Relationship between serum CHIP levels with cardiovascular disease in maintenance haemodialysis patients.

Many preclinical studies reported that the carboxyl terminus of Hsp70-interacting protein (CHIP) has cardiovascular protective effects. This study was designed to explore whether CHIP is related with cardiovascular disease (CVD) in maintanence haemodialysis (MHD) patients. 217 MHD patients and 150 healthy controls were recruited, serum CHIP concentration and clinical characteristics were measured. MHD patients were followed-up for 36 months and their cardiovascular events (CVEs) and survival conditions were recorded. Here, the data shows that serum CHIP concentrations in MHD patients were lower than those in healthy controls (31.69 ± 18.2 pg/mL vs 84.53 ± 22.1 pg/mL, p < 0.05). CHIP negatively correlated with age, C-reactive protein, B-type brain natriuretic peptide, phosphorus, parathyroid hormone, carotid intima-media thickness (CIMT) and left ventricular septal thickness (LVSTd), whereas it positively associated with albumin, haemoglobin, creatinine, Kt/V and ejection fraction (p < 0.05, respectively). Partial correlation and multiple linear regression analysis verified the negative relationship between CHIP with CIMT or LVSTd (p < 0.05, respectively). Using quartile method and Kaplan-Meier survival function, it indetified that the lower serum CHIP concentration predicted risk of CVEs, CVD and all-cause death (p < 0.001). Cox regression analysis manifested CHIP was negatively associated with CVEs (HR = 0.914, 95%CI 0.880-0.950, p < 0.001), CVD mortality (HR = 0.747, 95%CI 0.651-0.857, p < 0.001) and all-cause death (HR = 0.769, 95%CI 0.696-0.850, p < 0.001). In conclusion, the data of this study revealed that serum CHIP level is significantly correlated with multiple risk factors of CVD and may be one of the predictors of CVD risk and death in MHD patients.

Microbial composition of carapace, feces, and water column in captive juvenile green sea turtles with carapacial ulcers.

Introduction: Green sea turtles are endangered marine reptiles. Carapacial ulcers will develop on juvenile green sea turtles during artificial rescue, seriously affecting their health and potentially leading to death. Methods: To determine the pathogens causing ulcerative carapacial disease, we performed 16S and ITS high-throughput sequencing, and microbial diversity analysis on samples from carapacial ulcers, healthy carapaces, feces, and seawater of juvenile green sea turtles. Results: Our analysis showed that changes in microbial diversity of green sea turtle feces and seawater were not significantly associated with ulcerative carapacial disease. Discussion: Psychrobacter sp. is the dominant species in the carapacial ulcers of green sea turtles. The bacterium is present in both healthy turtles and seawater where carapacial ulcers did not occur and decreasing seawater temperatures are likely responsible for the infection of juvenile green turtles with Psychrobacter sp. This is the first study on carapacial ulcers in captive juvenile green sea turtles. Our research provides theoretical guidance for the prevention and control of carapacial ulcers in captive juvenile green sea turtles.

The regulation of macrophage polarization by hypoxia-PADI4 coordination in Rheumatoid arthritis.

BACKGROUND: Hypoxia, a common feature of rheumatoid arthritis (RA), induces the over-expression of peptidyl arginine deiminase 4 (PADI4) in fibroblast-like synoviocytes (FLSs) and macrophages. However, the roles of PADI4 and its inducer hypoxia in the regulation of macrophage polarization remain unclear. This study aimed to investigate the role of hypoxia-PADI4 for macrophage polarization in RA patients. METHODS: Synovial tissue (ST) and synovial fluid (SF) were collected from 3 OA patients and 6 RA patients. The distribution of M1 and M2 in ST and cytokines in SF were examined by immunohistochemical analysis and Bio-Plex immunoassays. THP-1 macrophages and BMDM polarization were determined under normoxic (21% oxygen) or hypoxic (3% oxygen) conditions. The effects of PADI4 on macrophages were determined by transfection of adenovirus vector-coated PADI4 (AdPADI4) and the use of PADI4 inhibitor. Finally, the roles of PADI4 in joint synovial lesions on macrophage polarization were investigated in collagen-induced arthritis (CIA) rats. RESULTS: We found increased macrophage polarization of M1 and M2 in the RA ST, compared with OA ST. The ratio of M1/M2 for RA and OA was 1.633 ± 0.1443 and 2.544 ± 0.4429, respectively. The concentration of M1- and M2-type cytokines was higher in RA than that in OA patients. Hypoxia contributed to the increase of the gene and protein expression of M1 and M2 markers. M1- but not M2-type gene expression showed a positive relationship with PADI4 expressionwhile the level of expression of M2-type genes showed no significant difference. The degree of joint swelling and destruction was effectively alleviated, and the number of macrophages especially M1 decreased in CIA rats after down-regulating PADI4 expression. CONCLUSION: Hypoxia is responsible for the co-polarization of M1 and M2. Hypoxia-associated PADI4 is responsible for M1 macrophage activation, implying that the inflammatory environment can be eased by decreasing PADI4 expression and improving the hypoxic environment.

Correlation of Serum Adropin Levels with Risk Factors of Cardiovascular Disease in Hemodialysis Patients.

Background: Many preclinical studies have shown that adropin has physiological effects such as regulating glucose, lipid, and energy metabolism, protecting endothelial cells and antiatherosclerosis. Our aim is to explore whether adropin is correlated with risk factors of cardiovascular disease (CVD) in hemodialysis (HD) patients. Methods: We recruited 170 HD patients and 120 healthy controls. The serum adropin concentration and clinical characteristics were measured. Results: The serum adropin concentration in HD patients was significantly lower than that in healthy controls and which in HD patients with CVD or diabetes mellitus (DM) was significantly lower than that in patients without CVD or DM. The correlation analysis showed that serum adropin levels were correlated negatively with Age, CVD history, DM history, C-reactive protein, type B natriuretic peptide, phosphorus, intact parathyroid hormone, carotid artery plaque amount and carotid intima-media thickness (CIMT), left ventricular septal thickness (LVSTd), and left ventricular posterior wall thickness, whereas it was correlated positively with albumin, hemoglobin, serum creatinine and Kt/V, and ejection fraction value. Partial correlation analysis verified that serum adropin levels were correlated negatively with CIMT, and multiple linear regression analysis revealed that low serum adropin levels may be one independent predictors of CIMT. However, the partial correlation analysis and multiple linear regression analysis did not identify the significant correlation between serum adropin levels and LVSTd. Conclusions: Our study revealed that serum adropin level is significantly correlated with risk factors of CVD and low serum adropin levels may be a potential predictor of CVD in HD patients.

Differentially expressed lnc-NOS2P3-miR-939-5p axis in chronic heart failure inhibits myocardial and endothelial cells apoptosis via iNOS/TNFα pathway.

Inflammatory cytokine-induced cell apoptosis is important for initiation and progression of chronic heart failure (CHF). Non-coding RNAs, including long non-coding RNAs and microRNAs, have emerged as critical regulators of this pathological process. The role in regulating inflammation and induction to cell apoptosis in CHF is not well understood. This study found CHF patients had elevated serum miR-939-5p, with greater increase in New York Heart Association (NYHA) I-II patients than in NYHA III-IV. Moreover, miR-939-5p was positively correlated with B-type natriuretic peptide (BNP) in NYHA III-IV patients, while not in NYHA I-II. Further study showed miR-939-5p mimics promoted cell proliferation and inhibited inflammatory cytokine-induced apoptosis of HUVECs and H9C2, while inhibition of endogenous miR-939-5p produced the opposite effects. Induced nitric oxide synthase (iNOS) and tumour necrosis factor α (TNFα) were identified as target genes of miR-939-5p. Additionally, lncRNA-NOS2P3 acted as an endogenous sponge RNA to inhibit miR-939-5p expression, regulate the expression of iNOS/TNFα and control inflammation-induced cells apoptosis. These suggest that CHF patients exhibited elevated serum miR-939-5p level especially in NYHA I-II grades. And lnc-NOS2P3-miR-939-5p-iNOS/TNFα pathway regulated inflammatory cytokine-induced endothelial and myocardial cells apoptosis and provided a promising strategy for diagnosis and treatment of CHF.