First Hospital of Shijiazhuang City

Shijiazhuang, China

First Hospital of Shijiazhuang City

Shijiazhuang, China
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Xie F.,University of Veterinary and Animal Sciences | Lei L.,University of Veterinary and Animal Sciences | Du C.,University of Veterinary and Animal Sciences | Li S.,Shanghai Entry Exit Inspection and Quarantine Bureau | And 2 more authors.
FEMS Microbiology Letters | Year: 2010

The limited information on the genetic differences among the 15 currently known serotypes of Actinobacillus pleuropneumoniae has significantly hampered the development of typing-based diagnostic methods and multivalent vaccines. In this study, we compared the genomic differences between A. pleuropneumoniae strains CVCC259 (serotype 1) and CVCC261 (serotype 3) by representational difference analysis. Of the eight differential DNA sequences in the CVCC259 strain and 11 differential DNA sequences in the CVCC261 strain that we identified, seven represent known virulent genes, 10 encode putative proteins, and two encode hypothetical proteins. We also investigated the distribution of these 19 sequences among the 15 serotypes, and each serotype showed a different distribution pattern. The autotransporter adhesin occurred as a novel putative virulence factor in serotypes 1, 5, 7, 8, 9, and 11. Notably, the presence of wzm and wzt in serotypes 1, 9, and 11 and the diverse distribution of wzz and wzy in the other serotypes suggest the presence of different O-antigen biosynthesis pathways among serotypes. The information on the differential distribution of these DNA sequences in the 15 serotypes of A. pleuropneumoniae may contribute to future research on the pathogenic mechanisms of different serotypes, typing-based diagnosis methods, and multivalent vaccines. © 2009 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.


Liu Y.,Hebei Medical University | Liu Y.,Key Orthopaedic Biomechanics Laboratory of Hebei Province | Peng M.,252 Hospital Of Peoples Liberation Army | Lin L.,Second Hospital of Cangzhou City | And 3 more authors.
Osteoporosis International | Year: 2015

Summary: This study retrospectively reviewed 327 nonagenarians who underwent hip fracture surgery at six hospitals. Functional status, postoperative complications, and 1-year mortality were evaluated, and relationships between these factors and American Society of Anesthesiologists (ASA) grade were analyzed. ASA grade was significantly associated with postoperative complications and 1-year mortality.Introduction: Few previous studies have reported outcomes after hip fracture in nonagenarians, and these studies did not report significant associations between ASA grade and mortality. However, most of these studies included only a small number of patients from a single hospital. This study aimed to evaluate the relationships between ASA grade and functional status, postoperative complications, and mortality rate in nonagenarians undergoing hip fracture surgery.Methods: This study included 327 nonagenarians who underwent hip fracture surgery between January 2000 and December 2012. Patients with open fractures, subtrochanteric fractures, polytrauma, and pathological fractures were excluded. The medical records and X-rays were retrospectively reviewed. The relationships between ASA grade and functional status, postoperative complications, and 1-year mortality were analyzed.Results: There were significant associations between the ASA grade and the rates of postoperative complications and 1-year mortality (both p < 0.05). All pairwise comparisons showed significant differences in postoperative complication rates between ASA grades (all p < 0.05). All pairwise comparisons, except for grades I vs. II and grades II vs. III, also showed significant differences in mortality rates between ASA grades (all p < 0.05). There were significant associations between the preoperative ability to manage activities of daily living and the rates of postoperative complications and 1-year mortality (both p < 0.05).Conclusions: ASA grade was significantly associated with the rates of postoperative complications and 1-year mortality in nonagenarians undergoing hip fracture surgery. The preoperative functional status was also significantly associated with these outcomes. © 2014, International Osteoporosis Foundation and National Osteoporosis Foundation.


Wang H.,First Hospital of Shijiazhuang City | Zheng Z.-M.,First Hospital of Shijiazhuang and Organ Transplantation Committee | Gao B.-L.,First Hospital of Shijiazhuang and Organ Transplantation Committee
Evidence-based Complementary and Alternative Medicine | Year: 2014

Purpose. To investigate the antiatherosclerotic effect of Guanxinkang (GXK) decoction on the apoptosis, mitochondrial membrane potential (MMP), and endoplasmic reticulum stress (ERS) of human umbilical vein endothelial cells (HUVEC) pretreated with homocysteinemia (HCY). Materials and Methods. HUVEC were randomly divided into 5 groups: (1) blank control group (control), (2) model control group (model), (3) GXK low dose group, (4) GXK medium dose group, and (5) GXK high dose group. For the three GXK groups, HCY was given to reach the concentration of 3.0 mmol/L after HUVEC had been incubated with rabbit serum containing GXK for two hours. At 3, 6, 12, and 24 h after HCY had been incubated with the cells, the HUVEC were collected for test of the apoptosis rate, MMP, and GRP78 protein (reflecting ERS). Results. In the model control group, the apoptosis rate and GRP 78 protein expression of HUVEC significantly increased (P < 0.05), while MMP significantly decreased (P < 0.05) compared with the blank control group. After GXK treatment of medium and high doses, the apoptosis rate and the GRP 78 protein expression significantly (P < 0.05) decreased, while MMP significantly increased (P < 0.05) in a time-dependent manner compared with the model control group. Conclusion. GXK can antagonize the injury of HUVEC caused by HCY and the antagonism effect increases with the concentration and treatment duration of GXK, with the possible mechanism of GXK antagonism being through inhibiting ERS caused by HCY. © 2014 Hao Wang et al.


Chen L.,Chinese People's Liberation Army | Chen G.,Chongqing Medical University | Guo Y.,Chinese People's Liberation Army | Liu L.,First Hospital of Shijiazhuang City | And 4 more authors.
Liver Transplantation | Year: 2014

Biliary fibrosis is a major complication after donation after cardiac death (DCD) liver transplantation. In this process, the roles of serotonin [5-hydroxytryptamine (5-HT)] and the 5-HT2A receptor subtype are still unknown. In this study, we analyzed markers of portal fibroblast (PF)/myofibroblast (MF) transdifferentiation such as transforming growth factor β1 (TGF-β1), phosphorylated smad2/3, α-smooth muscle actin (α-SMA), collagen I, and collagen III in a primary culture system of PFs after the administration of 5-HT or 5-HT plus ketanserin (a selective 5-HT2A receptor antagonist). A rat DCD transplant model was established with 30 minutes of warm ischemia and 4 hours of cold ischemia during organ procurement. Recipients were intraperitoneally injected with ketanserin (1 mg·kg-1·day-1) or normal saline. Grafts without in situ warm ischemia instead of minimal cold storage (30 minutes) served as controls. The serum biochemistry, the liver contents of 5-HT and hydroxyproline (HYP), and the expression of fibrosis-related genes (including TGF-β1, matrix metalloproteinase 2, procollagen α1, and α-SMA messenger RNA) were determined. The extent of biliary fibrosis was also assessed histopathologically. The results indicated that ketanserin inhibited 5-HT-activated TGF-β1-smad2/3 signaling in vitro and thereby depressed the MF conversion of PFs. Rats receiving DCD livers showed increased liver contents of 5-HT and HYP, impaired biliary function, up-regulation of fibrosis-related genes, and aggravated biliary fibrosis. However, these phenomena were alleviated by treatment with ketanserin. We concluded that the profibrotic activity of 5-HT occurred through the activation of TGF-β1 signaling and the 5-HT2A receptor. Thus, these data suggest that the 5-HT2A receptor may be a potential therapeutic target for ischemia-related biliary fibrosis after DCD liver transplantation. © 2014 AASLD.


PubMed | First Hospital of Shijiazhuang City and Chongqing Medical University
Type: Journal Article | Journal: Journal of Cancer | Year: 2016

Three-dimensional (3D) culture models represent a better approximation of solid tumor tissue architecture, especially cell adhesion, in vivo than two-dimensional (2D) cultures do. Here, we explored the role of architecture in chemosensitivity to platinum in colon cancer. Under the 3D culture condition, colon cancer cells formed multicellular spheroids, consisting of layers of cells. 3D cultures displayed significantly decreased sensitivity to platinum compared with 2D cultures. Platinum increased p53 in a dose-dependent and time-dependent manner. There was no detectable difference in basal p53 levels between 3D cultures and 2D cultures but cisplatin induced less p53 in both HCT116 3D cultures and LoVo 3D cultures. It was not due to cisplatin concentration because cisplatin induced similar -H2AX in 3D vs 2D. Knockdown of p53 significantly decreased sensitivity to platinum in 3D cultures. Knockdown of p53 decreased cleaved caspase 3 and apoptosis induced by cisplatin. These findings indicate that 3D architecture confers decreased chemosensitivity to platinum and p53 is involved in the mechanism. Knockdown of p53 decreased cisplatins induction of c-Jun N-terminal kinase 1/2 (JNK1/2) activation, whereas inhibition of JNK1/2 activation increased chemosensitivity. Inhibition of p38 activation decreased cisplatins induction of p53, but no difference in p38 activation by cisplatin was observed between 2D cultures and 3D cultures. Taken together, our results suggest that p53 is involved in a 3D architecture-mediated decrease in chemosensitivity to platinum in colon cancer. Mitogen-activated protein kinases (JNK1/2 and p38) do not play a dominant role in the mechanism.


Gao F.,First Hospital of Shijiazhuang City | Zheng Z.M.,First Hospital of Shijiazhuang City
Experimental and Clinical Endocrinology and Diabetes | Year: 2014

Diabetic neuropathy is a common complication of diabetes. It occurs in approximately 10-20% of patients with diabetes, or roughly 40-50% patients with diabetic neuropathy. However, the pathogenesis of diabetic neuropathic pain is still largely unknown. Several animal models have been used to study the underlying mechanisms for this complication. Some commonly used animal models include streptozotocin-induced rat and mouse models, diet/nutrition-induced models, combination of chemically- and nutrition-induced model, Zucker diabetic fatty rat model, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rat models, and transgenic/knock-out models. Even though the manifestations of diabetic neuropathic pain vary from thermal or chemical hyperalgesia, thermal or chemical hypoalgeia, allodynia, to spontaneous pain, some pathogenesis factors are shared among these symptoms. Increased AR activity, oxidative-nitrosative stress, protein kinase C, PARP and ACE activations, C-peptide deficiency, impaired neurotrophism, and proinflammatory responses have been identified in the development of diabetic neuropathic pain. This review discusses selected animal models for diabetic neuropathic pain, as well as some commonly shared pathways in these models. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart, New York.


Liu F.,Central South University | Liao F.,Central South University | Li W.,First Hospital of Changsha | Han Y.,First Hospital of Shijiazhuang City | Liao D.,Central South University
Molecular Medicine Reports | Year: 2014

Previous studies have demonstrated that progesterone has neuroprotective effects in the central nervous system (CNS) following traumatic brain injury (TBI). Numerous cellular mechanisms have been reported to be important in the neuroprotective effects of progesterone, including the reduction of edema, inflammation and apoptosis, and the inhibition of oxidative stress. However, the effect of progesterone on neuronal protection following TBI remains unclear. The present study aimed to investigate the effects of progesterone on the expression of Nogo-A, an inhibitor of axonal growth, glial fibrillary acidic protein (GFAP), a main component of the glial scar and growth-associated protein-43 (GAP-43), a signaling molecule in neuronal growth in TBI rats. The TBI model was produced by the weight drop method. In total, 75 rats were assigned to three groups: the sham group, TBI group with vehicle treatment and TBI group with progesterone treatment. The protein expression of Nogo-A, GFAP and GAP-43 in the cortex and the hippocampus was examined by immuno-cytochemistry. TBI rats significantly increased the expression of Nogo-A, GFAP, and GAP-43 at 1, 3, 7 and 14 days post-injury. Progesterone significantly decreased the expression of Nogo-A and GFAP, and upregulated the GAP-43 protein. Our findings suggested that progesterone promotes neuroprotection following TBI by inhibiting the expression of Nogo-A and GFAP, and increasing GAP-43 expression.


Yang J.,Central South University | Han Y.,Central South University | Han Y.,First Hospital of Shijiazhuang City | Ye W.,Central South University | And 3 more authors.
Journal of Surgical Research | Year: 2013

Background: Neurite outgrowth inhibitor-A (Nogo-A), myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein are three myelin-associated proteins that act as inhibitors to central nervous system regeneration. Neurite outgrowth inhibitor-A imposes the strongest effect on inhibiting axonal regeneration after traumatic brain injury. Alpha-tocopherol, a member of the vitamin E family, is recognized as an active antioxidative substance. Its use has not been well studied in brain injury research, especially in axonal regeneration research. Methods: We obtained 99 intact adult male Sprague-Dawley rats (200-250 g) from the Experimental Animal Center of Central South University. We used the modified method of Freeney to generate moderate brain injury in the rats. We injected 600 mg/kg α-tocopherol intraperitoneally daily as traumatic brain injury (TBI) treatment. Then, we performed behavioral tests in the corresponding time point, examined brain tissues after hematoxylin-eosin staining to identify changes in cell morphology, and performed immunohistochemical staining and quantitative real-time polymerase chain reaction to detect the expression of NoGo and Nogo receptor (NgR) in brain tissue. Results: For the Neurological Severity Scores of rats, there were obvious differences among the three groups at the corresponding time points. Standard hematoxylin-eosin staining showed that the brain structure of a sham-operated group of rats was clear, uniform, and compact. A TBI group exhibited hemorrhage, edema, inflammatory cell infiltration, condensed nuclei, and necrosis. We also saw glial cells and fibrous tissue proliferation. The α-tocopherol-treated TBI group had similar but less severe changes than the TBI group. Expression of Nogo-A and NgR increased after TBI compared with the sham-operated group. However, Nogo-A and NgR expression was significantly lower in the α-tocopherol-treated TBI group compared with the TBI group. Similarly, results showed that functional neurological deficits among rats in the α-tocopherol-treated TBI group were less pronounced than in the TBI group (model group). Conclusions: Our data demonstrate that α-tocopherol- treated rats had reduced microscopic evidence of brain damage. Alpha-tocopherol reduced Nogo-A and NgR expression in brain tissue after traumatic brain injury and promoted nerve regeneration. Alpha-tocopherol treatment of TBI rats had a neuroprotective role in their recovery. © 2013 Elsevier Inc. All rights reserved.


Zhang H.,First Hospital of ShiJiaZhuang City | Tang G.,First Hospital of ShiJiaZhuang City | Liu J.,First Hospital of ShiJiaZhuang City
Journal of Glaucoma | Year: 2016

Purpose: To assess the effects of phacoemulsification, intraocular lens implantation, and goniosynechialysis on patients with primary angle-closure glaucoma and cataract. Methods: A total of 145 eyes of 133 consecutively recruited patients were randomly divided into Phaco group and Trab group. Ocular parameters were measured before and after surgery. Results: The mean follow-up period was 13.2±5.6 months. The visual acuity in the Phaco group was significantly improved, whereas no alternation was found in the Trab group after surgery. The intraocular pressure (IOP) had no notable difference in 2 groups before surgery. Compared with preoperative IOP, there was significant decrease after surgery. No remarkable change in the IOP was measured in the 2 groups after surgery for 12 months. The anterior chamber depth was markedly augmented in the Phaco group compared with the Trab group after surgery for 3 months. Compared with the the Trab group, no obvious change in coefficient of outflow facility was found in the Phaco group before and after surgery, whereas there was a significant increase relative to its preoperation. The angle closure decreased from (290±25) to (60±35) degrees after surgery for 12 months in the Phaco group and no significant alteration was observed in the Trab group. The reduction extent of peripheral anterior synechiae was in direct proportion to the decreasing level of angle closure in the 2 groups. The change in the corneal endothelial cell density had no significant difference between 2 groups before and after surgery. Conclusions: The treatment of phacoemulsification, intraocular lens implantation, and goniosynechialysis is safe and effective for patients with primary angle-closure glaucoma and cataract. © 2015 Wolters Kluwer Health, Inc.


PubMed | First Hospital of Shijiazhuang City
Type: Case Reports | Journal: Journal of cancer research and therapeutics | Year: 2015

Mucoepidermoid carcinoma (MEC) is typically located in the salivary, lacrimal, and tracheobronchial glands and rarely presents in the esophagus. MEC is commonly characterized by squamous cells, mucus-secreting cells, and intermediate cells. This report presents the case of a 57-years-old male with a three months history of cough and shortness of breath. Computer tomography (CT) scans revealed a tumor locating in the left hilar. The histological report was squamous carcinoma. After three circles of chemotherapy, the patient complained of dysphagia. The electronic gastroscope showed a protrusion which 30-34 cm from the incisors. The tumor was histopathologically determined to be MEC of esophagus. The patient refused to surgery and concurrent chemoradiotheray; so, radiotherapy and sequential chemotherapy were performed, and after one year of follow up, the disease of esophagus recurrence; the patient was died of hemorrhage of esophagus for tumor progression. The literatures of MEC are also reviewed in this study.

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