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At least 1,027 records · Page 57Linked to original sources
PubMed1964

STUDIES ON THE PATHOGENESIS OF FEVER. XII. ELECTROLYTIC FACTORYS INFLUENCING THE RELEASE OF ENDOGENOUS PYROGEN FROM POLYMORPHONUCLEAR LEUKOCYTES.

The metabolic reactions responsible for the release of endogenous pyrogen from rabbit granulocytes incubated in 0.15 M NaCl are specifically inhibited by the presence of K(+) (and by related alkali metal ions, Rb(+) and Cs(+)) in the medium. The inhibitory action of K(+) apparently involves penetration of the cell membrane and is directly antagonized by the cardiac glycoside, ouabain. It is concluded, therefore, that the inhibition of pyrogen release by extracellular K(+) is due to transport of K(+) into the cell. Although the precise molecular mechanisms which are responsible for the release of pyrogen from granulocytes incubated in K-free saline have not been elucidated, further study of the process has revealed: (a) that it is preceded by the accumulation of pyrogen within the cell, (b) that it depends upon the catalytic action of one or more sulfhydryl-containing enzymes, (c) that it does not require energy, either from glycolysis or from reactions depending on molecular oxygen, and (d) that its inhibition by K(+) and by arsenite is qualitatively similar to the depression caused by these same reagents on the release of other leucocytic proteins; i.e., lysozyme and aldolase.

Aldehyde-Lyases↗
PubMedDate not supplied

Angiogenic factors and angiogenesis inhibitors in exudative pleural effusions.

The angiogenesis system has been implicated in inflammatory and neoplastic processes; nevertheless, it has been little studied in relation to the pleural space. Our aim is to analyze pleural and plasma levels of the activators--vascular endothelial growth factor, basic fibroblastic growth factor, and inhibitors--endostatin and thrombospondin-1 and to estimate the association between these factors and related biochemical markers. We analyzed pleural fluid from 105 patients with one of the following types of pleural effusion: empyema or complicated parapneumonic, non-complicated parapneumonic, tuberculous, neoplastic and transudative. Angiogenesis activators were higher in exudates than in transudates (p < 0.001) and in empyema than in non-complicated parapneumonic patients (p < 0.001). Endostatin showed no significant differences. Trombospondin-1 showed higher levels in exudates than in transudates and in empyema than in non-complicated parapneumonic effusions (p < 0.001). In pleural exudates there was a positive correlation of angiogenesis activators and trombospondin-1 with low glucose and pH and high LDH. There was no correlation between pleural and plasma levels of the angiogenesis factors. We conclude that exudative pleural effusions showed higher vascular endothelial growth factor, basic-fibroblastic growth factor and trombospondin-1 values than transudative effusions that associated to low glucose and pH, and high LDH. There was no correlation between pleural and plasma concentrations, suggesting a compartmentalized response.

Adolescent↗
PubMed2001

Adenosine deaminase levels in nontuberculous lymphocytic pleural effusions.

OBJECTIVES: Adenosine deaminase (ADA) can aid in the diagnosis of tuberculous pleural effusions, but false-positive findings from lymphocytic effusions have been reported. We studied the ADA levels in a variety of nontuberculous lymphocytic effusions and analyzed the relationships between ADA and conventional hematologic and biochemical parameters. METHODS: One hundred six lymphocytic pleural fluid samples (lymphocyte count > 50%) were analyzed. These included post-coronary artery bypass grafting (CABG) effusions (n = 45), malignant effusions (n = 27), miscellaneous exudative effusions (n = 10), and transudative effusions (n = 24). ADA levels were determined using the Giusti method. In 22 randomly selected cases, ADA was measured again on the same sample 6 weeks later. RESULTS: The ADA level reached the diagnostic cutoff for tuberculosis (40 U/L) in only three cases (2.8%): two lymphomas and one complicated parapneumonic effusion. There was no significant correlation between effusion ADA levels and the total leukocyte (r = 0.08), differential lymphocyte (r = 0.18) or monocyte (r = - 0.18) counts. ADA levels were significantly lower in the transudative effusions (7.2 +/- 3.5 U/L) than in post-CABG (16.6 +/- 7.2 U/L), malignant (15.3 +/- 11.2 U/L), and other exudative (15.4 +/- 13.1 U/L) effusions (p < 0.001). ADA measurements were consistent when assayed 6 weeks apart (r = 0.95; p < 0.00001; coefficient of variation, 14%). CONCLUSIONS: ADA levels in nontuberculous lymphocytic effusions seldom exceeded the diagnostic cutoff for TB. Effusion ADA levels cannot be predicted from total or differential leukocyte counts. Post-CABG pleural fluids had ADA levels similar to other nontuberculous lymphocytic effusions. ADA is stable in effusion fluids, and its measurement is reproducible.

Adenosine Deaminase↗
PubMed2002

[Diagnostic value of pleural fluid cytologic examination].

The study included 200 patients with pleural effusion. Pleural effusions were transudative in 48 (24%) and exudative in 152 (76%) of cases. Congestive cardiac failure (14.5%), nephrotic syndrome (5.5%), and liver cirrhosis (2.5%) were the most common etiological diagnoses of transudate cases. Malignant effusion (16.5%), pneumonia (13%), pleural empyema (9%), tuberculosis (6%), and pulmonary embolism (5.5%) were the most common etiological diagnoses of exudative cases. Thirty-two (16%) cases of exudative pleural effusions were of undertermined etiology. Polymorphonuclear leucocytes predominated in 48 patients with exudative pleural effusions. The most common etiological diagnoses were pneumonia (41.67%), pleural empyema (39.59%) and pulmonary embolism (10.42%). Lymphocytes in pleural fluid were predominant in 63 patients, with malignant (6.34%), tuberculous pleurisy (19.02%), pulmonary embolism (6.34%), trauma (6.34%), and (46.11%) cases in patients with pleural exudate undertermined etiology. Eosinophyls were predominant in 16 (8%) patients with exudative pleural effusions. The most common etiology of eosinophilic pleural fluid were pneumonia (37.5%), malignant pleural effusion (25%), pulmonary embolism (12.5%), pyopneumothorax (6.25%) and trauma 6.25%. From 16 patients with eosinophilic pleural exudate, in 31% cases air, in 12.5% blood in pleural fluid were determined and in 12.5% cases previous pleural puncture was performed. Pleural fluid eosinophilia is most commonly associated with the presence of air or blood in the pleural fluid (correalation index 0.82). Malignant pleural effusions were determined in 33 patients. Malignant cells in pleural fluid were identified in 25 cases. The diagnostic sensitivity of pleural fluid cytology for malignant pleural effusions were 76%. Hemoragic pleuritis was determined in 18 and hemothorax in 4 patients. Etiology of hemothorax were trauma (75%) and coaguliopathia (25%). Most common etiological diagnoses of hemoragic pleuritis were neoplasia (33.3%), pulmonary embolism (16.65%), trauma (16.65%), pneumonia (11.11%), and congestive cardiac failure (11.11%). Diagnostic sensitivity and specifity of hemoragic pleuritis is low, 58% and 45% respectively.

Eosinophils↗