the First Peoples Hospital of Xiaoshan District of Hangzhou City

Hangzhou, China

the First Peoples Hospital of Xiaoshan District of Hangzhou City

Hangzhou, China
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Xu J.,the First Peoples Hospital of Xiaoshan District of Hangzhou City | Huang B.,Dalian Medical University | Wang Y.,Dalian Medical University | Tong C.,Dalian Medical University | And 3 more authors.
Clinical and Experimental Pharmacology and Physiology | Year: 2016

The present study investigates the ameliorating effects of emodin on acute lung injury (ALI) induced by severe acute pancreatitis (SAP). An ALI rat model was constructed by sodium ursodeoxycholate and they were divided into four groups: SHAM, ALI, emodin and dexamethasone (DEX) (n=24 per group). Blood samples and lung tissues were collected 6, 12 and 24 hours after the induction of SAP-associated ALI. Lung wet/dry ratio, blood gases, serum amylase and tumor necrosis factor-α (TNF-α) were measured at each time point. The expressions of AQP1 and AQP5 in lung tissue were detected by immunohistochemical staining, western blotting and real-time PCR. As the results show, there were no statistical differences in the levels of serum amylase, lung wet/dry ratio, blood gases indexes, serum TNF-α and pathological changes between emodin and DEX groups. However, significant differences were observed when compared with the ALI group. AQP1 and AQP5 expressions were significantly increased and lung oedemas were alleviated with the treatment of emodin and DEX. The expressions of AQP1 and AQP5 were significantly decreased in SAP-associated ALI rats. Emodin up-regulated the expression of AQP1 and AQP5, it could reduce pulmonary oedema and ameliorate SAP-induced ALI. Regulations on AQP1 and AQP5 expression had a great value in clinical application. © 2016 John Wiley & Sons Australia, Ltd


Gu S.-J.,The first peoples Hospital of Xiaoshan District of Hangzhou City | Lu M.,The first peoples Hospital of Xiaoshan District of Hangzhou City | Xuan H.-F.,The first peoples Hospital of Xiaoshan District of Hangzhou City | Chen X.-Z.,The first peoples Hospital of Xiaoshan District of Hangzhou City | And 6 more authors.
Clinica Chimica Acta | Year: 2016

Background: Caspase-cleaved Cytokeratin-18 (CCCK-18) is released during apoptosis. Serum CCCK-18 concentrations are associated with prognosis of some critical illness. We investigated the potential relationships between serum CCCK-18 concentrations and disease severity and long-term clinical outcomes after intracerebral hemorrhage. Methods: Serum CCCK-18 concentrations were determined in a total of 102 patients and 102 controls. Multivariate models were used to predict high concentration of CCCK-18 and 6-month clinical outcomes. The predictive values were evaluated based on areas under receiver operating curve. Results: Compared with controls, serum CCCK-18 concentrations were increased in patients (245.8 ± 108.3 U/l vs. 23.6 ± 18.1 U/l, P< 0.001). National Institute of Health Stroke Scale scores [odds ratio (OR), 1.164; 95% confidence interval (CI), 1.027-1.320; P= 0.003] and hematoma volumes (OR, 1.079; 95% CI, 1.018-1.205; P= 0.008) were independent predictors of high concentration of CCCK-18. CCCK-18 was identified as an independent predictor of 6-month mortality (OR, 1.019; 95% CI, 1.010-1.038; P= 0.013) and 6-month unfavorable outcome (OR, 1.017; 95% CI, 1.008-1.029; P= 0.032) and possessed high predictive values. Conclusion: Increased serum CCCK-18 concentrations are associated with disease severity and clinical outcomes, suggesting that CCCK represent a novel prognostic predictive biomarker after intracerebral hemorrhage. © 2015 Elsevier B.V.


PubMed | The first peoples Hospital of Xiaoshan District of Hangzhou City
Type: | Journal: Clinica chimica acta; international journal of clinical chemistry | Year: 2015

Caspase-cleaved Cytokeratin-18 (CCCK-18) is released during apoptosis. Serum CCCK-18 concentrations are associated with prognosis of some critical illness. We investigated the potential relationships between serum CCCK-18 concentrations and disease severity and long-term clinical outcomes after intracerebral hemorrhage.Serum CCCK-18 concentrations were determined in a total of 102 patients and 102 controls. Multivariate models were used to predict high concentration of CCCK-18 and 6-month clinical outcomes. The predictive values were evaluated based on areas under receiver operating curve.Compared with controls, serum CCCK-18 concentrations were increased in patients (245.8108.3U/l vs. 23.618.1U/l, P<0.001). National Institute of Health Stroke Scale scores [odds ratio (OR), 1.164; 95% confidence interval (CI), 1.027-1.320; P=0.003] and hematoma volumes (OR, 1.079; 95% CI, 1.018-1.205; P=0.008) were independent predictors of high concentration of CCCK-18. CCCK-18 was identified as an independent predictor of 6-month mortality (OR, 1.019; 95% CI, 1.010-1.038; P=0.013) and 6-month unfavorable outcome (OR, 1.017; 95% CI, 1.008-1.029; P=0.032) and possessed high predictive values.Increased serum CCCK-18 concentrations are associated with disease severity and clinical outcomes, suggesting that CCCK represent a novel prognostic predictive biomarker after intracerebral hemorrhage.


PubMed | The first peoples Hospital of Xiaoshan District of Hangzhou City
Type: | Journal: Clinica chimica acta; international journal of clinical chemistry | Year: 2013

Visfatin, a proinflammatory mediator, has been associated with poor clinical outcomes after acute brain injury. The present study is designed to investigate the potential association between plasma visfatin levels and the risk of hematoma growth (HG) and early neurologic deterioration (END) after intracerebral hemorrhage.There were 85 patients as cases who presented with first-time hemorrhagic stroke that were assessed within 6h after the incident. The control group consisted of 85 healthy volunteers. HG was defined as hematoma enlargement >33% at 24h. END was defined as an increase of 4 points in National Institute of Health Stroke Scale score at 24h from symptoms onset. Plasma visfatin levels were determined using enzyme immunoassay.Plasma visfatin levels were significantly higher in patients compared to controls. Plasma visfatin level emerged as an independent predictor of HG [odds ratio (OR), 1.154; 95% confidence interval (CI), 1.046-3.108; P=0.009] and END (OR, 1.195; 95% CI, 1.073-3.516; P=0.005). For predicting HG, area under curve (AUC) of plasma visfatin level (0.814; 95% CI: 0.715-0.890) was similar to that of hematoma volume (0.839; 95% CI, 0.743-0.909) (P=0.703). For predicting END, AUC of plasma visfatin level (0.828; 95% CI: 0.730-0.901) was similar to that of hematoma volume (0.863; 95% CI, 0.771-0.928) (P=0.605). Visfatin did not improve AUC of hematoma volume for predicting HG and END (both P>0.05).Plasma visfatin level represents a novel biomarker for predicting HG and END.

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