Objective To investigate the histopathology of liver,spleen and heart in mice model with Chlamydia pneumoniae ( C pneumoniae ) pneumonia Methods The Icr mice were inoculated with C pneumoniae ,strain CWL 029,by the intranasal or intravenous routes After a single inoculation,mice were killed on the 1st,3rd,7th,14th,21st,28th and 60th day separately Specimens of spleen,liver and heart were obtained from the acute stage of C pneumoniae pneumonitis and stained with hematoxylin eosin Results After inoculation of C pneumoniae ,there were infiltration of neutrophils and macrophages in the spleen and necrosis of hepatocytes The histopathology of iv inoculation group was more serious than that of intranasal inoculation group No pathology changes were observed in heart Conclusions After iv inoculation of C pneumoniae ,the histopathologic changes appeared in the tissue of liver and spleen correspondingly,and the changes were more serious than that of iv inoculation group This study demonstrated that C pneumoniae was mainly limited to lungs and dissemination of C pneumoniae was seldom

Objectives: To evaluate mice as experimental animal for Chlamydia pneumoniae, a common cause of acute respiratory infections in human.　Methods: Intranasal inoculation of Icr mice with C. Pneumoniae induced a prolonged course of lung infection, as demonstrated by persistence of lung pathology(60 days).　Results: Icr mice were susceptible to C. pneumoniae. Lung pathology was characterized by patchy interstitial pneumonitis with predominately neutrophil leukocyte infiltration in the early(7 days) and lymphocytes infiltration in the later stages(14 days later) of infection.　Conclusions:Icr mice were susceptible to C. pneumoniae and the mouse model is useful for the investigation of the pathogenesis of C. pneumoniae infection.

Objective To investigate the effect of preptin on proliferation and differentiation of human osteoblasts. Methods After human osteoblasts were incubated with 10-10, 10-9, 10-8 , 10-7 mol/L preptin for 24 h,the proliferation of osteoblasts was determined by[3H]thymidine incorporation and alkaline phosphatase (ALP)activity was assayed by spectrophotometric measurement. The phosphorylation levels of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase ( MAPK), extracellular signal-regulated kinase (ERK) 1/2 were assayed by Western blot. ERK inhibitor PD98059, p38MAPK inhibitor SB203580, and JNK inhibitor SP600125were used for investigating the signal pathway of preptin-stimulated osteoblast proliferation and differentiation.Results Preptin dose-dependently increased human proliferation of osteoblasts and ALP activity with the maximum effect at the concentration of l0-9 mol/L (both P<0.01 ). Preptin stimulated ERK phosphorylation in human osteoblasts, but not p38 MAPK and JNK phosphorylation. PD98059 blocked preptin-sitmulated human osteoblasts proliferation and ALP activity (both P<0.05 ), while SB203580 and SP600125 had no effect. Conclusions Preptin promotes the proliferation and differentiation of human osteoblasts through ERK pathway.

，and 17.47%.Conclusions Xylitol can lower the blood glucose a littte but without significant difference.It has little effect on blood glucose variability of patients with type 2 diabetes mellitus and can be safely used for rehydration.

Objective To investigate the effect and mechnism of preptin on connect tissue growth factor (CTGF) in human osteoblasts. Methods Recombinant human preptin was used to treat primary human osteoblasts, and Western blot was used to detect CTGF protein level. Mitogen-activated protein kinase p38(p38MAPK), extracellular signal-regulated kinase (ERK1/2), c-jun N-terminal Kinase (JNK), and their phosphorylation levels were also detected by Western blot. MAPK inhibitors (PD98059, SP600125, or SB203580)were used to elucidate the mechnism of preptin induced expression of CTGF in human osteoblasts. Results Treatment of human osteoblasts with preptin caused a time and dose-dependent increase in CTGF secretion. Preptin induced activation of ERK, but not p38MAPK or JNK in human osteoblasts. Furhermore, pretreatment of human osteoblasts with the ERK inhibitor PD98059 abolished the preptin-induced CTGF secretion. Conclusion Preptin induces CTGF expression in human osteoblasts by means of ERK/MAPK pathway.

OBJECTIVETo evaluate mice as experimental animals for Chlamydia pneumoniae (C. pneumoniae) infection and investigate the pathogenesis of C. pneumoniae derived pneumonitis.

METHODSIcr mice were inoculated with the C. pneumoniae strain, CWL-029, either intranasally or intravenously. After a single dose inoculation, mice were killed on the 1st, 3rd, 7th, 14th, 21st, 28th and 60th days. The pathological changes in lung tissue were analyzed.

RESULTSThe Icr mice were shown to be susceptible to C. pneumoniae. Inoculation into mice with C. pneumoniae induced a prolonged course of lung infection, as demonstrated by persistence of lung pathology (up to 60 days). Via intranasal inoculation of mice, lung pathology was characterized by patchy interstitial pneumonitis with predominantly neutrophil leukocyte infiltration early (within the first 7 days) and lymphocyte infiltration in the later stages (14 days later) of infection. After intravenous inoculation, a similarly developed interstitial pneumonitis was observed, but it was milder and patchier, especially in early stages. C. pneumoniae DNA was detected by polymerase chain reaction (PCR) intermittently in the lung tissue. Inoculated mice developed serum IgG antibody responses.

CONCLUSIONThe Icr mice were susceptible to C. pneumoniae, resulting in a pulmonary infection characterized by interstitial pneumonitis, occurring most strongly via intranasal inoculation.

Animals ; Chlamydia Infections ; etiology ; pathology ; Chlamydophila pneumoniae ; DNA, Bacterial ; analysis ; Lung ; pathology ; Male ; Mice ; Mice, Inbred ICR ; Pneumonia, Bacterial ; etiology ; pathology ; Polymerase Chain Reaction