Plasma 25-hydroxyvitamin D deficiency in the peri-operative period is associated with survival outcome in colorectal cancer patients: a meta-analysis.

AIM: Surgery had a significant impact on 25-hydroxyvitamin D (25-(OH)D) levels. Uncertainty still existed regarding the effects of peri-operative 25(OH)D deficiency on colorectal cancer (CRC) patients' prognosis. The purpose of the present study was to explore the potential association between the peri-operative 25(OH)D deficiency and the survival outcome of CRC. METHODS: Seven electronic databases [including PubMed, EMBASE, Web of Science, The Cochrane Library, OvidMEDLINE(R), China National Knowledge Infrastructure (CNKI) and Wangfang data] were searched without language limitations. The primary outcomes were overall survival and all-cause mortality. Secondary outcomes were the incidence of 25(OH)D deficiency and risk variables for low 25(OH)D level in the peri-operative period. RESULTS: 14 eligible studies were obtained with 9324 patients for meta-analysis. In the peri-operative period, the pooled incidence of blood 25(OH)D deficiency was 59.61% (95% CI: 45.74-73.48). The incidence of blood 25(OH)D deficiency post-operatively (66.60%) was higher than that pre-operatively (52.65%, 95% CI: 32.94-72.36). Male (RR = 1.09, 95% CI: 1.03-1.16), rectum tumor (RR = 1.23, 95% CI: 1.03-1.47), spring and winter sampling (RR = 1.24, 95% CI: 1.02-1.49) were the risk factors for the 25(OH)D deficiency. The association between the low 25(OH)D post-operatively and short-term overall survival (HR = 0.43, 95% CI: 0.24-0.77) was most prominent, while a low 25(OH)D pre-operatively (HR = 0.47, 95% CI: 0.31-0.70) was more significantly associated with long-term all-cause mortality than that after surgery. CONCLUSION: Peri-operative 25(OH)D impacted the CRC patients' prognosis. Due to possible confounding effects of systemic inflammatory response (SIR), simultaneous measurement of vitamin D and SIR is essential for colorectal survival.

Factors Influencing Readiness for Hospital Discharge among Patients Undergoing Enterostomy: A Descriptive, Cross-sectional Study.

OBJECTIVE: To examine the factors influencing hospital discharge readiness among Chinese patients who have undergone enterostomy. METHODS: In this descriptive, cross-sectional study, researchers recruited patients with colorectal cancer who underwent enterostomy at a tertiary hospital in Guangdong Province, China, via convenience sampling between January 2021 and January 2023. Participants completed the Readiness for Hospital Discharge Scale, Ostomy Self-care Ability Scale, and Stoma-Quality of Life-Chinese Questionnaire (Chinese version) at the time of hospital discharge. Univariate, correlation, and multiple linear regression analyses were performed to explore the impact of self-care ability, quality of life, and other clinicodemographic characteristics on patients' readiness for hospital discharge. RESULTS: Of the 200 questionnaires distributed, 177 (88.5%) were completed and included in the final analysis. The median scores for the factors considered in this study were as follows: Readiness for Hospital Discharge Scale was 148.00 (interquartile range [IQR], 117.50, 164.00), self-care intention of the Ostomy Self-care Ability Scale was 36.00 (IQR, 34.00, 40.00), self-care knowledge of the Ostomy Self-care Ability Scale was 17.00 (IQR, 15.00, 19.00), self-care skill of the Ostomy Self-care Ability Scale was 5.00 (IQR, 3.00, 6.00), and the total score for quality of life was 60.00 (IQR, 49.00, 69.00). Multiple linear regression analysis identified several key factors explaining 48.2% of the variance in global readiness for hospital discharge: global quality of life (ß = .347, P < .001), self-care knowledge (ß = .259, P < .001), leakage during hospitalization (ß = -0.241, P < .001), monthly family income (ß = .148, P = .008), stoma siting before surgery (ß = .130, P = .020), and self-care intention (ß = .127, P = .035). CONCLUSIONS: The readiness for hospital discharge among patients undergoing enterostomy in this study was high. Factors such as quality of life, self-care knowledge, leakage during hospitalization, monthly family income, stoma siting before surgery, and self-care intention after undergoing enterostomy influenced the patients' readiness for hospital discharge. Therefore, future studies should focus on developing interventions to enhance patients' readiness for hospital discharge.

Effect of beraprost on pulmonary hypertension due to left ventricular systolic dysfunction.

Beraprost is used to treat peripheral chronic arterial occlusive disease. However, the efficacy and safety of beraprost in patients with pulmonary hypertension (PH) due to left ventricular systolic dysfunction (PH-HFrEF) remains unknown. The primary objective of this study was to determine the effects of beraprost on PH-HFrEF.We prospectively recruited patients with PH-HFrEF as determined by echocardiography and right cardiac catheterization. Beraprost sodium was given orally (1 µg/kg/d) added to the usual treatment, and patients were evaluated at 1-year follow-up.Twenty-five patients were recruited with baseline systolic pulmonary artery pressure (PAP) of 49.5 ±â€Š10.8 mm Hg. Systolic PAP results at 3, 6, 9, and 12 months were 39.1 ±â€Š8.1, 30.4 ±â€Š5.2, 27.7 ±â€Š3.0, and 27.0 ±â€Š4.7 mm Hg, respectively, which were all significantly lower than systolic PAP at baseline (P < .05). Left ventricular ejection fraction results at 6 months (43.5 ±â€Š7.0%), 9 months (47.0 ±â€Š5.5%), and 12 months (48.2 ±â€Š4.8%) were significantly higher than at baseline (34.7 ±â€Š9.2%) (P < .05). Six-minute walking distance at 3 months (282.8 ±â€Š80.6 m), 6 months (367.1 ±â€Š81.2 m), 9 months (389.8 ±â€Š87.1 m), and 12 months (395.7 ±â€Š83.4 m) increased with time, and all were significantly higher than baseline (190.1 ±â€Š75.5 m) (P < .05). One patient developed atrial fibrillation and recovered to sinus rhythm after intravenous administration of amiodarone. There were no instances of cardiac-related death, severe bleeding, or severe impairment of liver function.Routine oral administration of beraprost sodium added to the usual treatment may improve cardiopulmonary hemodynamics and exercise capacityin patients with PH-HFrEF.

Vitamin D Supplementation in the Treatment of Chronic Heart Failure: A Meta-analysis of Randomized Controlled Trials.

BACKGROUND: In recent years, there has been growing evidence that vitamin D deficiency is associated with the development and progression of chronic heart failure (CHF). HYPOTHESIS: Additional supplementation of vitamin D may have protective effects in patients with CHF. METHODS: We searched PubMed, Embase, and Cochrane databases through June 2015 and included 7 randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in patients with CHF. Then, we performed a meta-analysis of clinical trials to confirm whether vitamin D supplementation is beneficial in CHF patients. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated using fixed- or random-effects models. RESULTS: Our pooled results indicated that additional supplementation of vitamin D was not superior to conventional treatment in terms of left ventricular ejection fraction, N-terminal pro-B-type natriuretic peptide, and 6-minute walk distance. Moreover, vitamin D supplementation was associated with significant decreases in the levels of tumor necrosis factor-α (WMD: -2.42 pg/mL, 95% CI: -4.26 to -0.57, P < 0.05), C-reactive protein (WMD: -0.72 mg/L, 95% CI: -1.42 to -0.02, P < 0.05), and parathyroid hormone (WMD: -13.44 pg/mL, 95% CI: -21.22 to -5.67, P < 0.05). CONCLUSIONS: Vitamin D supplementation may decrease serum levels of parathyroid hormone and inflammatory mediators in CHF patients, whereas it has no beneficial effects on improvement of left ventricular function and exercise tolerance.

Association between serum corin levels and risk of acute myocardial infarction.

BACKGROUND: Accumulating evidence has indicated that corin plays critical roles in regulating salt-water balance, blood pressure and cardiac function by activating natriuretic peptides. The present case-control study was designed to evaluate the association of serum soluble corin with acute myocardial infarction (AMI). METHODS: We enrolled 856 consecutive AMI patients and 856 control subjects and explored the possible relation between serum corin levels and AMI risk using logistic regression model. RESULTS: Patients with AMI had higher BMI, were less physically active, and were more likely to have histories of hypertension, diabetes, hyperlipidemia and smoking compared with the controls. Serum levels of corin were remarkably reduced in AMI patients (825±263pg/ml) compared with those in healthy controls (1246±425pg/ml). Odds ratios of ST elevation (STEMI) and non-ST elevation myocardial infarction (NSTEMI) were significantly decreased with the increasing levels of serum corin in both men and women (P for trend, <0.001) after adjustment for body mass index, hypertension, diabetes, hyperlipidemia, smoking, and physical activity. CONCLUSIONS: Our study demonstrates that serum levels of corin are significantly decreased in AMI patients, and it is inversely associated with the incidences of STEMI and NSTEMI in both men and women.

Inverse Correlation Between Plasma Adropin and ET-1 Levels in Essential Hypertension: A Cross-Sectional Study.

Adropin is a recently identified bioactive protein that promotes energy homeostasis by affecting glucose and lipid metabolism. Recently, adropin has also been reported to be associated with endothelial dysfunction. Also, ET-1, as a biomarker for endothelial dysfunction, is a key regulator in hypertension. Accordingly, the aim of the present study was to detect the relationship between plasma adropin and ET-1 levels in hypertension. A total of 123 participants, diagnosed with primary hypertension on the basis of World Health Organization criteria (systolic blood pressure [SBP] ≥ 140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 mmHg), and 58 normotensive subjects were enrolled in the cross-sectional study from October 2011 to December 2013. All study participants were older than 18 years of age. Adropin and ET-1 levels were measured by enzyme-linked immunosorbent assay (ELISA). We found that plasma adropin levels were significantly lower in hypertensives compared with controls (3.18 ± 1.00 vs 4.21 ± 1.14 ng/mL, P < 0.001). Plasma ET-1 levels were higher in hypertensives than controls (2.60 ± 1.14 vs 1.54 ± 0.66 pg/mL, P < 0.001). Adropin had a negative correlation with DBP (r = -0.40, P < 0.001), SBP (r = -0.49, P < 0.001), and adjusted for age, body mass index, SBP, DBP, glucose, TC, TG, LDL, and Cr, there was a negative correlation between ET-1 and adropin (r = -0.20, P = 0.04). In multivariate logistic regression analysis of the variables, ET-1 (odds ratio [OR], 3.84; 95% CI, 2.16-6.81; P < 0.001) and adropin (OR, 0.99; 95% CI, 0.99 -1.0; P <  .001) were found to be independent predictors for hypertension.In conclusion, decreased plasma adropin levels are associated with increased blood pressure in hypertension. Adropin is an independent predictor for hypertension, and may influence blood pressure by protecting endothelial function.

Antioxidant effects of hydrogen sulfide on left ventricular remodeling in smoking rats are mediated via PI3K/Akt-dependent activation of Nrf2.

There is growing evidence that oxidative stress plays critical roles in the pathogenesis of cardiac remodeling. In the present study, we established a rat model of passive smoking and investigated the antioxidant effects of hydrogen sulfide (H2S) on smoking-induced left ventricular remodeling. Cardiac structure and function were evaluated using 2-dimensional echocardiography. Myocardial fibrosis was detected by Masson's trichrome staining and immunohistochemistry. Oxidative stress was assessed by measuring malondialdehyde levels, superoxide dismutase and glutathione peroxidase activities, and reactive oxygen species generation in the myocardium. Neonatal rat cardiomyocytes transfected with specific siRNA and exposed to cigarette smoke condensate and H2S donor sodium hydrosulfide were used to confirm the involvement of Nrf2 and PI3K/Akt signaling in the antioxidant effects of H2S. Our results indicated that H2S could protect against left ventricular remodeling in smoking rats via attenuation of oxidative stress. Moreover, H2S was also found to increase the phosphorylation of Akt and GSK3ß and decrease the nuclear expression of Fyn, which consequently leads to nuclear translocation of Nrf2 and elevated expression of HO-1 and NQO1. In conclusion, H2S may exert antioxidant effects on left ventricular remodeling in smoking rats via PI3K/Akt-dependent activation of Nrf2 signaling.

Etanercept attenuates myocardial ischemia/reperfusion injury by decreasing inflammation and oxidative stress.

The protective role of etanercept in myocardial ischemia/reperfusion is not well understood. The aim of this study was to investigate whether etanercept modulates neutrophil accumulation, TNF-α induction and oxidative stress in an ischemia/reperfusion injured rat heart model. Rats were randomly exposed to sham operation, myocardial ischemia/reperfusion (MI/R) alone, MI/R+ etanercept. The results demonstrated that compared to MI/R, etanercept reduced myocardial infarction area, myocardial myeloperoxidase (MPO) levels, serum creatinine kinase (CK) and lactate dehydrogenase (LDH) levels, and both serum and myocardial TNF-α production. Etanercept also markedly enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and reduced the level of malondialdehyde (MDA) in MI/R rats. In summary, our data suggested that etanercept has protective effects against MI/R injury in rats, which may be attributed to attenuating inflammation and oxidative stress.

[Correlation of serum adropin level with coronary artery disease].

OBJECTIVE: To explore the correlation of serum adropin level with coronary artery disease (CAD). METHODS: According to coronary angiography, 356 consecutive patients with chest complaints from January 2011 to July 2012 were divided into 2 groups of CAD (n = 264, with CAD) and control (n = 92, without CAD). The serum adropin level and other CAD related metabolic parameters were measured and SYNTAX score was calculated. RESULTS: Serum adropin level was significantly lower in group CAD than that in control group ((56 ± 15) vs (83 ± 10) ng/L, P < 0.01).Serum adropin levels in high, mild, low SYNTAX score group were (60 ± 22),(56 ± 12),(54 ± 10) ng/L respectively, and there was no significant difference among 3 groups(P = 0.116). Multivariate regression analysis revealed that adropin was an independent risk factor for CAD (OR = 0.849, 95%CI:0.817-0.882, P < 0.01). CONCLUSIONS: Lower serum adropin level is significantly associated with CAD. Thus it indicates a possible role of adropin in the prevention of CAD.

Inhibitory effects of hydrogen sulphide on pulmonary fibrosis in smoking rats via attenuation of oxidative stress and inflammation.

Accumulating evidence has demonstrated that hydrogen sulphide (H2 S) is involved in the pathogenesis of various respiratory diseases. In the present study, we established a rat model of passive smoking and investigated whether or not H2 S has protective effects against pulmonary fibrosis induced by chronic cigarette smoke exposure. Rat lung tissues were stained with haematoxylin-eosin and Masson's trichrome. The expression of type I collagen was detected by immunohistochemistry. Oxidative stress was evaluated by detecting serum levels of malondialdehyde, superoxide dismutase and glutathione peroxidase and measuring reactive oxygen species generation in lung tissue. Inflammation was assessed by measuring serum levels of inflammatory cytokines, including high-sensitivity C-reactive protein, tumour necrosis factor-α, interleukin (IL)-1ß and IL-6. The protein expression of Nrf2, NF-κB and phosphorylated mitogen-activated protein kinases (MAPKs) in the pulmonary tissue was determined by Western blotting. Our findings indicated that administration of NaHS (a donor of H2 S) could protect against pulmonary fibrosis in the smoking rats. H2 S was found to induce the nuclear accumulation of Nrf2 in lung tissue and consequently up-regulate the expression of antioxidant genes HO-1 and Trx-1 in the smoking rats. Moreover, H2 S could also reduce cigarette smoking-induced inflammation by inhibiting the phosphorylation of ERK 1/2, JNK and p38 MAPKs and negatively regulating NF-κB activation. In conclusion, our study suggests that H2 S has protective effects against pulmonary fibrosis in the smoking rats by attenuating oxidative stress and inflammation.

Hydrogen sulfide improves left ventricular function in smoking rats via regulation of apoptosis and autophagy.

The present study was designed to investigate the protective effects of hydrogen sulfide (H2S) against cigarette smoking-induced left ventricular dysfunction in rats. Left ventricular structure and function were assessed using two-dimensional echocardiography. Cardiomyocyte apoptosis was determined by Annexin V/PI and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Cardiac autophagy was evaluated by detection of autophagy-related protein expression and observation of autophagosomes. Our results indicated that administration of NaHS (a donor of H2S) could protect against smoking-induced left ventricular systolic dysfunction. H2S was found to exert anti-apoptotic effects in the myocardium of smoking rats by inhibiting JNK and P38 mitogen-activated protein kinases pathways and activating PI3K/Akt signaling. Moreover, H2S could also reduce smoking-induced autophagic cell death via regulation of AMPK/mTOR signaling pathway. In conclusion, our study demonstrates that H2S can improve left ventricular systolic function in smoking rats via regulation of apoptosis and autophagy.

Protective effects of valsartan against cigarette smoke-induced left ventricular systolic dysfunction in rats.

OBJECTIVES: To investigate the protective effects of valsartan against smoking-induced left ventricular dysfunction and explore the potential mechanisms involved. METHODS: Rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke), valsartan group (exposed to cigarette smoke and treated orally with valsartan), and control group. Transthoracic echocardiography was performed to evaluate left ventricular systolic and diastolic function. Oxidative stress was evaluated by detecting malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the supernatant of left ventricular tissue. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-α), and monocyte chemotactic protein-1 (MCP-1) were detected to reflect the extent of systemic inflammation. RESULTS: The echocardiographic data indicated that valsartan has protective effects against cigarette smoke-induced left ventricular systolic dysfunction (LVSD). Our findings showed a significant decrease in MDA level and increases in SOD and GSH-Px activities in the valsartan group compared to the smoking group. The apoptotic rate in the valsartan group was significantly lower than in the smoking group. The concentrations of hs-CRP, IL-6, TNF-α and MCP-1 in the valsartan group were significantly lower than in the smoking group. CONCLUSIONS: Our study demonstrates that valsartan has protective effects against smoking-induced LVSD by attenuating oxidative stress, apoptosis, and inflammation.

Overexpression of APRIN inhibits differentiation and proliferation and promotes apoptosis in P19 embryonal carcinoma cells.

We have previously demonstrated that androgen-induced proliferation inhibitor (APRIN) expression was upregulated in ventricular septum tissues from patients with ventricular septal defect (VSD). The present study was designed to investigate the effects of APRIN on P19 cell differentiation, proliferation and apoptosis. In this study, we established a stable APRIN-overexpressing P19 embryonal carcinoma cell line that can differentiate into myocardial cells when treated with 1 % dimethyl sulfoxide. Our data showed that mRNA expressions of myocardial cell differentiation-related genes (such as cTnT, α-MHC, GATA4, and MEF2C) in the APRIN-overexpressing P19 cells were downregulated compared to the empty-vector controls. Our findings also indicated that P19 cells overexpressing APRIN had a reduced growth rate and a decreased S phase of the cell cycle. Moreover, the apoptotic rate in P19 cells overexpressing APRIN was significantly higher than that in the controls. In conclusion, our study demonstrates that overexpression of APRIN inhibits differentiation and proliferation and promotes apoptosis in P19 cells, suggesting that APRIN may be involved in the pathogenesis of VSD.

Trimetazidine protects against smoking-induced left ventricular remodeling via attenuating oxidative stress, apoptosis, and inflammation.

Trimetazidine, a piperazine derivative used as an anti-anginal agent, improves myocardial glucose utilization through inhibition of fatty acid metabolism. The present study was designed to investigate whether trimetazidine has the protective effects against smoking-induced left ventricular remodeling in rats. In this study, Wistar rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke), trimetazidine group (exposed to cigarette smoke and treated with trimetazidine), and control group. The echocardiographic and morphometric data indicated that trimetazidine has protective effects against smoking-induced left ventricular remodeling. Oxidative stress was evaluated by detecting malondialdehyde, superoxide dismutase, and glutathione peroxidase in the supernatant of left ventricular tissue. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Gene expression and serum levels of inflammatory markers, including interleukin-1ß, interleukin-6, and tumor necrosis factor-α, were deteced by quantitative real-time PCR and enzyme-linked immunosorbent assay. Our results suggested that trimetazidine could significantly reduce smoking-induced oxidative stress, apoptosis, and inflammation. In conclusion, our study demonstrates that trimetazidine protects against smoking-induced left ventricular remodeling via attenuating oxidative stress, apoptosis, and inflammation.