Vertebroplasty with high-viscosity cement versus conventional kyphoplasty for osteoporotic vertebral compression fractures: a meta-analysis.

BACKGROUND: To evaluate outcomes following percutaneous vertebroplasty with high viscosity cement (PVP-HVC) and percutaneous kyphoplasty (PKP) with normal-viscosity cement in patients with osteoporotic vertebral compression fractures (OVCFs). METHODS: Pertinent studies were retrieved by searching five electronic databases up to July 2021. Additional records were identified via hand-searching of related references. Risk ratio (RR) and weighted mean difference (WMD), with their 95% confidence intervals (CIs), were calculated. A trial sequential analysis (TSA) was done for cement leakage. RESULTS: Twelve studies, embracing 1050 patients with OVCFs, were included. PVP-HVC was superior to PKP with normal-viscosity cement regarding risk of cement leakage (RR: 0.67, 95% CI: 0.54-0.83, I2 : 45.1%) and operation time (WMD: -11.26, 95% CI: -14.78 to -8.34, I2 : 88.8%). However, TSA revealed that a sufficient level of evidence for leakage reduction may have yet to be reached. PKP groups had a significant decrease in Cobb's angles postoperatively (within 1 month, WMD: 2.68, 95% CI: 1.85-3.48, I2 : 0%; after 1 year, WMD: 2.68, 95% CI: 1.35-4.01, I2 : 0%). There are no significant differences between the two procedures pertaining to injected cement volume, Visual Analogue Scale (VAS), Oswestry Disability Index (ODI) and risk of adjacent vertebral fractures. CONCLUSION: PVP-HVC and PKP with normal-viscosity cement are safe and effective treatments for the management of OVCF, but the former is superior to the latter in terms of procedure time. The potential of PVP-HVC in reducing cement leaks remains to be validated by more well-designed studies.

[Research advances in ecological risk of antibiotic resistance genes]. / æŠ—ç”Ÿç´ æŠ—æ€§åŸºå› çš„ç”Ÿæ€é£Žé™©ç ”ç©¶è¿›å±•.

Antibiotics have played an important role in the prevention and treatment of human and animal diseases as well as the improvement of animal products. However, the mass products and application of antibiotics, especially the abuse in animal industry and clinical medicine, led to the widespread of antibiotic resistance genes (ARGs) in the environment. They spread widely through conjugation, transposition, and transformation with the help of movable elements such as plasmid, transposon and integrons, resulting in the continuous enhancement of microbial medicinal properties and posing a serious threat to human health and ecological security. At present, great attention has been paid to the impacts of ARGs on human health, but limited research on the ecological risk of ARGs in the environment. Here, the status quo and ecological risks of ARGs pollution were summarized, and the future research priorities in this field were prospected. We hope it could pave the way for further studies and give references for the ecological control and prevention of ARGs pollution.

Weighted Gene Coexpression Network Analysis to Construct Competitive Endogenous RNA Network in Chromogenic Renal Cell Carcinoma.

AIM: This study is aimed at constructing the competing endogenous RNA (ceRNA) network in chromophobe renal cell carcinoma (ChRCC). METHODS: Clinical and RNA sequence profiles of patients with ChRCC, including messenger RNAs (mRNAs), microRNAs (miRNAs), and long noncoding RNAs (lncRNAs), were obtained from The Cancer Genome Atlas (TCGA) database. "edgeR" and "clusterProfiler" packages were utilized to obtain the expression matrices of differential RNAs (DERNAs) and to conduct gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Weighted gene coexpression network analysis (WGCNA) was performed to screen the highly related RNAs, and miRcode, StarBase, miRTarBase, miRDB, and TargetScan datasets were used to predict the connections between them. Univariate and multivariate Cox proportional hazards regressions were performed in turn to elucidate prognosis-related mRNAs in order to construct the ceRNA regulatory network. RESULTS: A total of 1628 DElncRNAs, 104 DEmiRNAs, and 2619 DEmRNAs were identified. WGCNA showed significant correlation in 1534 DElncRNAs, 98 DEmiRNAs, and 2543 DEmRNAs, which were related to ChRCC. Fourteen DEmiRNAs, 113 DElncRNAs, and 43 DEmRNAs were screened. Nine mRNAs (ALPL, ARHGAP29, CADM2, KIT, KLRD1, MYBL1, PSD3, SFRP1, and SLC7A11) significantly contributed to the overall survival (OS) of patients with ChRCC (P < 0.05). Furthermore, two mRNAs (CADM2 and SFRP1) appeared to be independent risk factors for ChRCC. CONCLUSION: The findings revealed the molecular mechanism of ChRCC and potential therapeutic targets for the disease.

Berberine alleviates visceral hypersensitivity in rats by altering gut microbiome and suppressing spinal microglial activation.

Accumulating evidence shows that agents targeting gut dysbiosis are effective for improving symptoms of irritable bowel syndrome (IBS). However, the potential mechanisms remain unclear. In this study we investigated the effects of berberine on the microbiota-gut-brain axis in two rat models of visceral hypersensitivity, i.e., specific pathogen-free SD rats subjected to chronic water avoidance stress (WAS) and treated with berberine (200 mg· kg-1 ·d-1, ig, for 10 days) as well as germ-free (GF) rats subjected to fecal microbiota transplantation (FMT) from a patient with IBS (designated IBS-FMT) and treated with berberine (200 mg· kg-1 ·d-1, ig, for 2 weeks). Before the rats were sacrificed, visceral sensation and depressive behaviors were evaluated. Then colonic tryptase was measured and microglial activation in the dorsal lumbar spinal cord was assessed. The fecal microbiota was profiled using 16S rRNA sequencing, and short chain fatty acids (SCFAs) were measured. We showed that berberine treatment significantly alleviated chronic WAS-induced visceral hypersensitivity and activation of colonic mast cells and microglia in the dorsal lumbar spinal cord. Transfer of fecal samples from berberine-treated stressed donors to GF rats protected against acute WAS. FMT from a patient with IBS induced visceral hypersensitivity and pro-inflammatory phenotype in microglia, while berberine treatment reversed the microglial activation and altered microbial composition and function and SCFA profiles in stools of IBS-FMT rats. We demonstrated that berberine did not directly influence LPS-induced microglial activation in vitro. In both models, several SCFA-producing genera were enriched by berberine treatment, and positively correlated to the morphological parameters of microglia. In conclusion, activation of microglia in the dorsal lumbar spinal cord was involved in the pathogenesis of IBS caused by dysregulation of the microbiota-gut-brain axis, and the berberine-altered gut microbiome mediated the modulatory effects of the agent on microglial activation and visceral hypersensitivity, providing a potential option for the treatment of IBS.

[Progresses on the effects and mechanisms of stress on gut microbiota].

Stress is the non-specific systemic response that occurs when the body is stimulated by various factors, and it can affect multiple systems of the body. Recent studies have shown that gut microbiota is an essential part of human microecology, and plays a pivotal role in keeping the body healthy. Stress can result in gut dysbiosis by affecting the function of intestinal mucosal barrier, intestinal immune and gastrointestinal motility. This article reviewed the alteration of gut microbiota caused by stress and the possible mechanisms involved.