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Biomedical subjects

R Polosa

Publications and source records attributed to R Polosa.

117 records · Page 7Linked to original sources
PubMedDate not supplied

[Smoking habits in health care workers: experience in two general hospitals of Eastern Sicily].

PURPOSE: The aim of our study was to assess the smoking habits in health care workers. MATERIALS AND METHODS: In concomitance with a medical examination for Health Care Surveillance requested by the Italian Laws (D. Lgs. 626/94), our operative units interviewed 2,000 persons (47.9% males, 52.1% females, mean age = 45 yrs (SD+/-9.41 yrs) working in two General Hospitals of Eastern Sicily. RESULTS: The prevalence of smokers was found to be higher in men (34.5%) than in women (33.6%), in Health Care Operators (36.4%) and professional nurses (36.2%) than in medical doctors (27.7%), in night-time workers (34,5%) then in day-time-workers (28,7%). The compliance with smoking restriction was found to be poor; in fact, 60% out of smokers declared to smoke during the working hours. CONCLUSIONS: This investigation has revealed the significant prevalence of tobacco smoking among the health care workers in general. We think that the inclusion of an anonymous questionnaire on smoking habits within the Services of Sanitary Surveillance may help in the national campaign against cigarette smoking.

Adult↗
PubMedDate not supplied

[Significance of tachyphylaxis induced by repeated bradykinin inhalation in bronchial asthma].

Bradykinin (Bk) is a potent bronchoconstrictor agent which may contribute to the pathogenesis of bronchial asthma. Recently we have shown that repeated bronchial challenge with this agonist in asthmatics produced a specific loss of responsiveness. In vitro studies suggest that this phenomenon may be due to generation of protective prostaglandins. In this study we investigated whether flurbiprofen (F) pretreatment inhibited Bk tachyphylaxis. The efficacy of F was demonstrated by the total suppression of whole blood TxB2 formation. In addition, a time-course study of the tachyphylactic response was carried out. Refractoriness in response to inhaled Bk occurred in all subjects. The mean PC20 Bk increased from 0.07 to 0.41 mg/ml with consecutive inhalation tests after placebo. Even in the presence of demonstrable cyclooxygenase inhibition, no effect of F was observed in inhibiting Bk tachyphylaxis the mean PC20 Bk still increasing from 0.10 to 0.47 mg/ml. Tachyphylaxis was still present at 6 h, but not in all subjects at 24 h. This study demonstrated that release of protective prostaglandins in the airway after Bk stimulation does not account for the loss of responsiveness following repeated exposure to Bk. At least 24 h should separate Bk inhalations to avoid tachyphylaxis. A possible mechanism of this phenomenon is discussed.

Administration, Inhalation↗
PubMedDate not supplied

[Role of adenosine in the pathogenesis of bronchial asthma].

Adenosine has been found to contract human bronchial smooth muscle in vitro and to induce bronchoconstriction in asthmatic patients when administered by inhalation. The importance of adenosine for bronchial tone and bronchial reactivity is still unclear. Adenosine seems unlikely to cause bronchoconstriction by a non-specific irritant effect. Some evidence suggests that the action of adenosine relates to a specific pharmacologic activity. Bronchoconstriction induced by adenosine is antagonized by theophylline and is potentiated by dipyridamole. Therapeutic concentrations of theophylline exhibit specificity for adenosine's bronchoconstrictor activity supporting the concept that the bronchospastic effect of adenosine is mediated through stimulation of cell surface receptors. Stimulation of afferent receptors producing vagally mediated reflex seems unlikely. A further explanation of adenosine bronchoconstriction is a release of mediators through potentiation of ongoing mediator release from bronchial luminal mast-cells.

Adenosine↗
PubMedDate not supplied

[Tachyphylaxis induced by repeated inhalation of bradykinin in asthmatic patients].

Bradykinin is a nonapeptide, which may act as a mediator in asthma since it is generated upon nasal immunological challenge in vivo and it has been shown to induce some asthma-like symptoms. In vitro studies suggest that refractoriness following bradykinin challenge may be due to release of contractile tachykinins. In this study it was shown that repeated bronchial challenge with bradykinin in atopic asthmatic subjects induced loss of response to the nonapeptide. Once achieved, reduced bradykinin responsiveness was not accompanied by loss of airways response to histamine. Moreover, repeated challenge with histamine failed to produce a significant loss of airways response to this agonist. In conclusion, either the depletion of contractile tachykinins or the down-regulation at the level of specific kinin receptors might account for the refractoriness following repeated inhalation of bradykinin in asthmatic subjects.

Adult↗
PubMedDate not supplied

[Mast cell mediator release after endobronchial challenge with adenosine 5'-monophosphate in asthmatic subjects].

Mediator release from activated mast cells is also likely to take place in the asthmatic airways in vivo during adenosine-induced bronchoconstriction. To test this hypothesis, we evaluated mast cell mediator release directly into the airways of 9 asthmatic subjects after endobronchial challenge with adenosine by bronchoalveolar lavage (BAL). The mediators measured were histamine, tryptase, and PGD2. When compared to the saline-challenged segment, the response to AMP instillation was characterized by a prompt reduction in airway calibre paralleled by a significant 4.2-fold increase in PGD2 levels in the BAL fluid (p = 0.004). There were also increases in median histamine (from 200.1 to 433.6 pg/mL) and tryptase levels (from 0.31 to 0.46 ng/mL) recovered after AMP challenge, although they were not significant. These findings support the view that acute bronchospastic response to AMP in asthmatic airways is paralleled by the local release of mast cells derived products, particularly PGD2.

Adenosine Monophosphate↗
PubMedDate not supplied

Renaissance of the effector role of the mast cell in bronchial asthma.

The mast cell, by virtue of its capacity to release a wide range of pro-inflammatory mediators, its abundant expression of the high-affinity receptor for immunoglobulin E and its strategic location in proximity to blood vessels, mucosal surfaces and smooth muscle, had long been considered as the central effector cell in asthma and other allergic diseases. In recent years there has been a tendency for less importance to be attached to this cell as a central effector in asthma. New findings, however, have led to a resurgence of interest in the mast cell and supported a reevaluation of its role. In particular the discovery that mast cells are a potential source of cytokines has suggested new ways in which mast cell activation could also participate in more persistent and even chronic inflammatory responses which we know are central to the pathophysiology of asthma. This review will address: 1) the main aspects of mast cell biology which are relevant to asthma with particular reference to mediators produced and their biological functions; 2) the evidence implicating the mast cell as an effector cell in both the immediate and delayed airway responses to allergen exposure; 3) how acknowledgement that mast cells act as a source of cytokines permits speculation on their involvement in the chronic inflammatory response of asthma.

Adenosine↗
PubMedDate not supplied

Anaphylactic reaction to oral prednisone: a case report and review of the literature.

Reports of corticosteroid anaphylactic reactions are rare in the medical literature. We describe the case of a nonatopic 17-year-old girl with bronchial asthma and aspirin intolerance who developed a dramatic anaphylactic reaction to oral prednisone. She recovered with shock therapy and intravenous administration of diphenhydramine and hydrocortisone. Intradermal testing with a wide range of steroid preparations gave positive results to prednisone. No reactions occurred to methylprednisolone and hydrocortisone. This case and the brief review of the literature which follows emphasize the danger of prednisone administration in patients who have asthma and a history of drug intolerance.

Administration, Oral↗
PubMedDate not supplied

Exposing the mast cell: its novel integrated role in allergy.

New discoveries have suggested that the mast cell has the potential to regulate allergic inflammation by inducing IgE synthesis from B cells. Under allergic inflammatory conditions, "primed" mast cells appear to express higher levels of the high affinity receptor for IgE and the ligand for the surface antigen CD40, involved in T/B cell interactions leading to immunoglobulin production, as well as Th2-type cytokines, IL-4 and IL-13. The critical role of these cells in the induction of IgE synthesis is supported by the findings that anti-ligand for the surface antigen CD40, anti-IL-4, and anti-IL-13 monoclonal antibodies inhibit IgE production. Mast cells also have the potential to function as antigen presenting cells with the ability to shift T cells into Th2 subtypes. These recent findings suggest that mast cells can modulate important regulatory functions of the allergic response by acting directly on B cells and inducing IgE production.

CD40 Antigens↗