[Therapeutic effect of scalp acupuncture combined with rehabilitation training on balance dysfunction in children with spastic hemiplegia].

OBJECTIVE: To investigate the therapeutic effect of scalp acupuncture and rehabilitation training on balance dysfunction in children with spasmodic hemiplegia so as to provide the reference to the optimization of treatment scheme. METHODS: A total of 60 children with spastic hemiplegia were divided into a routine group and a scalp acupuncture group, 30 cases in each one according to random number table. In the routine group, the rehabilitation training was provided, including exercise training, balance training, spasmotherapy apparatus, electromyography biofeedback apparatus and orthoses. In the scalp acupuncture group, on the base of the treatment as the routine group, scalp acupuncture was supplemented at motor area, foot motor sensory area, equilibrium area and parietal temporal anterior oblique line. Separately, before the treatment, after 3 months treatment and after 6 months treatment, the dimension D and E of the gross motor function measure-88 (GMFM-88) and Berg balance scale (BBS) were adopted to evaluate balance related motor functions and equilibrium function. The differences in the above 3 indicators at different time stages were compared in children between the two groups. RESULTS: Compared with the score before the treatment, BBS score was obviously increased after 3 and 6 months treatment in the patients of the two groups respectively (P<0.05). The score in the dimension D and E after 6-month treatment was increased significantly as compared with the score before treatment and after 3-month treatment in the same group respectively (P<0.05). Compared with the routine group, the score of dimension D and E of GMFM-88 as well as BBS score were all increased obviously in the scalp acupuncture group after 3 and 6 months treatment (P<0.05). CONCLUSION: On the base of routine rehabilitation training, scalp acupuncture can improve balance function of children with spastic hemiplegia better.

Prepubertal exposure to an oestrogenic mycotoxin zearalenone induces central precocious puberty in immature female rats through the mechanism of premature activation of hypothalamic kisspeptin-GPR54 signaling.

Sporadic epidemics and several researches in rodents indicated that zearalenone (ZEA) and its metabolites, the prevailing oestrogenic mycotoxins in foodstuffs, were a triggering factor for true precocious puberty development in girls. Nevertheless, the neuroendocrine mechanism through which ZEA mycoestrogens advance puberty onset is not fully understood. To elucidate this issue, hypothalamic kisspeptin-G-protein coupled receptor-54 (GPR54) signaling pathway that regulates the onset of puberty was focused on in the present study. Immature female SD rats were given a daily intragastric administration of corn oil (vehicle control), 50 µg/kg body weight (bw) of 17ß-estradiol (E2, positive control), and 3 doses (0.2, 1 and 5 mg/kg bw) of ZEA for consecutive 5 days starting from postnatal day 15, respectively. Puberty onset was evaluated by detecting the physiological and hormonal responses, and hypothalamic kisspeptin-GPR54 pathway was determined to reveal the neuroendocrine mechanism. As the markers of puberty onset, vaginal opening was significantly accelerated and uterine weight was increased in both E2 and 5 mg/kg ZEA groups. Serum levels of follicle stimulating hormone, luteinizing hormone and estradiol were also markedly elevated by E2 and 5 mg/kg ZEA, which is compatible with the changes in peripheral reproductive organs. The mRNA and protein expressions of hypothalamic gonadotropin-releasing hormone (GnRH) were both obviously elevated by E2 and 5 mg/kg ZEA. GnRH expression changes occurred in parallel with increased expressions of hypothalamic Kiss1 and its receptor GPR54 at both mRNA and protein levels. Most of these changes were also noted in 1 mg/kg ZEA group, but none in 0.2 mg/kg group. Therefore, within the context of this study, the No Observed Adverse Effect Level (NOAEL) for ZEA in terms of oestrogenic activity and puberty-promoting effect in immature female rats was considered to be 0.2 mg/kg bw per day, and the Lowest Observed Adverse Effect Level (LOAEL) was 1 mg/kg bw per day. In conclusion, prepubertal exposure to dietary relevant levels of ZEA induced central precocious puberty in female rats by premature activation of hypothalamic kisspeptin-GPR54-GnRH signaling pathway, followed by the stimulation of gonadotropins release at an earlier age, resulting in the advancement of vaginal opening and enlargement of uterus at periphery.

In ovo exposure of a Fusarium mycotoxin butenolide induces hepatic and renal oxidative damage in chick embryos, and antioxidants provide protections.

Butenolide is a mycotoxin produced by several toxigenic Fusarium species. It frequently invades many important grains, and evokes a broad spectrum of toxic effects. For these reasons, butenolide poses a health risk to both humans and animals. However, many toxicology issues of butenolide including targets and mechanisms of toxicity remain to be elucidated so far. The present study therefore attempts to reveal the toxic profile of butenolide from a viewpoint of oxidative damage, using chick embryos as an in vitro model. A single in ovo injection of butenolide resulted in significant oxidative injuries in embryonic livers and kidneys, as manifested by a dose-dependent depletion of sulfhydryl groups, reduction of glutathione peroxidase activity, and increase of thiobarbituric acid reactive substances production, an indicator of lipid peroxidation. In contrast, co-injections of butenolide with antioxidants sodium selenite, vitamin C and a representative antioxidative enzyme superoxide dismutase markedly abated these oxidative toxicities. In conclusion, the present study suggests that oxidative damage may serve as a mediator in the toxicity of butenolide, and amelioration of antioxidant defense capacity by exogenous supplementation may play a role in the prevention and treatment of butenolide intoxication.