Mammalian exocrine secretions. XVIII: Chemical characterization of interdigital secretion of red hartebeest, Alcelaphus buselaphus caama.

Gas chromatography, coupled gas chromatography-mass spectrometry (electron impact mode and chemical ionization with methane as reactant gas), gas chromatography-infrared spectroscopy, and derivatization techniques were used to identity 53 compounds in the interdigital secretion of the red hartebeest, Alcelaphus buselaphus caama. These compounds included alkanes, isoalkanes, alcohols, ketones, carboxylic acids, oxiranes, furanoid linalool oxides, and a large number of branched and unbranched saturated and unsaturated aldehydes. The secretion probably plays a role in demarcation of territories by dominant bulls.

Temporally and spatially restricted expression of apolipoprotein J in the developing heart defines discrete stages of valve morphogenesis.

During cardiac valve morphogenesis, a series of interactions between the mesodermal-derived myocardium and the overlying endothelium lead to condensed leaflet structure formation. At the atrioventricular (AV) canal, endocardial cells are transformed by specialized underlying myocardial cells into endocardial cushions, and then remodeled into mitral and tricuspid valves. Aortic and pulmonary valves develop by a similar mechanism in the primitive outflow tract. Few genes exhibit restricted spatiotemporal expression in these critical embryonic structures, thus limiting the clues to the sequence of molecular events necessary for valvulogenesis. Apolipoprotein J (ApoJ), a secreted glycoprotein expressed in a variety of cell types at tissue interfaces, exhibits a highly restricted and dynamic expression pattern in the developing heart. ApoJ transcripts were detected in mice at day 9.0 of gestation in the wall of the developing truncus arteriosus. By day 10, intense signal occurred in a thin layer of myocardial cells adjacent to developing endocardial cushions of both atrioventricular canal and truncus arteriosus. No apoJ mRNA was present in the overlying endocardial cushions until day 13.5 when prevalvular condensation begins. Intense expression occurred in the stromal connective tissue throughout leaflet formation. The highly restricted spatiotemporal expression pattern of apoJ in the developing heart implicates its role in the morphogenesis of the AV canal and outflow tract into cardiac valves.

Effects of acrivastine and terfenadine on skin reactivity to histamine.

The response to the histamine hydrochloride prick skin test was studied in 24 healthy volunteers who received, in random order and at least four days apart, acrivastine (8 mg), terfenadine (120 mg), and placebo. The tests were performed on either side of the back before and at the time of administration (single dose), then every 30 minutes for two hours, and every hour for the following four hours. Evaluation was based on the mean of two measurements of the surface area of the wheal-and-flare reaction accompanied by assessment of topical pruritus. The response to histamine was decreased markedly in the two active treatment groups. Although within one hour of injection, the activity of both antihistamines was consistently greater than that of placebo, the kinetics of action of the two products nevertheless differed; indeed acrivastine was active against flare and wheal earlier (within 30 minutes); terfenadine proved to be more active than acrivastine only on flare and only at the later times (four, five, and six hours). The safety study primarily demonstrated drowsiness in one-fourth of the patients receiving placebo and active treatment.

Intratracheal E. coli lipopolysaccharide induces platelet-dependent bronchial hyperreactivity.

Bronchial hyperresponsiveness (BHR) characterizes asthma and accompanies respiratory infections. Because endotoxin [lipopolysaccharide (LPS)] induces either hyper- or hyporesponsiveness of the guinea pig airways and protects against bronchopulmonary anaphylaxis in sensitized guinea pigs, we compared the effects of the intratracheal administration of Escherichia coli LPS on bronchopulmonary responsiveness to intravenous serotonin or acetylcholine in sensitized and nonsensitized guinea pigs. LPS (1 mg) induced BHR within 1-2 h, with a threefold increase in the bronchial response after serotonin challenge in both groups (n = 6; P < 0.005) and a marked influx of neutrophils into the perivascular and peribronchial connective tissue and the bronchoalveolar lavage fluid. This BHR was not leukocyte dependent, since it was still observed in animals depleted of circulating leukocytes with vinblastine and was not modified by antineutrophil serum, unless platelet counts were < 100,000/mm3. This suggested that LPS-induced BHR involves platelets, and indeed antiplatelet serum, which depleted platelets, or prostacyclin, which inhibited platelets, was effective in suppressing BHR. Neither aspirin, mepyramine, nor the platelet-activating factor antagonist WEB 2170, administered before LPS instillation, prevented BHR, whereas the association of methysergide, mepyramine, and aspirin was effective, without modifying platelet and leukocyte counts. This association has been shown to prevent the release of ATP by ex vivo platelets. Our results suggest that platelets or a platelet-derived product mediates LPS-induced BHR.

[Clinical effectiveness and tolerance of loratadine versus cetirizine in the treatment of seasonal allergic rhinitis]. / Efficacité clinique et tolérance de la Loratadine versus Cétirizine dans le traitement de la rhinite allergique saissonnière.

A double blind multicentre study of seasonal rhinitis (108 patients) has compared Loratadine and Cetirizine. The results of clinical scores are significantly good for both products. Only tolerance is different and in favour of Loratadine, since sleepiness was found in 9.5% of patients treated with Cetirizine, and 3.6% with Loratadine.

The house dust mite Dermatophagoides pteronyssinus is the most important allergen on the island of Mauritius.

To determine the relative importance of mites as a cause of allergic sensitivity and asthma on the western Indian Ocean island of Mauritius, we measured specific IgE antibodies to common inhalant allergens in sera from Mauritians claiming to have allergic symptoms and we examined house dust samples for evidence of mites and their allergens. Seventy-two of the 110 sera tested (65%) contained detectable IgE antibody to at least one mite, mould or pollen allergenic extract. By far the most prevalent was antibody to one or both of the common house dust mites, Dermatophagoides pteronyssinus and Dermatophagoides farinae, being present in 67 (61%) of the 110 sera. Allergy to pollens, including the locally prevalent Bermuda grass and sugar cane, was infrequent. Antibody to a limited number of moulds was detected in 22% of the sera tested. Of 81 subjects whose clinical history was known, 60 were asthmatic, and 75% of these asthmatic individuals had IgE antibody to mites. In contrast, only 35% of the subjects with rhinitis without asthma were sensitive to mites. Different mite species, including D. pteronyssinus but not D. farinae, were identified microscopically in samples of local house dust. Mite antigen Der p I but not antigen Der f I was detected with specific monoclonal antibodies in extracts of these dust samples. On the bases of this serological and environmental survey, we conclude that our data support the hypothesis that the house dust mite D. pteronyssinus is the principal cause of allergic sensitivity and asthma in that tropical environment.

Study of the allergenic fractions of latex.

Two latex (Hevea brasiliensis) raw materials, one from the cytosolic fraction, the other from the total natural latex have been characterised by immunoblotting techniques. The two latex fractions A and B were studied by immunoprints using eight sera from patients who were allergic to latex. They gave different profiles though there were also allergens of common molecular weights (60, 35, 30, 25, 20, 18, 15, and 10 kD). This study confirms the importance of allergic reactions to latex, that may in some patients cause anaphylactic shock.

Allergenicity suppression in natural latex surgical gloves.

By a revised manufacturing process we aimed to obtain latex surgical gloves without immediate allergenicity, and also to determine a simple physical technique by which to estimate this allergenicity. Five glove samples were evaluated for allergenicity by physical and biochemical methods and by skin tests at the University Allergy Centre. Three groups of allergic patients with documented anaphylaxis to surgical gloves, positive skin tests to latex extract and specific IgE to latex (RAST Pharmacia greater than or equal to class II), volunteered for the study. The protein content, the in vitro allergenic potency of glove supernatants (RAST inhibition) and the skin test results with glove supernatants were lower in washed gloves than in non-washed samples (P less than 0.02 to P less than 0.009). The supplementary effect of glove sterilization at 120 degrees C (for 1 h in saturated steam) was obvious. The protein content became undetectable in four of the five glove supernatants, and skin tests results with sample supernatants were decreased (M +/- SEM = 0.68 +/- 0.29 mm vs 3.06 +/- 0.61 mm with non-sterilized gloves), P less than 0.009 by Wilcoxon test. With the Spearman test there was a significant correlation (P = 0.029) between the mean wheal size, obtained with supernatants (Groups 1 and 2) and electrical conductivity. Skin tests through pieces of gloves randomly distributed and coded were decreased by sterilization: 0.66 +/- 0.25 mm vs 2.86 +/- 0.45 mm, P less than 0.0001. Thus, it is possible to decrease glove allergenicity by washing them after mould forming and then sterilizing with steam. Electrical conductivity may be a simple parameter for revealing allergenicity.

Blocking antibodies to inhalant allergens and asthma.

The mechanisms of specific immunotherapy are not still established. Among the lot of immunological changes, induced by immunotherapy, the increase of specific IgG 1, and then of IgG 4 antibodies, during the first months is well demonstrated. The skin-tests, the histamine-release and the human basophil degranulation are significantly decreased after incubation of allergen with the serum of desensitized patients. This antigen neutralizing capacity (blocking antibodies) disappeared when IgG 4 were suppressed from the serum by the mean of activated columns linked either with allergen, or protein A or antihuman IgG4 antibodies. Conversely, the total amount of serum blocking activity was found using pure IgG 4. However, the role of IgG 4 antibodies remains a subject of controversy. Since a clear correlation has yet to be established with symptom scores.

Dissociation between LPS-induced bronchial hyperreactivity and airway edema in the guinea-pig.

The interactions between LPS-induced bronchial hyper-reactivity (BHR) and lung inflammation (LI) were investigated. LPS-induced LI was assessed with the augmented alveolo-capillary permeability (ACP) and with the increased migration of neutrophils into the broncho-alveolar lavage fluid. BHR was defined as the increase in the response to a standard dose of serotonin. Mepyramine and the PAF antagonist WEB 2170 blocked LPS-induced increase of ACP, whereas aspirin was inactive. By contrast, neither LPS-induced neutrophil attraction to airways, nor LPS-induced HBR were inhibited by these agents. Our results indicate that LPS-induced edema and BHR are dissociated.

Reduced responsiveness of adenylate cyclase in alveolar macrophages from patients with asthma.

Alveolar macrophages from patients with asthma accumulated less cyclic adenosine monophosphate when these macrophages were exposed to isobutyl methylxanthine, salbutamol, or prostaglandin E2, compared to cells from control subjects without asthma, and the degree of the hyporesponsiveness was related to the severity of asthma. In addition, a significantly lower adenylate cyclase activity was observed in crude membrane fractions of macrophages from the group with asthma in the presence of salbutamol and prostaglandin E2. The refractoriness observed in patients with asthma is thus not accounted for by a specific beta-adrenergic desensitization at the adenylate cyclase receptor level but should rather be explained by a cyclic adenosine monophosphate-dependent postreceptor mechanism.