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The clinical characteristics, therapeutic effects and complications of 32 incipient patients with acute Vogt-Koyanagi-Harada ( VKH) syndrome admitted in Wuxi Second Hospital during October 2010 to September 2013 were retrospectively analyzed.There were 15 males and 17 females with a mean age of (41.3 ±14.1) years (22 -71 years), the time from the disease onset to treatment ranged from 3 to 20 days.Among 32 cases, 30 ( 94%) had premonitory symptoms. The multifocal bullous neurosensory detachment, optic disk hyperemia and edema in posterior pole of fundus were found in all cases, and exudative retinal detachment was found in 4 cases (6 eyes).The results of optical coherence tomography ( OCT) showed the macula neurosensory detachment, thick retinal neuroepithelial layer and wavy RPE layer in all patients.Fundus fluorescein angiography ( FFA) showed that scattered hyperfluorescence dots and cystic fluorescein reservoir was observed in early phase and later period respectively.Patients received intravenous methylprednisolone with the onset dose of 80 mg per day for 3-7 days and oral administration followed, which would gradually decrease later;the average treatment duration was (52.9 ±14.6) weeks. The visual acuity of 40 eyes (22 cases) was recovered to more than 0.8, and no blindness occurred after the treatment.During the treatment hair loss, depigmentation of skin and hair were found in 12 cases (38%) , and 2 cases showed short-term elevated intraocular pressure.These symptoms disappeared after drug therapy ceased.And no recurrence was found during the follow-up of 6 months.However, sunset glow fundus was found in 13 patients (26 eyes).The study shows that the diagnosis of VKH syndrome is based on the typical signs of the fundus presented on OCT and FFA.Early and systemic administration of glucocorticoids is important treatment for patients with VHK syndrome, which could decrease systemic and local complications effectively.
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Objective To investigate the expressions of protein kinase B (PKB/Akt) and glycogen synthase kinasc-3β in the hippocampus in mice with vascular dementia (VaD) induced by repetitive bilateral common carotid artery occlusion.Methods Forty-eight healthy adult male C57B1/6 mice were randomly allocated into 3 group:normal group,sham operation group,and model group (n =16 in each group).A mouse VaD model was induced by intermittent blocking the bilateral common carotid artery for 3 times in the model group.The sham group only separated the bilateral common carotid artery,but did not block it.The normal group did not receive any treatment.The behavioral changes of the mice were observed using the water maze and step-down tests at 4 weeks after procedure.HE staining was used to observe the histopathological changes of hippocampal tissue.The Western blotting was used to detect the expressions of Akt,p-Akt (Ser473),GSK3β and p-GSK3β (Ser9) proteins.Results In the water maze test,the time of swimming the entire distance was prolonged at the learning stage and memory stage (learning stage:F =19.389,P <0.05; memory stage:F =27.929,P < 0.05),the number of errors increased (learning stage:F =7.228,P < 0.05; memory stage:F =21.189,P<0.05) in the model group.In the step-down test,the response time was prolonged (F=19.162,P <0.05) at learning stage and the number of errors increased (F =6.562,P < 0.05),the latency time was shortened (F=10.634,P<0.05) and the number of errors increased (F=12.890,P<0.05) in the model group.At the same time,HE staining showed the reduction of neurons and the proliferation of glial cells in the hippocampal CA1 region in the model group; p-Akt (Ser473) (F=37.849,P<0.05) and p-GSK3β (Ser9)(F =67.725,P <0.05) protein expressions were up-regulated significantly (F =37.849,P <0.05; F =67.725,P<0.05) at 4 weeks after procedure compared to those in the sham operation group,while there were no significant differences in Akt (F =1.004,P >0.05) and GSK3β(F =0.329,P >0.05) total protein expressions among all groups.Conclusions The repetitive bilateral common carotid artery occlusion may result in learning and memory impairment and severe damage in the hippocampus in mice.The Akt and GSK3β expressions may be involved in the mechanism of VaD.
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Objective To investigate the expression of visfatin mRNA in abdominal omental adipose tissue and its relationship with blood lipid in type 2 diabetes mellitus.Methods 161 type 2 diabetic patients were divided into two groups according to triglyceride ( TG ),high triglyceride group ( TG ≥ 1.7mmol/L) and normal triglyceride group(TG < 1.7 mmol/L).The expression of visfatin mRNA in abdominal omental adipose tissue was measured with Northern Blot.Visfatin plasma concentration,fasting plasma glucose (FPG),blood lipid profiles and other biochemical indicators were also measured.Results Comparing with normal triglyceride group,the diabetic patients in high triglyceride group had significantly increased levels of visfatin plasma concentration [ ( 129.07 ± 21.35)ng/mL vs ( 101.65 ± 15.23 ) ng/mL,t =2.295,P <0.05]and mRNA expression in omental adipose tissue( P <0.05).Visfatin plasma concentration was positively correlated with TG( β =0.592,P <0.05 ) and FPG( β =0.763,P <0.01 ).Visfatin mRNA expression in omental adipose tissue had no correlation with FPG,TG and other biochemical indicators.Conclusions The plasma visfatin level in T2DM patients may be associated with triglyceride metabolism.
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Objective To investigate the association between -45C→G mutation at promoter of human urate transporter 1 gene and primary hyperuricemia. Methods The allele frequency and genotypo distribution of -45 C→G mutation at promoter of human urate trans-porter 1 gene were determined by PCR-RFLP in 217 patients with primary hyperuricemia and 419 normal controls. Results The frequencies of the G allele and CG genotype at promoter of human urate transporter 1 gene in patients were significantly higher than that in normal controls (P = 0. 031, P = 0.031). The levels of serum uric acid (UA) and triglyceride (TG) in subjects of CG genotype were significantly higher than those in the objects of CC genotype(t=3.058, t=3.699, P=0.002, P<0.001). There were no significant difference in the levels of total cholesterol (TC), fasting plasma glucose (FPG), urea nitrogen (BUN), creatinine (Cr) between the two groups (P>0.05). Conclusion The -45 C→G mutation at promoter of human urate transporter 1 gene may be related to primary hyperuricemia.
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Objective To evaluate the clinical and biochemical characteristics of type 2 diabetics with hyperuricemia and to investi-gate the association between serum uric acid and the number of metabolic syndrome components. Method In the cross-sectional study of 547 type 2 diabetics, we recorded body mass index (BMI), systolic blood pressure(SBP), diastolic blood pressure (DBP), and collected blood samples to measure serum uric acid (UA), fasting plasma glucose (FPG), glycosylated hemoglobin (HbAlc), creatinine (Cr) and blood lipid profile, including tfiglyceride (TG), total cholesterol (TC), low-density cholesterol LDL-C) and high-density cholesterol (HDL-C). Results Compared with the normal UA group, the diabetic patients in the high UA group had significantly increased levels of BMI, SBP, DBP, FPG, Cr, TG, TC and HbA1c (P <0.05, P <0.01, P <0.05, P <0.01, P <0.01), and decreased level of HDL-C(P < 0.05). There was no significant difference in the level of LDL-C between the two groups (P > 0.05). According to their possession of 1, 2, 3 or 4 components of metabolic syndrome, 547 cases were divided into four groups (MSI, MS2,MS3 and MS4). There were significant difference in the levels of UA, BMI, SBP, DBP, Cr, TG, TC, LDL-C and HDL-C among MSI, MS2, MS3 and MS4 (All P < 0.05). Multiple regression analysis showed that UA concentration was positively correlated with sex, TG and Cr (Beta:0. 088,0. 350, 0. 124; P < 0.05, P <0.01, P <0.01) and negatively correlated with HDL-C and HbA1 c(Beta: -0.107, -0.124 ; P <0.01, P <0.01). The con-centration of UA was strongly correlated with serum TG. Conclusions Serum UA level in type 2 diabetics was significantly elevated as the number of metabolic components increased. Abnormal TG had great influence on serum UA. Hyperuricemia was considered to be a dangerous factor of the metabolic syndrome.
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Objective To examine the effects of high-density lipoprotein(HDL) and lipoprotein-deficient serum(LPDS) isolated from patients with type 2 diabetes mellitus on cholesterol efflux through human skin fibroblast(HSF) and human hepatoma cell line(HepG2).Methods and Results Blood was collected from 13 patients with type 2 diabetes mellitus and 17 healthy volunteers,HDL and LPDS were isolated.Cholesterol efflux assays,RT-PCR and Western blot were performed with HSF and HepG2 cells.The HepG2 cells showed a high expression of scavenger receptor B1(SR-B1) and lack of functional ATP-binding cassette receptor A1(ABCA1) and ATP-binding cassette receptor G1(ABCG1) while HSF cells express SR-B1 at very low level and have a high expression of ABCA1 pretreated with 22-OH cholesterol.The cholesterol efflux from HepG2 cells to HDL isolated from patients with diabetes decreased significantly as compared to controls.However,cholesterol efflux from HSF cells to LPDS was not different between groups.Conclusion The function of HDL involving cholesterol efflux in type 2 diabetes mellitus was impaired while cholesterol efflux induced by LPDS from HSF cells was maintained,suggesting that HDL plays a critical role in mediation of intracellular cholesterol accumulation and progression of atherosclerosis inpatients with type 2 diabetes.
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Objective To investigate the relationship between plasminogen activator inhibitor-1(PAI-1) activity and PAI-1 promoter 4G/5G polymorphism in patients with type 2 diabetes from the coastal areas of Shandong province.Methods The 4G/5G allele polymorphism in the PAI1 gene promoter region were tested by allele specific PCR in 116 type 2 diabetes and 40 normal controls.The activity of plasma PAI-1 was assayed by chromogenic substrate method.Results The plasma PAI-1 activity in patients was higher than that in controls(P