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Objective@#To investigate the distribution characteristics of pathogens and related risk factors in patients with cardiovascular disease complicated with pulmonary infection.@*Methods@#From June 2015 to October 2017, 252 patients with cardiovascular disease who were treated in the People's Hospital of Shanxi Province were selected.The number of patients complicated with pulmonary infection in the treatment process was counted, the distribution characteristics of pathogens in patients with pulmonary infection was analyzed.The relationship between gender, age, time in bed, smoking history, invasive operation, chronic obstructive pulmonary disease(COPD) and pulmonary infection in patients with cardiovascular disease were analyzed.Logistic regression analysis was used to analyze the risk factors of pulmonary infection in patients with cardiovascular disease.@*Results@#There were 32 cases of pulmonary infection in 252 patients with cardiovascular disease, the incidence rate of pulmonary infection was 12.70%.Forty-one strains of pathogens were isolated from the patients with pulmonary infection, among them, there was Gram negative bacteria with 27 strains, accounting for 65.85%, Gram positive bacteria with 10 strains, accounting for 24.39%, and 4 fungi with 4 strains, accounting for 9.76%.The incidence of pulmonary infection in patients with cardiovascular disease was not related to the gender of the patients(χ2=0.267, P>0.05). The incidence rates of pulmonary infection in patients with age≥60 years old, time in bed for more than 2 weeks, smoking history, invasive operation, COPD were significantly higher than those of age<60, time in bed for less than 2 weeks, no smoking history, no invasive operation, no COPD(χ2=7.076, 7.066, 4.764, 12.603, 7.805, all P<0.05). The logistic regression analysis showed that age≥60 years old, time in bed for more than 2 weeks, smoking history, invasive operation, COPD were independent risk factors of patients with cardiovascular disease complicated with pulmonary infection(OR=4.229, 3.397, 3.504, 4.82, 3.804, all P<0.05).@*Conclusion@#The main pathogens of pulmonary infection in patients with cardiovascular disease are Gram negative bacteria, followed by Gram positive bacteria, only a few fungi.Excessive age, excessively long time in bed, smoking history, invasive operation, COPD are risk factors for pulmonary infection in patients with cardiovascular disease.
ABSTRACT
Objective To investigate the distribution characteristics of pathogens and related risk factors in patients with cardiovascular disease complicated with pulmonary infection.Methods From June 2015 to October 2017,252 patients with cardiovascular disease who were treated in the People ＇s Hospital of Shanxi Province were selected.The number of patients complicated with pulmonary infection in the treatment process was counted , the distribution characteristics of pathogens in patients with pulmonary infection was analyzed .The relationship between gender,age,time in bed, smoking history, invasive operation, chronic obstructive pulmonary disease ( COPD) and pulmonary infection in patients with cardiovascular disease were analyzed.Logistic regression analysis was used to analyze the risk factors of pulmonary infection in patients with cardiovascular disease .Results There were 32 cases of pulmonary infection in 252 patients with cardiovascular disease , the incidence rate of pulmonary infection was 12.70%.Forty－one strains of pathogens were isolated from the patients with pulmonary infection ,among them,there was Gram negative bacteria with 27 strains,accounting for 65.85%,Gram positive bacteria with 10 strains,accounting for 24.39%,and 4 fungi with 4 strains,accounting for 9.76%.The incidence of pulmonary infection in patients with cardiovascular disease was not related to the gender of the patients (χ2 ＝0.267,P＞0.05).The incidence rates of pulmonary infection in patients with age≥60 years old,time in bed for more than 2 weeks,smoking history,invasive operation,COPD were significantly higher than those of age ＜60,time in bed for less than 2 weeks,no smoking history, no invasive operation,no COPD(χ2 ＝7.076,7.066,4.764,12.603,7.805,all P＜0.05).The logistic regression analysis showed that age≥60 years old,time in bed for more than 2 weeks,smoking history,invasive operation,COPD were independent risk factors of patients with cardiovascular disease complicated with pulmonary infection ( OR ＝ 4.229,3.397,3.504,4.82,3.804,all P ＜0.05).Conclusion The main pathogens of pulmonary infection in patients with cardiovascular disease are Gram negative bacteria ,followed by Gram positive bacteria ,only a few fungi. Excessive age,excessively long time in bed ,smoking history,invasive operation,COPD are risk factors for pulmonary infection in patients with cardiovascular disease.
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Objective To study the effects of acetylcholine combined with vincristine (VCR) on A549 cells, furthermore to study the influence that is due to affecting the expression of the two proteins bcl-2 and p53. Methods MTT assay was used to analyze growth inhibition effect of acetylcholine alone and combined with IC50VCR on A549 cells.The expression of bcl-2 and p53 was measured by immunohistological chemistry technique(IHC) and Western blot.Results The inhibition rates for A549 cells with 0.1,1 and 10 μmol/L acetylcholine were (0.050±0.032)％,(0.101±0.021)％,(0.169±0.015)％.The inhibition rates for tumor cells with 0.1,1 and 10 μmol/L acetylcholine joint 0.2 μg/ml VCR were (0.529±0.023)％,(0.545±0.011)％,(0.589±0.015)％,the difference was statistically significant compared with the VCR group (q'values were 1.09,1.37,1.83,P＜0.05).Acetylcholine alone exerted inhibitory effect on A549 cells in a concentration dependent manner and significanrtly enhanced its sensitivity to VCR (P＜0.05).acetylcholibne (0.1-10 μmol/L)combined with IC50VCR decrased the expression of bcl-2 and p53 (P＜0.05).Conclusion Acetylcholine alone and combined with VCR can inhibit the growth of A549 cells. Significant synergistic effect between acetylcholine and VCR is found in inducing cell apoptosis by changing the expression of bcl-2 and p53.
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Objective To evaluate the effects and possible mechanism of endovascular irradiation using liquid 32 P-filled ballon catheter on restenosis after interventional therapy.Methods 54 Wistar rats were randomly divided into injured group, which received the balloon injury of thoracic aorta, and irradiated group, which received the balloon injury of thoracic aorta followed immediately by ionizing radiation using 20 Gy or 28 Gy liquid 32 p-filled balloon catheter. The expressions of proliferation cellular nuclear antigen(PCNA) in vascular cells and smooth muscle actin(?-SM actin) in the vascular adventitia were detected by immunohistochemical method, and were quantified by computer image analysis. The morphologic changes of thoracic aorta were analyzed by computer image analysis . Results ⑴14 days after injury, both the lumen area and external elastic lamina (EEL) area of thoracic aorta in the irradiated group were significantly larger than those in injuried group, but the neointima area was significantly smaller in the irradiated group. The above chanages were negative relation with the irradiation doses. ⑵At third day after injury, the cell proliferation activity in the adventitia and media of thoracic aorta in the irradiated group obviously decreased in dose dependent manner compared with the injured group. At the 7th day after injury,there was not significant difference in the cell proliferation in the adventitia and media of the vessels between the irradiated group and injury group. ⑶At 7th and 14th days after injury. The ?-SM actin expression level in the adventitia of thoracic aorta in the irradiated group was significantly lower than that in the injured group, which was negatively related with the irradiation dose.Conclusion To some extent, there was a correlation between the irradiation dose of using liquid 32 p-filled balloon catheter and the areas of lumen, EEL and neointima. The endovascular irradiation could contribute to inhibiting the neointima and improving the vascular remodeling by inhibiting vascular cell proliferation and adventititial ?-SM actin expression.