Objective To observe the expression of HBV-DNA and whether there were copy of HBV in the umbilical cord tissues of the died fetus delivered from puerpera with hepatitis virus B. Methods 40 cases such died fetus were collected by routine autopsy to obtain umbilical cord tissues.And using in situ molecular hybridization technique detected HBV-DNA. Results For the umbilical cord tissues, there were 40%(16/40) cases detected out HBV-DNA.HBV-DNA mainly localization in the surface of the umbilical cord vessel and in the cytoplasma of the cord vessel's endothelial cells. They were not in the cord vessel's endothelial cells nuclei. Conclusions There were HBV replication in the umbilical cord tissues of the died fetus. But the expression of HBV-DNA in the umbilical cord tissues of the died fetus is not related with the HBV replication status in the pregnant woman veins.

Objective This study is to identify the presence of superoxide anion-generating system in human lens epithelial cells using arachidonic acid (AA) as the stimulator.Design Experimental study.Participants Human lens epithelial cells B3 (HLE B3). Methods Confluent human lens epithelial cells (HLE B3) were subjected to stimulation by AA and its derivatives.The generation of su- peroxide anion was quantified with a luminometer (LumiStar BMG) immediately upon AA and its derivatives addition.Cells preloaded with superoxide dismutase (SOD) or mannitol were used as negative controls and cells mixed with 3% ethanol (solvent for AA) were used as baseline.Cells were preloaded with inhibitors 30 minutes before luminometer measurement.A time-and concentration-depen- dent study on the AA-stimulated activation of mitogen-activated protein kinase (MAPK) was carried out using western blot analysis. Main Outcome Measures Superoxide generation,phosphorylation of MAPK.Results AA at dosage of 30-150 mM proportionally in- duced luminescence in HLE B3 cells,but was ineffective in cells preloaded with SOD or mannitol.DPI,a non-specific NADPH oxidase inhibitor eliminated AA-induced superoxide anion generation partially.Leinoleic acid,stearic acid,eicosa-11Z,14Z,17Z-trienoic acid (20:3) and eicosa-11Z,14Z-dienoic acid (20:2) were ineffective.The generation of superoxide anion was not contributed by cyclooxyge- nase or the cytochrome p450 pathway since indomethacin (inhibitor for cyclooxygenase) or ketoconazole (inhibitor for cytochrome p450) could not eradicate the stimulatory effect of AA.While CDC,a specific inhibitor for lipoxygenase could eliminate superoxide generation partially.The specific inhibitor for 5-lipoxygenase AA861 completely blocked the generation of superoxide anion.Western blot analysis of the cell lysate showed that AA at the concentrations of 30-150 mM progressively activated ERK and JNK.They were transiently ac- tivated between 2.5-30 minutes.The activations of ERK and JNK were dose-dependent and time-dependent.Conclusions Inhibition of superioxide anion generation may be a new approach to block lens epithelial cell proliferation and post-capsule opacification.

A female patient with hair cell leukaemia was treated with human leukocyte interferon at a daily dose of 1.5 ? 104 for 27 days. The bone marrow cells were studied with electron microsepy. The follow up investigation of the bone marrow hair cells revealed that there were widening of the perinuclear space, disintegration of nuclear membrane, vaeuolization as well as expansion of the rough endoplasmic retieulum

The aim of the study is to provide an ideal animal model for the research in the field of molecular pathogenesis and experimental treatment of gastric carcinoma. By the microsurgical technique, 47 human gastric carcinoma specimens were orthotopically transplanted into the gastric mucosal layer in nude mice. Its oncogenicity, invasion, metastasis and morphologic characteristics were observed and the expression of oncogene P53, c erbB 2 and raSP 21 were assessed. Three models of human gastric carcinoma, were adenocarcinoma, squamous cell carcinoma, squamous adenocarcinoma were screened from 47 cases of patients. The oncogene proteins were positively expressed and related to the growth pattern, depth of invasion and lymph node metastasis. Its ultrastructural characteristic was similar to the human original gastric cancer cells. These models are suitable and helpful for the research of the molecular pathogenesis, invasion, metastasis and experimental treatment of gastric carcinoma.

Adolescent ; Adult ; Cat-Scratch Disease ; diagnosis ; therapy ; Child ; Child, Preschool ; Female ; Humans ; Lymphadenitis ; diagnosis ; etiology ; therapy ; Male ; Middle Aged ; Young Adult

0.05).At the eighth week of training and after ceasing the cognitive training for 4 weeks the NCSE scores and the FIM scores were improved in both groups,espeeially in the cognitive training group(P

Objective To explore the prevalence of sialorrhea and its clinical correlation with dysphagia in Chinese patients with Parkinson′s disease ( PD ).Methods One hundred and sixteen consecutive patients with a clinical diagnosis of PD were selected.Demographic data included sex , age, years of education, age at onset of PD, clinical genotype, disease duration, treatment, Hoehn and Yahr (H&Y) stage.Sialorrhea was assessed using the Unified Parkinson′s Disease Rating Scale (UPDRS) Ⅱitem number 6.All patients were studied with videofluoroscopic study of swallowing ( VFSS).Results The prevalence rate of sialorrhea in PD was 59.5% (69/116, 95% CI 50.6%-68.4%).Males were more likely to develop sialorrhea than females (47/70 vs 22/46,χ2 =4.298, P=0.038).PD patients′sialorrhea correlated with oral dysphagia:with food leaking from the mouth ( liquid r=0.229, P=0.014; juice r=0.197, P=0.034;pudding viscosities r=0.231, P=0.013;solid food r=0.255, P=0.006), with more than 1 ml of oral food residues (liquid r=0.319, P<0.01;solid food r=0.185, P=0.047), with delay in food transfer to the root of the tongue (liquid r=0.279, P=0.002; juice r=0.209, P=0.024), and delayed swallow transfer ( pudding viscosities r=0.257, P=0.005).Sialorrhea score was not related to H&Y stage, clinical course and levodopa equivalent doses (LED).The prevalence rate of dysphagia in PD was 87.1%(95% CI 81.0% -93.2%).Liquid was more likely to cause pharyngeal dysphagia ( P=0.03).With the increase in H&Y stage , so did the oral and pharyngeal stages of dysphagia.Late and mid-course was more likely to develop oral and pharyngeal dysphagia than those with early clinical course .Conclusions Sialorrhea and dysphagia are common non-motor symptoms in PD patients.Sialorrhea is more prevalent in males and correlates with oral phase of dysphagia.Liquid is more likely to cause pharyngeal dysphagia.With increase in H&Y stage , so did oral and pharyngeal dysphagia.Even though late clinical course is more likely to develop oral and pharyngeal dysphagia than early clinical course , the comparison between late and intermediate clinical courses does not reach statistical significance .

Autonomic Nervous System Diseases ; metabolism ; pathology ; surgery ; Colon ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Enteric Nervous System ; abnormalities ; pathology ; Hirschsprung Disease ; pathology ; Humans ; Infant, Newborn ; Intestinal Diseases ; metabolism ; pathology ; surgery ; Male ; Phosphopyruvate Hydratase ; metabolism ; S100 Proteins ; metabolism

This study is to investigate the effect of hydroxyethylpuerarin on the expression of tumor necrosis factor-alpha (TNF-α) and activity of nuclear factor kappa B (NF-κB) after middle cerebral artery occlusion (MCAO) in rats. Rats were subjected to cerebral ischemia-reperfusion injury induced by MCAO. Hydroxyethylpuerarin (10, 20, 40 mg·kg-1, iv) was administered just 30 min before occlusion and immediately after reperfusion. After a 24 h reperfusion following 2 h of MCAO, the number of viable neurons in hippocampal CA1 region was counted by hematoxylin and eosin (HE) staining. TNF-α protein and its mRNA expression were examined with radioimmunoassay (RIA) and reverse transcriptase-polymerase chain reaction (RT-PCR) respectively. NF-κB activity was observed by electrophoretic mobility shift assay (EMSA), and inhibition of NF-κB α (IκBα) protein expression was evaluated by Western blotting analysis. Animals treated with hydroxyethylpuerarin had a significant increase in neuronal survival in comparison with vehicle-treated group. Hydroxyethylpuerarin significantly reduced the protein and mRNA expression of TNF-α following 2 h of ischemia with 24 h of reperfusion. NF-κB DNA binding activity and the degradation of IκBα in the cytoplasm also decreased by hydroxyethylpuerarin treatment. The protective effects of hydroxyethylpuerarin against ischemia-reperfusion injury may be mediated by decreasing the expression of TNF-α and the activity of NF-κB in rats.

Objective To investigate the effect of different parts leukoencephalopathy on cognitive function in patients with acute cerebral infarction,and analyze the relationship between injury site of cholinergic pathways and cognitive function.Methods Ninety-seven patients with acute cerebral infarction were divided into leukoencephalopathy group (59 cases) and non-leukoencephalopathy group (38 cases)according to the cranial MRI T2 scanning.The all patients of 2 groups were evaluated by cholinergic pathways hyperintensities scale (CHIPS) and reforming Scheltens scale.The cognitive function of all patients were evaluated by Montreal cognitive assessment (MoCA).The difference of the cognitive function between 2 groups was observed,and the relationship between CHIPS score,reforming Scheltens scale score and MoCA score was investigated.Results There were statistical differences in MoCA total score and visuospatial/execution,memory,attention score between leukoencephalopathy group and non-leukoencephalopathy group [(20.86 ± 4.52) scores vs.(23.47 ± 4.49) scores,(3.80 ± 1.68) scores vs.(3.11 ± 1.47) scores,(2.78 ±1.57) scores vs.(1.95 ± 1.80) scores,(4.00 ± 2.08) scores vs.(3.87 ± 2.04) scores] (P ＜ 0.01 or ＜ 0.05).There were statistical differences in CHIPS score and reforming Scheltens scale score between cognitive dysfunction group (35 cases)and non-cognitive dysfunction group (24 cases)[(47.77 ± 12.36) scores vs.(39.83 ±7.98) scores,(5.14 ± 1.73) scores vs.(2.58 ±2.10) scores] (P ＜0.01).There was negative correlation between MoCA total score and frontal periventricular score,occipital periventricular score,parietal lobe score,periventricular total score,deep alba total score and reforming Scheltens scale total score (P ＜0.01).There was negative correlation between visuospatial/execution score,attention score,fixing score,MoCA total score and CHIPS score (P ＜ 0.01).There was negative correlation between attention score,fixing score,MoCA total score and reforming Scheltens scale score (P ＜ 0.01).Conclusions In acute cerebral infarction patients leukoencephalopathy is probably related to cognitive function,and the severity of leukoencephalopathy correlates with the degree of cognitive function impairment.Different parts leukoencephalopathy can induce different influence on cognitive function.The cognitive function impairment caused by leukoencephalopathy correlates with the impairment of cholinergic pathways,with main effects of visuospatial/execution function,and the severity correlates with the impairment of cholinergic pathways.