Résumé
Objective:To analyze the associations between attention deficit hyperactivity disorder (ADHD) and serum vitamin B levels in children.Methods:A total of 103 ADHD children who were diagnosed in the Department of Child and Adolescent Healthcare of Children′s Hospital of Soochow University from September 2018 to April 2019 were selected as the ADHD group, and 89 children of the same age who underwent routine physical examinations served as the healthy control group.The serum levels of vitamin B, including vitamin B 1, vitamin B 2, vitamin B 6, vitamin B 9, and vitamin B 12, were measured by the methods of electrochemistry.Weiss Functional Impairment Rating Scale-Parent Report (WFIRS-P) was applied to analyze the correlation between social function scores and vitamin B levels in ADHD children. Results:The levels of vitamin B 9[(12.55±2.22) nmol/L vs.(13.26±2.54) nmol/L] and vitamin B 12 [(278.54±32.00) ng/L vs.(288.90±31.32) ng/L] in ADHD children were significantly lower than those in healthy children( t=-2.064, -2.261, all P<0.05). No significant difference was observed in serum levels of vitamin B 1, vitamin B 2 and vitamin B 6 between the 2 groups (all P>0.05). Correlation analysis displayed that only vitamin B 12 level was significantly and negatively correlated with social function in the learning/school dimension ( r=-0.208, P=0.035), and no significant correlation was found between other vitamin B levels and social function (all P>0.05). Conclusions:The serum levels of vitamin B 9 and B 12 in ADHD children were obviously lower than those in healthy children of the same age.Serum vitamin B 12 deficiency had an influence on the social function of the learning/school in ADHD children.Attention to the monitoring and timely supplementation of vitamin B in childhood, especially vitamin B 9 and B 12, may be of positive significance in the prevention of the occurrence and development of ADHD to some extent.
Résumé
Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder among children and adolescents, and it is commonly accompanied with other developmental and psychological disorders.The prevalence of obesity in children continues to rise, and it is also a major social public concern that threatens human health.As a somatic comorbidity with ADHD, obesity is characterized by a high incidence.In this paper, the focus would be placed on the underlying mechanisms of ADHD accompanied with obesity from the aspects of genetics, perinatal period, environmental and neurobiological factors, which could provide a theoretical basis and intervention strategies for the early identification, rational treatment and long-term comprehensive management, as well as prevention and treatment effects of ADHD and its comorbidities.
Résumé
<p><b>OBJECTIVE</b>To observe the effect and mechanism of ginsenoside Rg1 in inducing senescence human leukemia K562 cell line.</p><p><b>METHOD</b>Proliferation of K562 cell line induced by Rg1 was detected by MTT colorimetric test for the purpose to screen optimal active concentration and time (20 micromol x L(-1) , 48 h). Impact of Rg1 on cell cycle was analyzed using flow cytometry. The percentage of staining positive cells was detected by SA-beta-Gal staining. The expressions of senescence-related genes such as p16, p53, p21, Rb, were detected by RT-PCR and the changes in ultramicro-morphology were observed by transmission electron microscopy.</p><p><b>RESULT</b>Rg1 can significantly inhibit the proliferation of K562 cells in vitro and arrest the cells in G2/M phase. The percentage of positive cells stained by SA-beta-Gal was dramatically increased (P < 0.05) and the expression of cell senescence-related genes were up-regulated. The observation of ultrastructure showed that cell volume increase, heterochromatin condensation and fragmentation, mitochondrial volume increase, lysosomes increase in size and number.</p><p><b>CONCLUSION</b>Rg1 can induce the senescence of leukemia cell line K562 and play an important role in regulating p53-p21-Rb, p16-Rb cell signaling pathway.</p>