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Biomedical subjects

S Sanjar

Publications and source records attributed to S Sanjar.

42 records · Page 3Linked to original sources
PubMed1985

Effects of serum albumin, indomethacin and histamine H1-antagonists on Paf-acether-induced inflammatory responses in the skin of experimental animals and man.

Cutaneous responses to synthetic platelet activating factor (Paf-acether) have been studied in guinea-pig and human skin. Intradermal injection of Paf-acether elicited an acute inflammatory response in guinea-pig skin (assessed by means of radioisotopic techniques) and acute oedema formation in human skin (assessed by means of weal volume and flare area). Acute inflammatory responses in guinea-pig and human skin are potentiated by the presence of serum albumin, a phospholipid carrier. Acute inflammatory responses induced by Paf-acether in guinea-pig and human skin are not significantly affected by concomitant administration of the cyclo-oxygenase inhibitor, indomethacin. Acute inflammatory responses induced by Paf-acether in guinea-pig and human skin are not significantly affected by concomitant administration of the cyclo-oxygenase inhibitor, indomethacin. Acute inflammatory responses induced by Paf-acether in guinea-pig and human skin are slightly modified by the H1-receptor antagonists, mepyramine and chlorpheniramine. These results indicate that the acute inflammatory response induced by Paf-acether is independent of cyclo-oxygenase products of arachidonic acid and that histamine release has a minor contribution to the inflammatory response induced by Paf-acether.

Adult↗
PubMed1985

Pharmacology of the late response to allergen and its relevance to asthma prophylaxis.

Inhalation of allergen by sensitised asthmatics results in an acute increase of airways resistance that, in some individuals, is succeeded by a response of late-onset. Late-onset responses are associated with an increased airway reactivity to constrictor stimuli that lasts for several days and hence may be akin to exacerbation of clinical asthma. For this reason, much attention has been given to inhibition of late-onset reactions by glucocorticosteroids or by cromoglycate. Such effects have been cited as evidence of anti-asthma efficacy for these drugs and also for ketotifen, as might be anticipated from prophylactic efficacy in clinical asthma. More recently, a similar inhibitory effect has been demonstrated for theophylline, which is in marked contrast to beta-adrenoceptor agonists, which have long been known not to inhibit expression of late-onset reactions. The profile of drug sensitivity observed for late-onset reactions precludes mast cell stabilisation as an adequate explanation, since late-onset reactions are unaffected by beta-adrenoceptor agonists, notwithstanding the potency of such drugs as inhibitors of mast cell secretion; furthermore, late-onset reactions can be inhibited by nonsteroidal anti-inflammatory drugs, even though such drugs can enhance mast cell secretion. Rather, present evidence favours platelet-activating factor (PAF, Paf-acether, AGEPC) as a primary determinant of late-onset reactions, especially since responses to this material can be inhibited by cromoglycate, glucocorticosteroids, ketotifen and theophylline, and since there is substantial evidence that PAF has properties that could account for exacerbation of asthma.

Airway Resistance↗
PubMed1984

Autonomic regulation of mucociliary transport rate in the oesophagus of the frog, Rana temporaria.

Transport of lead particles along the mucosal surface of the frog oesophagus has been measured by direct observation with the aid of video recording. Electrical stimulation of the vagus nerve increased the rate of particle transport. This acceleration was suppressed by atropine or by hexamethonium. Acetylcholine and other parasympathomimetic agents accelerated particle transport rate. Such acceleration was abolished by atropine. Nicotine increased the rate of particle transport and this effect was suppressed by hexamethonium or by atropine. Atropine did not significantly alter basal particle transport rate. Neither basal particle transport rate nor the response to vagal nerve stimulation were affected by eserine. Adrenaline, noradrenaline or isoprenaline did not affect basal particle transport rate. Adrenaline or noradrenaline were without effect on the increased particle transport rate due to electrical stimulation of the vagus.

Animals↗
PubMedDate not supplied

The potential roles of cytokines, IL-5 and IL-8, and plasma cortisol in the anti-inflammatory actions of phosphodiesterase inhibitors in sensitized guinea-pig airways.

Ovalbumin (OvA) inhalation by sensitized guinea-pigs caused a pronounced rise in interleukin (IL)-5 in bronchoalveolar lavage (BAL) fluid at both 3 and 24 h after antigen exposure. The increased levels at 24 h were attenuated by the phosphodiesterase inhibitors Ro 20-1724 and aminophylline and by dexamethasone, all of which also attenuated the concurrent lung eosinophilia. The rise in IL-5 at 3 h was additionally attenuated by the PDE3 inhibitor, siguazodan, which failed to attenuate the eosinophilia at 24 h. These results suggest a pivotal action of these compounds on the later rise in IL-5. Ro 20-1724, aminophylline, siguazodan and dexamethasone attenuated a rise in IL-8 levels in BAL fluid at 3 h and the subsequent neutrophilia at 24 h. There was no increase in plasma ACTH at 3 and 24 h after OvA challenge but cortisol levels were elevated at 3 h. This was inhibited by Ro 20-1724, siguazodan and dexamethasone. Thus, elevation of plasma cortisol does not explain the anti-inflammatory actions of these compounds. Aminophylline, however, did raise plasma cortisol at both 3 and 24 h after antigen challenge which may be an important further mechanism of action for this compound.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMedDate not supplied

Maintenance of the epithelial barrier in a bronchial epithelial cell line is dependent on functional E-cadherin local to the tight junctions.

Tight junctions (TJ) are essential components of polarized epithelia, and E-cadherin is important for their formation and maintenance. The bronchial epithelial cell line, 16HBE14o-expresses E- and P-cadherin, but not N-cadherin. E- and P-cadherin levels changed during culture, the former increasing after confluence, and the latter were markedly reduced. All detectable E-cadherin was bound to beta- and gamma-catenins. We investigated involvement of E-cadherin with epithelial integrity using an E-cadherin specific, function-blocking antibody, SHE78-7. Surprisingly, apical SHE78-7 exposure caused a prompt fall in transepithelial resistance (TER), while TER remained unchanged for 8 hrs after basal exposure then dropped. SHE78-7 exposure increased epithelial permeability to mannitol, inulin, and 9.5 kDa and 77 kDa dextrans and caused fragmentation and loss of the tight junction protein, ZO-1, from the cell borders in some areas. Ultrastructural studies showed that all junctional intercellular contact was lost in the center of SHE78-7 induced lesions. Near the lesion periphery, epithelial structure was maintained, but TJs were dysfunctional as shown by ruthenium red penetration. Analysis of epithelial penetration by SHE78-7 revealed discrete, local defects in the apical barrier at the top of some cell hills that permitted rapid access of the antibody to E-cadherin near the apical surface. In contrast, after basal exposure, antibody initially engaged with E-cadherin nearer the basal surface and only accessed apical E-cadherin later. Taken together with the TER measurements, these data suggest compartmentalization of E-cadherin function within 16HBE14o-cells, with only the apical E-cadherin adjacent to the tight junctions contributing to the function of the latter.

Animals↗