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Biomedical subjects

C A Wiley

Publications and source records attributed to C A Wiley.

At least 145 records · Page 8Linked to original sources
PubMed1989

The cerebellum in sagittal plane--anatomic-MR correlation: 1. The vermis.

Correlation of thin (5-mm) sagittal high-field (1.5-T) MR images of three brain specimens and 11 normal volunteers with microtome sections of the human cerebellar vermis and hemispheres demonstrates that proton-density-weighted (long TR/short TE) and T2-weighted (long TR/long TE) spin-echo pulse sequences provide the greatest contrast between gray and white matter. These images also can display (1) the corpus medullare and primary white-matter branches to the vermian lobules, including the lingula, centralis, culmen, declive, folium, tuber, pyramis, uvula, and nodulus; and (2) several finer secondary branches to individual folia within the lobules. Surface features of the vermis including the deeper fissures (e.g., preculminate, primary, horizontal, and prepyramidal) and shallower sulci are best delineated by T1-weighted (short TR/short TE) and T2-weighted images, which provide greatest contrast between CSF and parenchyma. Given that the width of the normal vermis varied from 6 to 12 mm in our volunteers, the acquisition of thin slices (less than or equal to 5 mm) was required to minimize volume averaging of the cerebellar hemispheres with the vermis on a midline sagittal MR section. Knowledge of the detailed normal anatomy of the cerebellar vermis on sagittal MR images can assist in the identification of various pathologic alterations.

Adolescent↗
PubMed1989

The cerebellum in sagittal plane--anatomic-MR correlation: 2. The cerebellar hemispheres.

Thin (5-mm) sagittal high-field (1.5-T) MR images of the cerebellar hemispheres display (1) the superior, middle, and inferior cerebellar peduncles; (2) the primary white-matter branches to the hemispheric lobules including the central, anterior, and posterior quadrangular, superior and inferior semilunar, gracile, biventer, tonsil, and flocculus; and (3) several finer secondary white-matter branches to individual folia within the lobules. Surface features of the hemispheres including the deeper fissures (e.g., horizontal, posterolateral, inferior posterior, and inferior anterior) and shallower sulci are best delineated on T1-weighted (short TR/short TE) and T2-weighted (long TR/long TE) sequences, which provide greatest contrast between CSF and parenchyma. Correlations of MR studies of three brain specimens and 11 normal volunteers with microtone sections of the anatomic specimens provides criteria for identifying confidently these structures on routine clinical MR. MR should be useful in identifying, localizing, and quantifying cerebellar disease in patients with clinical deficits.

Cerebellum↗
PubMed1989

Degeneration of oxidative muscle fibers in HTLV-1 tax transgenic mice.

The HTLV-1 tax gene under control of the HTLV-1 long terminal repeat (LTR) was introduced into transgenic mice. Previously tax protein expression in the muscle and peripheral nerves of three independent mouse lines was reported. Here the localization of this transgenic protein at a cellular and subcellular level is described. Tax protein was expressed in oxidative muscle fibers that developed severe progressive atrophy. It localized to the cytoplasma where it was associated with structures resembling degenerating Z bands. This pattern of muscle fiber involvement is similar to that observed in human retroviral associated myopathy. This transgenic mouse model suggests that preferential expression of the HTLV-1 viral promoter in oxidative muscle fibers may explain the productive infection of these fibers in HTLV-1 myopathy.

Animals↗
PubMed1988

Atypical retinitis in patients with the acquired immunodeficiency syndrome.

We examined three patients with AIDS who had large, sharply demarcated areas of thinned retina consistent with inactive cytomegalovirus retinitis and who were not treated with ganciclovir. These lesions appeared identical to clinically inactive areas of cytomegalovirus retinitis after effective antiviral treatment. All patients were receiving azidothymidine or ribavirin, or both, which have activity against the human immunodeficiency virus and which may improve immune function. All patients also received oral acyclovir at doses ineffective against cytomegalovirus retinitis.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Human immunodeficiency virus detected in bowel epithelium from patients with gastrointestinal symptoms.

Infectious human immunodeficiency virus (HIV) was recovered from two out of four bowel biopsy specimens from acquired immunodeficiency syndrome (AIDS) patients with chronic diarrhoea of unknown aetiology. In-situ hybridisation of biopsy specimens from rectum and duodenum of other AIDS patients with gastrointestinal complaints showed the presence of HIV-infected cells in both the base of the bowel crypts and the lamina propria. The type(s) of epithelial cell(s) infected could not be determined definitively. However, the association of in-situ labelling of HIV RNA in argentaffin staining cells strongly suggests that enterochromaffin cells derived from neural crest tissue are among the target cells. This evidence that HIV can directly infect the bowel raises the possibility that the virus causes some of the gastrointestinal disorders of AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Human immunodeficiency virus (HIV) and JC virus in acquired immune deficiency syndrome (AIDS) patients with progressive multifocal leukoencephalopathy.

Of the 93 acquired immune deficiency syndrome (AIDS) patients autopsied between 1983 and 1986, 27 had evidence of viral encephalitis of which 3 had progressive multifocal leukoencephalopathy (PML), confirmed by electron microscopy. Using in situ hybridization with biotinylated JC virus probes, paraffin sections from the brains of these 27 patients were examined. JC virus was found only in those patients with histologically proven PML, while no evidence of JC virus was detected in the brains of the other 24 AIDS patients despite the presence of white matter pathology. Brain biopsies of the PML patients demonstrated human immunodeficiency virus (HIV)-infected macrophages infiltrating regions of demyelination. When the patients died (2 to 6 months after diagnosis of PML), many more macrophages contained HIV antigens and some had fused to form multinucleated giant cells. These findings suggest that in AIDS patients, papovaviruses not only cause damage by directly infecting oligodendroglia but causes additional damage by eliciting the ingress of macrophages latently infected with HIV. As was seen with other infections (e.g., cytomegalovirus) of the CNS this might be a general mechanism of HIV entry into the brain.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Evidence for human immunodeficiency virus (HIV) infection of the brain in a patient with aplastic anemia.

A young female patient with a long history of intravenous drug abuse died after a fulminant course of aplastic anemia. At postmortem examination, she was found to have multinucleate giant cells and immunocytochemical evidence of human immunodeficiency virus (HIV) infection of the central nervous system. This case raises the possibility that HIV infection contributed to the patient's aplastic anemia, and suggests that HIV-associated giant cells might be found retrospectively or prospectively within the brains of patients who die of conditions other than those narrowly defined as acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC). It furthermore emphasizes that HIV infection of the nervous system is not necessarily accompanied by clinically apparent neurological disease.

Acquired Immunodeficiency Syndrome↗
PubMed1988

HIV and HCMV coinfect brain cells in patients with AIDS.

Direct interactions at the cellular level in vitro have been reported which suggest that opportunistic viruses may reactivate latent human immunodeficiency virus (HIV) in cells. The significance of these findings depends on whether coinfection of the same cell with these two different types of viruses occurs in vivo. Using various double-labeling techniques, we present evidence that human cytomegalovirus (HCMV) and HIV can coinfect the same cell in vivo in central nervous system tissue from AIDS patients. These observations indicate that direct cooperation at the single cell level could occur between HCMV and HIV. This new finding in the context of reports that herpesviruses can increase HIV transcription in vitro, suggest the possibility of a direct role for herpesviruses in the pathogenesis of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Pathogenesis of murine cytomegalovirus infection: identification of infected cells in the spleen during acute and latent infections.

Spleen cells which replicate murine cytomegalovirus (MCMV) during acute infection in vivo were identified by electron microscopy and combined immunocytochemical staining and in situ cytohybridization. Most infected cells, as defined by in situ hybridization for viral RNA with MCMV-specific probes, were shown to be positive for factor VIII-related antigen and negative for Ia, Thy-1, and F4/80 antigens. Electron microscopic ultrastructural observations indicated that the infected cells in the spleen are predominantly sinusoidal-lining cells. We also studied reactivation of MCMV from latently infected mice by cocultivation of spleen cells with mouse embryo fibroblasts. Virus was only recovered from cells in preparations of stromal (or reticular) fragments, and not from spleen cell suspensions. Neither removal of immunoglobulin-bearing cells from the stromal fragments by panning nor depletion of Thy-1- and Ia-bearing stromal cells by treatment with monoclonal antibodies and complement reduced the frequency of reactivation of MCMV. These data suggest that T lymphocytes, mature B lymphocytes, and other Ia-bearing cells are not predominant reservoirs of latent MCMV.

Acute Disease↗
PubMed1988

Role of human immunodeficiency virus and cytomegalovirus in AIDS encephalitis.

Approximately half of patients with advanced acquired immune deficiency syndrome (AIDS) develop a subcortical dementia. The brains of all autopsies on AIDS patients performed at UCSD between 1982 and 1986 (N = 93) were studied. Neuropathologic changes consistent with a viral encephalitis were present in 54 brains (58%). Human immunodeficiency virus (HIV) antigens were detected in 37 of the brains (40%), most frequently in macrophages, multinucleated giant cells, and endothelial cells. Cytomegalovirus (CMV) was detected in 31 of the brains (33%), 22 of which also contained HIV. Cellular localization of CMV antigens suggests that CMV disseminates to the central nervous system hematogenously where the virus can infect endothelial cells, glia, and neurons. While the temporal course of the appearance of these two viruses within the CNS is not clear, the common simultaneous occurrence of both viruses within the brains of AIDS patients suggests that in vivo interaction between them may play a role in the pathogenesis of AIDS-associated encephalitis. Given the significant neurologic symptoms described in AIDS patients, the paucity of viral antigens suggests a pathogenic mechanism of indirect CNS damage rather than direct viral infection.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Infantile neurodegenerative disease with neuronal accumulation of phosphorylated neurofilaments.

A caucasian male with a history of mental retardation and intractable epilepsy since birth, developed progressive wasting and weakness of skeletal muscles, leading to death at 4 years of age. A biopsy of gastrocnemius muscle at 2 years of age revealed severe neurogenic atrophy. Sural nerve biopsies at 2 and 3 years showed progressive atrophy and loss of large myelinated nerve fibers with a paucity of neurofilaments in remaining nerve fibers. Postmortem immunohistochemical and ultrastructural examination showed that neurons were markedly distended by phosphorylated neurofilaments. Whereas large lower motor neurons were most severely involved, dorsal root ganglia and neurons in the cerebral cortex and deep gray nuclei were also affected. It is suggested that this disease is caused by a disorder of neurofilament phosphorylation and transport.

Amyotrophic Lateral Sclerosis↗
PubMed1987

Relationship of adjuvants and swine influenza vaccine to experimental neuropathy in rabbits.

Experimental neuropathy, characterized by endoneurial edema and demyelination, was induced by inoculating rabbits with a combination of Freund's complete adjuvant (FCA), gangliosides, lecithin and cholesterol. A less severe demyelinating neuropathy could be induced by treatment with FCA alone but no significant change could be elicited by injection of swine influenza vaccine (SFV) alone. When FCA was combined with gangliosides, lecithins, cholesterol and SFV, neuropathy occurred, but the changes were less severe than if these agents were used without SFV. Sera were tested for myelin basic protein (MBP) and galactocerebroside (GC) antibodies in each experimental group. Neither SFV alone nor SFV combined with Freund's complete adjuvant, gangliosides, cholesterol and lecithin evoked significant antibody titers to MBP or GC. However, rabbits inoculated with FCA, gangliosides, lecithin and cholesterol had rising titers of antibody to both MBP and GC over the 3-month experimental period. One rabbit inoculated with FCA alone had significant antibody to MBP. The findings suggest that Freund's complete adjuvant alone can induce demyelination in the peripheral nerves of rabbits and that SFV may modulate the immune response acting either as an adjuvant or suppressant in the experimental demyelinating disease.

Animals↗
PubMed1987

Effects of regional spinal X-irradiation on demyelinating disease caused by Theiler's virus, mouse hepatitis virus or experimental allergic encephalomyelitis.

The effects of X-irradiation on the course of chronic demyelinating disease were examined in mice with experimental allergic encephalitis (EAE), mouse hepatitis virus (MHV) or Theiler's virus (DAV) infection. One month after the induction of EAE or 2-16 months after inoculation of DAV, exposure of the cervical spinal cord to 20 Gy X-rays caused local exacerbation of disease activity but spinal irradiation did not affect MHV-induced demyelination. In EAE, there was a significant increase in the number of inflammatory cells in the irradiated part of the cord. Mice infected with DAV showed locally increased demyelination and axonal degeneration but no change in the titer of infectious virus within the cord. Thus in DAV infection, as in EAE, the exacerbation of disease seemed to be due to vascular or immunological factors rather than viral reactivation.

Animals↗
PubMed1987

Peripheral nerve demyelination in rabbits after inoculation with Freund's complete adjuvant alone or in combination with lipid haptens.

The pathology of demyelination in rabbits with experimental allergic neuritis (EAN) or galactocerebroside-induced neuritis was compared to that in rabbits inoculated with either an emulsion of lipid haptens (gangliosides, lecithin and cholesterol) and Freund's complete adjuvant or Freund's complete adjuvant (FCA) alone. In rabbits inoculated with bovine peripheral myelin in FCA, perivenular demyelination associated with infiltrates of lymphocytes and macrophages occurred after 30 days, while those animals inoculated with galactocerebroside (GC) in Freund's adjuvant did not develop lesions until 60-90 days. GC rabbits had demyelination and severe nerve edema without cellular infiltrates. In rabbits inoculated with FCA alone, demyelination was restricted to ganglia and proximal nerve roots. Myelin basic protein (MBP) and GC antibodies from EAN, GC and lipid hapten-inoculated rabbits were detected by ELISA in sera at all post-inoculation time points. Appreciable P0 and P2 antibody titers were detected only in EAN animals. The results indicate that Freund's complete adjuvant alone or in combination with lipid haptens is capable of producing neuropathic effects in the rabbit independent of those produced by EAN or galactocerebroside neuritis.

Animals↗
PubMed1987

Optic nerve hypoplasia and the syndrome of nevus sebaceous of Jadassohn. A new association.

The nevus sebaceous of Jadassohn (NSJ) syndrome is a not uncommon pediatric dermatosis, with malignant potential. It is the cutaneous manifestation of another phakomatosis, characterized by neurologic, ophthalmic, cardiovascular, skeletal, and urogenital involvement. The features of this syndrome overlap those of the oculo-auriculo-vertebral dysplasia of Goldenhar and tuberous sclerosis. The extent of system involvement suggests a developmental insult during the first few weeks of gestation. A clearly genetic basis has not been established. An infant with NSJ syndrome is described who had associated optic nerve hypoplasia. His clinical, pathologic, and radiologic findings, including computed tomography (CT) and magnetic resonance imaging, are presented.

Humans↗