EGCG: Potential application as a protective agent against grass carp reovirus in aquaculture.

Grass carp reovirus (GCRV) is the primary cause of grass carp haemorrhagic disease. The major catechin in green tea, (-)-epigallocatechin-3-gallate (EGCG), has been found to have anti-GCRV activity in the C. idellus kidney cell line (CIK). The aim of this study was to test the potential application of EGCG as an anti-GCRV agent in aquaculture. Here, we demonstrate that various concentrations (99%, 50% and 35%) of EGCG could inhibit GCRV infectivity. EGCG (50%) + GCRV treatment significantly reduced the number of dead fish at 1-, 2-, 3-, 4 -and 5-day post-challenge compared with the negative control (GCRV challenge without EGCG treatment). The safety of EGCG compound products on cell survival was studied using four fish cell lines; we did not detect a significant change in cell viability within 24 hours of EGCG incubation. We also evaluated toxicity and concentrations of malondialdehyde (MDA), glutathione (GSH) and lysozyme (LZM) in the grass carp, and the results showed that even a high dose of EGCG did not induce toxicity. Following EGCG compound injection, the concentration of MDA decreased and the concentration of GSH and LZM increased compared with the control groups. We also detected EGCG concentration in grass carp plasma and kidney using HPLC with electrochemical detection after intraperitoneal injection at a dose of 150 mg/kg. The concentration of EGCG in the plasma and kidney reached the highest levels (20 µg/ml and 1.5 µg/ml) about 12 hr after injection and then decreased. Overall, EGCG is a safe, effective product that could inhibit GCRV infection and improve immunoactivity in aquaculture.

Measuring decreased serum IgG sialylation: a novel clinical biomarker of lupus.

INTRODUCTION: The aim of this work was to develop a simple assay to distinguish between patients with rheumatoid arthritis (RA) and patients with systemic lupus erythematosus (SLE) by measuring the serum sialylated IgG (SAIgG). METHODS: Using a newly established SNA-based ELISA method, we compared the sialylation of immunoglobulin G (IgG) from a healthy control group (n = 41), RA patients (n = 30), SLE patients (n = 45), patients with neuropsychiatric SLE (NPSLE) (n = 30) and patients with juvenile idiopathic arthritis (JIA) (n = 32). RESULTS: The average SAIgG level in healthy control individuals, RA patients, JIA patients, SLE patients and NPSLE patients was 0.64 ± 0.17, 0.82 ± 0.33, 0.69 ± 0.23, 0.12 ± 0.02 and 0.03 ± 0.01 mg/ml, respectively. The ratio of sialylated IgG to total IgG was significantly decreased in the SLE group (1.88 ± 0.32%) compared with the healthy population (4.64 ± 0.90%). CONCLUSION: In summary, while the mean serum SAIgG level of RA and JIA patients was similar to that of the healthy population, there was a significant decrease in the serum SAIgG of both SLE groups tested, whereby the level of the NPSLE population group was the lowest.

Effect of aerobic exercise on miRNA-TLR4 signaling in atherosclerosis.

Toll-like receptor 4 (TLR4)-tumor necrosis factor receptor 6 (TRAF6) signaling is activated in atherosclerosis (AS), inducing inflammatory mediators. Because miR-146a, a TLR4 microRNA (miRNA), can regulate TLR4 signaling during inflammatory responses, this study investigated the effects of aerobic exercise on TLR4-targeted miRNAs in AS. Apolipoprotein E-null mice fed a high-fat diet for 12 weeks were separated into 3 groups: (i) no treatment (AS), (ii) statin treatment (AD), or (iii) aerobic exercise (AE). Plaques and foam cells were observed in the untreated control and statin groups, respectively, but not in the AE group. Reduced angiotensin II (Ang II) and endothelin 1 (ET1) levels were observed in the AE group. Both treatment groups significantly altered the expression of inflammatory cytokine expression and reduced vascular TLR4 levels. Increased miR-146a and miR-126 and reduced miR-155 levels were observed in both treatment groups (all, P<0.001). miR-146a interacted with the 3' untranslated region of the TRAF6 gene, reducing its expression. Thus, aerobic exercise and statins may induce miR-146a expression, thereby reducing vascular TRAF and TLR4 signaling and vascular inflammatory injury in AS. Further analysis of this pathway may provide insight into the protective effects of aerobic exercise on vascular disease as well as new therapeutic targets.

Effects of beraprost sodium on renal function and inflammatory factors of rats with diabetic nephropathy.

Beraprost sodium (BPS) is a prostaglandin analogue. We investigated its effects on rats with diabetic nephropathy. There were 20 rats each in the normal control group (NC), the diabetic nephropathy group (DN), and the BPS treatment group. The rats in DN and BPS groups were given a high-fat diet combined with low-dose streptozotocin intraperitoneal injections. The rats in the BPS group were given daily 0.6 mg/kg intraperitoneal injections of this drug. After 8 weeks, blood glucose, 24-h UAlb, Cr, BUN, hs-CRP, and IL-6 levels increased significantly in the DN group compared with the NC group; however, the body mass was significantly reduced in the DN group compared with the NC group. Blood glucose, urine output, 24-h UAlb, Cr, hs-CRP, and IL-6 levels were significantly lower in the BPS group than in the DN group; the body mass was significantly greater in the DN group. Therefore, we concluded that BPS can improve renal function and protect the kidneys of DN rats by reducing oxidative stress and generation of inflammatory cytokines; it also decreases urinary protein excretion of rats with diabetic nephropathy.

MicroRNA-100/99a, deregulated in acute lymphoblastic leukaemia, suppress proliferation and promote apoptosis by regulating the FKBP51 and IGF1R/mTOR signalling pathways.

BACKGROUND: MicroRNAs alter multiple cell processes and thus influence tumour carcinogenesis and progression. MiR-100 and miR-99a have been reported to be aberrantly expressed in acute leukaemia. In this study, we focused on their functions in acute lymphoblastic leukaemia (ALL) and the molecular networks in which they are involved. METHODS: MiR-100 and miR-99a expression levels were measured in acute leukaemia patients by qRT-PCR. Kaplan-Meier analysis and log-rank tests were used to calculate the survival rate. Three human ALL cell lines were studied. Apoptosis and proliferation were analysed using siRNA transfection, western blot and flow cytometry. RESULTS: In vivo, miR-100 and miR-99a were down-regulated in 111 ALL patients, especially in high-risk groups; their expression levels were correlated with the patient's 5-year survival. In vitro, the restoration of miR-100 and miR-99a in ALL cells suppressed cell proliferation and increased dexamethasone-induced cell apoptosis. Ectopic expression of miR-100 and miR-99a targeted FK506-binding protein 51 (FKBP51) and, in turn, influenced glucocorticoid receptor (GR) activity. Meanwhile, miR-100 and miR-99a overexpression inhibited the expression of IGF1R and mTOR and their downstream oncogene MCL1. CONCLUSION: MiR-100 and miR-99a have critical roles in altering cellular processes by targeting both the FKBP51 and IGF1R/mTOR signalling pathways in vitro and might represent a potential novel strategy for ALL treatment.

Prognostic relevance and therapeutic implications of centromere protein F expression in patients with esophageal squamous cell carcinoma.

Centromere protein F (CENP-F), a cell cycle-regulated centromere protein, has been shown to affect numerous tumorigenic processes. This study aimed to clarify the prognostic significance of CENP-F expression in patients with esophageal squamous cell carcinoma (ESCC). The levels of CENP-F messenger RNA and protein were higher in ESCC cell lines than in the normal tissues. An immunohistochemical analysis of paired tissue specimens showed that the CENP-F expression was higher in tumorous tissues than in the adjacent non-tumorous tissues (P < 0.001). Moreover, there was a significant correlation between CENP-F expression and gender (P = 0.012), clinical stage (P = 0.039), and T classification (P = 0.026). Patients with higher CENP-F expression had shorter overall survival than those with lower CENP-F expression (P = 0.009). Multivariate Cox analysis indicated that CENP-F expression is an independent prognostic factor for overall survival (hazard ratio = 0.582, 95% confidence interval = 0.397-0.804, P = 0.041). Importantly, it was found that zoledronic acid (ZOL) could significantly enhance the chemotherapeutic sensitivity of ESCC cell lines with high CENP-F expression to cisplatin, although ZOL alone only exhibited a minor inhibitory effect to ESCC cells. In summary, these findings demonstrate that CENP-F may serve as a valuable molecular marker for predicting the prognosis of ESCC patients. In addition, the data indicate a potential benefit of combining ZOL with cisplatin in ESCC, suggesting that CENP-F expression may have therapeutic implications.

Screening and identification of the nucleic acid aptamers in nasopharyngeal carcinoma.

To screen the nucleic acid aptamers of the EB virus-positive nasopharyngeal carcinoma cells, we used SELEX technology and synthesized in vitro a 78-nucleotide random DNA library. We used normal nasopharyngeal epithelial cells and EB virus-positive low differentiated nasopharyngeal carcinoma cells as target to conduct 10 cycles of screening, cloning, sequencing, and identification of the aptamers. The fluorescence produced by the combination of the sub-library and the target cells gained intensity gradually with the increase in the number of screening cycles, indicating elevated binding capacity. The cluster analysis showed that the aptamers can be divided into three families, with two of the families having the common conserved sequence. In this study, by screening nucleic acid aptamers for affinity and specificity, we established an initial aptamer library for EB virus-positive nasopharyngeal carcinoma cells.

Synergistic effects of electroacupuncture and bone marrow stromal cells transplantation therapy in ischemic stroke.

OBJECTIVE: Animal studies and clinical trials demonstrated the effectiveness of a combination of transplanted bone marrow stromal cells (BMSC) and electroacupuncture (EA) treatment in improving neurological deficits. However, the ability of the BMSC-EA treatment to enhance brain repair processes or the neuronal plasticity of BMSC in ischemic stroke model is unclear. The purpose of this study was to investigate the neuroprotective effects and neuronal plasticity of BMSC transplantation combined with EA in ischemic stroke. MATERIALS AND METHODS: A male Sprague-Dawley (SD) rat middle cerebral artery occlusion (MCAO) model was used. Intracerebral transplantation of BMSC, transfected with lentiviral vectors expressing green fluorescent protein (GFP), was performed using a stereotactic apparatus after modeling. MCAO rats were treated with BMSC injection alone or in combination with EA. After the treatment, proliferation and migration of BMSC were observed in different groups by fluorescence microscopy. Quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemistry were performed to examine changes in the levels of neuron-specific enolase (NSE) and nestin in the injured striatum. RESULTS: Epifluorescence microscopy revealed that most BMSC in the cerebrum were lysed; few transplanted BMSC survived, and some living cells migrated to areas around the lesion site. NSE was overexpressed in the striatum of MCAO rats, illustrating the neurological deficits caused by cerebral ischemia-reperfusion. The combination of BMSC transplantation and EA attenuated the expression of NSE, indicating nerve injury repair. Although the qRT-PCR results showed that BMSC-EA treatment elevated nestin RNA expression, less robust responses were observed in other tests. CONCLUSIONS: Our results show that the combination treatment significantly improved restoration of neurological deficits in the animal stroke model. However, further studies are required to see if EA could promote the rapid differentiation of BMSC into neural stem cells in the short term.

Evaluation of status quo and determinants of catastrophic health expenditure among empty-nest elderly in China: evidence from the China health and retirement longitudinal survey (CHARLS).

OBJECTIVE: The aging society and the empty nest of the elderly have become issues that cannot be ignored by the Chinese government. Not only does the physical function of the empty-nest elderly (ENE) decline, and the incidence and prevalence of chronic diseases increase significantly, but they are also more likely to have loneliness, low life satisfaction, mental health problems, and even a much greater possibility of suffering from depression than the nonempty-nest elderly, besides the possibility of catastrophic health expenditure (CHE) which is also greatly increased. This paper aims to evaluate the status quo of dilemma and determinants of a vast sample of subjects based on the national level. SUBJECTS AND METHODS: Data were obtained from the latest 2018's data of the China Health and Retirement Longitudinal Study (CHARLS). Under the guidance of Andersen's model of health services utilization, this study clarified the overall and different demographic characteristics and prevalence of CHE among ENE and further built the Logit and Tobit model to explore the determinants of CHE occurrence and its intensity. RESULTS: A total of 7,602 ENE were included in the analysis, and the overall incidence of CHE among them was 21.20%. Poor self-reported health status (OR=2.03, 95% CI: 1.71-2.35), suffering from three or more chronic diseases simultaneously (OR=1.79, 95% CI: 1.42-2.15), low life satisfaction (OR=1.44, 95% CI: 1.20-1.68) and advanced age played the leading role in accounting for its high risk, and its intensity increased 0.0311 (SE=0.005), 0.0234 (SE=0.007), and 0.0178 (SE=0.005), respectively. In contrast, the leading drop in the probability of CHE among ENE was those whose monthly income was over 20,000 CNY (OR=0.46, 95% CI: 0.38-0.55), whose intensity declined 0.0399 (SE=0.005), whose monthly income was between 2,000 and 20,000 CNY (OR=0.78, 95% CI: 0.66-0.90) and whose intensity declined 0.021 (SE=0.005), and who were married during the survey period (OR=0.82, 95% CI: 0.70-0.94). Simultaneously, rural ENE showed more vulnerability and higher risk of CHE when confronted with these factors compared with the urban ones. CONCLUSIONS: More attention should be paid for ENE in China. The priority, including the relevant health insurance or social security measurements, should be further strengthened.

Risk factors for the development of hepatocellular carcinoma in Chengdu: a prospective cohort study.

OBJECTIVE: To investigate the incidence of hepatocellular carcinoma (HCC) in Chengdu, identify the risk factors for the development of HCC in Chengdu and provide a reference for the prevention of HCC. PATIENTS AND METHODS: The study population was recruited from Chengdu, Sichuan Province, China. The study group recruited volunteers in Chengdu from 2007 to 2012, conducted a baseline survey, and subsequently conducted long-term follow-up until December 31, 2019. A total of 22,525 study subjects were enrolled, excluding those who reported a previous history of liver disease, malignancy, and HCC within three months of enrollment. Cox proportional risk regression models were used to screen and determine the various risk factors and their hazard ratios (HR) for HCC in Chengdu, as well as to determine whether the association between other risk factors and HCC was modified by gender. RESULTS: The study population had a median follow-up of 5.35 years, and a total of 142 people developed HCC, with an incidence rate of 0.71%. Analysis of the multifactorial Cox proportional risk regression model showed that age (age 10 years for 1 group, HR= 1.98, 95% CI: 1.86-2.11, p<0.001), current smoking (HR= 1.25, 95% CI: 1.07-1.31, p=0.031), weekly consumption of pickled vegetables (HR= 1.70, 95% CI: 1.49-1.81, p=0.003) and consumption of pickled vegetables daily (HR= 1.36, 95% CI: 1.21-1.42, p=0.021) were risk factors for HCC, and women (HR= 0.39, 95% CI: 0.28-0.55, p=0.002) and the use of air conditioning (10 years for 1 group, HR= 0.79, 95% CI: 0.68-0.83, p=0.002) were protective factors against HCC. Further analysis revealed that the association between length of time using air conditioning and HCC was heterogeneous among men and women (p=0.007) and that there was an interaction between sex and use of air conditioning in the association with HCC development (p<0.001). CONCLUSIONS: The Chengdu population has a high incidence of HCC and numerous risk factors for HCC. There is a synergistic interaction between sex and length of time using air conditioning in their role in the development of HCC.

Systematic evaluation of influencing factors for Chinese rural doctors' job satisfaction and turnover intention: based on the two-factor theory.

OBJECTIVE: In China, rural doctors (RDs) perform crucial health care missions. However, they have received less attention than their colleagues in urban public hospitals. In this specific group, a severe challenge occurs in sync with a high turnover rate and deficient job satisfaction. MATERIALS AND METHODS: This study aims to systematically summarize and evaluate the influencing factors of job satisfaction and turnover intention among Chinese rural doctors. Seven databases, including PubMed, EMBASE, and China National Knowledge Infrastructure (CNKI), were systematically retrieved, and several experts were consulted to acquire holistic publications in this domain. RESULTS: A total of 20 full-text papers and 22,721 samples were included. In addition, 53 influencing factors were evaluated, of which 38 factors may play a significant role. Based on Herzberg's two-factor theory, together with China's cultural tradition and national conditions, we classified these influencing factors into sociodemographic characteristic factors (n=13), incentive factors (n=18), and health care factors (n=22). Meanwhile, we discussed and analyzed the influencing factors of turnover intention and job satisfaction in detail and put forward corresponding measures and suggestions for the government. CONCLUSIONS: We are confident that this research provides a holistic perspective to systematically evaluate the factors influencing the job satisfaction and intention to leave of Chinese rural doctors. Importantly, we hypothesize that the illumination of cases among Chinese rural physicians applies to other countries or regions, which has significant implications for the reformation of the medical system by governments or decision-makers worldwide.

Sixteen cases of pulmonary sclerosing haemangioma: CT findings are not definitive for preoperative diagnosis.

AIM: To describe and assess computed tomography (CT) imaging findings of pathologically confirmed pulmonary sclerosing haemangioma (PSH), a rare benign tumour, in 16 patients. MATERIALS AND METHODS: This study was approved by the human investigation committees of the two participating institutions, and the requirement of informed consent was waived. Findings from CT examinations in 16 patients with pathologically confirmed PSH were retrospectively reviewed. Two radiologists in consensus assessed the location, size, contour, and border of nodules, as well as the enhancement patterns. RESULTS: The study comprised 16 patients (two male and 14 female) aged 30-70 years. PSHs appeared as well-defined, round or ovoid masses with a diameter of 2.2±0.3cm, and were generally demonstrated as juxtapleural masses (94%) on CT. Calcification (13%), the air crescent sign (13%), and a prominent pulmonary artery (25%) in the tumours were also demonstrated in the cohort. The mean tumour attenuation value at CT was 30±3HU before intravenous administration of contrast media, and was significantly lower than that of the enhanced phase (79±3HU, p<0.05). Twelve tumours (75%) enhanced homogeneously compared with four tumours (25%) which enhanced heterogeneously. The diameters of the heterogeneously enhanced tumours were larger than those of the homogeneously enhanced tumours (p<0.05). CONCLUSION: The relatively characteristic CT findings include a markedly contrast-enhanced juxtapleural mass with homogeneous enhancement for the smaller tumours (<3cm in diameter) or heterogeneous enhancement for the larger tumours (>3cm). However, CT findings are not definitive for preoperative diagnosis of PSH.

Effect of NT-3 on repair of spinal cord injury through the MAPK signaling pathway.

OBJECTIVE: The aim of this study was to explore the effect of neurotrophin-3 (NT-3) on the repair of spinal cord injury (SCI) through the mitogen-activated protein kinase (MAPK) signaling pathway. MATERIALS AND METHODS: The rat model of SCI was first successfully established using the impactor (SCI group). Meanwhile, control group and NT-3 treatment group were set up as well. Basso-Beattie-Bresnahan (BBB) score was given and blood, and spinal cord tissues were collected from rats. Subsequently, serum indexes were detected, including glucose (Glu), creatinine (Cr), K+, Na+, the content of interleukin-6 (IL-6), IL-1ß, tumor necrosis factor-ß (TNF-ß), and the level of myeloperoxidase (MPO). Moreover, the morphological changes were observed via hematoxylin-eosin (HE) staining. The gene and protein expressions of glial fibrillary acidic protein (GFAP) and MAPK were determined through Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting, respectively. Furthermore, the effect of the MAPK signaling pathway on SCI was comprehensively observed. RESULTS: In SCI group, the rats could not crawl autonomously with the loss of motor function and paraplegia. Meanwhile, the levels of Glu, Cr, Na+, IL-6, IL-1ß, TNF-ß, and MPO were all significantly up-regulated. According to the results of HE staining, spinal nerve fibers disappeared with significant syringomyelia in SCI group. Meanwhile, the aggregation of nerve fibers was observed without apparent tissue bleeding, edema, and cell deformation in NT-3 group. QRT-PCR results demonstrated that SCI group showed remarkably higher levels of GFAP, MAPK, and c-Jun N-terminal kinase (JNK) (p<0.05), while it showed a markedly lower level of ERK2 than NT-3 group (p<0.05). In NT-3 group, the protein expression of MAPK in myocardial tissues was remarkably lower than that of SCI group (p<0.05). CONCLUSIONS: NT-3 can inhibit the MAPK signaling pathway, thereby promoting the repair of SCI.

LncRNA ROR1-AS1 promotes colon cancer cell proliferation by suppressing the expression of DUSP5/CDKN1A.

OBJECTIVE: The purpose of this study was to explore the possible role of ROR1-AS1 in the pathogenesis of colon cancer and the underlying mechanism. PATIENTS AND METHODS: The expression levels of ROR1-AS1 in 75 colon cancer tissue samples and adjacent ones, as well as in cell lines were examined by quantitative Polymerase Chain Reaction (qPCR). Then, ROR1-AS1 overexpression plasmid and siRNA were transfected into colon cancer cells using liposome method. After that, Cell Counting Kit-8 (CCK-8) and plate colony formation assays were conducted to analyze cell proliferation, while flow cytometry was applied for the analysis of cell cycle and apoptosis. At last, the mechanism of action of ROR1-AS1 was further explored by nuclear separation, RNA binding protein immunoprecipitation (RIP) and chromatin immunoprecipitation (CHIP) assays. RESULTS: ROR1-AS1 level in colon cancer tissues was remarkably higher than that in normal tissues, and the expression in tumors of stage III and IV was remarkably higher than those of stage I and II. Meanwhile, tumors with diameters more than 5 cm had a higher ROR1-AS1 expression than those less than 5 cm. After transfection with ROR1-AS1 overexpression plasmid, the cell proliferation ability was enhanced, the G0/G1 phase time of cell cycle was shortened, and the apoptosis was suppressed. However, the opposite result was observed after ROR1-AS1 was downregulated. Furthermore, RIP showed that ROR1-AS1 can bind to enhancer of zeste homolog 2 (EZH2) and inhibit the expression of DUSP5, and thus be engaged in the proliferation and apoptosis of colon cancer cells. CONCLUSIONS: ROR1-AS1 is highly expressed either in colon cancer tissues or in cell lines, which is able to enhance cell proliferation, accelerate cell cycle, and inhibit cell apoptosis. The mechanism of ROR1-AS1 to participate in the development of colon cancer may be the downregulation of DUSP5 via combination with EZH2.

Significance of white blood cell count and its subtypes in patients with acute coronary syndrome.

BACKGROUND: Inflammation plays a role in the pathogenesis of coronary atherosclerosis. MATERIALS AND METHODS: Six hundred twenty-three patients with acute coronary syndrome (ACS) referred for coronary angiography for the first time in our hospital were enrolled in this study. White blood cell and its subtypes were measured on admission. The study population was divided into three groups based on total white blood cell count and followed up. Clinical end points were major adverse cardiac events (MACEs), including cardiogenic death, stroke, heart failure, non-fatal myocardial infarction, rehospitalization for angina pectoris. RESULTS: The median age was 68 years (range 31-92) and 64.2% of the patients were men. The median white blood cell count was 6.48 x 10(9 )L(-1) (range 2.34-27.10 x 10(9 )L(-1)). The median follow-up duration was 21 months (range 1-116) and MACEs occurred in 167 patients. The multivariable Cox proportional hazards regression model revealed that neutrophil count [Relative risk = 1.098, 95% Confidence interval (CI): 1.010-1.193, P = 0.029) was a risk factor for MACEs. The logistic regression model revealed that lymphocyte count [Odds ratio (OR) = 1.075, 95% CI: 1.012-1.142, P = 0.018] and monocyte count (OR = 8.578, 95% CI: 2.687-27.381, P < 0.001) were predictive of stenosis >or= 75%; Neutrophil proportion (OR = 1.060, 95% CI: 1.007-1.115, P = 0.026), monocyte count (OR = 12.370, 95% CI: 1.298-118.761, P = 0.029) were predictive of the presence of multivessel disease. Kaplan-Meier analysis of short-term and long-term cumulative survival showed no significant statistical differences among three groups. CONCLUSIONS: Neutrophil count adds prognostic information to MACEs in ACS. Monocyte count and lymphocyte count are predictive of severity of coronary atherosclerosis.

Cisplatin induces apoptosis of A549 cells by downregulating peroxidase V.

The article "Cisplatin induces apoptosis of A549 cells by downregulating peroxidase V" by X. Chen, K.-W. Wang, Y.-Q. Chen, published in Eur Rev Med Pharmacol Sci 2018; 22(21): 7289-7295 has been withdrawn.

LINC01605 promotes the proliferation of laryngeal squamous cell carcinoma through targeting miR-493-3p.

OBJECTIVE: The purpose of this study was to elucidate the potential influence of LINC01605 on the progression of laryngeal squamous cell carcinoma (LSCC) and the underlying mechanism. PATIENTS AND METHODS: LINC01605 and microRNA-493-3p (miR-493-3p) levels in normal laryngeal tissues, LSCC tissues, and paired paracancerous tissues were detected. Regulatory effects of LINC01605 on proliferative ability and apoptosis in HEp-2 and AMC-HN-8 cells were assessed. Besides, the interaction between LINC01605 and miR-493-3p was evaluated by Dual-Luciferase reporter gene assay and Spearman's rank correlation analysis. Finally, rescue experiments were conducted to clarify the role of LINC01605/miR-493-3p axis in the progression of LSCC. RESULTS: LINC01605 was upregulated and miR-493-3p was downregulated in LSCC tissues. Knockdown of LINC01605 inhibited proliferative ability, and stimulated apoptosis in HEp-2 and AMC-HN-8 cells. Moreover, LINC01605 directly bound to miR-493-3p, and the former negatively regulated the level of the latter. In addition, miR-493-3p was able to reverse the regulatory effect of LINC01605 on proliferative ability in LSCC. CONCLUSIONS: LINC01605 is upregulated in LSCC tissues, and it promotes the malignant progression of LSCC via targeting miR-493-3p.

Systematic review and meta-analysis of randomized controlled trials comparing stapled haemorrhoidopexy with conventional haemorrhoidectomy.

BACKGROUND: This paper compares stapled haemorrhoidopexy with conventional haemorrhoidectomy for the treatment of haemorrhoids. METHODS: An electronic literature search was undertaken to identify primary studies and systematic reviews. Results on efficacy and safety were analysed. A meta-analysis was conducted to examine long-term outcomes. RESULTS: Twenty-nine randomized clinical trials recruiting 2056 patients were identified. Meta-analysis showed that stapled haemorrhoidopexy was less painful than conventional haemorrhoidectomy. Stapled haemorrhoidopexy required a shorter inpatient stay (weighted mean difference (WMD) -0.95 (95 per cent confidence interval (c.i.) -1.32 to -0.59) days; P < 0.001) and operating time (WMD -11.42 (95 per cent c.i. -18.26 to -4.59) min; P = 0.001). It was also associated with a faster return to normal activities (WMD -11.75 (95 per cent c.i. -21.42 to -2.08) days; P = 0.017). No significant difference was noted between the two techniques in terms of the total incidence of complications. Stapled haemorrhoidopexy was associated with a higher rate of recurrent disease (relative risk 2.29 (95 per cent c.i. 1.57 to 3.33); P < 0.001). CONCLUSION: Stapled haemorrhoidopexy offers some short-term benefits over conventional operation but the total complication rates are similar for both techniques. Stapled haemorrhoidopexy is associated with a higher rate of recurrent disease.

Cisplatin induces apoptosis of A549 cells by downregulating peroxidase V.

OBJECTIVE: The purpose of the study was to investigate the role of peroxidase V (Prx V) in Cisplatin-induced apoptosis of A549 cells and its underlying mechanism. MATERIALS AND METHODS: MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay was conducted to evaluate the regulatory effect of Cisplatin on the survival of A549 cells. ROS (Reactive Oxygen Species) level in A549 cells induced with 0, 2, 4, and 6 mol/L Cisplatin for 24 h was determined using immunofluorescence. Apoptosis of Cisplatin-induced A549 cells was determined by immunofluorescence and flow cytometry, respectively. Western blot was performed to detect protein levels of Prx V, Bcl-2 (B-cell lymphoma 2), BAD ,and caspase-3 in Cisplatin-induced A549 cells. RESULTS: Survival rate of A549 cells gradually decreased with the increased dose of Cisplatin. Immunofluorescence results elucidated that cellular ROS level in Cisplatin-induced A549 cells increases in a dose-dependent manner. Both immunofluorescence and flow cytometry results revealed that the apoptotic rate of A549 cells increases with the elevation of Cisplatin dose. Besides, the apoptotic rate and ROS level of A549 cells were reduced by NAC pretreatment. Western blot results showed that the protein level of Prx V remarkably decreased in a dose-dependent manner, whereas Prx II expression did not change. With the treatment prolongation of 4 µmol/L Cisplatin in A549 cells, Bcl-2 and caspase-3 were downregulated, while BAD upregulated. CONCLUSIONS: Cisplatin treatment induces the ROS production, increases the apoptotic rate and downregulates the Prx expression in A549 cells.

A novel mutation of dipeptidyl aminopeptidase-like protein-6 in a family with suspicious idiopathic ventricular fibrillation.

BACKGROUND: Sudden cardiac death (SCD) occurs in a broad spectrum of cardiac pathologies and is an important cause of mortality in the general population. Idiopathic ventricular fibrillation (IVF) is a rare but important factor resulting in SCD. It is diagnosed in a resuscitated cardiac arrest victim underlying unknown cause, with documented ventricular fibrillation. Previous studies have demonstrated that mutations in dipeptidyl aminopeptidase-like protein-6 (DPP6) and cardiac sodium channel Nav1.5 (SCN5A) are the most important genetic factors involve in IVF. AIM: By using whole sequencing to identify the genetic lesion of a family with suspicious idiopathic ventricular fibrillation. DESIGN: Prospective genetic study. METHODS: In this study, we employed whole-exome sequencing in combination with arrhythmia-related gene filtering to identify the genetic lesion for a family suffering from suspicious IVF, syncope and SCD. We then generated the plasmids of DPP6-pcDNA3.1+ (WT and c.1578G>C/p.Q526H). Kv4.3-pcDNA3.1+ was co-transfected together with/without DPP6-pcDNA3.1+ (WT and/or c.1578G>C/p.Q526H) into HEK293 cells to perform the patch clamp experiments. RESULTS: A novel missense mutation (c.1578G>C/p.Q526H) of DPP6 was identified and co-segregated with affected patients in this family. Patch clamp experiments suggested that this novel mutation might result in a gain of function and disturb the efflux of potassium ion. CONCLUSION: Our study not only reported the second missense mutation of DPP6 in heart disease and expanded the spectrum of DPP6 mutations, but also contribute to the genetic diagnosis and counseling of families with suspicious IVF, syncope and SCD.