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Biomedical subjects

B Wilson

Publications and source records attributed to B Wilson.

At least 235 records · Page 13Linked to original sources
PubMed1980

Studies on the retina and the pigment epithelium in hereditary canine ceroid lipofuscinosis. III. Morphologic abnormalities in retinal neurons and retinal pigmented epithelial cells.

Studies of the retina in 6- and 22-month-old English setters with progressive blindness, ataxia, and muscle weakness demonstrated a marked accumulation of abnormal cytosomes within neurons and retinal pigmented epithelial cells. Ganglion cells contained abundant cytosomes with evenly spaced stacks of membranes; bipolar and amacrine cell cytosomes consisted of dense, amorphous material with closely spaced configurations of light and dark lines; cytosomes within photoreceptor cells contained faintly staining curved profiles. All three cytosomes resembled those previously reported in brain neurons of CCL dogs. In retinal pigmented epithelial cells, there were prominent accumulations of lamellar fragments, either free in the cytoplasm or incorporated into melanin granules. These retinal abnormalities are likely to be related to deficiences of peroxidase and defects of lipid peroxidation. The pathologic and biochemical changes seen in these dogs are similar in many respects to those reported in human patients with Batten disease. As such, these dogs provide a convenient model for the study disease mechanisms and for therapeutic approaches to blindness in Batten disease.

Animals↗
PubMed1979

Induction of allergic encephalomyelitis in rhesus monkeys treated with anti monkey thymocyte sera.

Treatment with rabbit anti-moneky thymus cell sera whether limited (3 days) or extensive (15 days), did not alter the development of experimental allergic encephalomyelitis (EAE) in rhesus monkeys challenged with myelin basic protein or central nervous system tissue (CNS) when compared to similarly challenged control monkeys treated with normal rabbit serum. No consistent difference in disease incidence or intensity as measured by incubation period, neurologic signs or CNS pathology was observed between experimental and control monkeys. This finding is in contrast to previous reports on the efficacy of ATS treatment in prevention of EAE in rodents.

Animals↗
PubMed1978

Nosocomial meningitis and bacteremia due to contaminated amphotericin B.

Nosocomial Gram-negative bacillary meningitis and bacteremia occurred in a patient who was receiving intrathecal and intravenous amphotericin B. An epidemiologic investigation found the amphotericin B to be contaminated with Enterobacter agglomerans, Pseudomonas fluorescens, and P aeruginosa. These contaminants were traced to a lot ot sodium phosphate buffer that was added to all intrathecal and intravenous amphotericin B preparations. The phosphate buffer underwent prolonged storage at room temperature and was not subject to terminal sterilization nor sterility testing. This parenteral admixture prepared in the hospital is now steam autoclaved and sterility tested before use.

Adult↗
PubMed1977

Premature chromosome condensation and cell cycle analysis.

The application of the phenomenon of premature chromosome condensation for cell cycle analysis in HeLa and CHO cells has been examined. Random populations of HeLa and CHO cells pulse labelled with H3-TdR were separately fused with mitotic HeLa cells using U.V. inactivated Sendai virus. The resulting prematurely condensed chromosomes (PCC) were scored and classified into G1, S and G2-PCC on the basis of both morphological and autoradiographic data, The results of this study indicated that the G1, S and G2 phase cells are equally susceptible to virus-induced fusion with mitotic cells and subsequent induction into PCC. Hence the PCC method for cell cycle analysis is both practical and accurate. This study also revealed that the process of chromosome decondensation initiated during the telophase of mitosis continues throughout the G1 period reaching an ultimate state of decondensation by the end of G1, at which point the fusion of such cells with those in mitosis yield PCC with the most diffused morphology instead of the discrete single stranded structures characteristic of early G1-PCC. Thus, the decondensation of chromatin during G1 appears to be a prerequisite for the subsequent initiation of DNA synthesis.

Cell Division↗
PubMed1976

Casein-induced murine amyloidosis: amyloid and immunoglobulin production and proliferative capacity of splenocytes.

We have examined some aspects of lymphocyte and macrophage function in experimental murine amyloidosis. Casein-induced murine amyloidosis is a good model for studying secondary human amyloidosis while myeloma-associated murine amyloidosis is a poor model for human myeloma-associated amyloidosis. The amyloid of casein-induced and myeloma-associated murine amyloidosis cross-reacted immunologically. Neither form of amyloidosis was associated with L chain fragments or excess L chain production. Cellular immunologic reactivity of casein-induced amyloidotic mice, as assessed by lymphocyte transformation with mitogens, was abnormal using spleen lymphocytes but completely normal when thymus and peripheral blood lymphocytes were examined. The depressed activity could be attributed to splenic amyloid deposits. Intracellular amyloid was detected in the spleens of casein-injected mice prior to extracellular amyloid deposits. Amyloid containing cells could also be cultured from the spleen in a much higher proportion than that found in vivo. These cells may represent a subpopulation committed to amyloid synthesis.

Amyloid↗
PubMed1975

Experimental murine amyloidosis: a model system for studying amyloid formation.

Myeloma-associated and casein-induced murine amyloidosis were used as models to study the role of lymphocytes and macrophages in amyloid formation. Amyloidosis occurred rarely and in small amounts in Balb/C mice with immunoglobulin (Ig)-producing myeloma tumours but large amounts could be induced by injections of casein. Fluorescent staining of both forms of amyloid deposits by means of anti-casein- and anti-myeloma-amyloid antibodies indicated that they either crossreacted or coexisted. Nor abnormality of Ig biosynthesis was detected in amyloidosis, suggesting that abnormal degradation was responsible for production of the Ig form of amyloid. Although spleen lymphocytes of casein-injected mice with amyloidosis demonstrated diminished cellular immunologic responses, this did not indicate generalized immunologic incompetence. The non-Ig form of amyloid in casein-injected mice was shown to be produced by macrophages, and a technique was developed for increasing the yield of amyloid-containing cells.

Amyloid↗
PubMed1975

Immunoglobulin biosynthesis in myeloma-associated and casein- and endotoxin-induced murine amyloidosis.

Amyloidosis was induced in C57BL mice by daily injections of casein and in BALB/c mice by daily injections of endotoxin. There was no obvious disorder of immunoglobulin biosynthesis by spleen lymphocytes in these mice either before, during the development of, or in the amyloidotic stage. The pattern of immunoglobulin synthesis, assembly, and secretion was unaltered, the relative amount of heavy and light chains produced was normal, and there was an absence of immunoglobulin polypeptide chain fragments. Small amounts of amyloid were present in only 1 of 19 BALB/c and C3H mice (the IgG2a producing MOPC 173 tumor) bearing immunoglobulin-producing myeloma tumors and variants of these tumors. There was no relationship between excess light chain production by tumor plasma cells or spleen lymphocytes and the development of amyloidosis and there were no light chain fragments demonstrable. Antiserum prepared against casein-induced amyloid cross-reacted by immunofluorescence with the amyloid present in the MOPC 173 tumor-bearing mice, indicating the presence of common antigenic determinants in these two forms of amyloid. Attempts to study the biosynthesis of amyloid with incorporation of radioactively labeled amino acids were unsucessful.

Amyloid↗