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OBJECTIVE: Laparoscopic sleeve gastrectomy (LSG) is a widely recognized effective bariatric surgery. However, variable weight loss outcomes post-surgery remained a clinical challenge. Currently, there is no established consensus on the factors influencing weight loss failure following LSG. This study aimed to explore the association between preoperative cortisol secretion autonomy and postoperative weight loss in obese patients undergoing LSG. PATIENTS AND METHODS: A cohort of 181 patients with simple obesity (BMI ≥ 28 kg/m2) who underwent LSG and were followed up for one year was analyzed. Weight loss was measured by the percentage of excess weight loss (%EWL), and cortisol secretion autonomy was evaluated using a 1 mg dexamethasone suppression test (DST). Regression models were used to analyze the correlation between preoperative 1 mg DST results and %EWL one year after laparoscopic sleeve gastrectomy (LSG). RESULTS: Cortisol secretion autonomy was significantly lower in the %EWL ≥ 75% group and higher in the %EWL < 75% group, showing a negative correlation with %EWL (R = -0.336, p = 0.001). Logistic regression analysis indicated that high cortisol secretion autonomy was significantly correlated with %EWL < 75% after LSG. The likelihood of %EWL being < 75% was 10.47 times greater in patients with high cortisol secretion autonomy compared to those with low cortisol secretion autonomy (odds ratio 10.472, confidence interval: 1.660-66.048, p = 0.012). CONCLUSIONS: Cortisol secretion autonomy emerges as an independent predictor of weight loss outcomes in Asian patients undergoing LSG. This finding suggests the potential for cortisol secretion autonomy to inform preoperative assessments and personalized treatment strategies in bariatric surgery.

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Tumor-derived exosomes (TDEs) play critical roles in many aspects of cancer progression. There have been several advances in cancer immunotherapy in recent years. A major challenge, however, has been addressed to the role of TDEs in tumor cell immune escape through their influence on the antitumor immunity of natural killer (NK) cells, a key type of immune cell. In this review, we present our overview of the effects of different TDEs on NK cell activation and NK cell toxicity. Studies on mechanism suggest that TDEs mainly affect the immune response of NK cells by inhibiting activated receptors on the surface of NK cells and downregulating the NK recognition ligand MICA/B on the tumor cell surface. In addition, a summary was documented on how to restore the cytotoxicity of NK cells and improve the drug's ability to recognize tumor cells, and a detailed explanation was also provided on the mechanism of action of the drug.

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OBJECTIVES: There is little evidence in the literature about the relationship between frailty and falls in older adults. Our objective was to explore the relationship between frailty and falls, and to analyze the effect factors (e.g., gender, different frailty assessment tools, areas, level of national economic development, and year of publication) of the association between frailty and falls among older adults. DESIGN: Systematic review and meta-analysis. SETTING AND PARTICIPANTS: Cohort studies that evaluated the association between frailty and falls in the older adults were included. We excluded any literature outside of cohort studies. METHODS: We did a systematic literature search of English databases PubMed, Scopus, Web of Science, EBSCOhost, and SciElO, as well as the Chinese databases CNKI, WANFANG, and VIP from 2001 until October 2022. The eligible studies were evaluated for potential bias using the Newcastle-Ottawa Scale (NOS). Study selection, data extraction and assessment of study quality were each conducted by two investigators. In Stata/MP 17.0 software, we calculated pooled estimates of the prevalence of falls by using a random-effects model, Subgroup analysis was conducted based on gender, different frailty assessment tools, areas, level of economic development, and year of publication. The results are presented using a forest plot. RESULTS: Twenty-nine studies were included in this meta-analysis and a total of 1,093,270 participants aged 65 years and above were enrolled. Among the older adults, frailty was significantly associated with a higher risk for falls, compared with those without frailty (combined RR-relative risk = 1.48, 95% CI-confidence interval: 1.27-1.73, I2=98.9%). In addition, the results of subgroup analysis indicated that men had a higher risk for falls than women among the older adults with frailty (RR 1.94, 95% CI: 1.18-3.2 versus RR 1.44, 95% CI: 1.24-1.67). Subgroup analysis by different frailty assessment tools revealed an increased risk of falls in older adults with frailty when assessed using the Frailty Phenotype (combined RR 1.32, 95%CI: 1.17-1.48), FRAIL score (combined RR 1.82, 95%CI: 1.36-2.43), and Study of Osteoporotic Fractures index (combined RR 1.54, 95%CI: 1.10-2.16). Furthermore, subgroup analysis by areas and level of national economic development found the highest fall risk in Oceania (combined RR 2.35, 95%CI: 2.28-2.43) and the lowest in Europe (combined RR 1.20, 95%CI: 1.05-1.38). Developed countries exhibited a lower fall risk compared to developing countries (combined RR 1.44, 95%CI: 1.21-1.71). Analysis by year of publication showed the highest fall risk between 2013-2019 (combined RR 1.79, 95%CI: 1.45-2.20) and the lowest between 2001-2013 (combined RR 1.21, 95%CI: 1.13-1.29). CONCLUSION: Frailty represents a significant risk factor for falls in older adults, with the degree of risk varying according to the different frailty assessment tools employed, and notably highest when using the FRAIL scale. Additionally, factors such as gender, areas, level of national economic development, and healthcare managers' understanding of frailty may all impact the correlation between frailty and falls. Thus, it's imperative to select suitable frailty diagnostic tools tailored to the specific characteristics of the population in question. This, in turn, facilitates the accurate identification of frailty in older adults and informs the development of appropriate preventive and therapeutic strategies to mitigate fall risk.

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OBJECTIVE: The liver is a unique organ containing large populations of immune cells. Immunotherapy for liver cancer is a promising yet particularly challenging method. Therefore, it harbors great significance for the identification of immune-related subtypes and the potential therapeutic targets for hepatocellular carcinoma (HCC). MATERIALS AND METHODS: Firstly, we classified the HCC samples downloaded from the dataset of Cancer Genome Atlas (TCGA) into two clusters based on the immune cell infiltration. Thereafter, we identified the significant module and regulatory factors using the weighted gene co-expression network analysis (WGCNA). The immune competence of the regulatory factors was delineated through the ESTIMATE algorithm, the analysis of the tumor microenvironment, and pan-cancer analysis. In the single-cell RNA sequencing analysis, we further explored the immune competence of regulatory factors. We also collected the potential drugs targeting the regulatory factors. In addition, we constructed lncRNA-miRNA-mRNA interaction regulatory networks. Finally, western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to verify the protein expression of regulatory genes in HCC cell lines and tissues. RESULTS: According to the immune cell infiltration, two immune-related subtypes-cluster 1 and cluster 2-were found. Patients in cluster 2 had a more significant immune infiltration than in cluster 1. Afterward, six significant regulatory genes were identified through WGCNA, and the expression in cluster 2 was high in cluster 1. We performed a comprehensive analysis to clarify the immune signature. The results showed that the six genes had significant immunological competence. Moreover, the expression of the six genes was similar to the subtypes' classification. In the analysis of the prognosis value, patients in cluster 2 had a better prognosis. In addition, the lncRNA in the lncRNA-miRNA-mRNA interaction regulatory networks was located in the nucleus and cytoplasm. In the single-cell RNA sequencing analysis, the six genes were related to the immune cell. We also identified potential drugs for CD6 and CLEC12A, which may provide potential therapeutic drugs. Finally, the regulatory genes were verified in the western blot and quantitative real-time polymerase chain reaction. CONCLUSIONS: The classification into two clusters based on the immune cell infiltration may provide a promising prospect for HCC through immunotherapy. The six regulatory genes may be potential therapeutic targets in the treatment of HCC.

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Liver cancer is a malignant cancer with great harmfulness. Fenofibrate is a peroxisome proliferation activated receptor (PPARα) agonist widely used in the treatment of dyslipidemia. Previous studies have shown that fenofibrate may promote cell proliferation, but the underlying mechanism has not been fully characterized. The aim of this study was to investigate the role of PPARα agonist fenofibrate in cell proliferation of SMMC-7721 cells compared with that of THLE-2 cells. SMMC-7721 and THLE-2 cells were treated with different concentrations of fenofibrate. Cell proliferation was analyzed by MTT, using flow cytometry for cell cycle analysis, and CyclinD1, Cyclin-dependent kinases2 (CDK2) and Proliferating Cell Nuclear Antigen (PCNA) were analyzed by Western blotting. RT-qPCR method was used to assess CDK2, CyclinD1 and PCNA mRNA levels. The results showed that 10-9-10-4 mol/L fenofibrate could induce cell growth and 10-4, 10-5, 10-6 mol/L fenofibrate could reduce the number of G0/G1 phase cells and increased in the number of cells in S and G2/M phase of cell cycle in SMMC-7721 cells. Furthermore, fenofibrate could significantly increase the expression of cell cycle related protein (CyclinD1, CDK2)and cell proliferation related proteins (PCNA). The use of PPARα inhibitor MT886 inhibited cell cycle progression and promote tumor cell apoptosis. But fenofibrate had no obvious effect on THLE-2 cells. These results revealed the effect of fenofibrate on the cell cycle of liver cancer cells, and provided a reasonable explanation for studying how fenofibrate promotes cell proliferation.

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OBJECTIVE: This study aimed to evaluate the effects of genistein on glycolipid metabolism in postmenopausal women. METHODS: Electronic databases were searched and relevant reports were hand-screened. We included only randomized controlled trials of isolated genistein for glycolipid metabolism. The primary outcome for lipid metabolism included a changed value of low-density lipoprotein cholesterol (LDL-C), and for glucose metabolism was a changed value of homeostasis model assessment for insulin resistance (HOMA-IR). Secondary outcomes included a changed value of total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG), fasting blood insulin (INS), and body mass index (BMI). RESULTS: Ten trials with 11 articles were included. The level of LDL-C was not decreased in the genistein group compared with the placebo group (standardized mean difference [SMD] = -0.58; 95% confidence interval [CI] - 1.19, 0.02; p = 0.06). No statistical significance was found in subgroup analyses. HOMA-IR was obviously improved in the genistein group with SMD of -0.51 (95% CI -0.88, -0.14; p = 0.006). In subgroup analyses, HOMA-IR was improved more in women with BMI <30 kg/m2 and without metabolic disorders (p < 0.0001). For secondary outcomes, there were significant differences in total cholesterol, HDL-C, FBG, and INS, but not triglyceride or BMI. CONCLUSIONS: Genistein was effective in ameliorating glycolipid metabolism by increasing HDL-C levels and decreasing total cholesterol levels and improving insulin sensitivity.

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In this review, we assess the effectiveness of liposomal bupivacaine against the traditional bupivacaine infiltration in the postoperative management of total hip arthroplasty (THA). Various databases including PubMed Central, Medline, Scopus, Embase, Google Scholar, Cochrane library and ScienceDirect (inception date till August 2020) were searched. The quality of published trials was assessed using Cochrane risk of bias tool, and a random-effects model was used for meta-analysis. We report pooled Risk ratios (RR) or pooled Standardized Mean difference (SMD) with 95% confidence intervals (CIs). We analyzed a total of 13 studies with 62,582 participants. The majority of the studies were retrospective with lower bias risks. Liposomal bupivacaine was significantly associated with the reduction in opioid requirement at 48 hours (SMD = -0.25; 95% CI: -0.40 to -0.09; p=0.002) and length of hospital stay (SMD = -0.25; 95% CI: -0.43 to -0.07, p=0.006) following THA compared with the control group. However, there was no statistically significant difference between the effect of liposomal bupivacaine and other agents for pain score (24 and 48 hours), opioid requirement at 24 hours and incidence of nausea. Liposomal bupivacaine has selective benefits in terms of opioid consumption and length of hospital stay against the traditional bupivacaine among the patients undergoing THA.

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The article "LncRNA FEZF1-AS1 promoted chemoresistance, autophagy and epithelial-mesenchymal transition (EMT) through regulation of miR-25-3p/ITGB8 axis in prostate cancer, by Z.-H. Wang, J.-H. Wang, K.-Q. Wang, Y. Zhou, J. Wang, published in Eur Rev Med Pharmacol Sci 2020; 24(5): 2281-2293-DOI: 10.26355/eurrev_202003_20494-PMID: 32196579" has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20494.

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In December 2019, Coronavirus disease 2019 (COVID-19) emerged in Wuhan and rapidly spread throughout China and the rest of the world. COVID-19 is currently a global pandemic. There are cytokine storms in severe COVID-19 patients. Interleukin-6 plays an important role in cytokine storm. Tocilizumab is a blocker of interleukin-6 receptor, which is likely to become an effective drug for patients with severe COVID-19. Here, we reported a case in which tocilizumab was effective for a critical COVID-19 patient.

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OBJECTIVE: Accumulating evidence determined that lncRNA plays important roles in the development and occurrence of cancers. Prostate cancer is the second most common type of cancer and one of the top five cancers for the cause of male death in the world. Therefore, this study was to explore the regulatory mechanism of lncRNA in chemoresistance of PC. MATERIALS AND METHODS: qRT-PCR was used to detect the mRNA expression of FEZF1-AS1, miR-25-3p and ITGB8. Western blot was applied to measure the protein expression of ITGB8 E-cadherin, N-cadherin, Vimentin, LC3I, LC3II, ATG5 and Beclin-1. In addition, CCK-8 assay was used to assess cell proliferation of transfected cells. Luciferase reporter assay and RIP assay were used to determine the relationship among FEZF1-AS1, miR-25-3p and ITGB8. RESULTS: In this study, the expression of FEZF1-AS1 and ITGB8 was upregulated, whereas the expression of miR-25-3p was downregulated in PC tumor tissues and PC/PTX cells. Luciferase reporter assay and RIP assay determined that miR-25-3p was a target of FEZF1-AS1 and ITGB8 was a target mRNA of miR-25-3p. Interestingly, knockdown of FEZF1-AS1 could inhibit cell viability and EMT and promoted cell autophagy in PC/PTX cells, but inhibition of miR-25-3p or promotion of ITGB8 could reverse the effects of si-FEZF1-AS1 on PC/PTX cells. CONCLUSIONS: In this study, we found that lncRNA FEZF1-AS1 promoted chemoresistance, autophagy and epithelial-mesenchymal transition (EMT) through regulation of miR-25-3p/ITGB8 axis in PC, providing a new regulatory mechanism of PC and a novel therapeutic target.

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OBJECTIVE: Increasing evidence shows that long non-coding RNAs (lncRNAs) play important roles in the development and progression of human carcinoma. TDRG1 was a recently identified lncRNA which was reported to promote the progression of several carcinomas. However, its function in cervical cancer remains unknown. MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was performed to determine the mRNA expression. siRNA for lncRNA TDRG1, miR-330-5p, and the corresponding negative control were conducted. The cell function analysis was evaluated by CCK-8 assay, colony formation assay, transwell assay, scratch assay, and flow cytometry analysis. RNA-binding protein immunoprecipitation (RIP), Dual-Luciferase reporter assay, and RNA pull-down assay were used to determine the potential targets of TDRG1 or miR-330-5p. Western blot and Immunohistochemistry (IHC) analysis were used to examine the protein expression. The effect of TDRG1 on tumor growth was evaluated in vivo. RESULTS: LncRNA TDRG1 expression was notably increased in cervical cancer tissues and cancer cells. LncRNA TDRG1 promoted the proliferation and migration of cervical cancer cells. Mechanism investigation suggested that lncRNA TDRG1 up-regulated the expression of ELK1 by acting as a competing endogenous RNA (CeRNA) of miR-330-5p. Rescue experiments indicated that miR-330-5p-inhibitor reversed the si-TDRG1-induced cell activity changes. This in vivo study proved that the down-regulation of lncRNA TDRG1 inhibited cervical tumor growth by regulating miR-330-5p/ELK1. CONCLUSIONS: The present study reveals that lncRNA TDRG1 promotes cervical cancer progression by acting as a CeRNA of miR-330-5p to modulate the expression levels of ELK1 and may be explored as a novel target for developing therapeutic strategies for the treatment of cervical cancer.

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OBJECTIVE: Atrial fibrillation (AF) is independently associated with a higher risk of acute myocardial infarction (AMI). The occurrence of AMI in AF patients may lead to dismal prognosis. Risk assessment is a fundamental component of prevention for AMI. PATIENTS AND METHODS: 2419 consecutive patients with nonvalvular AF were enrolled in this retrospective study. A logistic regression analysis was performed on clinical variables to create a simple clinical prediction rule. The following nine variables and assigned scores (in brackets) were included in the prediction rule: age ≥65 years (1.0), heart failure (1.0), hypertension (1.0), diabetes mellitus (1.0), hyperlipidemia (0.5), history of stroke/TIA (0.5), vascular disease (1.0), current smoking (0.5), and resting heart rate >90 beats/min (1.0). Patients were considered to have a low probability if the score was ≤2.5, moderate if the score was 3.0 to 4.0, and high if the score was ≥4.5. The AMI unlikely was assigned to patients with scores <3.5 and AMI likely if the score was ≥3.5. To evaluate the score, we included an external validation cohort of 1810 nonvalvular AF patients from the Cardiology Center, Shandong Provincial Hospital affiliated to Shandong University, Jinan, China. RESULTS: The score showed a good ability in discriminating AF patients experiencing AMI both in the internal derivation cohort, with a c-index of 0.80 [95% Confidence Interval (CI) 0.77-0.83, p<0.001] and in the external validation cohort (c-index 0.73, 95% CI 0.69-0.77, p<0.001). Our scoring system offered significantly better predictive performance than the CHA2DS2-VASc score (c-index 0.80 vs 0.71, p<0.001). CONCLUSIONS: Our scoring system is a simple and accurate way of predicting the risk of AMI in AF patients. Therefore, more accurate targeting of preventive therapy will be allowed.

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OBJECTIVE: To investigate the potential role of long noncoding RNA (lncRNA) growth arrest specific transcript 5 (GAS5) in sepsis-induced podocyte injury and its underlying mechanism. MATERIALS AND METHODS: The sepsis model was established by lipopolysaccharide (LPS) induction in podocytes. The expression levels of Nephrin and GAS5 were detected by quantitative Real-time polymerase chain reaction (qRT-PCR) after LPS induction in podocytes for 12 h, 24 h and 36 h, respectively. Western blot was used to detect the expression level of Nephrin in sepsis-induced podocytes. The mRNA expressions of GAS5 and Nephrin in podocytes were detected after transfection of GAS5 siRNA. Albumin influx in podocytes after GAS5 knockdown was detected by Transwell assay. Western blot was used to detect the protein expression of Snail in sepsis after GAS5 knockdown. The target gene of GAS5 was predicted by bioinformatics analysis. QRT-PCR and Western blot were used to detect the protein and mRNA levels of PTEN (phosphatase and tensin homolog deleted on chromosome ten). Nephrin expression and the albumin inflow after PTEN knockdown were then measured. The expression of PI3K/AKT/GSK3ß was also detected after GAS5 was downregulated while PTEN was upregulated. RESULTS: LPS stimulation downregulated the mRNA expression of Nephrin in podocytes and achieved the lowest level at 24 h. The protein expression change of Nephrin was consistent with its mRNA expression. In the septic state, the albumin influx of podocytes remarkably increased, but the function of podocyte barrier was weakened. Besides, GAS5 expression decreased in a time-dependent manner in LPS-induced podocytes. After GAS5 knockdown by siRNA, Nephrin expression and the function of podocyte barrier were significantly reduced. Snail expression was also upregulated in septic state, and GAS5 knockdown increased the expressions of phosphorylated Snail and PI3K/AKT/GSK3ß. After knockdown of GAS5, the mRNA and protein levels of PTEN significantly decreased, which was contract to the expression of Snail. However, overexpression of PTEN could reverse the promotive effect of GAS5 on PI3K/AKT activation. CONCLUSIONS: GAS5 expression decreased in sepsis-induced podocyte injury, and GAS5 was involved in regulating sepsis-induced podocyte injury by reducing PTEN expression.

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OBJECTIVE: We investigate the mechanism of HOXB-AS3 in promoting the development of hepatocellular carcinoma. PATIENTS AND METHODS: The expression of HOXB-AS3 in tumor tissues and adjacent tissues of hepatocellular carcinoma was detected by quantitative real time-polymerase chain reaction (qRT-PCR), and the relationship between the expression of HOXB-AS3 and tumor tissues was analyzed. The effects of HOXB-AS3 and p53 on cell proliferation, cell cycle and apoptosis were detected by plate cloning experiment and flow cytometry. The binding relationship between HOXB-AS3 and DNMT1 and the regulation mechanism of DNMT1 on p53 were tested by RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) experiments, respectively. Western blot was used to detect the expression of p53 after knockdown of HOXB-AS3. The torsion experiment was performed to assess whether HOXB-AS3 regulated the proliferation and apoptosis of hepatoma cells by inhibiting p53 expression. RESULTS: The results of qRT-PCR showed that the expression of HOXB-AS3 was significantly higher in cancerous tissues of patients with hepatocellular carcinoma than in adjacent tissues. The expression of HOXB-AS3 in patients in stage III and IV was significantly higher than that in stage I and II. Inhibition of HOXB-AS3 expression in liver cancer cells including Hep3B and LM3 could promote cell proliferation, inhibit cell apoptosis and induce cell cycle arrest in the G0/G1 phase. The results of RIP and ChIP experiments showed that HOXB-AS3 inhibited the expression of p53 by binding to DNMT1, and overexpression of p53 in Hep3B cells could partially reverse the changes in cell proliferation and apoptosis induced by HOXB-AS3. CONCLUSIONS: Highly expressed HOXB-AS3 was confirmed to promote the proliferation of hepatocellular carcinoma cells and inhibit apoptosis, and the mechanism was related to the regulation role of HOXB-AS3 in p53 expression by binding to DNMT1.

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OBJECTIVE: This study aims at exploring the regulatory effects of miR-193a-5p on hepatocellular carcinoma (HCC). It might provide new insight into the improvement of clinical treatment of HCC. PATIENTS AND METHODS: A total of 50 HCC patients who did not receive any tumor treatments were recruited, and 50 paired tumor tissues and adjacent non-tumor tissues were obtained. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to validate the expression and significance of miR-193a-5p in HCC tumor tissues, adjacent non-tumor tissues and cell lines. Binding-site of the target gene of miR-193a-5p was predicted by bioinformatics and further verified by Dual-Luciferase reporter gene assay and Western blotting (WB) assay. To investigate the potential role of miR-193a-5p in HCC development, cell counting kit-8 (CCK-8) assay was performed to study the proliferation and viability capacities. Flow cytometric analyses were adopted to test the cell cycle distribution and quantify the apoptotic cell proportion. RESULTS: MiR-193a-5p expression was specifically up-regulated in HCC tissues and cell lines compared with paired adjacent non-tumor tissues and normal liver cell lines (HL-7702) respectively. BMF was considered as a downstream gene of miR-193a-5p, which was further proofed in Dual-Luciferase reporter gene assay and Western blot assays. In vitro experiments showed that miR-193a-5p overexpression could accelerate the proliferation, facilitate the G1/S transition and suppress the apoptosis of HCC cells. However, BMF overexpression could reverse the effects of miR-193a-5p on the cellular functions of HCC cells. CONCLUSIONS: This finding suggested that miR-193a-5p is strongly up-regulated in HCC. MiR-193a-5p promoted the abnormal proliferation of HCC cells and limited their apoptosis by targeting the downstream gene BMF. Thus, the miR-193a-5p/BMF axis might be a novel regulatory pathway of apoptosis which could be potential therapeutic sites in HCC treatment.

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OBJECTIVE: To discover the mechanisms of miR-154 affecting myocardial fibrosis. PATIENTS AND METHODS: Human cardiac fibroblasts (CFs) were cultured in medium containing 10% serum for 48 h. The expression of miRNA-154 in human CFs was detected by Real-time quantitative polymerase chain reaction (qRT-PCR). The miRNA-154 mimics and inhibitors were synthesized and transfected into fibroblasts, respectively. Cell proliferation rate was determined by cell counting kit-8 (CCK8). Collagen I and collagen III, myofibroblast marker (a-SMA) and ß-catenin were detected by Western blotting. Transwell migration assay was used to detect the changes of invasiveness of CFs. After the overexpression vector or siRNA of glycogen synthase kinase-3ß (GSK-3ß) was transfected into fibroblasts, we performed Western blot to detect a-SMA and ß-catenin expression. RESULTS: MiR-154 was overexpressed in cardiomyocytes, and when miR-154 was inhibited, the expression of collagen I, collagen III, a-SMA, ß-catenin, and the invasiveness of CFs decreased. Therefore, we considered that miR-154 could promote myocardial fibrosis by inhibiting the expression of GSK-3ß. CONCLUSIONS: MiR-154 can inhibit GSK-3ß expression by activating Wnt/ß-catenin signaling pathway, which promotes myocardial fibrosis.

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OBJECTIVE: In view of the high occurrence of avascular necrosis of the femoral head (ANFH) after femoral neck fracture and the difficulties in the treatment, our work aimed to explore the effects of platelet-rich plasma (PRP) combined with tri-calcium phosphate (TCP) on the repair of ANFH after femoral neck fracture and to provide reference for clinical treatment. MATERIALS AND METHODS: Thirty New Zealand white rabbits were randomly divided into control group, TCP group, and PRP+TCP group. The rabbit ANFH model was established and femoral head tissues were collected. HE staining was used for histological observation. Image analysis and statistical analysis were used to calculate the New Bone Area fraction (NBA %). The levels of bone morphogenetic protein (BMP)-7, transforming growth factor (TGF)-ß1, basic fibroblast growth factor (bFGF), interleukin (IL)-6 and tumor necrosis factor (TNF)-a in serum were detected by Enzyme-Linked ImmunoSorbent Assay (ELISA). RESULTS: The new bone area of TCP group was significantly lower than that of PRP+TCP group (p<0.05). Compared with the control group, the levels of BMP-7, TGF-ß1 and bFGF were significantly increased in both TCP and PRP+TCP groups (p<0.05), and the increase in PRP+TCP group was higher than that in TCP group. TCP and PRP+TCP can both significantly reduce the content of IL-6 and TNF-a (p<0.05); however, higher decrease was found in PRP+TCP group compared with the TCP group at 8 weeks after injection. CONCLUSIONS: PRP combined with TCP, which can promote new bone formation and inhibit inflammatory response, showed higher efficiency in repairing ANFH than internal fixation alone.

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This study aimed to investigate the protective effect of salvinorin A on the cerebral pial artery after forebrain ischemia and explore related mechanisms. Thirty Sprague-Dawley rats received forebrain ischemia for 10 min. The dilation responses of the cerebral pial artery to hypercapnia and hypotension were assessed in rats before and 1 h after ischemia. The ischemia reperfusion (IR) control group received DMSO (1 µL/kg) immediately after ischemia. Two different doses of salvinorin A (10 and 20 µg/kg) were administered following the onset of reperfusion. The 5th, 6th, and 7th groups received salvinorin A (20 µg/kg) and LY294002 (10 µM), L-NAME (10 μM), or norbinaltorphimine (norBIN, 1 μM) after ischemia. The levels of cGMP in the cerebrospinal fluid (CSF) were also measured. The phosphorylation of AKT (p-AKT) was measured in the cerebral cortex by western blot at 24 h post-ischemia. Cell necrosis and apoptosis were examined by hematoxylin-eosin staining (HE) and TUNEL staining, respectively. The motor function of the rats was evaluated at 1, 2, and 5 days post-ischemia. The dilation responses of the cerebral pial artery were significantly impaired after ischemia and were preserved by salvinorin A treatment. In addition, salvinorin A significantly increased the levels of cGMP and p-AKT, suppressed cell necrosis and apoptosis of the cerebral cortex and improved the motor function of the rats. These effects were abolished by LY294002, L-NAME, and norBIN. Salvinorin A preserved cerebral pial artery autoregulation in response to hypercapnia and hypotension via the PI3K/AKT/cGMP pathway.

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OBJECTIVE: The involvement of microRNAs in cancer and their potential as biomarkers of prognosis are becoming increasingly appreciated. The aim of this study was to evaluate the clinical importance and prognostic value of miR-342-3p in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: RT-PCR was used to detect the expression of miR-342-3p. The association with clinicopathologic features was analyzed. Kaplan-Meier survival analysis and Cox proportional hazards analysis were used to compare the overall survival between HCC patients with high miR-342-3p expression and those with low miR-342-3p expression. RESULTS: We found that miR-342-3p expression was significantly decreased in HCC tissues compared with paired adjacent non-tumor tissues (p < 0.001). MiR-342-3p expression was correlated with histologic grade (p = 0.008) and tumor TNM stage (p = 0.001). Kaplan-Meier survival analysis showed that patients in the high miR-342-3p expression group had better overall survival than those in the low miR-342-3p expression group (p < 0.001). Univariate analysis showed that miR-342-3p (p = 0.001), TNM stage (p = 0.002) and histologic grade (p = 0.006) were associated with poor survival rates. Multivariate analysis confirmed that miR-342-3p expression can be used as an independent predictor for HCC prognosis (p = 0.002). CONCLUSIONS: miR-342-3p may serve as a tumor suppressor during HCC progression, and its low expression may be a potential biomarker for poor prognosis of HCC.

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