Weifang Yidu Central Hospital

Weifang, China

Weifang Yidu Central Hospital

Weifang, China
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Wang S.,Weifang Peoples Hospital | Rui R.,Weifang Yidu Central Hospital | Zhang A.,Weifang Peoples Hospital | Liu X.,Weifang Peoples Hospital | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2017

Acute myocardial infarction (AMI) has a high incidence and causes severe consequences. Induced pluripotent stem (iPS) cells derives from patient’s own cells and has become one research focus for treating cardiovascular disease. The role and function of iPS cells on myocardial fibrosis after AMI, however, has not been illustrated. Healthy male Wistar rats were randomly divided into control, sham and AMI group. The AMI model was generated by occlusion of left anterior coronary artery. iPS cell transplantation group received mouse derived iPS cells after AMI model. M-type ultrasound was used to evaluate cardiac function of all rats. Immunohistochemistry staining was employed to evaluate the change of myocardial fibrosis. ELISA was adopted for measuring type I collagen content. Real time PCR and Western blotting were employed to quantify mRNA and protein levels of Bax or Bcl-2 in myocardial tissues, respectively. Left ventricular end-stage systolic dimeter (LVEDS), leaf ventricular end-stage diabolic diameter (LVEDD) and left ventricular mass index (LVMI) were all significantly increased in AMI model rats, which also showed elevated myocardial fibrosis, type I collagen content and Bax expression, along with decreased Bcl-2 mRNA or protein level (P<0.05 compared to sham group). iPS cell transplantation led to lower LVESD, LVEED and LVMI levels accompanied with fewer myocardial fibrosis, type I collage, Bax expression plus increased Bcl-2 expression (P<0.05 compared to AMI group). iPS cells can improve the condition of cardiac infarction and fibrosis via modulating apoptosis balance, protecting myocardial cells and suppressing type I collagen proliferation. © 2017, E-Century Publishing Corporation. All rights reserved.

Shi Y.-F.,Shanghai JiaoTong University | Ju W.-L.,Weifang Yidu Central Hospital | Zhu Y.-P.,Shanghai JiaoTong University | Xia S.-J.,Shanghai JiaoTong University | Sun X.-W.,Shanghai JiaoTong University
Urolithiasis | Year: 2017

Ureteric stenting is an effective drainage method in patients with acute urinary tract infection caused by ureteral calculi; however, the optimal ureteral stent indwelling time has not been clearly defined. The aim of this study was to evaluate the effect of ureteric stent indwelling time on the treatment of acute infection secondary to urinary tract calculi. A total of 142 patients with acute infection caused by urinary tract calculi were identified retrospectively from January 2011 to August 2015 at our institution. 63 patients were with ureteric stenting for 7 days (A group) and 79 patients with ureteric stenting for more than 7 days (B group). The patient characteristics of two groups were analyzed and the clinical data before and after stenting were compared. The postoperative complication outcomes were collected and analyzed. Effective drainage obtained from ureteral stenting clearly abated the infection after stenting for 7 days; WBC count, WBCs in urine, and positive rate of urine culture were significantly decreased compared with the condition of immediate stenting. Both groups showed similar stone clearance rates (96.8% vs. 96.2%, p = 0.841), and there was no significant difference in the rate of postoperative complications, especially related to urinary tract infection (6.3% vs. 6.3%, p = 1.000). It is safe and effective for patients with acute urinary tract infection secondary to urinary tract calculi to be treated by ureteroscopic lithotripsy after stenting for one week. Prolonging the stenting period achieves no added benefit for patients. © 2017 Springer-Verlag Berlin Heidelberg

Chen H.-Y.,Shandong University | Chen H.-Y.,Weifang Yidu Central Hospital | Li L.,Qingzhou Peoples Hospital | Fu Z.-J.,Shandong University
Pharmazie | Year: 2014

The pathophysiology of ventilator-induced lung injury (VILI) involves multiple mechanisms including inflammation. Histone deacetylase inhibitors have been shown to exert anti-inflammation activity. The purpose of this study was to examine the protecting roles and mechanisms of the histone deacetylase inhibitors trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA) in ventilator-induced lung injury in normal rat lung. Male Sprague-Dawley rats were divided into four groups: lung-protective ventilation (LV), injurious ventilation (HV), HV+TSA and HV+ SAHA groups. Mechanical ventilation (MV) settings were 7 ml/kg VT and 3 cm H2O positive end-expiratorypressure [PEEP], 40 breaths/min for LV group and 42 ml/kg VT, zero end-expiratoryvolume [ZEEP], 40 breaths/min for the HV, HV+TSA and HV+ SAHA groups. After 2 h of MV, acute lung injury (ALI) score, wet-to-dry (W/D) weight ratio and the activity of myeloperoxidase (MPO) were determined. The concentration of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-10(IL-6) in the homogenized lung were measured by ELISA. The expression ICAM-1 was measured by both realtime PCR and Western blot assays. In addition, survival of each group was also assessed. Our results indicated that administration of TSA or SAHA alleviated ventilator-induced lung injury. This was accompanied by reduced neutrophil infiltration, reduced MPO activity, decreased intercellular adhesion molecule-1 (ICAM-1) expression in lung tissue, and lower TNF-α, IL-1β and IL-6 levels. In addition, treatment with HDAC inhibitors significantly prolonged the survival time of ventilator-induced lung injury rats. Our data suggested that TSA and SAHA could significantly alleviate ventilator-induced rat lung injury and prolong the survival time of those rats by attenuate intrapulmonary inflammatory response. ©2014 Publishing Technology.

Feng A.-F.,Weifang Yidu Central Hospital | Liu Z.-H.,Weifang Yidu Central Hospital | Zhou S.-L.,Weifang Yidu Central Hospital | Zhao S.-Y.,Weifang Yidu Central Hospital | And 2 more authors.
BMC Cardiovascular Disorders | Year: 2017

Background: The meta-analysis was aimed to evaluate the effects of AMPD1 gene C34T polymorphism on cardiac function indexes, blood pressure and prognosis in patients with cardiovascular diseases (CVD). Methods: Eligible studies were retrieved through a comprehensive search of electronic databases and manual search. Then the high-quality studies met the rigorous inclusion and exclusion criteria, as well as related to the subject was selected for the study. Comprehensive data analyses were conducted using STATA software 12.0. Results: The study results revealed that CVD patients with CT + TT genotype of AMPD1 C34T polymorphism presented elevated left ventricular ejection fraction (LVEF) (%) and reduced left ventricular end diastolic dimension (LVEDD) (mm) as compared with CC genotype, moreover, the subgroup analysis found that the LVEF (%) was markedly higher in heart failure (HF) patients carrying CT + TT genotype than CC genotype. Besides, the systolic blood pressure (SBP) (mmHg) in CVD patients with CT + TT genotype was obviously decreased in contrast with the CC genotype. Patients suffered from HF with different genotypes (CT + TT and CC) of AMPD1 C34T polymorphism exhibited no significant differences in total survival rate and cardiac survival rate. Conclusions: Our current meta-analysis indicated that the T allele of AMPD1 gene C34T polymorphism may be correlated with LVEF, LVEDD and SBP, which plays a protective role in the cardiac functions and blood pressure in CVD patients, but had no effects on total survival rate and cardiac survival rate for HF. © 2017 The Author(s).

Chen L.,Peking University | Wu Y.,Weifang Yidu Central Hospital | Yu J.,Peking University | Jiao Z.,Weifang Yidu Central Hospital | And 4 more authors.
Knee Surgery, Sports Traumatology, Arthroscopy | Year: 2011

The increased use of allograft tissue in the reconstruction of anterior cruciate ligament has brought more focus to the effect of storage and treatment on allograft. The purpose of this study was to observe the effect of histology and biomechanics on Achilles tendon in rabbits through repeated freezing-thawing before allograft tendon transplantation. Rabbit Achilles tendons were harvested and processed according to the manufacture's protocol of tissue bank, and freezing-thawing was repeated three times (group 1) and ten times (group 2). Those received only one cycle were used as controls. Then, tendons in each group were selected randomly to make for histological observations and biomechanics test. Histological observation showed that the following changes happened as the number of freezing-thawing increased: the arrangement of tendon bundles and collagen fibrils became disordered until ruptured, cells disrupted and apparent gaps appeared between tendon bundle because the formation of ice crystals. There were significant differences between the experimental and control groups in the values of maximum load, energy of maximum load and maximum stress, whereas no significant differences existed in other values such as stiffness, maximum strain, elastic modulus, and energy density. Therefore, repeated freezing-thawing had histological and biomechanical effect on Achilles tendon in rabbits before allograft tendon transplantation. This indicates that cautions should be taken in the repeated freezing-thawing preparation of allograft tendons in clinical application. © 2010 Springer-Verlag.

Yang Y.-C.,Weifang Yidu Central Hospital | Li Y.,Weifang Yidu Central Hospital | Guo M.-T.,Shouguang Peoples Hospital | Zhao J.-M.,Jining No 1 Peoples Hospital
International Journal of Clinical and Experimental Pathology | Year: 2016

Present study aimed to investigate the effect of cantharidin on reduction in cell viability and induction of apoptosis in KOSC-2 oral cancer cells. Cantharidin treatment for 48 h caused a concentration dependent reduction in KOSC-2 cell viability. The IC50 of cantharidin against KOSC-2 cells was found to be 50 nM after 48 h. KOSC-2 cells showed reduction in size, protrusion of membrane and condensation of nuclear material on treatment with 50 nM concentration of cantharidin for 48 h. Flow cytometry using propydium iodide staining revealed significant (P<0.05) increase in the population of cells in G0/G1 phase of cell cycle in cantharidin treated compared to the control cells. Results from western blot analysis showed increase in the expression of pro-apoptotic BAD and decrease in the expression of anti-apoptotic protein Bcl-2 on treatment with cantharidin in KOSC-2 cells. Cantharidin treatment for 48 h also resulted in a significant increase in the expression of Apaf-1 and AIF as well as translocation of cytochrome c into the cytosol. The activation of caspase-3 in KOSC-2 cells was enhanced significant (P<0.05) in cantharidin treated compared to the control cells. Thus cantharidin treatment inhibits KOSC-2 cell viability and induces apoptosis through mitochondrial pathway. Therefore, cantharidin can be used for the treatment of oral cancer.

Chen H.,Weifang Yidu Central Hospital | Li L.,Qingzhou Peoples Hospital | Xia H.,Qingzhou Peoples Hospital
International Journal of Clinical and Experimental Medicine | Year: 2015

Ketamine is a commonly used short-acting anesthetic and recently attempted to treat pain which is a complication of diabetes. In this study we investigated the effect of ketamine on glucose levels of normal rats and diabetic rats. The results showed that no significance between the glucose levels in ketamine treatment group and saline treatment group at all time points was observed in normal rats. Ketamine did not produce hyperglycemia in normal fasted rats. However, ketamine dose dependently elevated glucose in diabetic rats from 80 mg/kg to 120 mg/kg at 1 hour after injection. The glucose did not return to the levels before treatment in streptozotocin (STZ) induced diabetic rats. Insulin revealed a powerful potency in decreasing glucose levels in diabetic rats. Ketamine did not induce acute hyperglycemia any more after diabetic rats pretreated with insulin. Serum corticosterone was significantly increased in all treatment groups including saline group after 1 hour treatment compared with baseline values. Then the corticosterone declined in both saline treatment groups. However, ketamine induced a more significant increase in corticosterone at 1 hour after injection compared with that of saline control group of diabetic rats. And no decline trend of corticosterone was observed after ketamine treatment 2 hours. Insulin did not reduce the elevated corticosterone level induced by ketamine either. The results suggested that the diabetic rats had a risk of hyperglycaemia when they were treated with ketamine. Pretreatment with insulin is a good symptomatic treatment for hyperglycaemia induced by ketamine. © 2015, E-Century Publishing Corporation. All rights reserved.

PubMed | Weifang Yidu Central Hospital
Type: Journal Article | Journal: European review for medical and pharmacological sciences | Year: 2016

The varied therapeutic approaches like radiotherapy, chemotherapy, surgery, etc. primarily aimed to target cancer cells specifically. Despite these efforts, they are not completely successful in eliminating this deadly pathological state. These failures ultimately lead to cancer reoccurrence, which is again, another burning problem associated with cancer. The prime reason for the above observation has been found to be the development of resistance by cancer cells towards cancer drugs or cancer-initiating cells (cancer stem cells) remain unaffected by existing treatment procedures. Recent research has evolved two drugs, salinomycin and apoptin, that hold great potential for the future of cancer treatment not only for restricting malignancy, but also in preventing tumor recurrence. The present review article will put light on these new upcoming cancer stem cell targeting agents.

PubMed | Weifang Yidu Central Hospital
Type: | Journal: Medical science monitor : international medical journal of experimental and clinical research | Year: 2016

BACKGROUND This study aimed to analyze the relationship of UGT2B7 and UGT1A4 polymorphisms with metabolism of valproic acid (VPA) and lamotrigine (LTG) in epileptic children. MATERIAL AND METHODS We administered VPA (102) and LTG (102) to 204 children with epilepsy. Blood samples were collected before the morning dose. Serum concentration of LTG was measured by high-performance liquid chromatography (HPLC). Serum VPA concentration was tested by fluorescence polarization immunoassay. UGT2B7 A268G, C802T, and G211T polymorphisms, as well as UGT1A4 L48V polymorphism, were assayed by direct automated DNA sequencing after PCR. Evaluation of efficacy was conducted using the Engel method. RESULTS The adjusted serum concentration of VPA was 4.26 g/mL per mg/kg and LTG was 1.56 g/mL per mg/kg. Multiple linear regression analysis revealed that VPA or LTG adjusted concentration showed a good linear relation with sex and age. UGT2B7 A268G and C802T polymorphisms were demonstrated to affect the serum concentration of VPA (F=3.147, P=0.047; F=22.754, P=0.000). UGT1A4 L48V polymorphism was not related with the serum concentration of LTG (F=5.328, P=0.006). In the efficacy analysis, we found that C802T polymorphism exerted strong effects on efficacy of VPA (=9.265, P=0.010). L48V polymorphism also showed effects on efficacy of LTG (=17.397, P=0.001). CONCLUSIONS UGT2B7, UGT1A4 polymorphisms play crucial roles in metabolism of VPA and LTG.

PubMed | Weifang Yidu Central Hospital
Type: | Journal: Hormones & cancer | Year: 2016

The microRNAs (miRNAs) have been suggested as a tumor suppressor in recent years. miR-15b was reported to exert an anti-oncogenic role in the proliferation, migration, and invasion of diverse tumor cells. However, the mechanisms underlying miR-15b-mediated biology of glioblastoma are still unclear. In the present study, the expression of miR-15b was down-regulated in glioblastoma tumor tissues and U87 and U251 cells, but insulin-like growth factor receptor 1 (IGF1R) expression became up-regulated in these tumor tissues and cells (all p<0.001). Furthermore, IGF1R expression was inversely associated with miR-15b expression. Notably, patients with lower miR-15b expression have a much shorter survival period compared with high expression (log-rank test p=0.045). In vitro data demonstrated that miR-15b mimics inhibited the proliferation, cell cycle arrest, and invasion of U87 and U251 cells. Besides, we validated IGF1R as a direct target of miR-15b using dual luciferase assays, and IGF1R plasmids partially abrogated miR-15b mimics inhibited cell proliferation. In vivo, miR-15b mimics indeed repressed cell proliferation in mouse xenograft model. In conclusion, our study demonstrated that miR-15b inhibits the progression of glioblastoma cells through targeting IGF1R, and miR-15b can be recommended as a tumor suppressor in the progression of glioblastoma.

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