Tongshan, China

Xuzhou Medical College

www.xzmc.edu.cn/
Tongshan, China

Xuzhou Medical College is a national university located in Xuzhou, Jiangsu province, China. Wikipedia.


Time filter

Source Type

OBJECTIVE:: The optimal time to initiate antihypertensive therapy among patients with acute ischemic stroke remains uncertain. We tested the effects of blood pressure reduction among patients with acute ischemic stroke according to time from onset to initiation of antihypertensive treatment. METHODS:: We randomly assigned 4071 acute ischemic stroke patients with elevated SBP to receive antihypertensive treatment or to discontinue all antihypertensive medications during hospitalization. The primary outcome was a combination of death and major disability, and secondary outcomes included the modified Rankin score, recurrent stroke, vascular disease events, and all-cause mortality. RESULTS:: At 24?h after randomization, the differences in SBP reductions were 8.7, 9.5, and 9.6?mmHg between the antihypertensive treatment and control groups among patients receiving treatment within less than 12, 12–23, and 24–48?h after stroke onset, respectively (P?


Lv X.-P.,Xuzhou Medical College
Oncology Letters | Year: 2017

Gastrointestinal (GI) tract cancers that arise due to genetic mutations affect a large number of individuals worldwide. Even though many of the GI tract cancers arise sporadically, few of these GI tract cancers harboring a hereditary predisposition are now recognized and well characterized. These include Cowden syndrome, MUTYH-associated polyposis, hereditary pancreatic cancer, Lynch syndrome, Peutz-Jeghers syndrome, familial adenomatous polyposis (FAP), attenuated FAP, serrated polyposis syndrome, and hereditary gastric cancer. Molecular characterization of the genes that are involved in these syndromes was useful in the development of genetic testing for diagnosis and also facilitated understanding of the genetic basis of GI cancers. Current knowledge on the genetics of GI cancers with emphasis on heritability and germ line mutations forms the basis of the present review. © 2017, Spandidos Publications. All rights reserved.


Zhang P.,Xuzhou Medical College
Experimental and Therapeutic Medicine | Year: 2017

Pathological remodeling of the myocardium is an integral part of the events that lead to heart failure (HF), which involves altered gene expression, disturbed signaling pathways and altered Ca2+ homeostasis and the players involved in this process. Of particular interest is the chronic activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) isoforms in heart, which further aggravate the injury to myocardium. Expression and activity of CaMKII have been found to be elevated in various conditions of stressed myocardium and in different heart diseases in both animal models as well as heart patients. CaMKII is a signaling molecule that regulates many cellular pathways by phosphorylating several proteins involved in excitation-contraction coupling and relaxation events in heart, cardiomyocyte apoptosis, transcriptional activation of genes related to cardiac hypertrophy, inflammation, and arrhythmias. CaMKII is activated by reactive oxygen species (ROS), which are elevated under conditions of ischemia-reperfusion injury and in a cyclical manner, CaMKII in turn elevates ROS production. Both ROS and activated CaMKII increase Ca-induced Ca release from sarcoplasmic reticulum, which leads to cardiomyocyte membrane depolarization and arrhythmias. These CaMKII-mediated changes in heart ultimately culminate in dysfunctional myocardium and HF. Genetic studies in animal models clearly demonstrated that inactivation of CaMKII is protective against a variety of stress induced cardiac dysfunctions. Despite significant leaps in understanding the structural details of CaMKII, which is a very complicated and multimeric modular protein, currently there is no specific and potent inhibitor of this enzyme, that can be developed for therapeutic purposes. © 2017, Spandidos Publications. All rights reserved.


Zhang P.-Y.,Xuzhou Medical College
Experimental and Therapeutic Medicine | Year: 2017

It is well recognized that the elevated plasma level of low-density lipoprotein-cholesterol (LDL-C) is a major risk factor for atherosclerosis and cardiovascular disease (CVD). Deposition of pro-atherogenic LDL-C, on the intima of arterial wall, contributes to plaque formation and atherosclerosis, which further leads to lowered blood flow to vital organs and increased risk of CVD. The most commonly used statin therapy is effective in reducing dyslipidemia and preventing cardiovascular events only in about half of the patient population. However, in patients with familial hypercholesterolemia, these drugs were not effective to meet the required goals of lower LDL-C, and to reduce the CVD risk. Furthermore, many patients even develop intolerability to statins and resistance. The identification of pro-protein convertase subtilisin/kexin type 9 (PCSK9) and the association of PCSK9 mutations with familial hypercholesterolemia led to the identification of PCSK9 as a new therapeutic target for lowering LDL-C and dyslipidemia-associated CVD. PCSK9 is found to promote the degradation of LDL-receptor (LDLR), thus rendering it unavailable for recycling to hepatocyte plasma membrane, leading to elevated levels of circulating LDL-C, as it cannot be taken up into cells. While gain-of-function mutations aggravate the degradation of LDLR as in familial hypercholesterolemia whereas loss of function mutations reduce the ability of PCSK9 to promote the degradation of LDLR and thus lower the plasma level of LDL-C and dyslipidemia. Monoclonal antibodies against PCSK9 are currently being tested in clinical trials and are found to be efficacious in countering the activity of PCSK9 and thus control the plasma LDL-C and triglycerides even in statin non-responsive patients and protect against dyslipidemia-related CVD. © 2017, Spandidos Publications. All rights reserved.


Li J.,Nanjing University | Li J.,Xuzhou Medical College | Zhu J.-J.,Nanjing University
Analyst | Year: 2013

Quantum dots (QDs) have been facilitating the development of sensitive fluorescence biosensors over the past two decades due to their high quantum yield, narrow and tunable emission spectrum and good photostability. The new emerging QDs with improved biocompatibility further promote their biological applications. In this review, we first briefly introduce the prevalently used QDs and their preparation and bioconjugation approaches. Then we summarize QDs-based fluorescent biosensing for proteins and nucleic acids, and QDs-based applications in cellular and in vivo targeting and imaging. Last but not the least, we envision the potential QDs-based applications in future perspectives. This journal is © 2013 The Royal Society of Chemistry.


Li J.,Xuzhou Medical College | Zhu J.-J.,Nanjing University | Xu K.,Xuzhou Medical College
TrAC - Trends in Analytical Chemistry | Year: 2014

Fluorescent metal nanoclusters (NCs) are a class of emerging fluorescent materials. They have excellent photostability and biocompatibility with sub-nanometer size and are easy to synthesize. Taking advantage of these features, fluorescent metal NCs have been involved in exciting developments of analytical methods for fluorescent biosensing and bioimaging. In this review, we first summarize the approaches to synthesis and bioconjugation for fluorescent metal NCs (Ag, Au, Cu and Pt). We then highlight their applications as fluorescent probes for metal ions, small molecules, nucleic acids, and protein detection. We also summarize the use of metal NCs in cellular and in-vivo targeting and imaging. Finally, we envision the various prospects for research on fluorescent metal NCs in the future. © 2014 Elsevier Ltd.


Tollini L.A.,University of North Carolina at Chapel Hill | Jin A.,University of North Carolina at Chapel Hill | Park J.,University of North Carolina at Chapel Hill | Zhang Y.,University of North Carolina at Chapel Hill | Zhang Y.,Xuzhou Medical College
Cancer Cell | Year: 2014

Mdm2 E3 ubiquitin ligase-mediated p53 degradation is generally accepted as the major mechanism for p53 regulation; nevertheless, the invivo significance of this function has not been unequivocally established. Here, we have generated an Mdm2Y487A knockin mouse; Mdm2Y487A mutation inactivates Mdm2 E3 ligase function without affecting its ability to bind its homolog MdmX. Unexpectedly, Mdm2Y487A/Y487A mice were viable and developed normally into adulthood. While disruption of Mdm2 E3 ligase function resulted in p53 accumulation, p53 transcriptional activity remained low; however, exposure to sublethal stress resulted in hyperactive p53 and p53-dependent mortality in Mdm2Y487A/Y487A mice. These findings reveal a potentially dispensable nature for Mdm2 E3 ligase function in p53 regulation, providing insight that may affect how this pathway is targeted therapeutically. © 2014 Elsevier Inc.


Zuo L.,Xuzhou Medical College
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2013

To investigate the antiviral and immuno-regulatory effects of Reduning injection on mouse cytomegalovirus (MCMV) pneumonia. BALB/c mice were divided randomly into five groups: blank control group, immunosuppressive control group, MCMV pneumonia group, Reduning treatment group, and ganciclovir treatment group. Acute MCMV interstitial pneumonia models were established in the latter three groups. Lung pathological changes were observed with HE staining, MCMV-DNA content in the lung tissue was detected by qRT-PCR, and the levels of interferon-γ (IFN-γ) and interleukin-6 (IL-6) in the lung tissue were determined by ELISA. Compared with MCMV pneumonia group, the lung injuries in Reduning treatment and ganciclovir treatment groups were ameliorated, and the MCMV-DNA expression in the two treatment groups decreased, and the changes in ganciclovir treatment group were more obvious (P < 0.05). Compared with MCMV pneumonia group, the levels of IFN-γ and IL-6 in Reduning treatment group rose by 1.4 times and dropped by 30.2%, respectively; and IFN-γ increased by 1.6 times and IL-6 decreased by 47.6% in ganciclovir treatment group (P < 0.05); the differences between the two treatment groups were statistically significant (P < 0.05). IFN-γ/IL-6 ratio in Reduning treatment group was higher than that in MCMV pneumonia group, and approached the level of immunosuppressive control group. Reduning injection might exert antiviral activity through inhibiting MCMV replication and proliferation in lung tissue directly, and down-regulating the expressions of IFN-γ and IL-6.


Zhao F.C.,Xuzhou Medical College
Orthopaedic surgery | Year: 2012

To explore the clinical characteristics of osteonecrosis of the femoral head (ONFH) induced by steroids. From January 2000 to October 2009, 497 hips in 270 cases of ONFH induced by steroids were studied. A questionnaire was administered when the patients were admitted; the questions concerned the underlying disease, duration of steroid usage, total dosage of steroid, incubation period (time interval between commencement of steroid therapy and onset of pain), severity of pain, location of initial complaint, primary diagnosis, time lag from onset of pain to final diagnosis and physical signs when admitted. The correlations between pain and Association Research Circulation Osseous (ARCO) stage, bone marrow edema (BME) and lesion size were analyzed. The median of time between commencing steroid medication and developing ONFH for the 269 cases was 18 months (range, 2-384 months). 78.82% cases presented with pain within three years of steroid initiation, only 10.41% patients first complained of pain six or more years after commencing steroid therapy. Fifty-six cases (20.82%) were misdiagnosed, lumbar disorders being the most frequent misdiagnoses. 79.29% of symptomatic hips presented with abnormal physical tests. Of 420 symptomatic hips, 166 hips were type C1, 223 hips type C2; 299 hips had collapsed; and there was BME in 209 hips. Most patients with ONFH induced by steroids complained of pain within 3 years of commencing steroid therapy. Pain was associated with lesion size, collapse and BME. Atypical location of pain, failure to perform a physical examination and MRI findings were the main causes of misdiagnoses. © 2012 Tianjin Hospital and Blackwell Publishing Asia Pty Ltd.


Strategies for increasing functional beta cell mass are effective for diabetes therapy. Although controversy remains on the existence of facultative beta cell progenitors in the adult pancreas, most evidence does not support such a possibility. One of the greatest physiological increases in beta cells has been detected in the maternal pancreas during pregnancy, following neonatal period and in the setting of insulin resistance. However, no systematical analysis on the beta cell growth in this period has been ever performed. Here we analyzed beta cell replication by quantifying BrdU incorporated beta cells at different time points in the pregnant mice. Similarly, we evaluated the possible involvement of beta cell neogenesis (differentiation from progenitor cells) by analyzing expression of Neurog3, a key determinant of pancreatic endocrine cell neogenesis during embryogenesis, in the exocrine pancreas. We found a dynamic increase in beta cell replication, but failed to detect beta cell neogenesis, demonstrating that beta cell growth in the maternal pancreas during pregnancy is predominantly attributable to beta cell replication, rather than beta cell neogenesis. © The Japan Endocrine Society.

Loading Xuzhou Medical College collaborators
Loading Xuzhou Medical College collaborators