96 resultados para persistent colonisation


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We report the case of a 68 year old immuncompetent woman with persisting fever. Symptomatic acute CMV infection with a partial thrombosis of the left portal vein branch was diagnosed.

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Tenofovir disoproxil fumarate (TDF) has been associated with proximal renal tubulopathy and reduction in estimated glomerular filtration rate (eGFR), without accounting for the tubular secretion of creatinine.

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Congenital peripheral nerve hyperexcitability (PNH) is usually associated with impaired function of voltage-gated K(+) channels (VGKCs) in neuromyotonia and demyelination in peripheral neuropathies. Schwartz-Jampel syndrome (SJS) is a form of PNH that is due to hypomorphic mutations of perlecan, the major proteoglycan of basement membranes. Schwann cell basement membrane and its cell receptors are critical for the myelination and organization of the nodes of Ranvier. We therefore studied a mouse model of SJS to determine whether a role for perlecan in these functions could account for PNH when perlecan is lacking. We revealed a role for perlecan in the longitudinal elongation and organization of myelinating Schwann cells because perlecan-deficient mice had shorter internodes, more numerous Schmidt-Lanterman incisures, and increased amounts of internodal fast VGKCs. Perlecan-deficient mice did not display demyelination events along the nerve trunk but developed dysmyelination of the preterminal segment associated with denervation processes at the neuromuscular junction. Investigating the excitability properties of the peripheral nerve suggested a persistent axonal depolarization during nerve firing in vitro, most likely due to defective K(+) homeostasis, and excluded the nerve trunk as the original site for PNH. Altogether, our data shed light on perlecan function by revealing critical roles in Schwann cell physiology and suggest that PNH in SJS originates distally from synergistic actions of peripheral nerve and neuromuscular junction changes.

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Plasmacytoid dendritic cells (pDCs) are the major producers of type I IFN in response to viral infection and have been shown to direct both innate and adaptive immune responses in vitro. However, in vivo evidence for their role in viral infection is lacking. We evaluated the contribution of pDCs to acute and chronic virus infection using the feeble mouse model of pDC functional deficiency. We have previously demonstrated that feeble mice have a defect in TLR ligand sensing. Although pDCs were found to influence early cytokine secretion, they were not required for control of viremia in the acute phase of the infection. However, T cell priming was deficient in the absence of functional pDCs and the virus-specific immune response was hampered. Ultimately, infection persisted in feeble mice. We conclude that pDCs are likely required for efficient T cell priming and subsequent viral clearance. Our data suggest that reduced pDC functionality may lead to chronic infection.

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The aim of this prospective cohort study was to identify modifiable protective factors of the progression of acute/subacute low back pain (LBP) to the persistent state at an early stage to reduce the socioeconomic burden of persistent LBP. Patients attending a health practitioner for acute/subacute LBP were assessed at baseline addressing occupational, personal and psychosocial factors, and followed up over 12 weeks. Pearson correlations were calculated between these baseline factors and the presence of nonpersistent LBP at 12-week follow-up. For those factors found to be significant, multivariate logistic regression analyses were performed. The final 3-predictor model included job satisfaction, mental health and social support. The accuracy of the model was 72%, with 81% of nonpersistent and 60% of persistent LBP patients correctly identified. Further research is necessary to confirm the role of different types of social support regarding their prognostic influence on the development of persistent LBP.

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To reduce the socio-economic burden of persistent low back pain (LBP), factors influencing the progression of acute/subacute LBP to the persistent state must be identified at an early stage.

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Persistent atrial fibrillation (AF) ablation may lead to partial disconnection of the coronary sinus (CS). As a result, disparate activation sequences of the local CS versus contiguous left atrium (LA) may be observed during atrial tachycardia (AT). We aimed to evaluate the prevalence of this phenomenon and its impact on activation mapping.