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Biomedical subjects

L Olmos

Publications and source records attributed to L Olmos.

At least 19 recordsLinked to original sources
PubMed1999

Usefulness of transthoracic echocardiography in detecting significant prosthetic mitral valve regurgitation.

To identify the transthoracic echo-Doppler (TTE) variables most predictive of significant mitral regurgitation (MR) of mechanical prosthetic valves, TTE and trans-esophageal echo (TEE) studies were independently reviewed in 57 patients (mean age [+/-SD] 59+/-12.5 years) undergoing both studies within 2+/-3 days. Several 2-dimensional and Doppler hemodynamic variables from the TTE studies were derived. Prosthetic MR was significant (moderate or severe) by TEE in 20 patients, whereas mild or no MR was seen in 37 patients. The best univariate predictors of significant MR by TTE were peak velocity of mitral inflow, mean gradient, tricuspid regurgitation velocity, isovolumic relaxation time, and ratio of time velocity integral of mitral inflow to time velocity integral in the left ventricular outflow (TVI(MV)/TVI(LVO)). Peak mitral velocity and TVI(MV)/TVI(LVO) were the best predictors of significant MR and performed similarly (area under the receiver-operating characteristic curve: 0.97 for both). A peak velocity of > or =1.9 m/s was 90% sensitive and 89% specific for significant prosthetic MR, whereas a TVI(MV)/TVI(LVO) > or =2.5 had a sensitivity and specificity of 89% and 91%, respectively. A decision tree was constructed to assess the conditional probabilities of having significant MR given all the possible outcomes of the 2 best predictors. None of the patients with peak velocity < 1.9 m/s and TVI(MV)/TVI(LVO) <2.5 by TTE had significant MR. Conversely, all patients with peak velocity > or =1.9 m/s and TVI(MV)/TVI(LVO) > or =2.5 had significant MR. The use of more complex algorithms did not further improve the results. Thus, measurements of hemodynamic Doppler variables on TTE examination can accurately identify a large number of patients without significant prosthetic MR, thereby reducing the need for further investigation with TEE.

Echocardiography, Doppler↗
PubMed1998

Autosomal dominant zonular cataract with sutural opacities is associated with a splice mutation in the betaA3/A1-crystallin gene.

PURPOSE: Congenital cataracts constitute a morphologically and genetically heterogeneous group of diseases that are a major cause of childhood blindness. Autosomal Dominant Zonular Cataracts with Sutural Opacities (CCZS) have been mapped to chromosome 17q11-q12 near the betaA3A1-crystallin gene (CRYBA1). The betaA3A1-crystallin gene was investigated as the causative gene for the cataracts. METHODS: The betaA3/A1-crystallin gene was sequenced in affected and control individuals. Base changes were confirmed and assayed in additional family members and controls using NlaIII restriction digestion of PCR amplified DNA sequences. Base changes were assessed for their effects on splicing by information analysis. RESULTS: The cataracts are associated with a sequence change in the 5' (donor) splice site of intron 3: GC(g->a)tgagt. The sequence change also creates a new NlaIII site. This base change cosegregates with the cataracts in this family, being present in every affected individual. Conversely, this base change was not seen in 140 chromosomes examined in 70 unaffected and unrelated individuals. Information theory mutational analysis shows that the base change lowers the information content of the splice site from 6.0 to -6.8 bits, so that splicing would not be expected to occur at the altered site. CONCLUSIONS: Taken together, these observations suggest that the observed mutation might be causally related to the cataracts in this family.

Amino Acid Sequence↗
PubMed1997

Biochemical characterization of myocardial damage in chronic Chagas' disease.

BACKGROUND: In the early asymptomatic stages of cardiomyopathy in chronic Chagas' disease, septal endomyocardial biopsies disclose multiple evidence of evolving myocardial damage. Detection of signs of an active myocardiopathic process may allow a better understanding of the evolution of this and other related dilated cardiomyopathies and provide a means for evaluation of the result of future therapeutic schemes. HYPOTHESIS: This study was designed to explore whether cellular damage caused by Chagas' disease is reflected by changes of certain serum electrolytes, enzymes, and glycoproteins associated with myocardial metabolism, especially in the coronary sinus into which the blood just metabolized by the heart is drained. METHODS: The study included 47 patients (35 men and 12 women, average age 40 years) with positive complement fixation reaction and hemagglutination test for Chagas' disease. The study protocol included medical records, electrocardiographic (ECG) recordings, routine laboratory analysis, chest x-rays, noninvasive cardiac examinations, and cardiac catheterization. RESULTS: In this study, we determined the concentration or activity of 9 electrolytes, 5 glycoprotein fractions, and 12 enzymes related to cardiac metabolism in blood from the coronary sinus, the superior vena cava, the pulmonary and femoral arteries, and found early release of inorganic phosphorus (p < 0.01) and isocitrate dehydrogenase (p < 0.01) from the heart and increased activity of serum alkaline phosphatase and aldolase (p < 0.05). Discriminant analysis suggested that the combination of the clinical picture, electrocardiographic findings, and peripheral activity of serum aldolase might be useful for the recognition of 86% of patients with Chagas' disease without segmental myocardial damage, 80% of those with early segmental abnormalities, and all patients with advanced myocardial damage or congestive heart failure. CONCLUSION: These results would make the application of more invasive techniques, such as left cineventriculography for detection of early myocardial compromise, unnecessary.

Adult↗
PubMed1996

Recovery of endothelium-dependent relaxations four weeks after ischemia and progressive reperfusion in canine coronary arteries.

The acute impairment of endothelium-dependent relaxations after ischemia and acute reperfusion injury has been studied extensively. However, less is known about the chronic status of the coronary endothelium following progressive reperfusion. Experiments were designed to characterize, after 60 min of ischemia followed by progressive reperfusion, the coronary endothelial function under acute and chronic conditions. Heartworm-free mongrel dogs were used. A percutaneous balloon catheter was inflated to occlude the left anterior descending coronary artery for 60 min, followed by progressive deflation. After 60 min or 4 weeks of reperfusion, the coronary arteries were dissected free, cut into rings, suspended in organ chambers, and exposed to endothelium-dependent and endothelium-independent agonists, both in the presence and absence of pertussis toxin. Left circumflex coronary arteries (from the same dogs) that had not been subjected to occlusion and reperfusion were studied in parallel as controls. The acute endothelium-dependent relaxations to serotonin, thrombin, and adenosine/diphosphate were impaired significantly following ischemia-reperfusion injury. Four weeks after ischemia-reperfusion injury, the endothelium-dependent relaxations to these substances were normal compared with those of controls. The endothelium-dependent relaxations to acetylcholine, bradykinin, and the calcium ionophore A23187 were unaffected either acutely or chronically. An early impairment of endothelium-dependent relaxations after ischemia-reperfusion injury occurs in response to serotonin, thrombin, and adenosine diphosphate. This early impairment is transient and is not evident 4 weeks after reperfusion. In contrast to the regenerated endothelium following balloon deendothelialization, the chronic endothelial pertussis toxin-sensitive G-protein function is not impaired selectively after ischemia-reperfusion injury, provided the reperfusion occurs gradually.

Acetylcholine↗
PubMed1995

cGMP mediates the desensitization to bradykinin in isolated canine coronary arteries.

The relaxation to bradykinin in canine coronary arteries is mediated by endothelium-derived nitric oxide (NO) and hyperpolarizing factor (EDHF). Desensitization to the kinin was induced by incubation of canine coronary arteries with endothelium with 10(-8) M bradykinin for 30 min. After washout, tissues were contracted with prostaglandin F2 alpha, and concentration-relaxation curves to bradykinin were obtained in control and desensitized arteries treated with indomethacin. After desensitization, there was a shift to the right of the concentration-relaxation curves to bradykinin. However, the elevation in guanosine 3',5'-cyclic monophosphate (cGMP) levels evoked by bradykinin was similar in both groups of tissues. The curves to bradykinin obtained in the presence of NG-nitro-L-arginine (an NO synthase inhibitor) were depressed, whereas those obtained in arteries contracted with potassium (to eliminate the EDHF-mediated relaxation) were not affected by the desensitization. Addition of NG-nitro-L-arginine, oxyhemoglobin, or methylene blue before the desensitization procedure preserved, whereas 3-morpholinosydnonimine (SIN-1, a donor of NO) and 8-bromoguanosine 3',5'-cyclic monophosphate impaired, the EDHF-mediated relaxation to bradykinin. Thus the selective impairment of the EDHF-dependent relaxation to bradykinin may be mediated by NO, acting mainly through increased production of cGMP.

Animals↗
PubMed1994

Effects of the Ca2+ antagonist RO 40-5967 on endothelium-dependent responses of isolated arteries.

Experiments were designed to determine whether the Ca2+ channel inhibitor RO 40-5967 [(1S,2S)-2-[2-[[3-(2-benzimidazolyl)propyl]methylamine]ethyl]-6- fluoro-1,2,3,4-tetrahydro-1-isopropyl-2-naphthyl methoxyacetate dihydrochloride] causes endothelium-dependent relaxations or inhibits endothelium-dependent contractions of isolated blood vessels. Rings of dog femoral, carotid, and basilar arteries and of rat aorta, with and without endothelium, were suspended in conventional organ chambers for measurement of isometric force. During contractions evoked by phenylephrine (full alpha 1-adrenergic agonist), St 587 (partial alpha 1-adrenergic agonist) and endothelin-1 (ET), RO 40-5967 caused concentration-dependent relaxations of rings of dog femoral arteries; the relaxations to RO 40-5967 were greater in rings with endothelium than in those without endothelium. Nitro-L-arginine (NLA) and methylene blue (MB) inhibited the endothelium-dependent component of the response to RO 40-5967 during contractions to phenylephrine (PE) St 587 and ET. The endothelium-dependent relaxations evoked by RO 40-5967 during contractions to PE were not affected by diltiazem in the femoral artery, suggesting that this effect of the compound may not be related to its calcium channel inhibitor properties. Under bioassay conditions, RO 40-5967 stimulated release of relaxing factors from the endothelium of canine carotid arteries; the response of the detector tissues was inhibited by MB. In strips of canine femoral artery with endothelium, in which membrane potential of vascular smooth muscle cells (VSMC) was recorded with glass microelectrodes, RQ 40-5967 did not cause endothelium-dependent hyperpolarizations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1989

[Wilson Jones angiosarcoma of the face and scalp].

Because of its rarity and its fast development, we report a case of a 84-year-old woman, who developed all the clinical and histopathological characteristics of the angiosarcoma of face and scalp, with a fatal evolution within four months and metastases to liver, lungs and bone marrow.

Aged↗
PubMed1981

[Morphology, morohogenesis, localization and diagnostic value of paramyxovirus-like particles].

Considering the most relevant features registered in the literature about the paramyxovirus-like structures, and based on personal investigations, it is allowed to accept that they are membranous structural differentiations of the endoplasmatic reticulum. They represent products of cellular degeneration towards the most heterogeneous stimuli. Their viral origin can be eliminated due to their presence in a variety of diseases non correlated physiopathologically. Their fast constant presence in the cases of lupus erythematosus and dermatomyositis allows to consider the paramyxovirus-like structures as an ultraestructural sign of diagnostic value in these diseases.

Dermatomyositis↗