Tuberculosis Pathogenesis Protection And Control

Original Research Article Objective: In this study our main goal is to evaluate the ascitic fluid fibronectin level to differentiate malignant from nonmalignant ascites. Method: This observational, cross sectional type study conducted in Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka from September 2014 to February 2017. During the study period of total 60 patients (30 patients with malignant ascites and 30 patients with nonmalignant ascites) were enrolled for the study. Results: Mean ascetic fluid fibronectin was found 0.50±0.15μg/ml in malignant ascites group and 0.22±0.07μg/ml in nonmalignant ascites group. Mean ascitic fluid fibronectin was found 0.64±0.11 μg/ml in positive for malignant cell group and 0.45±0.17 μg/ml in negative for malignant cell group. The mean difference was not statistically significant (p>0.05) between two groups. Sensitivity of cut off value of ascitic fluid fibronectin ≥0.22 μg/ml was 82.86%, specificity 96.0%, accuracy 88.33%, positive and negative predictive values were 96.67% and 80.0% respectively. Conclusion: The present study revealed on the usefulness of fibronectin in the differential diagnosis of ascites and these data and findings suggest that fibronectin may have potential value to differentiate malignant from nonmalignant ascites.

/pdf/the-ascitic-fluid-fibronectin-level-to-differentiate-2z9ar170e0.pdf

The Ascitic Fluid Fibronectin Level to Differentiate Malignant From Nonmalignant Ascites


 
 
 Dysbiotic intestinal microbiomes dominated by facultative anaerobes are strongly associated with inflammatory bowel disease (IBD). More recently, data from Baumler and colleagues support a model where mitochondrial dysfunction causes disease-associated dysbiosis by increasing oxygen (O2) availability to the microbiome. We posit that the restoration of epithelial mitochondrial respiration contributes to the restoration of a healthy microbiome dominated by facultative anaerobes such as Firmicutes [that produce short chain fatty acids (SCFA)]. Here, we tested a novel compound (AuPhos) that increases an O2 consumption in intestinal epithelial cells (IECs) thereby reducing O2 availability to the microbiome and promotes a healthy anaerobic environment (and blooms of firmicutes).
 
 
 
 Inbred C57BL/6 mice (n=3) were given oral vehicle (0.5% DMSO/Tween-80) or AuPhos (2.5 or 25mg/Kg;q3d) for two weeks, and colon and stool samples were extracted at day-15 sacrifice. Microbial DNA was isolated from stool samples using PoweFecal kit followed by 16S rRNA metagenomic sequencing. Linear Discriminant Analysis (LDA) and PICRUST2 were performed to reveal differentially abundant bacterial species and functional potentials of bacterial communities, respectively. Similar microbial profiling was performed on AuPhos-fed acute colitis mice (2% DSS-7d; Recovery-16d). Effect of AuPhos on microbial metabolism was determined by 1H NMR for detecting SCFA synthesis by gut microbiota in stool samples (n=3) collected after 3 consecutive doses. AuPhos-induced hypoxia in IECs was assessed by Hypoxyprobe-1 kit.
 
 
 
 Metagenomic analysis showed reduction in relative abundance of (O2 consuming) Proteobacteria and facultatively anaerobic Enterobacteriaceae in the gut, in AuPhos-fed mice. Conversely, AuPhos treatment dose- dependently increased the relative abundance of signature anaerobic bacteria e.g. Firmicutes including Clostridia (Faecalibacterium prausnitzii, Roseburia sp.), Bifidobacterium, etc. PICRUST2 and LDA revealed that AuPhos decreased bacterial LPS biosynthetic pathway and increased overall fatty acid biosynthesis pathways. AuPhos increased butyrate and propionate levels by >35% and acetate by 60% (n=3) compared to stools from vehicle-treated mice. In DSS-colitis mice, AuPhos reduced the relative abundance of inflammatory Proteobacteria, which includes facultative anaerobic Enterobacteriaceae family and increased Firmicutes over time (p<0.05). Interestingly, hypoxia staining showed AuPhos-induced O2 utilization in colonic surface IECs, facilitating obligate anaerobe-promoting environment in the gut.
 
 
 
 These finding suggest that AuPhos is a “first-in-class” oral therapeutic that has a potential to correct microbial dysbiosis in IBD by reducing epithelial oxygenation and thereby promoting a healthy microbiome dominated by obligate anaerobes.


/pdf/auphos-a-novel-drug-that-improves-colitis-by-microbiome-186i6o7h.pdf

Auphos, a novel drug that improves colitis by microbiome induced metabolic changes

562 auphos, a novel drug that restores intestinal homeostatis by correcting dysbiosis in inflammatory bowel diseases

Sa1852 ENHANCED EPITHELIAL MITOCHONDRIAL FUNCTION CORRECTS DYSBIOTIC METABOLOMICS IN HUMANIZED IL-10 KO MICE

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The Ascitic Fluid Fibronectin Level to Differentiate Malignant From Nonmalignant Ascites

Auphos, a novel drug that improves colitis by microbiome induced metabolic changes

562 auphos, a novel drug that restores intestinal homeostatis by correcting dysbiosis in inflammatory bowel diseases

Sa1852 ENHANCED EPITHELIAL MITOCHONDRIAL FUNCTION CORRECTS DYSBIOTIC METABOLOMICS IN HUMANIZED IL-10 KO MICE