IgE antibodies to penicillin in skin test negative patients.
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Biomedical subjects
Publications and source records attributed to A Romano.
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BACKGROUND: Peanut allergy is one of the five most frequent food allergies in children and in adults. Recently, we purified and evaluated the allergenicity of peanut oleosins, a family of small-sized proteins involved in the formation of peanut oil bodies. METHODS: Allergenicity of the purified native protein and of the recombinant protein was tested by Western blot and by IgE-RIA. RESULTS: We found IgE-binding with oleosin in 3 of 14 sera of patients who had suffered an allergic reaction to peanuts. Two sera reacted weakly against 16-18 kDa proteins corresponding to oleosin monomers, in Western blot. The main reacting bands had a molecular size estimated at approximately 34 kDa, approximately 50 kDa and approximately 68 kDa and could therefore correspond to oleosin oligomers. IgE reactivity was higher in extracts from roasted peanuts. The same phenomenon occurred with crude soybean oil fraction, with two bands of 16.5 and 24 kDa corresponding to monomers, and two bands of 50 kDa and 76 kDa corresponding to dimers and trimers, respectively. The 18 kDa band was observed in the 3 Western blots of a membrane-enriched fraction of recombinant oleosin produced in the Sf9-baculovirus expression system (performed with the 3 patient sera). CONCLUSIONS: We have characterized a new peanut allergen which belongs to the oleosins, a family of proteins involved in the formation of oil bodies. The protein may be involved in some of the allergic cross-reactions to peanuts and soybeans.
BACKGROUND: The release of histamine by iodinated contrast media (ICM) is higher in coronary artery disease patients than in noncoronary patients during coronary angiogram. METHODS: Eighty-eight patients who underwent a coronary angiography were classified either as having coronary artery disease or as noncoronary patients. Histamine concentration was higher than the 6.8 nM upper limit in 7 cases (group 1), of whom six were coronary artery disease patients. We compared the IgE and complement fractions in plasma of these patients to two control groups with normal histamine blood level, one (group 2) with and the other (group 3) without coronary artery disease. RESULTS: No difference of total IgE and C(3c) and C(4) complement fractions was found among the three groups. Anti-ioxaglate IgE-RIA was positive in only one patient from group 1. The affinity of drug-IgE binding in the serum of this patient was very low (Kd: 18.7 mM). The level of anti-ICM IgE detected by ioxitalamate- and iomeprol-Sepharose RIA was significantly higher in groups 2 and 3 than in group 1. CONCLUSIONS: The higher histamine release in ischaemic heart disease patients undergoing coronaroangiography is not mediated by IgE or complement activation. Further studies are needed to investigate the implication of histamine release factors.
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Penicillins are beta-lactam antibiotics able to generate several antigenic determinants that are recognized by the immune system. To study the differences in the antigen binding site of two monoclonal antibodies (Mab) specific to amoxicillin, polyclonal rabbit anti-idiotypic antibodies were produced. One Mab, AO3.2 (IgG2a), specific to a structure formed by the acyl-side chain structure and a part of the nuclear region of amoxicillin. The second one, AO6.2 (IgE), is specific to the side chain of amoxicillin, although it also recognizes the side chain of other penicillins (penicillin G and ampicillin). These antibodies were used to immunize rabbits in order to produce polyclonal anti-idiotypic antibodies, which were purified in several steps by affinity chromatography. The specificity and cross-reactivity studies were made by ELISA and ELISA inhibition. The results suggest that the anti-Id antibodies produced are the internal image of the antigen, since the binding to their specific idiotype is blocked mainly by the original hapten (amoxicillin): in 98% of the cases with anti-id-1 (induced against AO3.2) and in 59% with anti-id-2 (induced against AO6.2). The absence of cross-reactivity of each anti-idiotypic antibody with the different Mabs specific to amoxicillin shows that the idiotypes induced by the same hapten have differences that are reflected by the nonrecognition of these anti-idiotypes. We conclude that such a small molecule as amoxicillin can present several antigenic determinants that induce a panel of antibody specificities especially directed against the side chain.
BACKGROUND: A 41-kDa IgE-reactive protein (p41) was purified from raw cod extract. This protein is homologous to an aldehyde phosphate dehydrogenase (APDH). The present study aims to evaluate the IgE-binding and the cross-reactivity of this protein in 13 patients allergic to codfish. METHODS: IgE binding of sera from 13 patients allergic to codfish was tested by Sepharose RIA and by Western blot. RESULTS: Among the 13 patients, only 4 had specific IgE to APDH detected by APDH-Sepharose RIA. The two patients who had the highest level of specific IgE to human APDH also had a class 5-6 CAP-RAST IgE level to codfish, but two other patients with a class 5 had a negative APDH-Sepharose IgE-RIA. Relative content of APDH was higher in extracts of commercial nonfrozen fish, compared to pre rigor mortis, post rigor mortis and frozen commercial codfish. A high homology of codfish APDH was found with the corresponding human enzyme. A significant inhibition of APDH-Sepharose by human and, to a lesser extent, by rabbit APDH was observed. Western blot of APDH codfish extract showed two bands at 41 and 36 kDa, respectively. CONCLUSIONS: We have characterized a new allergen from codfish, which had a high level of homology in different species. The p41 relative content of extracts from nonfrozen codfish was higher than in the other samples assessed.
Extramedullary (EM) involvement occurs infrequently in acute promyelocytic leukemia (APL) and usually involves skin and CNS. We describe seven patients (four observed at a single institution) who relapsed in various sites of the auditory apparatus, including the external canal and middle ear (temporal bone). Front-line treatment included ATRA and chemotherapy (six patients) or chemotherapy alone (one patient). Three patients had concomitant hematologic relapse, two had molecular relapse and two were in hematologic and molecular remission when ear localization was documented. Local symptoms that stimulated further diagnostic studies included ear bleeding/discharge in the first patient, but were mild in the others (hypoacusia, five patients; earache, two patients). Ear involvement by leukemia was documented by histological and/or molecular studies after local surgery in five cases, and by CT scan or NMR in the remaining patients. We suggest that the ear might represent a specific sanctuary for disease involvement in APL.
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We have analyzed 18 families with high incidence of breast cancer or breast and ovarian cancer for the presence of BRCA1 mutations. We identified 4 mutations in the BRCA1 gene in 4 unrelated probands who belong to families with at least 1 case of breast and 1 case of ovarian cancer. Two of the mutations reported in this study are novel (GAA(1172)-->TAA in family Naples 14, GAA(1765)-->TAA in family Naples 20) whereas the others are already present in the Breast Cancer Information Core Electronic Database (http://nchgr.nih.gov/ Intramural research/Lab transfer/Bic/) (5382insC in family Naples 18 and 2080delA in family Naples 19). Conversely, no mutation in the BRCA1 gene was detected in 14 families characterized by 2 or more cases of breast cancer only, even if bilateral and with early-onset. These results indicate that germline mutations in the BRCA1 gene highly predispose for a cancer syndrome that involves the presence of both breast and ovarian cancer.
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We have studied two-body charmless decays of the B meson into the final states rho(0)rho(0), K(*0)rho(0), K(*0)K(*0), K(*0)K(*0), K(*+)rho(0), K(*+)K(*0), and K(*+)K(*-) using only decay modes with charged daughter particles. Using 9.7x10(6) BB pairs collected with the CLEO detector, we place 90% confidence level upper limits on the branching fractions (1.4-14.1)x10(-5), depending on final state and polarization.
We have measured the branching fraction and photon energy spectrum for the radiative penguin process b-->s gamma. We find Beta(b-->s gamma) = (3.21+/-0.43+/-0.27(+0.18)(-0.10))x10(-4), where the errors are statistical, systematic, and from theory corrections. We obtain first and second moments of the photon energy spectrum above 2.0 GeV, = 2.346+/-0.032+/-0.011 GeV, and - (2) = 0.0226+/-0.0066+/-0.0020 GeV(2), where the errors are statistical and systematic. From the first moment, we obtain (in the modified minimal subtraction renormalization scheme, to order 1/M(3)(B) and beta(0)alpha(2)(s)) the heavy quark effective theory parameter Lambda = 0.35+/-0.08+/-0.10 GeV.
We have measured the first and second moments of the hadronic mass-squared distribution in B-->X(c)l nu, for P(lepton)>1.5 GeV/c. We find = 0.251+/-0.066 GeV(2), <(M(2)(X)- )(2)> = 0.576+/-0.170 GeV(4), where M macro(D) is the spin-averaged D meson mass. From that first moment and the first moment of the photon energy spectrum in b-->s gamma, we find the heavy quark effective theory parameter lambda(1) (in the modified minimal subtraction renormalization scheme, to order 1/M(3)(B) and beta(0)alpha(2)(s)) to be -0.24+/-0.11 GeV(2). Using these first moments and the B semileptonic width, and assuming parton-hadron duality, we obtain absolute value of V(cb) = 0.0404+/-0.0013.
We observed a release of histamine, but not of tryptase, in arterial blood from 64 patients with ischemic heart disease and 24 patients without coronary disease, which was provoked by ioxaglate, a ionic compound, but was not provoked by iomeprol, a non-ionic radiocontrast compound. The release of histamine in arterial blood after ionic contrast medium injection was higher in patients with ischemic heart disease compared with patients without coronary disease, suggesting that an increased release from heart mast cells previously observed exists also for systemic blood basophils.
We evaluated the allele (and genotype frequencies in 60 Down syndrome (DS), 25 mothers and 57 controls from Sicily and its relation with mental retardation. DS patients and sex ratio (M:F) was 22.1+/-10.5 and 1.14, respectively. Allele varepsilon4 and varepsilon3 frequencies were respectively lower (P=0.015) and higher (P=0.005) in DS patients compared to controls. Genotype varepsilon3/varepsilon4 and varepsilon3/varepsilon3 were less (P=0.03) and more frequent (P=0.001) in DS patients, with respective odd ratios of 0.31 (CI at 95%: 0.18-0.49) and of 4.4 (CI at 95%: 3.4-5.7). No difference of allele (distribution was found in function of the grades of mental retardation according to DMS-IV. Our results show that the implication of Apo-E4 in the pathogenesis of Alzheimer disease cannot be extrapolated in that of dementia of DS.
We have measured the CP asymmetry A(CP) identical with[gamma(b-->sgamma)-gammab-->sgamma)]/[gamma(b-->sgamma)+gamma(b-->sgamma)] to be A(CP) = (-0.079+/-0.108+/-0.022) (1.0+/-0.030), implying that, at 90% confidence level, A(CP) lies between -0.27 and +0.10. These limits rule out some extreme non-standard-model predictions, but are consistent with most, as well as with the standard model.
We have measured the charge asymmetry in like-sign dilepton yields from B(0)B*(0) meson decays using the CLEO detector at the Cornell Electron Storage Ring. We find a(0)(ll) identical with[N(l(+)l(+))-N(l(-)l(-))]/[N(l(+)l(+))+N(l(-)l(-))] = +0.013+/-0.050+/-0.005. We combine this result with a previous, independent measurement and obtain Re(epsilon(B))/(1+ the absolute value of epsilon(B)(2)) = +0.0035+/-0.0103+/-0.0015 (uncertainties are statistical and systematic, respectively) for the CP impurity parameter, epsilon(B).