Biomedical subjects
Publications and source records attributed to J Dominguez.
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The protein domain responsible for the interaction of tau with tubulin has been identified. Biophysical studies indicated that the synthetic peptide Val187-Gly204 (VRSKIG-STENLKHQPGGG) from the repetitive sequence on tau binds to two sites on the tubulin heterodimer and to one site on each of the microtubule-associated protein-interacting C-terminal tubulin peptides alpha(430-441) and beta(422-434). The binding data showed a relatively stronger interaction of Val187-Gly204 with beta(422-434) as compared to that with alpha(430-441). The interaction of this tau peptide with either alpha or beta tubulin peptides appears to be associated with conformational changes in both the tau and the tubulin peptides. The beta tubulin peptide also appears to induce a structural change of tau fragment Val218-Gly235. Interestingly, tau peptides Val187-Gly204 and Val218-Gly235 induced tubulin self-assembly in a cold-reversible fashion, and incorporated into the assembled polymers. The specificity of the interaction of the tau peptide was supported by the competition of tau protein for the interaction with the tubulin polymer. In addition, the tau peptide appears to contain the principal antigenic determinant(s) recognized by anti-idiotypic antibodies that react with the tubulin binding domains on microtubule-associated proteins. The present findings together with the demonstration of the presence of multiple sites for the binding of the alpha(430-441) and beta(422-434) tubulin fragments to tau, and the existence of repetitive sequences on tau, strongly support the hypothesis that the region of tau defined by the repetitive sequences is involved in its interaction with tubulin.
Thirteen cases with loosening of THR treated by a massive prosthesis are reviewed. In previous years, with more conservative surgery, the loss of bone stock was most important. The results after a long follow-up were satisfactory. This was a desperate procedure during a period without a bone-bank. Despite the major problems with failure of this procedure, the author still recommends it in elderly patients who need early mobilization or when the use of a bank-bone is not possible.
A crossed comparative study was done with 248 extrinsic asthmatic children living either in polluted or non-polluted areas (mean emission per year of sedimentary material greater than or less than 300 mg/m2/day, respectively) to establish the influence of air pollution on childhood extrinsic asthma. The mean number of wheezing crises per year was significantly higher for the children living in polluted areas (10.4 versus 7.69). In addition, incidence of severe asthma (types II, III, and IV) in children living in polluted areas was markedly increased whereas the slight form of asthma (type I) was more frequent in children living in non-polluted areas. No correlation, however, between the wheezing episodes and levels of atmospheric contaminants (fumes and SO2) was detected when a group of 84 extrinsic asthmatic children living in polluted areas was studied longitudinally for a year. The data indicate that air pollution, as an isolated agent, plays a transient role in the appearance of wheezing episodes in subjects with extrinsic asthma. Results also suggest that the air pollution may potentiate wheezing episodes via alternative mechanisms.
In the eluted fractions of histone-treated crude extracts separated by Sephadex G-200 filtration, multiple protein kinase (PK) activities, including three from brain and two from skeletal muscle, were augmented by both S-100 protein and parvalbumin on the phosphorylation of endogenous substrates. One additional PK activity suppressed by both S-100 and parvalbumin was also found in muscle. In comparison, phosphoprotein phosphatases (PPase), which were also prepared by the same procedure of initial step of histone-treatment followed by the steps of Bio-Gel P-6DG for brain and DNA-cellulose for muscle, were all activated by S-100 while inhibited by parvalbumin and phosphatidylserine.
Inhalation of enzyme dusts can cause occupational asthma, and the list of enzymes able to induce asthma is increasing. We report two patients with asthma induced by occupational exposure to cellulase powder derived from Aspergillus niger. A type I hypersensitivity to this enzyme was demonstrated by means of skin test reactivity, positive passive transfer test, positive reverse enzyme immunoassay for specific IgE, and immediate bronchial provocation test response to cellulase dust. Skin tests with an A. niger extract were positive. Cross-reactivity between cellulase dust and an entire A. niger extract was also demonstrated.
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Four patients with occupational asthma were studied. All patients were exposed to African maple dust and two of them were also exposed to Ramin dust. Skin tests and bronchial provocation tests with African maple extracts revealed an immediate response in all patients, and the same tests performed with Ramin extracts again revealed an immediate reaction in either exposed or non-exposed patients to Ramin wood dust. Specific IgE antibodies against African maple extracts were demonstrated in all patients as measured by a reverse enzyme immunoassay. Cross reactivity between both woods was demonstrated by a reverse enzyme immunoassay inhibition study. Unexposed persons and exposed asymptomatic workers did not exhibit reactivity to both woods in any of the tests listed above. To the best of our knowledge, this is the first article in which occupational asthma due to Ramin is defined, and cross sensitivity between two different woods is demonstrated.
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Inhalation of wood dusts can cause immediate and/or late onset asthma, and the list of woods responsible for such reactions is increasing. We report two patients with asthma induced by exposure to the dust of African maple wood (Triplochiton scleroxylon). Type I hypersensitivity to this dust was demonstrated by means of immediate skin test reactivity, positive passive transfer test, positive reverse enzyme immunoassay for specific IgE, and an immediate bronchial provocation test response to an African maple-dust extract. Unexposed persons did not exhibit reactivity to this wood in any of the tests listed above.
We report two familial cases of Iso-Kikuchi sindrome, (mother and son). Patient one with small bone abnormalities under mycronychya, and patient two with atopic dermatitis. Literature cases are reviewed.
A microplate enzyme-immunoassay technique for the detection of specific anti-Lolium perenne IgE antibodies is described. This method consists of coating polystyrene wells with goat antihuman IgE (epsilon chain specific) and late selecting the IgE from the patients serum in order to finally reveal the bound specific IgE by means of a crude L. perenne extract conjugated with peroxidase. The optimal conditions necessary to achieve maximum sensitivity and specificity using this system have been studied. After testing 98 sera, the results showed a 97.9% correlation between our technique and the RAST.
A left upper lobe pneumonia developed in a patient who was receiving hemodialysis; he was treated intravenously with 1 g of erythromycin lactobionate every six hours. After five doses, hearing loss was noted; this was later documented by audiogram. Erythromycin serum concentrations as high as 100 mg/L and a half-life more than three times longer than normal were observed. To our knowledge, this represents the first report of reversible hearing loss associated with elevated serum erythromycin concentrations and prolonged serum half-life.
In the following paragraphs we describe a case diagnosed clinically and haemodynamically as a cardiomyopathy. Atrial flutter which was not in evidence in the standard ECG was diagnosed by the use of a new technique of amplification and filtering of special surface leads (T.A.F.). The diagnosis was later confirmed by means of special internal techniques (intra-atrial ECG and His bundle recording). The existence of a subpraventricular rhythm, probably sinusal, and also unapparent in the standard ECG, was observed by using the same method after electrical defibrillation. We comment on the extreme rareness of discovering concealed atrial rhythms and their possible explanation, and we emphasize the usefulness of the T.A.F. technique in their diagnosis.
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According to the authors the best designation of Ritter's disease would be "staphilococcic epidermal exfoliation" SEE. The physiopathological and agnoslogical basis for this denomination could be the following: 1st The "S. aureus" is the ehtiological agent of the SSE in man. The Koch postulates necessary to confirm this hypothesis have been accomplished. 2nd "Staphylococcus aureus" produces a thermostable toxin that is active indepently of the staphilococcus and gives rise to the separation of the cells of the stratum granulosus of the epidermis and eventually exfoliation in suckling babies and in the newborn mouse. 3rd The "Staphylococcus aureus" may be present on the skin or in other localisations such as the bowel or pharinx. 4th The viable "S. aureus" when administered subcutaneously to the adult mice gives rise to lesions clinically and histologically similar to the impetigo observed in children. 5th The "S. aureus" killed by means of autoclave (that is, the staphylococcic toxine by itself does not give rise to any lesion when administered to the healthy adult mouse). Neijther has the SEE been observed in healthy adult man. The authors reach the conclusion that the SSE and the toxic epidermal necrolysis are basically different according to the histopathology therapeutic response and prognosis and they must be considered as independant entities.