Biomedical subjects
Publications and source records attributed to C Ribeiro.
The authors describe the case of a twenty-nine-year-old female with the diagnosis of Maffucci's syndrome, since the age of five, with lower back and lower limb pain. The diagnosis was made of bone axial lesions, which are seldom found in this syndrome. Sarcomatous transformation was found in one of them.
We have previously shown that human urine contains substances that, like glycyrrhetinic acid, inhibit 11 beta-HSD1. We have named these substances "glycyrrhetinic acid-like factors" or GALFs. We now have found that human urine contains measurable quantities of both 11 beta(HSD1)- and 11 beta(HSD2)-GALF inhibitory substances. Both are markedly elevated in pregnancy. Their chemical and high-performance liquid chromatography (HPLC) characteristics suggest that several of the GALFs are steroidal. Large quantities of neutral 11 beta(HSD1)- and 11 beta(HSD2)-GALFs can be extracted directly from urine into ethyl acetate, yielding fraction EA1. Hydrolysis of the GALFs remaining in the aqueous phase by beta-glucuronidase markedly increases the total amounts of GALFs, with the majority now being ethyl acetate extractable (fraction EA2). These EA2 post-hydrolysis GALFs can be separated by HPLC resulting in at least six components with inhibitory activity against each isoenzyme. Only two GALF peaks are active against both 11 beta-HSD1 and 11 beta-HSD2. The others are peaks with specific 11 beta(HSD1)- and 11 beta(HSD2)-GALF inhibitory activity. The GALFs in the same posthydrolysis EA2 extract are also inhibitory toward the 11 beta-HSD1 that is present in vascular smooth muscle where they may play a role in the mechanisms controlling blood pressure. We have also found that 11 beta-HSD2 is selectively inhibited by 5 alpha- (but not by 5 beta-) reduced steroids. GC-MS analysis of the 11 beta(HSD2)-GALFs in EA2 is now being performed to determine whether this group includes 3 alpha,5 alpha-ring A-tetrahydro-reduced derivatives of steroids.
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AIMS: To study the circadian variation of BP in diabetics with chronic late complications (autonomic neuropathy, peripheral neuropathy and macroangiopathy of the lower limbs). PATIENTS AND METHODS: We studied 35 NIDDM patients, 22 male and 13 female, with a mean age of 62.17 +/- 8.66 years, all with hypertension (HBP) or with BP levels close to normal, many of them under anti-hypertensive therapy (mean BP in clinical measurements: 164 +/- 23.16 mmHg systolic and 92.14 +/- 11.06 mmHg diastolic). Twenty-four suffer from autonomic neuropathy, 23 from peripheral neuropathy and 11 from macroangiopathy of the lower limbs. The control group is composed of 10 patients with essential HBP without other observable pathology, with a mean age of 68.5 +/- 3.63 years and BP in clinical measurements: systolic 192 +/- 15.49 mmHg and diastolic 88 +/- 4.21 mmHg (without any previous therapy). The record of the BP circadian profile was made, with the use of a Spacelab monitor, model 90207, 5 days after anti-hypertensive therapy was suspended. RESULTS: The mean BPs in 24 hours were: control group-systolic BP 152.6 +/- 13 mmHg and diastolic 79.8 +/- 13 mmHg; diabetics-systolic BP 136.82 +/- 15 mmHg and diastolic 77.4 +/- 8 mmHg. The daily and nocturnal mean BPs were 158.5 +/- 8.5 and 146 +/- 8.4 mmHg (systolic) and 82.8 +/- 5.7 and 70.9 +/- 5.1 mmHg (diastolic) in the control group, while they were, in diabetics, 141.3 +/- 15.7 and 135.6 +/- 16.6 mmHg (systolic) and 79.6 +/- 7.1 and 72 +/- 8.2 mmHg (diastolic). In diabetic patients, considering the groups with and without autonomic neuropathy, the difference between daily and nocturnal mean BP was 1.6 vs 9.4 mmHg systolic and 4.9 vs 9.4 mmHg, diastolic. CONCLUSIONS: In both groups, the mean BP levels in 24 hours were notoriously lower than those obtained from the clinical measurements: the differences were 40 mmHg (control group) and 27.2 mmHg (diabetics) for systolic BP and 8.2 mmHg (control group) and 14.7 mmHg (diabetics) for diastolic. The BP circadian profiles show a lower variability, with absence of the nocturnal reduction, specially evident in diabetic patients with autonomic neuropathy versus other groups.
OBJECTIVE: To analyse the type and frequency of cranial CT and NMR imaging anomalies in children of short stature. PATIENTS AND INTERVENTIONS: We studied 57 children of short stature with a mean age (+/-SD) of 10.1 +/- 3.8 years, 34 boys and 23 girls, all of them with auxometric criteria of GH deficiency. After studying the pituitary function and determination of karyotype in the girls, the children were classified in to five groups:-Isolated GHD (IGHD) (n = 32), multiple pituitary hormone deficiency (MPHD) (n = 6), neurosecretory dysfunction (NSD) (n = 8), Turner syndrome (n = 7) and idiopathic short stature (ISS) (n = 4). The imaging methods used were cranial CT or NMR. RESULTS: Of the 57 children studied the CT/NMR was abnormal in 37(64.9%) children. We found anomalies in 65.6% of IGHD patients, 62.5% of NSD patients, 100% of MPHD patients and 57.1% and 25% in the Turner s. patients and ISS patients respectively. The most frequent anomaly was hypoplastic pituitary found in 50% of IGHD patients, 37.5% of NSD patients and 33.3% of MPHD patients. None of the cases of Turner s. or ISS had hypoplastic pituitary. An empty sella was the second most frequent anomaly found in 7 patients (IGHD-3, MPHD-3, DNS-1). Of the 25 children in which NMR was performed, 8 had hypoplastic pituitary and stalk and 2 had interruption of the pituitary stalk and ectopic neurohypophysis. CONCLUSION: These results strengthen the necessity for CT/NMR imaging in children of short stature which, besides allowing identification of tumors, also permits the diagnosis of idiopathic GHD because of its frequent association with cranial imaging anomalies, mainly hypoplastic pituitary.
OBJECTIVES: Analysis of the characteristics of acute myocardial infarction in female patients admitted to a coronary care unit during a 10 year period. DESIGN: Retrospective analysis of computerized data collected during a 10-year period in every patient with acute myocardial infarction admitted between 1986 and 1995. SETTING: A coronary care unit of a central hospital. PATIENTS AND METHODS: Data on 2439 patients were analyzed in what concerns gender, age and hospital mortality. In the restricted group of 655 patients admitted between 1993 and 1995 the prevalence of the following risk factors was assessed: arterial hypertension, dyslipidemia, smoking and diabetes mellitus. RESULTS: During a 10-year period, 1918 male (M) and 521 female (F) patients were admitted, originating a 3.5 to 1 M:F ratio. The M:F relation decreased from decade to decade from 11:1 in patients under 50 years old to 1.8:1 in patients over 70 years old. Hospital mortality was 25.9% in female patients and 12.0% in male patients (p < 0.001). Mortality was similar in males and females until 60 years of age; significant differences were found only in the seventh decade of life (25% in females vs. 12% in males, p < 0.001) and in patients over 70 years old (36% in females vs. 24% in males, p < 0.005). Hypertension was significantly move prevalent in females (66% in females vs 46% in males, p < 0.001) as well as diabetes mellitus (31% in females vs. 20% in males). Similarly, a previous history of dyslipidemia was more frequently found in females than in males, but the difference was not significant (24% vs. 19%, respectively). On the contrary, smoking was significantly less frequent in female patients (11% in female patients vs. 44% in male patients, p < 0.001). CONCLUSIONS: The probability of the occurrence of acute myocardial infarction is very low in premenopausal women. The M:F ratio decreases with aging. The risk of death progressively increases with age, and it is significantly higher in females in relation to males after the age of 60 years. Women, besides being older, have a higher prevalence of coronary artery disease risk factors, namely hypertension, diabetes mellitus and dyslipidemia.
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BACKGROUND: Left ventricular wall aneurysm is a complication of acute myocardial infarction which has been considered a precipitating factor of cardiac failure and ventricular arrhythmia. We have evaluated the relation between severe left ventricular wall motion abnormalities and ventricular arrhythmia. METHODS: During a two-year period 146 patients admitted to a coronary care unit with acute myocardial infarction were studied. Radionuclide angiography performed within the second and the fourth weeks was used to analyse phase and wall motility changes, and patients were divided into three groups: 1) Hypokinesia and/or akinesia localized to one segment: with no or slight changes in phase image--102 patients; 2) Aneurysm: left ventricular deformity with well-defined chromatic changes in phase image--19 patients; and 3) Dyskinesia and/or extensive akinesia of two or more segments: phase image with diffuse heterogeneous changes--25 patients. Ventricular arrhythmia was studied using Holter electrocardiography taken during the second week of acute myocardial infarction. Three rhythmic profiles were considered: no premature ventricular contractions--41 patients; with three or more than three premature ventricular contractions per hour--38 patients; repetitive premature ventricular contractions--20 patients. RESULTS: Premature ventricular contractions were absent in 31 (30%) of the patients with hypokinesia/localized akinesia vs 8 (42%) of the patients with aneurysm, and vs 2 (8%) of the patients with dyskinesia/extensive akinesia. Premature ventricular contractions were frequent (> or = 3/h) in 22 (22%) of the patients with hypokinesia/localized akinesia vs 4 (21%) of the patients with aneurysm (p = 0.35; NS), and vs 12 (48%) of the patients with dyskinesia/extensive akinesia (p=0.003). Repetitive premature ventricular contractions were present in 10 (10%) of the patients with hypokinesia/localized akinesia vs 2 (11%) of the patients with aneurysm, and vs 8 (32%) of the patients with dyskinesia/extensive akinesia (p=0.008). CONCLUSIONS: We conclude that the presence of aneurysm was not associated with a higher occurrence of ventricular arrhythmia, but patients with dyskinesia/extensive akinesia had a higher occurrence of ventricular arrhythmia, > or = 3 premature ventricular contractions per hour and repetitive premature ventricular contractions. Our results suggest that ventricular arrhythmia is related to functionally severe wall motion abnormalities, and not to anatomical discriminants. This finding leads us to suggest different electrophysiological mechanisms behind these two entities.
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Water and electrolyte transport in turtle urinary bladder closely resembles that present in the mammalian collecting tubule. Although cAMP is known to participate in the control of mucosal transport processes, the GTP-binding inhibitory Gi and stimulatory Gs proteins which link receptors on the cell surface to the adenylate cyclase system remain to be identified in this urinary epithelium. To this end, individual cells harvested from the mucosal surface of the turtle bladder were isolated using a discontinuous density Ficoll gradient. Examination by electron microscopy of the material from the different layers of the Ficoll gradient confirmed that bands II and III contained carbonic anhydrase-rich cells and granular cells, respectively. Identification of Gi and Gs in carbonic anhydrase-rich and granular cells was accomplished using pertussis (PT) and cholera toxins to promote [32P] ADP ribosylation of the proteins. Separation of Gi and Gs from other cell proteins was accomplished using polyacrylamide gel electrophoresis and autoradiography. Pretreatment of cells with 0.2% triton X-100 substantially magnified the ADP-ribosylation of Gi by PT. A doublet form of Gi was present in the 40-kD region and indicated heterogeneity of the PT substrate in granular and carbonic anhydrase-rich cells. Gs was observed as a single polypeptide at the 42-kD region in both cell types. A distinct 45-kD peptide not present in mammalian collecting tubule was identified by both toxins in granular cells and by cholera toxin in carbonic anhydrase-rich cells. In summary, this investigation identified and characterized Gi and Gs proteins in carbonic anhydrase-rich and granular cells from the mucosa of turtle urinary bladder.(ABSTRACT TRUNCATED AT 250 WORDS)
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New research about platelet and endothelial functions is allowing us to better understand the pathogenesis of myocardial ischemic episodes in patients with unstable angina, creating new perspectives for the rational utilization of therapies. In patients with unstable angina, the episodes of symptomatic and silent ischemia are caused by repeated reductions of coronary blood flow. They are the result of the mechanical effect of the growing thrombus, which causes intermittent episodes of partial obstruction of the arterial lumen, in association with vasoconstriction at the stenotic site and dependent coronary arterial bed, produced by the cyclic release of platelet derived vasoactive products, namely thromboxane A2 and serotonin. Several studies, many of them in animal models of thrombosis, suggest that serotonin and thromboxane A2 are mediators of platelet aggregation, adynamic obstruction and coronary artery thrombosis. Because they cause coronary cyclic flow reductions, they are implicated in the pathogenesis of myocardial ischemic episodes during unstable angina. Drugs that interfere with the arachidonate pathway, and the 5-HT2-receptor antagonists, have been proven to decrease or abolish coronary cyclic flow variations in animal models and man. However, further studies should be done to test the hypothesis that the association of a 5-HT2-receptor antagonist with aspirin may contribute to decrease myocardial ischemia and prevent coronary occlusion in patients with unstable angina. Continuous Holter monitoring during the first week after admission in the hospital should be a good method to evaluate the eventual efficacy of this new class of drugs in abolishing or decreasing the frequency, intensity and duration of myocardial ischemic episodes in patients with unstable angina. The central role of serotonin in the pathogenesis of thrombotic events, and the presumed preventive effect of ketanserin, were the bases of a national multicenter pilot controlled study designed to evaluate the safety and efficacy of ketanserin plus aspirin in the secondary prevention of patients with unstable angina and non-Q wave myocardial infarction (KATUA Trial).
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