugs against these viruses. METHODS: Twenty-two lung or heart-lung recipients were monitored for HHV-6, HHV-7 and cytomegalovirus (CMV) during 12 post-operative months. HHV-6- and HHV-7-specific antigens and CMV pp65 antigens were analyzed in blood leukocytes and bronchoalveolar lavage fluid cells by monoclonal antibodies. Ganciclovir or valganciclovir prophylaxis for a minimum of 3 months was given to 19 recipients at risk for CMV infection. RESULTS: HHV-6, HHV-7 and CMV antigenemia was detected in 20 (91%), 11 (50%) and 12 (55%) recipients (median 16, 31 and 165 days) after transplantation, respectively. HHV-6 antigenemia occurred in 15 (79%), HHV-7 antigenemia in 7 (37%) and CMV antigenemia in 1 (7%) of these patients during anti-viral prophylaxis. HHV-6 or HHV-7 antigenemia was frequently associated with CMV antigenemia, which was detected 3 to 12 months after transplantation. Ganciclovir or valganciclovir treatment of CMV infection was effective against the concomitant HHV-6 and HHV-7 antigenemia in 9 of 12 (75%) and 5 of 6 (83%) cases, respectively. One case of pneumonitis and 1 of encephalitis were temporally associated with HHV-6. No other clinical manifestations could be linked solely to HHV-6 or -7. CONCLUSIONS: HHV-6 and -7 antigenemia was common and appeared early after lung transplantation. CMV prophylaxis was not able to prevent the appearance of HHV-6 and -7 antigenemia.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB8535
    Nombre del producto:
    Anti-Herpes Virus 6 Antibody, 101kDa protein, clone C3108-103
  • The role of the substantia nigra pars compacta in regulating sleep patterns in rats. 17551593

    As of late, dopaminergic neurotransmission has been recognized to be involved in the generation of sleep disturbances. Increasing evidence shows that sleep disturbances in Parkinson's disease (PD) patients are mostly related to the disease itself, rather than being a secondary phenomenon. Evidence contained in the literature lends support to the hypothesis that the dopaminergic nigrostriatal pathway is closely involved in the regulation of sleep patterns.To test this hypothesis we examined the electrophysiological activity along the sleep-wake cycle of rats submitted to a surgically induced lesion of the SNpc by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We demonstrated that a 50% lesion of the substantia nigra pars compacta (SNpc) suffices to produce disruptions of several parameters in the sleep-wake pattern of rats. A robust and constant decrease in the latency to the onset of slow wave sleep (SWS) was detected throughout the five days of recording in both light [F((22.16)) = 72.46, pless than 0.0001] and dark [F((22.16)) = 75.0, pless than 0.0001] periods. Also found was a pronounced increase in the percentage of sleep efficiency during the first four days of recording [F((21.15)) = 21.48, pless than 0.0001], in comparison to the sham group. Additionally, the reduction in the SNpc dopaminergic neurons provoked an ablation in the percentage of rapid eye movement sleep (REM) during three days of the sleep-wake recording period with a strong correlation (r = 0.91; pless than 0.0001) between the number of dopaminergic neurons lost and the percentage decrease of REM sleep on the first day of recording. On day 4, the percentage of REM sleep during the light and dark periods was increased, [F((22.16)) = 2.46, pless than 0.0007], a phenomenon consistent with REM rebound.We propose that dopaminergic neurons present in the SNpc possess a fundamental function in the regulation of sleep processes, particularly in promoting REM sleep.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo
  • Sarcolemmal Na+/H+ exchanger activity and expression in human ventricular myocardium. 10933369

    OBJECTIVES: To determine sarcolemmal Na+/H+ exchanger (NHE) activity and expression in human ventricular myocardium. BACKGROUND: Although the sarcolemmal NHE has been implicated in various physiological and pathophysiological phenomena in animal studies, its activity and expression in human myocardium have not been studied. METHODS: Ventricular myocardium was obtained from unused donor hearts with acute myocardial dysfunction (n = 5) and recipient hearts with chronic end stage heart failure (n = 11) through a transplantation program. Intracellular pH (pHi) was monitored in enzymatically isolated single ventricular myocytes by microepifluorescence. As the index of sarcolemmal NHE activity, the rate of H+ efflux at a pHi of 6.90 J(H6.9)) was determined after the induction of intracellular acidosis in bicarbonate-free medium. Na+/H+ exchanger isoform 1 (NHE1) expression in ventricular myocardium was determined by immunoblot analysis. RESULTS: Human ventricular myocytes exhibited readily detectable sarcolemmal NHE activity after the induction of intracellular acidosis, and this activity was suppressed by the NHE1-selective inhibitor HOE-642 (cariporide) at 1 micromol/L. Sarcolemmal NHE activity of myocytes was significantly greater in recipient hearts (JH6.9 = 1.95+/-0.18 mmol/L/min) than it was in unused donor hearts (J(H6.9 = 1.06+/-0.15 mmol/L/min). In contrast, NHE1 protein was expressed in similar abundance in ventricular myocardium from both recipient and unused donor hearts. CONCLUSIONS: Sarcolemmal NHE activity of human ventricular myocytes arises from the NHE1 isoform and is inhibited by HOE-642. Sarcolemmal NHE activity is significantly greater in recipient hearts with chronic end-stage heart failure than it is in unused donor hearts, and this difference is likely to arise from altered posttranslational regulation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB3140
    Nombre del producto:
    Anti-Na+/H+ Exchanger-1 Antibody, CT, clone 4E9
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