OBJECTIVE: To study the correlation between vitamin D receptor genetic polymorphism FokⅠand vitamin D deficiency rickets in children between 1 to 3 years old, and to explore the significance of hereditary factors in the development of vitamin D deficiency rickets. METHODS: Sixty-two children with vitamin D deficiency rickets and 60 healthy children as a control group were enrolled. Serum levels of 25-hydroxyvitamin D3 were measured using ELISA. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genetic analysis method was used. A restriction fragment length polymorphism in the vitamin D receptor genetic polymorphism Fok I was tested. The frequencies of the vitamin D receptor genotype and allele were compared between the two groups. RESULTS: Serum 25-hydroxyvitamin D3 levels in the rickets group were significantly lower than those in the control group ( 9.1±4.1 ng/mL vs 16.1±6.9 ng/mL; P<0.05 ). FF genotype in the vitamin D receptor genetic polymorphism Fok I was more common in the rickets group than in the control group (53% vs 25%; P<0.05). F allele frequency in the rickets group was significantly higher than that in the control group (73% vs 57%; P<0.05). CONCLUSIONS: There is a correlation between vitamin D receptor genetic polymorphism Fok I and vitamin D deficiency rickets. This suggests that vitamin D receptor genetic polymorphism might play an important role in determining susceptibility to development of vitamin D deficiency rickets.[Chin J Contemp Pediatr, 2010, 12 (7):544-546]
OBJECTIVE: To investigate the impact of intrauterine infection induced by LPS injection on long-term brain development of premature rats. METHODS: Eighteen day-gestation pregnant rats were randomly assigned to a control group receiving an intraperitoneal injection of normal saline, and two infection groups that were intraperitoneally injected with 0.3 mg/kg or 0.6 mg/kg LPS. Twenty-four hours after injection, 7 pregnant rats of each group were sacrificed. The pathological changes of the placenta after hematoxylin and eosin staining were observed under a light microscope. The neural cell apoptosis of fetal brains was examined by the TUNEL assay. The remained pregnant rats were induced to labour before 21 gestation days. The long-term brain development of premature rats was tested with the Y type electric maze on postnatal day 42. RESULTS: Obvious pathological changes were observed in the placenta in the infection groups. The apoptotic neural cells in the fetal brain increased in the infection groups compared with that in the control group (32.41±5.36 in the 0.3 mg/kg infection group and 66.41±7.61 in the 0.6 mg/kg infection group vs 8.00±0.36 in the control group; P<0.01). The number of trials to criterion in the Y type maze test in the infection groups was much more than that in the control group [117.8±8.7 (0.3 mg/kg infection group) and 194.4±13.7 (0.6 mg/kg infection group) vs 56.8±3.7 (control group); P<0.01]. The number of correct reactions in memory retaining in the infection groups was lower than that in the control group (0.62±0.09 in the 0.3 mg/kg infection group and 0.37±0.09 in the 0.6 mg/kg infection group vs 0.92±0.06 in the control group; P<0.05). CONCLUSIONS: Intrauterine infection can cause fetal rats' neural cell apoptosis and affect adversely long-term brain development of neonatal rats.[Chin J Contemp Pediatr, 2010, 12 (7):569-572]