Human T-cell lymphotropic virus type I disease in Argentine intravenous drug users with human immunodeficiency virus type 1 infection.
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Biomedical subjects
Publications and source records attributed to L Lopez.
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Thirty-five patients with torsional nystagmus (TN) underwent vestibular and ocular motor assessment and magnetic resonance image (MRI) scanning of the head. Patients were divided into two groups according to whether TN was predominant and present in primary gaze (Group I, 23 patients) or elicited by head positioning or gaze deviation and less prominent than other concurrent nystagmus (Group II, 12 patients). The main aetiologies in both groups were demyelination, vascular disease and posterior fossa tumours. In Group I, a frequent pattern of findings, occurring in 30-50% of cases, was a caloric canal paresis contralateral to the direction of the fast phases ('beat') of the TN, whereas the duration of horizontal caloric/rotational nystagmus and the slow-phase eye velocity of pursuit and of optokinetic nystagmus were all reduced in the direction of beating. The TN was more frequently and consistently modulated by vertical canal stimuli (head oscillation in roll) than by otolith stimuli (static tilt). Statistical analysis of the MRI showed significant overlap of abnormal MRI signals in the area of the vestibular nuclei, on the side opposite to the beat direction of TN. These results suggest that TN originates in a central imbalance of vertical semicircular canal function, resulting from lesions involving the vestibular nuclei on the opposite side of the TN. Group II was heterogeneous with no consistent pattern of neuro-otological findings, although lesions ipsilateral to the TN were frequent occurrence; in these cases cerebellar system lesions may have produced ipsilateral vestibular nuclei disinhibition.
Herein we report the results of the first major prospective study directly comparing aneuploidy detection by fluorescence in situ hybridization of interphase nuclei with the results obtained by cytogenetic analysis. We constructed probes derived from specific subregions of human chromosomes 21, 18, 13, X, and Y that give a single copy-like signal when used in conjunction with suppression hybridization. A total of 526 independent amniotic fluid samples were analyzed in a blind fashion. All five probes were analyzed on 117 samples, while subsets of these five probes were used on the remaining samples (because of insufficient sample size), for a total of over 900 autosomal hybridization reactions and over 400 sex chromosome hybridization reactions. In this blind series, 21 of 21 abnormal samples were correctly identified. The remaining samples were correctly classified as disomic for these five chromosomes. The combination of chromosome-specific probe sets composed primarily of cosmid contigs and optimized hybridization/detection allowed accurate chromosome enumeration in uncultured human amniotic fluid cells, consistent with the results obtained by traditional cytogenetic analysis.
A case of tracheal agenesis diagnosed at birth is discussed in which surgical correction was attempted. Both main bronchi were divided and anastomosis of the main right bronchus to the larynx was attempted, after intrapericardial release of the right lung and severing of the lower pulmonary ligament: bronchoplastic reconstruction of the trachea was impossible. We think that tracheal agenesis, a rare cause of respiratory distress in the newborn, has no suitable therapy today. It is justified to attempt surgical correction if any promising device is at hand or if any doubt exists that an uncorrectable situation is present.
An external electric field applied parallel to longitudinal axis of neurons selectively depolarizes either end and thereby activates voltage-sensitive conductance changes in a large population of neurons. Here, we characterized such population responses in the in vitro turtle cerebellum. The responses were recorded and analyzed using a multimodal approach: the magnetic evoked field was measured using a Superconducting Quantum Interference Device (SQUID) magnetometer, and concurrently the electric field potentials were recorded. Laminar profile and current-source density analysis were used to uncover the pattern of activation due to the applied electric field. Intracellular recording provided further information for identifying the elements producing the observed responses. Finally, pharmacological manipulations confirmed the nature of the conductance changes. Our results show that it is possible to activate a defined cell population of the cerebellum by an applied field and obtain a magnetic response of the order of 0.5-2 pT. A field applied from the dorsal to the ventral side of cerebellum produced tetrodotoxin-sensitive population spikes. This component was followed by a kynurenic acid (KYNA)-sensitive postsynaptic response, most likely comprised of Ca(2+)-mediated action potentials occurring at the proximal pole of the Purkinje cell dendrites and evoked by climbing fiber inputs. The applied electric field directed from the ventral to the dorsal side of cerebellum gave rise to a complex of responses that was made up of a KYNA-sensitive component (presumably synaptically activated) and an Mn(2+)-sensitive but KYNA-insensitive component (probably due to a directly activated calcium conductance change). This study provides insights into the effects of electric and magnetic fields applied to the nervous tissue of experimental animal and human studies.
Gianturco self-expandable stents were used successfully in the management of 5 patients with tracheobronchial pathology. Placement was performed under endoscopic and fluoroscopic guidance. None of the patients has experienced complications secondary to the stent placement, and in all of them the clinical problems resolved satisfactorily. Longer follow-up is required to determine the place of tracheobronchial stenting in patients with respiratory compromise.
The use of postsclerotherapy compression was evaluated in 37 women with bilaterally symmetrical telangiectatic leg veins. Compressed vessels tended to achieve a greater clinical resolution when located on the distal leg and/or when greater than 0.5 mm in diameter. Postsclerotherapy hyperpigmentation fell from 40.5% to 28.5% with the use of compression. In addition, ankle and calf edema were lessened if a graduated compression stocking was worn immediately after sclerotherapy.
We report a case of vertical ocular motor apraxia in a 4-year old boy whom we have followed for 2 years. The patient had no upward and downward voluntary movements of the eyes since birth, but horizontal movements were normal. He achieved gaze changes in the vertical plane by combined blinks and head movements. Magnetic resonance imaging demonstrated bilateral lesions at the mesencephalic-diencephalic junction.
Lipid profiles were determined in 56 elderly patients with benign essential hypertension during an open-label 1-year study of the safety and efficacy of isradipine, a new calcium antagonist, in controlling blood pressure. Patients with diastolic blood pressures between 96 and 115 mm Hg were titrated with isradipine (mean dose of 11 mg/day) to reduce blood pressure to less than 90 mm Hg. Ten of these patients received concomitant hydrochlorothiazide (HCTZ) 50 mg/day for additional control. Sera were analyzed using standard methods at the end of a 2- to 4-week washout period, and at the end of Months 6 and 12, for total cholesterol (CHOL) and HDL- and LDL-cholesterol. Changes in lipid values (mg/dl) from baseline to 12 months with isradipine alone (n = 38) were as follows: CHOL, -7.5; HDL, +3.9 (p less than 0.05); LDL, -6.2; CHOL/HDL, -0.6 (p less than 0.05). For patients receiving concomitant HCTZ (n = 9), the changes were as follows: CHOL, -4.9; HDL, +3.4; LDL, -16.8; CHOL/HDL, -0.4. In conclusion, isradipine alone was associated with significant improvements in HDL cholesterol and total CHOL/HDL ratio. Lipid profiles of patients receiving isradipine and HCTZ were minimally affected. Favorable lipid changes with isradipine suggest that it may have advantages in the treatment of hypertensive patients.
The author performed a pilot study of nicardipine (NC), a Ca(+)+ channel blocker, to study its dosing, toxicity, and possible efficacy for hemispheric cerebral infarction within 12 hours (mean 6.9 hr) of onset to determine the advisability of proceeding with a multi-centered controlled trial. NC was administered IV (3 to 7 mg/hr) X 72 hours by titrating dose to mean arterial blood pressure (MABP not less than 10% of baseline), then orally X 30 days. Forty-three patients have been entered; mean age 63 (range 34-89), 25 male and 18 female. Only 3 had CT evidence of infarct on entry. Results have shown improvement in a 100-point (pt) graded exam (40 pts at entry, 68 pts at 3 months). Of 20 patients completing 3 months' evaluation, 17 improved and none worsened. Sixteen out of 20 were at home and 8 had minimal or no impairment. Mean Barthel's index was 72. Mean maximal serum NC level was 75 ng/mL. MABP decreased from 103 (entry) to 83 (72 hours). A larger controlled study is warranted to determine the efficacy of NC for acute cerebral infarct.
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Recent evidence suggests that ethanol initially causes an increase in receptor-dependent cAMP levels, followed by heterologous desensitization of receptors coupled to GS after chronic exposure. Here we investigated the role of adenosine in mediating these responses. We found that ethanol caused accumulation of extracellular adenosine in NG108-15 and S49 lymphoma cells. This adenosine activated adenosine receptors to increase intracellular cAMP levels. The addition of adenosine deaminase, to degrade accumulated extracellular adenosine, or isobutyl-methylxanthine, an adenosine receptor antagonist, completely blocked ethanol-induced increases in cAMP levels in NG108-15 cells. Chronic exposure of NG108-15 and S49 wild type cells to ethanol resulted in heterologous desensitization of adenosine receptor- and prostaglandin E1 receptor-dependent cAMP signal transduction. Coincubation of NG108-15 and S49 wild type cells with adenosine deaminase and ethanol for 48 hr prevented heterologous desensitization. Moreover, mutant S49 cells, which are unable to transport adenosine, did not accumulate extracellular adenosine after incubation with ethanol and did not develop ethanol-induced heterologous desensitization. Our results suggest that adenosine is an important mediator of both the acute and chronic effects of ethanol on cAMP signal transduction.
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Recombinant human erythropoietin produced in transfected Chinese hamster ovary cells is glycosylated much the same way as the erythropoietin present in human urine. To determine the role of carbohydrates in the stability of recombinant human erythropoietin in vivo, [125I]-labeled recombinant erythropoietin was intravenously infused into rats. The erythropoietin was slowly cleared from the blood with a half-life of approximately two hours. Asialoerythropoietin, which was produced by treatment of recombinant human erythropoietin with sialidase, was found to be cleared rapidly from circulation within ten minutes. These data suggest that the galactose binding protein of hepatic cells is involved in the clearance of asialoerythropoietin. Erythropoietin also contains N-glycans with a few N-acetyllactosamine repeats, which can be enriched by tomato lectin affinity chromatography. The lectin-bound fraction was cleared to a larger extent than was the unfractionated erythropoietin, while the component that did not bind the lectin was found to be stable in the circulation. Authentic N-acetyllactosamine repeats (polylactosaminoglycans) prepared from erythrocytes were similarly rapidly cleared from the circulation to the liver, and this clearance was inhibitable with asialo-alpha 1-acid glycoprotein. These results suggest that (a) the sialic acid of the recombinant erythropoietin is necessary for this glycoprotein hormone to circulate stably and (b) glycoproteins with more than three lactosaminyl repeat units may be cleared by the galactose binding protein of hepatocytes.
L-acetylcarnitine is a compound with cholinergic properties and putative action on the visual system and the glucose metabolism. Ten healthy, emmertropic volunteers (age range: 21 to 28 years) were studied. Each subject was administered 5, 10, and 30 mg/kg acute intravenous doses of L-acetylcarnitine and matching placebo. Retinal oscillatory potentials to full-field flash stimulation were recorded before and 30, 60, and 120 min after administration. A systematic reduction of the implicit time of the P2 and N2 oscillatory potential components was observed after administration of the 10 and 30 mg/kg doses: significant changes were not evident at the 5 mg dose or after placebo. The latency reduction was significantly correlated with the postdrug increment of the L-acetylcarnitine plasma concentration. No other systematic modification in latency of amplitude was observed.
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