Intrahepatic cholestasis of pregnancy (ICP), a pregnancy-related liver disease, leads to complications for both mother and fetus. Circulating microRNAs (miRNAs) have emerged as candidate biomarkers for many diseases. So far, the circulating miRNAs profiling of ICP has not been investigated. To assess the urinary miRNAs as non-invasive biomarkers for ICP, a differential miRNA profiling was initially analyzed by individual quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) assay in urinary samples from a screening set including 10 ICP and 10 healthy pregnancies. The selected candidate miRNAs were then validated by a validation set with 40 ICP and 50 healthy pregnancies using individual qRT-PCR assay. Compared with the expression in urine of healthy pregnant women, the expression levels of hsa-miR-151-3p and hsa-miR-300 were significantly down-regulated, whereas hsa-miR-671-3p and hsa-miR-369-5p were significantly up-regulated in urine from ICP patients (p < 0.05 and false discovery rate < 0.05). A binary logistic regression model was constructed using the four miRNAs. The area under the receiver operating characteristic curve was 0.913 (95% confidence interval = 0.847 to 0.980; sensitivity = 82.9%, specificity = 87.0%). Therefore, urinary microRNA profiling detection in ICP is feasible and maternal urinary miRNAs have the potential to be non-invasive biomarkers for the diagnosis of ICP.
Recent progress in high throughput sequencing technologies has provided an opportunity to probe T cell receptor (TCR) repertoire, bringing about an explosion of TCR sequencing data and analysis tools. For easier and more heuristic analysis TCR sequencing data, we developed a client-based HTML program (VisTCR). It has a data storage module and a data analysis module that integrate multiple cutting-edge analysis algorithms in a hierarchical fashion. Researchers can group and regroup samples for different analysis purposes by customized "Experiment Design File." Moreover, the VisTCR provides a user-friendly interactive interface, by all the TCR analysis methods and visualization results can be accessed and saved as tables or graphs in the process of analysis. The source code is freely available at https://github.com/qingshanni/VisTCR.
Inflammatory bowel disease ( IBD ) is a multifactorial disease involving defective immune responses against invasive microbiota. Genes associated with innate immune responses to microbes have been highlighted in the pathogenesis of IBD . To determine the role of Rab32 in the pathogenesis of IBD , we administered dextran sodium sulfate ( DSS ) to CD 11c + cell‐specific Rab32 knockout ( CD 11c ‐Cre + Rab32 f/f ) mice to induce colitis. Rab32 deficiency in CD 11c + cells resulted in more severe disease progression and increased mortality. Histopathological analysis showed extensive damage to the colon mucosa in DSS ‐treated CD 11c ‐Cre + Rab32 f/f mice, including more severe damage to the epithelial layer and crypts, as well as more inflammatory cell infiltration. The pro‐inflammatory cytokines IL 1A, IL 1B, IL 6, and CSF 3 and chemokines CXCL 1 and CXCL 2 were significantly increased, and the frequency of CD 11b + Ly6G + neutrophils was higher in CD 11c ‐Cre + Rab32 f/f colitis mice. Furthermore, CD 11c + cells deficient for Rab32 exhibited a significant increase in bacterial translocation in inflamed colon tissue. The present data demonstrate that Rab32 knockout in CD 11c + cells aggravates the development of DSS ‐induced colitis and suggest that the Rab32‐related antimicrobial pathway is involved in the pathogenesis of IBD .
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.