Central Hospital of Minhang District

Shanghai, China

Central Hospital of Minhang District

Shanghai, China
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Zheng L.,Central Hospital of Minhang District | Liu X.-L.,Shanghai JiaoTong University | Cao L.,Shanghai JiaoTong University
Chinese Journal of Contemporary Neurology and Neurosurgery | Year: 2017

Objective: To report 4 cases of ataxia-telangiectasia (AT) with ATM genetic mutation and to summarize the clinical and genetic characteristics of AT by literatures review. Methods: Clinical data of 4 patients from 3 AT families was collected in detail and genomic DNA of the patients and family members was extracted from peripheral blood. Whole exon sequencing (WES) and polymerase chain reaction (PCR) of Sanger sequencing was used to analyse ATM genic mutation. Results: Four patients were characterized by progressive cerebellar ataxia with onset in childhood, oculocutaneous telangiectasia, recurrent infection caused by immunodeficiency, α-fetoprotein (AFP) elevation and cerebellar atrophy shown in brain MRI were presented. Sequence analysis of ATM gene revealed two known compound heterozygous mutations c.8287C > T (p.Arg2763X) and c.9139C > T (p.Arg3047X) which were nonsense mutation in Case 1 and Case 2. In Case 3, there were two compound heterozygous mutations, including nonsence mutation c.8911C > T (p.Gln2971X) and deficit mutation c.7141_7151delAATGGAAAAAT (p.Asn2381GlufsX18) both of which were not reported previously. Case 4 carried homozygotic mutation c.1402_1403delAA (p. Lys468GlufsX18). Conclusions: Four patients were diagnosed as AT with typical clinical manifestations. Patients with variant AT present mild nervous system symptom, normal head MRI and less involvement other than nervous systemt. Definite diagnosis should be dependant on ATM genetic testing. Copyright © 2017 by the Editorial Board of Chinese Journal of Contemporary Neurology and Neurosurgery.


Wang L.,Shanghai JiaoTong University | Wang T.,Central Hospital of Minhang District | Song M.,Shanghai JiaoTong University | Pan J.,Shanghai JiaoTong University
Archives of Oral Biology | Year: 2014

Human periodontal ligament cells (hPDLCs) form specialised connective tissues that influence the lifespan of the tooth. Periodontal disease is a chronic infectious disease of the periodontal supporting tissues caused by a variety of factors, particularly the loss of hPDLCs. Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine known to play an important role in periodontal disease, but little is known about the effects of TGF-β1 on human PDL cells. To determine how TGF-β1 mediates the changes in hPDLCs, we characterised the effects of TGF-β1 treatment on hPDLCs. We then elucidated the signalling pathway that mediates these effects. Serum-starved hPDLCs were incubated with 10 ng/mL TGF-β1, and their proliferation was examined using the Cell Counting Kit-8, while their morphological changes were examined by phase-contrast microscopy. F-actin reorganisation was visualised by phalloidin staining and confocal microscopy. Protein expression was analysed by western blotting. We found that TGF-β1 treatment induced proliferation and cytoskeletal reorganisation, decreased Rho-GDIa protein expression, activated ROCK protein expression, and increased the phosphorylation of LIM kinase and cofilin. Proliferation and cytoskeletal rearrangement were suppressed by pre-treatment with the ROCK inhibitor Y-27632; additionally, expression of ROCK protein and phosphorylation of LIM kinase and cofilin were decreased by Y-27632, while Rho-GDIa knockdown by targeted siRNA transfection causes opposite effects. Therefore, we propose that TGF-β1 induces proliferation and cytoskeletal rearrangement in hPDLCs via Rho GTPase-dependent pathways that modulate ROCK, LIM kinase, and cofilin activity. © 2013 Elsevier Ltd.


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.


Wang L.,Shanghai JiaoTong University | Pan J.,Shanghai JiaoTong University | Wang T.,Central Hospital of Minhang District | Song M.,Shanghai JiaoTong University | Chen W.,Shanghai JiaoTong University
PLoS ONE | Year: 2013

Aim:Human periodontal ligament (PDL) cells incur changes in morphology and express proteins in response to cyclic strain. However, it is not clear whether cyclic strain, especially excessive cyclic strain, induces PDL cell apoptosis and if so, what mechanism(s) are responsible. The aim of the present study was to elucidate the molecular mechanisms by which pathological levels of cyclic strain induce human PDL cell apoptosis.Materials and Methods:Human PDL cells were obtained from healthy premolar tissue. After three to five passages in culture, the cells were subjected to 20% cyclic strain at a frequency of 0.1 Hz for 6 or 24 h using an FX-5000T system. Morphological changes of the cells were assessed by inverted phase-contrast microscopy, and apoptosis was detected by fluorescein isothiocyanate (FITC)-conjugated annexin V and propidium iodide staining followed by flow cytometry. Protein expression was evaluated by Western blot analysis.Results:The number of apoptotic human PDL cells increased in a time-dependent manner in response to pathological cyclic strain. The stretched cells were oriented parallel to each another with their long axes perpendicular to the strain force vector. Cleaved caspase-3 and poly-ADP-ribose polymerase (PARP) protein levels increased in response to pathological cyclic strain over time, while Rho GDP dissociation inhibitor alpha (RhoGDIα) decreased. Furthermore, knock-down of RhoGDIα by targeted siRNA transfection increased stretch-induced apoptosis and upregulated cleaved caspase-3 and PARP protein levels. Inhibition of caspase-3 prevented stretch-induced apoptosis, but did not change RhoGDIα protein levels.Conclusion:The overall results suggest that pathological-level cyclic strain not only influenced morphology but also induced apoptosis in human PDL cells through the RhoGDIα/caspase-3/PARP pathway. Our findings provide novel insight into the mechanism of apoptosis induced by pathological cyclic strain in human PDL cells. © 2013 Wang et al.


Pan J.,Shanghai JiaoTong University | Wang T.,Central Hospital of Minhang District | Wang L.,Shanghai JiaoTong University | Chen W.,Shanghai JiaoTong University | Song M.,Shanghai JiaoTong University
PLoS ONE | Year: 2014

Background: Although mechanical stimulations are known have a significant impact on cytoskeletal rearrangement, little is known regarding the behavioral alteration of human periodontal ligament cells (hPDLCs) under cyclic strain. The aim of this study was to elucidate the role of the Rho signaling pathway on cyclic strain-induced cytoskeletal rearrangement of hPDLCs. Methods: Healthy hPDLCs obtained from teeth extracted for orthodontic purposes were subjected to cyclic strain with physiological loading (10%) at a frequency of 0.1 Hz for 6 h or 24 h using a FX-5000T system. Changes in cell morphology were examined by phase-contrast microscopy, while F-actin reorganization was observed by phalloidin staining and confocal microscopy. Protein expression was analyzed through western blot analysis. Results: Significant enhancement of cytoskeletal reorganization was observed following exposure to the cyclic strain. In addition, a significant increase was noted in the expression levels of GTP-Rho, Rho-associated protein kinase (ROCK) and p-cofilin, whereas the expression levels of Rho GDP dissociation inhibitors alpha (Rho-GDIa) were reduced in the hPDLCs, compared with the static control cells. More importantly, the Rock inhibitor Y-27632 suppressed cyclic strain-induced cytoskeletal rearrangement of hPDLCs. Additionally, Y-27632 and overexpression of Rho-GDIa were found to lower p-cofilin protein expressions under cyclic strain, while Rho-GDIa siRNA transfection had the opposite effect on the hPDLCs. Conclusion: Cyclic strain promotes cytoskeletal rearrangement of hPDLCs by downregulating the expression levels of Rho-GDIa and upregulating the expression levels of GTP-Rho, Rock and p-cofilin. These observations may provide valuable insight into understanding orthodontic tooth movement as well as alveolar bone remodeling. © 2014 Pan et al.


Wu X.-B.,Central Hospital of Minhang District | Tao R.,Shanghai JiaoTong University
Hepatobiliary and Pancreatic Diseases International | Year: 2012

BACKGROUND: Liver cell transplantation and bioartificial liver may provide metabolic support of liver function temporary and are prospective treatments for patients with liver failure. Mesenchymal stem cells (MSCs) are expected to be an ideal cell source for transplantation or liver tissue engineering, however the hepatic differentiation of MSCs is still insufficient for clinical application. DATA SOURCES: A PubMed search on "mesenchymal stem cells", "liver cell" and "hepatocyte differentiation" was performed on the topic, and the relevant articles published in the past ten years were reviewed. RESULTS: Hepatocyte-like cells differentiated from MSCs are a promising cell source for liver regeneration or tissue engineering. Although it is still a matter of debate as to whether MSC-derived hepatocytes may efficiently repopulate a host liver to provide adequate functional substitution, the majority of animal studies support that MSCs can become key players in liver-directed regenerative medicine. However the clinical application of human stem cells in the treatment of liver diseases is still in its infancy. CONCLUSIONS: Future studies are required to improve the efficacy and consistency of hepatic differentiation from MSCs. It is necessary to better understand the mechanism to achieve transdifferentiation with high efficiency. More clinical trials are warranted to prove their efficacy in the management of patients with liver failure. © 2012, Hepatobiliary Pancreat Dis Int. All rights reserved.


Pan Y.,Shanghai JiaoTong University | Xu X.D.,Central Hospital of Minhang District | Guo L.L.,Shanghai JiaoTong University | Cai L.L.,Shanghai JiaoTong University | Jin H.M.,Shanghai JiaoTong University
Nephron - Clinical Practice | Year: 2012

Background/Aims: The association of the timing of dialysis initiation with mortality is controversial. We conducted a meta-analysis to determine the relationship between the risk of death and early initiation of dialysis, when the patient has a greater estimated glomerular filtration rate (eGFR). Methods: Prospective and retrospective cohort studies that independently measured the effect of early vs. late initiation of dialysis on risk of death were identified by review of several databases. Odds ratios (ORs) were estimated by comparison of the highest and lowest quartiles and combined by a random-effects model. Results: 15 studies (1,285,747 patients) met the inclusion criteria. Summary estimates indicated that early start of dialysis was associated with increased risk of mortality (OR = 1.33, 95% confidence interval (CI): 1.18-1.49, p < 0.00001). Subgroup analysis indicated that early starters were 6.61 years older (p < 0.00001) and more likely to have diabetes (OR = 2.23, 95% CI: 1.83-2.71, p < 0.00001) than late starters. Analysis of pooled results of early and late starters indicated that older age (OR = 1.18, 95% CI: 1.05-1.33, p = 0.006), diabetes (OR = 1.61, 95% CI: 1.38-1.87, p < 0.00001), and high comorbidity index score (OR = 2.38, 95% CI: 1.75-3.25, p < 0.00001) were strongly associated with increased risk of death. Conclusion: Our meta-analysis indicates that early initiation of dialysis (at higher eGFR) was associated with an increased risk of death. Older age, greater likelihood of diabetes, and the presence of severe comorbid disease(s) partly explain this effect. Copyright © 2012 S. Karger AG, Basel.


Wei R.,Shanghai JiaoTong University | Wang Q.-B.,Central Hospital of Minhang District | Chen Q.-H.,Central Hospital of Minhang District | Liu J.-S.,Central Hospital of Minhang District | Zhang B.,Shanghai JiaoTong University
Clinical Imaging | Year: 2011

Objective: To evaluate and describe computed tomographic (CT) and endoscopic (ES) imaging findings in patients with pathologically confirmed upper gastrointestinal (GI) tract heterotopic pancreas (HP). Methods: Findings from imaging examinations in 11 patients with pathologically confirmed HP were retrospectively reviewed (CT images obtained from 11 patients and ES images from 6 patients were available for review). Two radiologists evaluated lesion location, size, shape and border as well as growth pattern, enhancement pattern, enhancement grade and number of tumors. The presence of surface dimpling, prominent enhancement of overlying mucosa, and low intralesional attenuation were also evaluated. Results: HP in the upper GI tract showed typical features in CT imaging: submucosal masses, ill-defined borders, endoluminal growth patterns, bright enhancement similar to the normal pancreas, surface dimpling and low intralesional attenuation. Endoscopic photographs manifested an endoluminal, ill-defined, submucosal mass in the upper GI tract wall, typically with central umbilication. The LD (long diameter)/SD (short diameter) ratios were found to be significantly different between HP in the stomach and HP in the duodenum (P<.05 for each finding). In addition, HP in the duodenum tended to be small and round. Conclusions: HP exhibits typical pancreatic pathologic features. Images showed characteristic features in CT imaging: submucosal masses, ill-defined lesions with an endoluminal growth pattern, bright enhancement similar to the normal pancreas, surface dimpling and low intralesional attenuation. ES imaging showed an endoluminal, ill-defined, submucosal mass, typically with central umbilication. © 2011 Elsevier Inc.


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.


Deng X.,Central Hospital of Minhang District | Zhang Z.,Central Hospital of Minhang District | Gu W.,Central Hospital of Minhang District | Li Y.,Central Hospital of Minhang District | Liu M.,Central Hospital of Minhang District
Experimental Lung Research | Year: 2012

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung, and is the fifth leading cause of morbidity worldwide. A novel proinflammatory factor, interleukine-32 (IL-32), is suggested as a risk factor of COPD. Budesonide is widely used for COPD treatment as anti-inflammatory drug. However, the inflammatory inhibition mechanism of budesonide is not fully understood. In this study, we used a rat model with COPD to investigate the effect of budesonide on IL-32 expression in lung tissue. We found that cigarette smoking (CS) strongly induced IL-32 expression in lung tissue, seriously weakened lung function, and damaged pulmonary tissue. Budesonide inhibited the expression of IL-32 in lung tissue. In budesonide-treated rats, we observed no repair of damaged lung tissue but the pulmonary function was partly recovered. To our knowledge, this is the first report that budesonide inhibits the expression of IL-32 in lung tissues, which is strongly induced by CS. © Informa Healthcare USA, Inc.

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