Objective To verify the pathol ogical basis of high signal intensity on T 1 weighted image after brain ischemia by using the rat model. Methods Fifty-six male Wistar rats, weighing 250 to 300 g, were used for the model of middle cerebral artery occlusion(MCAO). 46 rats model were counted in the results. They were divided into two groups randomly, experimental group (T 1, n =39) and control group (T 0, n =7). Experimental group was further divided into 4 subgroups: 15 minute's MCAO (T 1-a, n =13), 30 minute's MCAO (T 1-b, n =12), 60 minute's MCAO (T 1-c, n =7), and permanent MCAO (T 1-d, n =7). Intraluminal filament technique was used with the method modified by Zea-Longa. Follow-up MRI was applied to observe the time and the position of short T 1 signal. H & E staining and electronic microscope were applied to observe the pathological changes in the position of short T 1 signal. Results In T 0 group ( n = 7), no short T 1 signal was observed in bilateral cerebral hemispheres. In T 1-a subgroup ( n =13), short T 1 signal was observed in 7 rats at the 14 th day. In T 1-b subgroup ( n =12), short T 1 signal was observed in the ischemic side in 8 rats. All of the rats in T 1-c subgroup ( n =7) and T 1-d subgroup ( n =7) were observed to have short T 1 signal. The histological changes of short T 1 signal were hemorrhage, lipid-laden macrophage, denatured protein, and myelinolysis. Earlier short T 1 signal in cortical region was mainly related with hemorrhage, short T 1 signal in the basal ganglia appeared at a later stage, which was induced by lipid-laden macrophages. The occurrence of short T 1 signal was prominently different in the time of MCAO (? 2=29.328, P

Objective:To observe the effects of orbital bone density on the stress distribution of implant-bone surface.Methods:The 3D finite element analysis craniofacial model with eight HU values(300 -1 0 000)was established.A force of 20 N along the im-plant axis was applied on the model.The stress values and distribution were calculated and analyzed.Results:The peak of stress val-ue and displacement discreased as HU value increased.In the range of HU value 800 -1 000 HU,the peak of stress value and dis-placement of bone interface did not significantly change with the increasing of HU value.Conclusion:Orbital bone density is an im-portant factor on orbital implant failure when HU value below 800.

Objective: To establish a method for the determination of gastrodine in Tianma Formula Granule. Methods: HPLC was used with LiChrospherR 100 column, MeOH-phosphate solution(contain KH2PO4 and Na2HPO4 each 0.1mol/L)-water(1.5:3:95.5) as mobile phase and detection wavelength at 270nm. Results: Gastrodine showed a good linearity in the range of 1.638～14.742?g. The average recovery was 98.17 %and RSD was 1.39 %(n=5). Conclusion: This method is simple, accurate and with good reproducibility, and can be used for the quality control of Tianma Formula Granule.

Objective To evaluate the effects of Deng Zhan Sheng Mai (DZSM) capsule, a compound made of Chinese herbs, on secondary and tertiary prevention of ischemic stroke. Methods A hospital-based randomized open-blinded clinical trial was conducted among people with a prior history of ischemic stroke. Hospitals were assigned to treatment group, in which all of the participants took DZSM capsules for 3 months, or control group, in which no DZSM capsules was administrated. The primary endpoint was the reduction of levels of blood lipids, fasting blood glucose (FBG) and fibrinogen in the 3rd month. The secondary endpoints were recurrence of stroke, incidence of cardiovascular event (CVD) and all-cause mortality in the 18th month. Results 495 people were enrolled in the treatment group and 504 in the control group, respectively. In the 3rd month, the levels of total cholesterol(TC),FBG and fibrinogen were significantly reduced by 1.7%,4.3 and 8.2%(t values were 4.13,6.65 and 8.50 respectively),and the levels of HDL-C and HDL-C/TC were increased by 7.6%and 1 1.6%(t values were 2.15 and 3.67)in the treatment group, respectively(all P＜0.05＝.The levels of TC,HDL-C and HDL-C/TC decreased significantly in the eontrol group(all P＜0.05＝.The incidence of recurrent stroke and CVD events were lower in the treatment group than those in the control group, but the differences did not reach the significant levels. The prevalence of post-stroke depression (PSD) was also decreased in the 3rd mouth while it remained stable in the controls (P for trend equals to 0.0027). The mortality was significantly lower in the treatment group (P=0.008). Conclusion The levels of TC,FBG and fibrinogen as well as the prevalence of PSD and all-cause mortality have decreased significantly in treatment group treated with DZSM capsule for 3 months as compared with the control group.

Objective To estimate the prevalence and related risk factors of post-stroke depression (PSD) in ischemic stroke survivors from community-based medical centers in urban areas of Beijing.Methods Five community-based medical centers in urban areas of Beijing were selected.Patients with first-ever or recurrent ischemic stroke were evaluated from January 2003 to December 2006. The prevalence of PSD was evaluated by Self-Rating Depression Scale (SDS), and the information on the onset of stroke, vascular risk factors and living style was also collected.Results Totally 1089 stroke patients were registered, 1074 cases among which had complete information and met inclusion criteria. The mean age of the patients was (65.0 ± 8.9) years with a median stroke course of 13.0 months. The overall prevalence of PSD was 49.9% (536/1074), and the proportions of mild, moderate and major PSD were 52.2%, 36.0% and 11.8%, respectively. There were no significant differences in prevalence of PSD among different stages of stroke and the prevalence of PSD was 51.3% within 6 months after stroke onset, 47. 1% during 6-18 months and 53.2% after 18months. Low education, activities of Daily Living (ADL) dependence, cognition impairment and recurrence of stroke were independent risk factors for PSD.Conclusions The prevalence of PSD among ischemic stroke patients is higher in community-based medical centers, but most of PSD patients are mild or moderate. More effective early intervention should be adopted to decrease PSD,promote the recovery of neural function and improve their quality of life.

Objective To investigate the expression of HSPA9 in hepatocellular carcinoma(HCC) and its relationship with clinicopathological features and prognosis.Methods Forty-nine cases HCC treated by operative resection and follow up data in our hospital from January 2006 to January 2010 were retrospectively analyzed.Immunohistochemistry was performed to determine the expression of HSPA9 in HCC and paratumor tissues.The relationship between HSPA9 expression and clinicopathological features and prognosis was statistically analyzed.Results The HSPA9 protein expression in tumor tissue was higher that that in the paratumor tissue(t=6.601,P＜0.01),moreover the over expression of HSPA9 was significantly correlated with lymph node metastasis (P =0.005),TNM-stage(P =0.015),tumor differentiation (P =0.033),microvascular invasion (P =0.009) and recurrence (P =0.047).In the survival analysis results,the patients with over expression of HSPA9 had a much lower total survival rate(P=0.002)and much higher postoperative cumulative recurrence rate(P =0.003).There were significant differences in TNM-stage,microvascular invasion,lymph node metastasis,tumor differentiation and HSPA9 staining for overall survival and cumulative recurrence rate based on a univariate analysis(P＜0.05).Conclusion HSPA9 has over expression in HCC.The over expression of HS-PA9 is closely related to invasion and metastasis pathological features and can serve as an independent prognostic risk factor for predicting the prognosis of HCC.

OBJECTIVETo observe the association between high-density lipoprotein cholesterol (HDL-C) level and rate of ischemic stroke recurrence.

METHODSA total of 1 059 patients with ischemic stroke were enrolled from 5 community health centers and underwent baseline surveys during the period of January 2003 to December 2006. After baseline surveys, patients were followed up every 6 months until December 31, 2008. The new stroke events were recorded as the primary study endpoint. The association between HDL-C, HDL-C/TC and ischemic stroke recurrence was analyzed by Cox regression analysis.

RESULTSThe proportions of stroke patients with high ( ≥ 1.55 mmol/L), moderate (1.04-1.54 mmol/L) and low (<1.04 mmol/L) HDL-C levels were 15.58% (165/1 059) , 54.58% (578/1 059) and 29.84% (316/1 059) respectively. During a mean of (3.21 ± 1.04) years follow-up, recurrent ischemic stroke was recorded in 137 patients. Compared with HDL-C ≥ 1.40 mmol/L group, multivariate Cox regression analysis showed that stroke recurrence rates of patients with HDL-C ≤ 1.00 mmol/L and ranged from 1.01 to 1.19 mmol/L increased by 0.944 (HR = 1.944, 95%CI:1.033-3.659, P = 0.039) and 1.027 (HR = 2.027, 95%CI:1.116-3.682, P = 0.020)fold , respectively. Recurrence rates increased 1.237 (HR = 2.237, 95%CI:1.208-4.144, P = 0.010) fold in patients with HDL-C/TC ≤ 0.19 mmol/L compared to patients with HDL-C/TC ≥ 0.28 mmol/L.

CONCLUSIONThe risk of ischemic stroke recurrence increases with decreasing HDL-C level or HDL-C/TC ratio.

Aged ; Cholesterol, HDL ; blood ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Recurrence ; Risk Factors ; Stroke ; blood ; epidemiology

Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.

Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.

Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.