12 research outputs found

    Renal Lesions Associated with IgM-Secreting Monoclonal Proliferations: Revisiting the Disease Spectrum

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    Background and objectives: Since the first description of pathology of the kidney in Waldenström disease in 1970, there have been few reports on kidney complications of IgM-secreting monoclonal proliferations. Here, we aimed to revisit the spectrum of renal lesions occurring in patients with a serum monoclonal IgM

    Single Dose Cefuroxime for Surgical Prophylaxis: Effects of Weight on Serum Concentrations and PK variables

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    Background:Altered pharmacokinetics (PK) of b-lactams in obese patients may result in inadequate serum concentrations when standard dosage regimens are administered. The aim of our study was to evaluate the effects of weight on cefuroxime (CEF) concentrations and PKs during surgical prophylaxis. Methods:Prospective observational study from 10/2012 to 4/2013 at Erasme hospital, including all consecutive adult patients undergoing gastric bypass or partial hepatectomy and receiving CEF for surgical prophylaxis. Patients were a priori stratified into 2 weight groups : 8 mg/L (EUCAST clinical breakpoint for Enterobactericaea spp.), and was evaluated 3H after administration of CEF (fCEF180) and at end of surgery (fCEFend). Results were expressed as median (ranges) and counts (percentage) for each group, and compared using chi-square tests and the Wilcoxon Rank-Sum Test. A p < 0.05 was considered statistically significant. Results: 19 patients were included. Eight (88.9%) and 7 (78%) patients in Group A had adequate fCEF180 and fCEFend, compared to 4 (40%) and 5 (50%) patients in group B (p=0.03 and NS, respectively). Conclusion:This is the first PK study of CEF in obese patients. As weight increased, CL and VD of CEF and CLcr(24H) increased, while fCEF180 decreased. Higher dosage regimens of CEF in patients weighing more than100 kg may be warranted to obtain effective prophylaxis :a second dose of CEF may be necessary if surgery lasts more than 180 minutes.info:eu-repo/semantics/publishe

    Time to the Most Recent Common Ancestor for mtDNA and Y-STR Types for the Mlabri and the Other Hill Tribes

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    <p>Posterior probability distribution of the time back to the most recent common ancestor for the mtDNA (A) and Y-STR haplotype (B) data for the Mlabri and six other hill tribes.</p

    Genetic Diversity in the Mlabri and Other Hill Tribes

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    <p>Genetic diversity based on mtDNA HV1 sequences, Y-STR haplotypes, and autosomal STR (A-STR) genotypes in the Mlabri, compared to the average genetic diversity for six other hill tribes. The haplotype diversity is indicated for the mtDNA and Y-STR data, while the average heterozygosity is indicated for the autosomal STR loci.</p

    Associations amongst Unlinked Autosomal STR Loci in the Mlabri and the Other Hill Tribes

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    <p>Probability values of the likelihood ratio test of association versus no association for nine unlinked autosomal STR loci in the Mlabri and six other hill tribes (average probability over the 36 pairs of loci in parentheses).</p

    Number of Founding Individuals in the Mlabri, Given No mtDNA Diversity

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    <p>Posterior probability distribution for the number of founding individuals <i>(k),</i> conditioned on the observation of no diversity in a sample of 58 mtDNA sequences and the time since the founding event. The prior probability is indicated by the dashed black line.</p

    Genetic inactivation of Semaphorin 3C protects mice from acute kidney injury

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    International audienceTo guide the development of therapeutic interventions for acute kidney injury, elucidating the deleterious pathways of this global health problem is highly warranted. Emerging evidence has indicated a pivotal role of endothelial dysfunction in the etiology of this disease. We found that the class III semaphorin SEMA3C was ectopically upregulated with full length protein excreted into the blood and truncated protein secreted into the urine upon kidney injury and hypothesized a role for SEAM3C in acute kidney injury. Sema3c was genetically abrogated during acute kidney injury and subsequent kidney morphological and functional defects in two well-characterized models of acute kidney injury; warm ischemia/reperfusion and folic acid injection were analyzed. Employing a beta actin-dependent, inducible knockout of Sema3c, we demonstrate that in acute kidney injury SEMA3C promotes interstitial edema, leucocyte infiltration and tubular injury. Additionally, intravital microscopy combined with Evans Blue dye extravasation and primary culture of magnetically sorted peritubular endothelial cells identified a novel role for SEMA3C in promoting vascular permeability. Thus, our study points to microvascular permeability as an important driver of injury in acute kidney injury, and to SEMA3C as a novel permeability factor and potential target for therapeutic intervention
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