PFKP is a prospective prognostic, diagnostic, immunological and drug sensitivity predictor across pan-cancer.

Phosphofructokinase, platelet (PFKP) is a rate-limiting enzyme of glycolysis that plays a decisive role in various human physio-pathological processes. PFKP has been reported to have multiple functions in different cancer types, including lung cancer and breast cancer. However, no systematic pancancer analysis of PFKP has been performed; this type of analysis could elucidate the clinical value of PFKP in terms of diagnosis, prognosis, drug sensitivity, and immunological correlation. Systematic bioinformation analysis of PFKP was performed based on several public datasets, including The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), Genotype-Tissue Expression Project (GTEx), and Human Protein Atlas (HPA). Prospective carcinogenesis of PFKP across cancers was estimated by expression analysis, effect on patient prognosis, diagnosis significance evaluation, and immunity regulation estimation. Then, pancancer functional enrichment of PFKP was also assessed through its effect on the signaling score and gene expression profile. Finally, upstream expression regulation of PFKP was explored by promoter DNA methylation and transcription factor (TF) prediction. Our analysis revealed that high expression of PFKP was found in most cancer types. Additionally, a high level of PFKP displayed a significant correlation with poor prognosis in patients across cancers. The diagnostic value of PFKP was performed based on its positive correlation with programmed cell death-ligand 1 (PD-L1). We also found an obvious immune-regulating effect of PFKP in most cancer types. PFKP also had a strong negative correlation with several cancer drugs. Finally, ectopic expression of PFKP may depend on DNA methylation and several predicated transcription factors, including the KLF (KLF transcription factor) and Sp (Sp transcription factor) families. This pancancer analysis revealed that a high expression level of PFKP might be a useful biomarker and predictor in most cancer types. Additionally, the performance of PFKP across cancers also suggested its meaningful role in cancer immunity regulation, even in immunotherapy and drug resistance. Overall, PFKP might be explored as an auxiliary monitor for pancancer early prognosis and diagnosis.

Clinical Impact and Risk Factors of Intensive Care Unit-Acquired Nosocomial Infection: A Propensity Score-Matching Study from 2018 to 2020 in a Teaching Hospital in China.

Purpose: Nosocomial infection (NI) is associated with poor prognosis. The present study assessed the clinical and microbiological characteristics of NI patients in the intensive care unit (ICU) and investigated the clinical impact and risk factors for NI in ICU patients. Patients and Methods: An observational study was conducted in an adult general ICU. The electronic medical records of all patients admitted to the ICU for >2 days from 2018-2020 were analyzed retrospectively. Multivariate regression models were used to analyze the risk factors for NI in ICU patients. Propensity score-matching (PSM) was used to control the confounding factors between the case and control groups, thus analyzing the clinical impact of NIs. Results: The present study included 2425 patient admissions, of which 231 (9.53%) had NI. Acinetobacter baumannii (33.0%) was the most common bacteria. Long-term immunosuppressive therapy, disturbance of consciousness, blood transfusion, multiple organ dysfunction syndromes (MODS), treatment with three or more antibiotics, mechanical ventilation (MV), tracheotomy, the urinary catheter (UC), nasogastric catheter, and central venous catheter (CVC) were risk factors for NI in the ICU patients. After PSM, patients with NI had a prolonged length of stay (LOS) in the ICU and hospital, significant hospitalization expenses (all p<0.001), increased mortality (p=0.027), and predicted mortality (p=0.007). The differences in the ICU and hospital LOSs among three pathogens were statistically significant (p<0.001); the results of the Escherichia coli infection group were lower than the other two pathogenic groups. Conclusion: NI was associated with poor outcomes. The risk factors for NI identified in this study provided further insight into preventing NI.

LncRNA SNHG6 inhibits autophagy of gastric carcinoma cells via PI3K/AKT/mTOR signaling pathway.

OBJECTIVE: To investigate the role of lncRNA SNHG6 (SNHG6) in gastric carcinoma (GC) and its relationship with the PI3K/AKT/mTOR signaling pathway in order to provide more comprehensive and reliable reference for the diagnosis and treatment of GC. METHODS: GC patients admitted to our hospital from May 2017 to August 2018 as well as healthy individuals who underwent physical examinations during the same time period were enrolled in this study. The serum SNHG6 level was quantified. Patients were followed up for 3 years to analyze the significance of SNHG6 in the diagnosis and treatment of GC. Finally, in vitro assays were performed to determine the influences of SNHG6 and PI3K/AKT/mTOR signaling pathway on biological behaviors and autophagy ability of GC cells. RESULTS: SNHG6 showed high expression in patients with GC and its expression decreased after therapy. SNHG6 also demonstrated a favorable predictive value for the development of GC and the death of patients. The survival curve suggested that increased SNHG6 indicated a higher risk of death. Additionally, mRNA of PI3K/AKT/mTOR pathway related molecules was highly expressed in GC patients. In in vitro assays, GC cells showed stronger viability and invasion activity and weaker apoptosis and autophagy ability after targeted up-regulation of SNHG6. According to the rescue assay, the effect of up-regulating SNHG6 on GC cells could be completely reversed by suppressing the PI3K/AKT/mTOR pathway. CONCLUSION: With high expression in patients with GC, SNHG6 can promote the development of GC by activating the PI3K/AKT/mTOR signaling pathway and suppressing the autophagy of cells. Therefore, it is a potential breakthrough in the diagnosis and treatment of GC in the future.

The Role of lncRNA PVT1 and hsa-miR-30a-3p in the Development of Gastric Cancer.

OBJECTIVE: Aberrantly expressed lncRNAs have been detected in gastric cancer (GC). LncRNA PVT1 is involved in numerous types of human malignant tumor. In this project, we demonstrated the relationship between PVT1 and Myc and tested the function of PVT1 and hsa-miR-30a-3p in the tumorigenesis of GC. METHODS: For experimental study, RNA-Seq datasets and equivalent clinical data for 367 samples were achieved from The Cancer Genome Atlas (TCGA)-STAD datasets. The online software clusterProfiler was used to perform Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway functional enrichment. The co-expression of YY1, PVT1, and Myc genes was evaluated by determining the Pearson correlation coefficients. Potential competing endogenous RNAs of PVT1-miRNA-Myc were predicted by the Cytoscape tool and Kaplan- Meier curves were generated for YY1, PVT1, and Myc genes. For clinical study, Human GC samples were taken from 26 pairs of GC tissue (GCT) and para-tumor tissue (PT, 5 cm from the edge of the tumor) in which no patient had previously undergone preoperative adjuvant chemotherapy or radiotherapy. RESULTS: For experimental study, a total of 1144 differential expression genes (DEGs) were identified consisting of 731 up-regulated genes and 413 down-regulated genes. DEGs were Myc, YY1, and PVT1 and PVT1 was significantly different (adj. P=1.11E-11). The correlation coefficient between PVT1 and Myc was 0.42. A ceRNA network model suggested the hsa-miR-30a-3p was interacted between PVT1 and Myc, playing the role of information transmission. Survival analysis of these genes suggested that lncRNA PVT1 might influence the GC case survival (p=0.06). PVT1 expression was upregulated in human gastric cancer tissues and its relative PVT1 expression of PT was increased two fold compared to GCT. The expressions of PVT1 from the tumor tissues were significantly upregulated in GCT. CONCLUSION: These discoveries imply that lncRNA PVT1 and hsa-miR-30a-3p has a responsibility in the GC development. Therefore, targeting PVT1 or/and hsa-miR-30a-3p as a strategy for gastric cancer should be explored.

The effectiveness of faecal collection devices in preventing incontinence-associated dermatitis in critically ill patients with faecal incontinence: A systematic review and meta-analysis.

OBJECTIVE: The objective of this study was to investigate the effects of different types of faecal collection devices on incontinence-associated dermatitis (IAD) in critically ill patients with faecal incontinence. REVIEW METHOD USED: This was a systematic review and meta-analysis. DATA SOURCES: A comprehensive electronic literature search was performed in PubMed, Embase, Cumulative Index of Nursing and Allied Health Literature (CINAHL), the Cochrane library, China Biology Medicine (CBM), China National Knowledge Infrastructure (CNKI), Wanfang, and WeiPu. All the databases were searched from their inception to July 31, 2019, and the data were updated on November 2, 2019. REVIEW METHODS: Randomised controlled trials (RCTs) and quasi-experimental studies were included. Participants were critically ill patients with faecal incontinence, and the interventions involved care with faecal collection devices. Comparisons were usual care, and the outcome was the incidence of IAD. Odds ratios (ORs) were used to calculate the pooled effect sizes. Heterogeneity was tested using the inconsistency index (I2) method. RESULTS: Nineteen studies were included in this systematic review including 16 RCTs and three quasi-experimental studies. Twelve RCTs were included in the meta-analysis, which showed that the use of faecal collection devices significantly reduced the incidence of IAD. Subgroup analyses based on device type showed significant effects for anal pouch collection devices (OR, 0.14; 95% confidence interval [CI], 0.07-0.26; P < 0.00001), anal pouch connected to negative-pressure suction devices (OR, 0.18; 95% CI, 0.08-0.42; P < 0.00001), anal catheter/tube collection devices (OR, 0.24; 95% CI, 0.13-0.44; P < 0.00001), and anal catheter/tube connected to negative-pressure suction devices (OR, 0.20; 95% CI, 0.07-0.59, P < 0.00001). CONCLUSIONS: Faecal collection devices can reduce the incidence of IAD in critically ill patients with faecal incontinence. It is suggested that when using a device to care for critically ill patients with faecal incontinence, an anal pouch connected to continuous low-negative-pressure suction device should be preferred. Further high-quality research is still needed regarding anal catheter/tube collection devices and anal catheter/tube connected to continuous low-negative-pressure suction devices.

Quantitation of nuclear factor kappa B activation in pancreatic acinar cells during rat acute pancreatitis by flow cytometry.

This study aimed to develop a specific and sensitive method for the rapid detection of NF-κB activity in pancreatic tissue. Male Wistar rats were randomly divided into two groups: (1) 16 rats in the acute pancreatitis (AP) group received retrograde injection of 5% sodium taurocholate (STC) into the biliopancreatic duct, and (2) 16 rats in the Control group received saline. NF-κB activation in rat pancreatic acinar cells was assessed by flow cytometry (FCM). We found that the NF-κB activity in the AP group significantly increased at 1.5 h (29.80%±7.83), had a peak at 3 h (65.17%±13.22), and then decreased gradually to 12 h time point, close to the level after 1.5 h stimulation of STC. The NF-κB activity of the Control group did not significantly vary at different time points (P>0.05). FCM is a specific and sensitive assay for the rapid detection of NF-κB activity in pancreatic tissue.