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Biomedical subjects

U Ruta

Publications and source records attributed to U Ruta.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Immediate hypersensitivity in the development of contact sensitivity to disinfectant agents].

In 53 female health service workers with contact allergy to disinfectants (formaldehyde, glutaraldehyde, benzalkonium, lisoformine) the results of skin prick tests using common environment allergens were analysed, and concentrations of total IgE in blood serum were identified. In 29 (54.7%) persons positive prick tests (Dermatophytes--21, pollens--21, latex--7, domestic dust--5, goose and duck feathers--3, dog hair--2, and cat hair--1) were noted. In the whole group mean IgE concentration accounted for 88.2 kU/1, whereas in the group with positive skin prick test the value increased to 136.1 kU/1. The authors are of the opinion that in patients with contact allergy to disinfectant some symptoms of atopic diathesis are observed.

Adult↗
PubMed1995

Latex allergy.

Over the last ten years allergy to latex has become a serious, life-threatening medical problem. Exposure to latex may result in immediate hypersensitivity reactions such as urticaria, dyspnoe, rhinitis, angioedema and anaphylactic shock in sensitized individuals. People occupationally exposed to latex--health care and rubber industry workers and children suffering from spina bifida--are the most important risk groups. Clinical manifestations, immunological mechanisms, trials for identifying latex allergens and laboratory testing are reviewed here. Moreover, the authors present two cases of latex allergy diagnosed with the use of a nasal challenge test. 0.0005% latex solution (Stallergen) and latex extract prepared at the Clinic were used. Nasal washings were performed before, 30 minutes, 3 and 24 hours after provocation. The test evaluation was based on changes in the number and type of cells present in the washings. As there is no laboratory test to be used in latex allergy diagnosis approved by the Food and Drug Administration (FDA) the nasal provocation test seems to be worthy of further investigation. Ways of reducing of the allergenicity of latex products and preventing hypersensitivity reactions are also presented.

Adult↗
PubMed1993

Changes in nasal lavage fluid due to formaldehyde inhalation.

The aim of the study was to characterize the nature of the formaldehyde-induced nasal response consisting in symptoms of rhinitis and changes in nasal lavage fluid. Eleven healthy subjects and nine patients with specific skin sensitization were provoked in a toxicological chamber with formaldehyde at a dose of 0.5 mg/m3 over 2 h. Nasal lavage was performed prior to and immediately after provocation and 4 and 18 h later. Provocation with formaldehyde caused transient symptoms of rhinitis and prolonged changes in nasal washings. There were increases in the number and proportion of eosinophils and elevated albumin and total protein levels in nasal lavage fluid 4 and 18 h after provocation. No difference in the nasal response to formaldehyde was found between patients with skin sensitization and healthy subjects. These data confirm the irritative effects of formaldehyde and are also suggestive of nonspecific proinflammatory properties when formaldehyde is inhaled at a low (0.5 mg/m3) dose.

Albumins↗
PubMed1993

Effect of ipratropium on nasal reactivity to histamine and eosinophil influx in perennial allergic rhinitis.

In a double-blind, placebo-controlled study nasal saline and histamine provocation tests were performed in patients with perennial allergic rhinitis in order to assess changes in eosinophil influx and non-specific nasal reactivity after 8 days of treatment with ipratropium bromide. A "nasal pool" method was used to trace changes in protein level and eosinophil influx into nasal secretions. Treatment with ipratropium 80 mg q.i.d. caused a significant decrease in the albumin and total protein level in saline washings and induced a five-fold increase in eosinophils as compared to the placebo treatment. The nasal mucosal response to histamine, assessed as the number of sneezes and protein level, was more responsive to ipratropium treatment than the mucosa from placebo-treated subjects. Since eosinophil numbers were correlated with an increase in the vascular and sneezing responses, it appears that ipratropium potentiates inflammatory mechanisms when used in subjects with an allergy in the nasal mucosa.

Adult↗
PubMed1993

Inhibitory effect of levocabastine on allergen-induced increase of nasal reactivity to histamine and cell influx.

For evaluation of the effect of levocabastine pretreatment on allergen-induced rhinitis symptoms, changes in nasal washings, and nasal responsiveness to histamine, 12 asymptomatic patients with documented allergic rhinitis participated in a single-blind, placebo-controlled study. Eight-day treatment with levocabastine (twice in each nostril, four times a day) caused significant reduction in nasal symptoms and inflammatory cell influx after allergen challenge, as compared with placebo administration. Levocabastine inhibited increased nasal reactivity to histamine induced by allergen provocation, as controlled by rhinitis symptoms and albumin level in nasal washings. These data reveal a high effectiveness of levocabastine in the prevention of allergen-induced rhinitis symptoms. Moreover, its inhibitory effect on inflammatory cell influx and hyperresponsiveness to histamine suggest that levocabastine is more than a simple H1-receptor antagonist.

Adult↗
PubMed1993

[Behavior of esterase inhibitor C1 in patients with urticaria due to aspirin hypersensitivity].

The aim of the study was to evaluate concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria. Deficiency of C1 INH is the basis for hereditary angioneurotic oedema. The study was performed in 32 subjects with aspirin-sensitive urticaria. The value of C1 INH in examined patients was the same as in control group. It seems there is no coexistence of aspirin-sensitive urticaria and C1 esterase inhibitor deficiency.

Adult↗
PubMed1992

[Principles of establishing the registries of chemical substances in the United States and Europe].

The paper presents the principles of building up the inventories of chemical substances in the USA, the countries belonging to European Economic Community (EEC) and Austria. In all countries, the appropriate legal regulations putting the manufacturers and importers of chemicals under obligation to provide some strictly determined information underlie the decision to build up these inventories. The data provided usually inform of: manufacturer's name and address, chemical substance identity, production volume and ways of distribution. The paper presents also the criteria of selection of substances to be placed in the inventory, organizational scheme of building up the inventory and the ways of exacting the respective regulations. The inventories of chemical substances issued in the USA and Austria may serve as banks of information on the place, kind and quantity of chemical substances on the territory of the whole country. Based on these data a map of chemical hazards zones may be prepared which may adversely affect either human health or environment. The inventory of EEC countries may serve only as lists of chemicals occurring in the common market.

Austria↗
PubMed1990

Nicotine increases human polymorphonuclear leukocytes chemotactic response--a possible additional mechanism of lung injury in cigarette smokers.

Human polymorphonuclear leukocytes (PMNL) which are a potential source of proteolytic enzymes and reactive oxidant species contribute to the development of pulmonary emphysema in cigarette smokers. We found that nicotine at concentrations that occur in smokers' plasma enhances human PMNL chemotactic response to zymosan-activated serum (ZAS) and n-formyl-methionyl-leucyl-phenylalanine (FMLP). Maximal increase in chemotactic migration was at nicotine concentration 1 mumol/l. Higher concentrations, above 0.1 mmol/l inhibited PMNL chemotactic response and spontaneous migration. Nicotine also enhanced PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of ZAS. The number of PMNL found in the pleural cavity was 1.9-fold higher (p less than 0.001, n = 5) when animals were pretreated with 0.15 mg of nicotine. However, this drug itself (concentrations of 0.1 mumol/l to 10 mmol/l) had weak chemotactic activity for PMNL. It seems that the stimulatory action of nicotine on PMNL chemotaxis may be partly responsible for increased PMNL numbers in the lower airways of cigarette smokers and following formation of the elastase/antielastase imbalance in lung tissue.

Animals↗
PubMed1990

Nicotine inhibits alpha-1-proteinase inhibitor inactivation by oxidants derived from human polymorphonuclear leukocytes.

Cigarette smoke can inactivate the alpha-1-proteinase inhibitor (alpha 1PI) by oxidative mechanisms and thus predisposes to the development of pulmonary emphysema. There are differences between the whole smoke and gas phase acting as alpha 1PI inactivators in vitro which suggests that the whole smoke is less oxidizing than the gas phase. Also studies on alpha 1PI oxidative inactivation in the lung of cigarette smokers gave controversial results. The reductive properties of cigarette tar which contains most of smoke nicotine may be some explanation of it. Therefore in this study we have investigated the effect of nicotine (0.4 mumol/l to 4 mmol/l) on the oxidative inactivation of human alpha 1PI by phorbol myristate acetate-activated polymorphonuclear leukocytes (PMNL), chloramine-T (15 mumol/l), hydrogen peroxide (15 mmol/l) and the superoxide radical (O2-.) generating system-xanthine (0.2 mmol/l)-xanthine oxidase (80 U/l). Nicotine at concentrations of greater than 40 mumol/l protected alpha 1PI from stimulated PMNL. The preincubation of PMNL with these concentrations of nicotine did not diminish their ability to inactivate alpha 1PI after stimulation. Nicotine (above 0.4 mumol/l) also protected alpha 1PI from chloramine-T but not from H2O2. The inhibition of O2-.-mediated alpha 1PI inactivation by nicotine was low and was observed only at a concentration of 4 mmol/l. This nicotine concentration did not affect xanthine oxidase activity. It is suggested that cigarettes with low nicotine contents can cause greater oxidative lung injury than their high nicotine counterparts and be a greater risk factor for the development of lung emphysema.

Humans↗
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↗
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↗