[Esthesioneuroblastoma of olfatory nerve. Study of a case (author's transl)].
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Biomedical subjects
Publications and source records attributed to E Pascual.
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Rosetting at 37 degrees ("warm" rosettes) was assayed as a technique to determine the degree of activation of T lymphocytes. Standard "cold" rosettes and an index of "warm" to "cold" rosettes were used to correct possible changes in the total percentage of T cells. Statistically higher numbers of "warm" rosettes were obtained in Pokeweed mitogen stimulated cultures when compared with unstimulated control; but not in old tuberculin stimulated cultures of lymphocytes from PPD positive individuals when compared with those of PPD negative. Also a significant rise was found in control cultures of 3 and 5 days when compared with those of day 1. We think that "warm" rosetting may be a useful technique for determining the degree of immunological activation of a lymphocyte population.
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Synovial fluid analysis for crystals represents one of the most important laboratory test for the evaluation of rheumatic diseases. The identification of monosodium urate and calcium pyrophosphate dihydrate crystals allows the prompt diagnosis of gout and pyrophosphate crystal-related arthropaties. Crystals are identified based on their shape and birefringence through a polarized light microscope equipped with a first order red compensator. Due to its simple execution and high diagnostic value, this examine should be always performed to complete synovial fluid analysis.
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Suppressor T cell hypofunction was found in active early rheumatoid arthritis (RA) (disease less than 3 months) and not in active late RA (greater than 6 months) or inactive RA. Active early RA patients when they were restudied 11-23 months later had normal suppressor cell function despite persistence of disease activity. Anti-suppressor cell antibody of the IgG class could be detected in plasma from active early RA patients and not in plasma from the other RA groups or the non RA controls. B cell targets for the Concanavalin A activated suppressor T cells were found to be functionally normal in early active RA. Suppressor cell hypofunction may contribute to the initiation, but not the persistence of rheumatoid synovitis.
OBJECTIVES: To analyze the effect of premedication with clonidine on postoperative sedation, anesthetic requirements and hemodynamic repercussions in patients undergoing craniotomy due to supratentorial intracranial pathology. PATIENTS AND METHODS: Twenty ASA I/II patients in a double-blind prospective study were assigned randomly to receive lorazepam (0.03 mg/kg/po, n = 10) or clonidine (0.005 mg/kg/po, n = 10) the night before and 90 minutes before surgery. Arterial pressure and heart rate were monitored continuously during and immediately after surgery (first 24 hours). Anesthetic induction was achieved with thiopental (maximum 6 mg/kg) and maintained with O2/N2O and an infusion of alfentanyl (1 microgram/kg/min). Hemodynamic response to surgical stimulus was treated with additional boluses of alfentanyl up to a maximum dose of 0.1 mg/kg and with an increase in infusion dosage to 2 micrograms/kg/min. When these were ineffective, isoflurane was given. All patients were extubated in the operating room. RESULTS: No differences in level of sedation were found between the two groups. The infusion dose and total amount of alfentanyl given were smaller for patients treated with clonidine (0.8 +/- 0.04 vs 0.6 +/- 0.01 microgram/kg/min and 22.4 +/- 5.3 vs 17.5 +/- 4.9 mg, respectively) (p < 0.05). No differences were found in isoflurane requirements (5/5 vs 2/8). Mean arterial pressure and heart rate were lower with clonidine from 3 minutes after intubation until the patient's arrival in the recovery room (p < 0.05), with marked bradycardia (49 +/- 5 vs 73 +/- 7 bpm) (p < 0.05) upon intubation. CONCLUSIONS: Premedication of neurosurgical patients with clonidine offers no advantages over lorazepam with respect to sedation. Nevertheless, clonidine may offer advantages with respect to the amount of alfentanyl required and attenuation of perioperative adrenergic response.
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