ABSTRACT
Objective To observe and analyze the pathological changes in BALB/c mice infected with herpes simplex virus typeⅡ (HSV-2) through nasal and genital inoculation. Methods Six-week old female BALB/c mice were divided into two groups, experimental and control groups. In the experimental group, the mice were infected with HSV-2 (104 CCID50/20μl per mouse) through nasal and genital tract in-oculation. Accordingly, the mice in the control group were injected with equal volume of PBS. Tissue speci-mens were collected from lung, nervous system and reproductive system for pathological analysis and viral load detection at different time points after infection. Lat gene expression in mouse trigeminal and sacral gan-glia was detected through in situ hybridization. In addition, the proliferation of viruses isolated form trigemi-nal and sacral ganglia of the infected mice was observed in vitro. Results Weight loss and histopathological lesions were observed in the mice of the experimental group 6 d after infection. Major pathological changes in the HSV-2-infected mice through nasal tract inoculation involved the lung and central nervous system( CNS) , including alveolar wall congestion, cerebrovascular cuff response and lymphocyte infiltration. How-ever, the major lesions in the infected mice through genital tract inoculation were found in the reproductive ducts, such as sacral ganglion necrosis, eosinophilia in the vagina and uterus, and ovarian congestion. Re-sults of the viral load detection in tissues and organs of the infected mice were consistent with the pathological changes. The mice infected through nasal tract inoculation had significantly higher viral loads in the nerves and lungs than those by genital tract inoculation, but lower viral loads in the genital tracts and sacral ganglia. Positive expression of lat gene at mRNA level was detected in the trigeminal and sacral ganglia of mice with HSV-2 latency 28 d after infection. In addition, both of the tissue fragments from trigeminal and sacral ganglia had cytopathic effects ( CPEs) on Vero cells. Enhanced expression of lat gene at mRNA level and much severer CPEs were induced by genital tract inoculation than by nasal tract inoculation. Conclu-sions HSV-2 could infect and cause histopathological damages in BALB/c mice through both nasal and genital tracts. In addition, the locations of the pathological lesions were closely related to the mode of infection.
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Objective: To study the chemical constituents of the aerial parts of Siegesbeckia pubescens. Methods: A systematic separation of chemical constituents was conducted. Detailed chemical investigation of S. pubescens led to the isolation of six compounds by comprehensive chromatographic Methods: (Extraction, Silic gel C.C, Sephadex LH-20, ODS C. C). The structures of them were fully determined based on spectroscopic analysis including IR, HR-ESI-MS, ESI-MS, 1H-NMR, 13C-NMR, DEPT, HSQC, and HMBC spectrum. Results: A total of six compounds were isolated from the fraction of n-butanol extract of S. pubescens including one new monoterpenoid glycoside named (2Z,5E)-7-hydroxy-3,7-dimethyl-2,5-octadiene-1-O-[α-L-rhamnpyranosyl (1→6)]-β-D-glucopyranoside (1), four known diterpenoid glucosides named pubeside D (2), ent-15,16,19-trihydroxypimar- 8(14)-en-2-one-19-O-β-glucopyranoside (3), ent-15,16-dihydroxypimar-8(14)-en-2-one-19-oic-β-glucopyranoside (4), and neodarutoside (5), and eleutherazine B (6). Conclusion: Compound 1 is a new compound, named as siegeside F, and compound 6 is isolated from this species for the first time.
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Objective To investigate 5-year survival after ST-segment elevation myocardial infarction(STEMI)in Beijing Yanqing district. Methods A total of 691 STEMI patients admitted to Beijing Yanqing hospital from August 2002 to December 2010 were followed up for as long as 5 years. The end point was all cause death. Five-year survival curve was computed for patients who had received primary percutaneous coronary intervention(pPCI)and patients who had not received pPCI. Predictors of death within 5 years were identified by multivariable cox regression analysis. Results In 691 patient,442 patients(64.0％)had not received pPCI,and 249 patients(36.0％)had received pPCI. The 5-year survival rates were 73.8％ and 93.6％in patients who had not received pPCI and patients who had received pPCI separately. The predictors of death within 5 years in patients who had not received pPCI were female,age,chronic obstructive pulmonary disease, Killip's class ≥ 2 in hospital,myocardial infarction of anterior wall and not receiving elective PCI,while the predictors in patients who had received pPCI were age and gastrointestinal bleeding. Conclusions The 5-year survival rate in patients who had received pPCI was obviously higher than in patients who had not received pPCI. The predictors of death within 5 years were different in the two groups.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes of NF-kappa B binding activity, the expression of PPARr and their correlation in the liver of rats with fatty liver disease (FLD) induced by different pathogenic factors and to investigate the molecular mechanism of the inflammation in FLD.</p><p><b>METHODS</b>40 Wistar rats were randomly divided into 4 groups of ten each: normal group, alcohol group, fat-rich diet group, alcohol adding fat-rich diet group. The rats were sacrificed at the end of the 16th week from the starting day of the experiment. Serum and liver specimens were collected. Histological specimens were stained with HE, SudanIV, and Masson and then studied microscopically. The ultrastructural changes were also checked under an electron microscope. NF-kappa B binding activity and the expression of PPARr mRNA were determined by electrophoretic mobility shift assay (EMSA) and RT-PCR respectively. The correlations between NF-kappa B binding activity and the expression of PPARr and the biochemical indexes were analyzed.</p><p><b>RESULTS</b>Steatosis, inflammation, necrosis and fibrosis were present in livers of the rats of all the experimental groups, and were most severe in the alcohol adding fat-rich diet group. NF-kappa B binding activity was markedly increased in the livers of the alcohol group (142+/-16.32) and of the alcohol adding fat-rich diet group (238+/-19.14) in comparison to the livers of the normal (73+/-9.24, F = 6.36, 17.93) and those of the fat-rich diet group (84+/-10.38, F = 5.96, 16.20). Binding activity was higher in the alcohol adding fat-rich diet group than that in the simple alcohol group, but there was no difference between those of the fat-rich diet and normal groups. The level of PPARr mRNA was lower in the livers of the alcohol, fat-rich diet, alcohol adding fat-rich diet groups (0.2530+/-0.069, 0.3647+/-0.082, 0.1226+/-0.054) than that of the controls (0.8097+/-0.094) (F = 15.43, 7.24, 21.45). NF-kappa B binding activity was correlated positively with the level of serum TNF alpha (r = 0.527, 0.639) and the content of MDA in the liver homogenates (r = 0.723, 0.537), but negatively with the expression of PPARr in the livers of the alcohol and the alcohol adding fat-rich diet groups (r = -0.568, -0.891).</p><p><b>CONCLUSION</b>The enhanced nuclear factors NF-kappa B binding activity and decreased expression of PPARr play a pivotal role in the inflammatory response of FLD induced by alcohol and fat-rich diet. It may provide a new idea for treating FLD effectively.</p>
