Inappropriate urinary catheterisation: a review of the prevalence, risk factors and measures to reduce incidence.

Urinary tract infections (UTIs) comprise the second most common type of healthcare-associated infections, with up to 80% of UTIs caused by indwelling urinary catheters. Current research suggests that the best way to prevent catheter-associated UTIs (CAUTIs) is to reduce unnecessary catheterisation. Few reviews have focused on the prevalence, risk factors and preventive measures for inappropriate catheterisation. This article, consequently, sought to evaluate the current evidence on the prevalence, risk factors and measures that can be taken to prevent inappropriate urinary catheterisation.

LncRNA CRNDE promotes the epithelial-mesenchymal transition of hepatocellular carcinoma cells via enhancing the Wnt/ß-catenin signaling pathway.

Colorectal neoplasia differentially expressed (CRNDE) is a significantly upregulated long noncoding RNA in hepatocellular carcinoma (HCC). CRNDE could promote cell proliferation, migration, and invasion, while its molecular mechanisms were still largely unclear. In this study, we investigated the expression and function of CRNDE. CRNDE was significantly upregulated in tumor tissues compared with adjacent normal tissues. In vitro, we revealed that knockdown of CRNDE inhibited cell proliferation, migration, and cell invasion capacities in HCC. Animal studies indicated that CRNDE knockdown represses both growth and metastasis of HCC tumors in vivo. Moreover, knockdown of CRNDE suppressed the cell epithelial-mesenchymal transition (EMT) process by increasing the expression of E-cadherin and ZO-1, whereas, decreasing the expression of N-cadherin, slug, twist, and vimentin in HCC cells. We also revealed that knockdown of CRNDE suppressed the Wnt/ß-catenin signaling in HCC. Thus, CRNDE could modulate EMT of HCC cells and knockdown of CRNDE impaired the mesenchymal properties. CRNDE increased invasion of HCC cells might be through activating the Wnt/ß-catenin signaling pathway.

Overexpression of JARID1B is associated with poor prognosis and chemotherapy resistance in epithelial ovarian cancer.

JARID1B, a histone demethylase, has been reported to be highly expressed in various human cancers. In the present study, we investigated the association of JARID1B level with epithelial ovarian cancer (EOC) and prognosis of patients with EOC. We analyzed JARID1B expression in 20 normal ovaries, 20 benign ovarian tumor (BOT) samples, and 45 epithelial ovarian carcinoma specimens by quantitative PCR (qRT-PCR) and western blotting analyses. JARID1B was further examined in 120 EOC specimens from patients with different histological stages via immunohistochemistry. Possible correlations between JARID1B levels and prognosis as well as chemotherapy resistance of EOC patients were determined by univariate and multivariate analyses. JARID1B level was significantly increased in EOC, as compared to normal ovaries and BOT. Among 120 EOC cases examined, the 5-year progression-free survival (PFS) rates were 17 and 85% in patients with high and low JARID1B expression, respectively (hazard ratio = 17.85, 95% confidence interval (CI) 6.31-50.51, P < 0.001). Similarly, the 5-year overall survival (OS) rates for patients with high and low JARID1B expression were 28 and 92% respectively (hazard ratio = 21.8, 95% CI 5.92-71.81, P < 0.001). Positive correlation between JARID1B level and chemotherapy resistance was observed in patients with EOC (odds ratio (OR) 36.81, 95% CI 4.84-280.11, P < 0.001). JARID1B could serve as an important biomarker for prognosis and chemotherapy resistance of EOC patients.

Circulating microparticles in patients with coronary heart disease and its correlation with interleukin-6 and C-reactive protein.

Microparticles (MPs) are vesicles released from activated or apoptotic cells. MP derive from various cells, most notably platelets, but also leucocytes, lymphocytes, erythrocytes, and endothelial cells. The aim of this study was to investigate endothelial MP (EMP), platelet MP (PMP), lymphocyte MP and monocyte MP and TF-positive MPs (TF+ MPs) in patients with coronary heart disease (CHD), and to evaluate the correlation of these MPs with Interleukin-6 (IL-6) and C-reactive protein (CRP). Different cell-derived MPs and TF+ MPs were analyzed by flow cytometry in 40 patients with myocardial infarction (MI), 30 unstable angina (UA), 20 stable angina (SA) and 20 healthy individuals, and IL-6 and CRP were determined by ELISA and special protein analyzer, respectively. Compared with SA and control, EMP and PMP was significantly elevated in MI and UA (P < 0.001), and TF+ MPs was significantly elevated in MI and UA (P < 0.001). EMP and PMP correlated with IL-6 (r = 0.822, P < 0.001 and r = 0.567, P < 0.001; respectively) or CRP level (r = 0.597, P < 0.001 and r = 0.66, P < 0.001; respectively). Different cell-derived MPs in CHD may indicate the different pathophysiological changes in vessels, and MPs may both participate in the development of thrombosis and enhance the vascular inflammation.

SARS-CoV-2 RNA detection on environmental surfaces in COVID-19 wards.

This study monitored the presence of SARS-Cov-2 RNA on environmental surfaces in hospital wards housing patients with mild, severe, and convalescent Coronavirus Disease 2019 (COVID-19), respectively. From 29 October to 4 December 2021, a total of 787 surface samples were randomly collected from a General Ward, Intensive Care Unit, and Convalescent Ward at a designated hospital for COVID-19 patients in China. All of the samples were used for SARS-Cov-2 detection. Descriptive statistics were generated and differences in the positivity rates between the wards were analyzed using Fisher's exact tests, Yates chi-squared tests, and Pearson's chi-squared tests. During the study period, 787 surface samples were collected, among which, 46 were positive for SARS-Cov-2 RNA (5.8%). The positivity rate of the contaminated area in the Intensive Care Unit was higher than that of the General Ward (23.5% vs. 10.4%, P<0.05). The positivity rate of the semi-contaminated area in the Intensive Care Unit (4.5%) was higher than that of the General Ward (1.5%), but this difference was not statistically significant (P>0.05). In the clean area, only one sample was positive in the Intensive Care Unit (0.5%). None of the samples were positive in the Convalescent Ward. These findings reveal that the SARS-Cov-2 RNA environmental pollution in the Intensive Care Unit was more serious than that in the General Ward, while the pollution in the Convalescent Ward was the lowest. Strict disinfection measures, personal protection, and hand hygiene are necessary to limit the spread of SARS-Cov-2.

High glucose upregulates myosin light chain kinase to induce microfilament cytoskeleton rearrangement in hippocampal neurons.

Chronic hyperglycemia leads to myosin light chain kinase (MLCK) upregulation and induces neuronal damage. However, the underlying molecular mechanism of neuronal damage in hyperglycemia has not yet been fully elucidated. In the present study, hippocampal neuronal cells were cultured and treated with a high glucose concentration (45 mmol/l). The results demonstrated that high glucose induced shrinking of the synapses, nuclear shape irregularity and microfilament damage. Filamentous actin (F­actin) filaments were rearranged, cell apoptosis rate was increased and the protein expression of MLCK and phosphorylated (p)­MLC was upregulated. The MLCK inhibitor ML­7 largely reversed the alterations in the microfilament cytoskeleton, inhibited F­actin depolymerization, reduced apoptosis and downregulated MLCK and p­MLC protein expression. Overall, these results indicated that high glucose upregulated MLCK to promote F­actin depolymerization, which induced microfilament cytoskeleton rearrangement in hippocampal neuronal cells.

LINC00052 upregulates EPB41L3 to inhibit migration and invasion of hepatocellular carcinoma by binding miR-452-5p.

Numerous studies have demonstrated that a class of long noncoding RNAs (lncRNAs) are dysregulated in hepatocellular carcinoma (HCC) and they are closely related with tumorigenesis. Our previous studies indicated that LINC00052 was a downregulated lncRNA in HCC and acted as a tumor suppressor gene. Using transcription microarray analysis, we found that knockdown of LINC00052 resulted in EPB41L3 downregulation. However, the function of EPB41L3 and the mechanism of LINC00052 downregulating EPB41L3 in HCC remain unclear. In this study, we found that overexpression of LINC00052 could upregulate the EPB41L3 expression and it might serve as a tumor suppressor gene in HCC. Database analysis showed that miR-452-5P could target LINC00052. The binding regions between LINC00052 and miR-452-5P were confirmed by luciferase assays. Moreover, LINC00052 inhibited cell malignant behavior by increasing miR-452-5P expression, suggesting that LINC00052 was negatively regulated by miR-452-5P. In addition, overexpression of miR-452-5P resulted in a decrease of EPB41L3 expression, suggesting that EPB41L3 was as a target of miR-452-5P. In conclusion, these results demonstrated that a novel pathway was mediated by LINC00052 in HCC.