Futterwertbeeinflussende Inhaltsstoffe in Rapssamen und Nebenprodukten der Rapsverarbeitung

Vytauto Didžiojo universitetasŽemės ūkio akademij

Pseudomonas aeruginosa bacteremia: Associations with a source of infection and antibiotic resistance

Aim of the study. To determine the associations between the source of infection and antibiotic resistance in patients with Pseudomonas aeruginosa bacteremia. Material and methods. A retrospective analysis of 50 patients with Pseudomonas aeruginosa bacteremia was carried out. If sepsis was suspected, blood culture was incubated in an automatic system BACTEC 9240. Then bacteria were identified, and their antibiotic resistance was estimated by disc diffusion method. If Pseudomonas aeruginosa strains were resistant to three or more antibiotics, they were considered as multidrug-resistant.Results. The origin of bacteremia was confirmed in 33 (66%) patients. Lower respiratory tract was the predominant source of Pseudomonas aeruginosa bacteremia (81.8%, n=27) as compared with infection of wound (39.4%, n=13), urinary tract (15.2%, n=5), and drain or cerebrospinal fluid (9.1%, n=3) (P<0.05). Eighteen percent (n=9) of strains, which caused bacteremia, were resistant to ceftazidime; 38% (n=19), to piperacillin; 22% (n=11), to imipenem; 26% (n=13), to meropenem; 24% (n=12), to ciprofloxacin; 40% (n=20), to gentamicin; and only 8% (n=4), to amikacin. Multidrug-resistant Pseudomonas aeruginosa strains were more frequently isolated if a source of infection was wound comparing to a source of other localization (61.5%, n=8 and 20.0%, n=4, respectively; P<0.05). Resistance of Pseudomonas aeruginosa strains to imipenem was associated with resistance to ciprofloxacin (13.2%, n=5 and 50.0%, n=6, retrospectively; P<0.05), but resistance to meropenem – both to ciprofloxacin and amikacin. Conclusions. The predominant source of Pseudomonas aeruginosa bacteremia was lower respiratory tract, and multidrug-resistant strains caused bacteremia more frequently if a source infection was wound. Pseudomonas aeruginosa resistance to carbapenems was associated with resistance to ciprofloxacin and resistance to meropenem – also to amikacin. Resistance of strains to ceftazidime and piperacillin was associated with resistance to gentamicin

Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD

Abstract Background Smoking activates and recruits inflammatory cells and proteases to the airways. Matrix metalloproteinase (MMP)-12 may be a key mediator in smoke induced emphysema. However, the influence of smoking and its cessation on airway inflammation and MMP-12 expression during COPD is still unknown. We aimed to analyse airway inflammatory cell patterns in induced sputum (IS) and bronchoalveolar lavage (BAL) from COPD patients who are active smokers and who have ceased smoking >2 years ago. Methods 39 COPD outpatients – smokers (n = 22) and ex-smokers (n = 17) were studied. 8 'healthy' smokers and 11 healthy never-smokers were tested as the control groups. IS and BAL samples were obtained for differential and MMP-12+-macrophages count analysis. Results The number of IS neutrophils was higher in both COPD groups compared to both controls. The amount of BAL neutrophils was higher in COPD smokers compared to healthy never-smokers. The number of BAL MMP-12+-macrophages was higher in COPD smokers (1.6 ± 0.3 × 106/ml) compared to COPD ex-smokers, 'healthy' smokers and healthy never-smokers (0.9 ± 0.4, 0.4 ± 0.2, 0.2 ± 0.1 × 106/ml respectively, p Conclusion The lower amount of BAL neutrophils in COPD ex-smokers, compared to COPD smokers, suggests positive alterations in alveolar compartment after smoking cessation. Smoking and disease itself may stimulate MMP-12 expression in airway compartments (IS and BAL) from COPD patients.</p

The effect of induced sputum and bronchoalveolar lavage fluid from patients with chronic obstructive pulmonary disease on neutrophil migration in vitro

Objective. The aim of study was to investigate a chemotactic effect of induced sputum and bronchoalveolar lavage fluid on blood neutrophils in patients with chronic obstructive pulmonary disease (COPD) and healthy individuals. Material and methods. Forty-three smokers with COPD, 19 ex-smokers with COPD, 13 healthy smokers, and 17 healthy nonsmokers were recruited to the study. Neutrophils were isolated from peripheral blood of study individuals. For the same experimental conditions, pooled induced sputum and bronchoalveolar lavage fluid of 20 COPD patients were used. Neutrophil chemotaxis in vitro was performed in cell-transmigration chamber. Substances tested for chemoattraction (interleukin-8, induced sputum, bronchoalveolar lavage fluid directly or in addition to interleukin-8) were added to lower wells. Upper wells were filled with 2.5×106/mL of neutrophil culture and incubated for 2 hours. Migration was analyzed by flow cytometry. Results. Interleukin-8 (10–100 ng/mL) induced a dose-dependant neutrophil migration in all the groups. Only 100 ng/L of interleukin-8 induced more intensive chemotaxis of neutrophils from COPD smokers as compared to ex-smokers (P&lt;0.05). Such difference between healthy individuals was obtained using 30 ng/mL of interleukin-8 (P&lt;0.05). Induced sputum/interleukin-8 (10–100 ng/mL), as well as induced sputum directly, induced neutrophil migration (P&lt;0.05). Chemotaxis of neutrophils isolated from COPD patients and healthy nonsmokers did not depend on additional interleukin-8 concentration. Bronchoalveolar lavage fluid/interleukin-8 (30–100 ng/mL) induced more intensive migration of neutrophils from COPD patients than bronchoalveolar lavage fluid (P&lt;0.05) alone. Conclusions. Migration of neutrophils isolated from patients with COPD was more intensive compared to healthy individuals. Induced sputum and bronchoalveolar lavage fluid directly and with addition of interleukin-8 stimulated chemotaxis, and it was higher in neutrophils from COPD patients. Migration of neutrophils did not depend on smoking status

Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

High frequency of the c.3207C>A (p.H1069Q) mutation in ATP7B gene of Lithuanian patients with hepatic presentation of Wilson’s disease

AIM: To investigate the prevalence of the ATP7B gene mutation in patients with hepatic presentation of Wilson’s disease (WD) in Lithuania

Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD-2

<p><b>Copyright information:</b></p><p>Taken from "Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD"</p><p>http://respiratory-research.com/content/8/1/81</p><p>Respiratory Research 2007;8(1):81-81.</p><p>Published online 14 Nov 2007</p><p>PMCID:PMC2200652.</p><p></p>OPD smokers, COPD ex-smokers and 'healthy' smokers

Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD-1

<p><b>Copyright information:</b></p><p>Taken from "Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD"</p><p>http://respiratory-research.com/content/8/1/81</p><p>Respiratory Research 2007;8(1):81-81.</p><p>Published online 14 Nov 2007</p><p>PMCID:PMC2200652.</p><p></p>-smokers, 'healthy' smokers and healthy never-smokers. Data are shown as mean ± SEM. *p < 0.05 compared to healthy never-smokers, #p < 0.05 compared to 'healthy' smokers

Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD-0

<p><b>Copyright information:</b></p><p>Taken from "Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD"</p><p>http://respiratory-research.com/content/8/1/81</p><p>Respiratory Research 2007;8(1):81-81.</p><p>Published online 14 Nov 2007</p><p>PMCID:PMC2200652.</p><p></p>ealthy' smokers and healthy never-smokers. Data are shown as mean ± SEM. *p < 0.05 compared to healthy never-smokers, #p < 0.05 compared to 'healthy' smokers