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51.
Satoshi Uchiyama Federica Andreoni Claudia Zürcher Katrin Schilcher Miriam Ender Jerzy Madon Ulrich Matt Partho Ghosh Victor Nizet Reto A. Schuepbach Annelies S. Zinkernagel 《Journal of molecular medicine (Berlin, Germany)》2013,91(7):861-869
Group A Streptococcus (GAS) is a human pathogen causing a wide range of mild to severe and life-threatening diseases. The GAS M1 protein is a major virulence factor promoting GAS invasiveness and resistance to host innate immune clearance. M1 displays an irregular coiled-coil structure, including the B-repeats that bind fibrinogen. Previously, we found that B-repeat stabilisation generates an idealised version of M1 (M1*) characterised by decreased fibrinogen binding in vitro. To extend these findings based on a soluble truncated version of M1, we now studied the importance of the B-repeat coiled-coil irregularities in full length M1 and M1* expressed in live GAS and tested whether the modulation of M1–fibrinogen interactions would open up novel therapeutic approaches. We found that altering either the M1 structure on the GAS cell surface or removing its target host protein fibrinogen blunted GAS virulence. GAS expressing M1* showed an impaired ability to adhere to and to invade human endothelial cells, was more readily killed by whole blood or neutrophils and most importantly was less virulent in a murine necrotising fasciitis model. M1-mediated virulence of wild-type GAS was strictly dependent on the presence and concentration of fibrinogen complementing our finding that M1–fibrinogen interactions are crucial for GAS virulence. Consistently blocking M1–fibrinogen interactions by fragment D reduced GAS virulence in vitro and in vivo. This supports our conclusion that M1–fibrinogen interactions are crucial for GAS virulence and that interference may open up novel complementary treatment options for GAS infections caused by the leading invasive GAS strain M1. 相似文献
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Sagüés María Federica Fusé Luis Alberto Iglesias Lucía Emilia Moreno Fabiana Carina Saumell Carlos Alfredo 《Parasitology research》2013,112(3):1047-1051
The large-scale production of nematophagous fungi as agents of biological control is one of the main challenges to be commercially used. In order to improve growth of microorganism in a culture medium, the addition of growth inducer is common. At the moment, the action of their addition in the mycelia growth and sporulation rate of nematophagous fungi is not known. The purpose of this trial was to evaluate the sporulation rate of Duddingtonia flagrans by adding two growth inducers, meso-inositol and Tween 80, both at 0.5 % in a traditional culture medium Sabouraud glucose agar (SGA) and also in a traditional culture medium enriched with wheat flour and milk powder. From a traditional sterile culture of D. flagrans, four groups were made: SGA; Sabouraud glucose agar–meso-inositol 0.5 %; Sabouraud glucose agar–Tween 80 0.5 %; and Sabouraud glucose agar-enriched (SGA-E). These media were placed at a constant temperature of 27 °C for 4 weeks. Following this, chlamydospores were gently rinsed off with sterile water and counted using a Neubauer haematocytometer to estimate the number of chlamydospores per millilitre of water. The addition of meso-inositol 0.5 % to SGA promoted a significant increase (p?<?0.05) in chlamydospore production obtaining an average of 51,715,000 chlamydospores per Petri dish. The highest chlamydospore concentration was observed in the SGA-E in comparison with SGA (p?<?0.01) obtaining an average of 208,760,000 chlamydospores. The aim of this study was to obtain basic knowledge regarding the effect of enriched culture medium and growth-inducing meso-inositol and Tween 80 on mycelial growth and production of chlamydospores. 相似文献
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IJ Collins J Cairns G Jourdain F Fregonese M Nantarukchaikul N Lertpienthum P Wannarit P Attavinijtrakarn P Layangool S Le Coeur M Lallemant;for the Program for HIV Prevention Treatment 《AIDS (London, England)》2012,26(15):1943-1952
OBJECTIVE:: To assess hospitalization trends in HIV-infected children on antiretroviral therapy (ART) in Thailand, an important indicator of morbidity, ART effectiveness, and health service utilization. DESIGN:: Prospective observational cohort METHOD:: Children initiating ART in 1999-2009 were followed in 40 public hospitals. Hospitalization rate per 100 person-years were calculated from ART initiation to last follow-up/death. Costs to the healthcare provider were calculated using WHO inpatient estimates for Thailand. Zero-inflated Poisson models were used to examine risk factors for early (<12 months of ART) and late hospitalization (≥12 months) and frequency of admissions. RESULTS:: A total of 578 children initiated ART, median follow-up being 64 months [interquartile range (IQR) 43-82]; 211 (37%) children were hospitalized with 451 admissions. Hospitalization rates declined from 63 per 100 person-years at less than 6 months to approximately 10 per 100 person-years after 2 years of ART, and costs fell from $35 per patient-month to under $5, respectively. Age less than 2 years, US Centers of Disease Control and Prevention stage B/C, and stunting at ART initiation were associated with early hospitalization. Among those hospitalized, baseline CD4 cell percentage less than 5%, wasting, initiation on dual therapy, late calendar year, and female sex were associated with higher incidence of early admissions (P?<0.02). There were no predictors of late hospitalization, although previous hospitalization in less than 12 months of ART was associated with three times higher incidence of late admissions (P?0.0001). CONCLUSION:: One in three children required hospitalization after ART. Admissions were highest in the first year of therapy and rapidly declined thereafter. Young age, advanced disease stage, and stunting at baseline were predictive of early hospitalization. Treatment initiation before disease progression would likely reduce hospitalization and alleviate demands on healthcare services. 相似文献
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Small Bowel Ultrasound beyond Inflammatory Bowel Disease: An Updated Review of the Recent Literature
Federica Cavalcoli Alessandra Zilli Mirella Fraquelli Dario Conte Sara Massironi 《Ultrasound in medicine & biology》2017,43(9):1741-1752
The use of bowel ultrasonography (US) for the evaluation of gut diseases has increased in recent years and has been proven to provide a widely available, non-invasive and inexpensive method for the initial work-up and follow-up of different intestinal diseases, limited mostly by technical challenges posed by the patient's anatomy. The present review aims to provide an extensive overview of the main pathologic features at US examination of intestinal diseases other than inflammatory bowel disease, both acute (e.g., acute appendicitis, colonic diverticulitis, infectious diseases and ischemic conditions) and chronic (e.g., celiac disease, cystic fibrosis and other enterocolites). The identification of typical US features may help in the diagnostic process and guide the treatment approach. Therefore, the application of knowledge of the US appearance of gastrointestinal diseases is of relevance in enabling greater diagnostic performance and better patient management. 相似文献
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Andreas Linkermann Jan Hinrich Br?sen Maurice Darding Mi Kyung Jin Ana B. Sanz Jan-Ole Heller Federica De Zen Ricardo Weinlich Alberto Ortiz Henning Walczak Joel M. Weinberg Douglas R. Green Ulrich Kunzendorf Stefan Krautwald 《Proceedings of the National Academy of Sciences of the United States of America》2013,110(29):12024-12029
Regulated necrosis (RN) may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated necroptosis, but it is currently unclear whether there is one common pathway in which CypD and RIPK1 act in or whether separate RN pathways exist. Here, we demonstrate that necroptosis in ischemia–reperfusion injury (IRI) in mice occurs as primary organ damage, independent of the immune system, and that mice deficient for RIPK3, the essential downstream partner of RIPK1 in necroptosis, are protected from IRI. Protection of RIPK3-knockout mice was significantly stronger than of CypD-deficient mice. Mechanistically, in vivo analysis of cisplatin-induced acute kidney injury and hyperacute TNF-shock models in mice suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis. We, therefore, generated CypD-RIPK3 double-deficient mice that are viable and fertile without an overt phenotype and that survived prolonged IRI, which was lethal to each single knockout. Combined application of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with mutant mice. The data demonstrate the pathophysiological coexistence and corelevance of two separate pathways of RN in IRI and suggest that combination therapy targeting distinct RN pathways can be beneficial in the treatment of ischemic injury. 相似文献
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