Calcium metabolism and celiac disease.
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Biomedical subjects
Publications and source records attributed to A Herrera.
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Fidel Pagés was born in Huesca on the 26th of January 1886. He completed his secondary studies in the same city, later receiving his degree in medicine and surgery from University of Zaragoza (1908) with high honors. The same year he joined the army medical corp, to be sent to serve in Melilla in 1909 with a rank of second medical officer. After being promoted in 1911 to first medical officer, he served in Tarragona, Toledo, Madrid (where received his doctoral degree), Ciudad Real, and once again in Madrid. In 1913 Pagés married and was destined to Mahón, only to return to work at the War Ministry in Madrid in 1915, after a brief sojourn in Alicante. The same year he placed first in competition for a staff position at Madrid's Hospital Provincial. In 1917, during World War I, he inspected POW camps in Austria and Hungary, while also serving in the military hospital in Vienna. In 1919 he became the founding editor of Revista Española de Cirugía, which published "Anestesia metamérica" in 1921, simultaneous to its publication in Revista de Sanidad Militar. In 1920 on he was assigned to Madrid's Hospital Militar de Urgencia, but was also briefly sent to Melilla in 1921 as a consequence of the military "Disaster at Annual". In 1922 he was promoted to the rank of Medical Commandant. On the 21st of September 1923, Pagés died in a traffic accident while returning to Madrid from San Sebastián. His work was soon forgotten, as can be seen from the credit long given to the Italian surgeon Dogliotti for the discovery of epidural anesthesia. Only with passing time, and through the effort of Argentinian and Spanish physicians, has the world come to recognize Pagés as the original author of this technique.
In Schizosaccharomyces pombe, MBF is a DNA-binding complex suspected to activate the transcription of genes necessary for entry into S phase. The MBF complex contains both p85cdc10 and p72res1/sct1. To obtain a better understanding of how the MBF complex regulates gene expression at the G1/S transition, we have performed a genetic analysis of p72res1. We determined that p72res1 can bind specifically to the cdc22 promoter, when analyzed by gel mobility shift assay, and that the N-terminal 157 amino acids of p72res1 are sufficient for this specific binding. When overexpressed in vivo, a fragment of p72res1 containing this DNA-binding domain could rescue a strain carrying a temperature-sensitive cdc10 allele at the restrictive temperature as well as a strain with a cdc10 null allele. We also determined that the C-terminal region of p72res1 is necessary and sufficient for binding to p85cdc10. Overexpression of the cdc10-binding domain of p72res1 leads to a G1 arrest with a cdc phenotype and a decrease on MBF activity. Overexpression of full-length p72res1 also leads to a growth arrest that can be rescued by overexpression of p85cdc10. These results imply that the MBF activity in vivo is dependent on the interaction of p85cdc10 with p72res1.
An enzyme immunoassay for the detection of serum IgG antibodies to H. pylori whole bacterial sonicate was used in a study of dyspeptic adult patients (n = 165), apparently healthy blood donors (n = 154), and children (n = 66) from Costa Rica, where a very high incidence of gastric carcinoma is observed. The mean antibody levels and frequency distributions were similar in the dyspeptic patients and the blood donors. Meanwhile lower antibody levels to H. pylori were more frequently observed in children than in adults, suggesting an age-dependent increase in seroprevalence, as described in studies from other populations.
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An incident involving central oxygen supply failure affecting 4 anesthetized patients in the operating theatre was analyzed by way of interviews with the anesthesiologists and a review of graphic records of anesthesia. The 4 ventilators involved had been checked by each anesthesiologist according to his own method. The oxygen supply failure alarm warned of the supply cutoff in 2 cases and the oxygen analyzer detected the other 2 within approximately 1 minute. After the failure, 2 patients were ventilated with ambient air through the ventilator, 1 was given medicinal air with the resuscitator. None suffered damage or recalled having awakened as a result of the incident. The cause of the failure in oxygen supply has not been determined but its duration has been estimated to be between 4 and 7 minutes. Our investigation shows that: 1) the operating rooms are not equipped with an alarm that warns of a drop in pressure within the tubes that supply central oxygen and in 2 cases the alarm warning of a cutoff in oxygen supply to the respirator did not sound correctly; 2) the ventilator equipment check did not follow a standard method and did not cover the possibility of oxygen supply failure, and 3) no alternative oxygen supply is available inside the operating theatre.(ABSTRACT TRUNCATED AT 250 WORDS)
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Analysis of gene expression in peripheral blood lymphocytes is of special interest because it could reflect physiological conditions. We have examined the expression and compared the relative amounts of specific mRNAs for interferons (IFN-alpha and IFN-beta), tumor necrosis factor-alpha (TNF-alpha) and interferon regulatory factors (IRF-1 and IRF-2) from interferon primed and Sendai virus induced peripheral blood leukocytes. Results obtained showed that IRF-1 was highly inducible by IFN treatment, IFN-alpha, TNF-alpha and IRF-2 were weakly induced by IFN treatment, and IFN-beta was not inducible by priming the cells with recombinant human IFN-alpha 2b. The IFN-alpha, IFN-beta, IRF-2 and TNF-alpha transcripts increased upon viral infection. The IRF-1 mRNA was rapidly induced by IFN treatment and decreased after Sendai virus infection. Our results show that, in peripheral blood lymphocytes, IFN-alpha and -beta genes have a different response to IFN induction, thus suggesting different regulatory mechanisms for IFN induction of type I IFN genes in peripheral blood lymphocytes.
The pyrethroid insecticide permethrin was tested for its ability to induce structural chromosome aberrations (CA) in human lymphocyte cultures and CHO cells, in order to confirm the clastogenic effect of itself and to compare the response of the two different cell types. Permethrin was tested in the range of 50-200 micrograms/ml in human lymphocyte cultures and in the range of 20-100 micrograms/ml in CHO cells. In both lymphocyte and CHO cultures, assays were performed in the absence and in the presence of a rat liver activation system (S9 mix). In the absence of S9 mix, two experiments with different duration of the treatment were carried out. Permethrin induced CA in both cultures when it was evaluated in the absence of a metabolic activation system. The activity of a given concentration of permethrin seemed to be decreased more by the reduction of the time of exposure than by the presence of S9 mix. Aberrations induced by permethrin were mainly chromosome-type aberrations in both cultures. Thus, permethrin can be characterised as an S-phase independent clastogenic agent. The response of both lymphocyte and CHO cultures was similar, indicating that both systems showed the same sensitivity for detecting the clastogenicity in vitro of permethrin.
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The concentrations of the plasminogen activators u-PA and t-PA as well as the inhibitor PAI-1 were studied immunohistochemically in 35 osteosarcoma specimens compared to 15 Ewing's sarcomas and various other bone lesions. The immunoreactivities of plasminogen activators in osteosarcoma specimens were significantly higher than PAI-1. Biochemically in cell cultures and immunohistochemically in the pathological specimens of the osteosarcomas u-PA was the dominant antigen, all factors showing a generally strong reactivity. Here a relation to the malignancy and invasivity of the tumors could be seen, which was comparable to the results in other tumors. This correlation, however, could not be detected in Ewing's sarcomas. On the whole low immunoreactivity of all enzymes, and of u-PA in particular, could be seen. In comparison in some benign lesions (fibrous dysplasias, aneurysmal bone cysts) the immunohistochemical reactions were distinctly stronger. Dominant antigens did not exist in Ewing's sarcomas. In all mesenchymal tumors studied the immunohistochemical localisation and concentration of the antigens showed a definite correlation with their histological differentiation. Chondroblastic differentiations in different tumors (chondrosarcomas, enchondromas, chondroblastic osteosarcomas) or chondroid parts were always negative for both activators and the inhibitor, especially in their central parts. Here, the biological malignancy was not decisive for the result.
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Chronic myelocytic leukemia is a particular subtype of leukemia characterized by increased myeloid precursor cells. It has been associated with the presence of the Philadelphia chromosome, described by Nowel and Hungerford in 1960, as a deletion of part of the long arm of a G group chromosome, the 22 chromosome. The present work reports the chromosomal abnormalities observed in 39 patients with chronic myelocytic leukemia, studied at the Genetic Unit, in the Faculty of Medicine of Zulia University, during the period from 1987 to 1991. Sixty per cent of the patients showed different abnormalities, such as 8 trisomy, t (8;22), and in the remaining 15%, no chromosomal changes were detected. The patients with t (9;22) as the only abnormality, had less relapses and longer survival. The clinical course of 50% of the patients with normal karyotype was similar to those with t (9;22) as the only abnormality; the other 50% had an accelerated course with frequent relapses and early death. The present findings confirm that the presence of the Philadelphia chromosome as the only karyotypical abnormality, is indicative of better prognosis, and its association with other chromosomal changes predicts a more accelerated course that will probably require a more aggressive treatment.