Objective To explore the clinical characteristics and risk factors of occult pneumonia in advanced elderly patients.Methods A total of 170 advanced elderly patients with community-acquired pulmonary infection in geriatric department of Xijing hospital from January 2014 to October 2017 were enrolled.Patients were divided into two groups:the observation group (with occult pneumonia,n=80)and the control group(without occult pneumonia,n =90).Clinical data of patients were collected,and clinical characteristics and related risk factors of occult pneumonia in elderly patients were analyzed.Results There was no statistically significant difference in the positive rate of sputum culture and the distribution of pathogenic bacteria between the two groups (P ＞ 0.05).Gram-negative bacteria predominated in pathogenic bacteria.The hospitalization time was longer in the observation group than in the control group[(17.3 ± 3.0) d vs.(10.3 ± 3.9) d,P ＜ 0.05].The mortality rate was higher in the observation group than in the control group(10.0 ％ vs.3.3 ％,P ＜ 0.05).The age was older in the observation group than in the control group[(87.0± 1.7) years vs.(82.0± 2.4) years,P ＜ 0.05].The incidences of diabetes,Alzheimer's disease,hypothyroidism and long-term bed rest were higher in the observation group than in the control group (P ＜ 0.05).Multivariate logistic regression analysis showed that age (OR =6.93),dementia (OR =4.32),hypothyroidism(OR =4.89) were independent risk factors for occult pneumonia (P ＜ 0.05).Conclusions The pathogenic bacteria in advanced elderly patients with occult pneumonia are mainly gram-negative bacteria.The positive rate of CT scan confirmed-occult pneumonia is much higher than that by chest X-ray.The advanced elderly patients with occult pneumonia have longer hospitalization time and higher mortality rates.Old age,senile dementia and hypothyroidism are independent risk factors for occult pneumonia in advanced elderly patients.

Objective:To establish cell lines stably expressing Rab5a and its the inactive mutant Rab5aN133I,analyze the effect of Rab5a on the expression of cytokines in LPS-stimulated RAW264.7 cells .Methods:RAW264.7 cells were transfected with Rab5a and its inactive mutant vector Rab5a N133I separately,and then screened by G418.Rab5a stable expressing cell lines were identified by Real time-PCR.The growth of the stable cell lines was analyzed by MTT assay.After the stable cell lines were stimulated by LPS for different time periods,the expression of iNOS,TNF-αand IL-6 was detected.Results:Rab5a and Rab5aN133I transfection resulted in elevated Rab5a mRNA expression compared with the control cells ( P<0.05 ).Rab5a overexpression enhanced the proliferation of RAW264.7 cells.However,the proliferation of Rab5aN133I cells was significantly slower than the control cells ( P<0.05).Overexpression of Rab5a promoted LPS-induced production of iNOS,TNF-αand IL-6 in RAW264.7 cells (P<0.01). Conversely,overexpression of Rab5aN133I abolished the stimulating effects of Rab5a.Conclusion: Rab5a promoted LPS-induced expression of iNOS,TNF-αand IL-6 in RAW264.7 macrophages in a GTP-binding ability-dependent manner.

Objective To investigate the effects of expression of mitochondria long-chain fatty acid oxidative enzyme (long-chain 3 hyroxyacyl CoA dehydrogenase,LCHAD) and p38 mitogen activated proteinkinase (p38MAPK) signal transduction pathway in severe preeclampsia.Methods Serum-free trophoblast cells cultured in vitro were stimulated by early onset severe preeclampsia serum (E-PE group),late onset severe preeclampsia serum (L-PE group),HELLP syndrome serum (HELLP group),and normal pregnancy serum (NP group) respectively; each group was added DMEM/F12 medium,reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor (NADPH-Ⅰ) and p38 MAPK inhibitor (p38-Ⅰ)to stimulate cells.Expression of mRNA and protein of LCHAD in trophoblast cells were detected by real-time PCR and western blot.Results (1) The expression of mRNA of LCHAD:the level of mRNA of LCHAD in NP+DMEM,E-PE + DMEM,E-PE + NADPH-Ⅰ,E-PE + p38-Ⅰ,L-PE + DMEM,L-PE + NADPH-Ⅰ,L-PE + p38-Ⅰ and HELLP + DMEM,HELLP + NADPH-Ⅰ,HELLP + p38-Ⅰ groups were 1.00 ± 0.03,0.14 ±0.08,0.95 ±0.20,1.43±1.02,0.37 ±0.18,1.51 ±0.36,1.60 ±0.31,0.10 ±0.04,0.49 ±0.10,0.44 ± 0.21,respectively.The relative expressions of mRNA of LCHAD were significantly reduced in E-PE + DMEM,L-PE + DMEM and HELLP + DMEM groups compared with the NP + DMEM group (P ＜0.05).Compared with the NP groups,the relative expressions of mRNA of LCHAD were significantly increased in L-PE + NADPH-Ⅰ and L-PE + p38-Ⅰ group (P ＜ 0.05),while reduced in HELLP groups (P ＜0.05).(2) The expression of protein of LCHAD:the relative expressions of protein of LCHAD in NP +DMEM,E-PE + DMEM,E-PE + NADPH-Ⅰ,E-PE + p38-Ⅰ,L-PE + DMEM,L-PE + NADPH-Ⅰ,L-PE +p38-Ⅰ and HELLP + DMEM,HELLP + NADPH-Ⅰ,HELLP + p38-Ⅰ groups were 19.4 ± 2.2,10.7 ± 1.1,17.9±3.3,19.1 ±2.9,16.4 ±2.3,20.3 ±2.3,20.9 ±4.3,12.4 ±2.3,17.6 ±2.6,17.7 ±2.0 respectively.Compared with the NP groups,the protein expressions of LCHAD were significantly remarkably reduced in E-PE + DMEM,L-PE + DMEM and HELLP groups (P ＜ 0.05).Compared with the DMEM groups,the protein expressions of LCHAD were significantly increased in NADPH-Ⅰ and p38-Ⅰ groups of E-PE,L-PE and HELLP groups (P ＜ 0.05).Conclusions These studies demonstrate that long chain fatty acid oxidation was involved in the pathogenesis and development of preeclampsia.The expressions of gene and protein of LCHAD were remarkably affected by early onset severe preeclampsia and HELLP syndrome.NADPH-Ⅰ and p38-Ⅰ may allay the disorder of fatty acid oxidation.p38MAPK signal transduction pathway may contributed in this process.

Aim To study the effect of 2,3,4′,5-tetrahydroxystilbene-2-O-?-D glucoside(TSG) on vascular smooth muscle cells(VSMCs) proliferation induced by fetal bovine serum and explore the underlying mechanisms.Methods VSMCs were cultured from rat aorta using explant technique.VSMCs proliferation was analyzed by 5-bromo-2-deoxyuridine(Brdu) incorporation assay.Cell cycle phase distributions were determined by flow cytometry.The expression of proliferating cell nuclear antigen(PCNA) was evaluated by Western blot analysis.The level of intracellular reactive oxygen species(ROS) was estimated through fluorescence assay.The intracellular activities of superoxide dismutase(SOD),catalase(CAT),and glutathi one peroxidase(GSH-px) were measured using biochemical method.Results TSG in the experimental concentration 0.1～100 ?mol?L~-1 exhibited no apparent cytotoxocity.10 ?mol?L~-1 and 100 ?mol?L~-1 TSG significantly inhibited the proliferation of VSMCs induced by serum,cell cycle transition from G0/G1phase to S phase,PCNA expression in nucleus of VSMCs and level of intracellular ROS.100 ?mol?L~-1 TSG markedly increased the activities of SOD and GSH-px.Conclusions Certain concentration of TSG can prevent VSMCs proliferation effect mediated by serum;the mechanism about TSG effect may be associated with arresting G0/G1 to S progression,decreasing PCNA expression and improving the antioxidation of VSMCs.