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Background: TNFAIP8L2 is a member of the tumor necrosis factor-alpha-inducible protein 8 (TNFAIP8) family shown to have oncogenic effects. However, no pan-cancer analysis has shown an association between TNFAIP8L2 and various tumor types. Methods: Using the Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and other bioinformatics tools, we performed a pan-cancer analysis of the TNFAIP8L2 gene. We investigated TNFAIP8L2’s function in 33 tumor types, exploring its gene expression, survival status, DNA methylation, genetic alterations, immune infiltration, and associated cellular pathways. Results: TNFAIP8L2 was strongly expressed in most malignancies and linked with patients' overall survival (OS) and disease-free survival (DFS). Missense mutations are the main type of mutation in the TNFAIP8L2 gene. TNFAIP8L2’s methylation levels were significantly different between tumors and normal tissues. In addition, infiltration of CD8+ T cells, cancer-associated fibroblasts, and macrophages has been linked to TNFAIP8L2 expression in various malignancies, including cervical cancer, breast-infiltrating cancer, and renal clear cell carcinoma. Mechanistically, Rac2, actin filament, and Fc gamma R-mediated phagocytosis are all implicated. Conclusion: TNFAIP8L2 may be a biomarker or treatment target for predicting the prognosis of cancer victims. In addition, it might interfere with Rac2-mediated pathways regulating macrophage M1 to M2 differentiation and metastasis. This could provide a new direction for tumor therapy.

Yoga is a mind and body practice that includes relaxation, meditation, breathing exercises, and body postures. It can be effective in enhancing the functioning of several body systems, including the lower urinary tract. Normal lower urinary tract functioning depends in part on the coordination of the bladder, urethra, pelvic floor and other muscles, and the nerves that control them. Lower urinary tract dysfunction can lead to symptoms, that is, stress urinary incontinence (UI), urinary frequency, nocturia, urinary urgency with and without incontinence, and mixed UI. Recent evidence suggests that yoga can improve lower urinary tract symptoms (LUTS). Thus, we performed a scoping review of the literature with regard to the evidence for the effects of yoga on LUTS and factors that may mediate yoga's effects on LUTS with the goal to identify gaps in knowledge regarding the relationship between yoga practice and LUTS.The authors employed the PRISMA extension for Scoping Reviews (PRISMA-ScR) methodological approach, proposed by Tricco et al., by searching the electronic databases, PubMed, Embase, and PsycINFO, for articles using the following keywords: yoga, urinary incontinence, urinary tract, bladder, and urethra. We assessed the quality of the studies using the Joanna Briggs Institute Critical Appraisal Checklist.Of the 172 articles we found, 8 articles met the inclusion criteria and were reviewed. We found that, despite the use of different protocols, yoga may reduce certain LUTS by increasing the strength of pelvic floor muscle and/or regulating the autonomic nervous system and activating the central nervous system.Yoga is a noninvasive practice that may improve some LUTS. Rigorous studies are needed to determine the specific mechanisms through which yoga may affect LUTS.

The purpose of the study was to compare the relative clinical efficacies of irradiation stent (IRS) and conventional stent (CVS) insertions for the treatment of patients with malignant biliary obstruction (MBO). Pubmed, Embase, and Cochrane Library databases were searched for relevant randomized controlled trials (RCTs) from the date of inception through to August 2020. Data analysis was performed using RevMan v5.3. This meta-analysis included eight RCTs which included a total of 319 patients who had undergone IRS insertion, and 328 who had undergone CVS insertion. No significant differences in pooled Δ total bilirubin values (MD 0.34; P = 0.92), incident rates of cholangitis (P = 0.47), hemobilia (P = 0.60), or pancreatitis (P = 0.89) were detected between two groups. The rate of stent dysfunction was significantly lower in the IRS group compared to the CVS group (22.2% vs. 37.7%, P = 0.02). The pooled stent patency (P < 0.00001) and survival (P < 0.00001) were significantly longer in the IRS group compared to the CVS group. Significant heterogeneity was detected in the endpoints of rate of stent dysfunction (I2 = 52%; P = 0.08) and survival (I2 = 77%; P = 0.0005). Subgroup analysis was performed based on the different IRS types and showed significantly longer survival in the IRS group based on both types of IRS. Funnel plot analyses did not detect any evidence of publication bias. This meta-analysis included eight RCTs which included a total of 319 patients who had undergone IRS insertion, and 328 who had undergone CVS insertion. No significant differences in pooled Δ total bilirubin values (MD 0.34; P = 0.92), incident rates of cholangitis (P = 0.47), hemobilia (P = 0.60), or pancreatitis (P = 0.89) were detected between 2 groups. The rate of stent dysfunction was significantly lower in the IRS group compared to the CVS group (22.2% vs. 37.7%, P = 0.02). The pooled stent patency (P < 0.00001) and survival (P < 0.00001) were significantly longer in the IRS group compared to the CVS group. Significant heterogeneity was detected in the endpoints of rate of stent dysfunction (I2 = 52%; P = 0.08) and survival (I2 = 77%; P = 0.0005). Subgroup analysis was performed based on the different IRS types and showed significantly longer survival in the IRS group based on both types of IRS. Funnel plot analyses did not detect any evidence of publication bias. Our meta-analysis demonstrates that IRS insertion can prolong stent patency and the survival of patients with MBO compared to CVS insertion.

Background: Interferon-lambda 4 (IFNL4) ss469415590 is a newly discovered polymorphism that could predict the treatment response in hepatitis C virus (HCV)-infected patients. This meta-analysis was performed in order to clarify its specific effect on the treatment response and to compare it with interleukin 28b (IL28B). Method: The commonly used literature databases were searched. Meta-analyses were performed with fixed/random-effects models using Stata 12.0. The sustained virological response (SVR) rate was summarized using R software. Publication bias was examined through Egger's test. Results: A total of seven studies were finally included in this meta-analysis. IFNL4 ss469415590 was demonstrated to be associated with SVR (odds ratio (OR) 3.83, 95% confidence interval (CI) 3.22–4.56, p

Professional identity is an important and universal concept in the field of nursing because it not only affects nurses' perceptions of their role in nursing, but it also affects retention rates. However, the influential factors that impact the professional identity of nursing students currently are not well known.This exploratory study aims to investigate the concept of professional identity and confirm its influencing factors among post-associate degree baccalaureate nursing students in China.We conducted a cross-sectional study of 198 first-year post-associate degree baccalaureate nursing students enrolled in full-time study at two provincial medical colleges in China. We used paper and pencil questionnaires to conduct the survey and obtain the results used in this study.The overall mean score for 'professional identity' of the sample was 3.63 ± 0.62 on a scale of 1 through 5, with the means for the five dimensions of professional identity ranging from 3.29 to 4.02. A clinical learning experience that is longer than eight months (ref. = 8 months) (β = 0.138, p 0.036) and a positive perception of the clinical learning environment (β = 0.476, p 0.001) are the dominant factors that we found to be positively associated with professional identity.Nurse educators should investigate the factors that influence professional identity among their students to help develop a stable and satisfied nursing workforce.

Uropathogenic Escherichia coli (UPEC), the primary uropathogen, adhere to and invade bladder epithelial cells (BECs) to establish a successful urinary tract infection (UTI). Emerging antibiotic resistance requires novel nonantibiotic strategies. Our previous study indicated that luteolin attenuated adhesive and invasive abilities as well as cytotoxicity of UPEC on T24 BECs through down-regulating UPEC virulence factors. The aims of this study were to investigate the possible function of the flavonoid luteolin and the mechanisms by which luteolin functions in UPEC-induced bladder infection. Firstly, obvious reduction of UPEC invasion but not adhesion were observed in luteolin-pretreated 5637 and T24 BECs sa well as mice bladder via colony counting. The luteolin-mediated suppression of UPEC invasion was linked to elevated levels of intracellular cAMP induced by inhibiting the activity of cAMP-phosphodiesterases (cAMP-PDEs), which resulting activation of protein kinase A, thereby negatively regulating Rac1-GTPase-mediated actin polymerization. Furthermore, p38 MAPK was primarily and ERK1/2 was partially involved in luteolin-mediated suppression of UPEC invasion and actin polymerization, as confirmed with chemical activators of p38 MAPK and ERK1/2. These data suggest that luteolin can protect bladder epithelial cells against UPEC invasion. Therefore, luteolin or luteolin-rich products as dietary supplement may be beneficial to control the UPEC-related bladder infections, and cAMP-PDEs may be a therapy target for UTIs treatment. © 2016 BioFactors, 42(6):674-685, 2016.

While miR-204 expression may be linked to renal cell carcinoma (RCC) progression, the detailed mechanisms remain unclear. In the present study, we demonstrated that miR-204 was differentially expressed in RCC tissues when compared with surrounding normal kidney tissues. Ectopic overexpression of miR-204 in human RCC cells suppressed cell proliferation and invasion in vitro and in vivo. Mechanism dissection revealed that miR-204 may function through RAB22A signals to inhibit RCC proliferation and invasion. Overexpression of RAB22A by oe-RAB22A was able to partially reverse the miR-204-mediated suppression of RCC tumor progression. Together, these results revealed that miR-204 suppressed RCC proliferation and invasion by directly targeting the RAB22A gene. Targeting newly identified RAB22A with miR-204 may aid in the suppression of RCC proliferation and invasion.

Alpinetin, a type of novel plant flavonoid derived from Alpinia katsumadai Hayata, has been reported to have anti-inflammatory effects. The aim of this investigation was designed to reveal the protective effects of alpinetin on Lipopolysaccharide (LPS)/ d -galactosamine (D-Gal)-induced liver injury in mice. Alpinetin (12.5, 25, 50 mg/kg) were given 1 h before LPS and D-Gal treatment. 12 h after LPS and D-Gal treatment, the liver tissues and serum were collected. Our results showed that alpinetin treatment improved liver histology, indicating a marked decrease of inflammatory cell infiltration and restore hepatic lobular architecture. Alpinetin also inhibited liver myeloperoxidase (MPO) activity and malondialdehyde (MDA) level. Furthermore, LPS/D-Gal-induced tumor necrosis factor-α (TNF-α) and Interleukin-1β (IL-1β) production were dose-dependently inhibited by alpinetin. Alpinetin also attenuated LPS/D-Gal-induced expression of phospho-NF-κB p65 and phospho-IκBα. In addition, alpinetin was found to increase the expression of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). In conclusion, these findings suggested that alpinetin inhibited liver injury through inhibiting NF-κB and activating the Nrf2 signaling pathway.

To examine whether poly-unsaturated fatty acid (PUFA) therapy is beneficial for improving nonalcoholic steatohepatitis (NASH).In total, 78 patients pathologically diagnosed with NASH were enrolled and were randomly assigned into the control group and the PUFA therapy group (added 50 mL PUFA with 1:1 ratio of EHA and DHA into daily diet). At the initial analysis and after 6 mo of PUFA therapy, parameters of interest including liver enzymes, lipid profiles, markers of inflammation and oxidation, and histological changes were evaluated and compared between these two groups.At the initial analysis, in patients with NASH, serum levels of alanine aminotransferase (ALT) and aspartase aminotransferase (AST) were slightly elevated. Triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol levels, markers of systemic inflammation [C-reactive protein (CRP)] and oxidation [malondialdehyde (MDA)], as well as fibrosis parameters of type IV collagen and pro-collagen type III pro-peptide were also increased beyond the normal range. Six months later, ALT and AST levels were significantly reduced in the PUFA group compared with the control group. In addition, serum levels of TG and TC, CRP and MDA, and type IV collagen and pro-collagen type III pro-peptide were also simultaneously and significantly reduced. Of note, histological evaluation showed that steatosis grade, necro-inflammatory grade, fibrosis stage, and ballooning score were all profoundly improved in comparison to the control group, strongly suggesting that increased PUFA consumption was a potential way to offset NASH progression.Increased PUFA consumption is a potential promising approach for NASH prevention and reversal.

Objectives Hepatocellular carcinoma (HCC) is one of the most common cancers and is a significant leading cause of cancer-related deaths worldwide. Emerging evidence has shown that microRNAs (miRNAs) are associated with cancer development and progression. However, up to now little has been known concerning the role of miR-709 in HCC. Materials and methods Real-time RT-PCR was performed to detect expression of miR-709 in HCC cell lines and tissues. To further understand its role in HCC, we restored its expression in HepG2 cell line through transfection with miR-709 mimics or inhibitors. CCK-8 proliferation assay, migration assay and invasion assay were used to detect functional roles of miR-709. Luciferase assay and western blotting were performed to detect the target gene of miR-709. Results We found that miR-709 was highly expressed in HCC tissues and in HCC cell lines by qRT-PCR. Re-expression of miR-709 in HCC cells remarkably promoted cell migration and invasiveness in vitro. Subsequent investigation revealed that glypican-5 (GPC5) was a direct and functional target of miR-709 in HCC cells where overexpression of miR-709 impaired GPC5-induced inhibition of proliferation and invasion. Finally, analysis of miR-709 and GPC5 levels in human HCC tissues revealed that miR-709 inversely correlated with GPC5 expression. Conclusions These results suggest that miR-709 may positively regulate invasion and metastasis of HCC through targeting GPC5.

Pyocyanin (PCN, 1-hydroxy-5-methyl-phenazine) is one of the most essential virulence factors of Pseudomonas aeruginosa (PA) to cause various cytotoxic effects in long-term lung infectious diseases, however the early effect of this bacterial toxin during PA infection and subsequent autonomous immune response in host cells have not been fully understood yet. Our results display that early onset of PCN stimulates Pseudomonas aeruginosa PAO1 adhesion and invasion in A549 cells via ROS production. Non-histone nuclear protein HMGN2 is found to be involved in the regulation of PCN-induced oxidative stress by promoting intracellular ROS clearance. Mechanistically, HMGN2 facilitates nuclear translocation of transcription factor Nrf2 upon PCN stimulation and in turn elevates antioxidant gene expression. We also found that actin cytoskeleton dynamics is targeted by ROS, which is to be exploited by PAO1 for host cell internalization. HMGN2 regulates actin skeleton rearrangement in both PCN-dependent and independent manners and specifically attenuates PCN-mediated PAO1 infection via ROS elimination. These results uncover a novel link between nuclear protein HMGN2 and Nrf2-mediated cellular redox circumstance and suggest roles of HMGN2 in autonomous immune response to PA infection.

Urinary tract infection (UTI), primarily caused by uropathogenic Escherichia coli (UPEC), is one of the most common infectious diseases worldwide. Emerging antibiotic resistance requires novel treatment strategies. Luteolin, a dietary polyphenolic flavonoid, has been confirmed as a potential antimicrobial agent. Here, we evaluated the sub-MICs of luteolin for potential properties to modulate the UPEC infection. We found that luteolin significantly decreased the attachment and invasion of UPEC J96 or CFT073 in human bladder epithelial cell lines T24. Meanwhile, obvious decreased expression of type 1 fimbriae adhesin fimH gene, lower bacterial surface hydrophobicity and swimming motility, were observed in luteolin-pretreated UPEC. Furthermore, luteolin could attenuate UPEC-induced cytotoxicity in T24 cells, which manifested as decreased activity of lactate dehydrogenase (LDH). Simultaneously, the inhibition of luteolin on UPEC-induced cytotoxicity was confirmed by ethidium bromide/acridine orange staining. Finally, the luteolin-pretreated UPEC showed a lower ability of biofilm formation. Collectively, these results indicated that luteolin decreased the attachment and invasion of UPEC in bladder epithelial cells, attenuated UPEC-induced cytotoxicity and biofilm formation via down-regulating the expression of adhesin fimH gene, reducing the bacterial surface hydrophobicity and motility.