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Biomedical subjects

R Rubenstein

Publications and source records attributed to R Rubenstein.

90 records · Page 5Linked to original sources
PubMed1979

Squamous cell carcinoma of the soft palate.

We performed a retrospective study of 106 patients with carcinoma of the soft palate who were treated at two university hospitals. Computer analysis using a new interactive data base program called MING was made to determine Berkson-Gage survival and Gehan tests of statistical significance. Statistically significant associations with an increased survival included the following: smaller lesions, a clinically negative neck examination. well- and moderately well-differentiated histopathologic features, radiation therapy dose of less than or equal to 6,300 rads, absence of a simultaneous primary, and surgical salvage. No statistically significant differences were seen with age, sex, stage, or the number of days during which patients were treated with radiation therapy. There appears to be a need for a prospective, multi-institutional, randomized therapy study to solidify treatment policy. Consideration should be given to combine surgery-radiation vs radiation therapy alone.

Adult↗
PubMed1976

Membrane transport properties of bovine articular cartilage.

The thermodynamic parameters which define transport of nonelectrolytes through bovine articular cartilage membranes were evaluated. H3HO, glucose and sucrose were used as permeants. These solutes permeate more readily through the upper layers (near the articular surface) than through the denser deeper layers approaching bone. Cartilage is similar in many respects to a swollen cellulose gel. Viscous-flow contributes importantly to transport within cartilage thus greatly enhancing the movement of nutrients.

Animals↗
PubMed1975

Fecal impaction following methadone ingestion simulating acute intestinal obstruction,.

A hitherto unreported clinical entity, namely fecal impaction following methadone ingestion simulating acute intestinal obstruction, is described. Five cases admitted to the Surgical Service of the Beth Israel Medical Center in New York City are discussed. The nature and pathogenesis of the obstruction are analyzed and a suggested method of managing these cases is presented. It is emphasized that with expansion and increasing acceptance of Methadone Maintenance Treatment Programs, the number of such cases will increase. It is thus important that physicians become aware of the existence of this syndrome since involvement in methadone maintenance may be a life-long commitment for persons involved, thus increasing the incidence of the complication. It is also imperative to avoid unnecessary, and possibly harmful surgical intervention in such cases.

Adult↗
PubMedDate not supplied

Scrapie strain infection in vitro induces changes in neuronal cells.

PC12 cells, in the presence of nerve growth factor (NGF), support replication of the mouse-derived scrapie strains 139A and ME7, with the former yielding 100-1000-fold higher levels of infectivity. Infectivity remained cell-associated and cells did not show any gross morphological alterations, although changes were observed by electron microscopy in the form of an increased number of lipid droplets in 139A-infected cultures. Analysis of phospholipid metabolism in 139A infected cells indicated that scrapie replication did not change the inositol phosphate levels, but did stimulate phosphoinositide synthesis. Replication was not detected in PC12 cells infected with either the hamster-derived 263K or rat-derived 139R scrapie strains. Since scrapie-infected cultures did not exhibit cell death or any gross changes, any scrapie-induced effects would probably be manifested in nonvital cellular functions. When compared to controls, infection with the 139A scrapie strain resulted in decreased activity of the cholinergic pathway-related enzymes, as well as the GABA synthetic pathway; however, the adrenergic pathway was unaffected by scrapie infection. The effects of the 139A scrapie strain on the cholinergic system appeared to be dose-dependent and were first detected prior to the detection of scrapie agent replication in these cells. No neurotransmitter-related enzymatic changes were detected in 263K- or 139R-infected PC12 cells. The enzymatic changes observed in ME7-infected PC12 cells and in Chandler agent-infected mouse neuroblastoma cells suggest that the significant changes in neurotransmitter levels in cultures exhibiting low infectivity titers must involve factors other than, but not excluding, replication of the agent. The role of additional factors is also suggested in studies of protein kinase C activity in 139A- and 139R-infected PC12 cells. These studies emphasize the value of the PC12 cell model system in examining the scrapie strain-host cell interaction and, in addition, support the concept of variation among scrapie strains.

Acetylcholinesterase↗
PubMedDate not supplied

The role of microglial cells and astrocytes in fibrillar plaque evolution in transgenic APP(SW) mice.

Ultrastructural reconstruction of 27 fibrillar plaques in different stages of formation and maturation was undertaken to characterize the development of fibrillar plaques in the brains of human APP(SW) transgenic mice (Tg2576). The study suggests that microglial cells are not engaged in Abeta removal and plaque degradation, but in contrast, are a driving force in plaque formation and development. Fibrillar Abeta deposition at the amyloid pole of microglial cells appears to initiate three types of neuropil response: degeneration of neurons, protective activation of astrocytes, and attraction and activation of microglial cells sustaining plaque growth. Enlargement of neuronal processes and synapses with accumulation of degenerated mitochondria, dense bodies, and Hirano-type bodies is the marker of toxic injury of neurons by fibrillar Abeta. Separation of amyloid cores from neurons and degradation of amyloid cores by cytoplasmic processes of hypertrophic astrocytes suggest the protective and defensive character of astrocytic response to fibrillar Abeta. The growth of cored plaque from a small plaque with one microglial cell with an amyloid star and a few dystrophic neurites to a large plaque formed by several dozen microglial cells seen in old mice is the effect of attraction and activation of microglial cells residing outside of the plaque perimeter. This mechanism of growth of plaques appears to be characteristic of cored plaques in transgenic mice. Other features in mouse microglial cells that are absent in human brain are clusters of vacuoles, probably of lysosomal origin. They evolve into circular cisternae and finally into large vacuoles filled with osmiophilic, amorphous material and bundles of fibrils that are poorly labeled with antibody to Abeta. Microglial cells appear to release large amounts of fibrillar Abeta and accumulate traces of fibrillar Abeta in a lysosomal pathway.

Alzheimer Disease↗
PubMedDate not supplied

Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt-Jakob disease in humans.

BACKGROUND: Solid evidence from experimentally infected animals and fragmentary evidence from naturally infected humans indicate that blood may contain low levels of the infectious agent of Creutzfeldt-Jakob disease (CJD), yet blood components have never been identified as a cause of CJD in humans. STUDY DESIGN AND METHODS: Blood components and plasma fractions were prepared from the pooled blood of mice that had earlier been infected with a mouse-adapted strain of human transmissible spongiform encephalopathy (TSE). Infectivity bioassays were conducted in healthy mice, and the brains of all assay animals dying during the course of the experiments were examined for the presence of proteinase-resistant protein. RESULTS: Infectivity in the blood during the preclinical phase of disease occurred in the buffy coat at infectious unit (IU) levels between 6 and 12 per mL and was either absent or present in only trace amounts in plasma and plasma fractions. Infectivity rose sharply at the onset of clinical signs to levels of approximately 100 IU per mL of buffy coat, 20 IU per mL of plasma, 2 IU per mL of cryoprecipitate, and less than 1 IU per mL of fractions IV and V. Plasma infectivity was not eliminated by either white cell-reduction filtration or high-speed centrifugation. Approximately seven times more plasma and five times more buffy coat were needed to transmit disease by the intravenous route than by the intracerebral route. CONCLUSION: Epidemiologic evidence of the absence in humans of disease transmission from plasma components can probably be explained by 1) the absence of significant plasma infectivity until the onset of symptomatic disease, and comparatively low levels of infectivity during the symptomatic stage of disease; 2) the reduction of infectivity during plasma processing; and 3) the need for at least five to seven times more infectious agent to transmit disease by the intravenous than intracerebral route. These and other factors probably also account for the absence of transmission after the administration of whole blood or blood components.

Animals↗
PubMedDate not supplied

The nature of the unconventional slow infection agents remains a puzzle.

Unconventional slow infections are progressive transmissible degenerative disorders of the central nervous system. The human diseases belonging to this group are Creutzfeld-Jakob disease, kuru, and Gerstmann-Straussler syndrome. Scrapie, transmissible mink encephalopathy, chronic wasting disease of mule deer and elk, and the recently discovered bovine spongiform encephalopathy are similar diseases found in animals. Unusual characteristics of the unconventional slow infections clearly distinguish these disorders from conventional infections. These include: unusually long incubation periods (from months to years); progressive CNS degeneration with characteristic histopathological lesions; the lack of an immune or inflammatory response; unconventional biological and physical properties of the etiologic agents. There has been considerable controversy concerning the nature of the causative agent. The 3 main hypotheses, virus, virino, and modified host protein, are reviewed relative to their ability to explain the properties of the agent and the unusual characteristics of the disease process. The discovery of an abnormal structure, termed scrapie associated fibrils (SAF) and an abnormally modified 33-37 kDa host-encoded glycoprotein unique to unconventional slow infections opened new areas of intense interest and investigation. SAF are abnormal filamentous structures which copurify with infectivity and possess characteristics of "amyloids." The major component of SAF is the host-encoded scrapie-specific protease resistant glyco-protein. Considerable data has accumulated on the biochemistry, immunology and molecular biology of this host coded scrapie protein. The relationship of SAF and the scrapie-specific protein to the infectious agent is discussed in the context of each of the "nature of the agent" hypotheses.

Animals↗
PubMedDate not supplied

Bovine spongiform encephalopathy: an overview.

Bovine spongiform encephalopathy (BSE), widely known as "mad cow disease," is a chronic, degenerative disease affecting the central nervous system of cattle. Worldwide, there have been more than 180,000 cases since the disease was first diagnosed in 1986 in Great Britain. Bovine spongiform encephalopathy has had a substantial impact on the livestock industry in the United Kingdom. The disease has also been confirmed in native-born cattle in Belgium, Denmark, France, Ireland, Luxembourg, Liechtenstein, The Netherlands, Northern Ireland, Portugal, and Switzerland. However, over 95% of all BSE cases have occurred in the United Kingdom. Bovine spongiform encephalopathy is not known to exist in the United States.

Animals↗
PubMedDate not supplied

Immunodiagnosis of prion disease.

The immunodiagnosis of prion diseases is of critical importance due to the transmissibility of these conditions and their fatal prognosis. A panel of monoclonal and polyclonal antibodies have been generated for use in the study and diagnosis of these diseases. This manuscript describes the generation and characterization of these antibodies as well as their diagnostic application.

Adult↗