Suzhou Health College

Suzhou, China

Suzhou Health College

Suzhou, China
SEARCH FILTERS
Time filter
Source Type

He Y.-C.,Nanjing University of Science and Technology | He Y.-C.,Suzhou Health College | Wu G.-Y.,Nanjing University of Science and Technology | Li D.,Nanjing University of Science and Technology | And 5 more authors.
Behavioural Brain Research | Year: 2012

The cerebellar fastigial nucleus (FN), together with the interpositus nucleus (IN), constitutes the two final output nuclei of the spinocerebellum and plays an important role in body and limb movements. Previous studies have revealed a direct histaminergic projection from the hypothalamus to the cerebellar nuclei and an excitatory effect of histamine on the IN neurons. However, role of hypothalamic histaminergic projection in the FN has been still little known. Here we show that histamine elicited the FN neurons of rats a concentration-dependent excitatory response in vitro. The histamine-induced excitation on FN neurons was mediated by postsynaptic histamine H 2 rather than H 1 receptors. In behavioral tests, microinjection of histamine into bilateral FNs remarkably improved motor performances of rats on both accelerating rota-rod and balance beam. Selective H 2 receptor antagonist ranitidine considerably declined those motor performances and selective H 2 receptor agonist dimaprit mimicked the facilitation effect of histamine on the movements. But selective H 1 receptor antagonist triprolidine and agonist 2-pyridylethylamine had no effect. Furthermore, microinjection of histamine into bilateral FNs narrowed stride width of footprint but did not influence wire suspension, whereas microinjection of histamine into bilateral INs increased stride length and promoted suspension. These results demonstrate that histamine enhances rat motor balance and coordination through modulation of both proximal and distal muscles by activation of histamine H 2 receptors in the cerebellar FN and IN, and suggest that the hypothalamocerebellar histaminergic projections may modulate the final outputs of the spinocerebellum and participate in the cerebellum-mediated motor control. © 2011 Elsevier B.V.


Luo X.,China Pharmaceutical University | Luo X.,Suzhou Health College | Yang H.,Chinese National Institute for the Control of Pharmaceutical and Biological Products | Liang C.,Chinese National Institute for the Control of Pharmaceutical and Biological Products | Jin S.,Chinese National Institute for the Control of Pharmaceutical and Biological Products
Toxicon | Year: 2010

Detailed structures of N-linked oligosaccharides of Defibrase, a highly active thrombin like enzyme (TLE) purified from the venom of Agkistrodon acutus, were successfully characterized using MALDI-TOF mass spectrometry in combination with sequential exoglycosidase digestion. Monosaccharide composition analysis was performed by high performance anion-exchange chromatography with pulsed amperometric detection (HPAEC-PAD). Galactose(Gal), mannose(Man), fucose(Fuc), N-acetylglucosamine (GlcNAc), and sialic acid (Neu5Ac) was detected and the total carbohydrate content was about 19.4% (w/w). The N-linked oligosaccharides were released by treatment with PNGase F, fluorescent labeled with 2-aminobenzamide, and fractionated by high performance liquid chromatography (HPLC). The main oligosaccharide fractions were collected and further digested with an array of exoglycosidase mixtures, and subsequent MALDI TOF MS analysis of the resulting products yielded information about structural features of the oligosaccharide. The combined data revealed the presence of five distinct oligosaccharide structures in Defibrase, which are mainly complex or hybrid type, with a small amount of oligomannosidic type. The complex type oligosaccharides are mostly tri-or bi-antennary and the hybrid oligosaccharides are all bi-antennary. Most oligosaccharides are also found to be fucosylated. © 2009 Elsevier Ltd. All rights reserved.


Sun H.-J.,Nanjing University | Rathinasabapathi B.,University of Florida | Wu B.,Nanjing University | Luo J.,Nanjing University | And 3 more authors.
Environment International | Year: 2014

Arsenic (As) and selenium (Se) are unusual metalloids as they both induce and cure cancer. They both cause carcinogenesis, pathology, cytotoxicity, and genotoxicity in humans, with reactive oxygen species playing an important role. While As induces adverse effects by decreasing DNA methylation and affecting protein 53 expression, Se induces adverse effects by modifying thioredoxin reductase. However, they can react with glutathione and S-adenosylmethionine by forming an As-Se complex, which can be secreted extracellularly. We hypothesize that there are two types of interactions between As and Se. At low concentration, Se can decrease As toxicity via excretion of As-Se compound [(GS3)2AsSe]-, but at high concentration, excessive Se can enhance As toxicity by reacting with S-adenosylmethionine and glutathione, and modifying the structure and activity of arsenite methyltransferase. This review is to summarize their toxicity mechanisms and the interaction between As and Se toxicity, and to provide suggestions for future investigations. © 2014.


Chavalitdhamrong D.,University of Florida | Donepudi S.,University of Florida | Pu L.,University of Florida | Pu L.,Suzhou Health College | Draganov P.V.,University of Florida
Digestive Endoscopy | Year: 2014

Endoscopic retrograde cholangiopancreatography (ERCP) has become a primary tool for the treatment of biliary and pancreatic ductal diseases. It is essential for the endoscopist carrying out the ERCP to have a thorough understanding of the potential adverse events. Typically, endoscopists are well familiar with common adverse events such as post-ERCP pancreatitis, cholangitis, post-sphincterotomy bleeding, post-sphincterotomy perforation, and sedation-related cardiopulmonary compromises. However, there are other less common adverse events that arecritical to promptly recognize in order to provide appropriate therapy and prevent disastrous outcomes. This review focuses on the presentation and management of the less common and rare adverse events of an ERCP from the perspective of the practicing endoscopist. © 2013 The Authors. Digestive Endoscopy © 2013 Japan Gastroenterological Endoscopy Society.


Xiang M.,Biotechnology Center | Wang J.,Suzhou Health College | Zhang Y.,Biotechnology Center | Ling J.,Suzhou Health College | Xu X.,Henan Provincial Institute of Food and Drug Control
Archives of Pharmacal Research | Year: 2012

Vascular complications are the leading causes of morbidity and mortality in diabetes mellitus (DM). The RAGE (receptor for advanced glycation end products)-NADPH oxidase-NF-κB signal transduction pathway plays an important role in the development of oxidative stressrelated vascular complications in DM. Ursolic acid (UA), a pentacyclic triterpenoid derived from plants, has been reported to have multiple pharmacological effects, including a potent antioxidant activity. This study aimed to investigate both the effect of UA on aortic injury in streptozotocin (STZ)-induced diabetic rats and the drug's mechanism of action. STZ-induced diabetic animals were randomized in one of the following 4 groups: no treatment (diabetic model group), aminoguanidine (AG, 100 mg/kg), high-dose UA (50 mg/kg), and low-dose UA (25 mg/kg). A non-diabetic control group was followed concurrently. After 8 weeks, the diabetic model rats exhibited: severe aortic arch injury, histologically elevated serum glucose, fructosamine, and glycosylated hemoglobin; and accumulation of advanced glycation end products (AGEs) in the arota. In addition, the levels of RAGE protein, transcription factor NF-κB p65, and the p22phox subunit of NADPH oxidase were increased, as were the serum levels of malondialdehyde and tumor necrosis factor-alpha (TNF-α; p < 0.01 vs control), suggesting that the mechanisms of oxidative stress contributed to vascular injury in the diabetic model group. In contrast, rats treated with UA (50 mg/kg) had a markedly less vascular injury and significantly improved biochemical parameters. Oxidative balance was also normalized in the UAtreated rats, and a marked reduction in the levels of RAGE and p22phox paralleled the reduced activation of NF-κB p65 and TNF-α (p < 0.01 and p < 0.05, respectively, vs diabetic model). These findings suggest that UA may suppress oxidative stress, thus blunting activation of the RAGE-NADPH oxidase-NF-κB signal transduction pathway, to ameliorate vascular injury in the STZ-induced DM rats.


Nicolae C.M.,Pennsylvania State University | Aho E.R.,Pennsylvania State University | Aho E.R.,Vanderbilt University | Choe K.N.,Pennsylvania State University | And 6 more authors.
Nucleic Acids Research | Year: 2015

Genomic instability, a major hallmark of cancer cells, is caused by incorrect or ineffective DNA repair. Many DNA repair mechanisms cooperate in cells to fight DNA damage, and are generally regulated by post-translational modification of key factors. Poly-ADP-ribosylation, catalyzed by PARP1, is a posttranslational modification playing a prominent role in DNA repair, but much less is known about mono- ADP-ribosylation. Here we report that mono-ADPribosylation plays an important role in homologous recombination DNA repair, a mechanism essential for replication fork stability and double strand break repair. We show that the mono-ADP-ribosyltransferase PARP14 interacts with the DNA replication machinery component PCNA and promotes replication of DNA lesions and common fragile sites. PARP14 depletion results in reduced homologous recombination, persistent RAD51 foci, hypersensitivity to DNA damaging agents and accumulation of DNA strand breaks. Our work uncovered PARP14 as a novel factor required for mitigating replication stress and promoting genomic stability. © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.


Liu Q.,Soochow University of China | Chen W.,Soochow University of China | Jiao Y.,Soochow University of China | Hou J.,Soochow University of China | And 4 more authors.
Journal of Surgical Research | Year: 2014

Background Many natural compounds possess antitumor growth activities. Pulsatilla chinensis is an herb used in traditional Chinese medicine to treat infectious diseases. More recently, extracts from P chinensis have been shown to contain antitumor activities. Materials and methods In this study, we isolated Pulsatilla saponin A as an active compound from P chinensis extracts and tested its anticancer activity in vitro and in vivo. Results In cell culture, Pulsatilla saponin A significantly inhibited the growth of human hepatocellular carcinoma SMCC-7721 cells and pancreatic BXPC3 and SW1990 cancer cells. Similar inhibitory activities were observed when the compound was tested in mouse xenograft tumor models using human hepatocellular carcinoma Bel-7402 and pancreatic cancer SW1990 cells. In Comet assay and flow cytometric analysis of cell cycle distribution and annexin V expression, DNA damage, G2 arrest, and apoptosis were identified in Pulsatilla saponin A-treated cancer cells. Based on the results of Western blotting, p53 and cyclin B protein levels were higher, whereas Bcl-2 protein levels were lower in Pulsatilla saponin A-treated cancer cells than in vehicle-treated cells. Conclusions Pulsatilla saponin A may exert its antitumor effect by inducing DNA damage and causing G2 arrest and apoptosis in cancer cells. Pulsatilla saponin A and its derivatives may be developed as a new class of anticancer agents. © 2014 Elsevier Inc. All rights reserved.


Yi L.X.,Suzhou Health College
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2012

To explore the mechanisms by which splicing factor SC35 regulates the costimulatory molecule B7-H3 expression in vitro through bioinformatic and molecular biological methods. We screened some regulatory proteins which might take part in regulating B7-H3 expression using bioinformatic methods. Then RNA interference (RNAi) and real-time PCR were performed to test if these proteins took part in the regulation. Splicing factor SC35, SRP40 and SF50 might play an important role in the regulation of B7-H3 expression. In PHA-activated T cells, B7-H3 was upregulated obviously and at the same time SC35 was also upregulated. When we suppressed SC35 expression using RNAi, we found B7-H3 was also downregulated. Splicing factor SC35 might take part in the regulation of B7-H3 expression, which could help understand B7-H3 biological function.


Lei J.,Suzhou Health College | Ye K.,Suzhou Municipal Hospital | Zhu T.-M.,Suzhou Health College
International Journal of Clinical and Experimental Medicine | Year: 2016

Purpose: Inflammation is reported to play an important part in mediating injury in neonatal hypoxic-ischemic encephalopathy (HIE). Whether inflammatory-related cytokine such as IL-6 and TNF-α is associated with risk of HIE remains unknown. Method: In this meta-analysis of 29 clinical trials published to date in Chinese VIP, Wangfang, CNKI, Pubmed, Google Scholar database using the keywords “IL-6”, “TNF-α” and “hypoxic-ischemic encephalopathy/HIE”, we selected eligible studies which met the inclusion criterion, extract interested information and analyzed outcomes using the Review Manage 5.3 software. Results: Meta-analysis including 1618 HIE newborns and 790 healthy controls showed that serum IL-6 was significant up-regulated in different states (mild, moderate, severe) of neonatal hypoxic-ischemic encephalopathy (HIE) with the value of IV was 2.62, 4.91, 6.55, 95% CI [2.03, 3.22], [4.01, 5.80], [5.46, 7.64] and P<0.01. Similarly, compared to healthy controls, elevated serum TNF-α was also found to be associated with risk of neonatal HIE, the value of Std. Mean. Difference was 4.00, 4.75, 8.24, 95% CI was [3.60, 4.40], [4.07, 5.43], [7.38, 9.11] and P value <0.01. Conclusion: Meta-analysis suggested that elevated serum IL-6 and TNF-α level in newborns is associated with high risk of hypoxic-ischemic encephalopathy (HIE)-induced brain injury. Further studies are needed to validate these observations. © 2016, E-Century Publishing Corporation. All Rights Reserved.


Ding M.,Suzhou Health College | Ding M.,Rush University Medical Center | Xu J.Y.,Nanjing Medical University | Fan Y.,Nanjing Medical University
Oral Diseases | Year: 2010

Objective: To explore a potential causal contribution of the transcription factor HIF-1α and its target gene, RTP801 and VEGF, to the development of oral lichen planus (OLP). Design relevant: Twenty-two adult OLP patients were enrolled in this study. All OLP diagnoses were verified by histopathological characteristics. Normal mucous specimens were collected from 12 controls after various oral surgeries. Material and method: RNA was isolated from OLP and control specimens. Microarray was performed using BiostarH-40s gene chip. Expression of HIF-1α, VEGF and RTP801 was evaluated using quantitative real-time polymerase chain reaction (qPCR). Unpaired t-test and one-way ANOVA was used for statistical analysis. Results: Microarray results showed that RTP801 expression was lower in OLP than in controls (779 vs 3090). qPCR further confirmed that expression of RTP801 was similarly lower in OLP than in controls (0.363 vs 1.473, P < 0.001); expression of VEGF was also lower in OLP (0.448 vs 1.74, P = 0.012). In contrast, expression of HIF-1α was higher in OLP than in controls (11.12 vs 1.628, P < 0.001). Conclusion: The oral mucosa of OLP is hypoxic. Genes that are activated by hypoxia, such as RTP801 and VEGF, and their signal cascades may be novel potential therapeutic targets for OLP. © 2010 John Wiley & Sons A/S.

Loading Suzhou Health College collaborators
Loading Suzhou Health College collaborators