[Adenosine deaminase in tumors: a marker of the pleural invasion of lymphoproliferative processes?].
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Biomedical subjects
Publications and source records attributed to C Rodríguez.
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We compared the prevalence of gastric metaplasia of the duodenal mucosa (GM) and its characteristics in 204 Peruvian patients from a low socioeconomic level with the corresponding prevalence reported in dyspeptic patients from a developed country, the United Kingdom. Gastric metaplasia was significantly less prevalent in the Peruvian than in the United Kingdom series. However, when present, GM was not significantly different in extent or frequency of colonization by Helicobacter pylori or association with active duodenitis, despite a higher prevalence of H. pylori-associated gastritis. Hypochlorhydria was markedly more frequent in the Peruvian than in the United Kingdom series. The finding of a low prevalence of H. pylori-colonized GM in patients with previously reported low prevalence of duodenal ulcer gives further support to a pathogenic link between both conditions.
Lymphoid follicles are the main B-cell areas in peripheral lymphoid tissues. These structures commonly consist of germinal centre (GC) and mantle zone (MZ) regions. In the present work, human tonsillar B cells belonging to these two compartments were purified by a combination of density centrifugation and separation techniques involving the recognition by monoclonal antibodies of specific surface molecules followed by panning and magnetic bead selection. These purified populations were identified as GC and MZ cells by three different criteria: (1) GC cells showed the phenotype IgD- CD20+bright CD38+ CD44- and peanut agglutinin (PNA)+, and MZ cells were IgD+ CD20+dim CD38- CD44+ and PNA-; (2) morphologically, MZ cells appeared as small resting lymphocytes whereas GC cells consisted of large blastic cells of the germinal centre; (3) functionally, most GC, but not MZ, cells underwent apoptosis early in culture. The isolation of GC and MZ cells allowed the study of their proliferative response. As a result of these studies, GC cells were demonstrated to inhibit the proliferation of MZ cells in response to B-cell mitogens (Staphylococcus aureus Cowan I and anti-mu plus BCGF) in a concentration-dependent way; 50% inhibition was reached at a GC/MZ cell ratio of 1/2. This effect did not require GC-cell DNA synthesis since similar results were obtained with irradiated GC cells. Neither was it due to a non-specific toxic effect since GC cells did not alter the proliferative response of autologous T cells to mitogens (phytohaemagglutin and anti-CD3). The inhibition required cellular contact between GC and MZ cells, and was not restricted by histocompatibility barriers. These data suggest the possible existence of a new regulatory pathway within peripheral B-cell areas.
Glucose tolerance and insulin effects on glucose production and utilization by various tissues were studied in 70-day-old anesthetized rats submitted to food restriction from the fetal stage. Basal and glucose-induced plasma insulin levels were reduced in food-restricted rats without alterations in glucose tolerance. Insulin action was quantified by using the euglycemic-hyperinsulinemic clamp technique. Glucose turnover rates were measured by using D-[6-3H]glucose. Exogenous insulin failed to decrease glucose production in food-restricted rats. Weight-related whole body glucose utilization was higher in restricted rats than in controls both in the basal (21.9 +/- 0.7 vs. 9.4 +/- 0.6 mg.min-1.kg-1) and hyperinsulinemic states (37.5 +/- 1.1 vs. 14.0 +/- 1.2 mg.min-1.kg-1). Local glucose utilization by peripheral tissues was estimated by a 2-deoxy-D-[1-3H]glucose technique. In both basal and hyperinsulinemic conditions glucose utilization was increased in various adipose and muscle tissues of the food-restricted rats as compared with the controls. Thus we conclude that food restriction leads to an increase in the insulin-mediated glucose uptake by various peripheral tissues and to insulin resistance in the liver.
The authors studied the epidemiology of the outbreak of cholera (due to Vibrio cholerae 01, Inabe serotype) which occurred in Panama in 1991, during which 1179 probable cases were reported, with 292 hospitalizations, 29 deaths and 51 confirmed cases. There was an average of 24.7% hospitalizations and a 2.5% mortality. The epidemic involved 21 of 24 "corregimientos' in Darién, 2 of 4 in San Blas, 5 of 15 in Panama East, 3 of 40 in Colón and one of 19 in the metropolitan area of Panama City. The incidence of infected patients was seen in infants less than 1 year old and in children 1 to 4 years of age. Taking into account the population in each 'corregimiento', it can be said that less than 1% of the population was infected, but that in San Blas, where few communities have aqueduct and latrines, 10% of the population was infected.
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Evidence is presented suggesting that infection by Helicobacter pylori triggers and continuously contributes to the pathophysiology of progressive gastric changes that can ultimately lead to gastric cancer. In Peru, especially in population groups of low socioeconomic status, infection by H. pylori begins earlier in life and is more prevalent and persistent than in developed countries. The infection produces a destructive lesion of the mucinous surface epithelium which probably enables other aggressive luminal factors to cause further mucosal damage. As a consequence, active chronic gastritis appears. The gastritis is of the superficial type at the beginning but may progressively change to atrophic. Chronic atrophic gastritis is found more frequently and at a younger age in dyspeptic patients with low socioeconomic status--that is, in patients having higher prevalence of persistent infection by H. pylori since earlier in life. When chronic atrophic gastritis becomes severe and extensive, hypochlorhydria ensues. Hypochlorhydria favors the appearance of bacterial overgrowth, nitrites, and N-nitroso compounds in the gastric lumen. N-nitroso compounds, because of their mutagenic-carcinogenic properties, probably induce gastric premalignant lesions like intestinal metaplasia and dysplasia of the gastric mucosa. Oral bismuth therapy apparently reverses H. pylori-associated gastric dysplasia. It is proposed that future programs designed for the control of gastric cancer would be incomplete if they do not include further evaluation of the many effects of infection by H. pylori on the gastric mucosa and of cost-effective methods to eradicate the infection.
Three cases of multiple simultaneous primary lung carcinomas are presented, in which diagnosis was established by post-surgery pathological exam. In all three cases, chest X-ray showed pulmonary masses suggestive or clinical malignancy, and pre-surgery pathological diagnosis or squamous lung carcinoma. During thoracotomy or in the resected segment, a second lesion we confirmed which made resection necessary being this second lesion classified as lung adenocarcinoma.
An 80 year-old woman presented subleukaemic acute monoblastic leukaemia (AML-M5a). Her bone marrow showed invasion by highly dysplastic histio-monocytic cells of great size and wide cytoplasm, with intense phagocytic activity (erythrophagocytosis was frequently seen), and with abnormal karyotype (50XX, +8, +8, +16, +21). The different malignant and reactive features of the mononuclear phagocytic system are commented, along with the haemophagocytic activity of the histio-monocytic cells in different states. The cytogenetic anomalies more frequently found in AML-M5 are also dealt with as compared to this patient's. The case reported here seems to correspond to subleukaemic acute "monophagocytic" leukaemia, with a biologic phenotype close to that of malignant histiocytosis.
We analyzed sera from 102 subjects older than 65 years of age with no clinical evidence of autoimmune disorders, inflammatory diseases or pharmacological interventions. Positive titers for antinuclear antibodies were found in 18.6%, anti-smooth muscle fibre in 16.6%, and rheumatoid factor in 11.8%. These values were significantly higher than those of a control group of healthy younger adults (p < 0.0001). Anti mitochondrial antibodies were present in 1% (NS). Thus, a greater proportion of autoimmune phenomena is demonstrated in the elderly.
The clinical and theoretical applications of contextual therapy for the treatment of drug abuse are presented. A case study illustrates intervention strategies, the therapy process, and a contextual-intergenerational view of drug addiction. Contextual concepts of intergenerational processes, loyalty, fairness, accountability, and trust are defined and applied. Four stages of brief contextual therapy are presented, and the process is examined using examples from transcribed transactions of the therapy sessions. It is suggested that contextual therapy offers conceptual and methodological tools for working with complex situations often involved in drug abuse cases.
A 51 year old man with acquired immune deficiency syndrome for 2 years developed a chronic leukemia/T cell lymphoma. Anti HTLV-1 antibodies were confirmed by Western Blot. In the last months he developed hypercalcemia and leukocytosis of 130,000. Necropsy confirmed the diagnosis of Leukemia/T cell lymphoma without cutaneous involvement.
The presence of neuron-specific enolase (NSF) and neurofilament proteins (NFP) immunoreactivities (IR) was investigated in dorsal root ganglia (DRG) of adult rats at cervical, thoracic, lumbar and sacral levels. All neurons display NSE-like IR with a variable intensity of immunostain which is not related to the neuronal size. Conversely, the antibody against all three proteic subunits of NFP no labelled the primary sensory neurons, whereas the intraganglionic axons and dorsal root of spinal nerves result positives. In the sciatic nerve the immunoreactivity was similar for NSE- and NFP-like IR. No regional differences were found among the different levels of DRG for NSE-like IR. The present results demonstrate heterogeneity in the neurons of the rat. DRG for NSE-like IR, and differences between sensory neurons and fibers in the distribution of NFP-like IR.
Thirty-four new cases of acute promyelocytic leukaemia (M3) were diagnosed at the authors' Centre between 1970 and 1988 (19 males and 15 females) with ages between 5 and 73 years (median age, 32 years). Three cases were of the hypogranular variant or M3-v (8.8%). The clinical picture included: haemorrhagic diathesis (85%), pallor/malaise (82%), fever/infection (41%), hepatomegaly (26%), splenomegaly (12%). Leucopenia of less than 5 x 10(9)/L was present in 23/34 cases, laboratory signs of DIC in 26/31, increased LDH, over 400 U/mL, in 6/31, and abnormal karyotype in 7/15. One of the patients rejected any treatment; two others died of brain haemorrhage before therapy was started, and seven died in the first two weeks of treatment. Of the 31 patients treated, complete remission (CR) was achieved in 21 cases (67.7%). Allogeneic BMT was carried out in two of them, with further relapse and death. Post-remission treatment was given to the remaining 19 patients, and there were 13 relapses. Six patients have been in CR, 5 of them after cessation of therapy, for the last 1.5-11.5 years. Age under 50 years and leucocyte count below 5 x 10(9)/L at diagnosis were favourable prognostic factors according to the univariate statistical analysis performed. The survival plateau of the actuarial curve was reached beyond 2.75 years by 15% of all the patients treated (33 cases), 23% of the patients who achieved CR (21 cases), 31% of the patients under 50 years of age and 5 x 10(9)/L leucocyte count at diagnosis (15 cases) and 36% of these last achieving CR (13 cases).
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One hundred and thirty-three cases of myelodysplastic syndromes studied during the last ten years were revised. Of them, 79 were males and 54 females, and their ages ranged between 15 and 91 years (median, 69 years). Five patients (3.7%) had secondary myelodysplasias. The haematological phenotype (FAB) of the cases was: RA, 41.3%; SRA, 24%; RAEB, 18%; RAEBT, 3.7%; CMML, 8.3%. Leucopenia/thrombocytopenia without initial anaemia was present in 4.5% of the cases. Abnormal karyotype was found in 54 patients (40.6%), MIKA in 41 cases and MAKA in 13 cases. The cytogenetic anomalies most commonly found were +8, 5q-, -7, 11q- and 13q-. Cytogenetic abnormalities were commonest amongst the RAEB (50%), and least frequent in CMML (18.2%). Thirty-one patients evolved into acute leukaemia (29 ANLL and 2 ALL). Such blastic changes were more frequent in RAEB (62.5%) and rarest in SRA (9.4%), and they appeared mostly in patients with complex karyotype (MAKA) (53.8%) as compared with those who had normal karyotype (17.7%). Short-lasting complete remission was achieved by 40% of the patients treated with conventional chemotherapy. The survival of the group as a whole (median 30 months) varied in accordance with the haematological phenotype: SRA, 81 months; RA, 65 months; CMML, 13 months; RAEB +/- T, 8 months. The finding of a MAKA karyotype significantly shortened the survival (4 months) with regard to MIKA (44 months) or normal karyotype (39 months). The following median survivals were attained after patients' staging (Bournemouth's criteria): stage A, 84 months; stage B, 22 months, and stage C, 5 months.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess whether the programs of diabetologic education (PDE) are effective to improve metabolic control in diabetes mellitus, depending on their inclusion in an overall therapeutic program and on the setting where they are imparted (hospital versus primary care center, PCC), we evaluated the changes in the HbA1 values in 230 insulin-treated diabetic patients, after receiving a PDE in a PCC (group A; n = 88) or as hospital inpatients (group B; n = 72) or outpatients (group C; n = 50). The remaining 20 patients (group D) received the same PDE, but their treatment did not depend on our Unit. The initial mean HbA1 levels were significantly reduced 3, 6 and 9 months after the PDE in group A patients (10.6% vs 9.6%, p less than 0.05; vs 9.4%, p less than 0.02; vs 9.1%, p less than 0.01), in group B patients (10.0% vs 9.5%, p less than 0.05; vs 9.1%, p less than 0.05; vs 9.0%, p less than 0.05) and group C patients (10.1% vs 9.5%, p less than 0.05; vs 9.1%, p less than 0.02; vs 8.9, p less than 0.01); however, they did not significantly change in group D patients (10.3% vs 10.7%, vs 10.3%, and vs 10.0%). Mean HbA1 in months 3, 6 and 9 were not different between groups A, B and C, but they were lower (p less than 0.05) than in group D. Our results confirm that PDE and treatment are effective to improve metabolic control in diabetic patients, whereas diabetological education alone is not useful. The place where PDE is given is not determinant for its effectiveness.
Carboxypeptidase H is a putative post-translational processing enzyme which removes basic amino acid residues from intermediates during protein hormone biosynthesis. A 2.2-kilobase pair cDNA was shown to contain the complete amino acid sequence of rat carboxypeptidase H. The deduced amino acid sequence revealed that the enzyme was synthesized as preprocarboxypeptidase H, a precursor form of 476 amino acid residues. Preprocarboxypeptidase H contained a putative hydrophobic signal peptide and a short propeptide which contained 5 adjacent Arg residues at its C terminus. Northern blot analysis identified a single carboxypeptidase H mRNA of approximately 2.3 kilobases in brain, pituitary, and heart, as well as in mouse AtT20 cells. No carboxypeptidase H mRNA was detected in rat liver, spleen, kidney, lung, and mammary gland. Sequence analysis of cDNAs obtained from different rat tissues suggested that a single mRNA encodes an identical carboxypeptidase in several tissues. Treatment of AtT20 cells with dexamethasone decreased the levels of both carboxypeptidase H and preproopiomelanocortin (POMC) mRNAs by approximately 30%. Exposure of the dexamethasone-treated cells to corticotropin-releasing factor effected a 2- to 3-fold increase in the carboxypeptidase H and POMC mRNA levels relative to those of dexamethasone-treated cells exposed to control medium. This suggests that the mRNA levels of POMC and one of its putative post-translational processing enzymes, carboxypeptidase H, are co-regulated by corticotropin-releasing factor and steroid hormones.