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1.
Chinese Journal of Infection and Chemotherapy ; (6): 140-143, 2017.
Article in Chinese | WPRIM | ID: wpr-511188

ABSTRACT

Objective To analyze the antibiotic resistance of pathogenic bacteria recovered from bronchial secretions by bronchofiberscope in bronchiectasis patients complicated with infection for improving antibacterial therapy. Methods A total of 97 bronchiectasis patients complicated with infection treated in Liyuan Hospital during the period from June 2013 to December 2015 were included in this analysis. The pathogens were recovered from bronchial secretions by bronchofiberscope and subjected to antimicrobial susceptibility testing by Kirby-Bauer disc method. The data were analyzed with WHONET 5.5 software. Results Pathogenic organisms were isolated from 53 (54.6%) of the 97 patients, including 49 (92.4%) strains of gram negative bacilli, mainly Pseudomonas aeruginosa, followed by Acinetobacter baumannii, Klebsiella pneumoniae, 3 (5.7%) strains of?gram?positive?cocci,?specifically?2?strains?of?S. aureus and 1 strain of S. pneumoniae, and 1 (1.9%) strain of Candida albicans. Antimicrobial susceptibility testing showed that most P. aeruginosa isolates (>71.8%) were susceptible to tobramycin, amikacin,cefepime, and aztreonam, but 100% resistant to levofloxacin. More A. baumannii isolates were susceptible to tobramycin and amikacin (both 85.7%), followed by imipenem (>42.9%). More than half (>50%) of the K. pneumoniae isolates were resistant to cefotaxime, gentamycin, ciprofloxacin, and levofloxacin.Conclusions Gram negative bacilli are dominant in the pathogenic organisms recovered from bronchial secretions in bronchiectasis patients complicated with infection. Most of the pathogens are relatively susceptible to tobramycin and amikacin, but resistant to ciprofloxacin?and?levofloxacin.

2.
Chinese Journal of Pathophysiology ; (12): 1327-1330,1335, 2016.
Article in Chinese | WPRIM | ID: wpr-604575

ABSTRACT

[ ABSTRACT] AIM:To observe the effects of long-term cigarette smoke exposure on pulmonary vascular remode-ling and the protein expression of transforming growth factor-β1 ( TGF-β1 ) in the rats, and to explore the mechanism. METHODS:SD rats (n=36) were randomly divided into control group, 2-week smoke exposure (S-2W) group and 12-week smoke exposure (S-12W) groups.HE staining andα-smooth muscle actin staining were performed to observe the pul-monary vascular remodeling.The protein expression of proliferating cell nuclear antigen ( PCNA) and TGF-β1 in the pulmo-nary arteries was determined by the method of immunohistochemistry.The mRNA expression of TGF-β1 in the pulmonary arteries was evaluated by RT-qPCR.RESULTS:Compared with control group, ratio of pulmonary vessel wall thickness to vessel diameter ( WT%) and percentage of muscularized vessels were significantly increased in S-2W group and S-12W group ( P<0.01) .Significant increases in the protein expression of PCNA and TGF-β1 in smoke exposure groups were ob-served compared with control group.There was significant difference between 2 model groups (P<0.01).Compared with control group, the mRNA expression of TGF-β1 in pulmonary artery walls obviously increased in smoke exposure groups. There was significantly difference between S-2W and S-12W groups (P<0.05).The mRNA expression of TGF-β1 was positively correlated with pulmonary vascular muscularization, WT% and the protein expression of PCNA.CONCLU-SION:Long-term cigarette smoke exposure results in pulmonary artery remodeling in rats.The possible mechanism is that cigarette smoking exposure induces the over-expression of TGF-β1 at mRNA level in pulmonary vessels and promotes the proliferation of pulmonary vascular smooth muscle cells in rats.

3.
Journal of Chinese Physician ; (12): 903-905,908, 2011.
Article in Chinese | WPRIM | ID: wpr-597998

ABSTRACT

Objective To explore the roles of IκBα and TGF-β1 on airway inflammation in rats with chronic bronchitis induced by smoking and study the effects and mechanism of anti-inflammation of pretreatment with ambroxol. Methods Sixty male wistar rats were randomly divided into four groups: Normal dosage group, model group, high dosage group and low dosage group. The rats with chronic bronchitis were established by smoking. For high and low dosage group, rats were pretreated respectively with ambroxol group, rats were pretreated with normal saline through peritoneal injection as much as the low dosage group.After 76 days, the histopathologic changes stained in hemotoxylin and eosin (H. E.) of bronchopulmonary tissues were observed under opticalmicroscope, white cell counts and differential analysis were performed in BALF, the expression of IκBα and TGF-β1 were detected by immunohistochemistry. Results The pathological changes of model group were in consistent with that of chronic bronchitis, but the degrees were significantly reduced in high and low dosage groups. Compared with those in normal group, the white cell count and the neutrophilic granulocyte count of BALF in model group were significantly increased and the macrophagocyte count decreased, and the expression of IκBαwas significantly decreased(t =3.24,3.31,3.29,3.48, P <0. 05) and the TGF-β1 significantly increased (P <0. 05). Compared with those in the model group, the white cell count and the neutrophilic granulocyte count of BALF in high and low dosage group were significantly decreased and the macrophagocyte count increased, the expression of IκBαwas significantly increased (t =2. 86,2. 97,2. 92,3.52,2.42,2. 88,2. 58,3.48, P <0. 05) and the TGF-β1 significantly decreased (P <0. 05) . Compared with those in low dosage group, the expression of TGF-β1 was decreased and the expression of IκBαincreased in high dosage group (t =2. 82,3.64, P <0. 05). Conclusions Down-regulating the expression of IκBα and up-regulating of TGF-β1 may be involved in the process of airway inflammation in rats with chronic bronchitis induced by smoking. Ambroxol might have better effects on ameliorating airway inflammation by up-regulating the expression of IκBα and down-regulating of TGF-β1.

4.
Journal of Chinese Physician ; (12): 494-496, 2009.
Article in Chinese | WPRIM | ID: wpr-395097

ABSTRACT

Objective To evaluate the effects and mechanism of valerian extract treatment on bleomycin-induced pulmonary fibrosis of rats. Methods After healthy Wistar rats(irrespective of sex)were given diethyl ether inhalation anesthesia, giving a single intratracheal instillation of bleomycin at a dose of 5 mg/kg to make a pattern of pulmonary fibrosis. 65 survival rats were randomly divided into four groups: Valerian high-dose groups(n = 16), Valerian low-dose groups(n = 16), Colchicine group(n = 16)and Model group (n = 17).Each group was given a dose of 100 mg/kg valeian extract everyday, a dose of 20 mg/kg valeian extract Valeian extract , a dose of 100μg/kg colchicine and a dose of 10ml/kg after second day. And in each groups, 6 rats were killed on day 7, 10 rats were killed on day 28 after instillation respectively. Rats in control group (n = 8) were instilled with saline intractracheally and saline was given everyday with a dose of 10ml/kg. Control group was killed on day 28. After rats were killed, The right lower pulmonary lobes were harvested for HE-staining, Masson-staining was used to observe the transformation of pulmonary tissue and immunohistochemistry was used to examine transforming growth factor-β1 (TGF-β1) which was analyzed by image analysis system. Results No obvious transformation were found in control group. The alveolitis in valerian and colchicine groups were ameliorated, compared with model group on day 7. The expressions of TGF-β1 in control group were lower than that in model group, and the mean integrated optical densities of TGF-β1 in control group were lower than that in mod-el group(P<0.05). The pulmonary fibrosis in valerian and colchicine group were ameliorated, compared with model group on day 28. The expressions of TGF-β1 in valerian and colchicine group were lower than that in model group. There were no significant differences between the valerian group and the colchicine group. Conclusion Valerian extract could reduce the degree of alveolitis and fibrosis induced by bleo-mycin through suppressing of TGF-β1.

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