Application of the Trivex system in the treatment of primary severe superficial varicose veins of the lower extremity.

PURPOSE: The aim of this study was to evaluate the clinical effects of the Trivex system in the treatment of primary severe superficial varicose veins of the lower extremity and compare Trivex to the point-form-stripping combined with foam sclerotherapy (FS). METHODS: A total of 64 patients (35 females, 29 males; mean age, 57 ±â€¯11 years [range, 29-79 years]) with primary severe superficial varicose veins of the lower extremity involving 64 legs were included between October 2015 and July 2019. The maximum diameter of the vein branches was >20 mm, which appeared to be cystic dilatation and forms large-scale in the crus or the thigh. All patients underwent high ligation and endovenous laser ablation or stripping of the trunk under general anesthesia. The surgical time, pain/phlebitis, number of incisions, amount of bleeding, recurrence of varicose vein, incidence of surgical site infections (SSIs), satisfaction score, and improvement in clinical symptoms were evaluated respectively with the patients in two groups: Group A, with patients who underwent treatment with the Trivex system, and Group B, patients who underwent treatment by point-form-stripping combined with FS. RESULTS: All procedures were performed successfully. The average operative time in Group A was 56 ±â€¯11 min, whereas that of Group B was 90 ±â€¯33 min, which was a significant difference (p < 0.05). Group A patients felt little pain after surgery, whereas in Group B the level of pain peaked on postoperative day 30, mostly due to thrombophlebitis after FS. There was no recurrence of varicose vein was observed in any patient, however, there were some residual effects in Group B, including the amount of bleeding volume, in-hospital stays, pain/phlebitis, and number of incisions (P < 0.05). There were no significant differences with respect to SSIs, improvement in clinical symptoms, and satisfaction scores observed (p>0.05). CONCLUSIONS: This study shows that patients benefited from both treatment options. However, primary severe superficial varicose veins of the lower extremity treated with the Trivex system suffered less pain with fewer incisions than severe branches treated with the point-form-stripping combined with foam sclerotherapy (FS). In summary, the Trivex system is a suitable treatment prior to point-form-stripping combined with foam sclerotherapy (FS) for those who demand a high level of appearance, and especially for young patients, the Trivex system is recommended.

Preoperative proteinuria and clinical outcomes in type B aortic dissection after thoracic endovascular aortic repair.

Background Proteinuria is a marker of poor outcomes in several diseases; however, few studies have been conducted to explore the prognostic value of proteinuria, assessed by urine dipstick test, for clinical outcomes in patients with type B acute aortic dissection (TBAD) undergoing thoracic endovascular aortic repair (TEVAR). Methods Consecutive patients with TBAD undergoing TEVAR were enrolled from January 2010 to July 2015. Proteinuria was defined as trace or higher, according to the results of urine dipstick testing. Associations among proteinuria and adverse events were evaluated. Results In total, 671 patients with a mean age of 44±15 years were included in the analysis. Proteinuria was detected in 281 patients (41.9%) before TEVAR. Multivariate logistic regression analysis showed that C-reactive protein and impaired renal function were independent predictors for proteinuria. During hospitalization, 21 patients died. In-hospital mortality was higher in patients with proteinuria (1.5% vs. 5.3%, p=0.005). After a median 3.4 years follow up, the post-TEVAR death rate was 10.4% (85 patients were lost to follow-up). The long-term cumulative mortality was significantly higher in patients with proteinuria (17.2% vs. 8.2%, log-rank=11.36, p=0.001). Multivariate Cox survival modeling indicated that proteinuria was significantly associated with long-term death, after adjustment for potential confounding risk factors (HR=1.92, p=0.012). Conclusions Pre-TEVAR proteinuria was identified as a prognostic marker in patients with TBAD and has potential for application as a convenient and simple risk assessment method before TEVAR.

Upregulated microRNA-16 as an oncogene in renal cell carcinoma.

MicroRNAs (miRs) are small, endogenous noncoding RNAs that serve a significant function in various biologic processes, including those involved in cancer. The present study aimed to determine the expression and function of miR-16 in renal cell carcinoma (RCC). Quantitative polymerase chain reaction was used to quantify the expression of miR-16 in 48 paired RCC tissues and adjacent normal tissues. The impact of miR-16 on cell proliferation, migration and apoptosis was analyzed by transfecting miR-16 mature molecules into the renal cancer cell lines 786-O and ACHN. The results indicated that miR-16 was significantly upregulated in RCC tissues (P<0.05). Downregulation of miR-16 resulted in reduced cell proliferation and migration and increased levels of apoptosis, while overexpression of miR-16 resulted in accelerated cellular proliferation and migration, suggesting that miR-16 may function as an oncogene in RCC. The present study demonstrated for the first time, to the best of our knowledge, that miR-16 is upregulated in RCC and acts as an oncogene by inducing cellular proliferation, migration and reducing apoptosis. Further study of miR-16 in RCC may clarify the molecular mechanisms of RCC carcinogenesis and aid in the development of novel biomarkers and therapeutic options.

Identification of miR­125a­5p as a tumor suppressor of renal cell carcinoma, regulating cellular proliferation, migration and apoptosis.

miR­125a­5p has been previously described as a tumor suppressor in numerous malignancies, however the expression and function of miR­125a­5p in renal cell carcinoma (RCC) remains to be elucidated. In the present study, to explore the potential role of miR­125a­5p in RCC, quantitative polymerase chain reaction was used to determine the expression levels of miR­125a­5p in renal cancer tissues. The influence of miR­125a­5p on cell proliferation, migration and apoptosis was also determined, using an MTT assay, a wound scratch assay and flow cytometry, respectively. The expression of miR­125a­5p was shown to be decreased in RCC and the restoration of miR­125a­5p by synthetic mimics was shown to suppress cell proliferation and migration, and induce apoptosis. The present results indicate that miR­125a­5p may function as a tumor suppressor in RCC. The present study is, to the best of our knowledge, the first to demonstrate the downregulation of miR­125a­5p in RCC, and to show the role it has in affecting cellular proliferation, migration and apoptosis. Further research is needed to define the target genes of miR­125a­5p and explore the potential of miR­125a­5p as a diagnostic or a prognostic biomarker for RCC.

MicroRNA-451a is associated with cell proliferation, migration and apoptosis in renal cell carcinoma.

MicroRNAs (miRNAs) are an important class of small, non­coding RNA molecules that regulate gene expression at the transcriptional or post­transcriptional level. They are involved in apoptosis, proliferation and migration and are known to have an important role in many types of cancer. Aberrant expression of miRNA­451a (miR­451a) has previously been reported in tumors, however its role in renal cell carcinoma (RCC) is currently unknown. The aim of the present study was to investigate the role of miR­451a in RCC. The expression of miR­451a was analyzed in 50 paired RCC and normal tissues by quantitative polymerase chain reaction. Furthermore, the effects of miR­451a on cell migration, proliferation and apoptosis were evaluated, using migration scratch, MTT and flow cytometric assays. The present study demonstrated that miR­451a was upregulated in RCC, as compared with paired normal tissues (P<0.05). Downregulation of miR­451a using a synthesized inhibitor, significantly suppressed cell migration and proliferation, and induced apoptosis of renal cancer cells in vitro, as compared with a negative control (P<0.05). In the present study, it was determined that miR­451a may have an important role as a tumor enhancer in RCC. These results imply that miR­451a may be a promising therapeutic target for the treatment of RCC.

miR­886­3p upregulation in clear cell renal cell carcinoma regulates cell migration, proliferation and apoptosis by targeting PITX1.

miR­886­3p has been discovered to be involved in the oncogenesis, progression and metastasis of several types of human cancer. The aim of the present study was to identify the biological function of miR­886­3p in clear cell renal cell carcinoma (ccRCC) and to determine its possible molecular mechanisms. miR­886­3p was found to be significantly upregulated in ccRCC tissues (P<0.05), in accordance with a previous sequencing result. Functional experiments revealed that forced downregulation of miR­886­3p significantly inhibited cellular migration, suppressed cell proliferation and induced cell apoptosis of renal cancer cells. Paired­like homeodomain 1 (PITX1), which has been identified as a tumor suppressor, was found to be downregulated in ccRCC tissues and identified as a target gene of miR­886­3p. Further experiments demonstrated that the protein level, and not the mRNA level, of PITX1 was significantly decreased or increased when miR­886­3p was upregulated or downregulated, respectively, indicating that miR­886­3p acted as an oncogene by directly regulating the protein expression of PITX1 at a post­transcriptional level. In conclusion, this study revealed that miR­886­3p was upregulated in ccRCC and was involved in cellular migration, proliferation and apoptosis of renal cancer cells by directly targeting the tumor suppressor gene, PITX1.

Expression and clinical significance of RCDG1 in renal cell carcinoma: a novel renal cancer­associated gene.

Recently identified molecular tumor markers have numerous potential applications in the diagnosis, therapy and prognostic prediction of renal cell carcinoma (RCC). Through bioinformatics­based screening approaches together with validation of western blot and immunohistochemical data, the present study identified a novel renal cancer­associated gene, preliminarily named Renal Cancer Differentiation Gene 1 (RCDG1), originally known as chromosome 4 open reading frame 46 (C4orf46). RCDG1 expression was evaluated by western blot analysis of RCC and adjacent normal tissues, renal cancer cell lines and normal kidney HEK293T cells. Additionally, RCDG1 expression was assessed in 124 RCC paraffin sections, including 92 paired adjacent normal tissues, by immunohistochemistry. The results showed that RCDG1 was significantly downregulated in RCC tissues as compared with normal adjacent tissues (P<0.001), and the expression of RCDG1 in clear cell (cc) RCC tissues was significantly lower as compared with that of non­ccRCC tissues (P=0.005). Furthermore, statistical analysis revealed RCDG1 expression was negatively correlated with the Fuhrman grade in ccRCC (P=0.008). A reduction in RCDG1 expression may be associated with the oncogenesis of RCC and the differentiation of ccRCC. Further studies may provide more information about the function of RCDG1 gene in RCC.

Expression of methionine adenosyltransferase 2A in renal cell carcinomas and potential mechanism for kidney carcinogenesis.

BACKGROUND: Methionine adenosyltransferase 2A (MAT2A) is an enzyme that catalyzes the formation of S-adenosylmethionine (SAMe) by joining methionine and ATP. SAMe is a methyl donor for transmethylation and has an important role for DNA and/or protein methylation. MAT2A is expressed widely in many tissues especially in kidney. Several studies have demonstrated that there are abnormal expressions of MAT2A in several kinds of cancers such as liver and colon cancers. But the relationship of MAT2A between renal cell carcinomas (RCC) is less understood. METHODS: The mRNA expression level of the MAT2A gene was determined in 24 RCC patients and 4 RCC cell lines, using real-time quantitative-polymerase chain reaction (RT-PCR). The MAT2A protein content was measured by western blotting and immunohistochemical analysis in 55 RCC patients. The mRNA levels of heme oxygenase-1 (HO-1) and cyclooxygenase-2 (COX-2) were also analysized in patients using RT-PCR. The correlations between the MAT2A and HO-1 as well as COX-2 were analyzed with nonparametric Spearman method. RESULTS: MAT2A transcript was significantly downregulated in cancer tissues compared to normal tissues (P < 0.05). Immunohistochemical analysis and western blotting indicated that level of MAT2A protein was decreased in cancer tissues. The statistical analysis reveals a negative correlation between MAT2A and HO-1 expression in RCC patients and cell lines (P < 0.01). CONCLUSIONS: This study demonstrated that MAT2A was lower expression in cancer tissues, suggesting that it may be involved in the development of RCC. MAT2A is a transcriptional corepressor for HO-1 expression by supplying SAM for methyltransferases, which may be one of potential mechanism of MAT2A as tumor suppressor in kidney carcinogenesis.

Identification of miR-7 as an oncogene in renal cell carcinoma.

MicroRNA-7 (miR-7) has been described as a tumor suppressor in several human cancers, but the results of a study to identify miRNAs associated with metastatic capability in breast cancer suggested that miR-7 may be characterized as an oncogene. The present study was to determine the expression and function of miR-7 in renal cell carcinoma. Quantitative real-time polymerase chain reaction was used to validate the expressions of miR-7 in 48 paired renal cell carcinomas (RCC) and normal tissues, based on the preliminary sequencing results of miRNAs. Furthermore, the impacts of miR-7 on cell migration, proliferation and apoptosis were analyzed using wound scratch assay, MTT and flow cytometry, respectively. The results demonstrated that miR-7 was up-regulated in RCC compared with normal tissues (p = 0.001). Down-regulation of miR-7 with synthesized inhibitor inhibited cell migration in vitro, suppressed cell proliferation and induced renal cancer cell apoptosis, prompting that miR-7 could be characterized as an oncogene in RCC. The present study was the first to reveal that miR-7 was up-regulated in RCC and it played an important role in RCC by affecting cellular migration, proliferation and apoptosis. Further researches should be conducted to explore the roles and target genes of miR-7 in RCC and other cancers.