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Background: The National Health and Family Planning Commission of China has issued more than 400 clinical pathways to improve the effectiveness and efficiency of medical care delivered by public hospitals in China. The aim of our study is to determine whether patient care is compliant with national clinical pathways in public general hospitals of Pudong New Area in Shanghai.Methods: We identified the clinical pathways established by the National Health and Family Planning Commission of China for 5 common conditions (community-acquired pneumonia, acute myocardial infarction (AMI), heart failure, cesarean section, type-2 diabetes). We randomly selected patients with each condition admitted to one of 7 public general hospitals in Pudong New Area in China in January, 2013. We identified key process indicators (KPIs) for each pathway and, based on chart review for each patient, determined whether the patient's care was compliant for each indicator. We calculated the proportion of care which was compliant with clinical pathways for each indicator, the average proportion of indicators that were met for each patient, and the proportion of patients whose care was compliant for all measures. For selected indicators, we compared compliance rates among hospitals in our study with those from other countries.Results: Average compliance rates across the KPIs for each condition ranged from 61 % for AMI to 89 % for pneumonia. The percent of patient receiving fully compliant care ranged from 0 for AMI and heart failure to 39 % for pneumonia. Compared to the compliance rate for process indicators in the hospitals of other countries, some rates in the hospitals that we audited were higher, but some were lower.Conclusions: Few patients received care that complied with all the pathways for each condition. The reasons for low compliance with national clinical pathways and how to improve clinical quality in public hospitals of China need to be further explored. [ABSTRACT FROM AUTHOR]

Background: Few population-based studies have examined the relationship between glycemic status and chronic kidney disease (CKD) in China. We examined the prevalence of CKD across categories of glycemia [diagnosed diabetes, undiagnosed diabetes (fasting plasma glucose [FPG] ≥ 126 mg/dL), prediabetes (FPG 100-126 mg/dL) and normal glycemia (FPG <100 mg/dL)] among Chinese adults and assessed the relative contribution of dysglycemia (prediabetes and/or diabetes) to the burden of CKD.Methods: 5,584 Chinese adults aged 20-79 years were selected from the Pudong New Area of Shanghai through a multistage random sampling. Demographic and lifestyle characteristics, anthropometry and blood pressure were measured. Biochemical assays included FPG, serum creatinine and lipids, urinary creatinine and albumin. Prevalence of albuminuria [urine albumin-to-creatinine ratio (ACR) ≥ 30 mg/g], decreased kidney function and CKD (either decreased kidney function or albuminuria) across levels of glycemia were estimated.Results: The prevalence of albuminuria, decreased kidney function and CKD each increased with higher glycemic levels (P < 0.001). Based on the MDRD Study equation, the unadjusted CKD prevalence was 30.9%, 28.5%, 14.1% and 9.2% in those with diagnosed diabetes, undiagnosed diabetes, prediabetes and normoglycemia, respectively. The corresponding age-, gender- and hypertension-adjusted CKD prevalence were 25.8%, 25.0%, 12.3% and 9.1%, respectively. In a multivariable analysis, the factors associated with CKD were hypertension (Odds ratio [OR] 1.70, 95% confidence interval [CI]: 1.42-2.03), dysglycemia (OR 1.65, 95% CI: 1.39-1.95), female gender (OR 1.48, 95% CI: 1.25-1.75), higher triglycerides (OR 1.14, 95% CI: 1.08-1.20 per mmol/L), higher body mass index (OR 1.08, 95% CI: 1.05-1.10 per kg/m2), and older age (OR 1.02, 95% CI: 1.01 -1.03 per year). The population attributable risks (PARs) associated with diabetes, prediabetes, dysglycemia (diabetes and prediabetes) and hypertension were 18.4%, 19.7%, 30.3% and 44.5% for CKD as defined by the MDRD study equation, and 15.8%, 24.4%, 29.2% and 10.0% with the CKD-EPI equation. Estimates of prevalence and ORs of the relative contribution of various risk factors to CKD obtained with the CKD-EPI equation were similar.Conclusions: As much as 30% of the CKD burden may be associated with dysglycemia among Chinese adults, independent of age, gender and hypertension status. Prevention and control of diabetes and prediabetes should be a high priority in reducing the CKD burden in China. [ABSTRACT FROM AUTHOR]

Background: The National Health and Family Planning Commission of China has issued more than 400 clinical pathways to improve the effectiveness and efficiency of medical care delivered by public hospitals in China. The aim of our study is to determine whether patient care is compliant with national clinical pathways in public general hospitals of Pudong New Area in Shanghai., Methods: We identified the clinical pathways established by the National Health and Family Planning Commission of China for 5 common conditions (community-acquired pneumonia, acute myocardial infarction (AMI), heart failure, cesarean section, type-2 diabetes). We randomly selected patients with each condition admitted to one of 7 public general hospitals in Pudong New Area in China in January, 2013. We identified key process indicators (KPIs) for each pathway and, based on chart review for each patient, determined whether the patient's care was compliant for each indicator. We calculated the proportion of care which was compliant with clinical pathways for each indicator, the average proportion of indicators that were met for each patient, and the proportion of patients whose care was compliant for all measures. For selected indicators, we compared compliance rates among hospitals in our study with those from other countries., Results: Average compliance rates across the KPIs for each condition ranged from 61 % for AMI to 89 % for pneumonia. The percent of patient receiving fully compliant care ranged from 0 for AMI and heart failure to 39 % for pneumonia. Compared to the compliance rate for process indicators in the hospitals of other countries, some rates in the hospitals that we audited were higher, but some were lower., Conclusions: Few patients received care that complied with all the pathways for each condition. The reasons for low compliance with national clinical pathways and how to improve clinical quality in public hospitals of China need to be further explored.

Background: A remolded microenvironment in hepatocellular carcinoma (HCC) caused by abnormally expressed matricellular proteins could promote HCC progression. The cell-matrix interactions mediated by integrins play an important role in tumor microenvironment. Epidermal Growth Factor-like repeats and Discoidin I-Like Domains 3 (EDIL3), an extracellular matrix (ECM) protein with angiogenic and anti-inflammatory effects, is abnormally highly expressed in HCC. Here we aim to analyze its expression in liver and HCC tissues, investigate the underlined mechanisms accounted for HCC progression., Methods: EDIL3 expression level is examined in normal liver, cirrhotic liver and HCC at both mRNA and protein level. The association between EDIL3 and clinical outcomes is analyzed. The pattern of EDIL3 expression and location is examined using Immunofluorescence and ELISA. Overexpression or knock-down of EDIL3 in a panel of cell lines are subjected to assays related to proliferation, invasion, and anoikis to investigate the mechanisms of this matrix protein in HCC progression. Recombinant EDIL3 treatment is applied to confirm the results., Results: Compared with normal liver and cirrhotic liver, EDIL3 is elevated in HCC. High level of EDIL3 protein is much more commonly in patients with larger tumor or portal vein tumor thrombus (PVTT) formation, associated with poor prognosis. EDIL3 is abundantly expressed in HCC cells and secreted by cancer cells. In vitro and in vivo studies indicate that EDIL3, probably in an autocrine manner, inhibits anoikis and promotes anchorage-independent growth of HCC cells. Further mechanistic studies suggest integrin ligation by EDIL3 and thus that the sustained activation of the FAK-Src-AKT signal is responsible for the anoikis resistance and anchorage independence. Both the administration of cilengitide, a RGD-containing integrin antagonist, and silencing of integrin αV, an important RGD-binding integrin, results in the blockade of anoikis-resistance induced by EDIL3., Conclusion: Our study suggests that high levels of autocrine EDIL3 may contribute to a receptive microenvironment for the survival of detached HCC cells and may involve in cancer cell spreading. We also highlight the importance of interaction between EDIL3 and integrin αV and suggest disrupting the ligation of EDIL3 to integrins via RGD-blocking in selected patients may bear potential therapeutic value.

Background: Gallbladder carcinoma is a malignant tumor with a very low 5-year survival rate because of the difficulty with its early diagnosis and the very poor prognosis of the advanced cancer state. The aims of this study were to determine whether curcumin could induce the apoptosis of a gallbladder carcinoma cell line, GBC-SD, and to clarify its related mechanism., Methods: First, the anti-proliferative activities of curcumin-treated and untreated GBC-SD cells were determined using the MTT and colony formation assays. Then, the early apoptosis of cells was detected by the annexin V/propidium iodide double-staining assay and Hoechst 33342 staining assay. Detection of mitochondrial membrane potential was used to validate the ability of curcumin on inducing apoptosis in GBC-SD cells. Cell cycle changes were detected by flow cytometric analysis. Finally, the expressions of the apoptosis-related proteins or genes caspase-3, PARP, Bcl-2, and Bax were analyzed by western blot and quantitative real time PCR assay. Statistical analyses were performed using the Student's t-test for comparison of the results obtained from cells with or without curcumin treatment., Results: The MTT assay revealed that curcumin had induced a dose- and a time-dependent decrease in cell viability. Colony counting indicated that curcumin had induced a dose-dependent decrease in the colony formation ability in GBC-SD cells. Cells treated with curcumin were arrested at the S phase, according to the flow cytometric analysis. A significant induction of both the early and late phases of apoptosis was shown by the annexin V-FITC and PI staining. Morphological changes in apoptotic cells were also found by the Hoechst 33342 staining. After treatment with curcumin fluorescence shifted from red to green as ΔΨm decreased. Furthermore, western blot and quantitative real time PCR assays demonstrated that the curcumin induced apoptosis in GBC-SD cells by regulating the ratio of Bcl-2/Bax and activating the expression of cleaved caspase-3., Conclusions: Taken together, the results indicate that curcumin may be a potential agent for the treatment of gallbladder cancer.

Background: HBO1 (histone acetyltransferase binding to ORC1) is a histone acetyltransferase (HAT) which could exert oncogenic function in breast cancer. However, the biological role and underlying mechanism of HBO1 in breast cancer remains largely unknown. In the current study, we aimed to investigate the role of HBO1 in breast cancer and uncover the underlying molecular mechanism., Methods: Immunohistochemistry was applied to detect HBO1 protein expression in breast cancer specimens (n=112). The expression of protein level was scored by integral optical density (IOD) for further statistical analyses using SPSS. Real-time PCR was used to simultaneously measure mRNA levels of HBO1. The HBO1 protein expression in breast cancer cells was confirmed by western blot., Results: HBO1 was highly expressed in breast cancer tissues and significantly correlated with estrogen receptor α (ERα) (p<0.001) and progestational hormone (PR) (p=0.002). HBO1 protein level also correlated positively with histology grade in ERα positive tumors (p=0.016) rather than ERα negative tumors. 17β-estradiol (E2) could upregulate HBO1 gene expression which was significantly inhibited by ICI 182,780 or ERα RNAi. E2-increased HBO1 protein expression was significantly suppressed by treatment with inhibitor of MEK1/2 (U0126) in T47 D and MCF-7 cells., Conclusions: HBO1 was an important downstream molecule of ERα, and ERK1/2 signaling pathway may involved in the expression of HBO1 increased by E2.

Background: The prevalence of metabolic syndrome (MS) has been increasing in China in recent years. The aim of this study is to estimate and compare the prevalence of MS among Chinese adults in Shanghai, one of the most economic developed areas in China, using definitions proposed by World Health Organization (WHO), National Cholesterol Education Program Adult Treatment Panel (modified ATP III) and International Diabetes Federation (IDF)., Methods: This cross-sectional study included 5,584 adults at age 20-79 randomly selected from Pudong New Area of Shanghai, China, through a three-stage sampling. All participants were interviewed in-person between April and July of 2008 to collect information on demographic and lifestyle characteristics. At the interview, anthropometry and blood pressure were measured and bio-specimens were collected., Results: The prevalence estimates for the MS increased with age for each definition in men and women, but the estimates varied greatly between the definitions and by sex. The prevalence of the MS was higher in men (20.2%) than in women (18.7%) using WHO definition but this sex difference was reversed when using the modified ATP III (28.4% for men vs. 35.1% for women) and the IDF (15.9% for men vs. 26.7% for women) criteria. The most common metabolic disorder in this population was dyslipidaemia, regardless of the definition used. Substantial agreement, estimated using the kappa statistic, was found between the modified ATP III and IDF definition, whereas the lowest agreement was observed between the WHO and ATP III criteria., Conclusions: The MS is highly prevalent among Chinese adults in Pudong New Area of Shanghai and the most prevalent component was dyslipidemia. These findings underscore the importance of prevention and control efforts for the MS in this area and the need for a unified predictive definition for the syndrome for use by clinical practitioners and public health agencies.

Background: Many in vitro studies have shown that adenosine (Ado) can induce vascular endothelial growth factor (VEGF) mRNA and protein expression and stimulate endothelial proliferation. In the present study, we seek to determine whether Ado can increase circulating levels of VEGF protein in the intact human., Methods: Five outpatients 49.3 +/- 6.7 years of age and weighing 88.2 +/- 8.5 kg were selected. They were given a 6 min intravenous infusion of Ado (0.14 mg kg-1 min-1) in conjunction with sestamibi myocardial perfusion scans. Mean blood pressure (MBP, calculated from systolic and diastolic values) and heart rate (HR) were determined before Ado infusion and every 2 min for the next 10 min. Plasma VEGF concentrations (ELISA) were determined immediately before Ado infusion and 1 h, 2 h, and 8 h after the infusion., Results: Plasma VEGF concentration averaged 20.3 +/- 2.0 pg ml-1 prior to Ado infusion, and increased to 62.7 +/- 18.1 pg ml-1 at 1 h post- infusion (p < 0.01). VEGF plasma concentration returned to basal levels 2 h after infusion (23.3 +/- 3.4 pg ml-1). MBP averaged 116 +/- 7 mmHg and heart rate averaged 70 +/- 7 prior to Ado infusion. MBP decreased by a maximum of approximately 22% and HR increased by a maximum of approximately 17% during the infusion., Conclusion: We conclude from these preliminary findings that intravenous infusion of adenosine can increase plasma levels of VEGF in humans.

Background: Physical inactivity increases the risk of atherosclerosis. However, the molecular mechanisms of this relation are poorly understood. A recent report indicates that endostatin, an endogenous angiostatic factor, inhibits the progression of atherosclerosis, and suggests that reducing intimal and atherosclerotic plaque tissue neovascularization can inhibit the progression atherosclerosis in animal models. We hypothesize that exercise can elevate the circulatory endostatin level. Hence, exercise can protect against one of the mechanisms of atherosclerosis., Results: We examined treadmill exercise tests in healthy volunteers to determine the effect of exercise on plasma levels of endostatin and other angiogenic regulators. Oxygen consumption (VO2) was calculated. Plasma levels of endostatin, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) were determined using ELISA. The total peak VO2 (L) in 7 male subjects was 29.5 +/- 17.8 over a 4-10 minute interval of exercise. Basal plasma levels of endostatin (immediately before exercise) were 20.3 +/- 3.2 pg/ml, the plasma levels increased to 29.3 +/- 4.2, 35.2 +/- 1.8, and 27.1 +/- 2.2 ng/ml, at 0.5, 2, and 6 h, respectively, after exercise. There was a strong linear correlation between increased plasma levels of endostatin (%) and the total peak VO2 (L) related to exercise (R2 = 0.9388; P < 0.01). Concurrently, VEGF levels decreased to 28.3 +/- 6.4, 17.6 +/- 2.4, and 26.5 +/- 12.5 pg/ml, at 0.5, 2, and 6 h, respectively, after exercise. There were no significant changes in plasma bFGF levels in those subjects before and after exercise., Conclusions: The results suggest that circulating endostatin can be significantly increased by exercise in proportion to the peak oxygen consumption under physiological conditions in healthy volunteers. These findings may provide new insights into the molecular links between physical inactivity and the risk of angiogenesis dependent diseases such as atherosclerosis.

Background: We have recently cloned and characterized a novel gene family named ancient conserved domain protein (ACDP) in humans. To facilitate the functional study of this novel gene family, we have cloned and characterized Acdp, the mouse homologue of the human ACDP gene family., Results: The four Acdp genes (Acdp1, Acdp2, Acdp3 and Acdp4) contain 3,631 bp, 3,244 bp, 2,684 bp and 2,743 bp of cDNA sequences, and encode deduced proteins of 951, 874, 713 and 771 amino acids, respectively. The mouse Acdp genes showed very strong homologies (>90%) in both nucleotide and amino acid sequences to their human counterparts. In addition, both nucleotide and amino acid sequences within the Ancient Conserved Domain (ACD) are highly conserved in many different taxonomic species. Particularly, Acdp proteins showed very strong AA homologies to the bacteria CorC protein (35% AA identity with 55% homology), which is involved in magnesium and cobalt efflux. The Acdp genes are widely expressed in all tissues tested except for Acdp1, which is only highly expressed in the brain with low levels of expression in kidney and testis. Immunostaining of Acdp1 in hippocampus neurons revealed a predominant localization on the plasma membrane., Conclusion: The Acdp genes are evolutionarily conserved in diverse species and ubiquitously expressed throughout development and adult tissues suggesting that Acdp may be an essential gene. Acdp showed strong homology to bacteria CorC protein and predominantly localized on the plasma membrane. These results suggest that Acdp is probably a family of proteins involved in ion transport in mammalian cells