Leukocyte Rho kinase activity and serum cystatin C affect cardiovascular events in acute coronary syndrome.

OBJECTIVE: This study was designed to investigate the effects of leukocyte Rho kinase activity and serum Cystatin C (Cys C) on cardiovascular events in patients with acute coronary syndrome (ACS). METHODS: A total of 48 patients with ST-segment elevation myocardial infarction (STEMI), 23 patients with non-ST-segment elevation myocardial infarction (NSTEMI), 25 patients with unstable angina (UA) and 20 patients with no-acute coronary syndrome as control from January 2017 to June 2018 in Tianyou Hospital affiliated to Wuhan University of Science and Technology were selected in this study. Western blot was used to detect the leukocyte Rho kinase activity and Elisa kit was used to measure serum Cys C. Univariate and multivariate analysis were used to analyze the influencing factors of cardiovascular events in ACS patients. RESULTS: The activity of leukocyte Rho kinase and serum Cys C were gradually reduced in the STEMI, NSTEMI and UA patients, but all significantly higher than that in No-ASC patients, and there was a positive correlation between leukocyte Rho kinase activity and serum Cys C in ACS patients (r = 0.516, P < .001). The activity of leukocyte Rho kinase was positively correlated with the levels of serum TNF-α (r = 0.634, P < .001), IL-6 (r = 0.578, P < .001), IL-8 (r = 0.582, P < .001) in ACS patients, and the level of Cys C was positively correlated with the levels of serum TNF-α (r = 0.634, P < .001), IL-6 (r = 0.578, P < .001), IL-8 (r = 0.582, P < .001) in ACS patients. Univariate and multivariate analysis showed that the leukocyte Rho kinase activity (HR = 2.994, 95%CI = 1.328-6.054, P < .0001) and the levels of serum Cys C (HR = 1.692, 95%CI = 1.028-2.124, P < .0001) were independent influencing factors of cardiovascular events in ACS patients. CONCLUSION: The leukocyte Rho kinase activity and serum Cystatin C are high in acute coronary syndrome patients, and are the independent influencing factors of cardiovascular events in ACS patients.

Impact of parental weight status on children's body mass index in early life: evidence from a Chinese cohort.

OBJECTIVES: To understand whether parents' weight status before conception predicts body mass index (BMI) of their offspring in early life and the differences between the mother-child and father-child associations. DESIGN: A birth cohort study. SETTING: Conducted at the Community Health Service Centre in Shenyang, Wuhan and Guangzhou. PARTICIPANTS: A total of 2220 live birth newborns were recruited randomly after consent of their parents, and 1178 were followed up until 2 years old. METHODS: Parental demographics, maternal characteristics during pregnancy, children's anthropometric data and feeding patterns at 1 month old were collected. BMI was calculated and BMI Z-scores (BMI_Z) were generated by referring to WHO growth standard. Parental weight status was categorised into underweight, normal weight, and overweight and obese according to the Working Group of Obesity in China. General linear models and generalised linear models were used to assess the associations between parents and offspring. OUTCOME MEASURES: The primary outcomes were descriptive data on child's sex-specific anthropometric variables. The secondary outcomes were BMI_Z and weight status of children at each time point. RESULTS: No gender difference was observed in BMI_Z or overweight or obesity rates from birth to 24 months old, although boys were significantly heavier and had a greater length/height than girls (P<0.05). The overweight and obesity rates of children peaked at 12 months old. Maternal BMI/weight status had a significant but small effect on BMI_Z at birth, but not on the paternal side. The impact of parental BMI on child's BMI_Z after birth was similar at each follow-up. Offspring with underweight mothers tend to have reduced BMI_Z after birth while overweight/obese fathers had children with a greater BMI_Z. CONCLUSIONS: Maternal weight status had small effect on both fetal and child growth after birth. Significant but mild paternal influence was only detected after birth.

Fibroblast growth factor 21 attenuates inflammation and oxidative stress in atherosclerotic rat via enhancing the Nrf1-ARE signaling pathway.

Inflammation and oxidative stress are associated with atherosclerotic progression. Fibroblast growth factor 21 (FGF21), a regulator of energy metabolism, has been reported to suppress the pathogenesis of atherosclerosis. However, the mechanism of anti-atherosclerotic effects of FGF21 remains unclear and needs to be further investigated. Transcription factor NF-E2-related 2 (Nrf2), a sensitive regulator of oxidative stress, is also associated with atherosclerotic progression. In this study, we investigated whether up-regulation of FGF21 affected inflammation and oxidative stress in atherosclerotic rats and whether the Nrf2-signaling pathway was involved in FGF21-mediated effects. Pathological changes were detected in arterial tissues of rats, and the expression of inflammatory and oxidative stress indicators, vascular endothelial markers, and Nrf2-signaling related protein were measured in the serum or/and arterial tissues of rats. As a result, expression of FGF21 and Nrf2-ARE signaling related proteins were markedly suppressed in arterial tissues of model rats. Thickness of endarteria and infiltrating cells obviously increased in atherosclerotic rats, whereas the increase of FGF21 expression could decrease thickness of endarteria. Moreover, the levels of ET-1, MDA, MCP-1, ICAM-1 and VCAM-1 were significantly higher in model rats than that in normal rats, whereas the levels of NO, GSH and T-AOC were significantly lower. Compared with model rats, up-regulation of FGF21 could increase the expression of Nrf2-ARE signaling related proteins and the level of anti-oxidative indicators, decrease the levels of endothelial dysfunction, and reduce inflammatory indicators. Down-regulation of FGF21 could reverse these actions. Therefore FGF21 reduces inflammation and oxidative stress in atherosclerotic rats via Nrf2-ARE signaling pathway.