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The mechanical microenvironment of cells plays a critical role in regulating the physiological function of cells. Cells in vivo are often subjected to a variety of mechanical forces from their mechanical micro-environment, such as shear, tension, and compression. At the same time, cells can adhere to the extracellular matrix (ECM) through adhesion molecules (such as integrin-ligand binding), and further sense the stiffness of the ECM. Cell mechanics mainly studies the properties and behavior of living cells under mechanical forces, and how they relate to cell functions. This review summarized the advances in cell mechanics in 2022, focusing on integrin-ligand interactions and the effects of matrix stiffness and mechanical forces on cell physiological behavior and morphogenesis.
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Objective To discuss the correlation between nutritional megaloblastic anemia and homocysteine,in order that e-valuate the application of homocysteine in some aspects that detection and treatment of megaloblatic anemia.Methods The study was divided into three groups,included case group (MA group,n=192,including megaloblatic anemia of vitamin B12 deficiency,n=60;megaloblatic anemia of folic acid deficiency,n=69;megaloblatic anemia of folic acid and vitamin B12 defi-ciency,n=63),matched group (heathy persons,n=200)and treated group (persons who recovered from megaloblatic ane-mia,n=192).Results The difference on homolevel in plasma between case group and matched group had statistical sidnifi-cance (t=3.56,3.21,2.78,P 0.05).The Hcy levels of folic acid deficiency vitamin B12 de-ficiency,vitamin B12 deficiency and folic acid and vitamin B12 deficiency had no statistical sidnificance (t=1.42,P >0.05). Conclusion The homocysteine level of patients who had nutritional megaloblatic anemia higher than heathy persons.High level of homocysteine had correction between the nutritional megaloblatic anemia.The lack of some nutrition facters (eg:fo-lic acid,vitamin B12)can lead to high homocysteine disease.Detecting the change of homocysteine level in plasma can guide the treatment of nutritional megaloblatic anemia.
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Background and purpose:Although cisplatin-based chemotherapies are used as the first-line treatment for ovarian cancers, the majority of patients eventually progress with platinum-resistant disease. miR-483-5p is overexpressed in lung cancer. However, the research on miR-483-5p in epithelial ovarian cancer (EOC) is still unclear. This study aimed to investigate the expression of miR-483-5p in EOC and its effects on cisplatin resistance in EOC cells.Methods:This study analyzed the expression of the miR-483-5p by real-time lfuorescent quantitative polymerase chain reaction (RTFQ-PCR) in EOC tissues, normal ovarian tissues, and EOC cells. The role of miR-483-5p in EOC was evaluatedin vitro by lentivirus-mediated knockdown of miR-483-5p or overexpression of miR-483-5p in EOC cell lines. Drug sensitivity assay was carried out by CCK-8 kit.Results:miR-483-5p was upregulated in EOC tissues as compared with normal tissues (P<0.01). Furthermore, miR-483-5p expression in advanced stage (Ⅲ–Ⅳ) EOC was significantly higher than that in early stage (Ⅰ–Ⅱ) EOC (P<0.05). Interestingly, miR-483-5p expression was higher in cisplatin-resistant A2780/CP cells than other cells. Increased miR-483-5p expression caused EOC cell resistance to cisplatin and downregulated the expression of p21 and Bcl-2, whereas reduced miR-483-5p expression induced its sensitivity and upregulated the expression of p21 and Bcl-2.Conclusion:The results suggest that miR-483-5p is highly expressed in EOC and contributes to cisplatin resistance. Thus, miR-483-5p is a potential therapeutic target for ovarian cancer.
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Objective: To investigate SIN ( Sinomenine) for TLR signal transduction pathway and MyD88 ( MyeloidDifferentiation Factor 88), TRAF-6 ( Tumor necrosis factor receptor associated factor-6) expression, clarifying SIN inhibit RA(Rheumatoid arthritis)-FLS(Fibroblast-like synoviocytes)proliferation leads to joint deformity of RA cartilage and subchondral bonedestruction caused by the role of mechanisms.Methods: RA-FLS cells for vitro were divided into a control group and(0.125,0.25,0.5,1 mmol/L)SIN group,within each group were detected by alkaline phosphatase(ALP)activity,to determine the best concentrationfor vitro drug;detect 0.5 mmol/L SIN group in CCK-8 method to detect cell proliferation rate;fluorescence quantitative PCR methodMyD88 SIN group and control group with 0.5 mmol/L TRAF-6 gene expression;Western blot method to detect MyD88 SIN group andcontrol group with 0.5 mmol/L TRAF-6 protein expression.Results: SIN the ALP activity of the lower than the control group,with theminimum ALP activity of 0.5 mmol/L SIN group(P<0.01).CCK 8 method,0.5 mmol/L RA-FLS cell proliferation rate SIN group wasobviously lower than the control group(P<0.01),SIN induce cell proliferation rate was highest,4 days into the plateau,after cell proliferationrate began to fall.Fluorescence quantitative PCR and Western blot method to detect,0.5 mmol/L SIN group of MyD88 andTRAF-6 gene and protein expression significantly lower than the control group,the difference was statistically significant(P<0.01). Conclusion: The SIN of TLR signalling pathways through effectively suppress the influence of RA-FLS MyD88 in the cell and theexpression of TRAF-6,this could be a treatment of RA prevent cartilage and subchondral bone damage cause joint deformity happened one of the important molecular mechanism.
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Objective To investigate the inhibitory effect of the mammalian target of rapamycin (mTOR) inhibitor, sirolimus on expression of hypoxia-inducible factor (HIF)1? protein and growth of ovarian carcinoma in an athymic mouse xenogeneic transplant model of ovarian cancer. Methods Four groups of female nude mice were inoculated subcutaneously with SKOV3 cells. After inoculation, mice were treated with saline, rapamycin alone, paclitaxel alone and sirolimus+paclitaxel. In each tumor protein expressions of HIF-1?,bcl-2 and apoptosis were determined by immunohistochemistry and RT-PCR. Results In sirolimus and sirolimus +paclitaxel groups protein expression of HIF-1? was inhibited. Tumor burden in rapamycin alone, sirolimus +paclitaxel, and paclitaxel alone was reduced by 47.9%( P 0.05) respectively compared with controls. Cell apoptosis inder in sirolimus alone(36), sirolimus +paclitaxel(40), paclitaxel alone(22),increased compared with control(15), while expression of bcl-2 decreased compared with control. Conclusion Sirolimus inhibited protein expression of HIF-1?, increased tumor apoptosis and decreased tumor growth.
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Objective To investigate the correlation of hypoxia-inducible factor (HIF)-1? and va scular endothelial growth factor (VEGF) or micro-vessel density ( MVD). Methods The ovarian cancer cell line SKOV3 was transplanted into nude mice to form xenog eneic tumor. Mice were treated with rapamycin 4mg/kg,sulindac 100 mg/(kg.d) a nd saline 200 ?l respectively. Expression of HIF-1? and VEGF proteins and MV D were determined by immunohistochemistry. The mRNA of Glut1 and VEGF was studi ed by RT-PCR. Results The positive expression of HIF-1? and VEGF was moderate to strong, and MVD was high (31?8) in control group. In rapamycin treated group, the expression of H IF-1? was inhibited to weak positive or negative (P