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1.
Frontiers of Medicine ; (4): 174-181, 2018.
Article in English | WPRIM | ID: wpr-772757

ABSTRACT

The relationship between vitamin D deficiency and idiopathic central precocious puberty (ICPP) has been recently documented. In this study, 280 girls diagnosed with ICPP and 188 normal puberty control girls of similar ages were enrolled and retrospectively studied. The ICPP group had significantly lower serum 25-hydroxyvitamin D (25[OH]D) levels than the control group. Furthermore, a nonlinear relationship was found between serum 25[OH]D and ICPP, and a cut-off point for serum 25[OH]D was found at 31.8 ng/ml for ICPP with and without adjusting the different confounding factors. Girls with serum 25[OH]D ≥ 31.8 ng/ml had a lower odds ratio (unadjusted: OR 0.36, 95% CI 0.15 to 0.83, P < 0.05; height and weight adjusted: OR 0.44, 95% CI 0.18 to 1.08, P = 0.072; BMI adjusted: OR 0.36, 95% CI 0.16 to 0.84, P < 0.05). The ICPP subjects with 25[OH]D deficiency had a higher body mass index (BMI) than the subjects from the two other subgroups. Correlation analysis showed that vitamin D level is correlated with BMI and some metabolic parameters in the ICPP group. Our study suggested that vitamin D status may be associated with ICPP risk and may have a threshold effect on ICPP.


Subject(s)
Child , Female , Humans , Body Mass Index , China , Linear Models , Logistic Models , Multivariate Analysis , Puberty, Precocious , Blood , Retrospective Studies , Vitamin D , Blood , Vitamin D Deficiency , Epidemiology
2.
The Journal of Practical Medicine ; (24): 176-179,183, 2018.
Article in Chinese | WPRIM | ID: wpr-697575

ABSTRACT

Objective To observe the effect of complement 5a receptor(C5aR)antagonist(PMX53)and palmitic acid(PA)on the inflammatory reaction of microglia,and to investigate the roles and mechanisms of com-plement C5a-C5aR in PA induced microglia inflammation.Methods Microglia from one day old mice was collect-ed,purified and identified by primary culture and immunohistochemical staining,and then was randomly divided into three groups including PA group,PA+PMX53 group and control group.The expressions of tumor necrosis factor-α(TNF-α),Iba-1 and ERK1/2 were determined by ELISA,Western blot and QT-PCR.Results In PA group, the levels of Iba-1 and TNF-α were higher significantly than the control group(P<0.001).Similarly,the levels of ERK1/2 mRNA(P = 0.005 6)and p-ERK1/2 protein(P < 0.001)in the PA group were higher significantly than that in control group in spite of no difference in ERK1/2 protein in all groups. However,the levels of Iba-1,p-ERK1/2 protein,ERK1/2 mRNA and TNF-α in the PA+PMX53 group were significantly lower than that in the PA group(P<0.001),although there was no difference in ERK1/2 protein in all groups.Conclusions C5a receptor antagonist suppresses inflammatory reaction of microglia induced byPA,suggesting that C5a-C5aR-ERK may par-ticipate in the inflammation of microglia induced byPA. Therefore,C5a receptor antagonist may protect the brain tissues from inflammation-induced damage.

3.
Chinese Journal of Perinatal Medicine ; (12): 222-226, 2015.
Article in Chinese | WPRIM | ID: wpr-469118

ABSTRACT

Objective To explore the febrile response and placental pathological inflammation of pregnant rats exposed to intrauterine infection in late gestation.Methods Pregnant Sprague-Dawley rats at gestational day 18 were randomly divided into control group and intrauterine-infected group with six rats in each.The intrauterine-infected group was intraperitoneally injected with 350 μ g/kg lipopolysaccharide to establish a rat model of intrauterine infection,while the control group was injected with sterile saline of the same dose.Core temperature was measured every 1 h after intraperitoneal injection of lipopolysaccharide or saline for 8 h.At gestational day 19,after anesthesia,the placentas were taken and stained with HE.The expression levels of tumor necrosis factor-α,interleukin-6,and interleukin-1β in the placenta were determined by enzyme linked immunosorbent assay.Student t test was used for statistical analysis.Results (1) There was no temperature difference between the two groups before experimental treatment (P > 0.05).Core temperature was increased 1 h after the lipopolysaccharide injection,reaching (37.67 ±0.08) ℃.The increase of temperature was significant compared with the control group [(37.13 ± 0.08) ℃,t=10.178,P < 0.01].Fever was lowered 2 h later and the rats became hypothermic with body temperature below 37 ℃ in the intrauterine-infected group.The body temperature in the intrauterine-infected group after 2-6 h was (37.70 ± 0.10),(37.23 ± 0.05),(36.57 ± 0.06),(36.60 ± 0.10) and (36.57 ± 0.08) ℃,respectively,compared with the control group [(36.83 ±0.12),(36.63 ± 0.12),(36.71 ± 0.07),(36.87±0.12),and (36.77±0.08) ℃,respectively],the differences being all statistically significant (t=11.402,11.163,-4.025,-4.000 and-4.243,all P < 0.01).(2) HE staining revealed large amounts of neutrophils infiltration,vascular enlargement and congestion in the placenta of the intrauterine-infected rats.No inflammatory cell infiltration was observed in the control placentas.(3) The expression levels of proinflammatory cytokine tumor necrosis factor-α [(0.62 ± 0.02) ng/g],interleukin-6 [(66.12 ± 5.11) ng/g],and interleukin-1β [(7.09± 1.23) ng/g] in the intrauterine-infected group were higher than those in the control group [(0.27±0.01),(16.71 ±1.55) and (2.86 ± 0.38) ng/g,respectively].The differences were all statistically significant (t=-26.608,-18.749 and-5.714,all P < 0.01).Conclusion After exposure to lipopolysaccharide in late gestation,pregnant rats show significant inflammatory response in the placenta,with suppression of febrile response and presence of hypothermia.

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