BACKGROUND: Differentiation of bone marrow mesenchymal stem calls(BMSCs) is associated with their microenvironment. After acute myocardial infarction (AMI), the necrosis of cardiomyocytes caused activation of complement, generation of free radical, and secretion of various cell factors. As a result, the ingredients of patients' serum also changed, so does the changes will influence the differentiation of BMSCs into cardiomyocytes? And what influence it will be? OBJECTIVE: To investigative effects of AMI rat serum on the differentiation of BMSCs into cardiomyocytes. DESIGN, TIME AND SETTING: The in vitro controlled cytology experiment was performed at the Laboratory of Center for Stem cells and Tissue Engineering, Sun Yat-sen University from September in 2005 to June in 2006. MATERIALS: SPF Sprague Dawley rats, weighing 50-80 g, aged 3-4 weeks, were used for culture of BMSCs, and SpragueDawley rats, weighing 200-300 g, aged 6-8 weeks, were used for making AMI models. METHODS: BMSCs were isolated and cultured with the adherent method. After making AMI rat models by deligating anterior descending of the left coronary artery, the serum were collected and centrifuged from AMI and normal rats. Then the passage 3 of BMSCs were divided into six groups, non-induction group, 5-azacytidine (5-aza) group, 5-aza plus serum from AMI rat group, 5-aza plus serum from normal rat group, serum from AMI rat group, and serum from normal rat group. MAIN OUTCOME MEASURES: Morphology changes in rat BMSCs after induction; Expression of cardiac troponin T of BMSCs after induction; Expression of GATA-4 and desmin mRNA of BMSCs after induction. RESULTS: After being induced by 5-aza and two kinds of serum, some cells became elongated and thinner. Two to three weeks after induction, some cells had a ball-like or rod-like appearance, and connection were formed between adjacent cells. It showed that some BMSC have differentiated into cardiac like cells. The expression of cardiac troponin T, GATA-4 and desmin were positive in cells differentiated from BMSCs. The troponin T expression in control group and simple serum induction group were negative, but GATA-4 and desmin expressed weakly. CONCLUSION: Serum from AMI rat cannot induce BMSCs to differentiate into cardiomyocytes alone, but it promotes BMSCs induced by 5-aza differentiating into cardiomyocytes and facilitates the differentiated calls into mature.

Objective To study the changes of serum free triiodothyronine (FT3), free tetraiodothyronine (FT4) and the relation between free thyroxine levels and serum tumor necrosis factor (TNK), albumin (ALB), urinary protein in children with primary nephrotic syndrome(PNS). Methods There were sixty children who were suffered from nephrotic syndrome in study group Serum FT3,FT4,TNF, Alb and urinary protein were detected. In the meantime compared with 25 health,cases. Results The levels of FT3, FT4 of the children who were suffered from nephrotic syndrome were lower. The difference between nephrotic syndrome and health cases were significantly (P

Objective To explore the clinical manifestations of hypermastigote detected from bronchoalveolar lavage fluid in children with mycoplasma pneumoniae pneumonia (MPP).Methods The clinical data from 18 cases (7 male cases,11 female cases;the age raged from 5 months to 13 years;13 case lived in rural cottage,5 cases lived in town building;the course ranged from 2 to 60 days) of MPP coinfected with hypermastigote were retrospectively analyzed,including the symptomatic and physical examination data, laboratory test, chest imaging features, bronchoscopic manifestation imaging,treatment and prognosis.The clinical characteristics and treatment of MPP coinfected with hypermastigote were analyzed.Results Clinical symptoms showed that 18 cases had cough, 14 cases had fever and 4 cases had asthma;laboratory blood routine test detected that 13 cases had increased leukocytes,5 cases with increased eosinophils;11 cases with increased C reactive protein and 8 cases with increased erythrocyte sedimentation rate.Eleven of 18 cases received immunological examination,which showed that 3 cases had increased IgG,2 cases with increased IgM,5 cases with increased IgA,and 11 cases with decreased ratio of CD4 and CD8;bronchoalveolar lavage fluid test showed that 1 case had increased eosinophils and hypermastigote were detected in 18 cases.High density spotty shadow were seen in chest imaging.Mucosal congestion, attached with white sputamentum, longitudinal folds, floc floating and sputum bolt obstructing within the lumen were seen under the bronchoscopy.The macrolides antibiotics combined with metronidazole (5 cases received metronidazole lung lavage) were effective.Conclusions Hypermastigote is a new type pathogen isolated from the lower respiratory tract in Liaocheng.For patients with MPP who have unsatisfactory response, hypermastigote should be taken into account and combined with metronidazole in therapy for better effect.

BACKGROUND:Human placental mesenchymal stem cells have been shown to be effective in inhibiting the development of pulmonary fibrosis,but the underlying mechanisms remain unclear. OBJECTIVE:To investigate the therapeutic effect and related mechanism of human placental mesenchymal stem cells on silica-induced pulmonary fibrosis in human embryonic lung fibroblasts(MRC-5). METHODS:CCK-8 assay was used to detect the effects of different mass concentrations of silica on the proliferation of MRC-5 at different time points.Immunofluorescence staining was used to screen out the best stimulating mass concentration and time of silica for subsequent experiments.MRC-5 cells were divided into blank group,silica group,and silica + human placental mesenchymal stem cell group.In the blank group,cells were not treated.In the silica group,MRC-5 cells were stimulated with 100 μg/mL silica for 48 hours.In the silica + human placental mesenchymal stem cell group,MRC-5 cells were stimulated with 100 μg/mL silica for 48 hours and then co-cultured with human placental mesenchymal stem cells for 24 hours.Immunofluorescence staining was used to detect the expression of α-smooth muscle actin and collagen type I in cells of each group.Western blot assay was used to detect the expressions of pulmonary fibrosis-related proteins and TGF-β1/Smad 3 signaling pathway-related proteins in cells of each group. RESULTS AND CONCLUSION:(1)CCK-8 assay results suggested that 100 μg/mL silica was the best mass concentration and time to stimulate MRC-5 cells for 48 hours.(2)Immunofluorescence staining results showed that the expression of α-smooth muscle actin and collagen type I in the silica + human placental mesenchymal stem cell group was significantly lower than that in the silica group.(3)Western blot assay results showed that compared with the silica group,the protein expression levels of α-smooth muscle actin,collagen type I,N-cadherin,fibronectin,transforming growth factor-β1,p-Smad3,and Smad3 in the silica + human placental mesenchymal stem cell group were decreased,and the expression of E-cadherin was increased.The difference was statistically significant(P<0.05).(4)The results showed that human placental mesenchymal stem cells had a significant therapeutic effect on silica-induced pulmonary fibrosis.Human placental mesenchymal stem cells can inhibit the development of pulmonary fibrosis by regulating transforming growth factor-β1/Smad3 signaling pathway.

Objective: To investigate the regulatory effect of miR-1297 on the malignant biological behaviors of breast cancer cells and its underlying mechanism. Methods: Twenty pairs of breast cancer tissues and para-cancer tissues resected at the Department of Thyroid and Breast Surgery of Leshan People′ s Hospital from May 2016 to May 2018, as well as breast cancer cell lines MCF-7, SW626, HCC1937 and human breast epithelial MCF-10A cells were collected for this study. qPCR was performed to evaluate the expression of miR-1297 in breast cancer tissues and cell lines. The experimental cells were divided into control group, miR-1297 inhibitor group; TET3 over-expression group and simultaneous over-expression of TET3 and miR-1297 group. CCK-8 assay was used to detect the cell proliferation of MCF-7 cells; Transwell assay was carried out to detect the migration and invasion of MCF-7 cells; and WB was used to measure the expressions of TET3 and EMT related proteins (E-cadherin, N-cadherin and vimentin). Dual luciferase reporter gene assay was used to verify the relationship between miR-1297 and TET3. Results: miR-1297 was up-regulated in both breast cancer tissues and cell lines (P<0.01 or P<0.05). Knockdown of miR-1297 dramatically repressed the proliferation, migration, invasion and EMT of MCF-7 cells (P<0.01 or P<0.05). Over-expression of TET3 significantly up-regulated the expression of TET3 in MCF-7 cells (P<0.05). Simultaneous over-expression of TET3 and miR-1297 could reverse the expression level of TET3 in MCF-7 cells and the inhibitory effect of TET3 on the proliferation, migration, invasion and EMT of MCF-7 cells. Dual luciferase reporter gene assay results showed that miR-1297 targetedly bound to the 3' UTR of TET3. Further experiment results demonstrated that miR-1297 targetedly down-regulated TET3 and promoted the malignant biological behaviors of MCF-7 cells. Conclusion: miR-1297 is up-regulated in breast cancer tissues and cells; it promotes the malignant biological behaviors such as proliferation, migration, invasion and EMT through targetedly down-regulating the expression of TET3.

BACKGROUND: Tumor recurrence and drug resistance are the main causes of death in tumor patients. The family of acetaldehyde dehydrogenase (ALDH) is closely related to the proliferation, migration, invasion and resistance of tumor cells, and different ALDH subtypes are expressed in different tumor cells. The aim of this study is to elucidate the ALDH subtype in human lung adenocarcinoma HCC-827/GR cells, which resistant to the gefitinib. METHODS: The human lung adenocarcinoma HCC-827 cells were used to generate the gefitinib-resistant HCC-827/GR cells; the expression of ALDH subtype in either HCC-827 or HCC-827/GR was detected by flow cytometry; The proliferative capacity and sensitivity to gefitinib of hcc-827/GR cells were analyzed by MTT assay before and after treatment with 100 μmol/L diethyllaminaldehyde (DEAB); Real-time quantitative PCR was used to detect the expression of ALDH subtypes at mRNA levels in hcc-827 cells and hcc-827/GR cells. RESULTS: Compared with HCC-827 cells, the positive rate of ALDH in HCC-827/GR cells increased. The proliferation ability of HCC-827/GR cells decreased after treatment with 100 μmol/L DEAB. Compared with HCC-827 cells, the expression of ALDH1A1 and ALDH1L1 mRNA was increased in hcc-827/GR cells, but the ALDH3B2 expression was decreased. CONCLUSIONS ALDH might be used as a molecular biomarker to test the gefitinib-resistant to lung adenocarcinoma cancer cells, and the ALDH1A1 may play a role in gefitinib resistance in lung cancer.
Adenocarcinoma ; pathology ; Adenocarcinoma of Lung ; Aldehyde Oxidoreductases ; antagonists & inhibitors ; genetics ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; genetics ; Enzyme Inhibitors ; pharmacology ; Gefitinib ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Lung Neoplasms ; pathology ; Quinazolines ; pharmacology