BackgroundThe short‐term and long‐term effect of Helicobacter pylori (H pylori) eradication on the gut microbiota is controversial; hence, this study aimed to clarify changes in the gut microbiome and microbial diversity after H pylori eradication.Materials and MethodsArticles published in PubMed, MEDLINE, and EMBASE were searched up to March 20, 2020, with English‐language restriction. The outcomes including gut microbiota and alpha diversity were extracted to analysis. And then, Review Manager 5.3 software was used to conduct the data analysis.ResultsAt phylum level, next‐generation sequencing was performed. Meta‐analysis results showed that Actinobacteria decreased compared with baseline throughout the follow‐up period. Proteobacteria increased during short‐term follow‐up and then returned to normal. In addition, Bacteroidetes decreased and Firmicutes increased only during long‐term follow‐up. At family or genus level, conventional microbiological culturing was performed. Enterobacteriaceae and Enterococcus both increased during the short‐term and interim follow‐up. In addition, Lactobacillus only showed a decreasing trend during short‐term follow‐up, but it appeared statistical decreasing during interim follow‐up. Moreover, relatively sufficient evidence showed that alpha diversity decreased during short‐term follow‐up, and no reliable data were obtained to confirm the change of alpha diversity during interim and long‐term follow‐up.ConclusionIn different follow‐up periods after H pylori eradication, changes in gut microbiota were inconsistent. Microbial diversity decreased in the short‐term follow‐up, while there was no data to confirm subsequent alterations. The results provided a basis for the rational selection of probiotics in the eradication process. However, further studies are needed to obtain more clues.
The aim of the present study was to investigate whether urinary kidney injury molecule-1 (KIM-1) presents a suitable early diagnostic biomarker of obstructive nephropathy-induced acute kidney injury (AKI), and to develop a rapid detection method for urinary KIM-1. Obstructive AKI was induced in an experimental rat model by a unilateral ureteral obstruction (UUO) operation. Macro- and micromorphological kidney alterations were determined by visual observation and hematoxylin and eosin (HE) staining, respectively. Kidney functions were evaluated by detecting urea nitrogen and creatinine levels in rat urine and blood. Urinary KIM-1 levels were measured using an enzyme-linked immunosorbent assay, and the protein expression levels of KIM-1, α-smooth muscle actin (α-SMA) and vimentin in kidney tissues were detected using immunohistochemical assays. In order to measure KIM-1 levels, colloidal gold immunochromatographic strips were developed based on the colloidal gold immunochromatographic assay. The results indicated that KIM-1 levels were significantly higher in the UUO group when compared with the Sham group. KIM-1 levels in the urine and kidney tissues exhibited a time-dependent increase, together with increasing obstructive AKI in the UUO group. In addition, KIM-1 levels were demonstrated to be a more sensitive biomarker of early obstructive AKI, when compared with α-SMA and vimentin. A colloidal gold-based immunochromatographic strip was developed, whereby the detection of urinary KIM-1 could be completed within 5–10 min. In conclusion, results of the present study demonstrated that urinary KIM-1 may be a valuable biomarker for the early diagnosis of obstructive AKI, and the use of a colloidal gold immunochromatographic strip may be a promising method for the rapid detection of urinary KIM-1.
Background. The aim of our study was to investigate whether serum cholinesterase (ChE) levels were associated with inflammatory bowel disease (IBD). Materials and Methods. We conducted a retrospective case-control study to clarify the relationship between serum ChE levels and IBD that included 142 patients with ulcerative colitis (UC), 60 patients with Crohn’s disease (CD), and 264 healthy controls (HCs). We used ROC curves to evaluate the diagnostic value of serum ChE levels for IBD. Results. Substantially lower serum ChE levels were detected in patients with UC than in HCs (6376 U/L versus 8418 U/L, P<0.001) and in patients with CD than in HCs (5181 U/L versus 8418 U/L, P<0.001). Additionally, patients with CD displayed significantly lower serum ChE levels than patients with UC (5181 U/L versus 6376 U/L, P<0.01). We also found that there was a negative association between serum ChE levels and the Crohn’s Disease Activity Index (CDAI) score of patients with CD (P=0.011) and the Simple Clinical Colitis Activity Index (SCCAI) score of patients with UC (P=0.018). The area under the curve (AUC) for serum ChE for the diagnosis of IBD was 0.826, and the AUCs of serum ChE for the diagnosis of CD and UC were 0.890 and 0.800, respectively. Conclusions. Serum ChE levels have important clinical significance in the diagnosis and assessment of clinical activity in patients with IBD, and the cholinergic anti-inflammatory pathway may provide new ideas for targeted treatment of IBD.
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