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Biomedical subjects

B F Trump

Publications and source records attributed to B F Trump.

At least 307 records · Page 17Linked to original sources

Adenocarcinoma of the kidney. II. Enzyme histochemistry of renal adenocarcinomas induced in rats by N-(4'-fluoro-4-biphenylyl)acetamide.

Activities of a broad spectrum of enzymes were studied histochemically in renal adenocarcinomas induced in young male F344 rats by chronic dietary administration of the carcinogen N(4'-fluoro-4-biphenylyl)acetamide. Enzymes included were: dehydrogenases of glucose-6-phosphate, lactate, succinate, malate, and alpha-glycerophosphate; peroxidase (catalase); glucose-6-phosphatase; alkaline and acid phosphatase; Mg2+ ATPase; 5'-nucleotidase; and aminopeptidase. Levels of enzyme activity were estimated visually and scored from 0 (not detectable) to a maximum of 5 (intense). Comparison of estimated activity for each enzyme was made between small neoplastic nodules (stage III tumors) and large adenocarcinomas (stage IV tumors) and between tumors and portions of normal proximal tubules in parenchyma of kidneys from untreated control rats. The results, which revealed nearly identical levels of activity for most enzymes in both stages III and IV tumors, suggested similar metabolic and biologic behavior of these lesions. However, when data for tumors were compared with data for normal proximal tubules, striking differences were observed consistent with: 1) a marked shift of energy metabolism from oxidative to glycolytic production of ATP, with a corresponding reduction in mitochondrial respiration; and 2) simplification of plasma membrane specializations that were possibly associated with a reduction or loss of transport function. These findings were compared with other histochemical, biochemical, and ultrastructural studies of renal adenocarcinomas in rats and man.

Adenocarcinoma↗

Post-traumatic hepatic dysfunction as a major etiology in post-traumatic jaundice.

Thirty-eight patients who had sustained acute trauma, profound hemorrhagic shock, and massive transfusion were studied prospectively to determine the predominant etiologic factors in the development of post-traumatic jaundice. An analysis of clinical and biochemical factors occurring in association with each bilirubin peak in the postoperative course found the jaundice related to transfusion and surgery in 11 instances, to sepsis and septicemia in 15 instances, and to hepatic dysfunction in 23 instances. Results indicated that admission estimates of SGOT and LDH levels, the height of the bilirubin peak and the postoperative day on which it occurs, and the white cell count and GGT at the time of the peak may be of use in the differential diagnosis. Four case reports were used to emphasize the fluctuating pattern of jaundice and the different etiologic factors that may predominate. Light and electron microscopy from three patients illustrated the structural alterations that accompany the biochemical impairment of liver function and enable a more precise appreciation of this syndrome. Hepatic dysfunction appears to be implicated in a high proportion of patients who develop post-traumatic jaundice, which frequently occurs as part of a spectrum of multiple organ failure.

Adolescent↗

Scanning electron microscopy of renal vascular casts.

The use of Cementex to form casts of the renal vascular system is described. These casts are useful in delineating the vascular microarchitecture of the kidney including that of the glomerular capillaries, but do not appear to reproducibly reflect physiological vascular tone. The postglomerular vascular system is often incompletely filled using this technique. The amount of filling can be altered by the techniques used in cast preparation. The effect of perfusion pressure, concentration of Cementex, fixation, and type of colour additive are compared with respect to the cast structure.

Animals↗

Long-term organ culture of human bronchial epithelium.

Human bronchial epithelium has been maintained in organ culture in serum-supplemented medium for 4 months. After 4 to 6 weeks in culture, various changes in morphology were apparent. There was an increase in autophagic vacuoles in mucous, ciliated, and basal cells, a reduction in the height of the columnar cells, a decrease in the number of goblet mucous cells, and an increase in cells with small mucous granules. After 3 months in culture, the basal lamina was frequently covered by 2 or 3 layers of epithelial cells consisting of nonkeratinizing squamous cells with short microvilli and small mucous granules. Less frequently, keratinizing squamous cells were seen. Differentiated epithelium incorporated precursors into macromolecules in serum-free medium, supplemented with vitamin A, at 1 week of culture. These explants exhibited changed epithelium by 2 weeks, similar to that described for epithelium in serum-supplemented medium after 4 to 6 weeks.

Bronchi↗

Binding of (3H)benzo(a)pyrene to DNA in cultured human bronchus.

The studies reported here demonstrate some of the factors affecting the binding of benzo(a)pyrene (BP) to macromolecules in cultured human bronchial mucosa. Bronchial specimens were obtained at either surgy or "immediate" autopsy from patients with and without lung cancer. Grossly normal-appearing pieces of bronchus were cultured in a chemically defined medium, i.e., CMRL 1066 medium containing 1 mug insulin per ml, 0.1 mug beta-retinyl acetate per ml,, 0.1 mug hydrocortisone hemisuccinate per ml, 2 mM L-glutamine, 100 units penicillin G per ml, and 100 mug streptomycin per ml. After 7 days, explant cultures were exposed to [3H]BP, usually for 24 hr, and then binding to total cellular macromolecules was studied by autoradiography, and binding to DNA was measured following isolation of DNA from bronchial mucosal cells. The extent of binding of [3H]BP was dependent on dose of BP, length of exposure to [3H]BP, and temperature. By autoradiography, bronchial epithelial cells bound more [3H]BP than stromal fibroblasts. Both 7,8-benzoflavone and butylated hydroxytoluene appeared to reduce the level of [3H]BP bound to DNA, while nicotine apparently did not alter the level of binding. These studies demonstrate that the bronchial mucosa, an important human cancer target tissue, has the capability to form metabolites of BP which bind to macromolecules including DNA. In addition, 7,8-benzoflavone and butylated hydroxytoluene, both known to alter the microsomal metabolism of BP, reduce the level of [3H]BP bound to DNA.

Benzopyrenes↗

Studies on the subcellular pathophysiology of ischemia.

The loss of ability to synthesize adenosine triphosphate (ATP) by mitochondria in ischemic cells even in a favorable medium correlates with the loss of cell viability. The early lesion at the molecular level needs further investigation but appears to involve an increased permeability of the mitochondrial membrane possibly promoting proton leak and obviating oxidative phosphorylation. The nature of this leak could involve changes in phospholipid-protein interactions, especially since the early release of free fatty acids and changes in phospholipid composition occur.

Adenosine Triphosphate↗

A clinicopathologic study of hepatic dysfunction following shock.

Nineteen patients who had profound hypotensive shock were studied to correlate the light and electron microscopic appearances of the liver with the clinical and biochemical evidence of hepatic dysfunction. Despite the multiple etiologic factors that can result in jaundice in these patients, a fluctuating pattern occurs which enables the correlation of a bilirubin peak with the predominating etiologic factor. Immediately after shock, there was enzymatic and light and electron microscopic evidence of hepatocellular damage, resulting in a jaundice peak on the eighth to tenth day after the shock episode. This was followed by repair and regeneration of the liver as well as an increase in cholestatic enzyme levels. Later, bilirubin peaks occurred when hepatocellular function was further decreased or overloaded against this background of dysfunction related to the episode of shock. Recovery of hepatic function could continue or be delayed by intercurrent disease, particularly systemic infection. Support of hepatic function, similar to that available for pulmonary and renal failure may, in the future, be used to effect the prognosis of these patients.

Bilirubin↗

Observations on small granule cells in adult human bronchial epithelium and in carcinoid and oat cell tumors.

Small granule cells are described in the segmental bronchi of adult humans. Rarely, these cells were seen abutting the lumen of the airway. A luminal location has been described for these cells in the bronchial epithelium of human fetuses and neonates and it is suggested that luminal small granule cells may be a rare, although normal component of the adult human bronchial epithelium. The dense core granules of the small granule cells stained intensely with phosphotungstic and at low pH suggesting that they contain glycoprotein. Granules present in a carcinoid and an oat cell tumor stained similarly. The role of the small granule cell in the genesis of bronchial carcinoid and oat cell tumors is recognized.

Adenocarcinoma, Bronchiolo-Alveolar↗

Histologic fixatives suitable for diagnostic light and electron microscopy.

The merits of formaldehyde, formaldehyde-glutaraldehyde combinations, and glutaraldehyde in phosphate buffers have been compared as fixatives that will give easy and satisfactory preservation of tissues for routine automated histologic processing and yet keep them suitable for electron microscopical studies after prolonged storage at room temperature. We recommend a combination of 4% commercial formaldehyde and 1% glutaraldehyde in a buffer of 176 mOsm/liter. Tissue sections should not exceed 3 mm in width, and tissues to be examined by electron microscopy should be taken from the outside of the tissue sections. All special stains performed at light microscopical level gave satisfactory results. The fixative should be stored at 4 C and is stable for at least three months. The superior cross-linking features of glutaraldehyde are retained, while the concentration of glutaraldehyde is low enough not to substantially obscure the PAS reaction.

Animals↗

Abnormal cilia in human bronchial epithelium.

Abnormal cilia are a common occurrence in human bronchial epithelium. Bronchial specimens were obtained at surgery or at "immediate autopsy" from patients with neoplastic and nonneoplastic diseases; these patients included smokers and one known nonsmoker. Areas of bronchial epithelium far removed from the tumor mass were studied. Ciliary abnormalities fell into four major categories: (1) cilia with a single axoneme and excess cytoplasmic matrix; (2) compound cilia; (3) intracytoplasmic microtubular doublets; and (4) cilia within periciliary sheaths.

Adenocarcinoma↗

Cellular pathophysiology of hepatitis.

This paper represents an analysis of the subcellular events that occur in the human liver in viral hepatitis. They involve both hepatocytes and sinusoidal lining cells, including Kupffer cells. We present a new hypothesis concerning the sequence of events that occurs in hepatic parenchymal cells. These events begin with a virus-hepatocyte interaction that involves primary damage to the cell membrane. This is assumed to trigger a complex sequence of events that results in the characteristic hepatocellular impairment of this disease. These events center around ionic shifts resulting from an altered plasma membrane, leading to interactive events in hepatocyte organelles, mostly reversible, but resulting in the characteristic hepatocellular impairment.

Bile Ducts↗

Cellular and subcellular effects of ischemia on the pancreatic acinar cell: in vitro studies of rat tissue.

Rat pancreatic slices were incubated at 37 degrees C in vitro, in order to determine if complete ischemia would reproduce the subcellular alterations seen in human pancreatic acinar cells following shock. The ultrastructural alterations observed were similar to those seen in humans and in animal models of hypovolemic shock. These changes ranged from dilated endoplasmic reticulum and swollen mitochondria (reversible changes) to mitochondrial flocculent densities and later stages (evidence of cell death). In this in vitro study the pancreas remained in an apparently reversible stage longer than liver, heart, kidney, and brain treated similarly. However, once the pancreatic cells died, necrotic breakdown occurred very rapidly, perhaps due to intracellular release of lysosomal and zymogen granule hydrolases.

Animals↗

Studies on the pathogenesis of ischemic cell injury. II. Morphological changes of the pars convoluta (P1 and P2) of the proximal tubule of the rat kidney made ischemic in vivo.

The pars convoluta of the proximal tubules of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of complete ischemia produced by clamping of the aorta. The same ischemia periods were also examined after 24 hrs of blood reflow. It was found that the vast majority of the cells of pars convoluta survived 60 min of ischemia as seen after 24 hrs of reflow. The following pattern of changes were observed at time intervals up to 60 min: progressive clumping of chromatin, progressive distortion of microvilli with bleb formation, increasing dilatation and finally vesiculation of rough-surfaced endoplasmic reticulum and initially condensation and later high amplitude swelling of mitochondria. It is concluded that these subcellular changes are compatible with cell survival. Also tubule cells containing swollen mitochondria with small flocculent densities are potential candidates for survival. 120 min of ischemia was associated with marked mitochondrial swelling with large flocculent densities, severe cell damage and necrosis and was not compatible with cell survival. A working hypothesis is presented relative to the pathogenesis of acute renal failure caused by complete ischemia.

Acute Kidney Injury↗

Studies on the pathogenesis of ischemic cell injury. III. Morphological changes of the proximal pars recta tubules (P3) of the rat kidney made ischemic in vivo.

The pars recta of the proximal tubule of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of ischemia produced by clamping of the aorta. Also the effects of 24 hrs of blood reflow following the same ischemia periods were determined. The maximal changes occurring after ischemic periods of up to 60 min included: marked cell swelling, swelling of the inner compartments of the mitochondria, swelling of the endoplasmic reticulum and of microvilli, pronounced chromatin clumping in the nuclei and distortion of the Golgi apparatus. These cell changes were reported to be reversible in the previous paper of this series. After 24 hrs of blood reflow it was found that with increasing periods of primary ischemia, ranging from 15 to 120 min, an increasing number of pars recta tubules cells were undergoing necrosis. Theses findings indicate that some additional mechanism other than the initial ischemia per se must be responsible for the progressive cellular damage leading to the necrosis. This is in contrast to the pars convoluta of the proximal tubule, which does not undergo further degenerative changes after the primary ischemia has been ended. The "no reflow" phenomenon may satisfactorily explain the necrosis seen in the pars recta segments following various periods of ischemia after 24 hrs of arterial renal reflow.

Animals↗

Amorphous calcium precipitations in human aortic valve.

Spheroidal, granular, and fibrillar particles were observed in human aortic valve calcifications. Spheroids were similar to amorphous calcium phosphate shown previously in syn thetic preparations and in bone. The frequent coexistence of needle shaped hydroxyapatite crystals with granular and fibrillar particles suggests that the latter are also amorphous calcium phosphate and may be precursors of hydroxyapatite. All three types of particles had a tendency to form laminated and spherular secondary and failed to give a crystalline pattern by electron diffraction.

Aging↗