Serum HBV DNA level is not correlated to histological grade or stage of liver disease in CHB patients with HBV DNA more than 10(5) copies/mL. Compared to HBeAg positive patients, HBeAg negative patients are older and have a lower HBV DNA level and a longer HBV infection history. There is no significant difference in sex ratio, ALT and AST levels and liver histology between the two groups.
Keloids are common abnormally raised fibroproliferative lesions that can occur following even minor cutaneous trauma. There are limited data on Chinese patients with keloids, and the purpose of our study was to investigate the clinical and epidemiological features of keloids in Chinese patients. Assessment was performed by unified, designed questionnaires. A total of 715 patients were enrolled and statistical analysis and heritability were performed using EPI INFO 6.0, SPSS13.0 and Falconer's method. Keloids occurred typically between the ages of 10 and 30 years, and the mean age of initial onset was 21.14 ± 13.45 years in females and 22.55 ± 11.36 years in males. The difference in the mean age of onset was not significant between males and females (p > 0.05). A greater severity of keloids was observed in the positive history family group than in the negative history family group, and this difference was statistically significant (χ (2) = 10.889, p < 0.05). The formation of keloids in multiple anatomical sites was found to be significant in the positive family history group. This difference was statistically significant (χ (2) = 15.47, p < 0.001). The prevalence of keloids in first-, second- and third-degree relatives of the proband with keloids was 7.62, 0.38 and 0.035 %, respectively. These results were higher than those in controls and the difference of the prevalence rates of first- and second-degree relatives between probands and controls was significant (χ (2) = 224.63 and 12.078, respectively, p < 0.001). The heritability of keloids in first-, second- and third-degree relatives was 72.45, 40.55 and 17.07 %, respectively. Our findings revealed that the most severe forms of keloids were observed in the probands with positive family history, and the heritability in first-degree relatives of probands was 72.45 %. It is certain, therefore, that genetic factors play a role in the hereditary composition of keloids.
Cisplatin resistance has long been a major problem that restricts its use. A novel paradigm in tumor biology suggests that gastric tumor chemo-resistance is driven by gastric cancer stem cell-like (GCSCs). Growing evidence has indicated that microRNAs (miRNAs) contributes to chemo-resistance in gastric cancer (GC). Here, Lgr5 cells derived from gastric cancer cell lines displayed stem cell-like features. Flow cytometry demonstrated the presence of a variable fraction of Lgr5 in 19 out of 20 GC specimens. By comparing the miRNA expression profiles of Lgr5 GCSCs and Lrg5 cells, we established the upregulation of miR-132 in Lgr5 GCSCs. The enhanced miR-132 expression correlated chemo-resistance in GC patients. Kaplan-Meier survival curve showed that patients with low miR-132 expression survived obviously longer. Functional assays results indicated that miR-132 promoted cisplatin resistance in Lgr5 GCSCs in vitro and in vivo. Further dual-luciferase reporter gene assays revealed that SIRT1 was the direct target of miR-132. The expression of miR-132 was inversely correlated with SIRT1 in gastric cancer specimens. Furthermore, through PCR array we discovered ABCG2 was one of the downstream targets of SIRT1. Overexpression of SIRT1 down-regulated ABCG2 expression by promoting the de-acetylation of the transcription factor CREB. CREB was further activated ABCG2 via binding to the promoter of ABCG2 to induce transcription. Thus, we concluded that miR-132 regulated SIRT1/CREB/ABCG2 signaling pathway contributing to the cisplatin resistance and might serve as a novel therapeutic target against gastric cancer.
The renin-angiotensin system (RAS) is a principal determinant of arterial blood pressure and fluid and electrolyte balance. RAS component dysregulation was recently found in some malignancies and correlated with poor patient outcomes. However, the exact mechanism of local RAS activation in tumors is still unclear. Here, we find that the local angiotensin II predominantly exists in the hypoxic regions of tumor formed by nasopharyngeal carcinoma CNE2 cells and breast cancer MDA-MB-231 cells, where these tumor cells autocrinely produce angiotensin II by a chymase-dependent rather than an angiotensin converting enzyme-dependent mechanism. We further demonstrate in nasopharyngeal carcinoma CNE2 and 5–8F cells that this chymase-dependent effect is mediated by increased levels of lactate, a by-product of glycolytic metabolism. Finally, we show that the enhanced angiotensin II plays an important role in the intracellular accumulation of HIF-1α of hypoxic nasopharyngeal carcinoma cells and mediates the radiation-resistant phenotype of these nasopharyngeal carcinoma cells. Thus, our findings reveal the critical role of hypoxia in producing local angiotensin II by a lactate-chymase-dependent mechanism and highlight the importance of local angiotensin II in regulating radioresistance of hypoxic tumor cells.
Background: Medial patellofemoral ligament (MPFL) reconstruction, MPFL repair, and nonoperative treatment are important treatments for patients with patellar dislocation. However, it is unclear which treatment leads to better outcomes. Purpose: To determine the efficacy and safety of the 3 treatments in the treatment of patellar dislocation and compare the effect of MPFL reconstruction with MPFL repair, MPFL reconstruction with nonoperative treatment, and MPFL repair with nonoperative treatment. Study Design: Systematic review; Level of evidence, 3. Methods: The PubMed, Web of Science, Cochrane Library, Embase, CNKI (China National Knowledge Infrastructure), and Wanfang databases were searched from inception to December 2020. Included were clinical studies that described the efficacy and safety of 2 of the 3 treatments, studies directly comparing the clinical effects of the 2 operative techniques, or studies comparing the effects of reconstruction or repair with nonoperative treatment. Two reviewers independently extracted data and assessed the quality of the included studies with the Cochrane risk-of-bias tools. The outcomes evaluated were postoperative redislocation rate, revision rate, complications, and Kujala score. We used traditional direct pairwise meta-analysis as well as network meta-analysis for comprehensive efficacy of all 3 treatment measures. Results: Twelve studies were included: 5 compared MPFL reconstruction with MPFL repair, 2 compared MPFL reconstruction with nonoperative treatment, and 5 compared MPFL repair with nonoperative treatment. The risk of bias was serious in 4, moderate in 4 and low in 4 articles. MPFL reconstruction led to significantly reduced redislocation and improved Kujala scores compared with MPFL repair and nonoperative treatment. MPFL repair led to reduced redislocation rates compared with nonoperative treatment but did not show an obvious benefit in primary dislocations. There was no significant difference among the 3 treatments in terms of revision rate and incidence of complications, although we found that treatment-related complications were least likely to occur in nonoperative treatment. Conclusion: The results of this review indicate that MPFL reconstruction decreases recurrent dislocation compared with MPFL repair or nonoperative treatment, but it has a higher possibility of complications. MPFL repair resulted in less postoperative redislocation than nonoperative treatment but did not show an obvious benefit in primary dislocation.
Recently, long noncoding RNAs (lncRNAs) have emerged as new gene regulators and prognostic biomarkers in several cancers, including gastric cancer (GC). In this study, we investigate the role of lncRNA ZEB1 antisense1 (ZEB1-AS1) on GC progression. In the present study, we found that ZEB1-AS1 expression was upregulated in GC tissues and cell lines. High ZEB1-AS1 expression was significantly correlated with advanced TNM stage, lymph node metastasis, and poor overall survival in GC patients. ZEB1-AS1 suppression reduced GC cell proliferation and invasion in vitro. Tumor formation assay in nude mice showed that ZEB1-AS1 inhibition suppressed GC cell growth. Quantitative real-time PCR showed that miR-335-5p expression was downregulated and negatively correlated with ZEB1-AS1 expression in GC tissues. And miR-335-5p expression was directly regulated by ZEB1-AS1. Furthermore, we found that inhibition of miR-335-5p abrogated the suppression of proliferation and invasion of GC cells induced by ZEB1-AS1 depletion. Collectively, ZEB1-AS1 is critical for the proliferation and invasion of GC cells by regulating miR-335-5p. Our findings indicated that ZEB1-AS1 might offer potential novel therapeutic targets for GC patients.
Two strains of Methanogenium bourgense, strains MS2T (T = type strain) and LX1, were characterized, and, based in part on previously published DNA hybridization data, this species was transferred to a new genus, Methanoculleus, as Methanoculleus bourgense comb. nov. Methanogenium marisnigri JRIT and a new strain of Methanogenium marisnigri, strain ANS, were also characterized. This species was also transferred to the genus Methanoculleus as MethanocuUeus marisnigri comb. nov. et emend., and its description was emended to indicate that the species has a temperature optimum near 40°C, is halotolerant, and is slightly alkaliphilic; in contrast, the previous description of this organism indicates that it has a temperature optimum of 20 to 25"C, is halophilic, and is slightly acidophilic. We also propose the transfer of two other phylogenetically related species, Methanogenium thermophilicum and Methanogenium olentangyi, to the genus Methanoculleus as Methanoculleus thermophilicum and Methanoculleus olentangyi, respectively. Methanogenium cariaci JRIT was also further characterized, and its description is emended.
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