Jinhua Peoples Hospital

Jinhua, China

Jinhua Peoples Hospital

Jinhua, China
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Chen G.-Z.,Tongde Hospital of Zhejiang Province | Shan X.-Y.,Jinhua Municipal Central Hospital | Cheng G.-P.,Jinhua Peoples Hospital | Tao H.-M.,Zhejiang University of Science and Technology
Journal of Molecular Neuroscience | Year: 2013

Background: Cyclooxygenase-2 (COX-2) catalyzes the formation of prostaglandins that contribute to the inflammation in atherosclerosis. The aim of the present study was to investigate the relationship between two polymorphisms (-1195G>A and -765G>C) in the COX-2 gene and subtypes of ischemic stroke in a Chinese population. Methods: Genomic DNA of 224 patients with large artery atherosclerosis (LAA), 329 patients with small vessel occlusion (SVO), and 450 controls were genotyped for the COX-2 1195G>A (rs689466) and -765G>C (rs20417) polymorphisms using polymerase chain reaction-restriction fragment length polymorphism. Chi-square test and logistic regression analysis were performed for association analysis. Results: The frequencies of variant allele with -1195G>A and -765G>C polymorphisms were 0.46 and 0.22, respectively. The -1195GA genotype and 1195A allele carriers were identified independently to be related with ischemic stroke (adjusted OR = 1.51, 95 % CI: 1.09-2.10, P = 0.02; OR = 1.45, 95 % CI: 1.06-1.97, P = 0.02) and SVO (adjusted OR = 1.57, 95 % CI: 1.07-2.30, P = 0.02; OR = 1.50, 95 % CI: 1.05-2.16, P = 0.03). In contrast, the 1195G>A polymorphism was not associated with LAA. No relationship between the -765G>C polymorphism and risk of either ischemic stroke was observed. The linkage disequilibrium analysis showed that -1195G>A and -765G>C SNPs are moderate linkage disequilibrium in this study population (D′ = 0.72, r 2 = 0.16). Compared with G-1195-G-765 haplotype, the haplotype of A-1195-G-765 showed significant increased risk of ischemic stroke (OR = 1.27, 95 % CI: 1.05-1.54, P = 0.02) and SVO (OR = 1.27, 95 % CI: 1.02-1.58, P = 0.03) but not LAA. Conclusions: In conclusion, we found that -1195G>A polymorphism and A-1195-G-765 haplotype of COX-2 were associated with susceptibility to ischemic stroke in a Chinese population. The effects were confined to SVO among the stroke subtypes rather than to LAA. © 2013 Springer Science+Business Media New York.


Shan X.-Y.,Jinhua Municipal Central Hospital | Chen G.-Z.,Tongde Hospital of Zhejiang Province | Cheng G.-P.,Jinhua Peoples Hospital
Journal of Molecular Neuroscience | Year: 2013

Cyclooxygenase-2 (COX-2) is a key enzyme involved in the conversion of arachidonic acid into prostaglandins, which are important mediators of inflammation. To clarify the role of inflammation in the pathogenesis of cerebral small vessel disease (SVD), we investigate the possible modulating effect of the functional COX-2 polymorphisms -1195G > A (rs689466) and -765G > C (rs20417) on the risk for development of cerebral SVD in a Chinese population. Genomic DNA of 116 patients with lacunar infarction (LI), 334 patients with leukoaraiosis (LA) and 450 control subjects was genotyped for the COX-2 -1195G > A and -765G > C polymorphisms using polymerase chain reaction-restriction fragment length polymorphism. Distribution of genotypes and haplotypes in patients and controls were compared. The genotype distribution of the -765G > C polymorphism was not different between the patients with LI or LA and the control group. The 1195A allele carriers was identified independently to be related with LA (adjusted OR = 1.41, 95 % confidence interval (CI) = 1.09-2.10, P = 0.03) but not associated with LI. The linkage disequilibrium analysis showed that -1195G > A and -765G > C SNPs are moderate linkage disequilibrium in this study population (D′ = 0.70, r 2 = 0.16). Compared with G-1195-G-765 haplotype, the haplotype of A-1195-G-765 showed significantly increased the risk of LA (OR = 1.24, 95 % CI = 1.10-1.55, P = 0.04) but not LI. In conclusion, we found that -1195G > A polymorphism and A-1195-G-765 haplotype of COX-2 were associated with susceptibility to LA in a Chinese population. © 2013 Springer Science+Business Media New York.


Fang T.,Jinhua Peoples Hospital | Dong Y.,Zhejiang Economic and Trade Polytechnic | Zhang X.,Zhejiang University | Xie K.,Zhejiang University | And 3 more authors.
International Journal of Pharmaceutics | Year: 2016

Liposomal nanoassemblies have been used extensively as carriers for the delivery of both lipophilic and hydrophilic drugs. They represent a mature, versatile technology with considerable potential for improving the pharmacokinetics of drugs. However, the formulation of many chemotherapeutics into liposome systems has posed a significant challenge due to their incompatible physicochemical properties, as was the case with camptothecin-based chemotherapeutics. Here, we present a rational paradigm of potent chemotherapeutics that were reconstructed and subsequently integrated into liposomal nanoassemblies. Using SN38 (7-ethyl-10-hydroxy camptothecin) as a model drug, a lipophilic prodrug 1 (designated as LA-SN38) was constructed by tethering the linoleic acid (LA) moiety via esterification, which was further facilitated to form liposomal nanoparticles (LipoNP) through supramolecular nanoassembly. The resulting 1-loaded LipoNP exhibited sustained drug release kinetics and decreased cellular uptake by macrophage cells. Uptake by tumor cells was enhanced relative to our previous supramolecular nanoparticles (SNP 1), which were derived from the self-assembling prodrug 1. Notably, LipoNP outperformed SNP 1 in terms of pharmacokinetics and in vivo therapeutic efficacy in both human BEL-7402 hepatocellular carcinoma (HCC) and HCT-116 colorectal cancer-derived xenograft mouse models. These results were likely due to the improved systemic circulation and preferential accumulation of nanodrugs in tumors. Hence, our results suggest that the combination of liposomal delivery platforms with rational prodrug engineering may emerge as a promising approach for the effective and safe delivery of anticancer chemotherapeutics. © 2016 Elsevier B.V.


Wang H.,Jinhua Peoples Hospital | Fei Z.,Wenzhou University | Jiang H.,Zhejiang Hospital
Journal of Pharmacological Sciences | Year: 2017

Blockade of EGFR with reversible EGFR tyrosine kinase inhibitors (TKIs) is considered the frontline strategy for advanced NSCLC with EGFR mutations. However, acquired resistance to EGFR-TKI has been observed, resulting in disease progression and limited clinical benefit. Polyphyllin VII is the main member of polyphyllin family, which has been demonstrated to show strong anticancer activity against carcinomas. The sensitizing effect and underlying mechanism of Polyphyllin VII against acquired EGFR-TKI resistant NSCLC are still unexplored. In the present study, we aim to examined the sensitizing effect of Polyphyllin VII to gefitinib by modulating P21 signaling pathway in gefitinib acquired resistant NSCLC in vitro and in vivo. Gefitinib sensitive PC-9 cells and gefitinib acquired resistant H1975 cells were used. Cell proliferation and Clonogenic assay, Cell cycle analysis, Western blotting analysis and xenograft treatment were carried out. Polyphyllin VII enhanced the anti-proliferative effects of gefitinib and gefitinib-induced G1 phase arrest by modulation of P21 signaling pathway in acquired gefitinib resistant cells in vitro and in vivo. Polyphyllin VII elevated sensitization of gefitinib acquired resistant NSCLC cells to gefitinib through G1 phase arrest and modulation of P21 signaling pathway. It provides a potential new strategy to overcome gefitinib acquired resistance for EGFR-TKI resistant NSCLC. © 2017 The Authors


Cheng G.-P.,Jinhua Peoples Hospital | Shan X.-Y.,Jinhua Central Hospital
Canadian Journal of Neurological Sciences | Year: 2012

Background: Transforming growth factor beta1 (TGFβ1) is a multifunctional cytokine involved in inflammation and pathogenesis of atherosclerosis. The aim of the present study was to investigate the relationship between human TGFβ1 gene +869T>C (rs1800470), -509C>T (rs1800469) single nucleotide polymorphisms (SNPs) and haplotypes and cerebral infarction (CI) in a Chinese population. Methods: The genetic association study was performed in 450 Chinese patients (306 male and 144 female) with CI and 450 control subjects (326 male and 124 female). TGFβ1 gene +869T>C and -509C>T polymorphisms were identified with amplification refractory mutation system polymerase chain reaction and DNA sequencing method. Results: The individual SNPs analysis showed the +869T and -509C in an additive model (+869T vs +869C; -509 C vs T), +869TT genotype in a recessive model (TT vs TC+CC) and 509CC genotype in a dominant model (CC+ CT vs TT) were identified to be related to CI (P<0.05). +869T>C and -509C>T SNPs were in strong linkage disequilibrium (d'=0.87, R2=0.75). Haplotype analysis showed that +869C/-509T haplotype was associated with a significant decreased risk of CI (OR= 0.86, 95%CI, 0.70-0.92; P=0.007). Furthermore,+869T/-509C haplotype was associated with a significant increased risk of CI (OR=1.31, 95%CI, 1.10-2.03; P=0.019). Conclusions: The results of this study indicate that polymorphisms and the haplotypes in the TGFβ1 gene might be genetic markers for CI in the Chinese population.


Tan H.,Jinhua Peoples Hospital | Wang R.,Jinhua Peoples Hospital | Chen Z.,Jinhua Peoples Hospital | Ding S.,Zhejiang University
Molecular Medicine Reports | Year: 2012

The aim of this study was to investigate the effect of vascular endothelial growth factor-C (VEGF-C) expression in tumor-associated macrophages (TAMs) on lymphatic microvessel density (LMVD) and lymphatic endothelial cell proliferation (LECP) and to determine the role of VEGF-C expression in lymphangiogenesis in patients with breast cancer. Breast cancer tissue specimens confirmed by pathological analysis were obtained from 75 patients. Samples were observed by microscopy analysis after immunohistochemical double-staining. The total number of TAMs and the number of VEGF-C-positive TAMs were determined. LMVD and LECP were calculated for the intratumoral and peritumoral areas. Correlation analysis was performed among these indexes, lymph vessel invasion (LVI) and lymph node metastasis in the peritumoral regions. Immunohistochemical double-staining demonstrated that VEGF-C was markedly expressed in TAMs. The number of TAMs, LMVD and LECP in the peritumoral areas was significantly higher than that in the intratumoral areas (P<0.001). We observed positive correlations between the following parameters: the number of TAMs and the peritumoral LMVD (P<0.001), the percentage of TAMs expressing VEGF-C and the peritumoral LMVD (P<0.001), the number of TAMs and the peritumoral LECP (P<0.001), and the percentage of TAMs expressing VEGF-C and the peritumoral LECP (P<0.001). Furthermore, the total number of TAMs and VEGF-C-positive TAMs, LMVD and LECP in cases with lymph node metastasis or LVI were significantly higher compared to those in cases without lymph node metastasis or LVI (P<0.01 or P<0.05). Our findings suggest that TAMs play a critical role in tumor-induced lymphangiogenesis through upregulating VEGF-C, which may contribute to lymphatic invasion in breast cancer.


Chen Y.-H.,Jinhua Peoples Hospital | Cheng Z.-Y.,Jinhua Peoples Hospital | Shao L.-H.,Jinhua Peoples Hospital | Shentu H.-S.,Jinhua Peoples Hospital | Fu B.,Jinhua Peoples Hospital
Clinica Chimica Acta | Year: 2017

Background Macrophage migration inhibitory factor (MIF) has been implicated in inflammation. We clarified whether serum MIF could be used as a marker of inflammation, brain damage and outcome after aneurysmal subarachnoid hemorrhage (aSAH). Methods Serum samples from 102 aSAH adults and 102 healthy controls were determined. The World Federation of Neurological Surgeons (WFNS) scale was used for neurological evaluation and radiological severity was estimated in accordance with the Fisher scale. Results Serum MIF, C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and S100B concentrations were significantly higher in patients than in controls. Serum MIF concentrations correlated with WFNS scores and Fisher scores and serum concentrations of CRP, IL-6, TNF-α and S100B. Serum MIF was identified as an independent predictor for 6-month unfavorable outcome (defined as Extended Glasgow Outcome Scale score of 1–4). Area under receiver operating characteristic curve of serum MIF concentrations was similar to those of WFNS scores, Fisher scores and serum S100B concentrations and significantly exceeded those of serum CRP, IL-6 and TNF-α concentrations. Conclusions Serum MIF provides information about inflammation, brain injury severity and outcome after aSAH, which can be useful as a complement to clinical data. © 2017


Du X.-W.,Jinhua Peoples Hospital | Wu H.-L.,Jinhua Peoples Hospital | Zhu Y.-F.,Jinhua Peoples Hospital | Hu J.-B.,Jinhua Peoples Hospital | And 5 more authors.
Neurourology and Urodynamics | Year: 2013

Objective: To explore the myoblast formation around the urethra and increase in urethral resistance of bone marrow mesenchymal stem cells or muscle-like cells/calcium alginate composite gel injection therapy and effect on LPP in SUI rat model. Methods: Isolation, cultivation, and identification of SD rat bone marrow mesenchymal stem cell were performed. 5-Azacytidine was introduced to induce muscle-like cells. SUI was produced in 72 6-week-old female Sprague-Dawley rats, which were divided into four groups: stem cell-gel group, muscle-like cell-gel group, Gel group, and mock control group. One, 4, and 8 weeks after injection, the leak point pressure (LPP) was measured. HE staining of Desmin and α-skeletal muscle actin (α-SMA) were performed. Results: At 4 and 8 weeks after injection in stem cell-gel group and muscle-like cell-gel group, growth of blood vessels gradually increased at gel edge, BMSC, and muscle-like cells gathered around the new blood vessels observed by fluorescence tracer, muscle-like cells grew into elongated spindle-like cells, Desmin, and α-SMA staining were obviously positive expression. LPP determinations of the mock control group compared with the Gel groups were significantly different. Conclusions: Compound of BMSC, muscle-like cells, and calcium alginate composite gel has the potential to differentiate into muscle cells in the microenvironment of SUI rat model. It is found by LPP measurement that the correlation between the increase in urethral resistance and the volume effect of calcium alginate gel is high. © 2012 Wiley Periodicals, Inc.


Ke H.-Y.,Lingan Peoples Hospital Of Hangzhou City | Qian Y.,Jinhua Peoples Hospital
World Chinese Journal of Digestology | Year: 2015

AIM: To assess the efficacy of Mamiai in the prevention of childhood diarrhea secondary to pneumonia. METHODS: One hundred and eight children with pneumonia treated at Ling’an People’s Hospital from January 2013 to January 2015 were randomly divided into either an observation group or a control group, with 54 cases in each group. The control group was given symptomatic treatment (e.g., antibiotic therapy), and the observation group was additionally given Mamiai on the basis of symptomatic treatment. The total duration of diarrhea, time to diarrhea control, hospitalization time, and the incidences of abdominal pain, diarrhea, tenderness, loss of appetite, dehydration, and abnormal bowel sounds were compared for the two groups. RESULTS: The total duration of diarrhea, time to diarrhea control, and hospitalization time were significantly shorter in the observation group than in the control group (P < 0.05). The incidences of abdominal pain, diarrhea, tenderness, loss of appetite, dehydration, and abnormal bowel sounds were significantly lower in the observation group than in the control group (P < 0.05). CONCLUSION: Mamiai can better prevent childhood diarrhea secondary to pneumonia, reduce hospitalization time and duration, and has high security. © 2015 Baishideng Publishing Group Inc. All rights reserved.


Bao H.,Jinhua Peoples Hospital | Chen L.,Dongyang Hospital of Traditional Chinese Medicine
Zhongguo Zhongyao Zazhi | Year: 2011

Objective: To investigate the effects of icariin on cardiac functions and mitochondrial oxidative stress in streptozotocin (STZ)-induced diabetic rats. Method: Male SD rats were randomly divided into normal control group, icariin control group, diabetic group, and diabetic groups administered with a low dose (30 mL·kg -1·d -1, ig) or a high dose (120 mL·kg -1·d -1, ig) of icariin for 8 weeks. The body weight, blood glucose, cardiac functions, left ventricular weight, and myocardial collagen level were assayed. The cardiac mitochondrial reactive oxygen species (ROS) level, malondialdehyde (MDA) level, and superoxide dismutase (SOD) activity were measured. Result: Treatment with icariin reduced the losing of body weight in diabetic rats. Icariin markedly reduced the ratio of ventricular weight and body weight, increased the left ventricular develop pressure and ±dp/dt max, and decreased the left ventricular end diastolic pressure in diabetic rats. The myocardial collagen and the level of cardiac mitochondrial ROS in diabetic rats were all markedly reduced by icariin. Furthermore, high dose of icariin significantly decreased the mitochondrial MDA level and increased SOD activity in diabetic rat hearts. Conclusion: Treatment with icariin for 8 weeks markedly improved the cardiac function, which may be related to reducing mitochondrial oxidative stress injuries in diabetic rats.

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