Objective To investigate the effect and mechanism of melatonin on bioactivity of fibroblasts from human hypertrophic scar.Methods Fibroblasts from hypertrophic scar were cultured and incubated with melatonin,melatonin and Luzindole,and Luzindole,respectively,for 24 h,and the media as control.XTT/PMS assay was used to measure the proliferation of fibroblasts,ELISA assay to detect the TGF-β1 production of fibroblasts,and the expression of cell a-SMA,collagen Ⅰ,collagen Ⅲ mRNA were determined with real-time PCR method.Results Compared with the control,melatonin at the concentration of 10-5mmol/L,10-3mmol/L,and 1 mmol/L could inhibit the proliferation of fibroblasts in a does-dependent manner (P＜0.05); melatonin at the concentration of 10-3 mmol/L could significantly decrease the TGF-β1 production and expression of a-SMA mRNA and collagen Ⅰ mRNA in fibroblasts from human hypertrophic scar (P＜0.05) ; the effect of melatonin on fibroblast was significantly blocked by Luzindole (P＜0.05),but melatonin could not inhibit collagen Ⅲ mRNA expression (P＞0.05).Conclusions Melatonin can significantly regulate the biological activity of fibroblasts from human hypertrophic scar through a receptor pathway.

Objective To investigate of the tissue TGF-β changes at early stage of hypertrophic scar formation and the value of scar blisters in hypertrophic scar.Methods The TGF-β1 content in the blister fluid and the blood were quantified with ELISA,patients(n=15)with hypertrophy scar after depth burn were included,three time point(each n=5)on early　stage(<3 months)of hypertrophy scar formationwere monitored.and normal skin blister fluid and the blood(n=5)was used as control.Results The serum TGF-β1 in the both hypertrophic scar patients and normal skin group was not elevated(P>0.01),the TGF-β1 in the blister of normal skin was also not elevated(P>0.01),but TGF-β1 level in the scarblisters hypertrophic scar was elevated significantly[<60 d(158.5±69.8)pg/L,60-90 d,(181.1±40.1)pg/L,>90 d,(534.4±125.9)pg/L,P<0.01] and higher than the normal skin blister and the blood(P<15.6 pg/L.P<0.01),the increased TGF-β1 1evel in the hypertrophic scar blisters were persisted for at least three months.the TGF-β1 level of scar blister on the 3th month of hypertrophic scar formation reached a peak [(534.4±125.9)pg/L,P<0.01].Conclusions The data in this study indicates that TGF-β production at the early stage of hypertrophic scar formation is increased and may play an important role in scar formation;scar blisters is a valuable approach in hypertrophic scar study.

Objective To explore the clinical features,electroneurophysiology,neuroimaging and gene characteristics of one juvenile dentatorubral-pallidoluysian atrophy (DRPLA) pedigree with an onset of epilepsy.Methods The clinical data of the elder sister and younger brother in a family with juvenile DRPLA were collected.Furthermore,their clinical manifestations,electroneurophysiology results,neuroimaging characteristics and atrophin-1 gene CAG repeat numbers were detected and analyzed in detail.Results There were four patients in this family in total.The probands were two siblings,and they both had the onset manifestation of epilepsy.The younger brother had frequently epileptic seizure,marked cerebellar ataxia,involuntary movement and mental retardation.Compared with her younger brother,the sister had light symptoms such as mild memory deterioration without ataxia and involuntary movement,and she could undertake some simple work.The spike wave and sharp wave complex can be detected in electroencephalogram (EEG) examination,the cortical center segment lesions pathological changes were revealed in somatosensory evoked potentials (EP),and the latency period of P300 was prolonged in the both siblings.Magnetic resonance imaging (MRI) showed that the younger brother had marked atrophies in the cerebral cortex,brainstem and cerebellum.Furthermore,MRI showed that the elder sister had only mild atrophies in the cerebral cortex,brainstem and cerebellum,and that on the contrary some abnormally high signals were observed in cerebral cortex but not white matter.DRPLA gene detection revealed that the numbers of CAG repeats were 15/68 (the younger brother) and 15/64 (the elder sister),respectively.Conclusions Epilepsy,especially the myoclonus,is a common clinical manifestation for juvenile DRPLA,and many other types of epileptic seizures may arise with the development of DRPLA.DRPLA has diverse clinical heterogeneity.EEG,EP and brain MRI examination are great for DRPLA diagnosis and differential diagnosis,and the specific gene detection can be helpful for a definitive diagnosis.