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B W Volk

Publications and source records attributed to B W Volk.

At least 19 recordsLinked to original sources
PubMed1993

Morphologic basis for loss of regulated insulin secretion by isolated rat pancreatic islets.

Laboratories engaged in secretory studies of rat pancreatic islets often encounter high baseline insulin secretion with poor secretory response to secretagogues, such as glucose. The specific morphologic abnormalities that accompany this unregulated release have not been described. We isolated islets comparing two approaches. Both used stationary digestion with collagenase. In method I, we distended the biliary duct extracorporeally with collagenase and minced the pancreas after a 28 min digestion (37 degrees C). In method II, we distended the pancreas intracorporeally and digested for 40 min without mincing. Both methods utilized a similar collagenase concentration (2 micrograms/ml in Hank's balanced salt solution (HBSS). Both methods yielded over 300 islets/rat. Islets from both methods appeared intact, when viewed under the dissecting microscope. We found that adequate secretion from incubated islets was evoked with method I, i.e., low basal insulin levels at low glucose (3.3 mM), tripling at 11.0 mM glucose, and nearly quadrupling in response to higher glucose (16.7 mM). In contrast, method II was characterized by high basal levels without response to higher glucose. Ultramicroscopic examination of islet B cells in method I revealed normal cytological features, while B cells in method II showed marked degranulation, profiles of swollen endoplasmic reticulum, and swollen mitochondria. Morphometric analysis of B cells confirmed quantitatively a decrease in secretory granule density and mitochondrial enlargement in method II compared to method I. Anatomic changes, largely confined to the B cells of islets may account for functional alterations of responses. Defects cannot be predicted from gross appearance of islets.

Animals↗
PubMed1977

Light and electron microscopic studies of "nude" mice CNS after subcutaneous administration of the E variant of the encephalomyocarditis (EMC) virus.

Sixteen 3 month old "nude" mice, 24 of their litter mates and 30 Swiss mice were injected subcutaneously with 0.1 ml suspension of the E variant of the encephalomyocarditis (EMC) virus. While the mortality rate of the litter mates and Swiss mice during 5-7 days after inoculation was more than 40%, none of the "nude" mice died during the experiment. The surviving animals were sacrificed at 24 h intervals from day one to seven days after injection. Brain suspensions assayed for the presence of the virus yielded significant titers at 24 h in all groups, which increased during 7 days. The litter mates and Swiss mice showed proliferation of lymphocytes and microglial cells in the perivascular areas of the brain during the fifth to the seventh day. The "nude" mice, on the other hand, displayed no perivascular lymphocytic infilteration during the same periods. Ultrastructurally, all groups showed aggregates of ribosomes in the cytoplasmic matrix on the third day, which became enlarged in size on the 5th day. At 7 days, both litter mates and Swiss mice showed an increased number of necrotic cells, while these changes were not observed in the "nude" mice. These findings suggest that the high mortality rate in immunologically normal mice was related to the efforts of T cells to eliminate virus-infected cells and to produce extensive necrosis, while T cell-depleted animals showed good survival rates.

Animals↗
PubMed1977

Modification of streptozotocin-induced diabetes in rats by pretreatment with cortisone.

Cortisone pretreatment considerably enhances the mortality of young, male, streptozotocin-injected Holtzman rats. In those that survive, cortisone pretreatment decreases the ensuing hyperglycaemia, extends the period during which streptozotocin-induced B cell damage can be observed from less than two to as much as four to seven days and permits the persistence of poorly granulated B cells in such animals. These effects are at least partially attributable to a cortisone-induced augmentation of the total B cell mass. Compared with the high degree of protection against alloxan-induced damage afforded the pancreatic B cells of cortisone-pretreated rabbits, the protective effect of cortisone against B cell destruction in streptozotocin-injected rats is thus much more limited in scope. Species differences as well as differing pathogenetic mechanisms may account for these results.

Animals↗
PubMed1977

Gaucher disease in mice induced by conduritol-B-epoxide: morphologic features.

Morphologic changes were studied in mice in which Gaucher disease was induced by the administration of conduritol-B-epoxide. Sixteen newborn Swiss mice received a daily subcutaneous dosage of 100 mg/kg of body weight of conduritol-B-epoxide from one day after birth to 28 days. Light microscopically, no Gaucher cells were noted in the viscera, bone marrow, and the CNS during this study. Ultrastructurally, the spleen and liver showed irregular granules and fibrils in histiocytes and Kupffer cells during the second to fourth week. In the CNS, the neurons showed fibrils and tubular structures within the cisternae of the endoplasmic reticulum at three to four weeks. During the fourth week, they frequently contained well-organized inclusion bodies that were membrane-bound and contained tubular structures that varied from 250 to 500 A in diameter. These inclusion bodies were similar to Gaucher bodies seen in human cases.

Animals↗
PubMed1976

Ultrastructure and biochemical studies of rat CNS and viscera after subcutaneous injection of chlorphentermine.

Ultrastructural and biochemical studies were carried out on three groups of experimental models which were induced by a single subcutaneous daily dose of 10 to 40 mg./kg. body weight of chlorphentermine hydrochloride. The first group consisted of 20 young adult rats which were sacrificed at intervals of from one to four weeks. The liver and lungs showed concentrically arranged memberanous bodies in the hepatocytes and alveolar cells during the first week after the first injection, while the CNS and pancreas showed no ultrastructural alterations. During the fourth week, the pancreas displayed abnormal cytoplasmic inclusion bodies in the A and B cells of the islets of Langerhans as well as in the exocrine portion. The brain showed various neuronal alterations at four weeks which consisted of irregular dense bodies to well-developed membranous structures which were similar to those of Tay-Sachs disease. Biochemically, thin layer chromatograms showed that the major ganglioside fraction in the brain at four weeks had an RF value similar to that of GM1-ganglioside. In an analysis of the total N-acetyl neuraminic acid the brains in the experimental group contained 90.9% GM1-gandlioside as compared with 44% in the controls. The total and fractions of phospholipids in the brains and livers of the experimental animals were within normal limits.

Animals↗
PubMed1976

Nodular intercapillary glomeruloscerosis in diabetes secondary to chronic calcific pancreatitis.

Nodular (specific) intercapillary glomerulosclerosis (Kimmelstiel-Wilson) was found at autopsy in a 47-year-old man who had been diabetic for 20 years. The family history for this disease had been negative. Both the clinical course and the autopsy findings strongly suggest that this patient's diabetes was secondary to chronic fibrocalcific pancreatitis. This is only the fourth recorded case of histologically documented nodular glomerulosclerosis occurring in a patient with pancreatogenic diabetes.

Calcinosis↗
PubMed1976

Fine structure of pancreas in cortisone-treated guinea pigs and rabbits.

Twenty-eight male rabbits and 28 male guinea pigs received daily intramuscular injections of cortisone acetate for four to 31 days (rabbits, 5 mg/kg; guinea pigs, 10 mg/animal). Moderate hyperglycemia ensued. Insulin concentrations of the pancreatic tissue varied but were higher in cortisone-treated animals than in untreated controls. In rabbits, degranulation of beta cells, hyperplasia of islets, and proliferation of ductular structures were the major light microscopic findings. Ultrastructural studies suggested that beta cell neogenesis took place mainly within pre-existing islets but probably also within ductular structures. Mixed (acinar-islet) cells were not identified. In guinea pigs, ductular proliferation was not noted, and beta cell neogenesis appeared to take place exclusively within preexisting islets and islet cell nests. In both species, cells of several types contained glycogen deposits.

Animals↗
PubMed1975

Ultrastructural alterations of tissue cultures from human fetal brain infected with the E variant of EMC virus.

Explant outgrowths from human fetal brain were infected with 104 plaque forming units of the E variant of the encephalomyocarditis virus. Ultrastructurally, the majority of the cultured cells were astrocytes containing a moderate amount of glial fibrils. The earliest alterations at 44 hrs after infection of the culture consisted of dilatation of the rough endoplasmic reticulum (ER) and moderate enlargement of the mitochondria with increased density of their matrix. Twenty hours thereafter, increased amounts of the rough ER and of free ribosomes were observed in the infected cells. This was followed by aggregates of larger dense particles which developed into a parallel lattice-like pattern within the cytoplasm, presumably presenting viral particles, without obvious cytonecrosis. The present observations of the continuous development of the crystalloid formation of the virus within the cytoplasmic matrix as well as the mode of formation of the free ribosomes adjacent to the ER support the previous hypothesis that, after the uptake of the virus into the cytoplasmic matrix, it associates with the ER, where production of viral RNA polymerase and of viral RNA is initiated.

Astrocytes↗
PubMed1975

The gangliosidoses.

The gangliosidoses are hereditary diseases with a recessive mode of inheritance and are caused by a genetically induced enzymatic block, which results in the accumulation of gangliosides in various tissues of the body, mainly in the brain. Although Tay-Sachs disease, the most commonly occurring of the gangliosidoses, has been known for nearly 100 years, additional variants of ganglioside "storage" disorders have been discovered during the past 15 years. Considerable progress in the knowledge of these disorders has been made with the advent of electron microscopy and with the elaboration of new biochemical and enzyme-chemical techniques. At the present the gangliosidoses are not amenable to therapy. Therefore the foreseeable future the pragmatic approach involves identification of the high-risk pregnancy and antenatal diagnosis.

Axons↗
PubMed1975

EMC virus and cultured human fetal pancreatic cells. Ultrastructural observations.

Tissue cultures of pancreatic acinar cells of seven human fetuses were infected with either the M or the E variant of the encephalomyocarditis (EMC) virus. Between the third and fifth days after infection, severe ultrastructural damage was noted. Margination, condensation, and fragmentation of the nuclear chromatin and the appearance of numerous cytoplasmic vesicles filled with finely granular material were the major changes observed. Viral particles were not identified. One hundred plaque-forming units (PFU) were sufficient to induce these alterations with the M variant while 10,000 PFU were needed to obtain the same results with the EMC-E virus. The described lesions are qualitatively similar to those induced in vivo in experimental CD-1 mice infected with the virus.

Cell Nucleus↗