Summary We prospectively examined bone growth patterns in 894 children aged 6–17 years at the baseline visit, with a 6-year follow-up.
Results show bone “tracking” over a six-year interval and sexual dimorphism of bone attained levels and timing of peak bone
growth. Our findings underscore childhood and adolescence as critical periods for building bone and developing gender differences.
Introduction Bone growth patterns were prospectively examined in 894 Chinese children (496 males), aged 6–17 yrs, from a population-based
twin cohort. Whole-body bone area (BA), bone mineral content (BMC), and bone mineral density (BMD) were measured by DEXA at
baseline and a 6-yr follow-up.
Methods Graphic smoothing plots and generalized estimating equations were used to model bone attained levels, growth, and “tracking”.
Results Attained levels of BMC and BA increased curvilinearly with age. Male attained levels were higher than females after age ∼15 yr,
but BMD was lower between 13–17 yrs (Tanner stage I to IV). In both genders, peak BMC and BMD growth lagged ∼2 yrs behind
peak BA growth, which lagged 2 yrs behind peak height growth. Peak bone growth occurred 1–3 yrs later in males. Over the 6-yr
follow-up, all bone measurements “tracked”, but “shifting” across ranks also occurred, and baseline tertile ranking influenced
bone growth. Females with early menarche had higher attained levels than females with late menarche at age 12–13 yrs.
Conclusion Our findings confirm and expand previous studies on peak bone growth conducted in Caucasian cohorts, particularly sexually
dimorphic and maturational effects. The significant “tracking” of bone measurements in this 6-yr follow-up study underscores
the importance that osteoporosis prevention should begin in childhood and adolescence.
Fengxiu Ouyang and Binyan Wang contributed equally to this article.
Source(s) of support: This study is supported in part by grant R01 HD049059, R01 HL0864619 and R01 AR045651 from the National
Institute of Health and by the Food Allergy Project. 相似文献
Background: Preconditioning the brain with relatively safe drugs seems to be a viable option to reduce ischemic brain injury. The authors and others have shown that the volatile anesthetic isoflurane can precondition the brain against ischemia. Here, the authors determine whether isoflurane preconditioning improves long-term neurologic outcome after brain ischemia.
Methods: Six-day-old rats were exposed to 1.5% isoflurane for 30 min at 24 h before the brain hypoxia-ischemia that was induced by left common carotid arterial ligation and then exposure to 8% oxygen for 2 h. The neuropathology, motor coordination, and learning and memory functions were assayed 1 month after the brain ischemia. Western analysis was performed to quantify the expression of the heat shock protein 70, Bcl-2, and survivin 24 h after isoflurane exposure.
Results: The mortality was 45% after brain hypoxia-ischemia. Isoflurane preconditioning did not affect this mortality. However, isoflurane preconditioning attenuated ischemia-induced loss of neurons and brain tissues, such as cerebral cortex and hippocampus in the survivors. Isoflurane also improved the motor coordination of rats at 1 month after ischemia. The learning and memory functions as measured by performance of Y-maze and social recognition tasks in the survivors were not affected by the brain hypoxia-ischemia or isoflurane preconditioning. The expression of Bcl-2, a well-known antiapoptotic protein, in the hippocampus is increased after isoflurane exposure. This increase was reduced by the inhibitors of inducible nitric oxide synthase. Inducible nitric oxide synthase inhibition also abolished isoflurane preconditioning-induced neuroprotection. 相似文献