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Abstract

Background

To investigate the serum level of hepcidin and its relationship with cardiovascular disease (CVD) in maintenance hemodialysis (MHD) patients.

Methods

Blood was obtained from 75 MHD patients before undergoing hemodialysis and 20 healthy controls. Serum hepcidin, advanced oxidation protein products (AOPP) and interleukin (IL)-6 were measured by enzyme-linked immunosorbant assay (ELISA). Spearman correlation, and binary logistic regression linear regression analyses were used to assess the relationship between serum hepcidin and other parameters.

Results

The serum level of hepcidin, AOPP and IL-6 was significantly up-regulated in MHD patients compared with the control (P < 0.05). Furthermore, serum hepcidin levels in patients with CVD were higher than those in patients without CVD (P < 0.05). In all MHD patients, serum hepcidin level was correlated positively with erythropoietin (EPO) dose per week (ρ = 0.251, P = 0.030), EPO resistance index (ρ = 0.268, P = 0.020), ferritin (ρ = 0.814, P < 0.001), transferin saturation (TSAT, ρ = 0.263, P = 0.023), AOPP (ρ = 0.280, P = 0.049), high sensitive C reactive protein (ρ = 0.151, P = 0.006), IL-6 (ρ = 0.340, P = 0.003) and left ventricular mass index (LVMI, ρ = 0.290, P = 0.033). Moreover, it was negatively correlated with serum pre-albumin (ρ = −0.266, P = 0.021), total iron-binding capacity (TIBC, ρ = −0.458, P < 0.001), unsaturated iron-binding capacity (UIBC, ρ = −0.473, P < 0.001) and transferrin (ρ = −0.487, P < 0.001). Linear regression analysis showed that ferritin (β = 0.708, P < 0.001), TIBC (β = −0.246, P = 0.032) and IL-6 (β = 0.209, P = 0.041) were independently associated with hepcidin. Results of binary logistic regression analysis suggested that higher serum hepcidin level (>249.2 ng/mL) was positively and independently related to CVD (OR = 1.32, 95% CI [1.20–9.56], P = 0.043).

Conclusions

Serum hepcidin level is associated with CVD in MHD patients, indicating that hepcidin may be a novel biomarker and therapeutic target for CVD.

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Objectives

Impaired intestinal barrier function has been demonstrated in the pathophysiology of diarrhea-predominant irritable bowel syndrome (IBS-D). This study aimed to describe the intestinal ultrastructural findings in the intestinal mucosal layer of IBS-D patients.

Methods

In total, 10 healthy controls and 10 IBS-D patients were analyzed in this study. The mucosa of each patient’s rectosigmoid colon was first assessed by confocal laser endomicroscopy (CLE); next, biopsied specimens of these sites were obtained. Intestinal tissues of IBS-D patients and healthy volunteers were examined to observe cellular changes by transmission electron microscopy (TEM).

Results

CLE showed no visible epithelial damage or inflammatory changes in the colonic mucosa of IBS-D compared with healthy volunteers. On transmission electron microscopic examination, patients with IBS-D displayed a larger apical intercellular distance with a higher proportion of dilated (>20 nm) intercellular junctional complexes, which was indicative of impaired mucosal integrity. In addition, microvillus exfoliation, extracellular vesicle as well as increased presence of multivesicular bodies were visible in IBS-D patients. Single epithelial cells appeared necrotic, as characterized by cytoplasmic vacuolization, cytoplasmic swelling, and presence of autolysosome. A significant association between bowel habit, frequency of abdominal pain, and enlarged intercellular distance was found.

Conclusion

This study showed ultrastructural alterations in the architecture of intestinal epithelial cells and intercellular junctional complexes in IBS-D patients, potentially representing a pathophysiological mechanism in IBS-D.

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The p38 MAP kinases are stress-activated MAP kinases whose induction is often associated with the onset of heart failure. This study investigated the role of p38 MAP kinase isoforms in the regulation of myocardial contractility and ischemia/reperfusion injury using mice with cardiac-specific expression of kinase dead (dominant negative) mutants of p38α (p38αdn) or p38β (p38βdn). Hearts were subjected to 20 min ischemia and 40 min reperfusion. Immunofluorescence staining for p38αdn and p38βdn protein was performed on neonatal cardiomyocytes infected with adenovirus expressing flag-tagged p38αdn and p38βdn protein. Basal contractile function was increased in both p38αdn and p38βdn hearts compared to WT. Ischemic injury was increased in p38βdn vs. WT hearts, as indicated by lower posti-schemic recoveries of contractile function and ATP. However, despite a similar increase in contractility, ischemic injury was not increased in p38αdn vs. WT hearts. Immunohistological analysis of cardiomyocytes with comparable levels of protein overexpression show that p38αdn and p38βdn proteins were co-localized with sarcomeric α-actinin, however, p38αdn was detected in the nucleus while p38βdn was exclusively detected in the cytosol. In summary, attenuated p38 activity led to increased myocardial contractility; specific isoforms of p38 and their sub-cellular localization may have different roles in modulating ischemic injury.

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The aim of this study was to investigate postprandial effects of two Chinese liquors on s elected cardiovascular disease risk factors in humans. Sixteen healthy men were randomized into three groups in a three-way crossover study: tea-flavor liquor (TFL), traditional Chinese liquor (TCL) and water control (WC). Every subject consumed 60 mL of either liquor (45% (v/v) ethanol) or water together with a high-fat meal, respectively. Compared with baseline, serum uric acid was significantly increased in TFL group (0.5-hour: P = 0.012; 1-hour: P = 0.001; 2-hour: P = 0.008) and it was significantly decreased in WC group (1-hour: P = 0.001; 2-hour: P = 0.001; 4-hour: P < 0.001), while uric acid was non-significantly increased in the TCL group. High-sensitive C-reactive protein (hs-CRP) was significantly increased in the TCL (P = 0.014) and WC (P = 0.008) groups at postprandial 4 hours compared with baseline. There was no significant difference between groups during the postprandial period for these two parameters or other biochemical parameters. In conclusion, both liquors increased postprandial uric acid, and no significant difference was observed for the effects of TFL and TCL on the measured biochemical parameters.

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