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Qu Y.-G.,The Central Hospital of Enshi Autonomous Prefecture | Zhang Q.,Wuhan Nano Tumor Diagnosis Engineering Research Center | Pan Q.,Traditional Chinese Medical Hospital of Wenling | Zhao X.-D.,Hubei University | And 3 more authors.
International Journal of Nanomedicine | Year: 2014

Background: Epidermal growth factor receptor (EGFR) mutation status plays an important role in therapeutic decision making for non-small cell lung cancer (NSCLC) patients. Since EGFR mutation-specific antibodies (E746-A750del and L858R) have been developed, EGFR mutation detection by immunohistochemistry (IHC) is a suitable screening test. On this basis, we want to establish a new screening test, quantum dots immunofluorescence histochemistry (QDs-IHC), to assess EGFR gene mutation in NSCLC tissues, and we compared it to traditional IHC and amplification refractory mutation system (ARMS).Materials and methods: EGFR gene mutations were detected by QDs-IHC, IHC, and ADx-ARMS in 65 cases of NSCLC composed of 55 formalin-fixed, paraffin-embedded specimens and ten pleural effusion cell blocks, including 13 squamous cell carcinomas, two adenosquamous carcinomas, and 50 adenocarcinomas.Results: Positive rates of EGFR gene mutations detected by QDs-IHC, IHC, and ADx-ARMS were 40.0%, 36.9%, and 46.2%, respectively, in 65 cases of NSCLC patients. The sensitivity of QDs-IHC when detecting EGFR mutations, as compared to ADx-ARMS, was 86.7% (26/30); the specificity for both antibodies was 100.0% (26/26). IHC sensitivity was 80.0% (24/30) and the specificity was 92.31% (24/26). When detecting EGFR mutations, QDs-IHC and ADx-ARMS had perfect consistency (κ =0.882; P˂0.01). Excellent agreement was observed between IHC and ADx-ARMS when detecting EGFR mutations (κ =0.826; P˂0.01).Conclusion: QDs-IHC is a simple and standardized method to detect EGFR mutations with its high sensitivity and specificity, as compared with real-time polymerase chain reaction. In addition, the development of specific antibodies against EGFR mutation proteins might be useful for the diagnosis and treatment of lung cancer. © 2014 Qu et al. Source


Zhu X.Q.,Fujian Medical University | Hong H.S.,Fujian Medical University | Lin X.H.,Fujian Medical University | Chen L.L.,Fujian Medical University | Li Y.H.,The Central Hospital of Enshi Autonomous Prefecture
Brazilian Journal of Medical and Biological Research | Year: 2014

The physiological mechanisms involved in isoproterenol (ISO)-induced chronic heart failure (CHF) are not fully understood. In this study, we investigated local changes in cardiac aldosterone and its synthase in rats with ISO-induced CHF, and evaluated the effects of treatment with recombinant human brain natriuretic peptide (rhBNP). Sprague-Dawley rats were divided into 4 different groups. Fifty rats received subcutaneous ISO injections to induce CHF and the control group (n=10) received equal volumes of saline. After establishing the rat model, 9 CHF rats received no further treatment, rats in the low-dose group (n=8) received 22.5 μg/kg rhBNP and those in the high-dose group (n=8) received 45 μg/kg rhBNP daily for 1 month. Cardiac function was assessed by echocardiographic and hemodynamic analysis. Collagen volume fraction (CVF) was determined. Plasma and myocardial aldosterone concentrations were determined using radioimmunoassay. Myocardial aldosterone synthase (CYP11B2) was detected by quantitative real-time PCR. Cardiac function was significantly lower in the CHF group than in the control group (P<0.01), whereas CVF, plasma and myocardial aldosterone, and CYP11B2 transcription were significantly higher than in the control group (P<0.05). Low and high doses of rhBNP significantly improved hemodynamics (P<0.01) and cardiac function (P<0.05) and reduced CVF, plasma andmyocardial aldosterone, and CYP11B2 transcription (P<0.05). There were no significant differences between the rhBNP dose groups (P>0.05). Elevated cardiac aldosterone and upregulation of aldosterone synthase expression were detected in rats with ISO-induced CHF. Administration of rhBNP improved hemodynamics and ventricular remodeling and reduced myocardial fibrosis, possibly by downregulating CYP11B2 transcription and reducing myocardial aldosterone synthesis. Source


Zhang Y.,Wuhan University | Ye M.,The Central Hospital of Enshi Autonomous Prefecture | Chen L.J.,Texas Tech University Health Sciences Center | Li M.,Wuhan University | And 2 more authors.
Endocrine Journal | Year: 2015

The ubiquitin-proteasome system (UPS and autophagy are two conserved intracellular proteolytic pathways, responsible for degradation of most cellular proteins in living cells. Currently, both the UPS and autophagy have been suggested to be associated with pathogenesis of insulin resistance and diabetes. However, underlying mechanism remains largely unknown. The purpose of the present study is to investigate the impact of the UPS and autophagy on insulin sensitivity in serum-starved 3T3-L1 adipocytes. Our results show that serum depletion resulted in activation of the UPS and autophagy, accompanied with increased insulin sensitivity. Inhibition of the UPS with bortezomib (BZM, a highly selective, reversible 26S proteasome inhibitor induced compensatory activation of autophagy but did not affect significantly insulin action. Genetic and pharmacological inhibition of autophagy dramatically mitigated serum starvation-elevated insulin sensitivity. In addition, autophagy inhibition compromised UPS function and led to endoplasmic reticulum (ER stress and unfolded protein response (UPR. Inability of the UPS by BMZ exacerbated autophagy inhibition-induced ER stress and UPR. These results suggest that protein quality control maintained by the UPS and autophagy is required for preserving insulin sensitivity. Importantly, adaptive activation of autophagy plays a critical role in serum starvation-induced insulin sensitization in 3T3-L1 adipocytes. © The Japan Endocrine Society. Source


Li X.,China Three Gorges University | Gong Z.,Wuhan University | Zhang L.,Wuhan University | Zhao C.,Wuhan University | And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

Cervical cancer is a leading cause of cancer death among women in the world. The specific etiopathogenesis of cervical cancer is indeed complex. Even so, we should make arduous efforts to have a precise understanding of the complicate cellular/molecular mechanisms underlying initiation, progression and/or prevention of the cervical cancer. The high-risk human papillomavirus (hrHPV) is considered as the major causative agent of cervical cancer. But with the existence of hrHPV only is not sufficient, autophagy plays a vital character in the development of cervical cancer. Autophagy is the endogenous, tightly regulated cellular “housekeeping” process responsible for the degradation of damaged and dysfunctional cellular organelles and protein aggregates. Our aims in this review were (1) to provide a brief synopsis of process of autophagy (including an overview of the key molecular mediators of this catabolic process and its relationship with hrHPV infection) and (2) most importantly, summarize the current evidence for autophagy-mediated cervical carcinogenesis. One of the latest opinions about the etiopathogenesis is that hrHPV leads to the occurrence of cervical cancer via inhibiting the host’s autophagy. The infection of hrHPV will cause the autophagy of cancerous cells, resulting in autophagic cell death, which will suppress the further infection of HPV in return. But the autophagy would be knocked down by the hrHPV, which means the protecting action would end with failure. What’s worse, the negative denouement will enhance the infectivity of HPV ultimately, which leads to accelerate cervical carcinogenesis. © 2015 E-Century Publishing Corporation. All rights reserved. Source


Zhang D.,Wuhan University | Zhang Y.,Wuhan University | Ye M.,The Central Hospital of Enshi Autonomous Prefecture | Ding Y.,Wuhan University | And 4 more authors.
Molecular and Cellular Endocrinology | Year: 2016

Previous study has shown that curcumin directly or indirectly suppresses insulin signaling in 3T3-L1 adipocytes. However, the underlying mechanism remains unclear. Here we experimentally demonstrate that curcumin inhibited the ubiquitin-proteasome system (UPS) function, activated autophagy, and reduced protein levels of protein kinase B (Akt) in a dose- and time-dependent manner in 3T3-L1 adipocytes, accompanied with attenuation of insulin-stimulated Akt phosphorylation, plasma membrane translocation of glucose transporter type 4 (GLUT4), and glucose uptake. These in vitro inhibitory effects of curcumin on Akt protein expression and insulin action were reversed by pharmacological and genetic inhibition of autophagy but not by inhibition of the UPS and caspases. In addition, Akt reduction in adipose tissues of mice treated with curcumin could be recovered by administration of autophagy inhibitor bafilomycin A1 (BFA). This new finding provides a novel mechanism by which curcumin induces insulin resistance in adipocytes. © 2016 Elsevier Ireland Ltd. Source

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