Bonded-phase extraction of plasma tricyclic antidepressant drugs for gas chromatographic analysis.
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Biomedical subjects
Publications and source records attributed to R Martinez.
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Phosphorylation on tyrosine residues mediated by pp60src appears to be a primary biochemical event leading to the establishment of the transformed phenotype in Rous sarcoma virus (RSV)-infected cells. To identify the cellular proteins that undergo tyrosine phosphorylation during transformation, a 32P-labeled RSV-transformed chicken embryo cell extract was analyzed by electrophoresis on a polyacrylamide gel. After slicing the gel into approximately 60 slices, phosphoamino acid analyses were carried out on the protein recovered from each gel slice. Phosphotyrosine was found in every gel slice, with two major peaks of this phosphoamino acid around M(r)'s of 59 and 36 kilodaltons. When the same analysis was performed with cells infected with a transformation-defective src deletion mutant of RSV (tdNY101), significant and reproducible peaks of phosphotyrosine were found in only 2 of 60 gel slices. These gel slices corresponded to M(r)'s of 42 and 40 kilodaltons. Identical results were obtained with normal uninfected chicken embryo fibroblasts. We conclude from these observations that pp60src or the combined action of pp60src and pp60src-activated cellular protein kinases cause the tyrosine-specific phosphorylation of a very large number of cellular polypeptides in RSV-transformed cells. In addition, untransformed cells appear to possess one or more active tyrosine-specific protein kinases which are responsible for the phosphorylation of a limited number of proteins. These proteins are different from the major phosphotyrosine-containing proteins of the transformed cells.
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We analyzed the results obtained in 163 consecutive patients with "pure" mitral stenosis who underwent operation by the open approach exclusively. Calcification was found in the mitral valve leaflets in 11% of the patients and left atrial thrombus, in 13.2%. A statistically significant relationship was discovered between history of previous systemic embolism and cardiac rhythm (p less than 0.005). The subvalvular apparatus was affected in 66.6% of patients; most of them were in New York Heart Association Functional Class III (p less than 0.005). The frequency with which annuloplasty had to be performed because of mitral insufficiency after commissurotomy was statistically higher (p less than 0.025) among patients in Functional Class III. Early mortality was 1.2% and late mortality, 0.2% per patient-year. Two patients required late reoperation (0.4% per patient-year). One was in Functional Class III and the other, Functional Class IV before the first operation. Three patients sustained a late systemic embolism (0.6% per patient-year). All survivors but 1 are in Functional Class I (84.4%) or II (14.9%).
Alterations in the pancreatic secretion of fluid and of enzymes in response to either pilocarpine (15 mg/kg) or an octapeptide of cholecystokinin (0.1 microgram/kg) have been found in rats that received daily injections of reserpine (0.5 mg/kg) for 7 days. During a 3-hr secretory period, significant reductions in the volume of pancreatic juice and in the total output of protein, amylase, and trypsin were observed in these animals. In the first hour of the secretory response, however, protease output was increased in the treated animals, particularly that of chymotrypsin, which was also increased in the longer secretory period following pilocarpine, but not cholecystokinin, stimulation. Zymogen granules isolated from the pancreas of the treated rats by differential centrifugation in a 0.3 M sucrose buffer had increased specific activities of the proteases when compared to those of untreated controls. Ultrastructurally, zymogen granules isolated from the pancreas of the treated rats showed changes in density, with bizonal and trizonal configurations being frequently observed, and had less distinct limiting membranes. In some, the membrane appeared broken at intervals, and there was granular material, presumably derived from the granule contents, lining the surface of the granule. It is concluded that pretreatment with reserpine inhibits fluid secretion and alters enzyme secretion in the rat exocrine pancreas. The latter effect is related to a nonparallel storage of amylase and proteases in the secretory granules induced by the drug treatment, probably through an action on protein synthesis or intracellular transport. An accumulation of proteases may lead to activation of these enzymes and to granule lysis. Inasmuch as the reserpine-treated rat has been proposed as an experimental model for cystic fibrosis, these findings are relevant in terms of possibly pathogenetic mechanisms in this disease.
An intracavernous aneurysm of the left internal carotid artery arose following transsphenoidal surgery in this patient. The pathogenic, clinical, and therapeutic aspects of the case are discussed. Only four other iatrogenic intracavernous carotid aneurysms have been reported previously.
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The authors have conducted a retrospective statistical study in a series of 45 patients with craniopharyngiomas in order to assess the value of different therapeutic approaches. All the patients included in the study were placed in three groups according to their method of treatment: 1) total excision; 2) subtotal excision; and 3) surgery followed by a course of radiotherapy (RT). Symptomatic recurrence was used to define failure of treatment. Of the patients subjected to total excision, 30% experienced recurrence after a mean time of 2 years. Tumors recurred in 71% of those treated by subtotal excision, with a mean time of 2.6 years. Of patients receiving RT in addition to surgery, only 6% had recurrence, after a mean time of 1 year. The authors conclude that the elective treatment for craniopharyngiomas is controlled subtotal surgery plus RT. Total excision should be attempted only if there is a negligible danger of mortality.
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According to Powers et collaborators the hypothesis that intramyocardial vessels may be collapsed in artificially ventilated patient with added PEEP, could be arisen. So, myocardial ischemia may explain why in some of those ones there appear signs of left ventricular failure. To test whether this reasoning was correct we measured LVEDP in normal dogs submitted to increasing levels of PEEP up to 40 cm H2O. Our results seem to point towards the following conclusions: a) In normal dogs, Starling relation is not altered and remains within the same hypercontractility pattern. b) As PEEP increases, ventricular function remains within the same curve up to 30 cm H2O and jumps to a higher contractility curve at 40 cm H2O of PEEP. All of this would suggest that under our experimental conditions it does not seem reasonable to assume the existence of left ventricular failure due to PEEP influence.
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