[Pregnancy and smoking: significance of the problem and health-service based prevention].
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Biomedical subjects
Publications and source records attributed to E Castellanos.
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The application of nerve growth factor (NGF) to primary adrenal medulla chromaffin cell cultures induces phenotypic changes characterized mainly by the presence of neurites. A similar effect has been seen when these cells are stimulated by extremely low frequency magnetic fields (ELFMF). In this study, newborn rat chromaffin cells were cultured and subjected to NGF or ELFMF in order to compare their histological and ultrastructural characteristics. Cells cultured in the presence of NGF developed cytoplasmic projections and their distal ends showed growth cones as well as filopodia. With scanning and transmission electron microscopy, an increased submembranous electron density was observed in the nuclei of cells as well as irregular, wavy neuritic projections with a moderate number of varicosities, as well as the prevalence of intermediate filaments among the cytoskeleton components. Cells stimulated with ELFMF presented straighter neuritic extensions with a greater number of varicosities. With the transmission electron microscope, numerous neurotubules were observed, both in the cell soma and in their neuritic extensions. In both groups, growth cones were clearly identified by their ultrastructural characteristics. The differences seen in the cytoskeleton of cells stimulated with NGF or ELFMF suggest differential stimulation mechanisms possibly determining the biochemical, electrophysiological, and morphological characteristics in both types of cell cultures.
BACKGROUND: Failure to differentiate supraventricular from ventricular arrhythmias is the most frequent cause of inappropriate implantable cardioverter-defibrillator therapies. Although a sudden-onset criterion is available to differentiate sustained monomorphic ventricular tachycardias (SMVTs) and sinus tachycardias (STs), SMVTs arising during ST and SMVTs gradually accelerating above the cutoff rate can remain undetected. Regular paroxysmal atrial tachycardias (ATs) also can be undetected by onset and stability algorithms. We hypothesized that the first postpacing interval (FPPI) variability after overdrive right ventricular pacing may differentiate SMVTs from STs and ATs. METHODS AND RESULTS: FPPI variability was measured in 23 SMVTs (cycle length [CL] 366+/-50 ms [VT group]), 27 supraventricular tachycardias, 15 episodes of induced or simulated ATs (CL 376+/-29 ms [AT group]), and 12 exercise-related STs (CL 381+/-24 [ST group]). Sequences of trains of 5, 10, and 15 beats were delivered with a CL 40 ms shorter than the tachycardia CL. An FPPI absolute mean difference between consecutive trains of 5 and 10 beats (deltaFPPI) < or =25 ms identified all VTs (mean difference 5+/-7 ms). In the AT group, the deltaFPPI was >25 ms in all sequences (mean difference 129+/-60 ms, P<0.01). In the ST group, the deltaFPPI was >50 ms in all STs (mean difference 118+/-47 ms, P<0.01). CONCLUSIONS: FPPI variability may differentiate SMVT from AT and ST. This criterion is potentially useful in implantable devices that use a single ventricular lead.
Several experimental models have been proposed to explain the electrocardiographic and electrophysiological characteristics of atrial flutter. In animal models based on anatomical obstacles, intercaval crush or Y like shaped lesion located in the right atrium, it has been possible to induce sustained atrial arrhythmias in which the entrainment criteria could be demonstrated. Additionally these tachycardias presented an atrialwave morphology similar to the F waves of type 1 or typical atrial flutter. Flutter type 2 could better be explained by models based on functional reentry like the leading circle. Typical atrial flutter in human, saw teeth morphology in inferior ECG leads, is though to be a circus movement located in the right atrium, as deduced of the analysis of activation sequence, resetting and entrainment phenomena from right and left atrium. Moreover the successful results of RDF ablation procedures confirm this idea. Nevertheless the delimitation of the anatomical boundaries of the reentry pathway remains inconclusive.
In the present manuscript the information concerning electrical therapy of atrial fibrillation (AF) to prevent its development and to control its consequences (excluding ablation which will be covered in separate manuscripts of this series) is reviewed. Both presently conventional approaches and those undergoing investigation will be considered, under three general headings. Electrical stimulation to prevent the development of AF. Based on non controlled studies comparing VVI stimulation with other modalities that include stimulation of the atria, it was suggested that atrial stimulation could prevent AF recurrences in patients with sinus node dysfunction. This concept has been questioned in recent studies. In contrast, the hypothesis that specific ways of atrial stimulation (stimulation at sites other than the high right atrium, multisite simultaneous or with certain "delays" atrial stimulation) may be more efficacious is presently under enthusiastic assessment. Electrical stimulation to control ventricular response. Despite the evidence that ventricular stimulation may contribute to regularization and rate control during AF, its quantitative value seems to be scarce and, thus, is not of regular use in practice. Automatic implantable atrial defibrillator. Both animal experiments and clinical studies have demonstrated that the atria can be defibrillated using intracavitary electrodes with less than 3 joules in most cases, and without risk of inducing ventricular tachyarrhythmias as long as shocks are synchronized to the R wave and the preceding R-R interval is not short. Although an implantable atrial defibrillator is already undergoing clinical evaluation, the subject of tolerability of patients to shocks for non malignant arrhythmias is still controversial, since even low energy shocks seem to be painful.
Intermittent aortic regurgitation is an unusual complication following a mechanical prosthesis replacement in the early postoperative period. Arterial pressure recording and echocardiographic assessment were enough to diagnose the prosthetic dysfunction. Reexploration of the valve confirmed the dysfunction, which was caused by a pannus of previous aortic valve replacement with the pulmonary valve. The pannus impeded normal closure of the leaflet in an intermittent way during diastole. Reorientation of the valve corrected the aortic insufficiency. Doppler ultrasound was a very useful noninvasive technique in order to evaluate the suspected prosthetic valve dysfunction in the immediate postoperative period.
We observed a case of hyperammonaemic encephalopathy in a patient without liver dysfunction which revealed meningeal involvement of IgD multiple myeloma. We have reviewed briefly the hyperammonaemic syndrome and we believe that this diagnosis has to be considered in differential diagnosis of encephalopathies in patients with multiple myeloma.
Intimal thickening in the aorta and carotid artery of rats was induced by repeated intraperitoneal injections of ovalbumin, 2.5 mg/kg BW, given weekly 5 times after initial subcutaneous sensitization, and/or feeding with a cholesterol-rich diet. The intimal thickening was apparent in immune-challenged rats fed with either a cholesterol-rich or a basal diet (p less than 0.01), whereas it was mild in non-immunized rats fed a cholesterol-rich diet. The ultrastructural changes in the thickened intima were characterized by leukocytic (mainly monocytic) adhesion and migration, and minor endothelial cell damage. Morphometric evaluation of leukocyte adhesion to the intima of the thoracic aorta revealed that the immunized rats fed either a cholesterol-rich or a basal diet showed greater leukocytic adhesion (p less than 0.01 and p less than 0.001, respectively) than that in non-immunized rats fed a cholesterol-rich diet, which in turn also showed an increased degree of leukocyte adhesion (p less than 0.05) than control rats. This immunological approach to the arteriosclerotic process could explain the earlier and more severe arteriosclerosis found in patients with immunological disorders, and the development of arteriosclerosis in the absence of hypercholesterolemia, hypertension and other risk factors.
In order to learn about the influence of dietary factors and obesity on prostatic cancer in our environment, a case-control study was performed. The group of cases consisted of 90 men histologically diagnosed with prostatic cancer in the 'La Paz' hospital (Madrid) during the 4-year period of 1983-1987. The controls were 180 men selected to obtain a random sample of males from the same hospital, stratified according to age and date of admission as compared with the prostatic cancer patients. The results of the study revealed that a diet rich in animal fats as well as high in meat consumption increased the risk of prostatic cancer. Low ingestion of vitamin A or vitamin C and obesity were unassociated to the disease.
In this paper the following findings were described: 1) Murine arteriosclerosis induced by immune challenge was ultrastructurally characterized by intimal monocyte-macrophage recruitment and minor endothelial alterations; 2) Atherosclerotic lesions of human coronary arteries exhibited frequently segmental or patchy neovascularization, probably representing a response to intimal injury as an example of repair process. Newly formed blood vessels in the intima were derived from both adventitial and luminal endothelial growth; 3) Angiogenesis in vitro was related to the activation of fibrinolytic system especially via the autocrine production of u-PA from endothelial cells, and this process was modulated by cytokines and TGF beta. These findings add more evidence for the hypothesis that the chronic inflammation-repair process plays an essential role in the initiation and progression of atherosclerosis.
An epidemiological case-control study was performed to know the factors involved in the development of prostatic cancer. Ninety patients diagnosed of prostatic cancer in La Paz Hospital (Madrid) from January, 1981 to December, 1987, comprised the study group. The controls were 180 male patients from the same hospital and with no personal or familial antecedents of urologic disease or malignant tumours. The cases and controls were matched by age, and year of admission to the hospital. The results of the study revealed that the disease is strongly associated to familial antecedents of prostatic cancer. The risk for the patients with these antecedents is 3.14. The disease was statistically associated to a fatherhood of more than 5 children. No association between the disease and antecedents of tonsillectomy, rheumatic fever, educational level, place of residence, or marital status was found.
OBJECTIVE: To assess the evolution of cytologic atypia on cervical cytologic smears as an attempt to better understand the natural history of these lesions and to establish a follow-up protocol. STUDY DESIGN: The study group consisted of 76 patients with a diagnosis of cytologic atypia on cervical cytologic smears performed at the gynecology Outpatient Clinic, Hospital del Mar, between December 1989 and June 1993. Patients with inflammatory atypia, a reparative process or findings consistent with human papillomavirus infection had been excluded. Follow-up smears were reviewed. Compliance with follow-up recommendations was also evaluated. RESULTS: Thirty-nine patients returned to the clinic for follow-up after a diagnosis of atypia (51.3%). Progression from atypia to dysplasia was found in 38.5% of patients with at least a follow-up smear. Changes consistent with intraepithelial neoplasia were found in 17 patients: low grade dysplasia was found in 10 patients (mild dysplasia in 8 and atypia in 2) and high grade dysplasia in 7 (moderate in 4 and severe in 3). This progression was most commonly found at the first follow-up visit and within the first year. CONCLUSION: Patients with cytologic atypia were at higher risk of developing dysplasia than those with reparative atypia. Our results support the theory of progression from atypia to dysplasia in a considerable percentage of patients. Follow-up compliance in our patient population was low. One should emphasize the importance of this diagnosis and encourage close cytologic follow-up, especially within the first year after the diagnosis of atypia.
This report describe a 69-year old woman with a congenital aneurysm of the non-coronary sinus of Valsalva ruptured in the right atrium, causing severe hemodynamic derangement of the right ventricle. The site of the communication between the aneurysm and the receiving chamber was accurately diagnosed by two-dimensional color flow Doppler imaging which provided more valuable preoperative information than conventional aortography.
This is a study of 199 consecutive patients who survived isolated mitral or aortic valve replacement with a Björk-Shiley (B-S) or St. Jude Medical (SJM) prostheses. Mean follow-up was 36 months. Preoperative status was similar for both groups (B-S or SMJ). Five year survival rates for mitral valve replacement (MVR) were 91% for B-S and SJM, and for aortic valve replacement (AVR) 96% vs 91% for SJM (p less than 0.06). Linearized incidence of thromboembolism in MVR was 5.62% patient year for BS and 5.23% patient year for SJM (p = NS). Classical risk factors for thromboembolism were evaluated on a univariate analysis: no single risk factor was identified. Only the association of two or more was possibly significant. The presence of inadequate anticoagulation (prothrombin index greater than 50%) was the main risk factor for thromboembolism, as the incidence rate was 19% per patient year when poorly anticoagulated versus 4.6% per patient year incidence in the whole series (p less than 0.01).
Four cases of anomalous origin of the left coronary artery from the pulmonary artery, three of which were operated upon in our Centre, are presented. An aortocoronary bypass with reversed autologous saphenous vein was carried out in both of the children; and in the adult, the anomalous ostium was closed from the interior of the pulmonary artery. After 84, 72, and 4 months of evolution, respectively, they were found to be asymptomatic, the mitral insufficiency had disappeared and the venous graft remained patent. In this paper, the clinical form of presentation, diagnostic possibilities and surgical treatment are analysed.
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