Shenyang, China
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Sun Y.,General Hospital of Shenyang Military Command | Xu K.,General Hospital of Shenyang Military Command | Jiang T.-M.,College of Logistics | Yang L.-X.,Kunming General Hospital of Chengdu Military Command | And 15 more authors.
Medical Journal of Chinese People's Liberation Army | Year: 2016

Objective To explore the correlation between the degree of target vessel occlusion and in-hospital mortality in patients with acute ST-elevated myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). Methods To retrospectively analyze the data collected from the Management System of Cardiovascular Interventional Treatment in Military Hospitals. A total of 8170 patients with STEMI and PCI were enrolled, and the endpoint of present study was in-hospital mortality. The degree of target vessel occlusion were stratified to determine the effects of occlusion degree on in-hospital mortality. Results According to the degree of target vessel occlusion, the enrolled patients were divided into 2 groups: 75%-99% occlusion group and 100% occlusion group. The in-hospital mortality in the 2 groups were 2.2% and 3.0%, respectively (P=0.077). The patients were then further divided into 3 groups according to the symptom-onset-to-balloon time <3h, between 3h and 6h, and ≥6h. The in-hospital mortality in duration <3h group were 2.5% and 3.3%, respectively (P=0.436); duration between 3h and 6h group were 2.0% and 2.9%, respectively (P=0.147); and duration ≥6h group were 2.4% and 2.8%, respectively (P=0.430). Conclusion The in-hospital mortality in STEMI patients may be no relation with the degree of target vessel occlusion. © 2016, People’s Military Medical Press. All rights reserved.


Li P.,General Hospital of Shenyang Military Command | Liang L.-L.,General Hospital of Shenyang Military Command | Zhang S.-W.,202 Hospital of PLA | An L.,210 Hospital of PLA | And 9 more authors.
Medical Journal of Chinese People's Liberation Army | Year: 2014

Objective: To investigate the integrated control levels of hemoglobin A1c(HbA1c), systolic and diastolic blood pressure (BP), low-density lipoprotein cholesterol (LDL-C) in retired army cadres suffering from type 2 diabetes (T2DM) in northeast China.Methods: Four hundred and seventy-seven retired army cadres (aged ≥50 years) with T2DM were interviewed using questionnaire. The subjects were assigned into two groups according to the presence (n=350) or without (n=127) cardiovascular disease (CVD), and then the control levels of HbA1c, fast blood glucose (FBG), 2-hour postprandial blood glucose (2hPG), BP, blood cholesterol (TC), triglycide (TG), high-density lipoprotein cholesterol (HDL-C) and LDL-C were compared between the two groups.Results: The overall successful rate of control of HbA1c(<7%) was 65.8%. The overall successful rate of controling HbA1cin diabetic patients without CVD was significantly higher than in those with CVD (74.8% vs 56.9%, χ2=13.857, P<0.05). The overall successful rate for controling LDL-C in enrolled subjects (<2.6mmol/L) was 47.8%. The overall successful rate for controling LDL-C in patients without CVD (<2.6mmol/L) was significantly higher than in those with CVD (<1.8mmol/L) (47.2% vs 23.9%, χ2=6.77, P<0.05). In 85.5% of patients the target of controling blood pressure (<140/80mmHg) was achieved. The successful rates were almost identical between the with- and without-CVD groups (85.1% vs 86.4%, χ2=0155, P>0.05). The comprehensive attainment rate for controling HbA1c, BP and LDL-C among all the subjects was 23.5%, and no significant difference was found between with- and without-CVD subjects (22.9% vs 25.1%, χ2=0.284, P>0.05).Conclusions: Under the military health care management system, the unique and comprehensive successful rate for controling HbA1c, BP and LDL-C was higher among retired army cadres in northeast China as compared with that in non-military Chinese populations, and it is close to, even higher than the reported levels abroad. The successful rate shows no difference between with- or without-CVD subjects. © 2014, People's Military Medical Press. All rights reserved.


Guo S.-J.,Sun Yat Sen University | Sun Z.-J.,202 Hospital of PLA | Li W.,PLA Fourth Military Medical University
Medical Hypotheses | Year: 2012

Of all men consulted for infertility, around 30% appear to have a varicocele, therefore, this male dysfunction has been considered as a potential cause of infertility in many patients. Emerging studies point out spermatozoa progressive motility as the most important predictor of fertility provided that the analysis was carried out with infertility duration, thus leaving unsolved problem to evaluate the spontaneous testicular damage during the very early phase in varicoceles. Given the deterioration of testicular function caused by varicoceles is progressive, the early and efficient evaluation of testicular damage would be of great importance for the future medical intervention in this population. The resultant mechanism by which varicoceles affect testicular function remains unclear, but the increase in testicular temperature is most commonly accepted aetiology. In this context, we hypothesize that metastasis-associated protein 1 (MTA1), an intrinsic DNA damage response component, possessing transient protective effect in primary spermatocytes against heat stress, bears the potential to be a diagnostic biomarker for the assessment of early testicular damage in varicoceles. The facet that the decrease of MTA1 expression appears much earlier than the beginning of apoptotic wave after heat stress warrants its theoretical rationality and technical accessibility for biochemical application. Basically, MTA1 participates in the maintenance of early apoptotic balance induced by hyperthermal stimulation by elevating the deacetylation level of p53, a master regulator responsible for the initial phase of germ cell apoptosis induced by hyperthermia. These knowledges collectively promote our belief that information from future experiments designed to further study MTA1 during spermatogenesis will provide a scientific basis for the development of a novel biomarker for early diagnosis of testicular detriment in varicoceles, which should lead to improved outcomes in this progressive pathology. © 2012 Elsevier Ltd.


Wei J.-H.,PLA Fourth Military Medical University | Feng X.,PLA Fourth Military Medical University | Sun Z.-J.,202 Hospital of PLA | Cheng P.,PLA Fourth Military Medical University | And 5 more authors.
Reproduction, Fertility and Development | Year: 2016

Our previous study showed that the chemokine regulated upon activation normal T-cell expressed and secreted (RANTES) originating from the mouse epididymis bound to the midpiece of luminal spermatozoa. The present study was undertaken to investigate the association between RANTES and epididymal spermatozoa and to determine whether the association is mediated by the RANTES receptors CCR1, CCR3 or CCR5. The use of reverse transcription polymerase chain reaction (RT-PCR), immunohistochemical staining and immunofluorescent staining demonstrated that RANTES secreted by apical and narrow cells of mouse epididymal ducts was associated with luminal spermatozoa. Flow cytometric analysis and immunofluorescent labelling revealed that the association between RANTES and spermatozoa of different regions weakened gradually as the spermatozoa moved along the epididymis. Moreover, CCR1, CCR3 and CCR5 were expressed in epididymal spermatozoa and located on the head of epididymal spermatozoa, while RANTES was generally located at the midpiece. In conclusion, RANTES and its receptors were not in the same sperm location, suggesting that RANTES binding to mouse epididymal spermatozoa is independent of CCR1, CCR3 and CCR5. © CSIRO 2016.


Li W.,PLA Fourth Military Medical University | Wu Z.-Q.,PLA Fourth Military Medical University | Zhang S.,PLA Fourth Military Medical University | Cao R.,PLA Fourth Military Medical University | And 3 more authors.
Cell and Tissue Research | Year: 2016

An increasingly pro-oxidant environment has been widely implicated in causing dysfunction of testicular steroidogenesis, but little progress has been made in understanding the underlying molecular mechanism. Here, we report that gamma-glutamyl transferase 5 (GGT5), a key metabolism component responsible for the catalysis of important anti-oxidant glutathione (GSH), is predominantly expressed in mammalian Leydig cells (LCs). Deregulated GGT5 expression negatively correlates with testosterone deficiency in the testes of type 2 diabetic mice. Consistently, overexpression of GGT5 potentiates the susceptibility of TM3 LCs to spontaneous oxidative stress during luteinizing hormone (LH)-stimulated steroidogenesis. From a mechanistic standpoint, the deleterious effect of GGT5 overexpression on testicular steroidogenesis may stem from an alteration of the local redox state because of GSH deficiency. The above-mentioned response might involve the impairment of extracellular signal-related kinase activation mediated directly by oxidative injury or indirectly by abnormal P38 activation, which in turn inhibits steroidogenic acute regulatory protein abundance in mitochondria and thus significantly sabotages the rate-limiting step during LH-induced steroidogenesis. Alternatively, GGT5 overexpression induces heme oxygenase 1 (HO-1) expression, which, as a key catalyst responsible for the oxidative degradation of heme, may inhibit the activities of the cytochrome P450 monooxygenases, thus substantially impairing testicular steroidogenesis. These results, coupled with the differential roles of mitogen-activated protein kinases and HO-1 signaling in spermatogenesis, lead us to propose a model in which a delicate balance between these two pathways modulated by the GGT5/oxidative stress cascade plays a central role during LH-stimulated steroidogenesis. © 2016 Springer-Verlag Berlin Heidelberg


PubMed | PLA Fourth Military Medical University and 202 Hospital of PLA
Type: Journal Article | Journal: Cell and tissue research | Year: 2016

An increasingly pro-oxidant environment has been widely implicated in causing dysfunction of testicular steroidogenesis, but little progress has been made in understanding the underlying molecular mechanism. Here, we report that gamma-glutamyl transferase 5 (GGT5), a key metabolism component responsible for the catalysis of important anti-oxidant glutathione (GSH), is predominantly expressed in mammalian Leydig cells (LCs). Deregulated GGT5 expression negatively correlates with testosterone deficiency in the testes of type 2 diabetic mice. Consistently, overexpression of GGT5 potentiates the susceptibility of TM3 LCs to spontaneous oxidative stress during luteinizing hormone (LH)-stimulated steroidogenesis. From a mechanistic standpoint, the deleterious effect of GGT5 overexpression on testicular steroidogenesis may stem from an alteration of the local redox state because of GSH deficiency. The above-mentioned response might involve the impairment of extracellular signal-related kinase activation mediated directly by oxidative injury or indirectly by abnormal P38 activation, which in turn inhibits steroidogenic acute regulatory protein abundance in mitochondria and thus significantly sabotages the rate-limiting step during LH-induced steroidogenesis. Alternatively, GGT5 overexpression induces heme oxygenase 1 (HO-1) expression, which, as a key catalyst responsible for the oxidative degradation of heme, may inhibit the activities of the cytochrome P450 monooxygenases, thus substantially impairing testicular steroidogenesis. These results, coupled with the differential roles of mitogen-activated protein kinases and HO-1 signaling in spermatogenesis, lead us to propose a model in which a delicate balance between these two pathways modulated by the GGT5/oxidative stress cascade plays a central role during LH-stimulated steroidogenesis.


Liu C.-Y.,202 Hospital of PLA | Li Q.-Y.,202 Hospital of PLA | Wang L.,202 Hospital of PLA | Jiang J.,202 Hospital of PLA | And 2 more authors.
Medical Journal of Chinese People's Liberation Army | Year: 2015

Objective To investigate the protective effect of prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2) and platelet activating factor (PAF) receptor antagonist on endotoxin-induced acute gastric mucosal injury in young rats. Methods Eighteen-day old Wistar rats were randomly divided into 4 groups: normal control group, model group (LPS group), PAF antagonist prevention group, and PAF antagonist treatment group. The model of endotoxemia in young rats was reproduced by intraperitoneal injection of endotoxin (5mg/kg of O55:B5 lipopolysaccharide). The rats in PAF prevention and treatment group received PAF antagonist BN52021 (Ginkgolide B, 5mg/kg) 0.5h before or after modeling. The rats in control group were given intraperitoneal injection of same amount of normal saline (1ml/kg). The animals were sacrificed 1.5, 3, 6, 24, 48 and 72h after intraperitoneal injection of endotoxin (8 in each group). The pathologic changes in gastric mucosa were observed after HE staining. The content of PGE2was measured by radioimmunoassay, the expression of COX-2 protein was determined by immunohistochemistry SP method, and the expression of COX-2 mRNA was assessed with RT-PCR method. Results Pathological changes in gastric mucosa were found to be edema of epithelial cells at 1.5h, and hyperemia and edema 3h after intraperitoneal injection of endotoxin in LPS group. The changes were most marked at 6h, including bleeding, karyorrhexis, pyknosis and apoptosis of epithelial cells of gastric mucosa. Exfoliation of the epithelium and neutrophil infiltration were observed at 24h, thinning of mucosa and a decrease in glands were observed at 48h, but no further changes were observed at 72h. However, all the above changes were significantly alleviated in prevention and treatment groups. The PGE2 content of gastric mucosa was lowered at 3h (P<0.05), and it was lowest at 6h (P<0.01) after endotoxin injection in LPS group, and significant difference was found between LPS group and control group. The PGE2 content of gastric mucosa was obviously increased at 3h and 6h in prevention group (P<0.05), and at 6h in treatment group (P<0.05). The differences at 6h were significant (P<0.01) among prevention group, treatment group and LPS group. No expression of COX-2 protein or mRNA was seen in gastric mucosal tissue of control group. In contrast with control group, cytoplasm COX-2 protein of gastric mucosal tissue was seen to express at 6h after endotoxin injection in LPS group, and it was obviously enhanced at 24, 48 and 72h (P<0.01), and the COX-2 mRNA level was also elevated. The expressions of COX-2 protein and mRNA were increased obviously at 6h in PAF antagonist prevention group and treatment group (P<0.01). The expressions of COX-2 protein at 6h and COX-2 mRNA at 24h were obviously elevated in prevention group and treatment group compared with those of LPS group (P<0.01). Conclusion PAF receptor antagonist may up-regulate the expression level of COX-2 protein and mRNA, increase PGE2 content, alleviate acute gastric mucosal injury, and promote the healing of gastric mucosal injury. © 2015 People's Military Medical Press.


Su X.,Liaoning Province Tumor Hospital | You Z.,202 Hospital of PLA | Zheng Z.,Liaoning Province Tumor Hospital
Chinese Journal of Clinical Oncology | Year: 2011

Objective: To investigate and discuss the relationship between the expressions of E-cadherin and S100A2 genes in gastric cancer tissues, as well as their clinical characters. Methods: Semi-quantitative RT-PCR and immunohistochemistry were performed in the tumor tissues with various grades, paracancerous, and normal gastric tissues to observe the functions of E-cadherin and S100A2 in gastric cancer tissues. Sixty-four cases of tumor tissues with various grades were collected from July 2006 to December 2006 in the Liaoning Province Tumor Hospital, and 15 gastric para-neoplastic and normal gastric tissues were collected as controls. Statistical methods were used to analyze the relationship between the clinical characters of E-cadherin and S100A2 and their roles in tumor progression. Results: The length of the amplified products of E-cadherin and S100A2 was 487 bp and 362 bp, respectively. The positive expression of E-cadherin and S100A2 genes in normal gastric tissues was both 100%, whereas the expression was lower in gastric cancer tissues. Moreover, same results were obtained in the positive expression of E-cadherin and S100A2 proteins. The expression of E-cadherin and S100A2 had high consistency in gastric cancer tissues. The positive expression of E-cadherin and S100A2 proteins was statistically significant in clinical characters, such as gross type, differentiation, invasion depth, and lymph node metastasis. Conclusion: E-cadherin and S100A2 are tumor-inhibiting factors, and their expression in gastric cancer tissues decreased. The expression was negatively correlated with to tumor differentiation grade, lymph node metastasis, and invasion grade.


Yu Y.,202 Hospital of PLA | Li J.,202 Hospital of PLA | Chen J.,202 Hospital of PLA | Fan B.-J.,202 Hospital of PLA | Yan Y.-B.,202 Hospital of PLA
Medical Journal of Chinese People's Liberation Army | Year: 2013

Objective To observe the influence of reperfusion after adnexal torsion (AT) on malondialdehyde (MDA), glutathione peroxidase catalase (GSH-Px) and catalase (CAT) contents of ovarian tissue in rabbits. Methods Forty female Japanese long-eared white rabbits were randomly divided into study group (n=32) and control group (n=8). The left adnexa of rabbits in the study group was clockwise twisted three laps, and then fixed on the left abdominal walls. Adnexal detorsion was then done 24 hours after adnexal torsion in the study group, and then the rabbits were divided into 4 groups (8 each). Both ovaries of each group were removed 24h, 48h, 72h and 96h, respectively, after reperfusion. The rabbits in the control group received sham-operation and both ovaries were removed 96h later. The removed left ovaries were used for biochemical detection of GSH-Px, CAT and MDA. All the right ovaries were used as experimental internal-control. Results The activity of GSH-Px declined significantly 24h to 72h after adnexal detorsion (P<0.01), and no significant difference was found when compared with that of control group 96h later (P>0.05). The activity of CAT declined significantly 24h and 48h after adnexal detorsion (P<0.01), then it began to increase after 72h, and it became significantly higher in 96h group as compared with that in control group (P<0.05). MDA content in study groups increased obviously 24h and 48h after adnexal detorsion (P<0.01), and it declined 72h later albeit still significantly higher than that of control group (P<0.01), and then it continuously declined to reach the level of control group 96h later (P>0.05). Conclusions Detorsion after adnexal torsion can affect the degree of oxidative stress injury in rabbits' ovaries as shown by the changes in the activities of GSH-Px, CAT and MDA. With the elongation of detorsion time, ovarian injury will be gradually alleviated.

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