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Biomedical subjects

B Gonzalez

Publications and source records attributed to B Gonzalez.

At least 55 records · Page 3Linked to original sources
PubMed1994

Tuberculin reactivity in families of infants who failed to develop tuberculin reactivity after BCG immunization at birth.

SETTING: Some infants immunized with BCG in the newborn period fail to develop any measurable tuberculin reactivity despite a local reaction at the site of immunization. OBJECTIVE: We wished to determine the possibility of a genetic regulation of this phenomenon by comparing the tuberculin reactivity of BCG-immunized parents and siblings of infants who failed to respond to BCG, and of infants who developed tuberculin reactivity after immunization. DESIGN: We studied 65 parents and siblings of 33 nonresponder infants, and 35 parents and siblings of 14 infants who had developed tuberculin reactivity. Tuberculin reactivity was analyzed by multiple regression analysis considering the BCG immunization status of each individual, and the 2 groups were compared by analysis of covariance. RESULTS: 96 of these family members had one or more BCG scars. The percentages of tuberculin reactors and non-reactors among BCG-immunized family members of both index infant groups were not significantly different. CONCLUSION: These observations suggest that maturational differences among newborns, rather than genetic regulation, account for the lack of development of cellular immunity against tuberculin after BCG immunization in some infants.

Adult↗
PubMed1994

Invasive micropapillary carcinoma of the breast. A new special type of invasive mammary carcinoma.

After reviewing 986 consecutive cases of breast carcinoma from our files, 27 ductal infiltrating cancers showing micropapillary differentiation in invasive areas (MP) were selected. Special immunohistological and ultrastructural techniques were used, and their characteristics compared to those of the Not Otherwise Specified type of carcinomas (NOS). Diagnostic areas of MP were easily identified in H&E sections and were composed of solid or tubular neoplastic cell groups inside a spongy background, where they appeared to swim in aqueous or mucinous material. Neoplastic cells displayed the reverse polarity typical of the papillary phenotype. This was revealed by the detection of acid mucinous rims, lineal deposits of EMA substances, and microvilli in a peripheral position, even in areas where the micropapillae resembled tubules. Histologically, most MP were mixed with N0S, Papillary, or Mucinous patterns, but regardless of the extension of their micropapillary diagnostic component, their tumour size, or their WHO histological grade, two thirds had extensive lymphatic vessel invasion and all the cases presented massive axillary lymph node metastasis. Six of the twelve patients followed died within a mean of 22 months. In conclusion, we propose the recognition of "Invasive Micropapillary Carcinoma of the Breast" as a new special entity with a potentially high degree of aggressiveness.

Breast Neoplasms↗
PubMed1994

Evaluation of tuberculin reactivity in BCG-immunized siblings.

The purpose of the present study was to determine in BCG-immunized sibships < or = 14 yr of age whether the correlations of intensity of tuberculin reactivity support a genetic regulation of the response to BCG immunization. The study population consisted of 659 healthy children living in 265 households exposed to an adult with tuberculosis: 38 children did not have a BCG scar, 327 children had one BCG scar, and 294 had two BCG scars from vaccinations at birth and at 6 yr of age. There were 603 full siblings, 16 half-siblings, and 40 unrelated children. Tuberculin testing was performed by one trained nurse. Sibling correlations of the intensity of the tuberculin response were calculated after adjusting for various nongenetic covariates that could be important in predicting it. The sibling correlations were significant at the 1% significance level. There was no significant correlation of tuberculin reactivity among unrelated children in the same household. These results are consistent with genetic regulation of the development and persistence of tuberculin reactivity after BCG immunization.

Adolescent↗
PubMed1993

Disseminated bacillus Calmette-Guérin infections in patients with primary immunodeficiencies.

The pathologic findings from biopsy or autopsy material in four patients, who were vaccinated with bacillus Calmette-Guérin (BCG) at birth in Chile, are presented. Two patients had severe combined immunodeficiency, and two had more restricted cellular (T-cell) immunodeficiency with no evidence of human immunodeficiency virus infection. The patients had distinct skin nodules and nodular lesions in systemic organs and bone marrow. Three patients had regional BCG lymphadenitis. One patient with severe combined immunodeficiency, however, had disseminated BCG without any local reaction. In all cases BCG strains of Mycobacterium were identified in a reference mycobacteriology laboratory. The histologic lesions in most patients usually consisted of diffuse histiocytic infiltrates with poorly formed granulomas and variable or no necrosis. Histiocytes were plump and engorged with numerous acid-fast bacilli (AFB). In some areas the massive histiocytosis resembled a spindle cell neoplasm. Other histologic findings supported the underlying immunodeficiency. The pattern of histiocytic response and degree of microbial killing depend on the host's immunocompetence. In the later stages of disease or in severe immunodeficiency, there is a lack of granuloma formation and unimpeded proliferation of AFB. These findings are reminiscent of nontuberculous mycobacterial infections in AIDS patients. Bacillus Calmette-Guèrin dissemination has to be considered in immunocompromised individuals when the patient comes from other countries in which such vaccinations are practiced.

BCG Vaccine↗
PubMed1992

Somatostatin receptors are expressed by immature cerebellar granule cells: evidence for a direct inhibitory effect of somatostatin on neuroblast activity.

Somatostatin and somatostatin receptors are transiently expressed in the immature rat cerebellar cortex but virtually undetectable in the cerebellum of adults. Although somatostatin binding sites have been visualized during the postnatal period in the external granule cell layer, the type of cell that expresses somatostatin receptors has never been identified; thus, the potential function of somatostatin in the developing cerebellum remains unknown. In the present study, we have taken advantage of the possibility of obtaining a culture preparation that is greatly enriched in immature cerebellar granule cells to investigate the presence of somatostatin receptors and the effect of somatostatin on intracellular messengers on cerebellar neuroblasts in primary culture. Autoradiographic labeling revealed the occurrence of a high density of binding sites for radioiodinated Tyr-[D-Trp8]somatostatin-(1-14) on 1-day-old cultured immature granule cells. Saturation and competition studies showed the existence of a single class of high-affinity binding sites (Kd = 0.133 +/- 0.013 nM, Bmax = 3038 +/- 217 sites per cell). Somatostatin induced a dose-dependent inhibition of forskolin-evoked cAMP formation (ED50 = 10 nM), and this effect was prevented by preincubation of cultured immature granule cells with pertussis toxin. Somatostatin also caused a marked reduction of intracellular calcium concentration. These results show the presence of functionally active somatostatin receptors on immature granule cells. Our data suggest the possible involvement of somatostatin in the regulation of proliferation and/or migration of neuroblasts during the development of the cerebellar cortex.

Adenylyl Cyclases↗
PubMed1992

Somatostatin receptors in the human cerebellum during development.

The ontogeny of somatostatin receptors (SRIF-R) was studied in the human cerebellum from mid-gestation to the 15th month postnatal. The brains were collected 3-26 h after death, from 18 fetuses and infants, and from 4 adults aged from 48 to 82. SRIF-R were characterized by membrane-binding assay and their localization was determined by in vitro autoradiography. Both techniques were conducted with two radio-ligands: [125I-Tyr0, DTrp8]S14 and D-Phe-Cys-125I-Tyr-DTrp-Lys-Thr- ol (125I-SMS 204-090). Membrane-binding studies carried out with each radioligand showed the presence of a single population of saturable, high affinity binding sites. Neither were the Kd values for either ligand (assessed by Scatchard analysis) changed appreciably during development, mean Kd values being 0.36 +/- 0.04 nM and 0.56 +/- 0.11 nM for [125I-Tyr0,DTrp8]S14 and 125I-SMS 204-090, respectively. Although inter-individual fluctuations of the Bmax were observed, the concentration of SRIF-R in the cerebellum of fetuses and infants up to 8 months appeared to be at least 2- to 10-fold higher than in the adult cerebellum. No appreciable differences in the Bmax values were found using either radioligand. The highest density of SRIF-R was observed in the cerebellar cortex of fetuses, in particular in the external granule cell layer (EGC), where stem cells of the granule cells are generated and enter the differentiation process. A high density of SRIF-R also occurred in the internal granule cell layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Zidovudine induces molecular, biochemical, and ultrastructural changes in rat skeletal muscle mitochondria.

Zidovudine (AZT) inhibits HIV-1 replication in AIDS. A limiting side effect is AZT-induced toxic myopathy. Molecular changes in a rat model of AZT-induced toxic myopathy in vivo helped define pathogenetic molecular, biochemical, and ultrastructural toxic events in skeletal muscle and supported clinical and in vitro findings. After 35 d of AZT treatment, selective changes in rat striated muscle were localized ultrastructurally to mitochondria, and included swelling, cristae disruption, and myelin figures. Decreased muscle mitochondrial (mt) DNA, mtRNA, and decreased mitochondrial polypeptide synthesis in vitro were found in parallel. Mitochondrial molecular changes occurred in absence of altered abundance of cytosolic glyceraldehyde-3-phosphate dehydrogenase, or sarcomeric mitochondrial creatine kinase mRNAs. Quadriceps mitochondrial DNA polymerase gamma activity was similar in both AZT-treated and control rats. In vivo findings with rats support the hypothesis that AZT-induced inhibition of mtDNA replication has an effect of depressing the abundance of striated muscle mtDNA, mtRNA, and mitochondrial polypeptide synthesis. This experimental approach may be useful to examine mitochondrial or toxic myopathies.

Animals↗
PubMed1991

Identification and distribution of microglial cells in the cerebral cortex of the lizard: a histochemical study.

The histochemical demonstration of nucleoside diphosphatase as a specific microglial marker was used to study the distribution of this glial cell type in the cerebral cortex of Podarcis muralis and Podarcis hispanica. Our results showed that in both species, NDPase staining was specific for the microglial cell population and that microglial cells displayed a specific localization pattern in the different cortical areas. In the medal cortex, microglial cells were principally found in the outer and inner plexiform layers in the strata adjacent to the granular layer. Moreover, some microglial cells were found near the ependymal layer, but no microglial cells were normally present near the brain surface and never in the deep inner plexiform layer. In the dorsomedial cortex, microglial cells were found near the brain surface in the outer plexiform layer, in the upper part of the granular layer, and near the ependymal layer. No microglial cells were found, however, in the outer and inner plexiform layers adjacent to the granular layer. Finally, in the dorsolateral cortex, microglial cells were located in the upper part of the outer plexiform layer, in and bordering the granular layer, and scattered in the inner plexiform layer. This layered-pattern distribution of microglial cell population in the cerebral cortex of the lizard differs from the apparently homogeneous distribution of microglia in the brain of mammals.

Acid Anhydride Hydrolases↗
PubMed1991

Stress-induced gastroduodenal lesions and total parenteral nutrition in critically ill patients: frequency, complications, and the value of prophylactic treatment. A prospective, randomized study.

OBJECTIVE: To assess the frequency, complications, and value of prophylactic treatment of stress-induced gastroduodenal lesions. DESIGNS: Patients were prospectively randomized to treatment with total parenteral nutrition, either alone, with sucralfate, or with ranitidine. SETTING: A multidisciplinary ICU from a tertiary care referral center. PATIENTS: Ninety-seven patients submitted to prolonged mechanical ventilation, with normal hepatic and renal function, in metabolic stress, and receiving total parenteral nutrition. INTERVENTIONS: On admission, we determined the Acute Physiology and Chronic Health Evaluation II score and the catabolic index score. We also performed an endoscopic examination on day 3, every 7 days subsequently, and whenever needed. Thirty patients received total parenteral nutrition alone. Twenty-four patients received total parenteral nutrition and sucralfate (1 g by nasogastric tube every 4 hrs). Nineteen patients received total parenteral nutrition and ranitidine (50 mg iv every 6 hrs). MAIN RESULTS: The overall occurrence rate of gastroduodenal mucosal damage was 29.6%. The overall frequency rate for stress ulcerations was 15.6% and was 6.2% for stress hemorrhage. There were no deaths secondary to stress hemorrhage. The difference in the frequency of stress-induced mucosal lesions and stress hemorrhage between the studied groups was not statistically significant. CONCLUSIONS: Additional prophylaxis to total parenteral nutrition in the form of sucralfate and ranitidine to prevent acute upper gastrointestinal bleeding is not required in this group of ICU patients.

Adolescent↗
PubMed1991

Mitochondrial ultrastructural and molecular changes induced by zidovudine in rat hearts.

Zidovudine (azidothymidine (AZT)) inhibits human immunodeficiency virus replication, prolongs survival, and delays progression of acquired immune deficiency syndrome. We determined AZT-induced molecular and ultrastructural changes in the rat heart. Rats (3 per group) were given drinking water with or without AZT (0.2 to 1.0 mg/ml; 29 to 102 mg/kg/day). After 21, 35, or 49 days, hearts were glutaraldehyde-fixed by abdominal aortic perfusion, processed, and examined by transmission electron microscopy. In parallel, myocardial RNA was extracted from hearts (AZT dose: 1 mg/ml; 35 days) and subjected to Northern analysis using cDNA probes for: alpha c-actin, troponin C, mitochondrial creatine kinase and malate dehydrogenase, a portion of the mitochondrial genome containing cytochrome b coding region (pMM26), and glyceraldehyde-3-phosphate dehydrogenase. Results showed marked and widespread cardiac mitochondrial swelling with fractured and disrupted cristae after 35 days of 1 mg/ml AZT. After a 14-day recovery, these ultrastructural defects did not reverse. Changes were not present in myocardium after 21 days of AZT nor after 35 days of lower dose AZT (0.2 mg/ml). Mitochondrial cytochrome b mRNA expression was depressed in AZT-treated rat hearts (35 days; 1 mg/ml AZT). mRNAs encoding glyceraldehyde-3-phosphate dehydrogenase, alpha c-actin, troponin C, mitochondrial creatine kinase, malate dehydrogenase, and mitochondrial ribosomal RNAs remained unchanged. AZT disrupts cardiac mitochondrial ultrastructure and expression of mitochondrial cytochrome b mRNA in a dose- and time-dependent fashion. The mechanism of AZT cardiotoxicity may relate to inhibition of mitochondrial DNA replication (at the level of DNA polymerase gamma) as postulated by others.

Animals↗
PubMed1990

Immunological and serological markers predictive of progression to AIDS in a cohort of HIV-infected drug users.

We have performed a prospective 33-month follow-up of the evolution of HIV infection in a cohort of 76 HIV-positive intravenous drug users (IVDUs). We report on immunological and serological variables that proved to be highly predictive of development to AIDS. In a stepwise multivariate analysis of the actuarial progression rate we found the number of CD4+ lymphocytes to be the most powerful predictor of progression to AIDS. We found no independent predictive effects associated with any other variable with predictive power: loss of antibody to p24 antigen, anergy, HIV p24 antigenaemia, loss of antibody to p53 (reverse transcriptase), decreased number of CD8+ T cells, loss of antibody to p31, loss of antibody to p17, beta 2-microglobulin level, loss of antibodies to gp41 and p64, or immunoglobulin A level. We have found that our data differ from those obtained in studies in homosexual men in the different prognostic value of those predictive markers. Our findings should help to identify high risk of progression to clinical AIDS among IVDUs, thereby assisting in the selection of patients for prophylaxis and therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Actin isoform mRNA alterations induced by doxorubicin in cultured heart cells.

Cultured rat myocardial cells (CMC) were incubated with adriamycin (ADR), an antineoplastic which causes dilated cardiomyopathy (COCM). CMC were exposed to 10(-7) M to 10(-5) M ADR for 24 hours, harvested, and CMC RNA was extracted. Extracted RNA underwent electrophoresis, transfer to nitrocellulose filters, and hybridization with radiolabeled cDNA probes which were specific for the actin isoforms (alpha, beta, and gamma) and isotypes (alpha sk = alpha skeletal; alpha c = alpha cardiac). RNA from CMC exposed to 10(-7) M ADR yielded a strong signal for mRNA coding for alpha c actin when probed with the isotype-specific cDNA. Hybridization signal was reduced in CMC extracts at 10(-6) M ADR. In CMC extracts at 10(-5) M ADR, the alpha c actin mRNA again hybridized. The cDNAs which were specific for beta and gamma actin isoforms yielded hybridization signals in extracts from CMC exposed to 10(-7) M and 10(-6) M ADR. These signals were reduced in extracts of CMC at 10(-5) M ADR. ADR's dose-related effect on the expression of alpha c actin in CMC is specific and suggests that ADR may have effects on regulation of CMC alpha c actin polypeptides and mRNA.

Actins↗
PubMed1989

Cytochemical demonstration of TPPase in myelinated fibers in the central and peripheral nervous system of the rat.

Thiamine pyrophosphatase (TPPase) activity was demonstrated by means of cytochemistry and electron microscopy in association with myelinated fibers in the central and peripheral nervous system of the rat. The areas studied included corpus callosum, hippocampus, cerebral cortex, cervical spinal cord and sciatic nerves. In the myelin sheaths, the enzymatic activity was found in 3 locations: (1) within oligodendroglial and Schwann cytoplasmic clefts between myelin lamellae; (2) in the major dense line of myelin; and (3) within the periaxonal space. In addition to this myelin-associated TPPase, enzymatic activity was also observed in specific cytoplasmic localizations in myelinogenic cells. Oligodendrocytes displayed TPPase activity within the nuclear envelope and the endoplasmic reticulum cisternae, whereas Schwann cells displayed TPPase activity within the endoplasmic reticulum and Golgi saccules. The results are discussed in relation to the role that TPPase might play in myelinated fibers, including roles in the conduction of nerve impulses or roles in the maintenance of structural configuration of myelin sheaths.

Animals↗
PubMed1989

Clinical presentation of Bacillus Calmette-Guérin infections in patients with immunodeficiency syndromes.

Nine children with immunodeficiency syndromes who developed persistent or disseminated Bacillus Calmette-Guérin (BCG) infections after BCG vaccination at birth were observed in Santiago, Chile, over a period of 10 years. This represents a risk for persistent or disseminated BCG infections of 3.4/1,000,000 vaccinated newborns. This may closely reflect the incidence of severe combined immunodeficiency syndromes, cellular immunodeficiency syndromes and chronic granulomatous disease in the study area. The clinical presentation and course of the infection varied considerably depending on the underlying immunodeficiency syndrome. Two patients with severe combined immunodeficiency presented with cutaneous nodules in the absence of any local reaction at the site of BCG vaccination. Both patients died of disseminated BCG infection within the first year of life. Four patients with cellular immunodeficiency syndromes presented with regional lymphadenitis resistant to treatment after the fifth month of life. Three of these patients had specific unresponsiveness to tuberculin and survived from 5 to 6 years of age. Two boys with X-linked chronic granulomatous disease presented with regional lymphadenitis in the first 3 months of life. A girl with autosomal recessive chronic granulomatous disease presented at 18 months of age with regional lymphadenitis. All three patients with chronic granulomatous disease had positive tuberculin reactions and died from infections other than BCG.

BCG Vaccine↗
PubMed1988

Lactate dehydrogenase activity in cultured neonatal rat heart cells exposed to doxorubicin.

Doxorubicin (Adriamycin, ADR) is an anthracycline antineoplastic with the serious side effect of dose-related cardiomyopathy. A model of ADR cardiotoxicity was created to examine some subcellular toxic effects of ADR with cultured cardiac myocytes (CMCs) exposed to 1 x 10(-7) to 1 x 10(-5) M ADR for 24 to 48 hr. Lactate dehydrogenase (LDH) activity was monitored in the CMC medium to monitor CMC damage as a function of ADR concentration. A four- to eightfold elevation of LDH activity in medium of CMCs exposed to 1 x 10(-6) to 1 x 10(-5) M ADR was found. No change in LDH activity was detected in medium of CMCs exposed to 1 x 10(-7) M ADR or in control CMCs after 24 or 48 h ADR exposure. Data suggest a dose-dependent effect of ADR on LDH activity in CMC medium. Serial monitoring of LDH in media of ADR-exposed CMCs may correlate with other evidence of ADR cardiotoxicity in vitro.

Animals↗
PubMed1988

Biochemical and genetic studies of bacteria metabolizing lignin-related compounds.

The ability of bacterial strains to metabolize lignin model compounds was studied. Strains examined were non-filamentous bacterial isolates obtained from decaying wood and the actinomycete Streptomyces viridosporus T7A. Model compounds included dimers containing either the beta-1 (1,2-diarylethane) or the beta-O-4 (arylglycerol-beta-aryl ether) type of linkage. Pseudomonas fluorescens biovar I A1 proliferated on anisoin (4,4'-dimethoxybenzoin) accumulating anisic acid temporarily. Cleavage at the beta-1 bond was also observed with crude extracts prepared from the same strain. In turn, cleavage of the beta-O-4 linkage of veratrylglycerol-beta-guaiacyl ether was detected in cultures of Pseudomonas acidovorans D3. In this case, main degradation intermediates were beta-hydroxypropioveratrone, acetoveratrone and guaiacol. S. viridosporus T7A reduced the carbonyl group of some beta-1 dimers and did not modify the beta-O-4 model compounds tested. Attempts to ascribe a catabolic character to large molecular weight extrachromosomal DNA present in some strains were unsuccessful. Gene banks of P. fluorescens biovar I A1 and P. acidovorans D3 were prepared utilizing the broad host range cosmid pLAFR1 as vector.

Bacteria↗
PubMed1988

Alpha-actin synthesis changes in cultured cardiac myocytes: relationship to anthracycline structure.

Four anthracyclines (AAs) were examined comparatively to determine effects on actin isoform synthesis in vitro. Cultured cardiac myocytes (CMCs) were incubated for 24 hours with 35 microCi sulfur 35-labeled methionine and 10(-10) to 10(-5) mol/L doxorubicin hydrochloride (Adriamycin) (ADR), daunomycin (DM), 5-iminodaunorubicin IDR), or 3'-deamino-3'-(3-cyano-4-morpholinyl)doxorubicin (MRA-CN). CMCs were harvested in buffered Triton X-100 and homogenized. Proteins in the extracts were fractionated by centrifugation. Equal protein quantities were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, to two-dimensional electrophoresis, and to autoradiography. AAs caused a dose-dependent decrease in radiolabeling of CMC proteins in Triton-soluble and -insoluble fractions of the extracts. ADR and DM (10(-6) mol/L each) and IDR (10(-5) mol/L) decreased radiolabeling of CMC polypeptides including alpha-actin. In polypeptides extracted in the Triton X-100-soluble pool, the effect on CMC alpha-actin synthesis was greater than the effect on beta- or gamma-actin. CMC alpha-actin synthesis was susceptible to ADR and to DM in a dose-dependent fashion. Contrastingly, alpha-actin radiolabeling was not altered by exposing CMCs to 10(-5) mol/L MRA-CN. Decreased sarcomeric actin isoform synthesis in vitro may reflect forms of subcellular damage in this model of anthracycline cardiomyopathy.

Actins↗