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Biomedical subjects

N Ge

Publications and source records attributed to N Ge.

24 records · Page 2Linked to original sources
PubMed1993

Persistence of tick-derived Anaplasma marginale in cultured bovine turbinate and endothelial cells.

Anaplasma marginale from salivary glands of Dermacentor andersoni was used to inoculate monolayers of bovine turbinate and endothelial cells. Monolayers were passaged at 2 or 4 week intervals and monitored with light and electron microscopy and with an A. marginale-specific DNA probe. Intracellular inclusions were observed in turbinate cells after 2-4 weeks. The number of inclusion-bearing cells increased over 1-2 weeks and gradually disappeared. A radiolabeled fragment from within the msp1 beta gene of the erythrocytic stage of A. marginale hybridized to DNA extracted from bovine turbinate cell cultures as late as 7 weeks post inoculation (passage 4). Individual rickettsiae were observed with electron microscopy in samples taken at this time. Susceptible calves inoculated with suspect cultures did not develop clinical anaplasmosis but did develop significant antibody titers as detected with ELISA. DNA from endothelial cell cultures at 9 weeks post inoculation also bound the Anaplasma-specific DNA probe. Anaplasma marginale from salivary glands of D. andersoni appears to persist in cultured bovine turbinate and endothelial cells but typical development and infectivity for bovines do not occur.

Anaplasma↗
PubMed1992

Amyloid precursor protein is localized in growing neurites of neonatal rat brain.

Previous studies have indicated that amyloid precursor protein (APP) might be a trophic agent in the nervous system, possibly through the regulation of cell adhesion and the protease/protease inhibitor activity. Additionally, APP is upregulated during the development of the nervous system. In order to further study the role of APP in neuritic outgrowth, we examined the patterns of distribution of APP in the immature neonatal rat brain (P1). Laser-scanning confocal imaging of double-immunolabeled sections showed that a subpopulation of the anti-GAP43-immunoreactive outgrowing neurites contained APP immunoreactivity in the neocortex and hippocampus. These fine, long neuritic processes were also positive with antibodies against phosphorylated neurofilaments and were glial fibrillary acidic protein (GFAP) negative. In addition, anti-APP strongly immunolabeled neurons in the inner cortical layers, while GAP43 strongly immunolabeled the neuropil surrounding them. These observations are consistent with a previous study where APP was localized to aberrant sprouting neurites and suggest a possible role for APP in neuritic outgrowth in plaques of patients with Alzheimer's disease (AD), which might explain the abnormal neuritic response found in AD.

Amyloid beta-Protein Precursor↗
PubMed1992

Spectrum of human immunodeficiency virus-associated neocortical damage.

A spectrum of neurocognitive defects, termed human immunodeficiency virus type 1 (HIV-1)-associated cognitive/motor complex, has been described in patients with acquired immunodeficiency syndrome (AIDS). AIDS dementia complex (ADC) is a severe form of this disease seen in 20 to 30% of terminally ill patients. The etiology of this complex is distinct from commonly observed opportunistic infections seen in brains of patients with AIDS and has been attributed to HIV infection within the brain. At autopsy, the brains of patients with ADC contain numerous HIV-infected macrophages/microglia with prominent subcortical damage, together termed HIV encephalitis. We retrospectively analyzed all 107 brains from a three-year period (1988-1990) of AIDS autopsies using immunocytochemistry to detect HIV. Rather than breaking into distinct groups of HIV encephalitis versus non-HIV encephalitis, the specimens revealed a spectrum of severity of HIV infection. Although only 16% of the brains showed the histological hallmarks of HIV encephalitis, more than 50% of the autopsies showed moderate to severe HIV infection. In a subset of 23 AIDS autopsies during which short postmortem times and absence of significant opportunistic infection permitted quantitative analysis of dendritic and synaptic complexities, we identified a strong correlation between neocortical dendritic and presynaptic damage and abundance of HIV envelope protein in the neocortical gray and deep white matter. This correlation suggests that the presence of HIV-1 in the neocortex may be responsible by direct or indirect mechanisms for dendritic and synaptic damage.

AIDS Dementia Complex↗
PubMed1992

Selective neuronal vulnerability in HIV encephalitis.

Recent studies of human immunodeficiency virus type 1 (HIV-1) encephalitis have shown that in addition to well established white matter damage, the neocortex shows thinning, loss of large neurons and dendritic damage. In order to identify neuronal populations affected in HIV encephalitis and to determine how neuronal damage relates to the severity of HIV infection within the nervous system, we quantified parvalbumin (PV+) and neurofilament (NF+) immunoreactive neurons in the frontal cortex and hippocampus. We found that in the neocortex, the density of NF+ and PV+ neurons was independent of severity of HIV encephalitis, and therefore changes in these neuronal subsets did not account for previously reported neuronal loss. However, neuritic processes of PV+ neurons were fragmented, atrophic and in some cases distended. In contrast to the frontal cortex, there was a trend toward decreased density of PV+ neurons in the hippocampus which only reached significance in the CA3 layer where there was a 50-90% decrease in PV+ neurons. This decrease was closely correlated with the severity of HIV encephalitis. Double-label immunocytochemical analysis confirmed neuritic damage to interneurons. These results suggest that HIV encephalitis differentially involves specific subpopulations of neurons. Since direct HIV infection of neuronal cells was not detected, damage to PV+ cells and fibers may be indirectly mediated by cytokines released by HIV-infected microglia.

AIDS Dementia Complex↗
PubMed1992

Cortical dendritic pathology in human immunodeficiency virus encephalitis.

Previous neuropathological and morphometric studies of the cerebral cortex of patients with human immunodeficiency virus encephalitis (HIVE) have shown a decrease in the population of large neurons, moderate loss in synaptophysin immunoreactivity, and pathological changes in dendrites. To further characterize and quantify alterations in the dendritic tree of neocortical pyramidal neurons, we performed a modified Golgi impregnation technique on Formalin fixed blocks from the frontal cortex of 5 HIVE cases, 5 human immunodeficiency virus seropositive control cases without encephalitis, and 5 human immunodeficiency virus seronegative controls. Apical dendrites of HIVE cases were dilated, vacuolated, and tortuous with decreased length and branching. Basal and oblique dendrites also showed these alterations, but to a lesser extent. Some dendrites presented lacunae and filopodia consistent with remodeling. Computer aided quantification of HIVE cases showed a 40-60% decrease in spine density throughout the entire length of dendrites. Laser confocal imaging of Golgi impregnated sections displayed aberrant spines in regions of abnormal second order dendritic branches. These observations support the role of primary dendritic damage in HIVE in contrast to other neurodegenerative disorders where the primary pathology is presynaptic.

AIDS Dementia Complex↗