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Biomedical subjects

K G Bensch

Publications and source records attributed to K G Bensch.

At least 73 records · Page 4Linked to original sources
PubMed1978

Malignant mesothelioma arising after direct application of asbestos and fiber glass to the pericardium.

A case of mesothelioma, apparently arising in the pericardium, is reported in a patient who, 15 years previously, had been treated for angina pectoris by dusting of the pericardial cavity with a mixture of fibrous dusts. At autopsy, transparent fibers and ferruginous bodies were present within the pericardium. Electron diffraction and microprobe analysis indicated that approximately two thirds of the fibers were tremolite and anthophyllite asbestos, and the remainder, fiber glass. Development of mesothelioma in laboratory animals has been reported after intrapleural deposition of asbestos and other fibers, but in humans, the link between exposure to asbestos and mesothelioma has always been based on epidemiologic data and the retrospective finding of asbestos in tissues. To our knowledge, this is the first example of a malignant mesothelioma in a human associated with direct mesothelial contact with fibrous dusts.

Angina Pectoris↗
PubMed1978

Prolongation of G1 and S phase in C-6 glioma cells treated with maple syrup urine disease metabolits. Morphologic and cell cycle studies.

Metabolites accumulating in maple syrup urine disease, a disease attributable to an inborn error in the catabolism of branched-chain amino acids, were administered to rat C-6 glioma cells maintained in monolayer culture in order to study the morphologic and cell kinetic changes caused by these metabolites. Computer analysis of fraction-labeled mitoses in combination with flow microfluorometric analysis was used to analyze the effects of these metabolites on the cell cycle. The maple syrup urine disease metabolites, i.e., L-leucine, L-isoleucine, and L-valine and their corresponding ketoacids caused a prolongation of the G1 and S phases, when administered in combination at concentrations corresponding to approximately the highest recorded plasma levels in patients with the disease (1 x level). This effect was not reversible. Ketoleucine (alpha-ketoisocarproic acid or AKICA) alone, the compound that accumulates in maple syrup urine disease and that has previously been shown to be the most important metabolite associated with it, caused marked prolongation of the G1 and, to a lesser extent, the S phase at concentrations of 200 mg. per 100 ml. Return of the AKICA-treated growth-arrested cells to a standard medium caused complete reversal of grwoth inhibition. Consistent fine structural changes were found in cells treated with AKICA at concentrations of 300 mg. per 100 ml. or with the combined maple syrup urine disease metabolites at a 2 x level. These included marked cell process elongation and the appearance of numerous bundles of cytoplasmic filaments.

Caproates↗
PubMed1978

Myoglobinuria associated with herpes-group viral infections.

Two cases of myoglobinuria were associated with herpes-group viral infection (herpes simplex and Epstein-Barr). Muscle atrophy and acute renal failure were important complications. No evidence of direct invasion of muscle fibers by virus was found, nor was the severity of myoglobinuria correlated with histologic appearance of muscle.

Acute Kidney Injury↗
PubMed1977

Pulmonary alveolar cell carcinoma. Fine structural and in vitro study of a case and critical review of this entity.

Alveolar cell carcinoma is an unusual pulmonary neoplasm composed of cells with the ultrastructural features of granular pneumocytes. In the past this lesion has been grouped with peripheral well-differentiated mucin-secreting adenocarcinomas under the heading of bronchiolo-alveolar cell carcinoma. Because the existence of alveolar cell carcinoma as a distinct entity has been disputed, we examined a case ultrastructurally and confirmed that the neoplastic cells exhibit granular pneumocyte differentiation (lamellar bodies and abundant surface microvilli). In addition, we have growth this tumor in organ culture for up to 5 months and have documented the persistence of granular pneumocyte differentiation during this period. The accumulated evidence from human and animal studies that the granular pneumocyte may undergo neoplastic transformation is briefly reviewed. We conclude that alveolar cell carcinoma is a distinct entity; however, the elucidation of its natural history must await series that separate this lesion from other pulmonary carcinomas.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1976

Peripheral pulmonary carcinoid tumors.

The light microscopic and ultrastructural features of five asymptomatic peripheral carcinoids presented as distinct pulmonary solitary nodules are described. By conventional microscopy the tumors displayed a variety of histologic patterns, the most unusual one showing tumor cells embedded in a richly vascular hyalinized stroma and forming papillary structures or cystic spaces lined by low cuboidal cells which ultrastructurally bore a strong resemblance to intermediate or transitional forms between types I and II pneumocytes. A striking feature of these tumors was their rich vasculature associated with a marked perivascular sclerosis composed of basement membrane-like material and collagen fibrils most likely produced by the increased numbers of pericytes surrounding these sclerotic vessels. The clinical implications, biologic behavior, and association of these tumors with other pulmonary neoplasms are also discussed.

Adult↗
PubMed1976

Pulmonary carcinoid tumors is tissue and organ culture.

Pulmonary carcinoid tumors arise from cells whose function is yet to be defined. Conditions for maintenance of cells of these tumors for prolonged periods of time in tissue and organ cultures were established in order to gain insight into their supposed endocrine activity. We succeeded in growing explants of these tumors in organ culture for as long as 5 months without the cells losing their ability to produce large numbers of neurosecretory-type granules.

Carcinoid Tumor↗
PubMed1976

On the origin of the so-called tumorlets of the lung.

A light and electron microscopic study of multiple tumorlets in a 66 year old female is presented. Clinically the patient had had chronic obstructive lung disease with bronchiectasis of the right upper lobe. Aside from severe bronchiectatic alterations, the resected lobe showed typical tumorlets. On electron microscopic study, these were shown to consist of cells containing large numbers of a neurosecretory type of granule, which was identical to those present in the bronchial counterpart of the intestinal argentaffin (Kulchitsky) cell, as well as in pulmonary carcinoid and oat cell carcinoma cells. Our studies suggest the possibility of a histogenetic relationship between tumorlets, bronchial carcinoid tumors, and oat cell carcinoma, the cell of origin in each case being the bronchial counterpart of the intestinal argentaffin cell.

Aged↗
PubMed1976

Bronchopulmonary dysplasia: the pulmonary pathologic sequel of necrotizing bronchiolitis and pulmonary fibrosis.

A light and electron microscopic study was carried out in 21 infants in whom the pathologic diagnosis of bronchopulmonary dysplasia had been made. All the infants except two had the respiratory distress syndrome at birth, and all 21 had been treated with respirator and oxygen therapy for various periods of time. The pathologic alterations observed in all the infants studied were primarily damage of the bronchial and bronchiolar ciliary apparatus and mucous membranes, severe necrotizing bronchiolitis, and marked bronchiolar and alveolar fibrosis. These changes were more pronounced in infants who survived the longest period of time. Such inflammatory and fibrotic changes are known to predispose to destruction of lung tissue, emphysema, and pulmonary hypertension. Six of these 21 infants developed symptoms and signs of cardiac atrial or ventricular stress, including cor pulmonale, prior to their demise. These infants were among those that survived the longest periods of time, had the longest exposure to supplemental oxygen, and showed histopathologically severe pulmonary fibrosis and emphysema.

Bronchial Diseases↗
PubMed1976

Oxygen toxicity in the newborn lung: reversal of inhibition of DNA synthesis in the mouse.

Continuous exposure to 100% oxygen at atmospheric pressure for two weeks causes significant alterations in the growth of the lung and the body of newborn mice. These changes can be divided into three phases. The initial phase, which lasts 96 hours, is characterized by inhibition of lung DNA synthesis, diminished total lung DNA, and a decrease in the ratio of lung DNA to body weight. The intermediate phase from 96 to 144 hours is characterized by a sharp increase in mortality, a plateau in body weight, and a minimal lung DNA/body weight ratio. During this period, however, surviving animals show a reversal of the inhibition of DNA synthesis and thus an increase in total lung DNA. The third phase, occurring after 144 hours, is characterized by a continued increase in DNA synthesis and total lung DNA, a gain in body weight, a return of the lung DNA/body weight ratio to control levels, and a sharp decline in mortality. The survival rate of 54% in newborn mice over two weeks contrasts with the near total mortality reported for adult experimental animals similarly exposed. The reversal of the inhibition of lung DNA synthesis in surviving mice suggests either that some newborn animals are inherently resistant to pulmonary oxygen toxicity or that they develop, during a critical exposure period, an adaptive process necessary for their survival.

Animals↗
PubMed1976

Oxygen toxicity in the newborn. The effect of chronic continuous 100 percent oxygen exposure on the lungs of newborn mice.

Continuous exposure of newborn mice of a single, highly inbred strain to 100% oxygen at normal atmospheric pressure for up to 6 weeks resulted in a progressive evolution of pulmonary changes which consisted of dense fibrous tissue deposition, chronic bronchitis and bronchiolitis, and emphysema. Survival of the experimental animals decreased with the duration of exposure, and it was 18% after the sixth week. While the pulmonary changes were evolving, lung growth was markedly inhibited in the experimental animals, whereas lung weight increased significantly. The present study indicates that in contrast to the adult mouse, survival of a substantial percentage of newborn mice for at least 6 weeks is possible, but it is associated with severe changes in pulmonary structure that doubtlessly lead to serious derangement of cardiopulmonary functions.

Animals↗
PubMed1975

The normal human thymic vasculature: an ultrastructural study.

Electron microscopy of the normal human thymus demonstrates a characteristic vascular-parenchymal relationship. The vascular lumen is always separated from the thymic parenchyma by: the endothelial cell cytoplasm, a muscular coat in arterioles and veins, the vascular basal lamina, a perivascular space containing collagen fibers and cells, the epithelial-reticular cell basal lamina and the epithelial-reticular cell cytoplasm. The width of this perivascular space is proportional to the size of the vessel it surrounds; it is wide around the vessels in the septa and at the cortical-medullary junction, but narrow around capillaries. While many cells are present in this space around larger vessels, only collagen is observed around the capillaries. Lymphocytes are the predominant cell type in the space; however, plasma cells, eosinophils, histiocytes, polymorphonuclear leukocytes, mast cells and unidentified granulated cells are also seen. The vascular complex described above may function as a blood-thymus barrier, as the initial site of exposure of the lymphocytes to circulating antigen and as the route of lymphocytes from the thymus.

Arteries↗
PubMed1975

Energized endocytosis in human erythrocyte ghosts.

The mechanism of endocytosis in resealed human erythrocyte ghosts was studied. The energy for endocytosis or micropinocytosis appears to be derived from Mg-ATP, and membrane internalization is preceded by activation of a membrane-associated Ca,Mg-ATPase and by the active efflux of Ca. Endocytosis, Ca,Mg-ATPase activity, and active Ca efflux all require the presence of Mg. Furthermore, these three phenomena, endocytosis, Ca,Mg-ATPase activity, and active Ca extrusion, all have a concentration dependence on Ca such that low concentrations stimulate and higher concentrations inhibit the phenomena. The optimal concentration of Ca is identical for endocytosis, active Ca efflux, and Ca,Mg-ATPase. Morphologic studies indicated that while active Ca efflux and activation of the Ca,Mg-ATPase activity occurred promptly upon onset of incubation, there was a significant time delay before endocytosis occurred, which suggests that endocytosis additionally involved a more slowly functioning mechanicochemical mechanism. Ruthenium red, a specific inhibitor of Ca,Mg-ATPase and Ca transport, inhibited endocytosis in a concentration-related manner. Prostaglandins E1 and E2 had no measurable effect on ghost endocytosis, active Ca efflux, or Ca,Mg-ATPase activity.

Adenosine Triphosphatases↗
PubMed1975

Oxygen toxicity in the newborn. The effect of prolonged 100 per cent O2 exposure on the lungs of newborn mice.

A comprhensive morphologic study of pulmonary oxygen toxicity was undertaken on 78 newborn mice of a single, highly inbred strain continuously exposed to 100 per cent oxygen at normal atmospheric pressure for 7 days. The survival rate was 95 per cent through the first 4 days and 75 per cent through the 7th day. Our findings indicate that response to continuous exposure to 100 per cent oxygen can be divided arbitrarily during the first 7 days into three different phases. During the first, or acute toxic, phase (which generally extends into the 3rd day of exposure), mechanisms, probably adaptive in nature, are sufficiently developed in some of the newborn animals to permit them to survive a continuous 7-day exposure. The acute toxic phase is followed by the critical, high mortality phase, which lasts 3 to 4 days. During this phase, which can be subdivided into a continuum of several stages, the changes seen in the initial, acute toxic phase may progress to more pronouced injury. If the injury is severe, massive pulmonary edema and hemorrhage occur, accounting probably for the deaths of most of the animals in previous similar experimental studies and of 25 per cent of our animals by the 7th day. The second stage of this high mortality phase, being more clearly reactive, consists of a progression of reactive mitochondrial changes, proliferation of granular pneumocytes, and a return to normal of the features of the membranous pneumocytes. The beginning of the third phase, the chronic injury and repair phase, is characterized by the appearance of fibroblasts and a concomitant moderate increase in the amount of collagen.

Animals↗