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Sun S.-N.,Fudan University | Yao Z.-Z.,Central Hospital of Minhang District | Jiang Q.,Shanghai Institute of Cardiovascular Diseases | Gui Y.-H.,Fudan University
Fudan University Journal of Medical Sciences | Year: 2016

Objective: To observe ethanol-induced cardiac phenotypes and identify ethanol-sensitive stages during embryonic development, and to explore the optimal period during which the administration of folic acid can effectively rescue the ethanol-induced heart and outflow tract (OFT) defects and its underlying mechanisms. Methods: Ethanol was administrated to zebrafish embryos in a series of developmental stages (7-12 h) and the abnormal heart and OFT phenotypes were observed after ethanol exposure. The embryos which were given ethanol at 7-12 hpf was defined as ethanol treated group. Administrating folic acid to ethanol-treated zebrafish embryos in different stages (7-12 h) was conducted to rescue the abnormal cardiac defects. The ethanol-treated embryos which were given folic acid at 7-12 hpf was defined as folic acid rescue group. The survival percentage, the malformation percentage, the heart rate and the ventricular shortening fraction (VSF) were recorded. The OFT phenotypes were evaluated using fluorescein micro-angiography. Whole-mount in situ hybridization and Real-time PCR were conducted to analyze the expression of bmp2b and tbx1. Results: Ethanol exposure produced heart and OFT defects, including the abnormal cardiac shapes, the hypogenesis of OFT and the reduced heart rate and VSF. The teratogenic effect of ethanol was observed most obviously at the early embryonic development. Supplementation of folic acid at 7-12 hours post-fertilization partially rescued the developmental defects in ethanol-induced zebrafish embryos. The expressions of bmp2b and tbx1 were reduced in ethanol-treated group, and they were partially recovered after administration of folic acid. Conclusions: Folic acid supplementation can effectively rescue ethanol-induced heart OFT defects, possibly by enhancing the expressions of bmp2b and tbx1. © 2016, Editorial Department of Fudan University Journal of Medical Sciences. All right reserved. Source

Chen Y.,Central Hospital of Minhang District | Liu J.,Central Hospital of Minhang District | Chen S.,Shanghai JiaoTong University
Chinese Journal of Gastroenterology | Year: 2015

Background: There are seldom studies on effect of long-term proton pump inhibitor (PPI) on gastric mucosal histology (including atrophy, intestinal metaplasia and dysplasia) in patients with gastroesophageal reflux disease (GERD). Aims: To investigate the effect of long-term PPI on histological changes of gastric mucosa in GERD patients with and without Helicobacter pylori (Hp) infection. Methods: A prospective, randomized, controlled study was conducted. One hundred patients with endoscopically confirmed reflux esophagitis (RE) were enrolled. Patients were given esomeprazole 20 mg bid as initial therapy for 8 weeks and followed by esomeprazole on-demand therapy for 10 months. Hp infection was detected, GERDQ score, gastroscopy and histological examination of gastric mucosa were performed before and after treatment. Results: After long-term PPI, GERDQ score was significantly reduced than that before treatment (P=0.000). The healing rate of RE was 81.0%, and no significant difference in healing rate was found between Hp positive group and Hp negative group (P=0.323). Chronic inflammation in gastric corpus and antrum was significantly reduced after treatment (P<0.05), active inflammation almost disappeared and no worsening of gastric atrophy, intestinal metaplasia, dysplasia was seen (P>0.05). Significant difference in active inflammation and dysplasia in gastric antrum was found between Hp positive group and Hp negative group after treatment (P=0.021, P=0.028). In Hp positive group, improvement of inflammation in gastric antrum was much lower than in gastric corpus (P=0.041). Conclusions: Long-term PPI can significantly improve clinical symptoms and mucosa healing of GERD, and significantly reduce the inflammation of gastric corpus and antrum. COPYRIGHT © 2015 by the Editorial Office of Chinese Journal of Gastroenterology. Source

Wang H.,Central Hospital of Minhang District | Chen Y.-Q.,Central Hospital of Minhang District | Wei R.,Central Hospital of Minhang District | Wang Q.-B.,Central Hospital of Minhang District | And 4 more authors.
American Journal of Roentgenology | Year: 2013

OBJECTIVE. The purpose of this study was to assess the feasibility of using CT to differentiate malignant from benign lesions in patients with pathologically confirmed appendiceal mucoceles. MATERIALS AND METHODS. CT scans of 18 consecutively registered patients (11 men, seven women; age range, 21-78 years) with pathologically confirmed appendiceal mucocele were reviewed retrospectively. Patients were classified into three groups according to pathologic results: nonneoplastic mucocele (n = 3), mucinous cystadenoma (n = 10), and mucinous cystadenocarcinoma (n = 5). The nonneoplastic and mucinous cystadenoma groups were formed into a benign group, and the mucinous cystadenocarcinoma constituted the malignant group. Two experienced radiologists working in consensus assessed the shape, short diameter, density, contour, and wall thickness of the masses. The presence of calcifications, internal septations, soft-tissue thickening, periappendiceal fat stranding, intraperitoneal free fluid and pseudomyxoma peritonei were also evaluated. The CT results were compared for malignant and benign appendiceal mucoceles. RESULTS. CT showed statistically significant differences in wall irregularity and softtissue thickening between malignant and benign cases (p < 0.05). Short diameter of mucoceles, attenuation of intraluminal contents, maximal wall thickness, calcifications, internal septations, periappendiceal fat stranding, intraperitoneal free fluid, and pseudomyxoma peritonei in the lesions did not differ significantly between the benign and malignant groups (p > 0.05). CONCLUSION. Differentiating. © American Roentgen Ray Society. Source

Lian W.,Central Hospital of Minhang District | Ma D.J.,CAS Shanghai Institute of Organic Chemistry | Ma D.J.,University of Chinese Academy of Sciences | Xu X.,CAS Shanghai Institute of Organic Chemistry | And 2 more authors.
Journal of Digestive Diseases | Year: 2012

Objective: To develop a rapid, high-performance liquid chromatography (HPLC) method for the determination of tryptophan in gastric juice to help the differentiation between gastric cancer and benign gastric disease. METHODS: HPLC was performed on a restricted access material Shiseido Capcell Pak MF SCX SG80 column. Phosphate buffered solution (90mmol/L, pH 3.5)-acetonitrile (ACN; 80/20, V/V) was chosen as the mobile phase. Separation was done at room temperature using a constant flow rate of 1.0mL/min. Fluorescence emission signal intensity at 330nm excited by 288nm ultra violet light was detected and measured. RESULTS: Thirty-eight gastric juice samples from patients with gastric cancer and 48 gastric juice samples of patients with benign gastric disease were tested. A linear relationship in the range of 0.20-100mg/L was obtained between the concentration of tryptophan and its fluorescence emission signal intensity at 330nm. The limit of detection was 0.05mg/L. The recovery rate was 77.4-90.6%. CONCLUSIONS: An HPLC method based on strong cation-exchange restricted access columns for determination of concentration of tryptophan in gastric juice was developed. The method has excellent precision and stability. It is compatible with the analysis of gastric juice and has the potential to be used for gastric cancer screening. © 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd. Source

Liu L.,Shanghai JiaoTong University | Jin X.,Shanghai JiaoTong University | Zhou Z.,Central Hospital of Minhang District | Shen C.,Shanghai JiaoTong University
International Journal of Molecular Sciences | Year: 2016

Background: Most mesenchymal stem cells (MSCs) die shortly after transplantation into a myocardial infarcted area. Dead MSCs (dMSCs) are phagocytized by macrophages (pMΦ) in vivo and in vitro; however, the effects of pMΦ on cardiac stem cells (CSCs) remain unknown. Methods: MSCs, CSCs, and macrophages were obtained from bone marrow, hearts, and peritoneal cavity of mice, respectively. dMSCs were harvested after hypoxia for 24 h, and incubated with macrophages (2:1) for another 2 days with or without lipopolysaccharide (LPS, 50 ng/mL) and sorted by flow cytometry to obtain pMΦ. Viability and apoptosis of CSCs were respectively evaluated with the cell counting kit-8 (CCk-8) assay and Annexin V-PE/7-AAD staining at 0, 6, 12, and 24 h of culture with supernatant fluids from macrophages (MΦ), LPS-stimulated macrophages (LPS-pMΦ), pMΦ, and MSCs. GATA-4 and c-TnI expression was measured by flow cytometry on the seventh day. Expression of inflammation and growth factors was assessed by real-time polymerase chain reaction (RT-PCR) in MΦ, LPS-pMΦ, and pMΦ cells. Results: pMΦ expressed higher levels of interleukin-10 (IL-10) and transforming growth factor-β (TGF-β)and lower levels of tumor necrosis factor-α(TNF-α)and IL-6 than LPS-pMΦ, higher levels of growth factors and of GATA-4 and c-TnI at the 7th day, which were similar to those in MSCs. CSCs cultured with supernatant fluids of pMΦ exhibited higher proliferative, anti-hypoxic, and differentiation activities. Conclusion: The supernatant fluids of macrophages that had phagocytized dead MSCs encouraged changes in phenotype and growth factor expression, enhanced proliferation, differentiation, and anti-hypoxic activity of CSCs, which is relevant to understanding the persistent therapeutic effect of MSCs after their massive demise upon transplantation in myocardial infarction. Furthermore, some miRNAs or proteins which were extracted from the supernatant fluids may give us a new insight into the treatment of myocardial infarction in the future. © 2016 by the authors; licensee MDPI, Basel, Switzerland. Source

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