The association of C789A polymorphism in the dopamine beta-hydroxylase gene (DBH) and aggressive behaviour in dogs

The genetic basis of aggressive behaviour has been examined extensively, including analysis of genes encoding neurotransmitters, signalling molecules and regulatory enzymes, as well as their synthesis and degradation. Dopamine beta-hydroxylase, an enzyme catalysing the conversion of dopamine into norepinephrine in synaptic endings, significantly affects the modulation of emotional states and behaviour. The aim of this study was to determine the association of C789A polymorphism in the canine dopamine beta-hydroxylase gene (DBH) and aggressive behaviour in dogs. A total of 110 dogs of different breeds were analysed. All animals were classified according to their individual behavioural characteristics, defined by a veterinary interview and observation. Polymorphism was analysed using ACRS-PCR (amplification created restriction site-polymerase chain reaction) method. Significant differences in DBH genotypes and allele frequency between aggressive and non-aggressive dogs were observed (χ2 = 16,232, P = 0.0003). In aggressive dogs, the CC genotype (0.788) and C allele (0.815) were most frequent while in non-aggressive dogs, their frequencies were significantly lower (0.361 and 0.404, respectively). The obtained results indicate that DBH is a promising candidate gene for canine behavioural study.

Construction of Nursing Intervention Model and Clinical Empirical Study on Dopamine Beta Hydroxylase Gene Polymorphism in Children with ADHD

ADHD is a common disease in children, and the pathogenesis is still unclear. Attention deficit is the main manifestation of ADHD, which has a serious impact on children’s learning and growth. The treatment of ADHD is mainly western medicine, supplemented by psychotherapy. More and more studies have shown that ADHD has similar characteristics to psychological diseases, and dopamine beta hydroxylase gene abnormality is the common feature of most mental diseases. In view of the potential relationship between ADHD and dopamine β hydroxylase gene, this paper will study the polymorphism of dopamine β hydroxylase gene in children with ADHD under the nursing intervention mode. This paper is divided into three parts. The first part is theoretical research. In this part, we deeply analyze ADHD. We think that the pathogenesis of ADHD mainly comes from four factors: heredity, environment, nutrition, and behavior. In order to further test the relationship between ADHD and dopamine beta hydroxylase gene, the corresponding experimental model was established in the second part of this paper. All the samples in the experiment are from real cases. The experimental principle and specific operation steps are given in detail. In order to facilitate comparison, the same number of control groups was established in addition to the real disease. The third part is the experimental results and analysis. After a number of comparative experiments, through the analysis of experimental data, we believe that ADHD is closely related to the gene of dopamine beta hydroxylase. Among them, the A2 gene in the patient group was significantly more than that in the normal group, which further verified that ADHD has the characteristics of common psychological diseases.

Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss

Myocardial infarction (MI) can result in sympathetic nerve loss in the infarct region. However, the contribution of hypo-innervation to electrophysiological remodeling, independent from MI-induced ischemia and fibrosis, has not been comprehensively investigated. We present a novel mouse model of regional cardiac sympathetic hypo-innervation utilizing a targeted-toxin (dopamine beta-hydroxylase antibody conjugated to saporin, DBH-Sap), and measure resulting electrophysiological and Ca2+ handling dynamics. Five days post-surgery, sympathetic nerve density was reduced in the anterior left ventricular epicardium of DBH-Sap hearts compared to control. In Langendorff-perfused hearts, there were no differences in mean action potential duration (APD80) between groups; however, isoproterenol (ISO) significantly shortened APD80 in DBH-Sap but not control hearts, resulting in a significant increase in APD80 dispersion in the DBH-Sap group. ISO also produced spontaneous diastolic Ca2+ elevation in DBH-Sap but not control hearts. In innervated hearts, sympathetic nerve stimulation (SNS) increased heart rate to a lesser degree in DBH-Sap hearts compared to control. Additionally, SNS produced APD80 prolongation in the apex of control but not DBH-Sap hearts. These results suggest that hypo-innervated hearts have regional super-sensitivity to circulating adrenergic stimulation (ISO), while having blunted responses to SNS, providing important insight into the mechanisms of arrhythmogenesis following sympathetic nerve loss.