ERCC5 abnormal expression influences the biological behaviour of ovarian cancer by Wnt pathway

Nucleotide excision repair (NER) is the most important repair pathway of DNA, and a variety of cancers are closely related to the gene abnormal expression and the deletion or downregulation of gene function in NER pathway. In this study, we investigated the differential expression of ERCC5 in different ovarian cancer cells and its potential mechanism. By detecting the expression of ovarian in both SKOV3 and Caov4 cell lines, we found that the expression of ERCC5 in SKOV3 was significantly higher than that in Caov4. We further constructed the SKOV3 cell line with low ERCC5 expression by RNA interference and Caov4 cell line with high ERCC5 expression by transient transfection, then comparing the effect of ERCC5 abnormal expression on the biological behaviour of ovarian cancer cells. The results showed that high expression of ERCC5 could significantly promote proliferation and migration of ovarian cancer but inhibit apoptosis. However, low expression of ERCC5 could significantly promote apoptosis but inhibited proliferation and migration. We further observed the effect of ERCC5 abnormal expression on potential regulation pathway by Western blot and noticed that ERCC5 abnormal expression could activate the Wnt pathway. Overall, the results revealed that ERCC5 abnormal expression could influence the proliferation, apoptosis and migration ability of ovarian cancer cells by activating the Wnt pathway.

miR-135a inhibits airway inflammatory response in asthmatic mice via regulating JAK/STAT signaling pathway

The objective of this study was to investigate the inhibitory effect of miR-135a in regulating JAK/STAT signaling pathway on airway inflammation in asthmatic mice. An asthma model was established by sensitization and stimulation with ovalbumin (OVA), and the corresponding drug intervention was given from the day of stimulation by means of nasal drops. Airway hyperresponsiveness was tested. The content of miR-135a in the lung tissue of mice was detected by RT-PCR. The pathological changes of lung tissue were evaluated by HE staining. Tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-5, and eotaxin in bronchoalveolar lavage fluid (BALF) and lung tissue were detected by ELISA and immunohistochemistry, respectively. The expression of JAK/STAT signaling pathway-related protein in lung tissue was detected by western blot. To further validate the effect of miR-135a overexpression on the JAK/STAT signaling pathway, pathway activators and inhibitors were added. Compared with the OVA group, the airway hyperresponsiveness of the mice was significantly decreased after treatment with the miR-135a agonist. The expression of miR-135a was significantly increased in the lung tissue and the pathological changes of the lung tissue were alleviated. The contents of TNF-α, IL-6, IL-5, and eotaxin in BALF and lung tissues were decreased. The expression of JAK/STAT signaling pathway-related proteins p-JAK3/JAK3, p-STAT1/STAT1, and p-STAT3/STAT3 were significantly reduced in lung tissue (P<0.05). Addition of JAK inhibitor AG490 reduced airway inflammation in asthmatic mice. miR-135a agonists inhibit airway inflammation in asthmatic mice by regulating the JAK/STAT signaling pathway.

Screening of molecular markers in gastric cancer based on GEO database / 中国肿瘤生物治疗杂志

@#[Abstract] Objective: Bioinformatics combined with Gene Expression Omnibus (GEO) was used to screen key genes involved in the development of gastric cancer in order to obtain molecular markers for diagnosis, target selection and prognosis prediction of gastric cancer. Methods: The chip data sets related to gastric cancer (GC) from the GEO database were downloaded, and differentially expressed genes (DEG) were screened. Functional enrichment analysis on DEG was performed, and protein-protein interaction network (PPI) was constructed to screen key genes. Then, co-expression networks were further constructed, and survival curves were drawn and hierarchical clustering analysis was performed. Results: A total of 261 GC-related DEGs were selected, and 14 key genes were obtained through analysis, which were PLOD1, PLOD3, COL1A1, COL1A2, COL2A1, COL3A1, COL4A1, COL4A2, COL8A1, COL12A1, COL15A1, ITGA2, LUM and SERPINH1. Key genes are mainly involved in biological processes such as generation of collagen fiber tissues, extracellular matrix tissues, extracellular structure tissues, skin morphogenesis, collagen biosynthesis and vascular development. Survival curve analysis showed that the change in the expression of COL3A1 (P=0.0241) significantly reduced the overall survival rate of patients with gastric cancer; the change in the expression of ITGA2 (P=0.0679) also showed a correlation with the reduction of disease-free survival in gastric cancer patients. Compared with normal gastric tissues, hierarchical cluster analysis showed that the expressions of genes PLOD1, PLOD3, COL3A1, ITGA2, COL1A2, COL1A1, COL4A1, LUM, COL12A1, SERPINH1 and COL8A1 in GC tissues were up-regulated. Conclusion: The key genes obtained after screening can be used as potential molecular markers for early diagnosis, treatment target selection and prognosis judgment of gastric cancer, which provide reference for subsequent research.

Utility and Safety of Tolvaptan in Cirrhotic Patients with Hyponatremia: a Prospective Cohort Study

Abstract: Introduction and aim. Hyponatremia is common in patients with decompensated cirrhosis and is associated with increased mortality. Tolvaptan, a vasopressor V2 receptor antagonist, can increase free wáter excretion, but its efficacy and safety in cirrhotic patients remain unclear. Material and methods. We studied the usage and safety of tolvaptan in cirrhotic patients in a real-life, non-randomized, multicenter prospective cohort study. Forty-nine cirrhotic patients with hyponatremia were treated with tolvaptan 15 mg daily, and 48 patients not treated with tolvaptan in the same period served as controls. Improvement in serum sodium level was defined as an increase in serum sodium from < 125 to ≥ 125 mmol/L or from 125-134 to ≥ 135 mmol/L on day 7. Results. Twenty-three (47%) patients in the tolvaptan group and 17 (35%) in the control group had normal serum sodium on day 7 (p = 0.25). Serum sodium improved in 30 (61%) patients in the tolvaptan group and 17 (35%) patients in the control group (p = 0.011). Adverse events occurred in 46-47% of patients in both groups, and tolvaptan was not associated with worsened liver function. No patient with normal serum sodium on day 7 died within 30 days of treatment, whereas 16% of those with persistent hyponatremia died (p = 0.0019). Conclusion. In conclusion, short-term tolvaptan treatment is safe and can improve serum sodium level in cirrhotic patients with hyponatremia. Normalization of serum sodium level is associated with better survival.

Value of non-sexual penile erection for penile rehabilitation in men with erectile dysfunction / 中华男科学杂志

Erectile dysfunction (ED) is a common male disease. Some related studies show that the prevalence of ED is nearly 52% in men aged 40 to 70 years and is increasing among younger males. Hypoxia is now considered to be an independent risk factor for ED and the mechanisms of hypoxia inducing ED are varied and complicated. Recently, an idea in penile rehabilitation has attracted much attention, which aims at improving erectile function by increasing oxygen supply to the cavernosum and reducing tissue fibrosis and apoptosis. The approaches to achieve non-sexual penile erection by increasing oxygen supply to the cavernosum, such as behavior therapy, medication, vacuum constriction device, and intracavernous injection, can simulate normal sexual erection and help patients with penile rehabilitation. This review focuses on the strategies for non-sexual penile erection in penile rehabilitation.

Expression of ALEX1 in breast cancer and its clinical significance / 中国病理生理杂志

AIM: To detect the expression of ALEX 1 in the breast cancer tissues in order to verify whether ALEX1 has correlation with clinical pathological features in breast cancer .METHODS:Real-time PCR and immmunohis-tochemistry were applied to detect the expression of ALEX 1 at mRNA and protein levels in the breast tissues .The statistical analysis were performed for determining the correlation with the level of ALEX 1 and the clinical pathological features in breast cancer .RESULTS:The protein levels of ALEX1 in the breast cancer tissues were lower than that in the non-breast cancer tissues (P<0.01).The expression of ALEX1 had correlations with pathological grade , clinical stage, molecular type (P<0.05) but had no correlation with the patients ’ age, tumor size and tumor types in breast cancer .Furthermore, the result of real-time PCR showed that mRNA expression of ALEX 1 was also significantly reduced in the breast cancer tis-sues (P<0.01).CONCLUSION:The expression of ALEX1 in the breast cancer tissues is lower than that in non-breast cancer tissues .The pathological grade and clinical stage in breast cancer are negatively correlated with the expression of ALEX1.

Identification of reference genes for gene expression normalization in safflower (Carthamus tinctorius)

ABSTRACT Safflower (Carthamus tinctorius L., Asteraceae) is an important oil crop and medicinal plant. Gene expression analysis is gaining importance in the research of safflower. Quantitative PCR has become a powerful method for gene study. Reference genes are one of the major qualification requirements of qPCR because they can reduce the variability. To identify the reference genes in safflower, nine candidate genes of the housekeeping genes were selected from the EST library of safflower constructed by our lab: CtACT (actin), CtGAPDH (glyceraldehyde 3-phosphate dehydrogenase), CtE1F4A (elongation factor 1 alpha), CtTUA (alpha-tubulin), CtTUB (beta-tubulin), CtPP2A (serine/threonine-protein phosphatase), CtE1F4A (eukaryotic initiation factor 4A), CtUBI (Ubiquitin), and Ct60S (60S acidic ribosomal protein). Expression stability was examined by qPCR across 54 samples, representing tissues at different flowering stages and two chemotype of safflower lines. We assessed the expression stability of these candidate genes by employing four different algorithms (geNorm, NormFinder, ΔCt approach, and BestKeeper) and found that CtUBI and Ct60S were the highly ranked candidate genes. CtUBI and Ct60S were used as reference genes to evaluate the expression of CtFAD2-10 and CtKASII. Our data suggest CtUBI and Ct60S could be used as internal controls to normalize gene expression in safflower.

Effect of salidroside on the expression of connexin43 in the corpus cavernosum smooth muscle cells of hypoxic rats / 中华男科学杂志

<p><b>Objective</b>To investigate the effect of salidroside on the expression of the connexin43 (Cx43) protein in the corpus cavernosum smooth muscle cells (CCSMCs) of hypoxic SD rats.</p><p><b>METHODS</b>CCSMCs were cultured in vitro and identified by immunofluorescence staining. The cells were divided into six groups: normal control (21% O2), hypoxia (1% O2), hypoxia+salidroside (HS) 8 μg/ml,HS 16 μg/ml, HS 32 μg/ml, and HS 64 μg/ml, and cultured for 48 hours. Then the relative expression of Cx43 in different groups was detected by Western blot.</p><p><b>RESULTS</b>The in vitro cultured CCSMCs grew well and 90% of the cells showed positivity for α-SMA and desmin on immunohistochemistry. Salidroside ≤64 μg/ml produced no obvious toxicity on the CCSMCs. The expressions of Cx43 and phosphorylated proteins were dramatically increased in the hypoxia group as compared with the normal control (P<0.01 and P<0.05). The HS groups all showed significantly higher expression of Cx43 than the hypoxia group (P<0.01), but the phosphorylation rate of the Cx43 proteins was remarkably decreased (P<0.01).</p><p><b>CONCLUSIONS</b>Hypoxia increases the expression of Cx43 in the CCSMCs of SD rats. Salidroside ≤64 μg/ml cannot reverse the hypoxia-induced change but can reduce the dephosphorylation of Cx43 in CCSMCs. It is deduced that salidroside can protect CCSMCs by decreasing the phosphorylation of Cx43 and suppressing hypoxia-induced formation of the gap junction channel.</p>

Natural killer cells in hepatitis B virus infection

Natural killer cells are a unique type of lymphocytes with cytotoxic capacity, and play important roles against tumors and infections. Recently, natural killer cells have been increasingly valued in their effects in hepatitis B virus infection. Since hepatitis B virus is not cytopathic, the subsequent antiviral immune responses of the host are responsible for sustaining the liver injury, which may result in cirrhosis and even hepatocellular carcinoma. Many studies have confirmed that natural killer cells participate in anti-hepatitis B virus responses both in the early phase after infection and in the chronic phase viacytolysis, degranulation, and cytokine secretion. However, natural killer cells play dichotomic roles: they exert antiviral and immunoregulatory functions whilst contribute to the pathogenesis of liver injury. Here, we review the roles of natural killer cells in hepatitis B virus infection, introducing novel therapeutic strategies for controlling hepatitis B virus infection viathe modulation of natural killer cells.