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EN
Glucocorticoid (GCs) hormones are widely used in the treatment of bronchial asthma. However, not all aspects of their pharmacological effects are well understood as yet. It is know that the effects of GCs are mediated through GC receptors (GCRs). We sought to evaluate the effect of short-term and chronic GC therapy on GCR number in peripheral blood lymphocytes, the relationship between GCR number and cortisol concentrations in asthma patients treated with GCs as well as the response to GC therapy in various pictures of this disease. Sixty-nine patients with bronchial asthma were investigated. Thirty-five of them had received steroid therapy: 18 patients for 1 to 15 years and 17 patients for 13 days after a prior 3 month discontinuation of steroid treatment. The control group consisted of 28 healthy, age matched volunteers. GCR numbers were determined using tritriated dexamethasone as a ligand. The scatchard method was applied to calculate the maximal specific binding and the dissociation constant. The number of receptor sites per lymphocyte was calculated. Cortisol was measured by radioimmunoassay. Lymphocyte GCR numbers in patients with bronchial asthma who were not treated with steroids, did not differ from age-matched healthy persons (means 8115+- 812 and 7905+- 832). A significant decrease in receptor number was seen in patients receiving steroid therapy. There was also a significant difference in receptor number between the groups with short-course (mean 3741+- 549) and chronic steroid therapy (mean 4885+- 1095). The number of GCRs did not correlate with age, sex, clinical state or serum cortisol concentration in either group.
EN
It is known that NO is involved in a variety of physiological functions including the regulation of blood pressure. Dysregulation of L-arginine/NOS/NO biological activity occurs in blood hypertension. The present review will focus on a significance of NO in pathogenesis of essential hypertension.
EN
This article describes the potential regulatory role of the low-affinity receptor for immunoglobulin E, CD23 and soluble form of the CD23 antigen, sCD23 in immune inflamatory processes and its relevance to clinical disorders, particularly allergy.
EN
The article is the review of the data from literature concerning the role of neutrophil elastase in pathophysiology of bronchial obturative diseases. The function of elastase and its inhibitors in airways remodelling and in development of asthmatic responses are discussed.
EN
NO is an important mediator of immune and inflammatory responses. NO is produced from L-arginine by three isoforms of nitric oxide synthase (NOS), neuronal (nNOS; NOS1), endothelial (eNOS; NOS3) and inducible (iNOS). Exhaled NO has been shown to be increased in asthma and has been put forward as a marker of airways inflammation. Moreover, increased production of NO and peroxynitrite may be responsible for the oxidative damage and fibrosis seen in interstitial lung diseases. The present review focuses on clinical and laboratory studies that are aimed at identifying the role of NO in the physiopathology of these disorders.
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