AIM: To characterize the prevalence of rotavirus(RV) and adenovirus(Ad V) infections in immunocompromised patients with acute gastroenteritis. METHODS: The presence of RV and Ad V(serotypes 40 and 41) was evaluated in...
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AIM: To characterize the prevalence of rotavirus(RV) and adenovirus(Ad V) infections in immunocompromised patients with acute gastroenteritis. METHODS: The presence of RV and Ad V(serotypes 40 and 41) was evaluated in 509 stool samples obtained between January 2009 and December 2010 from 200 immunocompromised patients(83 females and 117 males; median age 21 years old, range 0-72. The diagnosis of infection was performed as a routine procedure and the presence of RV and Ad V(serotypes 40 and 41) was determined by immunochromatography using the RIDA® Quick Rota-Adeno-Kombi kit(r-Biopharm, Darmstadt, Germany). The data analysis and description of seasonal frequencies were performed using computer software IBM® SPSS®(Statistical Package for Social Sciences) Statistics version 20.0 for Mac. The frequencies of infection were compared into different age and gender groups by χ2 ***: The study revealed 12.4% Ad V positive samples and 0.8% RV positive samples, which correspond to a prevalence of 6.5% and 1.5%, respectively. Ad V was more frequent between October 2009 and April 2010, while RV was identified in April 2010 and July 2010. The stool analysis revealed that from the 509 samples, 63(12.4%) were positive for Ad V and 4(0.8%) positive for RV, which by resuming the informationof each patient, lead to an overall prevalence of Ad V and RV of 6.5%(13/200 patients) and 1.5%(3/200 patients), respectively. The stratification of the analysis regarding age groups showed a tendency to an increased prevalence of infection in paediatric patients between 0-10 years old. Considering the seasonal distribution of these infections, our study revealed that Ad V infection was more frequent between October 2009 and April 2010, while RV infection was characterized by two distinct peaks(April 2010 and July 2010). CONCLUSION: The overall prevalence of Ad V and RV infection in immunocompromised patients with acute gastroenteritis was 8% and Ad V was the most prevalent
Current anti-epileptic drugs mostly control convulsions with a limited efficacy, and do not seize epileptogenesis. One of the structural-functional modifications occurring during epileptogenesis is an abnormal axonal ...
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Current anti-epileptic drugs mostly control convulsions with a limited efficacy, and do not seize epileptogenesis. One of the structural-functional modifications occurring during epileptogenesis is an abnormal axonal sprouting. The hippocampal mossy fiber(MF) sprouting found in patients and in animal models of temporal lobe epilepsy(TLE)(Neuroscience14, 375-403) generates an aberrant excitatory feedback circuit in granule cells that is thought to contribute to the hyperexcitability underlying the seizure-prone state(Neurochem. Res.28, 1649-58). However, the mechanism underlying this aberrant re-wiring is still poorly understood. There is now a growing evidence for a sustained increase in extracellular ATP levels in different pathological conditions, prompting ATP as a danger signal in the brain(Front. Neurosci.9:148). Accordingly, we now measured a sustained increase of the evoked release of ATP from hippocampal nerve terminals of Sprague-Dawley rats subjected to Status Epilepticus(SE) induced by pilocarpineinjection. Concomitantly, we found in developing rat hippocampal neurons that the pharmacological activation of adenosine A receptors(ARs) with the selective agonist CGS21680(30 n M) induces the formation of abnormal secondary axons. This prompted us to propose that this abnormal sprouting is due to an abnormal reactivation of the developmental-related AR-driven axon formation and outgrowth. We have now found in hippocampal organotypic slices that the spontaneous MF sprouting was attenuated by the pharmacological blockade of ARs, since the current densities(p A/p F) recorded were significantly lower in the slices cultured in the presence of the selective AR antagonist SCH58261(100 n M). More importantly, we found that the animals subjected to a long-term systemic treatment with SCH58261(0.1 mg/kg, i.p.), beginning 10 hours after pilocarpine-induced SE in rats, displayed significantly less hippocampal MF sprouting. Interestingly, CD73 knockout(CD73 KO) mice(lackin
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