Biomedical subjects
Publications and source records attributed to C Calvo.
A collective intoxication with chlorine gas in 76 children (21 males, 55 females; the median age was 9.9 years) is reported. They were treated with a combination of oxygen gas (O2) and corticosteroids until the symptoms disappeared.
Two Yersinia enterocolitica strains were able to utilize the products of cephalothin degradation. The utilization of these products was shown by an increase of oxygen uptake by Y. enterocolitica with cephalothin as the only substrate, and by the growth of both strains with the hydrolysis products of cephalothin as sole energy and carbon sources. Nuclear magnetic resonance analysis of the cephalothin degradation reaction demonstrated the progressive disappearance of hydrolysis products. However, the products of benzylpenicillin degradation could not be utilized by Y. enterocolitica.
The incidence of the Reye syndrome in Spain has been retrospectively reviewed from 1980 to 1984. A survey of 57 cases has been available to study. It is pointed out the low frequency (0.12/10(5) 15 years); the low mean age (12 month) due to a higher prevalence in infants; the high mortality rate (49%), proportional to the great number of III and IV Lovejoy's stages; the low correlation with chicken-pox and salycilate-intake in the prodromic period and a better prognosis in patients when barbituric coma was established along with other measures.
The presence of receptors to bacteriophage I of Y. enterocolitica in Y. enterocolitica cells grown at 37 degrees C was investigated. Protein extracts obtained from bacterial cells (strain 4052) grown at 25 degrees or 37 degrees C produced a diminution of free bacteriophage. Cultures of this strain inactivated phage I at 37 degrees C, and high titre suspensions of this phage showed bacteriocin-like activity. According to these results receptor sites must be present in Y. enterocolitica cells incubated at 37 degrees C.
The membrane phenotype of human T cell colony progenitors and that of their clonal progeny was studied for expression of the T4 and T8 determinants. Using clonal culture conditions, the colonies were grown in semi-solid agar medium from peripheral blood cells. Clonality was assessed using the glucose-6-phosphate-dehydrogenase isoenzyme marker. Combination of this marker with the culture of sorted cell fractions allowed us to ascribe the colony progenitors to a subset of OKT4+ lymphocytes. The progeny consisted of the mixture of single OKT4+, single OKT8+ and double OKT4+8+ cells, as determined by double staining. Double staining was performed on mass-harvested colony cells and on individual colonies expanded in liquid culture with fresh interleukin 2. Expression of the OKT8 positivity on colony cells deriving from OKT4+ progenitors required an interaction with radioresistant OKT8+ cells that were co-cultured with these progenitors. Furthermore, the functional capacities of the cell progeny were assayed on the pokeweed mitogen-driven immunoglobulin production by B cells. It was found that OKT4+ colony cells were helper whereas OKT8+ colony cells were suppressor cells. It is concluded that a subset of OKT4+ peripheral blood T lymphocytes can generate colonies containing both helper OKT4+ cells and suppressor OKT8+ cells.
Sixty-eight sera from 36 children with celiac disease (CD) were collected in a 4-year study, and the levels of beta2-microglobulin (beta2M), orosomucoid, alpha1-antitrypsin, and C-reactive protein (CRP) were measured. A simultaneous intestinal biopsy was taken in all the patients and used to classify them. The values of beta2M were 1.94 +/- 0.49 mg/L in group A (inactive CD with normal intestinal biopsy) and 2.58 +/- 0.76 mg/L in group B (active CD with flat mucosa). These levels were higher than in the normal controls (1.87 +/- 0.49 mg/L, p less than 0.005) and in the other 19 patients with chronic diarrhea of another cause (1.72 +/- 0.63 mg/L, p less than 0.005). CRP values were generally normal; orosomucoid and alpha1-antitrypsin were variable and they did not correlate with beta2M levels. Beta2M was increased at the time of diagnosis in seven of eight (87.5%) of the CD children and only in three of 19 (15.7%) of nonceliac patients with chronic diarrhea of another cause (p less than 0.005). In 12 children with CD, serial studies were possible. The highest beta2M level coincided with a flat mucosa in 10 cases. The increase of beta2M could be related to the intestinal infiltration or even to the lymphocyte activation. It may also be a useful noninvasive method for evaluating the activity of CD.
The effects of long-term treatment with mouse interferon on the phenotype of untransformed C3H/10T1/2 cells and cloned derivatives transformed by methylcholanthrene (MCA) and Simian virus 40 (SV40) were investigated. Continuous presence of interferon induced morphologic reversion, with the development of thick, submembranous filaments in MCA-transformed cells, whereas no morphological effects were detected in SV40-transformed cells. Interferon inhibited the proliferation of all three cell lines and maintained low saturation densities. However, prolonged treatment of MCA-transformed cells with interferon rendered them tolerant toward the anti-proliferative and antiviral activities of interferon although 2-A synthetase activity was induced. Interferon treatment reduced the capacity of both MCA and SV40-transformed cells to form colonies in agar and decreased the tumorigenicity of MCA-transformed but not SV40-transformed cells in mice. These results indicate that the same cell type transformed by different means has different sensitivities to a number of interferon-induced changes in the cell phenotype.
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Three cases (one, newborn infant and two infants--one of them recently published--) who present electrocardiographic and enzymatic alterations comparative with diagnosis of ischemia and myocardial infarction are reported. Rarity of this entity in infants is stressed as most of published cases are secondary to ananomolous coronary artery. Etiology of the cases presented shows a myocardiac fibrosis with Schwachman's syndrome in one case, a coronary thrombosis secondary to a disseminated intravascular coagulation in a second case, and finally a generalized hypoplasia of coronary arteries. Hypoxia appears in these cases a factor acting in favour of myocardial ischemia. Diagnostic criteria of acute myocardial infarction are based on typical electrocardiogram and rise of isoenzymes of LDH and CPK-MB. Although rare, it is a diagnosis to be considered in cases of unknow cardiac insufficiency in newborns and infants.
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Seven bacteriophages active on Yersinia enterocolitica (YE) were isolated from surface water samples collected in Granada, Spain. A comparison of the respective host ranges of these new phages and of reference phages used for YE phage typing showed that YE strains belonging to various phage types, grown at either 37 or 25 degrees C, expressed susceptibility to reference sewage water phages whereas susceptibility to new waterborne phages, as well as to reference phages from lysogenic YE, was only demonstrated in YE strains grown at 25 degrees C. A YE strain isolated by stool culture from a pig was lysogenic for a bacteriophage which behaved like waterborne phages and reference phages from lysogenic YE strains. The possibility that the isolation of waterborne bacteriophages might, in certain circumstances, reflect the presence of lysogenic YE was raised.
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Ninety-six sera from coeliac children were studied, 55 were taken during a normal diet and 41 with a gluten-free diet. C'3, C'4, C'5, C'3, PA, C'1 INH and C'3b INA were measured. No significant differences were found between coeliac patients and normal controls. Results were also similar for gluten-free diet coeliac childrens and for active patients. A challenge was performed with 20 g. of gluten in 14 active patients. The levels of C'3, C'3 PA had a large variability, increasing and decreasing, but no similar and constant pattern was found. Activation products of C'3 appeared, specially between 4 and 24 hours, and disappeared about 48 hours. These results support an alteration of complement in coeliac patients but there is not a constant and steady pattern. Our hypothesis is that complement activation is not a pathogenic mechanism of coeliac disease. Maybe is just a consequence or epiphenomenon.