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Biomedical subjects

G Rona

Publications and source records attributed to G Rona.

At least 19 recordsLinked to original sources
PubMed1988

Neutrophil elastase alpha 1-proteinase inhibitor complexes in pleural effusions.

Polymorphonuclear (PMN) granulocyte derived neutrophil elastase (NE) is rapidly antagonized by alpha 1-proteinase inhibitor (alpha 1 PI) in vivo. To determine the clinical value of elastase alpha 1-proteinase inhibitor complexes (E-alpha 1 PI) in pleural effusions, fluid samples of 99 patients were examined. Fifty-six had malignant effusions, 30 had non-malignant exudates (pleural protein above 3 g/dl) mainly of inflammatory origin, and 13 patients had low protein transudates (below 3 g/dl) due to congestive heart failure. Nonmalignant exudates showed significantly higher (P less than 0.001) concentrations of E-alpha 1 PI compared with malignant effusions or low protein transudates (P less than 0.001). Malignant exudates secondary to lung cancer were characterized by higher (P less than 0.001) median pleural E-alpha 1 PI concentrations compared to malignant exudates due to primarily extrathoracic malignancies. Total pleural leukocyte counts and pleural neutrophil counts were performed in 68 effusions. By this means no clear-cut differentiation between malignant and nonmalignant exudates seems possible except for marked empyema. In conclusion, E-alpha 1 PI complexes in pleural fluid may better reflect the stage of inflammation of pleural effusions rather than mere pleural leukocyte counts. Low levels of E-alpha 1 PI complexes (less than 75 ng/ml) in pleural exudates with protein values above 3 g/dl are characteristic of malignant exudates. Determination of E-alpha 1 PI in pleural exudates may serve as a sensitive marker of inflammation and useful adjunct to pleural cytology in aspects of differential diagnosis of pleural effusions.

Blood Proteins↗
PubMed1987

Histopathologic evaluation of the effects of etodolac in established adjuvant arthritis in rats: evidence for reversal of joint damage.

Histopathologic evaluation of hindpaws from control rats with established adjuvant arthritis showed severe alterations in soft tissue and bone, as well as progressive, moderate-to-severe articular changes. Following treatment with etodolac for 28 days, soft tissue and articular changes were rated mild, and bone changes were rated moderate, but with remodeling. These findings indicate that etodolac partially reversed the joint damage in these rats.

Acetates↗
PubMed1986

[Diagnostic value of the combined determination of carcinoembryonic antigen (CEA) in pleural effusion and serum with an enzyme immunoassay (EIA). Sensitivity, specificity and relation to tumor type].

Measurement of carcinoembryonal (CEA) levels in pleural fluid are suggested to improve the unsatisfactory sensitivity of pleural cytology in the differential diagnosis of malignant pleural effusions. We evaluated simultaneously determined pleural and serum CEA levels in 117 patients with pleural effusions of different aetiology (74 malignant, 30 inflammatory exudates and 13 transudates) by use of an enzyme immunoassay (EIA). Despite considerable scatter, pleural levels of CEA in malignant effusions were significantly higher (p less than 0.001) than the values in benign effusions. Using a cut off level of 5 ng/ml, 41% (= sensitivity) of malignant pleural effusions showed elevated concentrations of CEA. Only one out of 43 benign effusions showed a level of 5 ng/ml, which is equivalent to a specificity of 98%. However, malignant effusions due to small cell lung cancer, pleural mesothelioma and metastasising ovarian carcinoma never showed elevated levels of CEA. Highest pleural values of CEA were observed in cases of alveolar cell or adenocarcinoma of the lung or metastasising breast cancer. Although pleural and serum CEA levels correlated significantly (rs = 0.77), the evaluation of serum CEA levels alone yielded a lower sensitivity (36%) and specificity (93%) than pleural levels. 77% of cases with malignant pleural effusions showing elevated pleural CEA levels were characterized by an increased ratio Pleura/Serum greater than 1, particularly in effusions due to lung cancer. The CEA ratio was significantly higher (p less than 0.05) in patients with malignant than with benign effusions. EIA appears to be more specific by avoiding false positive results in benign effusions as compared with determination by conventional RIA. In conclusion, evaluation of pleural CEA levels in patients with malignant effusions by using an EIA because of its high specificity is a valuable adjunct to pleural cytology in improving the diagnosis of malignant effusions. However, a normal CEA level in either pleural effusion or in serum is of no clinical significance. Simultaneous measurement in pleural effusion and serum is of greater value.

Breast Neoplasms↗
PubMed1985

Catecholamine cardiotoxicity.

The morphologic-functional correlative studies that we have carried out in the past 25 years with the various catecholamines have served as an example for analyzing myocardial reaction patterns and the reactions of the cardiac muscle cells to insult. These studies disclosed the unique nature of isoproterenol in producing 'infarct-like' myocardial necrosis. It appears that the pathogenesis of the catecholamine-induced myocardial necrosis is multifactorial. Our early studies suggested the role of relative hypoxia. Later studies by using extracellular fine structural protein tracers demonstrated the importance of microcirculatory effects as well as, in the norepinephrine model, that of early sarcolemmal membrane permeability alteration. The Ca2+ overload theory is supported not only by the experimental observations but also by its successful application in clinical cardiology. A new contribution is the recognition of catecholamine oxidation products in producing myocardial injury. Experimental data indicate that catecholamines play an important role in reperfusion and ischemic myocardial injuries. The sequence of events demonstrated by our studies with catecholamines might represent a common pathway in the evolution of myocardial changes in humans who develop myocardial lesions without narrowing or obstruction of coronary arteries. Investigation in the field of molecular and cellular cardiology has led to a better understanding of current clinical problems and helped to devise procedures for the prevention and management of human myocardial disorders. The isoproterenol-induced myocardial necrosis served as model to Professor A. Fleckenstein to formulate the Ca2+ overload theory of myocardial injury and develop a series of now widely used Ca2+ antagonistic drugs for the management and the prevention of human myocardial diseases.

Animals↗
PubMed1978

A three month inhalation toxicity study in the squirrel monkey (Saimiri sciureus) with terbutaline sulfate (Bricanyl).

A study of the subacute toxicity of inhaled terbutaline sulfate was performed in the Squirrel monkey (Saimiri sciureus). 3 groups of monkeys were exposed 1 h daily 7 days/week for 3 months to terbutaline sulfate aerosols at concentrations of 0.039, 0.185 and 0.799 mg terbutaline/litre of air respectively. A fourth group was a chamber control receiving air only. The following clinical parameters were evaluated: physical appearance and behavior, weight gain, ophthalmoscopic appearance, electrocardiograms, hemograms, blood biochemical profiles and urinalyses. At termination necropsies were conducted and organ weights determined. A variety of staining techniques was employed in the histopathological examination of tissues. Special attention was given to heart and lung. The distribution of goblet cells in sections from the main bronchi and trachea was also investigated. Occasionally a few animals in both the intermediate and high dose groups showed small amounts of exudate and frothing around the mouth during exposure to their respective terbutaline aerosols. No other changes that could be attributed to the exposure to terbutaline aerosols were seen in any parameter.

Aerosols↗
PubMed1976

Permeability alteration of sarcolemmal membrane in catecholamine-induced cardiac muscle cell injury. In vivo studies with fine structural diffusion tracer horse radish peroxidase.

Cardiac muscle cell injury was produced in male Sprague-Dawley rats weighing 300 to 450 gm. with catecholamines, norepinephrine, and isoproterenol; sarcolemmal membrane alteration was tested in vivo using the extracellular macromolecular tracer, horseradish peroxidase. Norepinephrine was administered in continuous intravenous infusion in a dose of 4 to 6 mug. per 100 gm. of body weight per minute, whereas isoproterenol was given as a single subcutaneous injection in a dose of 8.5 mg. per 100 gm. of body weight. Horseradish peroxidase was injected intravenously and localized in the right ventricular myocardium following 6 and 30 minutes of circulation time by light and electron microscopy. As early as 10 minutes after norepinephrine infusion, horseradish peroxidase appeared within cardiac muscle cells possessing normal fine structure. Selective deposition of the tracer on normal and altered myofilaments was noted. Similar observations were made in the isoproterenol model at 60 to 90 minutes. The results indicate that sarcolemmal membrane permeability alteration is an early event in catecholamine-induced cardiac muscle injury. The possible functional significance of the findings is discussed.

Animals↗
PubMed1976

Plasma hormone profiles in populations at different risk for breast cancer.

Evidence suggests that the reliability of urinary androgens or estrogens as prognostic discriminants for breast cancer may vary with different populations and may bear little relation to changes in plasma hormone levels. In this study the plasma estradiol level was significantly lower in Bantu, but did not in Caucasian, women with breast cancer, while the proportion of plasma androstenedione to dehydroepiandrosterone increased in Bantu patients. These changes in the plasma hormone profile in Bantu patients, a low-risk population for breast cancer, imply a change in ovarian and/or adrenal activity. Lack of similar hormone changes in Caucasian patients may be due to the initial differences in the hormone profile between the healthy Caucasian and Bantu women and to the different environmental factors that promote the breast disease in Western women.

Adult↗
PubMed1976

Plasma hormone levels in different ethnic populations of women.

It has been suggested that the urinary hormone profile is subject to environmental changes, such as urbanization and Westernization, and that the composition of the hormones can be used as a discriminate in determining the patient at risk for breast cancer. In this study, a comparison of the plasma hormone levels in Bantu and Japanese women, low-risk populations, and Caucasian women, a high-risk population, showed a higher level of 17 beta-estradiol in prepubertal girls and young Bantu and Japanese women. The higher estrogen level in the Bantu was evident in the early luteal and late follicular phases of the menstrual cycle. The difference in the dehydroepiandrosterone and testosterone levels in Bantu young women and prepubertal Bantu girls, suggests differences in adrenal activity between Bantu and Caucasian women. A fall in the plasma androstenedione was evident in postmenopausal Bantu and Japanese but not Caucasian women. Data suggest that the hormone profile is different among the 3 ethnic groups in both the pre- and postmenopausal women. Since the daily life-style of the women is comparable, it is suggested that the composition of the hormone profile is partially dependent on dietary on dietary factors.

Adrenal Glands↗
PubMed1976

Prolactin levels in populations at risk for breast cancer.

The basal plasma concentration of prolactin was determined by radioimmunoassay in Caucasian women at different risk for breast cancer and in three cases of women at risk for breast cancer. Samples taken under comparable conditions showed similar basal levels at birth and in prepubertal Bantu and Caucasian girls, or in healthy pre- and postmenopausal Bantu, Caucasian, or Japanese women. Elevated plasma prolactin levels were found in women castrated prior to 35 years of age and in women whose first pregnancy occured after 35 years. Evidence indicates that the prolactin/estrogen relationship may not be similar in women 35 to 45 years of age as compared to young women and suggests that elevation of serum prolactin per se does not appear to be related to an increased risk of breast cancer. The prolactin level was increased only in Caucasian women with breast cancer. If a high prolactin/estradiol ratio increases the susceptibility of the mammary epithelium to neoplastic growth, the lack of changes in prolactin levels in premenopausal Japanese patients and in postmenopausal patients of the three ethnic groups indicates that other factors are involved. Further study of the effects of life-style and diet on the basal level and stimulated release of prolactin is required to resolve the relationship of prolactin to breast cancer.

Adult↗
PubMed1975

Cytoplasmic contractile apparatus in aortic endothelial cells of hypertensive rats.

Hypertension was produced in male Wistar rats (150 gm. body weight) by complete ligature of the aorta between the renal arteries. Electron microscopic examination revealed that 1 week later the amount of cytoplasmic microfilaments in the endothelial cells of the aortic segment above the coarctation (mean blood pressure 160 mm. Hg) was strikingly increased as compared with normal animals. The endothelial cells in the segment below the coarctation (mean blood pressure 25 mm. Hg) contained few filaments and were similar to the cells in the aortic endothelium in controls (mean blood pressure 105 mm. Hg). Microfilaments measured 40 to 70 angstrom in diameter and were mostly located close to the endothelial clefts, where they formed longitudinal bundles or a network. The bundles of microfilaments contained electron-dense areas similar to the "attachment sites" of the underlying smooth muscle. By using en face preparations of aortic endothelial cells treated with antiactin autoantibodies (AAA) followed by anti-human IgG, it was seen that in hypertensive animals the cells above the ligature were intensely fluorescent when compared with those of the aortic portion below the ligature or those of the controls. The fluorescence was abolished after incubation of the AAA sera with thrombosthenin A. The correlation between electron microscopic and immunologic findings suggests that the microfilaments present in the endothelial cells of hypertensive animals are composed, at least in part, of actin. Endothelial cells so modified may play a role in permeability or may be related to other phenomena such as electrotonic coupling and synchronized contraction of aortic cells during hypertension.

Actins↗
PubMed1975

Membrane permeability alterations as manifestation of early cardiac muscle cell injury.

Studies with extracellular fine structural diffusion protein tracers, horseradish peroxidase and ferritin, were carried out on catecholamine-induced cardiac muscle cell injury. Epinephrine, norepinephrine, and isoproterenol were administered in a dose of 4- 6 mug/100g body weight by continuous intravenous infusion. For follow-up studies, isoproterenol was also given subcutaneously in a dose of 8.5 mg/100 g body weight as a single injection. In contrast to saline-infused controls and following epinephrine infusion, where these tracers always remained extracellular, norepinephrine- and isoproterenol-infused animals exhibited alteration of sarcoplasmic membrane permeability to macromolecules in the early stage of evolution preceding fine structural changes of cardiac muscle cells. This was reflected by the intrasarcoplasmic presence of peroxidase in some cardiac muscle cells which otherwise showed no ultrastructural alteration. Deposition upon and selective binding of the extracellular protein tracer, peroxidase, to intact myofilament was also a characteristic early change that may affect the contraction-relaxation mechanism of the myofilaments and may contribute to the evolution of necrobiotic alteration. In structurally altered cells, peroxidase showed similar affinity to contraction bands and fragmented myofilaments. Furthermore, these studies disclosed different sensitivities of various membrane components of the cardiac muscle cell. While in the early pahse of cell damage no peroxidase could be detected in various intrasarcoplasmic compartments, with increasing severity of the lesion the external and internal mitochondrial membranes as well as the sarcoplasmic reticulum were also affected. When the large molecular tracer, ferritin, was used, the sequence of events in altered cardiac muscle cells followed that outlined for peroxidase. However, free ferritin molecules could not be demonstrated in the sarcoplasm of cardiac muscle cells which exhibited normal ultrastructure.

Animals↗