Objective To investigate the circadian change of autonomic nervous system in hyperthyroidism (HT) patients. Methods Recording 24 h dynamic electrocardiography from 33 HT patients( HT group) and 35 controls (control group). The cardiac autonomic nervous function was evaluated by the time domain and frequency domain analysis of heart rate variability( HRV). Results Comparing with control group, the SDNN, SDANN, ASDNN and rMSSD were significantly lower in HT group[ (82.3 ± 29.0)ms vs. (139.4±40.2 ) ms, ( 75.0 ± 27.4) ms vs. ( 130.3 ± 43.9) ms, (29.9 ± 14.9 ) ms vs. (57.3 ± 14.4) ms,( 19.8 ± 10.9 ) ms vs. (29.5 ± 9.4) ms ] (P ＜ 0.01 or ＜ 0.05 ), the long term total power (TP), high frequency (HF), low frequency (LF) and very low frequency (VLF) were significantly lower in HT group [ (566.1±573.2) ms2/Hz vs. ( 1894.2 ± 984.3)ms2/Hz, (68.1 ± 88.9 ) ms2/Hz vs. (232.7 ± 155.5 ) ms2/Hz, ( 127.4 ±163.0) ms2/Hz vs. (551.3 ± 390.6) ms2/Hz, (330.3 ± 300.6) ms2/Hz vs. (1073.2 ± 570.2) ms2/Hz] (P ＜0.01 ). Comparing with control group, short term VLF was higher in HT group during most time in 24 hours (P＜ 0.05 ). Short term LF was higher in HT group mainly in day time (P＜ 0.05 ). Short term HF was higher in HT group occasionally in the whole day (P＜0.05). Short term LF/HF didn't show significant difference between HT group and control group at most time points (P＞0.05).Conclusion In HT patients, cardiac chronotropic property is impaired, sympathetic activity increases in whole day, vagal activity increases correspondently but the increase in day is more marked than that in night.

Objective To investigate the relationships of nuclear factor кB (NF-кB) activation with protein kinase B (Akt) and glycogen synthase kinase 3β (GSK-3β) during amyloid-β (Aβ) (25-35) -induced apoptosis in pheochromocytoma cells (PC12 cells) of rats. Methods Apoptosis in PC12 cells was induced by A(25-35). The activities of Akt, GSK-3β and NF-кB were analyzed in this process. The Akt and GSK-3β pathways were blocked by their specific inhibitors, respectively, and the relationships of Akt and, GSK-3β with NF-кB during Aβ(25-35)-induced apoptosis in PC12 cells were determined. Results Aβ(25-35) induced apoptosis was in a dose-dependent manner. With 0, 5, 10, 20 μmol/L and 40 μmol/L Aβ(25-35) treaing for 48 h, the apoptosis rates of PC12 cells were (3. 01 ± 0.03)%, (3.08 ±0.03)%, (25.32 ± 0.76)%, ( 42.88 ± 0.60 )% and ( 60.85 ± 2.39 )% , respectively. Compared to control, both Akt and GSK-3β were suppressed during apoptosis, at meantime NF-кB was activated. The inhibited Akt activity by wortmannin leaded to decreased NF-кB activatity and increased GSK-3β activatity. Suppression of GSK-3β with its specific inhibitor LiCl caused the decreased activation of NF-кB too, but it had no significant influence on Akt activity. Conclusions These results suggest that both Akt and GSK-3β are upstream regulators of NF-кB. They co-regulate the activation of NF-кB during Aβ(25-35)-induced apoptosis in PC12 cells. This study contributes to the theoretical base for the pathogenesis of Alzheimer disease (AD) , and provides a new idea to AD prevention and therapy.

OBJECTIVE: To investigate the characteristics of adductor spasmodic dysphonia phonatory break in mandarin Chinese and select the stimuli phrases. METHOD: Thirty-eight patients with adductor spasmodic dysphonia were involved in this study. Standard phrase " fù mŭ xīn" and a speech corpus in mandarin Chinese with 229 syllables covering all vowel and constant of mandarin Chinese were selected. Every patient read the phrases above twice in normal speed and comfortable voice. Two auditory perpetual speech pathologists marked phonatory break syllables respectively. The frequency of phonatory break syllables and their located phrases were calculated, rated and described. The phrases including the most phonatory break syllables were selected as stimuli phrases, the phonatory break frequency of which was also higher than that of standard phrase "fù mŭ xīn". RESULT: Phonatory break happened in the reading of all patients. The average number of phonatory break syllables was 14 (3-33). Phonatroy break occurred when saying 177 (77.3%) syllables in the speech corpus. The syllables "guŏ, rén, zāng, diàn, chē, gè, guăn, a, bā, ne, de" broke in 23.1%-41.0% patients. These syllables belonged to the phrases "pĭng guŏ, huŏ chē, shì de, nĭ shì gè hăo rén, wŏ mén shì yŏu zŏng shì bă qĭn shì nong dé hĕn zāng, wŏ mén nà biān yŏu wăng qiú yùn dong chăng, cān gŭan, jiŭ bā hé yī gè miàn bāo dìan, tā shì duō me kāng kăi a,wŏ yīng gāi zài xìn lĭ xiĕ yī xiē shén mē ne?". Thirty-seven patients (97.3%) had phonatory break in above mentioned words. Ratios of these words phonatory break also were more than "fù mŭ xīn". CONCLUSION Adductor spasmodic dysphonic patients exhibited different degrees of phonatory break in mandarine Chinese. The phrases" shì de, pĭng guŏ, huŏ chē, nĭ shì gè hăo rén, wŏ mén nà biān yŏu wăng qiú yùn dong chăng, cān gŭan, jiŭ bā hé yī gè miàn bāo dìan, tā shì duō me kāng kăi a" were recommended as stimuli phrases for adductor spasmodic dysphonia evaluation.
Dysphonia ; diagnosis ; physiopathology ; Female ; Humans ; Language ; Male ; Phonation ; Spasm ; diagnosis ; physiopathology ; Voice

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ObjectiveTo evaluate the effects of angiotensin Ⅱ (Ang Ⅱ )infusion on renal c-Abl expression in vivo,and on podocyte c-Abl expression change in cultured mouse podocytes.Methods Twenty four male Sprague-Dawley rats (Group C,D,E and F) were assigned to receive Ang Ⅱ(400 ng· kg-1 min-1) by osmotic minipump and of which 12 rats (Group D and F) were assigned to receive telmisartan (3 mg·kg-1·d-1),six rats received normal saline(Group B),and six rats were used as normal control(Group A).Animals were sacrificed at day 14 (Group C and D),day 28 (Group E and F) respectively.Conditionally immortalized mouse podocytes were used in vitro.Podocytes were studied 2 weeks after thermoswitching from 33℃ to 37℃.Cells were fetal bovine serum(FBS) starved for at least 12 hours prior to stimulation.The cultured podocytes were treated withAngⅡdosesranging from10 -9 mol/L to10 -6 mol/L andfor differenthours.Expression of renal and podocytes c-Abl was examined by immunofluorescence staining,real-time PCR and Western blotting.Results(1) Distribution of c-Abl expression was mainly in the cytoplasm and nuclear of the podocytes in vivo and in vitro. (2) Expressions of c-Abl mRNA and protein wereincreasedinAng Ⅱ-infusedratpodocytesandAng Ⅱ-inducedculturedmouse podocytes(P＜0.05),and the effects of Ang Ⅱ were dose-dependent and time-dependent in vitro.Conclusion There are c-Abl mRNA and protein expression in podocytes,and c-Abl may play a critical role in the pathogenesis of Ang Ⅱ -induced podocyte injury.

ObjectiveTo investigate whether aldosterone infusion induces glomerular or podocyte injury in rats and to evaluate the effects of eplerenoen (EPL), andodipine (CCB) and telmisartan (ARB) on aldosterone- induced injury. MethodsThirty male Sprague-Dawley rats were divided into 5 groups: control, subcutaneous infusion of aldosterone (1.5 μg/h, ALD group) and aldosterone infusion plus eplerenone (100 mg·kg-1·d-1, EPL group), amlodipine(10 nag·kg-1·d-1 CCB group), telmisartan (3 mg·kg-1·d-1, ARB group), respectively. Systolic blood pressure(SBP) and urinary albumin excretion ratio(UAER) were measured at day 0, 7, 14, 21, 28. Blood samples were harvested to detect plasma angiotensin Ⅱ, plasma aldosterone, serum sodium, serum potassium and serum creatinine at day 28. Glomerular damge was quantified by morphological glomerular injury score (GIS). Immunohistochemistry and RT-PCR were performed to evaluate podocyte lesion, and apoptosis ratio of pedocyte (ARP) in a glomerular cross section was analyzed by TUNEL. ResultsALD infusion progressively increased SBP and UAER compared with CTL (P＜0.01). SBP was significantly reduced in EPL, CCB or ARB-treated animals, meanwhile, UAER was decreased in EPL and ARB group, but not in CCB group. The ALD-infused rats exibited hypernatremia and hypopotassaemia, which were blocked by EPL adminstration but not by CCB or ARB treatment. ARB group had a significant increase in plasma angiotensin Ⅱ compared with ALD, CCB and EPL groups(P＜0.01). The ALD-infused animals developed hyperaldosteronemia compared with CTL, but with no difference of plasma aldosterone among ALD, EPL, CCB and ARB-treated rats. Treatment with EPL prevented an increase of GIS and ARP compared with CCB and ARB (P＜0.05, P＜0.01). Protein and mRNA expression of nephfin was up-regulated in ALD group (P＜ 0.01), but was significantly prevented by EPL treatment(P＜0.01), whereas CCB and ARB therapy had no such effect. Conclusion ALD infusion significantly induces glomerular and pedocyte injury which is blocked by EPL but not by CCB or ARB independently on systemic hemodynamics.

ObjectiveTo evaluate the effects of Ang Ⅱ on apoptosis of podocytes and explore the signaling pathwayof nephrin in preventingAng Ⅱ-inducedpodocyte apoptosis.MethodsDifferentiated mouse podocytes were exposed to Ang Ⅱ at different concentrations for 18 h or at 10-8 mol/L for variable incubation times.Undifferentiated mouse pedocytes were transfected using lipofectamine 2000 with the pcDNA3.1-mNPHS1 plasmid and stably transfected cell lines were generated with G418 selection.In separated experiments,untransfected mouse podocytes (MPC) and stably transfected podocytes with pcDNA3.1-neo and PcDNA3.1-mNPHS1 were exposed toAng Ⅱ(10-8 mol/L) or LY294002(a selective Akt inhibitor,50 μmol/L) for indicated times.Apoptosis was evaluated by flow cytometry.The expression of nephrin was assessed by quantitative real-time PCR,immunofluorescence and Western blotting.The phosphorylation level of Akt was determined by Westem blotting.Results(1) AngⅡ promoted podocyte apoptosis in a dose-and time-dependentmanner. PretreatmentwithlosartansignificantlypreventedAngⅡ -induced apoptosis. (2) Nephfin mRNA and protein were obviously decreased in podocytes exposed to 10-8 mol/L Ang Ⅱ for at least 12 h than those in vehicle-treated cells (P＜0.05).(3) Ang Ⅱ exposure for more than 15 min inhibited the phosphorylation of AKT in MPC,which was dramatically reversed by pcDNA3.1-mNPHS1 transfection,but not by pcDNA3.1-neo transfection. (4) Podocyte apoptosis was promoted byLY294002. Conversely,Ang Ⅱ-induced podocyteapoptosis was significantly alleviated by pcDNA3.1-mNPHS1 transfection.ConclusionAng Ⅱinduces mouse podocyte apoptosis which is suppressed by overexpression of nephrin through PI3K-Akt signaling pathway.

Objective To observe whether dermal multipotent stem cells (dMSCs) treated with platelet-derived growth factor-AA ( PDGF-AA )could distribute more frequently to the bone marrow in rats of total body irradiation (TBI).Methods Male dMSCs were isolated and 10 μg/L PDGF-AA was added to the culture medium and further cultured for 2 h.Then the expression of tenascin-C were examined by Western blot, and the migration ability of dMSCs was assessed in transwell chamber.The pre-treated dMSCs were transplanted by tail vein injection into female rats administered with total body irradiation, and 2 weeks after transplantation, real-time PCR was employed to measure the amount of dMSCs in bone marrow.Non-treated dMSCs served as control.Results PDGF-AA treatment increased the expression of tenascin-C in dMSCs, made (1.79 ± 0.13) × 105 cells migrate to the lower chamber under the effect of bone marrow extract, and distributed to bone marrow in TBI rats, significantly more than ( 1.24 ± 0.09) ×105 in non-treated dMSCs (t = 8.833, P ＜ 0.0l ).Conclusions PDGF-AA treatment could enhance the migration ability of dMSCs and increase the amount of dMSCs in bone marrow of TBI rats after transplantation.

Objective To investigate the HBV reactivation status and clinic outcomes in the renal allograft recipients with inactive HBsAg carriers,and explore the preventive measures.Methods A retrospective analysis of clinical manifestation was processed in 88 cases of inactive HBsAg carriers before and after renal transplantation.Preoperative liver function in all cases was normal and serum HBsAg positive,HBV DNA＜106 copies/L.Tacrolimus (or cyclosporine A) + mycophenolate mofetil (MMF) + prednisone were given in prevention of rejection after transplantation.In 88 cases,56 cases were given nucleoside analogues (acid) for prophylactic antiviral therapy,in which 31 cases were given lamivudine (LAM) (LAM group),25 cases were given entecavir (ETV) (ETV group) ; The rest 32 cases were not given prophylactic antiviral therapy,only receiving routine liver-protecting therapy (inosine,glucurolactone) (control group).Incidence of HBV re-activation,liver function,response to treatment and the pathological changes of hepatic tissue were observed.Results During the follow-up period,the incidence of HBV reactivation in LAM group and ETV group was 45.2％ and 28.0％ respectively,significantly lower than in control group (84.4％,P＜ 0.05).In prophylactic treatment groups,HBV reactivation occurred later,liver function damage was milder,and HBV DNA load peak was lower (P＜0.05).In LAM group,HBV reactivation occurred in 14 cases,including 10 cases occurred during administration of LAM,and ETV treatment was given for about 2 months,serum HBV DNA levels in 7 cases were under detection line;in the rest 4 cases,HBV reactivation occurred in patients with treatment less than 1 year and noncompliance,who withdrew medicine blindly.After the original scheme of antiviral therapy was done,serum HBV DNA levels in 3 cases were under detection line,and the effect was not obvious in one case.In control group,HBV reactivation occurred in 27 cases.Fourteen cases therefore accepted nucleoside (acid) analogs antiviral therapy,and HBV DNA levels in 10 cases were under detection line.Histological examination revealed the liver with fibrotic cholestatic hepatitis changes in 9 patients,including 8 cases in control group,and 1 case in LAM group due to blind withdrawal of medicine.Conclus(i)on LAM and ETV prophylactic use may decrease the HBV reactivation rate in inactive HBsAg carriers after renal transplantation,reduce the severity of liver damage and the occurrence of fibrotic cholestatic hepatitis.

Objective To assess the safety among acute ischemic stroke patients with asymptomatic intracranial aneurysm after the administration of intravenous thrombolysis.Methods We searched database including Wanfang,CNKI,VIP,Pubmed,EMBASE,EBSCO HOST and Metstr data for all the cohort studies on the use of thrombolysis for acute ischemic patients with asymptomatic intracranial aneurysm,and ascended the correlated references listed on the articles.Meta-analysis was conducted based on the methods recommended by the Cochrane collaboration.The outcomes of the meta-analysis were intracerebral hemorrhage (ICH),symptomatic intracerebral hemorrhage (sICH),subarachnoid hemorrhage (SAH).Results Four cohort studies included 707 patients,of whom 48 patients had asymptomatic cerebral aneurysms.The risk ratio prevalence of ICH among those patients did not differ statistically with those without aneurysms (RR =1.17,95％ CI 0.69-1.99,P =0.56).No statistical differences were found in both odds ratio prevalence of sICH (OR =1.70,95％ CI 0.44-6.59,P =0.45) and SAH (OR =1.13,95％ CI 0.20-6.27,P =0.89) between the patients with asymptomatic cerebral aneurysms and those without.Conclusion Current evidence did not indicate that the risk of hemorrhage increased in acute ischemic stroke patients with asymptomatic intracranial aneurysm after the administration of intravenous thrombolysis.