ABSTRACT
Objective@#To examine pubertal timing across body mass index (BMI) trajectory under polygenic susceptibility in boys and girls,and to provide a reference basis for children’s adolescent development deviation form early intervention strategies.@*Methods@#All the participants were recruited from 1 to 3 grade in 2016 from 2 Bengbu primary school and were followed up for 3 consecutive years. The study comprised 997 children (418 boys) with available data for height, weight, BMI, breast Tanner stages and testicular volume annually. The polygenic risk score (PRS) was computed based on 17 SNPs derived from published genome-wide association studies for early pubertal timing. Group-based trajectory model (GBTM) was used to identified BMI trajectory in children. Accelerated failure time model (AFT) was used to examine associations of different BMI trajectory and polygenic risk with pubertal development in boys and girls.@*Results@#Classes of BMI trajectory were persistently healthy weight, persistently overweight and persistently obesity. Adjusted concomitant variables, boys with persistently obesity exhibited 6.10-mo delay of testicular volume in low polygenic risk group (adjusted TR=1.05，P=0.04). Compared with the girls in persistently healthy weight group, the girls with low PRS were persistently overweight or obesity, which was associated with thelarche age 3.42 and 6.84-mo earlier, respectively (adjusted TR=0.97，0.94,P<0.01). Persistently overweight or obesity in girls with moderate PRS was associated with an earlier age of thelarche timing of 6.72 and 8.96-mo, respectively (adjusted TR=0.94，0.92, P<0.01). At high PRS groups, the persistently obese girls were found to have a more advanced age (10.80 and 12.96-mo, respectively) of thelarche (adjusted TR=0.90，0.88, P<0.01).@*Conclusion@#Persistently overweight and obesity is associated with early thelarche in girls, but persistently obesity may increase delayed puberty risk in boys with low polygenic risk.
ABSTRACT
Objective:To observe the effects of toadpoison and arsenic on the ultrastructure of dental pulp,Methods :Dental pulp of 36 teeth in 3 dogs was exposed by operation and then direct dressing with toadpoison paste or arsenic paste was performed. 1,2,6 and 24 hours after operation ,the pulps were processed and examinedunder a trasmission electron microscope (JEM-2000EX). Results:In toadpoison treated group ,the deformityof the basernembrane of pulp nerve ,swelling of metochondrion,degeneration of nerve axite were observed 1 h after dressing,and were more obvious in 2, 6 and 24 h. Damage of capillary and pulp cells were alsoobserved.In arsenic treated group ,swelling and break of capillaries ,deformity and degeneration of mitochondrion and endoplasmic reticulum in endoepithelial cells were observed,and were more obvious following time lasting. Damages of pulp nerve and pulp cells were also observed. Conclusion:Toadpoison and arsenic are toxic to pulp tissues. But the angiotoxicity of arsenic is stronger than that of toadpoison,the neurotoxicity and protoplasmic toxicity of toadpoison are stronger than those of arsenic.
ABSTRACT
Linolenic acid containing selenium was synthesized and brought into emul- sion(82). Its aatitumor effects were tested in vitro and in vivo. As a result, when 82 was injected peritoneally into mice(200mg?kg-1?d-1), its inhibitory rate on mouse S180 was 42.6%(P