Adult ; Antigens, CD1 ; metabolism ; Female ; Histiocytosis, Langerhans-Cell ; complications ; metabolism ; pathology ; surgery ; Humans ; Mediastinoscopy ; Myasthenia Gravis ; complications ; metabolism ; pathology ; surgery ; S100 Proteins ; metabolism ; Thymus Gland ; metabolism ; pathology ; surgery

Adolescent ; Humans ; Male ; Parasomnias

Objective To investigate the extracellular regulated protein kinases (ERKs) pathway of hepatitis B virus(HBV) X protein(HBx) on glomerular mesangial cell(GMC) proliferation of rat and tumor necrosis factor(TNF)-? expression.Methods The HBV X gene was amplified by polymerase chain reaction(PCR),inserted into the eukaryotic expression vector PCI-neo and confirmed by restrict endonuclease digestion and sequence analysis.PCI-neo contained HBV X gene (PCI-neo-X) was transfected into cultured GMC via liposome.GMC proliferation,TNF-? and its mRNA expression were investigated in the condition of with or without U0126 in the culture media.HBx,ERK1/2 and phosphorynated-ERK1/2 (p-ERK1/2) expression in GMC were assessed by Western blot.TNF-? mRNA expression was assessed by semi-quantitative reverse transcriptase-PCR (RT-PCR).TNF-? level in supernatants was measured by enzymelinked immunosorbent assay(ELISA).GMC proliferation was assessed by methyl thiazolyl tetrazolium(MTT).Results HBx expression was found in transfected GMC,and became prominent at 36 and 48 hours after transfection whether with or without U0126 in culture media.TNF-? mRNA expression was significantly decreased in U0126 group compared with U0126-free group.TNF-? levels in supernatants in PCI-neo-X transfection without U0126 group were (189.0?18.1) ng/L at 36 hours and (172.3?24.3) ng/L at 48 hours after transfection,respectively.In contrast,TNF-? levels in supernatants with U0126 were (65.6?11.6) ng/L and (84.0?24.6) ng/L,respectively.The TNF-? le-vels in the latter groups were significantly lower than the formers (Pa

Adolescent ; Child ; Child, Preschool ; Electroencephalography ; Female ; Humans ; Infant ; Retrospective Studies ; Rett Syndrome ; pathology ; physiopathology

Objective To investigate the effect of angiotenisn ⅡI (Ang Ⅱ) on RIN-m β-cell,and to explore the mechanism of β-cell function impairment caused by Ang Ⅱ.Methods RIN-m cells were cultured with various concentrations of AngⅡ (0.1,1,10,100 nmol/L).After incubation for 24 hours,the basal(3.3 mmol/L) and glucose-stimulated(16.7 mmol/L) insulin secretion(GSIS)were detected by radioimmunoassay,mRNA and protein expressions of uncoupling protein 2(UCP2)were determined by RT-PCR and Western blot,respectively.The intracellular ATP content was measured by luciferase bioluminescence.The mitochondrial membrane potential and cellular Ca~(2+) concentration were detected by flow cytometry.Results (1) Various concentrations of Ang Ⅱ had no significant influence on the basal insulin secrection of RIN-m cell(F=0.644,P = 0.634).Except for 0.1 nmol/L AngⅡ,the other concentrations of Ang Ⅱ markedly reduced GSIS of RIN-m cells(F= 118.528,P = 0.000).(2) Compared with the control group,Ang Ⅱ significantly increased mRNA and protein expression of UCP2(F= 1 370,P = 0.000;F=675.175,P = 0.000).(3)Except for 0.1 nmol/L Ang Ⅱ,the other concentrations of Ang Ⅱ significantly decreased the mitochondrial membrane potential,cellular ATP content,and cellular Ca2+ concentration of RIN-m cell(F=4.035,P=0.008;F=3.353,P = 0.013;F=5.867,P = 0.001).Conclusion Ang Ⅱ impairs GSIS of p-cell,the mechanism of impairment may be interpreted that Ang Ⅱ can increase the expression of UCP2,furthermore,it can reduce mitochondrial membrane potential,decrease the content of cellular ATP and the concentration of cellular Ca~(2+),can finally impair the function of β-cell.

The paper introduced the general picture of Xiangya Hospital in the past five years in its development of ahigh-level research hospital of international influence.Aiming at this strategic goal, the hospital proceeds by means of discipline development,talent training,research platform building, international academic exchange,performance appraisal and incentive,budget guarantee and system development.All these efforts contribute to the building of a mutual-supportive,efficient and sustainable medical science innovation system tailored to large hospitals.

Objective To investigate the effect of angiotensin Ⅱ(AngⅡ) and losartan on ? cells,and its related molecular mechanisms.Methods Normally cultured RIN-m cells were divided into three groups:control group(cultured with RPMI 1640 medium),AngⅡ group(treated with 100 nmol/L AngⅡ),losartan group(treated with 1 ?mol/L losartan 15min before addition of 100nmol/L AngⅡ).After incubation for another 48h,the apoptosis rate of RIN-m cells was quantified by flow cytometry(FCM) with Annexin-V FITC/PI dual staining.The expressions of Bcl-2 and Bax mRNA and protein were determined by RT-PCR and Western blotting,and the activities of Caspase 3 and Caspase 9 were detected by spectrophotometry.Results The apoptosis rate of RIN-m cells was significantly higher in AngⅡgroup than in both control and losartan group(P0.05).In comparison to the control group,the expressions of Bcl-2 mRNA and protein significantly declined,while of Bax mRNA and protein increased obviously in AngⅡ group(P0.05),but the expressions of Bcl-2 mRNA and protein were significantly higher(P0.05).Conclusion AngⅡ may induce the apoptosis of ? cells through mitochondrial pathway,and pre-intervention with losartan,which partly reverses the effect of AngⅡ,may play a protective effect on ? cells.

1 ?mol?L-1,and it was defined as "delayed" MTX elimination.Intra-patient variability in C48 was significant(P=0.000).Risk factors that correlated with increased C48 of MTX were boys,abnormal urine routine tests within 1 week before infusions,concurrent infections within 2 weeks before infusions,and co-administration of ceftriaxone(P