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Biomedical subjects

R Guerra

Publications and source records attributed to R Guerra.

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

Variation at the hepatic lipase and apolipoprotein AI/CIII/AIV loci is a major cause of genetically determined variation in plasma HDL cholesterol levels.

Genetic factors have been shown to play an important role in determining interindividual variation in plasma HDL-C levels, but the specific genetic determinants of HDL cholesterol (HDL-C) levels have not been elucidated. In this study, the effects of variation in the genomic regions encoding hepatic lipase, apolipoprotein AI/CIII/AIV, and the cholesteryl ester transfer protein on plasma HDL-C levels were examined in 73 normotriglyceridemic, Caucasian nuclear families. Genetic factors accounted for 56.5 +/- 13% of the interindividual variation in plasma HDL-C levels. For each candidate gene, adjusted plasma HDL-C levels of sibling pairs who shared zero, one, or two parental alleles identical-by-descent were compared using sibling-pair linkage analysis. Allelic variation in the genes encoding hepatic lipase and apolipoprotein AI/CIII/AIV accounted for 25 and 22%, respectively, of the total interindividual variation in plasma HDL-C levels. In contrast, none of the variation in plasma HDL-C levels could be accounted for by allelic variation in the cholesteryl ester transfer protein. These findings indicate that a major fraction of the genetically determined variation in plasma HDL-C levels is conferred by allelic variation at the hepatic lipase and the apolipoprotein AI/CIII/AIV gene loci.

Apolipoprotein A-I↗
PubMed1994

Bifascicular block complicating blunt cardiac injury. A case report and review of the literature.

A thirty-five-year-old horse trainer presented to the emergency room of the authors' hospital with minimal nonpenetrating chest injury after having been kicked by a horse. No rib or sternum fractures were demonstrated. The admission ECG demonstrated a right bundle branch block and a left anterior hemiblock that were previously absent. The authors are aware of only two similar reports, but analogous conduction disturbances might have been classified as intraventricular conduction defects. The rarity of these defects may be explained by the anatomic pathways of the bundle of His and its bifurcations.

Adult↗
PubMed1994

The use of the EEG to predict outcome in premature infants with positive sharp waves.

The goal of this study was to investigate the factors that could predict prognosis in 51 premature infants with positive sharp waves on their EEGs (gestational age 23-36 wks) with 114 tracings. Follow-up clinical examinations were conducted, up to 10 yrs later. Death occurred in 18%, from a non-CNS cause, either sepsis or a congenital cardiac or pulmonary defect. A severe outcome was seen in 8% and was related to maternal i.v. drug abuse (IVDA) and the presence of many positive sharp waves. A moderate outcome, noted in 29%, was associated with a Grade III-IV intracerebral hemorrhage (ICH) or periventricular leukomalacia (PVL) and maternal IVDA. A mild outcome seen in 20% was related to infrequent positive sharp waves, vaginal delivery and an improving EEG over time, while a normal outcome (26%) was also related to infrequent discharges, a normalized EEG over time, a normal sonogram and the absence of clinical seizures. The addition of negative sharp waves to the positive ones and the addition of central to temporal positive sharp waves were associated less often with a normal outcome. The general conclusion of this study was that various aspects of positive sharp waves in premature infants, in addition to other factors, can be used to predict outcome in these neonates.

Child↗
PubMed1994

Genetic analysis of a polymorphism in the human apolipoprotein A-I gene promoter: effect on plasma HDL-cholesterol levels.

Previous studies have indicated that a G to A substitution at position -76 in the gene encoding apolipoprotein A-I (apoA-I) confers increased plasma high density lipoprotein cholesterol (HDL-C). Increased HDL-C may be a direct consequence of the A allele, or may reflect the action of a locus in linkage disequilibrium with the A allele. To elucidate this question, we examined the effect of this polymorphism in a large sample (n = 409) of unrelated Caucasians and their nuclear families (n = 22). To eliminate the confounding effects of hypertriglyceridemia, individuals with triglyceride levels greater than 150 mg/dl were excluded from the study. ApoA-I genotype was determined by polymerase chain reaction (PCR) amplification of genomic DNA and restriction digestion with Msp I. Individuals were grouped by genotype (GG, GA or AA) and mean adjusted HDL levels of the three groups were compared by one-way analysis of variance. Our analysis indicates that HDL-C levels do not vary by genotype, and no gene dosage effect is apparent in men or in women. Analysis of 22 informative Caucasian nuclear families showed no significant difference between individuals with the A allele and their GG siblings. These data suggest that polymorphism at -76 in the apoA-I gene does not directly affect HDL levels. Therefore, the increased HDL-C levels reported in other populations must reflect linkage disequilibrium between the A allele and a putative HDL-raising allele. As we find no evidence for association between the A allele and high HDL levels, this putative allele must occur at a low frequency in the population sampled in this study.

Adenine↗
PubMed1993

Intestinal helminths and risk of anaemia among Nepalese children.

Relationships between hookworm, A. lumbricoides and anaemia were studied utilising egg count in faecal specimens and haemoglobin levels from a cross-sectional sample of 641 Nepalese children, 6 to 120 months of age. Additional analyses were performed to assess the level of risk by age and worm load. Kato thick-smear technique was used to perform faecal analyses, recording the number of hookworm eggs and A. lumbricoides eggs in each sample of 50 mg of faeces. Haemoglobin levels were assessed by the Sahli method. The presence of eggs for each parasite was significantly associated with lower levels of haemoglobin (P < 0.001). Children infected with both parasites or hookworm alone presented higher depletion of haemoglobin. The presence of A. lumbricoides was more closely related with anaemia in the age group 72 to 119 months and for an intensity of infection higher than 8000 eggs per gram of faeces. Hookworm, correlated with lower levels of haemoglobin, affected less than 4% of the children in the sample and appear to be a serious risk factor at the individual level. A. lumbricoides, present in 51% of the children, was associated with moderate anaemia and represents a more important risk factor at the community level, especially if coupled with inadequate food and iron intake. Any public health intervention aimed at reducing anaemia prevalence in Nepal should consider effective measures for the control of soil-transmitted helminths.

Age Factors↗
PubMed1993

[The echo-nitrate test for the detection of viable myocardium after a myocardial infarct: a comparison with delayed-acquisition thallium scintigraphy].

BACKGROUND: The aim of this study was to evaluate the ability of echocardiography, associated with nitroglycerin infusion, in the detection of myocardial viability in patients with recent infarction. PATIENTS AND METHODS: Fourteen patients (11 male, 3 female, mean age 59 +/- 8 years) with first acute myocardial infarction (12 Q wave, 2 non-Q wave) underwent predischarge (18 +/- 3 days) nitrate echocardiography. All patients underwent delayed planar thallium scintigraphy within four weeks from AMI. Nitrate echocardiography was performed with a nitroglycerin infusion starting from 0.4 mcg/Kg/min every 5 minutes up to 2.0 mcg/Kg/min; the test was terminated with an improvement of wall motion abnormalities or with a drop of systolic blood pressure > or = 20%. Wall motion abnormalities were evaluated with a 16-segment wall motion score index (WMSI). Thallium was performed after a symptom-limited exercise test, after 3 and 24 hours. The left ventricle was divided in 15 regions. Thallium was considered the gold standard for myocardial viability. RESULTS: Basal echo identified 59 dyssynergic segments: of these, 12 (20%-6 patients) showed improvement in contractility during nitrate echocardiography at a mean dose of 0.9 +/- 0.3 mcg/Kg/min. WMSI decreased from 1.42 +/- 0.22 to 1.27 +/- 0.13 (p = 0.022), with no significant change of haemodynamic data (mean systolic blood pressure from 125 to 112 mmHg; mean heart rate from 66 to 76 beats/min; mean rate/pressure product from 8415 to 8848; all p = ns). Thallium scintigraphy showed 40 fixed defects (19%-7 patients) and 10 (4.7%-7 patients) late reversible defects. 20% of the 3-hour fixed defects improved at 24-hour imaging. 5/7 patients with echo improvement had 24-hour reversible defects, while 6/7 with no WMSI improvement had 24-hour fixed defects. Therefore, nitrate echocardiography demonstrated 71% sensitivity, 86% specificity, 83% positive predictive value, 75% negative predictive value and 78% accuracy. CONCLUSIONS: Nitrate echocardiography may be a feasible and low cost method in the detection of myocardial viability after myocardial infarction, but awaits further validation.

Aged↗
PubMed1992

Epikeratophakia: histopathological and cultural study.

Three epikeratoplasty buttons (one aphakic and two myopic) prepared by the freeze technique were removed two to nineteen months after surgery. A complete morphological and immunohistochemical study was performed on these buttons in order to gain insight into the reasons for epikeratophakia failure. Histopathological studies with light microscopy and scanning and transmission electron microscopy were performed. All three cases showed an anomalous process of re-epithelialization: in the first, the epithelium over the donor cap was almost completely absent, with many abnormalities; in the second, the epithelium was irregular, with a varying number of cell layers and poor adhesion between cells; in the third, the development of an epithelial cyst between the tissue lens and the cornea of the host caused the failure of the epikeratoplasty. The specimens were cultured 'in vitro' and the cells grown typed for HLA antigens. The antigen panel was the same as that of the host. Immunohistochemistry showed CD3- and CD8-positive cells in the stroma, proving the activity of T-suppressor lymphocytes in a cell-mediated immunoreaction.

Adult↗
PubMed1992

Release of multiple endothelium-derived relaxing factors from porcine coronary arteries.

Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187. Total NOX was compared with the bioactivity of endothelium-derived relaxing factors (EDRF) by a biodetector ring preparation before and after inhibition of L-arginine-dependent nitric oxide synthesis and in the presence of indomethacin. Under basal conditions, arterial segments released NOX and relaxed biodetector rings. Bradykinin, ADP, and A23187 elicited vasorelaxation greater than that observed basally; A23187, but not bradykinin or ADP, caused additional release of NOX greater than that measured basally. Hemoglobin completely reversed vasorelaxation elicited by all three agonists. We compared the amount of nitric oxide released under basal conditions and after stimulation with bradykinin, ADP, and A23187 with the amount of authentic nitric oxide necessary to elicit a bioequivalent response. Authentic nitric oxide did not account for the observed bioactivity as compared with the amount of nitric oxide actually measured in arterial segment effluent. To investigate whether a second non-nitric oxide-containing compound was responsible for the increased bioactivity and the discrepancy between the bioactivity and quantity of nitric oxide measured, we exposed arterial segments to omega-nitro-L-arginine methyl ester to inhibit L-arginine-dependent synthesis of nitroso compounds. The drug completely abolished the nitric oxide signal derived from both basally released and A23187-stimulated relaxing factor and completely reversed vasorelaxation. In contrast, omega-nitro-L-arginine methyl ester only partially reversed bradykinin-stimulated vasorelaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1992

Voluntary intake of "Tiquira", an alcoholic beverage prepared from fermented manioc, decreases immunoglobulin production and increases self-reactivity in mice.

UNLABELLED: We studied the effects of chronic voluntary ingestion of "Tiquira" (50%)--an alcoholic beverage prepared from fermented manioc, widely consumed in Maranhão,--on the natural immunological activity of young adult (2-3 months old) C57B1/6J mice (16-17 g) by evaluating the number of plaque-forming cells (PFCs) in the spleen and by titrating serum antibodies by ELISA. Voluntary ingestion of "Tiquira" for 30 days decreased immunoglobulin secretion in serum ( CONTROL: 1600 +/- 30 vs EXPERIMENTAL: 193 +/- 20), caused an impressive reduction in the total number of PFCs in the spleen ( CONTROL: 482 +/- 22 vs EXPERIMENTAL: 58 +/- 3) and increased the proportion of self-reacting antibody molecules in serum ( CONTROL: 119 +/- 16 vs EXPERIMENTAL: 800 +/- 20) and self-reactive PFCs to mouse red blood cells (MRBC) in the spleen ( CONTROL: 183 +/- 14 vs EXPERIMENTAL: 272 +/- 16; N = 10 animals per group). These preliminary results suggest that the voluntary ingestion of "Tiquira" for 30 days may interfere with immunological relations by decreasing the total number of immunoglobulin secreting cells and increasing the anti-self antibody production. Experiments are in progress to determine if ethanol or other substances present in "Tiquira" are responsible for the effects documented here.

Alcoholic Beverages↗
PubMed1991

Nitric oxide generation from nitroprusside by vascular tissue. Evidence that reduction of the nitroprusside anion and cyanide loss are required.

Nitric oxide (NO) was produced from sodium nitroprusside in the presence of vascular tissue but was not released spontaneously from the nitroprusside anion. In the absence of tissue in the dark nitroprusside did not release NO. When solutions of nitroprusside alone were irradiated with visible light, nitric oxide was released at rates linearly proportional to nitroprusside concentration and light intensity. Nitric oxide was produced from solutions of nitroprusside in the dark after the addition of vascular tissue, including lengths of rabbit aorta, subcellular fractions of aorta, and human plasma. NO was also released from nitroprusside after reaction with various reducing agents including cysteine and other thiols, ascorbic acid, sodium dithionite, ferrous chloride, hemoglobin, myoglobin, and partially purified cytochrome P450 with an NADPH-regenerating system. HCN was simultaneously produced in these solutions, and addition of KCN blocked NO release. Iodine oxidized intermediate cyanoferrates and blocked nitric oxide release. KCN or iodine also blocked NO production by tissue, but had no effect upon photochemical NO release. These results show that, apart from photolysis which makes no physiological contribution, release of nitric oxide from nitroprusside, in simple solutions and in biological tissue, occurs after nitroprusside has undergone reduction and lost cyanide.

Animals↗
PubMed1991

Role of the endothelium in modulation of the acetylcholine vasoconstrictor response in porcine coronary microvessels.

STUDY OBJECTIVE: The aim was to investigate the role of the endothelium in modulating the acetylcholine response in porcine coronary microvessels and compare the results with simultaneously studied large coronary arteries. DESIGN: Coronary microvessels [104 (SEM 3.3) microns; range 38-150] were removed from fresh porcine hearts and studied in vitro during no flow constant pressure conditions. Endothelium derived relaxing factor (EDRF) activity and the role of the endothelium in modulating the acetylcholine response in microvessels was assessed by measuring changes in intraluminal diameter using a video tracking device. Large coronary arteries were simultaneously studied using conventional isometric ring techniques. EXPERIMENTAL MATERIAL: Fresh porcine hearts were obtained from a local slaughterhouse. MEASUREMENTS AND MAIN RESULTS: Acetylcholine was a potent vasoconstrictor (EC50 = 0.17 microM) of passively distended microvessels. The effects of EDRF were studied by either inactivation with haemoglobin or inhibition of EDRF synthesis with N-omega-nitro-L-arginine. Preconstricted microvessels exposed to either N-omega-nitro-L-arginine or haemoglobin constricted further, consistent with basal release of EDRF. Neither drug affected passively distended microvessels. The acetylcholine vasoconstrictor response was potentiated after exposure of microvessels to either drug. Atropine, but not indomethacin, blocked the acetylcholine response in microvessels. As with microvessels, acetylcholine was a vasoconstrictor (EC50 = 0.3 microM) of large coronary arteries. In contrast to microvessels, indomethacin antagonised acetylcholine vasoconstriction in vessels with intact endothelium. Bioassay experiments using indomethacin-treated large epicardial donor artery segments showed basal release of EDRF but no EDRF release in response to acetylcholine. CONCLUSIONS: The results show the microvessels and large coronary arteries are similar in their vasoconstrictor response to acetylcholine, that both release EDRF basally, and that vasoconstriction to acetylcholine is importantly modulated by the endothelium. In large arteries, acetylcholine does not stimulate EDRF release and, in contrast to microvessels, a cyclo-oxygenase product influences the vasoconstrictor action of acetylcholine.

Acetylcholine↗
PubMed1991

Specific antibodies in mouse milk after ovalbumin ingestion.

C57B1/6J mice received ovalbumin (Ova) orally, 20 mg/day, from day of parturition for 3, 5, 7, 10 or 15 days. Anti-Ova antibodies were titrated in plasma and milk by passive hemagglutination, and Ova-specific plaque-forming cells (PFC) were counted in the spleen and mesenteric lymph nodes. Anti-Ova antibodies in milk and antibody-secreting cells in mesenteric lymph nodes and spleen were detected on day 3, increased on day 5 and peaked on day 10. In contrast, anti-Ova antibodies in serum and PFC in spleen were low on day 7 and decreased on days 10 to 15. Although the oral administration of this antigen has been used to induce oral tolerance or secretory immune responses in the mouse, the present study demonstrates that the repeated ingestion of ovalbumin results in the development of circulating and secretory antibodies.

Animals↗
PubMed1991

Testicular function in active ankylosing spondylitis. Therapeutic response to human chorionic gonadotrophin.

Testicular function was studied in 22 patients with ankylosing spondylitis (AS) with serum measurements of hormone levels, seminal fluid analysis and testicular reserve test. Results were correlated with disease activity. The abnormal findings were elevated luteinizing hormone (LH), inversion of estradiol/testosterone ratio (E2:T) and diminished testicular reserve for testosterone (T) and slightly increased for estradiol (E2). Nine patients with severe active AS received biweekly 2,500 IU of human chorionic gonadotrophin injections with a resulting increase in E2 serum levels. When the values of E2 reached 40 pg/ml or higher, there was a decrease of the sedimentation rate (p less than 0.05) and a reversal to normal of the E2:T ratio. This was accompanied by an improvement in AS at the 10th week that lasted up to 9 weeks after discontinuation of treatment. Our findings suggest a possible role of sex hormones in the physiopathogenesis of AS and offers a possible therapeutic alternative.

20-alpha-Dihydroprogesterone↗
PubMed1990

Vasorelaxant properties of the endothelium-derived relaxing factor more closely resemble S-nitrosocysteine than nitric oxide.

Studies of cultured bovine aortic endothelial cells using quantitative chemiluminescence techniques have shown that the amount of nitric oxide released under basal conditions, or in response to either bradykinin or the calcium ionophore A23187 is insufficient to account for the vasorelaxant activities of the endothelium-derived relaxing factor (EDRF) derived from the same source. This observation contradicts previous suggestions that nitric oxide and EDRF are the same compound, but may be explained if EDRF is a compound that contains nitric oxide within its structure but is a much more potent vasodilator than nitric oxide. Such a molecule could be one of several nitrosothiols which may yield nitric oxide after a one-electron reduction. The present experiments were carried out to test the possibility that the biological activities of the endothelium-derived relaxing factor might more closely resemble those of one of these compounds, S-nitrosocysteine, than nitric oxide. Nitric oxide release from cultured bovine aortic endothelial cells was detected by chemiluminescence and bioassay experiments compared the vasodilator potencies of nitric oxide, S-nitrosocysteine, and EDRF. The results suggest that EDRF is much more likely to be a nitrosylated compound such as a nitrosothiol than authentic nitric oxide.

Animals↗
PubMed1990

Diet-induced atherosclerosis increases the release of nitrogen oxides from rabbit aorta.

We examined the hypothesis that impaired endothelium-dependent vasodilation in atherosclerosis is associated with decreased synthesis of nitrogen oxides by the vascular endothelium. The descending thoracic aortae of rabbits fed either normal diet, a high cholesterol diet for 2-5 wk (hypercholesterolemic, HC), or a high cholesterol diet for 6 mo (atherosclerotic, AS) were perfused in a bioassay organ chamber with physiologic buffer containing indomethacin. Despite a dramatic impairment in the vasodilator activity of endothelium-dependent relaxing factor (EDRF) released from both HC and AS aortae (assessed by bioassay), the release of nitrogen oxides (measured by chemiluminescence) from these vessels was not reduced, but markedly increased compared to NL. Thus, impaired endothelium-dependent relaxation in atherosclerosis is neither due to decreased activity of the enzyme responsible for the production of nitrogen oxides from arginine nor to arginine deficiency. Because the production of nitrogen oxides increased in response to acetylcholine in both hypercholesterolemic and atherosclerotic vessels, impairments in signal transduction are not responsible for abnormal endothelium-dependent relaxations. Impaired vasodilator activity of EDRF by cholesterol feeding may result from loss of incorporation of nitric oxide into a more potent parent compound, or accelerated degradation of EDRF.

Animals↗