Ventricular asystole during upper gastrointestinal endoscopic electrocoagulation.
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Adenocarcinoma, Mucinous↗
Biomedical subjects
G J Rubeiz
Publications and source records attributed to G J Rubeiz.
Changes in tumor necrosis factor in postpneumonectomy lung growth.
So that changes in production and binding of tumor necrosis factor-alpha during postpneumonectomy lung growth could be determined, rats underwent left lung resection and were killed 3, 7, or 14 days later, 1 hour after the injection of 3H-thymidine. Serum was collected, and the lungs were lavaged and perfused in vitro. Lung volumes were measured. Lungs were homogenized, and changes in lung weight, protein content, deoxyribonucleic acid content, deoxyribonucleic acid synthesis, and tyrosine kinase activity of different lobes were recorded. Tumor necrosis factor-alpha content of serum, lavage fluid, and perfusate was measured by an enzyme-linked immunoassay. The binding of tumor necrosis factor-alpha to membrane extracts of lung homogenates was measured by immunoblots. Whereas the cardiac lobe of the remaining right lung demonstrated larger increases in size than other lobes after pneumonectomy, there was no difference in any growth parameter between it and the other lung lobes. Serum tumor necrosis factor-alpha was detectable in sham-operated animals and increased significantly after pneumonectomy. However, by day 14, it was not different from the level in sham-operated animals. In contrast, tumor necrosis factor-alpha in lavage fluid remained significantly elevated, and its binding increased gradually throughout the study period. Tumor necrosis factor-alpha in perfusate did not demonstrate any rise. We conclude that lung growth after pneumonectomy is uniform among various lobes, which suggests that it is regulated by humoral factors. Because tumor necrosis factor-alpha, a cytokine known to stimulate cellular proliferation and matrix synthesis, is produced and bound to the lung during this process, it may be one of the humoral factors implicated in postpneumonectomy lung growth.
Animals↗
Association of hypomagnesemia and mortality in acutely ill medical patients.
OBJECTIVE: To test the hypothesis that the mortality rate of acutely ill patients admitted to a medical ward or medical ICU is higher for those patients who present with hypomagnesemia than for those patients who do not present with hypomagnesemia. DESIGN: Prospective, observational study. SETTING: Emergency Department admissions to the medical ward and medical ICU of a tertiary care teaching hospital serving an inner city patient population. SUBJECTS: A total of 381 consecutive acutely ill patients. MEASUREMENTS: Serum magnesium concentrations and other metabolic variables were measured on admission from the Emergency Department. Acute Physiology and Chronic Health Evaluation (APACHE II) scores were computed for all patients, and mortality rates were determined for hypomagnesemic and normomagnesemic groups. MAIN RESULTS: Hypomagnesemic and normomagnesemic groups had comparable APACHE II scores and other variables. However, the mortality rates of the hypomagnesemic ward and medical ICU groups were approximately twice (p < .01) the rate of the normomagnesemic groups. Additionally, the duration of hospital survival in those patients who died was approximately 8 days less for hypomagnesemia than normomagnesemia, but not for ward admissions. Other associated metabolic abnormalities were frequently observed in both hypomagnesemic and normomagnesemic groups, including hypokalemia and hypocalcemia. CONCLUSIONS: Hypomagnesemia detected at the time of admission of acutely ill medical patients is associated with an increased mortality rate for both ward and medical ICU patients.
Adolescent↗
Steroid responsiveness of fibroblasts of paraquat injured lungs.
We evaluated the effect of dexamethasone on the synthesis of fibronectin by rat lung fibroblasts. A dose dependent inhibition was observed in fibroblasts isolated from normal lungs and in fibroblasts isolated early (4 days) and late (14 days) after the administration of endobronchial paraquat, and was more pronounced in fibroblasts exposed to dexamethasone for longer durations of time. Fibroblasts isolated early were more responsive to the inhibitory effects of dexamethasone on fibronectin synthesis. In addition, the distribution of fibronectin between the cellular and the extracellular compartments in these cells was altered. We conclude that fibroblasts of repairing lungs undergo changes in their responsiveness to corticosteroids during the repair process and are more susceptible to such therapeutic agents during the acute phase of injury.
Animals↗
Dynamic changes in the functional characteristics of the interstitial fibroblast during lung repair.
To evaluate the mechanisms involved in the regulation of fibroblast function during the repair of fibrotic lung injury, we isolated lung fibroblasts from adult male Fischer-344 rats before the induction of severe unilateral paraquat lung injury, as well as 1 and 14 days later. Fibroblasts were utilized at an early generation time to avoid senescence. In general, fibroblasts of injured lungs displayed significant increases in proliferative and matrix synthesis properties, with more pronounced increases detected early after the induction of injury. This was true of DNA synthesis, which increased by 3- and 1.4-fold on days 1 and 14, respectively; tyrosine kinase activity, which increased by 4- and 3.5-fold; fibronectin synthesis, 14- and 8-fold, respectively; and glycosaminoglycans synthesis, 4.4- and 3-fold, respectively. The increase in function of fibroblasts isolated from the immediate influence of extrinsic growth factors suggests that fibroblast function during repair may be under intrinsic as well as extrinsic control. In the early phases of repair, intrinsic changes may be more dominant and may result in autoregulation of fibroblast function. In the later phases of repair, despite some reduction in intrinsic fibroblast activation, exposure to extrinsic growth factors may result in maintaining the state of activation and in sustaining the repair process.
Animals↗