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Biomedical subjects

O M Pitts

Publications and source records attributed to O M Pitts.

At least 19 recordsLinked to original sources
PubMed1995

Con A cytotoxicity: a model for the study of key signaling steps leading to lymphocyte apoptosis in AIDS?

Lymphocytes respond to mitogens, viruses and other activation agents with hydrogen peroxide or reactive oxygen bursts which may originate at or near the cell membrane. It has been shown that a very small increase in the ratio of Con A cells results in a rapid switchover from mitogenicity to cytotoxicity. It is hypothesized that the change from mitogenicity to cytotoxicity correlates with the strength and duration of the hydrogen peroxide or reactive oxygen bursts which in turn depends on the number of molecules of the activation agent bound per cell. This hypothesis is presented and discussed in the context of the apoptosis (programmed cell death) and pro-oxidant-antioxidant hypothesis of CD4+ T-cell and B-cell subpopulation depletion in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1993

A reconsideration of the measles-adherent leukocyte phenomenon and multiple sclerosis.

Some studies have shown that more mononuclear leukocytes (MNLs) from multiple sclerosis (MS) patients adhere to cells persistently infected (PI) with measles virus than do MNLs from controls. Some studies have shown no difference in adherence. It is suggested that the conflict between studies is merely technical. The net effect of this conflict has been to obscure the possibility of cell surface differences which underlie this adherence phenomenon and discourage further investigation of them. Given the current interest in the molecular basis of cell-cell adhesion and the new methods and reagents available to study it, the problem of identifying cell surface differences between normal and MS leukocytes can now be more readily approached. An investigation of the MS MNL cell surface using these new methods is suggested.

Cell Adhesion↗
PubMed1991

Astrocytes: a possible primary site for colchicine-mediated neurotoxicity in the rat striatum.

Ultrastructural changes in rat astrocytes including endfoot swelling and rupture of plasma membranes were seen as early as 1 h after injection of 6.0 micrograms colchicine (CO) into the striatum. Significant change in neuronal morphology was not seen by 24 h. Astrocytes may therefore be primary targets for CO-mediated damage, which then may have secondary neurotoxic consequences.

Animals↗
PubMed1988

Retrovirus induced motor neuron degeneration.

Neurotropic retroviruses are capable of infecting and altering the function of dividing populations of neuron-like cells such as the PC-12 cell line. However, histological, immunohistochemical, and ultrastructural studies have failed to implicate direct infection of neurons by MuLV as the etiologic mechanism responsible for MuLV induced neurodegenerative disease. Indirect mechanisms such as the physical or biochemical disruption of endothelial cell basement membranes or the production of toxic cytokines by virus infected cells may play a role in the development of retrovirus induced neurodegeneration.

Animals↗
PubMed1987

Ultrastructural changes associated with retroviral replication in central nervous system capillary endothelial cells.

Widespread ultrastructural alterations in the vascular basal lamina were found in the central nervous system of symptomatic mice infected with three different neuropathogenic murine leukemia viruses. These changes appeared to progress in frequency and severity in parallel with the progression of spongiform lesions and clinical symptoms. Accumulations of pleomorphic, apparently degenerating, virions were frequently seen within areas that showed marked aberrations from the normal basal lamina ultrastructure. We suggest that the observed retrovirus-associated ultrastructural changes in the endothelial basal lamina may alter normal physiologic functions and thus play a primary role in the pathogenesis of retrovirus-induced spongiform disease.

Animals↗
PubMed1986

Characterization of a progressive neurodegenerative disease induced by a temperature-sensitive Moloney murine leukemia virus infection.

A progressive neurodegenerative disease occurred following infection of mice with a temperature-sensitive (ts) isolate of Moloney (Mo) murine leukemia virus (MuLV), ts Mo BA-1 MuLV. This NB-tropic ecotropic MuLV, which was ts for a late function, induced a syndrome of tremor, weakness of the hind limbs, and spasticity following infection of several strains of laboratory neonatal mice, including NFS, C3H/He, CBA, SJL, and BALB/c. The latent period of 8 to 16 weeks was considerably longer than that observed for the acute paralytic diseases observed following neonatal infection with other ts Mo-MuLV, rat-passaged Friend MuLV, and some wild mouse ecotropic MuLVs. Spongiform pathology without inflammation and degeneration of neurons devoid of budding virions occurred in the cerebellar grey matter, brain stem, and upper spinal cord; but lower spinal cord anterior horn cells were less obviously affected than in other MuLV-associated neuroparalytic syndromes. ts Mo BA-1 MuLV differed from other ts Mo-MuLV mutants that are capable of inducing a neuroparalytic syndrome in that while infected nervous system tissue contained high levels of MuLV p30 and gp70, no evidence of precursor accumulation or abnormal processing of MuLV p30 or gp70 could be demonstrated. The localization of virus within the nervous system suggests that direct neuronal infection may not be the etiologic mechanism in this MuLV-induced neurodegenerative disease.

Animals↗
PubMed1985

Greying with age in mice: relation to expression of murine leukemia viruses.

Some strains of C57BL/10 H-2-congenic mice were found to exhibit greying with age, whereas others did not. Two patterns of greying were observed, diffuse greying beginning at 4 to 6 months of age and patterned greying beginning at 4 to 6 weeks. Strains exhibiting either greying pattern expressed high levels of infectious ecotropic and mink cell focus-inducing murine leukemia viruses (MuLV) in tests of thymus and spleen and in cultures from skin or tail biopsies, whereas nongreying strains expressed little virus until late in life. Electron microscopy demonstrated large accumulations of MuLV in grey, but not in black areas, of skin from a mouse with patterned greying. Infectious MuLV was produced spontaneously by embryos of greying, but not of nongreying, mice and pups of nongreying strains fostered on greying mothers turned grey after 3 months. These results suggest that greying with age results from melanocyte dysfunction that occurs subsequent to pre- or early postnatal infection with MuLV.

Aging↗
PubMed1983

Vascular neoplasms induced in rodent central nervous system by murine sarcoma viruses.

Mice and rats were injected intracerebrally with Harvey or Kirsten murine sarcoma viruses at 2 or 10 days after birth. Animals exhibited neurologic symptoms at 10 to 30 days postinjection. Brains, livers, and spleens were examined grossly and by light and electron microscopy. Mice injected at 2 days and rats injected at 10 days developed multiple brain neoplasms derived from endothelial cells. This conclusion was reinforced by immunofluorescence studies showing factor VIII expression on transformed cells both in vivo and in vitro. Brains of rats injected at 2 days contained both transformed endothelial and astroglial elements. Ultrastructural evidence for murine sarcoma virus replication was found in endothelial and glial cells of animals injected at 2 days; however, such evidence was not found in those injected at 10 days of age. The type of neoplasm induced appeared to be independent of concentration of inoculum, genetic strain within a species, or type of helper virus pseudotyped with the murine sarcoma virus. This system may facilitate the investigation of endothelial function and neoplasia.

Animals↗
PubMed1982

Retrovirus antigens in brains of mice with scrapie- and murine leukemia virus-induced spongiform encephalopathy.

Wild mouse ecotropic virus-induced spongiform encephalomyelopathy pathologically similar to scrapie was associated with the expression of retrovirus antigens in mouse brains. However, scrapie-infected mice with spongiform encephalopathy showed no increased expression of retrovirus antigens in brain. Thus, the pathogenesis of the scrapie spongiform lesion does not appear to involve activation of endogenous retrovirus.

Animals↗
PubMed1976

An evaluation of a procedure for the isolation of myelin basic protein (BP).

A detailed description and stepwise evaluation of a procedure that can be used to obtain myelin basic protein (BP) from whole brain is presented. The procedure involved the 0.001 MHC1 extraction of whole brain pre-treated in a sequential manner with chloroform-methanol (2:1 v/v), acetone, and deionized water. This is followed by a precipitation of the extract at pH 9.0, and gel filtration of the supernatant in 0.01 M HC1. Yields of canine and porcine BP and their disc gel evaluations are presented at several key points in the procedure. The final products possessed a high degree of homogeneity when examined on SDS gels stained with commonly used protein stains. When compared with six SDS-gel marker-protein standards, the canine and porcine final products had mobilities that correspond to an apparent molecular weight of 18,5000 +/- 5%. Quantitative binding of 125I-labeled canine and porcine BPs with standardized rabbit anti-BP antisera gave comparable results. Immunoelectrophoretic and immunodiffusion examinations demonstrated single components and complete identity. The canine and porcine BP's also reacted fully with syngeneic anti-BP antisera raised in Lewis-strain rats. The canine BP was tested for encephalitogenicity in Lewis-strain rats and found to be comparable to rat BP in producing experimental allergic encephalomyelitis.

Animals↗
PubMed1975

The antibody responses to myelin basic protein (BP) in Lewis rats: the effects of Bordetella pertussis.

A time-course study was made of the systemic humoral immune response of Lewis rats to myelin basic protein (BP) as influenced by the dosage of ancillary pertussis adjuvant. Peak activities were observed 5 to 7 weeks after injection. When injected proximal to BP and Mycobacterium butyricum in complete Freund's adjuvant (CFA), Bordetella pertussis at the level of 4 billion organisms doubled the antibody-binding activity of rat sera for 125I-labeled BP as compared to activities obtained with 0, 2, 6, or 8 billion. The severity of clinical symptoms of experimental allergic encephalomyelitis (EAE) at the end of the 2nd week was greatest in rats receiving 64 billion organisms, the very same rats that displayed a severely dampened humoral immune response to BP 5 weeks later. When pertussis was injected i.p. rather than proximal to the CFA mixture, the time-course of the humoral immune response displayed a different profile--unusually high binding activities at the time of onset of EAE that fluctuated back and forth from high to low and that eventually dampened to an intermediate level.

Animals↗