First Hospital of Jiaxing

Jiaxing, China

First Hospital of Jiaxing

Jiaxing, China
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Yu J.-Y.,First Hospital of Jiaxing | Wang J.-Y.,First Hospital of Jiaxing
World Chinese Journal of Digestology | Year: 2017

The acid phosphatase 5, tartrate resistant or tartrate-resistant acid phosphatase (ACP5/TRACP/TRAP) is a metalloproteinase of the acid phosphatase family, which is a good marker of bone resorption and osteoclast activity. It has recently been found that the expression of ACP5 in a variety of tumors is significantly higher than that in matched normal tissues. These suggest that ACP5 may play an important role in the occurrence and development of tumors. © The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.

PubMed | First Hospital of Jiaxing, Hangzhou Hospital of Traditional Chinese Medicine, Tongde Hospital of Zhejiang Province and Zhejiang University
Type: Journal Article | Journal: Oncology reports | Year: 2016

5-Aza-2-deoxycytidine (5-Aza-CdR) is currently acknowledged as a demethylation drug, and causes a certain degree of demethylation in a variety of cancer cells, including pancreatic cancer cells. Emodin, a traditional Chinese medicine (TCM), is an effective monomer extracted from rhubarb and has been reported to exhibit antitumor activity in different manners in pancreatic cancer. In the present study, we examined whether emodin caused demethylation and increased the demethylation of three tumor-suppressor genes P16, RASSF1A and ppENK with a high degree of methylation in pancreatic cancer when combined with 5-Aza-CdR. Our research showed that emodin inhibited the growth of pancreatic cancer Panc-1 cells in a dose- and time-dependent manner. Dot-blot results showed that emodin combined with 5-Aza-CdR significantly suppressed the expression of genome 5mC in PANC-1 cells. In order to verify the effect of methylation, methylation-specific PCR (MSP) and bisulfite genomic sequencing PCR (BSP) combined with TA were selected for the cloning and sequencing. Results of MSP and BSP confirmed that emodin caused faint demethylation, and 5-Aza-CdR had a certain degree of demethylation. When emodin was combined with 5-Aza-CdR, the demethylation was more significant. At the same time, fluorescent quantitative PCR and western blot analysis results confirmed that when emodin was combined with 5-Aza-CdR, the expression levels of P16, RASSF1A and ppENK were increased more significantly compared to either treatment alone. In contrast, the expression levels of DNA methyltransferase 1 (DNMT1) and DNMT3a were more significantly reduced with the combination treatment than the control or either agent alone, further proving that emodin in combination with 5-Aza-CdR enhanced the demethylation effect of 5-Aza-CdR by reducing the expression of methyltransferases. In conclusion, the present study confirmed that emodin in combination with 5-Aza-CdR enhanced the demethylation by 5-Aza-CdR of tumor-suppressor genes p16, RASSF1A and ppENK by reducing the expression of methyltransferases DNMT1 and DNMT3a.

Xu D.,Anhui Medical University | Xu D.,Anhui Provincial Childrens Hospital | Chen M.,First Hospital of Jiaxing | Ren X.,Nanjing University | And 2 more authors.
Fitoterapia | Year: 2014

Acute kidney injury (AKI) is an abrupt loss of kidney function. Severe AKI requires renal replacement therapy and has high mortality. Leonurine (LEO), an alkaloid isolated from Leonurus cardiaca, has shown biological effects such as antioxidant, anticoagulant, and anti-apoptosis. We have examined the effect of LEO on lipopolysaccharide (LPS)-induced AKI in mice and further studied the mechanism involved. Blood urea nitrogen (BUN), creatinine and cytokine were estimated in the serum or tissue. Kidney tissue specimens were used for biochemical estimations of lipid peroxides (LPO), reduced glutathione (GSH), and reactive oxygen species (ROS). The effects of LEO on LPS-induced renal tissue damage were detected by hematoxylin and eosin (HE) stain and electron microscopy. The production of cytokines in the tissue and blood was measured by ELISA. Protein phosphorylation and protein subcellular localization were tested by Western blot. LEO is protected against LPS-induced AKI, improved animal survival and maintained the redox balance. The beneficial effects of LEO were accompanied by the down-regulation of TNF-α, IL-1, IL-6, IL-8, KIM-1 expression and by the inhibition of the phosphorylation of IκBα and p65 translocalization. These results suggest that LEO may suppress NF-κB activation and inhibit pro-inflammatory cytokine production via decreasing cellular ROS production. Accumulating studies have demonstrated that LEO reduces kidney injury and protects renal functions from LPS-induced kidney injury. © 2014 Elsevier B.V.

Chen J.,Zhejiang University | Lu X.-Y.,Zhejiang University | Wang W.-J.,Hangzhou Cancer Hospital | Shen B.,First Hospital of Jiaxing | And 4 more authors.
Journal of Pain and Symptom Management | Year: 2014

Context. Cancer treatment capacity in China is severely limited relative to the enormous size of the population; and many aspects of treatment, such as opioid protocols for pain control, are not standardized. To improve the quality of drug treatment, clinical pharmacists are taking a more active role in patient care.Objectives. This study compared the effectiveness of opioid treatment between cancer patients receiving interventions from Clinical Pharmacist-Led Guidance Teams (CPGTs) and a comparable control group.Methods. This was a prospective, multicenter, double-Arm, controlled study conducted in China. Multidisciplinary guidance teams were established and led by clinical pharmacists with expertise in cancer pain therapy. The CPGTs provided pre-Therapy consultation and drug education to physicians, monitored prescriptions during treatment, and conducted patient follow-up. The process and outcome parameters of therapy were collected and analyzed with overall statistics and logistic regression.Results. A total of 542 patients were enrolled, 269 in the CPGT intervention group (CPGT group) and 273 controls. Standardization of opioid administration was improved significantly in the CPGT group, including more frequent pain evaluation (P < 0.001), more standardized dosing titration (P <0.001), and less frequent meperidine prescriptions (P <0.001). The pain scores in the CPGT group were significantly improved compared with the control group (P <0.05). The incidences of gastrointestinal adverse events were significantly lower in the CPGT group (constipation: P = 0.041; nausea: P = 0.028; vomiting: P = 0.035), and overall quality of life was improved (P = 0.032). No opioid addiction was encountered in the CPGT group. Risk analysis revealed that patient follow-up by pharmacists and the controlled dosing of opioids were the major factors in improving treatment efficacy.Conclusion. The CPGTs significantly improved standardization, efficiency, and efficacy of cancer pain therapy in China. In a country where clinical pharmacy is still developing, this is a valuable service model that may enhance cancer treatment capacity and efficacy while promoting recognition of the clinical pharmacy profession. © 2014 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.

Zhou H.,Ningbo University | Zhou H.,First Hospital of Jiaxing | Xiao B.,Ningbo University | Zhou F.,Ningbo University | And 6 more authors.
Biomarkers | Year: 2012

The detection of circulating tumor cells (CTCs) has recently received great attention. To evaluate if miR-421 could be used as a specific marker for CTCs, the level of miR-421 in mononuclear cells (MNCs) from peripheral blood were determined by reverse transcription-polymerase chain reaction. Transfection of miR-421 inhibitor significantly suppressed tumor growth in vivo. The level of miR-421 in MNCs from gastric cancer was significantly higher than in those from healthy controls. The area under the receiver operating characteristic curve was 0.773±0.0736. In conclusion, miR-421 may be used as a biomarker for monitoring CTCs in patients with gastric cancer. © 2012 Informa UK, Ltd.

Zhang W.,Nantong University | Zhang W.,First Hospital of Jiaxing | Chen D.-Q.,Nantong University | Chen D.-Q.,First Hospital of Jiaxing | And 4 more authors.
Journal of Cardiovascular Pharmacology | Year: 2010

Calcium-calmodulin-dependent protein kinase II (CaMKII) is one of the main protein kinases mediating intracellular Ca changes. It is also involved in the process of cardiac diseases, such as cardiac hypertrophy, but its effects on myocardial fibrosis remain unclear. The present study investigates whether CaMKII is involved in cardiac fibroblast proliferation and extracellular matrix (ECM) secretion induced by angiotensin II (AngII) or electrical field stimulation (EFS) in cultured neonatal rat cardiac fibroblasts. Cardiac fibroblast proliferation was assessed by a cell survival assay (MTT) and manual cell enumeration. Cellular matrix production was demonstrated by matrix metalloproteinases (MMP) 1, 2, 9, and collagen I/III messenger RNA expression, MMP-2, 9 protein expression, and secretion of transforming growth factor β1 and tumor necrosis factor α. Either AngII or EFS promoted cardiac fibroblast proliferation and ECM secretion, while also up-regulating expression of CaMKII δB and δC. More importantly, CaMKII inhibitors, autocamtide-2-related inhibitory peptide (AIP 5 μM) or KN93 (0.5 μM), suppressed cardiac fibroblast proliferation, inhibited the excretion of transforming growth factor β1 and tumor necrosis factor α, decreased the messenger RNA expression of MMP-1, 2, 9 and collagen I/III, and decreased the protein expression of MMP-2, 9. These results suggest that CaMKII mediates cardiac fibroblast proliferation and ECM secretion induced by either AngII or EFS. Copyright © 2010 by Lippincott Williams & Wilkins.

Xu L.,Soochow University of China | Xu L.,First Hospital of Jiaxing | Pan Y.,Soochow University of China | Zhu Q.,Soochow University of China | And 4 more authors.
Journal of Neurophysiology | Year: 2012

The tyrosine kinases of Src family play an important role in the central sensitization following peripheral inflammation. However, whether the Src family in the arcuate nucleus (ARC) of mediobasal hypothalamus is involved in central sensitization remains unknown. The aim of this study was to investigate the role and mechanisms of tyrosine kinases of Src family in N-methyl-D-aspartate (NMDA) receptor activity in the ARC following peripheral inflammation. Peripheral inflammation was induced by unilateral injection of complete Freund's adjuvant (CFA) into rat hindpaw. The neuronal activities of the ARC were recorded using electrophysiological field recording from the in vitro mediobasal hypothalamic slices from control and CFA rats. Expression of total and phosphorylated Src and NR2B subunit protein was analyzed by Western blot and immuoprecipitation. Our results showed that CFA injection resulted in an increase in mechanical and thermal sensitivity, which was partially blocked by neonatal monosodium glutamate treatment. CFA injection also enhanced spontaneous firings of ARC neurons, which were reversed by the NMDA receptor NR2B subunit specific antagonist Ro25-6981 and by PP2, an Src family tyrosine kinase inhibitor. In addition, peripheral inflammation enhanced Src phosphorylation and NMDA receptor NR2B subunit phosphorylation without alteration of total NR2B subunit expression in the ARC. Peripheral inflammation also increased the association of NR2B protein with p-Src protein in the ARC. Administration of PP2 blocked the upregulation of NR2B phosphorylation induced by CFA injection. Taken together, our present results suggest that the arcuate Src activation-induced tyrosine phosphorylation of NR2B NMDA subunit may contribute to inflammatory pain. © 2012 the American Physiological Society.

Shen P.,Jiaxing University | Zong Y.-M.,Jiaxing University | Shu J.,Jiaxing University | Shi Y.-C.,Jiaxing University | And 4 more authors.
Critical Care | Year: 2013

H7N9 influenza is a new emerging infection and has high mortality. Both chest radiography and computed tomography (CT) had some limitations in assessing such patients. We performed daily lung ultrasound in a patient with H7N9 influenza. Lung ultrasound and lung ultrasound score showed high consistency with CT and the progression of pneumonia. Ultrasound can be adjutant to chest radiography and CT in caring for patients with H7N9 influenza. © 2013 BioMed Central Ltd.

To explore the therapeutic feasibility of percutaneous puncture and neurolytic thoracic sympathetic nerve block under the guidance of computed tomograph (CT). From September 2009 to August 2010, 23 cases with primary palmar hyperhidrosis underwent percutaneous puncture and neurolytic thoracic sympathetic nerve block at our hospital. The puncture of thoracic sympathetic nerve was guided by CT through the gap of T3-4. The screen showed the direction of needle and the location of needle tip at the upper joint of costal head beside T3 body and outside of costal pleura. A mixed injection of 1% lidocaine and 30% iohexol was administered. On CT, lidocaine was found to cover the area where the thoracic sympathetic nerve was located. And after several minutes, the patient's palms turned warm and dry from cool and wet without the onset of Horner's syndrome. Then 2.5 ml of absolute alcohol was injected to block the thoracic sympathetic nerve. CT could guide the needle to the right position. And the injectate spreaded to the site of thoracic sympathetic nerve. At 5 min after anesthetic injection, the palmar temperature raised an average of 2.86°C and the amplitude of pulse rose over 55%. Palmar hyperhidrosis was cured in 19 patients by one attempt and 4 patients required a second block with absolute alcohol. No complication occurred and there were 2 patients with tendency of recurrence during a follow-up period of 8 - 18 months. The CT-guided therapy of percutaneous puncture and chemical neurolysis of thoracic sympathetic nerve block is both feasible and efficacious for palmar hyperhidrosis.

Xiao C.,First Hospital of Jiaxing | Sun J.-L.,First Hospital of Jiaxing
National Medical Journal of China | Year: 2013

Objective: To explore the effect of dexmedetomidine in acute postoperative pain and remifentanil-induced hyperalgesia. Methods: From January 2011 to June 2012, 120 patients scheduled for elective abdominal surgery under general anesthesia were included in this study. All patients received intravenous remifentanil infusion during operation, and dexmedetomidine was given after anesthesia induction. The postoperative mechanical pain threshold, pain visual analog scale (VAS) score, morphine consumption, and score of sedation (Ramsay) was recorded. Results: Relatively large-dose intraoperative remifentanil resulted in lower mechanical pain threshold and higher dose of postoperative morphine consumption. Dexmedetomidine reduced postoperative morphine consumption significantly, and increased Ramsay scores, but had no effect on mechanical hyperalgesia. Conclusion: Dexmedetomidine can alleviate the acute postoperative pain effectively, but the effect is not dependent on inhibiting remifentanil-induced hyperalgesia. Copyright © 2013 by the Chinese Medical Association.

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