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Notes: Permanent magnetic materials containing the intermetallic compound Nd2Fe14C were obtained by annealing melt-spun flakes. As quenched flakes with compositions close to the stoichiometric composition consist of α-Fe, Nd2Fe17 with some dissolved carbon, and an amorphous phase. At approximately 700 °C Nd2Fe14C is formed in a solid-state reaction. The amount of Nd2Fe14C formed, the presence of secondary phases, and the magnetic properties depend strongly on the composition. Samples with the composition Nd13.5Fe79.6C6.9 contain only a small fraction of secondary phases. The remanence and intrinsic coercive field are 0.72 T and 800 kA/m, respectively. The kinetics of the phase transformation, as well as the thermodynamics of the phase equilibria in the relevant part of the Nd-Fe-C system are discussed.

Notes: The effect of vaccinating lactating Pakistani mothers with a combination of live oral typhoid vaccine and parenteral inactivated cholera vaccine on specific milk and serum IgA antibodies in both monomeric (m) and polymeric (p) forms was analysed. IgA antibody titres peaked for both antigenic specificities 2 weeks after the first dose of vaccine. 82±7% of anti-Vibrio cholerae and 72±17% of anti-Salmonella typhi IgA were in the polymeric form. These serum pIgA antibodies were mainly dimeric IgA, not complexed with the secretory component. They disappeared more rapidly from serum than mIgA antibodies. Anti-V. cholerae IgA responses were parallel in serum and milk samples, whereas anti-S. typhi responses were dissociated. In milk, IgA antibodies were secretory IgA for both antigenic specificities, being probably of local origin in the mammary gland. Our results indicate that both oral and parenteral vaccinations can induce pIgA antibodies in serum and secretions, confirming that the presence of pIgA in serum does not necessarily reflect an immune stimulation only at the mucosal level.

Notes: Previously we have reported that in asthmatics an inhalation of 20 μg lipopolysaccharide (LPS) produces a bronchial obstruction associated with an inflammatory blood response. The aim of the present study was to evaluate this response in normal subjects. Eight normal non-atopic subjects were challenged by inhalation of a solution containing 20 μg LPS (from Escherichia coli 026:B6) a week after bronchial challenge with control solution. The lung function response was evaluated by the changes in forced expiratory volume in one second (FEV1), in specific conductance and in airway resistance while the blood inflammatory response was evaluated by serial measures of total white blood cells (WBC) and polymorphonuclear neutrophils (PMN) count, luminol enhanced-chemiluminescence (luminol-CL, as a marker of the PMN degree of activation), C-reactive protein (CRP), haptoglobin, complement fraction C3, tumour necrosis factor-α (TNF-α) and adrenocorticotropic hormone (ACTH). No response in lung function was observed for 6 h after the LPS inhalation. The count in WBC and PMN increased 300 (P 〈 0.01) and 360 (P 〈 0.01) min after the LPS challenge associated with an increase in the level of luminol-CL (P 〈 0.001). This rise in luminol-CL level was significant at 120 min (P 〈 0.05) before any change in the PMN count. After 24 and 48 h the acute-phase protein CRP raised significantly (P 〈 0.01), the other proteins C3 and haptoglobin being unchanged. A slight increase in ACTH was observed 240 and 360 min (P 〈 0.05) after the LPS challenge while the TNFα detectable level was not modified. In conclusion, in normal subjects, inhalation of a pro-inflammatory agent is able to induce a systemic inflammatory response in the absence of any effect on lung mechanics, while in asthmatics the same bronchial challenge has been reported to induce a similar blood inflammation associated with a significant response in lung function.

Notes: Background Immune response lo inhaled antigens differs in allergic patients and healthy individuals, mostly in the quality of T cell help provided (i.e. Th2 or Th l dominant subset). However, while different in many functional aspects, both groups of T cells shared the capacity to support the synthesis of antigen-specific immunoglobulin G (IgG) antibodies detected in different amounts in the serutn of atopic and healthy individuals.Objective The present study investigates whether these IgG responses display similar or different epitopic dominance in the mite sensitization model.Methods Antibody specilicity was evaluated by comparing the IgG binding to native Der p1 (nDer p1) and its products of pepsin hydrolysis (dDer p1) in 56 mite-allergic patients and 148 healthy individuals, including 24 mite-sensitized individuals in a solid enzyme linked immunosorbent assay (ELISA). Antibody specificity was also studied in competitive ELISA using streptavidin biotin technology.Results Mite-allergic sera showed a higher degree of binding to nDer p1 than to dDer p1, whereas control sera and mite-sensitized sera bound at a similar level to the two forms of the antigen. Allergic sera and control sera, including mite-sensitized sera, showed distinct capacities to prevent the binding to nDer p1 of pooled IgG from each group as well as murine monoclonal antibodies specific to Der p1.Conclusion The IgG response to Der p1 of mitc-allergic patients differs from that of healthy controls and mite-sensitized subjects, not only in its increased titres but also in its consistant pattern of modified specificity, displaying a marked preference lor conformational epitopes. Cross-competition experiments confirm the clinically associated, restricted specificity, allowing almost complete discrimination between groups, particularly between mite-sensitized and mite-allergic subjects, which is currently impossible with routinely available assays.

Notes: Endotoxins are potent pro-inflammatory substances present in several natural environments and in commercial house dust extracts. To investigate the possible effect of chronic endotoxin exposure on asthma, 28 patients with perennial chronic asthma (20 allergic to house dust mite and eight intrinsic asthmatics) were evaluated during a 4-month period (lung function, clinical and immunological criteria). At the same time, two house dust samples were collected from each patient's home to determine total house dust weight (mg/m2), endotoxin concentration and house dust mite antigen content (evaluated indirectly by guanine content with HPLC method). The mean (± s. d.) endotoxin concentration, as measured by quantitative Limulus assay was 2.59 (± 3.41) ng/mg house dust, ranging from 0.12 to 20 ng/mg. The mean guanine content was 0.13 (± 0.16) mg/100 mg house dust. There was no correlation between endotoxin and house dust mite concentrations. Patients were compared according to the low or high grade exposure to dust, endotoxins and guanine. Compared with patients with low grade (≤ 5.6 ng/ml) exposure, subjects exposed to high endotoxin concentrations (〉 5.6 ng/ml) showed a significant increase in dyspnea (median 2.6 vs 3.3; P〈0.05) and treatment (median 14 vs 44.3; P〈0.01) scores, oral corticosteroid (median 0.0 vs 13.5 mg/24 hr; P〈0.01) and β2-mimetics (median four vs eight puffs/day; P〈0.01) intake, and a significant decrease in FEV1/FVC (median 84.5 vs 67% of predicted value; P〈0.01). In contrast, no differences were found between the two groups exposed to low (〈 0.07 mg/100 mg house dust) and high (≥ 0.07 mg/100 mg house dust) concentrations of guanine, respectively. We conclude that endotoxins are present in normal domestic environment and could have a deleterious effect on the chronic asthmatic disease.

Notes: Background The evolution of the IgG response during venom immunotherapy (VIT) has been previously investigated in terms of antibody titres and subclasses.Objectives The present work studied the evolution of IgG antibody fine specificity in wasp allergic patients treated with rush VIT.Methods Antibody specificity was evaluated in 51 wasp allergic patients in competitive ELISA using streptavidin biotin technology. Patients were tested before and during specific rush immunotherapy (at 15 days, 6 months, 12 months) and compared with 44 patients treated by venom injections for at least 2 years.Results The capacity of sera to prevent the antigen binding of pooled IgG from allergic patients changed rapidly with mean percentage inhibitions (± sd) falling from 70 ± 11–51 ± 18% after 15 days of treatment (P 〈 0.001 by one way anova). Similarly, the antigen binding capacity of pooled IgG from VIT patients was differently prevented by sera with mean percentage inhibitions increasing from 37 ± 12–65 ± 8 after 15 days of treatment (P 〈 0.0001 by one-way anova).Conclusions The immunodominance pattern of IgG epitopes recognized on wasp venom antigens by sera from wasp allergic patients changes soon after initiating rush VIT. Further studies will indicate whether, instead of measuring IgG titres, this marked change could be used as the basis of a new test for monitoring the outcome of VIT.

Notes: Manifestations of fish allergy can include near-fatal anaphylactic reaction. In very sensitive patients, fish odors and cooking vapors may have some al-lergenic activity. We reported a case of life-threatening fish allergy in a girl of 39 months referred for three episodes of Quincke edema with wheezing, cyanosis and severe urticaria after fish consumption or inhalation. Reagins were found against codfish and direct skin prick test with fresh food (cod fish) showed important local reaction. Strict avoidance of fish in the diet is usually the only recommended procedure. However, in this particular case, the life-threatening nature of the allergic reaction was the major considera tion to perform a desensitization. The child was treated by RUSH immuno therapy using codfish extracts from BENCARD company, following the schedule for insect venom allergy described by Pharmacia. Immunotherapy was performed immediately after determination of the threshold of sensi tivity by specific skin prick tests and intra-dermal injections. Desensitiza tion was initiated with a 1/10 dilution of the cut-off solution and 5 subcuta neous injections were administered daily. When important local reactions were observed, additional doses were necessary to obtain tolerance. After the RUSH therapy, the child was submitted to uncooked codfish odors without any reaction. No reaction has been observed even when the child has accidentally eaten a little piece of codfish.

Notes: Background: We have previously shown in several allergy models that allergic and tolerance status with respect to allergens is associated with a somewhat different dominant specificity of IgG antibodies. The objective was to test this hypothesis in the compelling model of ultrarush venom immunotherapy (VIT), which induces clinical tolerance after only a few hours of treatment. Methods: Antibody titers and specificity were evaluated through solid-phase ELISA using streptavidin-biotin technology in 12 patients allergic to wasp venom before and during the ultrarush procedure (at 12 h, 24 h, and 15 days). The results were compared with those from another group of 20 patients treated with venom injections for at least 2 years. Results: No significant change was observed in IgG titers during the early phase of VIT. The capacity of individual sera to prevent the antigen binding of pooled IgG from allergic patients changed rapidly, with mean percentage inhibitions falling from 80±15%, before starting VIT, to 26±14%, 35±15%, and 34±5% after 12 h, 24 h, and 15 days of treatment, respectively (P〈0.001 by one-way ANOVA). The capacity of individual sera to prevent the antigen binding of pooled IgG from patients receiving prolonged VIT changed, with mean percent inhibitions increasing from 47±8%, before starting VIT, to 76±7%, 83±6%, and 87±6% after 12 h, 24 h, and 15 days of treatment, respectively (P〈0.001 by one-way ANOVA). Conclusions: During the initial phase of ultrarush VIT, a change in IgG specificity, i.e., a change in the set of epitopes dominantly recognized by IgG on wasp-venom antigens, occurred concomitantly with early clinical tolerance and was already detectable a few hours after the onset of treatment. Although it may be an epiphenomenon, this change represents the earliest humoral modification described so far during this procedure. The mechanism is unknown, but it appears to be a selective depletion of the highest avidity antibody fraction by the venom injected in large doses at this stage of therapy. Finally, our data now show the previously documented association between a particular IgG specificity and the clinical status (allergy vs tolerance) to be true also with ultrarush VIT, a model in which the clinical ability to display allergic symptoms is rapidly reversed.