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Objective To investigate the pubertal growth patterns and anthropometric characteristics of the patients with adolescent idiopathic scoliosis(AIS) by anthropometry measurements. Methods The anthropometric data of 256 AIS girls were collected. The mean age of diagnosis was 14.1 years old(from 12 to 16 years old). The children with more than 10 degree of the scoliosis angle at coronal level were diagnozed as AIS. The control group consisted of 462 age-matched health girls. Four variables were measured: height, sitting height, arm span and menstrual states. Height and sitting height were adjusted using Bjure formula to make up the height loss from spinal deformity. The above variables were analyzed between AIS group and the controls. Results There were no differences in the composition of age between two groups. There were no significant differences in height,sitting height and arm span between the 256 cases of AIS girls and the 462 controls. However, the corrected height and sitting height were significantly higher in AIS than those of the controls. The menstrual onset time was earlier in AIS than that in controls. There were no statistical differences in corrected height, corrected sitting height and arm span between AIS girls and the controls at the age group of 12 years old. On the contrary, the AIS girls showed shorter uncorrected height than the controls did at this age. However, the scoliotic girls were found in the corrected height, the corrected sitting height and the arm span significantly taller than the controls between ages of 13 and 15 years. There were significant differences in corrected height and corrected sitting height between AIS girls and the controls at the age of 16 years old, while no difference were found in the variables of height, sitting height and arm span. Conclusion There is an abnormal growth pattern in AIS during pubertal growth spurt, which may be related to the pathogenesis of AIS.

9.Hyperthermia aggravates focal cerebral ischemia-reperfusion injury in rats by down-regulating claudin-1 expression

Chunli ZHANG ; Zengyun QIU ; Qiang MENG

International Journal of Cerebrovascular Diseases 2013;21(10):775-780

Objective To investigate the impact of hyperthermia on the expression of claudin-1 in focal cerebral ischemia-reperfusion injury in rats and its mechanism in ischemic cerebral injury.Methods A total of 100 male Sprague-Dawley rats were randomly divided into 3 groups:sham operation,normothermia and hyperthermia groups.Both the normothermia and hyperthermia groups were redivided into 3 time points:Ischemia (1 hour) and reperfusion for 3,6,and 24 h.A model of middle cerebral artery occlusion was induced by the intraluminal suture method.At 24 h after reperfusion,brain water content was measured by the wet and dry weight method.The volume of cerebral infarction was assessed by 2,3,5 triphenyl tetrazolium chloride staining.At 3,6,and 24 h after reperfusion,the claudin-1 expression in ischemic brain tissue was measured by Western blot and immunohistochemical staining Results At 24 h after reperfusion,the mean neurological function score in the normothermia group was significantly lower than that in the hyperthermia group (2.3 ± 0.48 vs.3.2 ± 0.63; t =3.576,P =0.002).The brain water content on the operated sides in the sham operation,normothermia and hyperthermia groups was 79.31％ ± 0.60％,81.13％ ± 0.12％,and 84.4％ ± 0.55％,respectively.There were significant differences (F=147.115,P=0.000).Western blot analysis showed that at 3,6,and 24 h after reperfusion,the expression levels of claudin-1 in the normothermia and hyperthermia groups were significantly lower than the sham operation group (all P =0.000),and the expression levels of claudin-1 progressively decreased with the extension of ischemia-reperfusion time (all P ＜ 0.05).At the same time point,the expression level of claudin-1 in the hyperthermia group was significantly lower than that in the normothermia group (all P ＜ 0.01).At 3 and 6 h after reperfusion,the positive expression of claudin-1 among the cerebrovascular endothelial cells was observed in the sham operation,normothermia and hyperthermia groups,while at 24 h after reperfusion,no claudin-1 positive cells were observed.Compared to the sham operation group,at 3 h after reperfusion,the numbers of claudin-1 positive cell and claudin-1 IOD/area (integrated optical density/accumulated positive cell area) in the normothermia and hyperthermia groups begin to decrease,they decreased significantly at 6 h and disappeared at 24 h (P=0.000).At 3 and 6 h after reperfusion,claudin-1 IOD/area in the hyperthermia group was significantly lower than that in the normothermia group (all P ＜ 0.01).Conclusions During cerebral ischemia-reperfusion,hyperthermia may aggravate ischemic brain edema and brain injury by down-regulating the expression of claudin-1 in blood-brain barrier.