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Kallmann syndrome ( KS) is a rare disease and characteristic of an absence of puberty, infertility, and a defective sensation of smell (anosmia or hyposmia). Here, we analyze the features of a case of KS diagnosed clinically. In addition, the etiology, genetic features, clinical manifestations, diagnosis, and treatment of KS were reviewed.
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Objective To explore the effect of arsenic trioxide (As2O3) on the migration of neurons and the potential mechanism through the establishment of primary neuron culture from the brains of neonatal rats.Methods Brain tissues were selected from SD neonatal rats for primary neuron calture.The cells were divided into 4 groups based on the addition of As2 O3:normal control group,1 μmol/L As2O3 group,10 μmol/L As2O3 group and 20 μmol/L As2O3 group.The primary neurons were treated with different concentrations of As2O3 and cultured for 24 hours.Boyden chamber assay was used to detect the effect of As2O3 on neuronal migration.Immunofluorescence laser confocal microscope was used to observe the structure of actin.Results In the control group,the cultured neurons showed a regular pattern of distribution.In the 3 groups treated with As2O3,the distribution of neurons was loose and disordered,which was most obvious in the 20 μmol/L As2O3 group.The results showed that the higher concentration of As2O3,more difficult it was for the neurons to survive.The number of neuronal migration was 64.6 ± 4.3 for normal control group,63.0 ± 7.0 for 1 μmol/L As2O3 group,54.8 ± 3.6 for 10 μmol/L As2O3 group,and 21.6 ± 3.9 for 20 μmol/L As2O3 group.The results showed that As2O3 might inhibit the migration of primary neurons in a dose-dependent manner (F =49.31,P ＜0.001).The normal actin skeleton was destroyed under the laser confocal microscope in 10 μmol/L As2O3 group and 20 μmol/L As2O3 group,while they remained unaffected in normal control group and 1 μmol/L As2O2 group.Conclusion As2 O3 exposure can reduce the neuron migration in a dose-independent manner probably through disrupting the organization of acting cytoskeleton.
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Objective To explore the effect of thyroxine (TH) on the migration of hippocampal neurons in newborn rat exposed to tritiated water (HTO).Methods The hippocampal neurons from neonatal rats were primarily cultured,7 days later,randomly divided into control group,HTO group,TH group and HTO + TH group(3.7 × 105 Bq/ml HTO and 0.3 μg/ml TH were simultaneously added).After 24 h,the distance of neuronal migration was measured with Leica AF 6000,the expressions of BDNF and Reelin mRNA in neurons were analyzed with reverse transcription polymerase chain reaction (RT-PCR),the expression of β-tubulin protein in neurons was assayed with Western blot and immunocytochemical staining.Results Compared with control group,the expression of Reelin mRNA,BDNF mRNA and β-tubulin in HTO group were significantly reduced(t =5.80,5.48,5.47,P ＜ 0.01),but those in HTO + TH group and TH group were obviously increased (t =7.75,12.06,13.65,P ＜ 0.01 ;t =4.34,5.47,5.65,P ＜0.01)and higher than that in HTO group (t =2.92,10.32,8.76,P ＜ 0.01 ;t =18.07,20.55,40.13,P ＜0.01).Accordingly,the neuronal migration distance in HTO group was much shorter than that in control (t =8.62,P ＜ 0.01),and in HTO + TH group and TH group was far longer than that in control(t =7.64,4.93,P＜0.01).Moreover,the neuronal migration distance in HTO + TH group was notably elongated in comparison with that in HTO group(t =11.32,12.31,P ＜ 0.01).Conclusions Thyroxine may promote the migration of hippocampal neurons in newborn rat exposed to HTO.