The Fifth Peoples Hospital

Xining, China

The Fifth Peoples Hospital

Xining, China
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PubMed | Fengxian District Psychiatric Center, The 175th Military Hospital of the Peoples Liberation Army, Peoples Hospital, Tuberculosis Hospital and 17 more.
Type: Journal Article | Journal: PloS one | Year: 2015

On July 1, 2011, the Chinese government launched a national Action Plan for antibiotic stewardship targeting antibiotic misuse in public hospitals. The aim of this study was to evaluate the impacts of the Action Plan in terms of frequency and intensity of antibiotic utilization and patients costs in public general hospitals.Administrative pharmacy data from July 2010 to June 2014 were sampled from 65 public general hospitals and divided into three segments: (1) July 2010 to June 2011 as the preparation period; (2) July 2011 to June 2012 as the intervention period; and (3) July 2012 to June 2014 as the assessment period. The outcome measures included (1) antibiotic prescribing rates; (2) intensity of antibiotic consumption; (3) patients costs; and (4) duration of peri-operative antibiotic treatment in clean surgeries of thyroidectomy, breast, hernia, and orthopedic procedures. Longitudinal and cross-sectional analyses were conducted.Longitudinal analyses showed significant trend changes in the frequency and intensity of antibiotic consumption, the patients costs on antibiotics, and the duration of antibiotic treatment received by surgical patients undergoing the 4 clean procedures during the intervention period. Cross-sectional analyses showed that the antibiotic prescribing rates were reduced to 35.3% and 12.9% in inpatient and outpatient settings, that the intensity of antibiotic consumption was reduced to 35.9 DDD/100 bed-days, that patients costs on antibiotics were reduced significantly, and that the duration of peri-operative antibiotic treatment received by surgical patients undergoing the 4 types of clean procedures decreased to less than 24 hour during the assessment period.The Action Plan, as a combination of managerial and professional strategies, was effective in reducing the frequency and intensity of antibiotic consumption, patients costs on antibiotics, and the duration of peri-operative antibiotic treatment in the 4 clean surgeries.


PubMed | Shanghai JiaoTong University, Chongqing Medical University, The Fifth Peoples Hospital and Luzhou Medical College
Type: | Journal: Evidence-based complementary and alternative medicine : eCAM | Year: 2015

Esophageal carcinoma is a major public health problem worldwide and one of the most aggressively malignant neoplasms. Although considerable diagnostic and therapeutic progress has been made in recent years, the prognosis of EC patients still remains dismal due to high rates of recurrence/metastasis and invasion. Previous studies have demonstrated that Epithelial mesenchymal transition (EMT) is proposed as a critical mechanism for the acquisition of malignant phenotypes by epithelial cells. Several lines of evidence have shown that Cripto-1 plays an important oncogenic role during tumorigenesis by promoting EMT. The aim of our study was to evaluate the significance of Cripto-1 which plays a role in EMT and its metastasis in esophageal carcinoma. Data of this study suggest that Cripto-1 overexpression is connected with the tumorigenesis and progression of esophageal carcinoma; shRNA might be feasible for the inhibition of the invasion and metastasis of esophageal carcinoma.


PubMed | Centers for Disease Control and Prevention, Case Western Reserve University and The Fifth Peoples Hospital
Type: Journal Article | Journal: Journal of AIDS and immune research | Year: 2016

Although the process of reverse transcription is well elucidated, it remains unclear if viral core disruption provides a more cellular or viral milieu for HIV-1 reverse transcription. We have devised a method to require mixing of viral cores or core constituents to produce infectious progeny virus by a bipartite subgenomic RNA (sgRNA) system, in which HIV-1 cplt_R/U5/gag/pol and nfl sgRNAs are complementary to each other and when together can complete viral reverse transcription. Only the heterodiploid virus containing both the nfl and cplt_R/U5/gag/pol sgRNAs can complete reverse transcription and propagate infectious virus upon de novo infection. Dual exposure of U87.CD4.CXCR4 cells with high titers of the homodimeric nfl and cplt_R/U5/gag/pol virus particles did not result in productive virus infection. On the other hand, in early endosomes, the HIV-1 sgRNAs released from viral cores can retain function and complete the reverse transcription and result in productive infection. These findings confirm the assumptions that, in natural infection, HIV-1 cores, and likely other retrovirus cores, remain largely intact and do not mix/fuse in the cytoplasm during the reverse transcription process, and circulating cytoplasmic HIV-1 sgRNA (produced through transfection) could not help the complementary sgRNA in the viral core to complement the reverse transcription process.


Wang Y.,Shandong University | Zhang P.,Shandong University | Liu Z.,The Fifth Peoples Hospital | Wang Q.,Shandong University | And 4 more authors.
Molecular Cancer | Year: 2015

Background: CUL4A has been proposed as oncogene in several types of human cancer, but its clinical significance and functional role in human non-small cell lung cancer (NSCLC) remain unclear. Methods: Expression level of CUL4A was examined by RT-PCR and Western blot. Forced expression of CUL4A was mediated by retroviruses, and CUL4A silencing by shRNAs expressing lentiviruses. Growth capacity of lung cancer cells was measured by MTT in vitro and tumorigenesis in vivo, respectively. Results: We found that CUL4A was highly expressed in human lung cancer tissues and lung cancer cell lines, and this elevated expression positively correlated with disease progression and prognosis. Overexpression of CUL4A in human lung cancer cell lines increased cell proliferation, inhibited apoptosis, and subsequently conferred resistance to chemotherapy. On other hand, silencing CUL4A expression in NSCLC cells reduced proliferation, promoted apoptosis and resulted in tumor growth inhibition in cancer xenograft model. Mechanistically, we revealed CUL4A regulated EGFR transcriptional expression and activation, and subsequently activated AKT. Targeted inhibition of EGFR activity blocked these CUL4A induced oncogenic activities. Conclusions: Our results highlight the significance of CUL4A in NSCLC and suggest that CUL4A could be a promising therapy target and a potential biomarker for prognosis and EGFR target therapy in NSCLC patients. © 2014 Wang et al.; licensee BioMed Central Ltd.


Zhao C.-M.,The Fifth Peoples Hospital | Shang C.-X.,The Fifth Peoples Hospital
World Chinese Journal of Digestology | Year: 2014

AIM: To investigate the quality of life, social support and self-care self-efficacy in patients with digestive system tumors, and to analyze their correlation.METHODS: A total of 153 patients with digestive system tumors were surveyed using the general information questionnaire, strategies used by people to promote health, social support rating scale and quality of life questionnaire-C30.RESULTS: The score of self-care self-efficacy was 86.03 ± 14.23, and the score of social support was 40.28 ± 6.63. There was a significant positive correlation between social support and quality of life (P < 0.05), and between self-care selfefficacy and quality of life (P < 0.05).CONCLUSION: Health care professionals should pay attention to making patients have high quality of cancer self-care self-efficacy and fully utilize the sources of social support to improve the quality of life of patients with digestive system tumors. © 2014 Baishideng Publishing Group Inc. All rights reserved.


Wang Y.,Shandong University | Zhang P.,Shandong University | Liu Z.,The Fifth Peoples Hospital | Wang Q.,Shandong University | And 4 more authors.
Molecular Cancer | Year: 2014

Background: CUL4A has been proposed as oncogene in several types of human cancer, but its clinical significance and functional role in human non-small cell lung cancer (NSCLC) remain unclear. Methods: Expression level of CUL4A was examined by RT-PCR and Western blot. Forced expression of CUL4A was mediated by retroviruses, and CUL4A silencing by shRNAs expressing lentiviruses. Growth capacity of lung cancer cells was measured by MTT in vitro and tumorigenesis in vivo, respectively. Results: We found that CUL4A was highly expressed in human lung cancer tissues and lung cancer cell lines, and this elevated expression positively correlated with disease progression and prognosis. Overexpression of CUL4A in human lung cancer cell lines increased cell proliferation, inhibited apoptosis, and subsequently conferred resistance to chemotherapy. On other hand, silencing CUL4A expression in NSCLC cells reduced proliferation, promoted apoptosis and resulted in tumor growth inhibition in cancer xenograft model. Mechanistically, we revealed CUL4A regulated EGFR transcriptional expression and activation, and subsequently activated AKT. Targeted inhibition of EGFR activity blocked these CUL4A induced oncogenic activities. Conclusions: Our results highlight the significance of CUL4A in NSCLC and suggest that CUL4A could be a promising therapy target and a potential biomarker for prognosis and EGFR target therapy in NSCLC patients. © 2014 Wang et al.; licensee BioMed Central Ltd.


To investigate the incidence of new-onset amiodarone-induced hypothyroidism (AIH) and the associated risk factors.We performed a systematic search in MEDLINE, Embase, the Cochrane Library and the Chinese database from 1995 to 2015. Studies that investigated amiodarone-related adverse reactions on the thyroid were included. A random-effect model was used for the meta-analysis to investigate the incidence rate of AIH and associated risk factors.We identified 465 studies, of which data from 9 studies were included, comprising 1,972 patients. The incidence of AIH was 14.0% (95% confidence interval, CI, 8.7-21.7%) as a whole; it was higher in areas with a high than a low iodine content in the environment (20.3 vs. 8.7%, p < 0.001); subgroup analysis showed that AIH occurred in 19.2% (95% CI 10.2-33.1%) of women and 13.3% (95% CI 7.9-21.7%) of men (p < 0.001). Meta-regression analysis indicated a positive correlation with the mean age and percentage of women.The occurrence of AIH is a relatively frequent complication of amiodarone, and older women are more likely to develop AIH, especially in areas with a high iodine content in the environment, and restriction of total exposure to iodine might decrease the incidence of AIH.


PubMed | The Fifth Peoples Hospital
Type: Journal Article | Journal: Cardiology journal | Year: 2016

The factors and the mechanism contributing to an increase in cardiac troponin I (cTnI) in patients with chest pain, at least one cardiovascular risk factor, and no evidence of coronary heart disease remains elusive.Excluding patients with acute coronary syndrome and chronic myocardial isch-emia, we selected 362 consecutive patients with normal coronary angiography or computed tomography coronary angiography results or lesions causing < 50% stenosis in any of the coronary arteries from January 2012 to June 2015. Using a cut-off value of 0.01 ng/mL, patients with cTnI levels 0.01 ng/mL (164 patients) were compared with those with cTnI levels < 0.01 ng/mL. Logistic regression analysis was used to evaluate associations between elevated cTnI and patient characteristics.Other than history of diabetes mellitus (DM) (18.90% vs. 8.08%, p = 0.002), the characteristics of the patients with and without elevated cTnI levels were similar. History of DM predicted elevation of cTnI level (OR 3.34, 95% CI 1.55-7.20, p = 0.002) in logistic regression analysis.In total, 45.30% of patients with chest pain had elevated cTnI levels with a mean level of 0.07 0.10 ng/mL. History of DM rather than blood glucose level itself was associated with elevated cTnI levels, whereas female gender was protective against increases in cTnI levels.


PubMed | Shandong University and The Fifth Peoples Hospital
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2015

Metformin, a widely prescribed antidiabetic drug, has previously been shown to lower the risk of certain types of cancer, including that of breast cancer, and to improve prognosis. Its anticancer effects, which are mediated by the activation of AMP-activated protein kinase (AMPK), have become notable. The Sonic hedgehog (Shh) signaling pathway is involved in changes in mammary ducts and malignant transformation. The aim of the present study was to elucidate the role of the Shh pathway in mediating the anticancer effects of metformin and the correlation between AMPK and the Shh pathway. We investigated the effectiveness of metformin in inhibiting the proliferation, migration, invasion and stemness of breast cancer cells in vitro using RNA extraction and reverse transcriptionpolymerase chain reaction (RT-PCR), western blot analysis, cell proliferation assay, scratch-wound assay (cell migration assay), cell invasion assay, mammosphere culture and flow cytometry. In in vivo experiments, a tumor xenograft model was used to detect the effects of metformin on cancer cell proliferation. The results revealed that the treatment of breast cancer cells with metformin led to the inhibition of the Shh signaling pathway. Importantly, metformin inhibited recombinant human Shh (rhShh)induced cell migration, invasion, and stemness, and impaired cell proliferation both in vitro and in vivo. Furthermore, the small interfering RNA (siRNA)mediated downregulation of AMPK reversed the inhibitory effects of metformin on rhShhinduced Gli-1 expression and stemness. Our findings identified a role of the Shh signaling pathway in the anticancer effects of metformin in breast cancer. Furthermore, we revealed that the metformin-mediated inhibition of the Shh signaling pathway may be dependent on AMPK.


PubMed | Renmin University of China, The Fifth Peoples Hospital and Hubei University
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

To investigate the expression level of NEK2 in 40 tissue specimens of primary liver cancer and to search for clues whether the effect of NEK2 depletion plays a role on biological behaviors of HepG2 cells and the relevant molecular mechanism are the objectives of this study. Real-time PCR and immunohistochemistry assessed expression level of NEK2 in specimens of cancerous tissues and carcinoma-adjacent tissues. The NEK2 expression level in HepG2, Huh7, SMMC, and 7402 cells was detected by real-time PCR and western blot to screen experimental cell line. To assess the expression levels of NEK2 mRNA and protein, an effective siRNA transfected into the HepG2 cells was designed. CCK8 and colony-forming assays were performed to verify short-term and long-term proliferative activities, respectively. Capacity of apoptosis and cell cycle changes were assessed by flow cytometry. Ability of transference and invasion was measured by Transwell Chambers. Western blot approach was used to determine the protein expression levels. There was significantly high expression level of NEK2 in cancerous tissues compared to adjacent tissues. The expression of NEK2 was higher in HepG2 cells than other cell lines. Real-time PCR and western blot shown there were obviously down-regulated NEK2 expression in the NEK2-siRNA group compared to control groups. The capacity of amplification and invasion was inhibited distinctly, and FCM revealed the apoptosis rate was increased and G1 phase was arrested in NEK2-siRNA group. Western blot indicated that low expression of NEK2 in HepG2 cells could increase the expression levels of Bax, caspase-3, P21, and TIMP-1, but significantly suppressed the c-myc, c-jun, Bcl-2, cyclinD1, CDK4, MMP2, and MMP9 expression levels and the phosphorylation levels of ERK, JNK, and P38 compared with the control groups. Our findings demonstrated that NEK2 could be a valuable carcinogenic factor and a promising therapeutic target for primary liver cancer; NEK2 may regulate proliferation, apoptosis, and other biological behaviors of HepG2 cells via MAPK signal pathway.

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