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Objective:To investigate the protective effects and related mechanisms of Astragaloside Ⅳ(ASⅣ)alleviating Angiotensin II-induced cardiomyocyte hypertrophy.Methods:H9c2 cardiomyocytes were divided into six groups: normal control group, ASⅣ group(ASⅣ 100 μmol/L), AngⅡ group(AngⅡ 1 μmol/L), and three ASⅣ dose experiments(AngⅡ 1 μmol/L + ASⅣ 25 μmol/l group, AngⅡ 1 μmol/L+ ASⅣ 50 μmol/l group, AngⅡ1 μmol/L+ ASⅣ 100 μmol/L group), and simultaneously cultured for 24 hours.Cardiomyocyte viability was assessed by CCK8 assay, and surface area of culturedcardiomyocytes in each group was assessed by immunofluorescence assay.Atrial natriuretic peptide(ANP)mRNA expression was assessed by fluorescence real-time quantitative RT-PCR.And LC3 protein expression, an autophagy related protein, was assessed by Western blotting as well as immunofluorescence.Results:(1)AngⅡ decreased cardiomyocyte H9c2 viability in a dose-dependent manner( P<0.05). ASⅣ could inhibit the decrease of cardiomyocyte H9c2 viability in response to AngⅡ in a dose-dependent manner( P<0.05). (2)H9c2 cardiomyocytes induced by AngⅡ showed a significantly larger cell area and significantly higher ANP mRNA and ANP protein expression compared with controls.Different concentrations of ASⅣ intervention could reverse the increase of cardiomyocyte H9c2 area induced by AngⅡ and also decreased the expression of ANP protein induced by AngⅡ in a dose-dependent manner(all P<0.05). (3)Compared with the control group, the autophagy level and the expression of autophagy marker LC3II/I of H9c2 cardiomyocytes induced by AngⅡ were significantly increased(all P<0.05). ASⅣ could inhibit AngⅡ-activated autophagy, and the difference was statistically significant( P<0.05). ASⅣ inhibited the expression of LC3II/I in H9c2 cardiomyocytes stimulated by AngⅡ, and the difference was statistically significant( P<0.05). Conclusions:ASⅣ inhibits AngⅡ-induced cardiac hypertrophy by inhibiting autophagy of cardiomyocytes.
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Background@#In China, secondary cytoreductive surgery (SCR) has been widely used in ovarian cancer (OC) over the past two decades. Although Gynecologic Oncology Group-0213 trial did not show its overall survival benefit in first relapsed patients, the questions on patient selection and effect of subsequent targeting therapy are still open. The preliminary data from our pre-SOC1 phase II study showed that selected patients with second relapse who never received SCR at recurrence may still benefit from surgery. Moreover, poly(ADP-ribose) polymerase inhibitors (PARPi) maintenance now has been a standard care for platinum sensitive relapsed OC. To our knowledge, no published or ongoing trial is trying to answer the question if patient can benefit from a potentially complete resection combined with PARPi maintenance in OC patients with secondary recurrence. @*Methods@#SOC-3 is a multi-center, open, randomized, controlled, phase II trial of SCR followed by chemotherapy and niraparib maintenance vs chemotherapy and niraparib maintenance in patients with platinum-sensitive second relapsed OC who never received SCR at recurrence. To guarantee surgical quality, if the sites had no experience of participating in any OC-related surgical trials, the number of recurrent lesions evaluated by central-reviewed positron emission tomography–computed tomography image shouldn't be more than 3. Eligible patients are randomly assigned in a 1:1 ratio to receive either SCR followed by 6 cyclesof platinum-based chemotherapy and niraparib maintenance or 6 cycles of platinum-based chemotherapy and niraparib maintenance alone. Patients who undergo at least 4 cycles of chemotherapy and must be, in the opinion of the investigator, without disease progression, will be assigned niraparib maintenance. Major inclusion criteria are secondary relapsed OC with a platinum-free interval of no less than 6 months and a possibly complete resection. Major exclusion criteria are borderline tumors and non-epithelial ovarian malignancies, received debulking surgery at recurrence and impossible to complete resection. The sample size is 96 patients. Primary endpoint is 12-month non-progression rate.
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Objective To modify recombinant plasmid construction of BPO trimer,and establish the detec-tion of M2 type anti-mitochondrial antibody (AMA-M2) using ELISA.To modify the recombinant expression vector of the target gene triplet of AMA-M2,and to establish and evaluate an enzyme linked immunosorbent assay (ELISA) for the detection of AMA-M2.Methods The expression vector pGEX 4T 1 BPO was con-structed through the gene amplification of triplet BPO by polymerase chain reaction (PCR),and expressed in E.coli BL21,and the recombinant protein was induced by isopropyl Thioglucoside (IPTG).The target protein was purified by affinity chromatography,and ELISA was established to detect AMA-M2.Results The recom-binant protein with a purity greater than 95% was obtained.326 cases of clinical samples was examined,and in 43 cases of primary biliary cirrhosis (PBC),41 cases showed AMA-M2 positive,the sensitivity was 95.3%(41/43),the specificity was 98.2%(278/283),and the difference of AMA-M2 detection rate between PBC group and non PBC group was statistically significant.Conclusion The target protein obtained by the im-proved technology can be used for AMA-M2 detection.AMA-M2 has high sensitivity and specificity for the clinical diagnosis of PBC.
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Objective To analyze and study the relationship between plasma adhesion molecules,free amino acids and ovarian cancer.Methods A total of 67 patients with ovarian cancer in our hospital during the time of March 2015 to May 2016 were selected as the observation group,and 67 healthy women at the same time were selected as the control group.The plasma adhesion molecules and free amino acids levels of two groups were detected and compared,The detection levels of observation group with different stages and degree of differentiation of ovarian cancers were compared.The relationship between plasma adhesion molecules,free amino acids and ovarian cancer were analyzed by the Logistic analysis.Results The plasma adhesion molecules levels of observation group were all higher than those of control group (P ＜ 0.05),the plasma free amino acids levels were all lower than those of control group (P ＜ 0.05),and the detection levels of observation group with different stages and degree of differentiation of ovarian cancer plasma adhesion molecules and free amino acid levels had significant differences (P ＜ 0.05).The Logistic analysis showed that the plasma adhesion molecules and free amino acids had close relationship to the ovarian cancer (all P ＜ 0.05).Conclusions The plasma adhesion molecules and free amino acids of the patients with ovarian cancer show abnormal expression state,and the expression levels of patients with different stages and degree of differentiation of ovarian cancer have certain differences,so the detection value of those indexes in the patients with ovarian cancer is higher.
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BACKGROUND:In recent years a large number of studies have suggested that bone marrow mesenchymal stem cells can ease hyperglycemia of diabetic rats, but the related mechanism is unclear and controversial. OBJECTIVE:To investigate the relevant mechanism of bone marrow mesenchymal stem cells on pancreas microenvironment in vivo in diabetic rats. METHODS:Bone marrow mesenchymal stem cells were transfected with enhanced green fluorescent protein (EGFP) and administered to diabetic rats via the subcapsular pancreas. Blood glucose levels were monitored. The expressions of the key genes in islet development in these EGFP positive pancreatic cells were analyzed by Real-time quantitative PCR at different times. EGFP and insulin double-positive cells were detected by immunofluorescence. Flow cytometry was performed to analyze cellcycle and DNA ploidy. RESULTS AND CONCLUSION:Blood glucose levels were effectively reduced after transplantation. The expressions of the key genes in islet development reached their own peak values at different times after transplantation:Nestin at week 1, Nkx 2.2 at week 3, Pax 4 and Ngn 3 at week 4, insulin and glucagon at week 12, PDX-1 at week 8 until week 12. The cells double-positive for EGFP and insulin cells were observed. In the pancreas, EGFP positive cells at S+G 2/M phase were significantly increased, and there were no polyploid and aneuploid cells. In pancreas microenvironment, the bone marrow mesenchymal stem cells transplanted into the diabetic pancreas can differentiate into isletβ-like cells under gene control, but not through the fusion with tissue cells.
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Objective To investigate the pathogenesis,high risk factors,clinical characteristics,methods of diagnosis and treatment,and prognosis of vaginal intraepithelial neoplasia (VAIN).Methods The clinical data of thirteen cases of VAIN treated in Zhejiang Provincial Cancer Hospital dated Mar.2002 through Dec.2008 were reviewed and analyzed retrospectively.Results Twelve of 13 VAIN cases were performed the human papillomavirus(HPV) detection with 92% (11/12) HPV positive rate.None of the cases shown specific clinical manifestation.Among the 13 cases,6 of them accompanied with cervical cancer,4 cases with cervical intraepithelial neoplasia (CIN ),and 3 cases with vulvar intraepithelial neoplasma (VIN).Five cases synchronously diagnosed with cervical lesion and 3 with vulva lesion were underwent surgery,while the other 5 cases were diagnosed metachronously.Among 8 cases underwent surgery,1 case with CIN underwent argon plasma coagulation (APC) after surgery,1 case with the positive edge of VIN underwent APC.During follow up,1 case with locally advanced cervical cancer underwent radiotherapy again,3 cases with VAIN received APC,while 1 cervical cancer cases with VAIN received no treatment.The average follow-up time was 25.6 months (range 6-87 months).Two cases died of cervical cancer metastasis.The other 11 cases were normal and still alive.None of them progressed to invasive carcinoma.Conclusions The main reason of VAIN is HPV infection.There are not specific clinical manifestations,usually diagnosed when reviewing cervical or vulva lesions and rarely progressed to invasive carcinoma.The main treatment of VAIN is surgery with the adjuvant treatment of APC.