Objective To evaluate the efficacy and safty of BaileMian capsulae on treatment of insomnia in aged people. Methods 40 aged people with insomnia were randomly divided into the research group (BaileMian capsule group,n= 20) and the control group (Zaorenanshen capsule group,n=20) treated for 14 days.The clinical effects were esti- mated with SDRS before and after 1 w and 2 w treatment.Results The total SDRS scores after treatments in both groups were significantly decreased comparing with scores before treatments respectively (P

60 years old) in a community of Beijing were investigated by telephone visit, physical examination and Doppler examination. The rates of hypertension, coronary artery disease, diabetes and stroke were evaluated according to the patient whether had PAOD. Results Among 1730 people, 263 cases were diagnosed as POAD. The prevalence of hypertension, coronary heart disease, diabetes and stroke in PAOD population (59.3%,40.3%,29.3% and 22.3%) was higher than those in non-PAOD population (48.1%,32.6%,23.0%and 15.2%)( P

Objective To investigate the pathogenesis of the syringomyelia in Chiari I malformation by measuring the posterior cranial fossa structures. Methods The posterior cranial fossa structures on mid sagittal MR image were measured in 50 normal subjects,and 24 Chiari I malformation patients associated with syringomyelia and 26 Chiari I malformation patients without syringomyelia. The t test was used for statistical analysis. Results In Chiari I malformation patients and normal subjects, the width of the CSF space anterior to the medulla oblongata was (4 2?1 8) mm and (6 6?1 4) mm respectively( t =7 30, P 0 05). In Chiari I malformation with syringomyelia group and without syringomyelia group, the width of the CSF space anterior to the medulla oblongata was (2 9?1 4) mm and (5 5?1 1) mm respectively( t =7 30, P

Objective To study the effects of mild hypothemia therapy on coagulatic-fibrinolytic functions of the severe head injury patients.Methods 35 severe head injured patients from Jan 1998 to May 2000 were treated by mild hypothermia therapy and compared with past 30 patients.All patients's coagulate and fibrinolytic index was measured.Results All patients have coagulate- fibrinolytic disorders, mild hypothermia therapy can reduce consume of coagulate factors and inhibit secondary fibrinolytic function.Conclusion Mild hypothermia therapy is important to the severe head injury patients.

Objective To investigate the mechanism of the protective effects of olanzapine against apoptosis of PC12 cells induced by ?-amyloid peptide 25-35 (A?_ 25-35 ). Methods Based on the model of apoptosis of PC12 cells induced by A?_ 25-35 , cell viability was determined by MTT assay. The expressions of Bax, Caspase-3 of PC12 cells induced by A?_ 25-35 and olanzapine were assessed by Western blot. Results 10 -14 -10 -5 mol/L A?_ 25-35 lowered the cell viability of PC12 cells, 50?mol/L and 100?mol/L olanzapine pretreatment enhanced the cell viability of PC12 cells, and there was significant difference compared with olanzapine non-pretreated groups (P

BACKGROUND: β-amyloid has been proved to be capable of inducing cell apoptosis and play a vital role in Alzheimer disease (AD).OBJECTIVE: To probe into olanzapine's protective effect and mechanism of PC12 cell apoptosis induced by β-amyloid 25-35.SETTING: Department of Neurology, Southern Building of the General Hospital of Chinese PLA.DESIGN: Randomized design.MATERIALS: This experiment was carried out in the Neuropsychopathic Research Institute, Medical College of the University of Saskatchewan(Canada), between May 2002 and March 2003.METHODS: P12 cells were cultured with RPMI1640 culture medium.100 μL cell suspension was inoculated in each well of 96-well culture plate, and 5 mL suspension was inoculated in 25 cm2 culture bottle covered with collagen and cultured for 24 hours, then with additional 50 μmol/L and 100 μmol/L olanzapine, respectively, for 24 hours, and β-amyloid 25-35 of different concentrations (0.01 μmol/L, 2 μmol/L and 20 μmol/L) for 24 hours. PC12 cell apoptosis was induced by β-amyloid 25-35 in 96-well culture plate and cells were harvested to assay their survival rate with MTF colorimetric assay. PC12 cells in 25-cm2 culture bottles were also harvested to detect the effect of olanzapine on Bax and caspase-3 expression in PC12 cells using Western blot assay.MAIN OUTCOME MEASURES: ① Cell survival rate; ② the expression of Bax and caspase-3 in PC12 cells.RESULTS: ① Cell survival rate: cell activity was found declined from 75% to 35% in PC12 cells induced by β-amyloid 25-35, but obviously increased in PC12 cells due to pretreatment with olanzapine of 50 μmol/L and 100 μmol/L. ② Olanzapine's effects on Bax expression in PC12 cell apoptosis induced by β-amyloid 25-35: Bax expression increased in PC12cells due to exposure to β-amyloid 25-35 of 0.01 μmol/L, 2 μmol/L and 20 μmol/L, but it could be suppressed if pretreated with olanzapine of 50 μmol/L. ③ Effect of olanzapine on caspase-3 expression in PC12apoptotic cells induced by β-amyloid 25-35: There was no change in PC12cells induced by 0.001 μmol/L or 0.01 μmol/L of β-amyloid, as well as in PC12 cells pretreated with 50 μmol/L olanzapine. However, caspase-3 expression obviously increased in PC12 cells exposed to 2 μmol/L and 20 μmol/L of β-amyloid 25-35, and it could be suppressed by pretreatment with 50 μmol/L of olanzapine.CONCLUSION: ① β-amyloid 25-35 can induce the high expression of cell apoptosis related Bax and caspase-3 in vitro cultured PC12 cells. ②Olanzapine can reduce the expression, thus enhancing the survival rate of PC 12 cells.

BACKGROUND: Many studies have indicated that amyloid beta-protein (Aβ) plays an important role in the pathophysiology of Alzheimer disease (AD), the reduction of production of Aβ can slow down the deterioration of AD, so to reduce Aβ production could become an important therapeutic target in AD. Many AD patients present behavioral disturbance and psychotic symptoms, and are treated with antipsychotics. Olanzapine and quetiapine can significantly improve the clinical global impressions(CGI) severity-of-Alzheimer scores, clinical studies suggest that early and prolonged intervention can improve long-term outcome.OBJECTIVE: To investigate the effect of olanzapine and quetiapine on the secretion of Aβ42 in Swedish amyloid precursor protein(APP) gene and presenilin 1 gene transfected murine N2a neuroblastoma cells.DESIGN: A completely randomized controlled trial based on N2a cells.MATERIALS: Setting was at Neuropsychiatry Research Institute of Medical College, University of Saskatchewan. The murine N2a and double transfected N2a cell was provided by department of neurology and neuroscience, Cornell university medical college.INTERVENTIONS: The double transfected murine N2a neuroblastoma cells were treated for 24 hours with 200 μmol/L olanzapine and 50 μ mol/L quetiapine respectively, then intracellular and extrocellular levels of Aβ were determined. The MTT assay was used to determine cell viability; the BCA assay was used to determine the protein content of cells; the western blot analysis was used to determine the APP expression; and the Enzyme-Linked-Immuno-Sorbent Assay(ELISA) was used to determine the Aβ produced by double transfected murine N2a neuroblastoma cells.MAIN OUTCOME MEASURES: The levels of intracellular and extracellullar Aβ 42 secreted by double transfected murine N2a neuroblastoma cells were detected using ELISA.RESULTS: The double transfected N2a cells produced more APPs than the naive N2a cells. The extracellular Aβ[ (4.78 ± 0.54) nmol/L] of cells treated with olanzapine decreased significantly comparing to the vehicle [(7.69±0.62) nmol/L] (t=3.52, P ＜0.05); and theextracellular Aβ[ (4. 09 ±0. 18) nmol/L] of cells treated with quetiapine decreased significantly comparing to the vehicle[ (7.50 ±0.50) nmol/L] ( t =5.61,P ＜ 0.05) . The intracellular Aβ of cells treated with olanzapine did not change significantly conpared with the vehicle ( P ＞ 0.05 ); the intracellular Aβ of cells treated with quetiapine did not change significantly compared with the vehicle ( P ＞ 0.05 ).CONCLUSION: The result suggests that olanzapine and quetiapine can decrease the production of Aβ42 in double transfected murine N2a neuroblastoma cells and clinically may be helpful in slowing down the progression of AD by decreasing the extrocellular secretion of Aβ42.

Objective To explore histopathological features in the nigrostriatal tissues of Parkinson’s disease (PD)and Parkisonism plus syndrome. Methods The substantia nigra and the striatum of 5 PD cases, 3 progressive supralnuclear palsy (PSP) cases and 3 multiple system atrophy (MSA) cases, and 5 normal aging control cases were examined by routine neuropathological methods and Gallyas-Braak staining and tau, ubiquitin and ?-synuclein immunohistochemistry. Pigmented neurons in the substantia nigra of PD, PSP, MSA cases and normal aging control cases were counted. The neuronal and glial cytoplasmic inclusions in the nigrostriatal tissues were observed. Components of the abnormal proteins were identified. Results Nerve cells in the substantia nigra of PD,PSP and MSA groups showed severe loss in number,especially the ventrolateral zone and the ventromedial zone. Compared with those in the normal aging control group,numbers of nerve cells in the ventrolateral zone of PD, PSP and MSA groups decreased to 37.5%, 24.2%, 33.8% in the right side, and 48.0%, 25.8%, 33.9% in the left side respectively. There were ?-synuclein and ubiquitin-positive Lewy bodies in the substantia nigra of PD. A lot of tau-positive, argyrophilic globous neurofibrinary tangles, tuft-shaped astrocytes and coiled bodies in the substantia nigra and the striatum of PSP were observed.Severe loss of neurons and gliosis in the caudate nucleus and putamen of MSA were found. In addition, ?-synuclein and ubiquitin-positive glial cytoplasmic inclusions were found in the substantia nigra and striatal region of MSA. Conclusions Lewy bodies in PD and glial cytoplasmic inclusions in MSA are related to abnormal depositions of ?-synuclein and ubiquitin.Neuronal and glial cytoplasmic inclusions in PSP are related to abnormal aggregation of tau.

In order to study the effect of chronic noise exposure on auditory center, seven guinea pigs were .exposured to 105 dB A noise 8h daily for 45 d. Then the animals were killed by decapitation. The superior olive and inferior colliculus were taken immediately to make the samples of electron microscope. The mitochondria swelling, membrane rupture, cristae breaking, ballooning degeneration were found. The rough surfaced endoplasmic reticulum was swollen and expanded. The lysosome and secondary lysosome were increased. The cell interstitial edema and synaptic besicle decrease were observed. The nuclear chromatid was decreased and nucleolus was kept to the side. The laminae of neurilemma of nerve fibers were dissociated, swollen and broken. The results indicate that the ultrastructure, neural cells and fibers in the auditory center are damaged by chronic noise exposure and most of these damages are irreversible.

Objective:To investigate the effect of hypoxia on the expression of forkhead box P3 (FOXP3) in human oral squamous cell carcinoma (OSCC) cells,and to clarify its possible epigenetic mechanism.Methods:Two kinds of OSCC cell lines,FaDu and OECM-1,were cultured under normoxic or hypoxic conditions for 18 h.The relative expression levels of FOXP3 mRNA and protein in the cells were detected by Real-time RT-PCR and Western blotting method.The histone modification levels on the FOXP3 gene promoter,including acetylation of histone 3 lysine 4 (H3K4ac),trimethylation of histone 3 lysine 4 (H3K4me3) and lysine 27 (H3K27me3),were analyzed by Chromatin Immunocipitation (ChIP) and quantitative PCR (ChIP-qPCR).The relative expression levels of histone deacetylase 3 (HDAC3) mRNA and inhibitory rates of FOXP3 mRNA expression in the HDAC3-knockdown FaDu cells were investigated by Real-time qPCR and ChIP-qPCR.Results:Compared with normoxic condition,the relative expression levels of FOXP3 mRNA in FaDu and OECM-1 cells under hypoxic condition were decreased by 65.6% and 75.7% (P<0.01).The Western blotting results indicated that compared with normoxic condition,the expression levels of FOXP3 protein in FaDu and OECM-1 cells under hypoxic condition were decreased.The ChIP experiment results showed that compared with normoxic condition,the levels of H3K4ac and H3K4me3 on FOXP3 gene promoter in FaDu cells were decreased under hypoxic condition (P<0.01),while the H3K27me3 level was not changed.In HDAC3-knockdown FaDu cells,compared with control cells,the inhibitory rates of the expressions of H3K4ac and H3K4me3 on FOXP3 gene promoter under hypoxia condition were decreased (P<0.05),so did expressions the FOXP3 mRNA expression (P<0.05).Conclusion:Hypoxia could suppress the expression of FOXP3 by HDAC3-mediated down-regulation of H3K4ac on FOXP3 gene promoter in the human OSCC cells.