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Biomedical subjects

J Rozniecki

Publications and source records attributed to J Rozniecki.

At least 55 records · Page 3Linked to original sources
PubMed1991

[Alpha 1-antitrypsin and its phenotype in patients with asthma and aspirin hypersensitivity].

Alpha-1 antitrypsin (A-1-AT) levels were determined in 46 patients with aspirin sensitive asthma using the Eriksson method. The control group was made up of 17 asthmatics without aspirin sensitivity and 78 healthy volunteers. In 30 patients with aspirin asthma the phenotype of A-1-AT was determined using the Laurell method. The serum A-1-AT level was significantly higher in asthmatics in comparison with the healthy subjects. In the 30 subjects in whom the phenotype of A-1-AT was determined none of the phenotypes characteristic for lowered A-1-AT level were found more frequently than in groups without sensitivity to aspirin.

Adult↗
PubMed1991

[Effect of aspirin on FMLP (formyl-meth-leu-phe)-stimulated leukocytes in patients with asthma and hypersensitivity to aspirin].

In order to determine if aspirin sensitivity effects leukocyte reaction in aspirin sensitive asthma patients the authors studied the influence of aspirin on chemiluminescence in 12 aspirin sensitive asthmatics and 13 non-aspirin asthmatics. Leukocyte suspension were carried out according to Böyum. Chemiluminescence was determined using the LKB--Wallac counter. No statistical differences in leukocyte chemiluminescence was found in both groups.

Adult↗
PubMed1989

The effect of preseasonal immunotherapy on the production of histamine-releasing factor (HRF) by mononuclear cells from patients with seasonal asthma: results of a double-blind, placebo-controlled, randomized study.

The effect of immunotherapy on the production of histamine-releasing factor (HRF) by mononuclear cells (MNC) from patients with seasonal asthma was investigated in a double-blind, placebo-controlled, randomized study. Twenty-four patients with asthma were randomly divided into a placebo-treated group and a grass pollen-treated group. In vitro production of HRF by MNCs and the provocative concentration of histamine that causes 20% fall in FEV1 were measured before and after immunotherapy, and symptoms were monitored during the pollen season. MNCs from the patients were either cultured alone, spontaneous HRF production (spHRF), or in the presence of grass allergens (grass-stimulated HRF production), and the supernatants were assayed for HRF activity with basophils from a single donor after the study. We found that MNCs from patients with seasonal asthma to grass pollen spontaneously produce substantial amounts of HRF. The group of patients treated with placebo developed typical symptoms in the pollen season and also an increase in HRF production. In contrast, patients treated with grass pollen demonstrated reduced symptoms and no increase in spHRF production. A high degree of correlation between spHRF productions and symptom scores in both treated groups was noted. After 2 years of immunotherapy, allergen-stimulated HRF production decreased significantly, whereas spHRF production decreased significantly only in the patients who were clinically benefitted. The change in the provocative concentration of histamine that causes 20% fall in FEV1 during the pollen season highly correlated with the change in HRF production. The results of this study suggest that HRF might be involved in the pathogenesis of atopic asthma.

Adult↗
PubMed1989

[Role of fungi in house dust allergy in patients with bronchial asthma].

The aim of the study was to evaluate the contribution of skin hyperreactivity to fungi in patients with bronchial asthma and demonstrating skin sensitivity to house dust. In 50 patients skin tests with 24 allergen solutions of fungi found most often in house dust. Positive skin tests were found in 92% of the evaluated patients. Reactions to fungi allergens were seen more often than to Dermatophagoides pteronyssimus. Most often skin reactivity toward the following fungal allergens were seen: Candida albicans, Aspergillus fumigatus, Fusarium culmorum and Aureobasidium pullulans. It seems that skin hypersensitivity to fungi is very common in patients with bronchial asthma and sensitive to house dust. Clinical verification of this hypersensitivity should be studied further.

Adult↗
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↗
PubMed1988

Effect of autogenic bacterial antigens on the production of histamine releasing factor by mononuclear cells from intrinsic asthmatic patients.

The production of histamine releasing factor (HRF) by mononuclear cells (MNC) from intrinsic asthmatic patients has previously been reported. In this study, we investigated the effect of preincubation of lymphocytes with autogenic killed bacteria upon the production of HRF. Bacteria were isolated from the sputum, and nasopharyngeal swab obtained from patients and control subjects. MNC from intrinsic asthmatics and healthy controls were preincubated with killed bacteria for 4 h, then washed and cultured for 18 h. HRF activity of the cell-free supernatants was assayed in the histamine release test using basophils from normal subjects. We found that MNC from the patients spontaneously produce significant amounts of HRF. Preincubation of the cells with autogenic bacterial antigens enhanced HRF production in 12 of 25 patients and only in one of 15 control subjects. No specific bacterial strain was identified as having the sole stimulatory property for HRF production; rather, individual susceptibility predisposes to the ability to produce HRF in response to some common bacteria. When MNC from healthy subjects were preincubated with bacterial antigens isolated from the patients, no enhancement in HRF production was observed. We concluded that MNC from some intrinsic asthmatics are specifically sensitized to certain bacterial antigens and release HRF upon contact with these antigens.

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↗
PubMed1987

The magnitude of the spontaneous production of histamine-releasing factor (HRF) by lymphocytes in vitro correlates with the state of bronchial hyperreactivity in patients with asthma.

In our previous studies we reported that lymphocytes from patients with asthma spontaneously produce histamine-releasing factor (HRF) in vitro. In an effort to examine whether spontaneous HRF production (SpHRF) by lymphocytes from patients with asthma is related to the state of bronchial hyperreactivity (BHR), 20 patients with mild to severe asthma were studied. Peripheral blood lymphocytes were cultured alone in a serum-free medium for 24 hours, and culture supernatant was assayed for HRF activity in two separate histamine-release tests with autologous basophils and normal basophils from known healthy donors. BHR was measured as bronchial reactivity to inhaled histamine and was expressed as a provocation concentration of histamine required to induce a 20% fall in FEV1 (PC20). The result of this study demonstrated that lymphocyte supernatant from all patients with asthma released significant amount of histamine from both autologous and normal basophils. Very high histamine release was usually induced by lymphocyte supernatant from severely ill patients who had PC20 less than 2 mg/ml. Statistical analysis demonstrated that the magnitude of the SpHRF significantly correlated (r = -0.86; p less than 0.001) with PC20. Since mast cell- and basophil-derived mediators have been implicated in the pathogenesis of BHR, high correlation between PC20 and SpHRF by lymphocytes suggests that the latter may contribute to the development of BHR. Further studies are required to disclose the exact relationship between SpHRF and BHR.

Adult↗
PubMed1987

Tolerance to acetylsalicylic acid (ASA) induced in ASA-sensitive asthmatics does not depend on initial adverse reaction.

A state of tolerance to aspirin (ASA) was induced in 10 aspirin-sensitive patients by daily administration of incremental doses of ASA. No adverse reactions were reported. The initial dose (from 5 to 60 mg) was gradually increased each day up to 300 mg and then doubled. 50 mg indomethacin given the day after administration of 600 mg ASA did not elicit any symptom of intolerance. The authors discuss a possible mechanism of tolerance to aspirin in ASA-sensitive asthmatics after ASA administration, suggesting that it might be connected either with inhibition of the lipooxygenetic pathway of arachidonic acid metabolism or with blockade of the cyclooxygenase supplementary binding site by salicylic acid, a product of acetylsalicylic acid hydrolysis. This would prevent aspirin from binding with the catalytic cyclooxygenase site.

Adult↗