Factors associated with trait anger level of juvenile offenders in Hubei province: A binary logistic regression analysis.

The risk factors of high trait anger of juvenile offenders were explored through questionnaire study in a youth correctional facility of Hubei province, China. A total of 1090 juvenile offenders in Hubei province were investigated by self-compiled social-demographic questionnaire, Childhood Trauma Questionnaire (CTQ), and State-Trait Anger Expression Inventory-II (STAXI-II). The risk factors were analyzed by chi-square tests, correlation analysis, and binary logistic regression analysis with SPSS 19.0. A total of 1082 copies of valid questionnaires were collected. High trait anger group (n=316) was defined as those who scored in the upper 27th percentile of STAXI-II trait anger scale (TAS), and the rest were defined as low trait anger group (n=766). The risk factors associated with high level of trait anger included: childhood emotional abuse, childhood sexual abuse, step family, frequent drug abuse, and frequent internet using (P<0.05 or P<0.01). Birth sequence, number of sibling, ranking in the family, identity of the main care-taker, the education level of care-taker, educational style of care-taker, family income, relationship between parents, social atmosphere of local area, frequent drinking, and frequent smoking did not predict to high level of trait anger (P>0.05). It was suggested that traumatic experience in childhood and unhealthy life style may significantly increase the level of trait anger in adulthood. The risk factors of high trait anger and their effects should be taken into consideration seriously.

Factors Associated with Trait Anger Level of Juvenile Offenders in Hubei Province: A Binary Logistic Regression Analysis / 华中科技大学学报（医学）（英德文版）

The risk factors of high trait anger of juvenile offenders were explored through question naire study in a youth correctional facility of Hubei province,China.A total of 1090 juvenile offenders in Hubei province were investigated by self-compiled social-demographic questionnaire,Childhood Trauma Questionnaire (CTQ),and State-Trait Anger Expression Inventory-Ⅱ (STAXI-Ⅱ).The risk factors were analyzed by chi-square tests,correlation analysis,and binary logistic regression analysis with SPSS 19.0.A total of 1082 copies of valid questionnaires were collected.High trait anger group (n=316) was defined as those who scored in the upper 27th percentile of STAXI-Ⅱ trait anger scale (TAS),and the rest were defined as low trait anger group (n=766).The risk factors associated with high level of trait anger included:childhood emotional abuse,childhood sexual abuse,step family,frequent drug abuse,and frequent internet using (P＜0.05 or P＜0.01).Birth sequence,number of sibling,ranking in the family,identity of the main care-taker,the education level of care-taker,educational style of care-taker,family income,relationship between parents,social atmosphere of local area,frequent drinking,and frequent smoking did not predict to high level of trait anger (P＞0.05).It was suggested that traumatic experience in childhood and unhealthy life style may significantly increase the level of trait anger in adulthood.The risk factors of high trait anger and their effects should be taken into consideration seriously.

Association of ß-adrenergic receptor genes polymorphisms with incidence of subsequent cardiovascular events in Han Chinese patients with coronary artery disease.

BACKGROUND: Sequence variants in the ß-adrenergic receptor (ADRB) genes have a close relationship with the development of coronary artery disease (CAD) and the patient's prognosis. However, there is a lack of data on the role of the variants in ADRBs genes in Han Chinese patients with CAD. We aimed to investigate the association of genetic variants in the ADRB1 and ADRB2 genes with the incidence of major adverse cardiac event (MACE) in Han Chinese patients with CAD. METHODS: A total of 545 Han Chinese patients with CAD undergoing percutaneous coronary intervention (PCI) were recruited to the study and followed for one year. Three variant sites in ADRB1 (rs1801253) and ADRB2 (rs1042713 and rs1042714) were genotyped. The effect of the ADRB1 and ADRB2 genotypes on MACE within one year was assessed. RESULTS: There were 47 cases of MACE during follow-up. There was no significant difference in the incidence of MACE among patients carrying different genotypes of the three variants in ADRB1 and ADRB2 (Log-rank, all P > 0.05). Cox regression analysis showed no association between three variants in ADRB1 and ADRB2 genes and the incidence of MACE during one-year follow-up, the adjusted hazard ratios (95% confidence interval) for rs1801253, rs1042713 and rs1042714 were 1.05 (0.54-2.02), 1.24 (0.58-2.64) and 1.66 (0.81-3.42), respectively. CONCLUSION: Our data did not support a relationship between the three polymorphisms of ADRB1 (rs1801253) and ADRB2 (rs1042713 and rs1042714) genes and risk of subsequent cardiovascular events after PCI in Han Chinese patients with CAD.

Lack of association between lipoprotein(a) genetic variants and subsequent cardiovascular events in Chinese Han patients with coronary artery disease after percutaneous coronary intervention.

BACKGROUND: Elevated lipoprotein(a) [Lp(a)] levels predict cardiovascular events incidence in patients with coronary artery disease (CAD). Genetic variants in the rs3798220, rs10455872 and rs6415084 single-nucleotide polymorphisms (SNPs) in the Lp(a) gene (LPA) correlate with elevated Lp(a) levels, but whether these SNPs have prognostic value for CAD patients is unknown. The present study evaluated the association of LPA SNPs with incidence of subsequent cardiovascular events in CAD patients after percutaneous coronary intervention (PCI). METHODS: TaqMan SNP genotyping assays were performed to detect the rs6415084, rs3798220 and rs10455872 genotypes in 517 Chinese Han patients with CAD after PCI. We later assessed whether there was an association of these SNPs with incidence of major adverse cardiovascular events (MACE: cardiac death, nonfatal myocardial infarction, ischemic stroke and coronary revascularization). Serum lipid profiles were also determined using biochemical methods. RESULTS: Only the rs6415084 variant allele was associated with higher Lp(a) levels [41.3 (20.8, 74.6) vs. 18.6 (10.3, 40.9) mg/dl, p < 0.001]. During a 2-year follow-up period, 102 patients suffered MACE, and Cox regression analysis demonstrated that elevated Lp(a) (≥30 mg/dl) levels correlated with increased MACE (adjusted HR, 1.69; 95% CI 1.13-2.53), but there was no association between LPA genetic variants (rs6415084 and rs3798220) and MACE incidence (p > 0.05). CONCLUSIONS: Our data did not support a relationship between genetic LPA variants (rs6415084 and rs3798220) and subsequent cardiovascular events after PCI in Chinese Han CAD patients.

Irbesartan and emodin on myocardial remodeling in Goldblatt hypertensive rats.

OBJECTIVE: Interactions between the renin-angiotensin system and transforming growth factor-beta 1 (TGF-ß1) have been well documented. The aim was to explore the effect of irbesartan combining with emodin on myocardial remodeling in Goldblatt (2K-1C) hypertensive rats. METHODS: All 60 Sprague-Dawley rats were randomly divided into 5 groups as follows: the sham-clipped without any drugs; 2K-1C without any drugs; the 2K-1C with irbesartan (50 mg/kg/day); the 2K-1C with emodin (80 mg/Kg/day); and the 2K-1C with irbesartan and emodin together for the last 8 weeks of a 12-week period of study. The outcome measures included left ventricular mass index, TGF-ß1 and angiotensin II in the left ventricle, mRNA expression of TGF-ß1, and connective tissue growth factor (CTGF). RESULTS: Compared with 2K1C group, the 2K1C/irbesartan group and 2K-1C/emodin plus irbesartan group had significantly lower systolic blood pressure and local angiotensin II (P < 0.05). The left ventricular mass index in each of the 3 treatment groups was significantly lower than that in the 2K1C group, especially in the combined group. The mRNA/protein TGF-ß1 and the mRNA CTGF of 2K1C/irbesartan group, 2K1C/emodin group, and 2K-1C/emodin plus irbesartan group were significantly decreased compared with 2K-1C group (P < 0.05). CONCLUSIONS: Irbesartan or emodin or 2 drugs together can inhibit myocardial remodeling in renovascular hypertension rats probably by reducing TGF-ß1 and CTGF expression. The combination of irbesartan and emodin is better than single drug application.