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Biomedical subjects

D Nowak

Publications and source records attributed to D Nowak.

At least 217 records · Page 12Linked to original sources
PubMed1989

Roles of hyperresponsiveness and airway inflammation in bronchial asthma.

Bronchial hyperresponsiveness is one important feature of bronchial asthma, and evidence has been accumulated that airway inflammation contributes to the specific airway response in asthmatic patients. Increase in airway responsiveness following viral infection, exposure to allergen, ozone or chemical sensitizers supports the evidence for a link between hyperresponsiveness and airway inflammation. However, as only some respiratory tract infections induce an increase in hyperresponsiveness, and patients with chronic bronchitis and cystic fibrosis have less airway hyperresponsiveness than asthmatics, airway inflammation is considered to be only one of many factors contributing to the hyperresponsiveness of asthmatic airways.

Allergens↗
PubMed1989

Chemotactic activity of elastin-derived peptides for human polymorphonuclear leukocytes and their effect on hydrogen peroxide and myeloperoxidase release.

The chemotactic activity of elastin-derived peptides (EP) for human polymorphonuclear leukocytes (PMNL) was investigated using the under agarose method. The EP were produced by digesting the bovine ligament elastin with porcine pancreatic elastase. Thus prepared digest had weak chemotactic activity for PMNL. The mean chemotactic index for all tested EP concentrations did not exceed 1.30 and was lower than that obtained with zymosan-activated serum (ZAS, n-formyl-methionyl-leucyl-phenylalanine (FMLP) 2.2 +/- 0.40, 3.1 +/- 0.32, (n = 10) respectively. However, EP (50 micrograms) after injection to the mouse pleural cavity induced PMNL influx. The mean PMNL number found in this cavity was 0.09 +/- 0.03 x 10(6) for PBS and 0.18 +/- 0.03 +/- 10(6) for EP injection (p less than 0.01 n = 6). Human PMNL during 60 min incubation with EP (1 to 10 micrograms/ml) or with EP and cytochalasin B (CB 4.8 micrograms/ml) released myeloperoxidase and low amounts of hydrogen peroxide. At 1 micrograms/ml and in presence of CB elastin digest was nearly as active in myeloperoxidase release as FMLP (300 ng/ml). The values reached 17.1 +/- 2.5 and 19.7 +/- 2.1% of the total activity of whole cell lysate, respectively. The obtained results suggest that EP produced in vivo in the site of inflammation could modulate to some extent its course by enhancing PMNL influx and their activation. It seems that such mechanism of enhancement of the inflammatory response may occur in the lungs which are rich in elastin fibers.

Animals↗
PubMed1989

Ascorbic acid inhibits polymorphonuclear leukocytes influx to the place of inflammation--possible protection of lung from phagocyte-mediated injury.

Ascorbic acid as a scavenger of oxidants derived from human polymorphonuclear leukocytes (PMNL) may have clinical significance in antioxidant prevention of emphysema. However, there is a risk relevant to its administration because this drug was reported to enhance PMNL chemotactic response and thus could create protease burden in the lower airways. In this study we have investigated the effect of ascorbic acid on the PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of zymosan-activated serum (ZAS). We also evaluated the influence of ascorbic acid on human PMNL spontaneous migration, chemotaxis to ZAS and n-formyl-methionyl-leucyl-phenylalanine (FMLP) under agarose. The previous ascorbic acid intraperitoneal administration (single dose 10 mg per day for 3 following days) inhibited leukocyte influx. Total number of cells found in the cavity, number of PMNL and lymphocytes was 2.4, 3.5, 1.7-fold lower than in animals without ascorbic acid, respectively. In vitro ascorbic acid (concentrations of 1 to 10 mg/dl) enhanced PMNL spontaneous migration, concentrations 10 mg/dl and higher inhibited PMNL chemotaxis to ZAS and had no influence on migration of the cells toward FMLP. These results suggest that ascorbic acid may be useful for prevention of lung oxidant injury not only as oxidant scavenger but also as an inhibitor of PMNL influx to the pulmonary tissue.

Animals↗
PubMed1989

[Experimental studies on the effect of tobacco smoke, vitamin C and vitamin E on elastase-induced pulmonary emphysema].

In this study the authors tried to evaluate the effect of tobacco smoke (source of oxidants) vitamin C and E (antioxidants) on elastase induced pulmonary emphysema in hamsters. Using morphometry the internal area of pulmonary alveoli was calculated. The results of this study differ from other similar studies because no effect of tobacco smoke could be demonstrated. The authors discuss this finding.

Animals↗
PubMed1989

[The prognosis of bronchial asthma in childhood].

The prevalence of childhood asthma is about 10% as compared to 6% in adults. 40% to 80% of asthmatic children become symptom-free during adolescence, but asymptomatic bronchial hyperreactivity may persist. About one third of those patients who have become symptom-free during adolescence will have relapses in adult life. Some factors seem to predict a worse prognosis of the disease: positive family history, concomitant allergic diseases, eczema, severe symptoms at the onset of the disease and during adolescence, a high degree of non-specific bronchial hyperreactivity, active and passive smoking. Questionable prognostic factors include sex, age of onset and breast-feeding.

Asthma↗
PubMed1988

Formation of DNA adducts and water-soluble metabolites of benzo[a]pyrene in human monocytes is genetically controlled.

Formation of DNA adducts and of water-soluble metabolites was studied in monocytes of 86 first-degree relatives of 15 families. Tests were performed with blood monocytes using (G-3H)-benzo[a]pyrene as a model pro-carcinogen. Variance analysis revealed significantly higher inter-familial than intra-familial variations. From these data we conclude that the formation of DNA adducts is genetically controlled. Therefore the enhanced formation of benzo[a]pyrene DNA adducts in lung cancer patients found in earlier studies may reflect a genetic predisposition for lung cancer in some patients.

Adolescent↗
PubMed1988

The influence of aminophylline on human neutrophils--possible protection of lung from proteolytic injury.

Protease-antiprotease imbalance in the lung is considered to be a likely pathogenetic mechanism in the development of lung injury--particularly emphysema. Aminophylline is often used in bronchitis, bronchial asthma and emphysema. To assess, whether aminophylline indeed affects this mechanism we evaluated in vitro its influence at therapeutical concentrations (12 and 20 micrograms/ml) on phagocytosis, release of total protein and lysosomal enzymes after phagocytosis, spontaneous migration and chemotaxis of human neutrophils to zymosan-activated serum. There were no significant differences in phagocytosis, release of leukoprotease and acid phosphatase between neutrophils with and without aminophylline at both concentrations. However, the release of total protein was different (p less than 0.02, 12 micrograms/ml) and lower (p less than 0.02, 20 micrograms/ml) than the control. The mean decrease in protein release was 13.5 +/- 6% of the control and aminophylline inhibited the release of the protein with molecular weight below 35.000 daltons. Significant migration inhibition was found in 22% cases (12 micrograms/ml, n = 9) and in 53% (20 micrograms cm-3, n = 13). Neutrophil chemotaxis was different (p less than 0.02, 12 micrograms/ml) and lower (p less than 0.05, 20 micrograms/ml) than the control. The obtained results suggest that high doses, of aminophylline may diminish inflammatory recruitment of neutrophils--a rich source of elastase to the lung, and thus diminish proteolytic pulmonary injury.

Acid Phosphatase↗
PubMed1988

The comparative study of reactive oxygen species generated by polymorphonuclear leukocytes as alpha 1-proteinase inhibitor inactivators-possible application for antioxidant prevention of emphysema.

The oxidative inactivation of alpha 1-proteinase (alpha 1AP) inhibitor is a one of mechanisms that may lead to the pulmonary emphysema. This process is caused by oxidants derived from atmosphere and released from lung phagocytes. These cells produce various oxidants hydrogen peroxide (H2O2), hypochlorous acid (HClO), hydroxyl (OH.) and superoxide (O2-) radicals after inflammatory stimulation. In this study I have investigated the effects of H2O2 (1.5 x 10(-5) to 1.5 x 10(-2) M) alone or with addition of FeCl2 (50 microM) in order to generate OH., chloramine-T (1.5 x 10(-5) to 1.5 x 10(-3) M) which generates HClO, glucose 10 mg/ml-glucose oxidase (12.5 to 80 mU/ml)-H2O2 generating system, xanthine 0.2 mM-xanthine oxidase (12.5 to 80 mU/ml)-O2-2 generating system on the elastase inhibitory activity of alpha 1AP in vitro. H2O2 was weak in alpha 1AP inactivation--only concentration of H2O2 1.5 x 10(-2) caused severe loss of its activity to 23 +/- 8% inhibition of elastase. Addition of FeCl2 to H2O2 and following OH. generation did not enhance its alpha 1AP inactivation. O2-2 generating system inhibited moderately alpha 1AP. The % inhibition of elastase at concentration of xanthine oxidase 80 mU/ml was 65 +/- 7. HClO was most effective as an alpha 1AP inactivator. All used chloramine-T concentrations completely suppressed alpha 1AP activity. The obtained results and in vivo consumption of H2O2 by polymorphonuclear leukocyte myeloperoxidase for HClO production suggest that scavenging of these reactive oxygen species may be useful in prevention of emphysema.

Antioxidants↗
PubMed1988

Quantitative analysis of the tomographic thallium-201 myocardial bullseye display: critical role of correcting for patient motion.

Single photon emission computed tomography (SPECT) myocardial 201TI imaging appears to offer major improvements over planar imaging. Quantitative analysis of the 201TI images appears to offer major advantages over subjective analysis in planar imaging, but the three-dimensional data available in SPECT images requires special approaches to analysis and display. Thus the myocardial "bullseye" display was developed to summarize and analyze the three-dimensional images of the left ventricle in two dimensions. The relative 201TI distribution to each region of the left ventricle of an individual patient can be displayed as the number of s.d.s away from normal that the region falls. We found that patient motion during the 22 min required for SPECT imaging appeared to produce artifactual defects. Thus, computer programs were developed to quantitate motion between consecutive frames of a [201TI] SPECT myocardial imaging study, simulate nonreturning vertical motion in normal patients, and correct the acquired data for motion. Motion as small as 0.5-1.0 pixel (3-6 mm) in the vertical (axial) direction caused artifactual defects in the quantitative bullseye display that resulted in a false-positive rate of up to 40% for a +1.0 pixel shift. Patient motion of magnitude greater than the threshold value for artifact-production (0.5 pixel) occurred at a rate of 10%, and should be corrected before tomographic reconstruction.

Heart↗
PubMed1987

[Chemotherapy of pulmonary tuberculosis. Sputum culture conversion in 8 weeks in 84% of patients].

Conversion rate to negativity of sputum culture and microscopy in 50 patients, previously untreated, with open cavernous pulmonary tuberculosis was analysed. Treatment consisted of isoniazid, rifampicin and pyrazinamide for three months, followed by administration of isoniazid and rifampicin. Conversion to a negative sputum culture had occurred after four weeks in 30% of patients, after eight weeks in 84%, and after 14 weeks in all patients. In 76% of patients the cultural conversion preceded the microscopic one. Treatment was well tolerated; only one patient had side effects requiring a short interruption of drug administration. The results confirm that this regimen is effective against pulmonary tuberculosis without significant side effects.

Adolescent↗