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Biomedical subjects

M Perez

Publications and source records attributed to M Perez.

At least 181 records · Page 10Linked to original sources
PubMed1985

Anti-SSA(Ro) antibody: a connective tissue disease marker.

The characteristics of 100 patients with anti-SSA(Ro) antibody were studied. By accepted criteria 34 patients had systemic lupus erythematosus, 25 had other known connective tissue diseases (CTD) and 9 had no significant evidence of a CTD. Thirty-two patients had an unclassified CTD characterized in most instances by arthritis, dermatitis, and a positive fluorescent antinuclear antibody test. The results support the concept of a continuous spectrum of autoimmune disease in which anti-SSA(Ro) antibody may be a marker and in which a variety of disorders may be found that cannot be classified by accepted criteria.

Adult↗
PubMed1984

Leukopenia in Still's disease.

Two patients, one a 14-year-old girl and the other a 20-year-old man, with typical manifestations of juvenile rheumatoid arthritis had leukopenia and thrombocytopenia, two heretofore unreported findings. The presence of leukopenia should not be used to exclude a diagnosis of Still's disease.

Adolescent↗
PubMed1984

Rotavirus shedding by newborn children.

We studied the shedding of rotavirus by newborn children in the nurseries of a large maternity hospital in Caracas, Venezuela, throughout the year 1982. Sixty-two (57%) of 108 children examined shed the virus within the first few days of life. Four (6%) of the 62 children who shed rotavirus had diarrhea but only one of them required oral rehydration therapy. The rotavirus specimens were identified as subgroup 2 in an ELISA subgrouping assay that employs monoclonal antibodies. Analysis of the RNA extracted from 52 of the samples by electrophoresis revealed a similar migration pattern in all the specimens; their identity was confirmed by crosshybridization analyses which revealed a strong degree of genomic homology among the strains studied.

Diarrhea↗
PubMed1984

Relative frequency of rotavirus subgroups 1 and 2 in Venezuelan children with gastroenteritis as assayed with monoclonal antibodies.

Monoclonal antibodies recently developed against the 42,000-dalton protein of two rotavirus strains were used in an enzyme-linked immunosorbent assay to determine the subgroup specificity of 252 specimens collected during a 45-month period from Venezuelan children with rotavirus gastroenteritis. Subgroup 2 rotavirus was shed by 85% of the children, whereas only 14% shed subgroup 1 rotavirus (one-half of them in a 3-month period). No differences were found in the occurrence of fever and vomiting between children shedding either rotavirus subgroup, but it appeared that the syndrome tended to last longer in children shedding subgroup 2 rotavirus. The monoclonal subgrouping enzyme-linked immunosorbent assay seemed to be more sensitive than an immune adherence hemagglutination assay, an enzyme-linked immunosorbent assay with polyclonal antibodies, or the electrophoretic analysis of RNA extracted from the virus. Overall, 99% of the specimens could be subgrouped by this assay.

Antibodies, Monoclonal↗
PubMed1984

High out-put congestive heart failure as first manifestation of Osler-Weber-Rendu disease.

We present two cases of hemorrhagic hereditary telangiectasia (HHT) or Osler-Weber-Rendu disease which started as heart failure. Both had multiple arteriovenous fistulas, one of them in a rare localization in this disease, a lower extremity. We conclude stressing the importance of thinking of HHT in the presence of obscure heart failure or arteriovenous fistulas and of looking for internal fistulas when faced by a HHT.

Aged↗
PubMed1983

Inhibition of brain adenylate cyclase by A1 adenosine receptors: pharmacological characteristics and locations.

When tested under conditions reducing the endogenous production of adenosine (presence of adenosine deaminase (ADA) 1.6 IU/ml; and deoxyadenosine triphosphate (d-ATP), and in the presence of both NaCl and GTP, the ADA-resistant analog phenylisopropyladenosine (PIA) inhibited the adenylate cyclase of several brain tissues. These tissues included: (1) 5 brain areas of adult rats (frontal and parietal cortex, cerebellum cortex, hippocampus and striatum)--hypothalamus and mid-brain adenylate cyclases were not inhibited by PIA; (2) astrocytes in primary cultures prepared from cerebral cortex of newborn mice; and (3) neurons in primary cultures prepared from striata of 15-day-old mouse embryos. The specificity profile of the adenosine receptor involved in the inhibition was determined in astrocytes. It was typical of an A1 adenosine receptor (high affinity of PIA; Ka app: 9 +/- 5 X 10(-9) M (n = 4) compared to the affinity of 5'-N-ethylcarboxamide adenosine (NECA); Ka app: 1.3 +/- 0.6 X 10(-7) M (n = 3). There was an excellent correlation between the affinities of several adenosine agonists and antagonists for A1 receptors coupled with an adenylate cyclase in astrocytes and for the receptors labeled with N6-cyclohexyl-[3H]adenosine in brain cortex. In adult rat striatum as well as in astrocytes and striatal neurons in culture the adenylate cyclase was inhibited by low PIA concentrations through A1 receptors and stimulated by higher concentrations through A2 receptors. In contrast, A2 receptors were not detected in adult rat cerebral cortex. In adult rat striatum, A1 and dopamine receptors coupled with an adenylate cyclase seemed to be located on different cell populations. In contrast, in astrocytes A1 and beta-adrenergic receptors coupled with adenylate cyclase were apparently located on the same cells.

Adenosine↗
PubMed1982

Preliminary crystallographic data on cytochrome P-450CAM.

The cytochrome P-450CAM monooxygenase from Pseudomonas putida has been crystallized in three forms designated orthorhombic I, tetragonal I, and orthorhombic II. Conditions and parameters of crystal growth are presented along with the preliminary x-ray diffraction data including heavy atom derivatives.

Cytochrome P-450 Enzyme System↗
PubMed1982

Autoradiographic detection and characterization of a Chinese hamster ovary cell mutant deficient in fucoproteins.

Autoradiography of colony replicas immobilized on filter paper was used to isolate a Chinese hamster ovary cell line deficient in incorporation of radiolabeled fucose into a trichloroacetic acid-insoluble fraction. This cell line, called 62.1, has the same growth rate at 37 degrees C as wild-type cells, but incorporates five times less fucose into acid-insoluble radioactivity. Chemical analysis of fucose bound to macromolecules also showed a fivefold reduction in the mutant. The fucoproteins of the mutant cell line differ qualitatively from those of wild-type cells as visualized by SDS gel electrophoresis fluorography; no differences were detected between total proteins as visualized by coomassie blue staining. The macromolecular sialic acid content of the mutant was somewhat higher than the wild type (20%). Studies of the synthesis of the glycoprotein of vesicular stomatitis virus in mutant and wild-type cells showed that the mutant is unable to synthesize complex-type N-linked oligosaccharides. Enzyme assays show that ths defect in the mutant is due to reduction in UDP-N-acetylglucosamine-glycoprotein N-acetyl-glucosaminyltransferase, a key enzyme in the assembly of complex glycopeptides. Hybridization studies have shown that mutant 62.1 has common mutations belonging to the same complementation group as mutant PhaR1-1. This latter mutant was previously isolated using lectin resistance by Stanley et al. (1975) and was also deficient in the above N-acetyl-glucosaminyltransferase.

Animals↗
PubMed1982

Genetic relatedness among human rotaviruses as determined by RNA hybridization.

Viral RNAs from human rotaviruses were compared by gel electrophoresis and by hybridization to probes prepared by in vitro transcription of two well-characterized laboratory strains (Wa and DS-1). Also, the viral RNAs were compared by hybridization to probes prepared from three of the test viruses. Thirteen specimens (diarrheal stools) were obtained from infants and children 5 to 21 months old on a single day at the emergency ward of the Caracas Children's Hospital, and an additional specimen was obtained from the same hospital 6 months before. When the electrophoresed viral RNAs were stained with ethidium bromide and examined by UV light, five different migration patterns (electropherotypes) were distinguished on the basis of differences in mobility of the RNA segments. The hybridization technique that was employed permitted only qualitative comparisons of corresponding genes of different human rotaviruses. Ten of the specimens contained enough virus to yield sufficient RNA for hybridization studies. Eight of the viruses studied by hybridization contained 4 to 11 genes that reacted specifically with the Wa probe to yield double-stranded RNA segments with a mobility similar to that of Wa viral RNA or test virus RNA. The other two viruses contained 11 genes that reacted specifically with the DS-1 hybridization probe to yield double-stranded RNA segments with a mobility similar to DS-1 viral RNA or test virus RNA. A more complex picture emerged when hybridization probes were prepared from three of the test viruses and used to compare the different electropherotypes. Corresponding genes that exhibited similar migration did not necessarily exhibit homology when studied by hybridization. Also, some corresponding genes that exhibited homology did not have the same mobility by gel electrophoresis.

Child, Preschool↗
PubMed1982

[Syndromic diversities in Creutzfeldt-Jakob disease: neurophysiological and histopathological correlates].

Two syndromatic forms of Creutzfeldt-Jakob disease are illustrated with data from two cases confirmed by necropsy and studied by means of electroencephalogram, evoked potential recording and neuropathological techniques. One of the cases presented the typical hypersynchronous periodic discharges through to be characteristic of this disease. The other did not exhibit epileptiform discharges, showing an evolution in which progressive diffuse slowing was the prominent feature. Cortical spongyosis, gliosis, and neuronal lose were intense in the case showing spikes, and moderate in the one without spikes. Subcortical involvement was similar in both cases. This different topography of pathological involvement might explain, in addition to electroencephalographic findings, the different behavior of somatosensory evoked potentials, which were of larger amplitude in the case showing epileptiform discharges, although in both cases deterioration of clinical state was accompanied by a progressive amplitude decrement in the evoked potential. Sleep induced by barbiturates was disrupted in the case with spikes, its pattern being closer to normal in the case with less severe cortical involvement. A Wada test demonstrated that discharges in the hemispheres were independent. Spike periodicity is discussed. It is postulated that the heavier involvement of cortical layers II to IV deprive the remaining pyramidal cells of inhibitory influences, a condition which might explain the generation of periodic spike discharges.

Adult↗
PubMed1982

[Actinic granuloma. Presentation of 3 cases].

Three cases of actinic granuloma which presented anular lesions with central atrophy in the frontotemporal region are reviewed. Microscopy changes showed the center of the lesion devoid of elastic fibers, an inflammatory reaction at the edge of the lesion and normal elastic fibers in the surrounding area. We discuss the differential diagnosis with granuloma annulare and the possible etiological role of previous actinic damage.

Aged↗
PubMed1981

Apoprotein formation and heme reconstitution of cytochrome P-450cam.

Apoprotein suitable for heme reconstitution has been prepared by an acid/butanone extraction of cytochrome P-450cam at pH 2.5. Absorption spectra of apo-P-450cam indicate less than 2% residual holoenzyme. Four tryptophan residues per molecule were estimated from the aromatic absorbance region of denatured apoprotein. Heme-reconstituted holoprotein was purified in 30% yield to a specific activity equivalent to the native enzyme. Absorption and EPR spectra of 57Fe- and 54Fe-heme-enriched P-450cam reveal complete restoration of the native active site.

Apoproteins↗
PubMed1981

Neuronal, glial and meningeal localizations of neurotransmitter-sensitive adenylate cyclases in cerebral cortex of mice.

The neurotransmitter-sensitive adenylate cyclases, respectively present in the dissociated cells of new-born mouse cerebral cortex (containing both neuronal and glial cells) and in a homogeneous population of glial cells, were compared. The dissociated cells from the cerebral cortex of new-born mice were found to contain Ca2+-, dopamine-, serotonin- and purinergic-sensitive adenylate cyclases. The dopaminergic receptor involved was extensively characterized and was similar to that described in adult animals. Beta-adrenergic-sensitive adenylate cyclase was present but was poorly active. After 3 weeks in culture, the neurons disappeared and a homogeneous population of glial cells was obtained (96% of the cells synthetized glial fibrillary acidic protein). These glial cells contained a highly potent beta-adrenergic-sensitive adenylate cyclase, and adenosine- adn Ca2+-sensitive enzymes. Ca2+ stimulation of the adenylate cyclase was due to the presence of calmodulin. We suggested that the dopaminergic- and serotoninergic-sensitive adenylate cyclases which disappeared during culture are probably localized in neuronal cells. The presence of Ca2+-, adenosine- and beta-adrenergic-sensitive adenylate cyclases in glial cells does not exclude their presence in neuronal cells. For comparison, the same experiments were conducted on meningeal layers of new-born mice and on meningeal cells in culture. They both contained beta-adrenergic- and purinergic-sensitive adenylate cyclases.

Adenylyl Cyclases↗
PubMed1981

Characteristics of the beta 1-and beta 2-adrenergic-sensitive adenylate cyclases in glial cell primary cultures and their comparison with beta 2-adrenergic-sensitive adenylate cyclase of meningeal cells.

The agonist specificity pattern of the beta-adrenergic adenylate cyclase in glial primary cultures was not typical of either beta 1- or beta 2-adrenergic receptors. The dose-response curves for adrenaline did not correspond to simple mass action kinetics and their computer analysis suggests the presence of both beta 1- and beta 2-adrenergic-sensitive adenylate cyclase (58 plus or minus 17% and 42 plus or minus 17% respectively). Similar properties of beta 1- and beta 2-adrenergic-sensitive adenylate cyclases were found by computer analysis of the dose-response curves for isoprenaline in the presence of a constant concentration of practolol (a selective beta 1 antagonist) (55 plus or minus 10% and 45 plus or minus 10% of beta 1- and beta 2-sensitive adenylate cyclase respectively). The curves for displacement of [3H]dihydroalprenolol by practolol confirm these results. For purpose of comparison, the beta-adrenergic receptors of meningeal cells in cultures were subjected to similar analysis. The results clearly showed that these cells exclusively contained beta 2-adrenergic receptors.

Adenylyl Cyclases↗
PubMed1981

Alpha 1 and alpha 2 Adrenergic receptors in mouse brain astrocytes from primary cultures.

Mouse brain astrocytes from primary cultures were found to contain both alpha 1 and alpha 2 adrenergic receptors. 3H WB 4101 labeled one category of binding site (KD = 1.5 +/- 0.39 nM, Bmax = 64 +/- 7.9 fmoles/mg protein) with typical alpha 1 adrenergic specificity (WB 4101 greater than prazosin greater than yohimbine). The density of alpha 1 adrenergic receptors was 2-3 times higher in mouse cerebral cortex than in glial cells. Like rat brain [U'Pritchard et al, 1979; Rouot et al, 1980], mouse glial cells were found to contain two categories of 3H clonidine binding sites: high affinity sites, which were identical to the high but not to the low affinity sites found in rat brain, since 1) they displayed the same affinity for 3H clonidine (KD = 1.2 +/- 0.13 nM, n = 4) and the same typical alpha 2 adrenergic specificity (yohimbine greater than WB 4101 greater than prazosin); 2) the dissociation rate constant for clonidine binding was equal to 0.06 min-1, a value close to that found previously for the high affinity 3H clonidine binding sites in rat brain (0.05 min-1); and 3) divalent cations augmented and guanyl nucleotides reduced 3H clonidine binding as in rat brain. Na+ decreased 3H clonidine binding in a complex manner. The number of high affinity sites in glial cells (52 +/- 9.4 fmoles/mg protein, n = 4) was half the number found in mouse cerebral cortex (98 fmoles/mg protein). Low affinity 3H clonidine binding sites (KD = 81 +/- 18 nM, Bmax = 96 +/- 5.8 fmoles/mg protein, n = 3) were not fully characterized. In conclusion, glial cells contained the same alpha adrenergic receptors as those described in brain, but their physiological function is not yet known.

Adrenergic alpha-Antagonists↗
PubMed1981

Selection of mutant Chinese hamster ovary cells altered glycoproteins by means of tritiated fucose suicide.

Mutant Chinese hamster ovary cells altered in glycoproteins have been isolated by selecting for ability to survive exposure to [6-3H]fucose. Mutagenized wild-type cells were permitted to incorporate [3H]fucose to approximately 1 cpm of trichloroacetic acid-insoluble radioactivity per cell and then frozen for several days to accumulate radiation damage. The overall viability of the population was reduced by 5- to 50-fold. Four consecutive selection cycles were carried out. The surviving cells were screened by replica plating-fluorography for clones showing decreased incorporation of fucose into trichloroacetic acid-insoluble macromolecules. Considerable enrichment for cells deficient in fucose uptake or incorporation into proteins (or both) was found in populations surviving the later selection cycles. Two mutant clones isolated after the fourth selection cycle had the same doubling time as the wild type, but contained only 30 to 40% as much fucose bound to proteins as the wild type. Sialic acid contents of the mutants and the wild type were similar. The mutants differed quantitatively and qualitatively from the wild type and from each other with respect to total glycoprotein profiles as visualized by sodium dodecyl sulfate gel electrophoresis. Differences were also found in resistances to cytotoxicity of lectins such as concanavalin A and wheat germ agglutinin.

Animals↗