Ocular bobbing in hepatic encephalopathy.
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Biomedical subjects
Publications and source records attributed to M Scanlon.
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The growth hormone (GH), thyrotrophin (TSH) and prolactin response to growth hormone releasing factor (GRF) was investigated in 18 patients suffering from major depression with melancholia and in 18 age- and sex-matched normal controls. There was no significant difference in the GH response to GRF stimulation between the patients and controls and in neither subject group was there a demonstrable TSH or prolactin response to GRF. These findings indicate that the pathophysiology underlying the blunted GH response to pharmacological challenge, demonstrated in other studies, must lie at a suprapituitary level.
Microsporidia of the genus Encephalitozoon undergo merogony and sporogony in a parasitophorous vacuole within the host cell. Cultured green monkey kidney cells infected with Encephalitozoon hellem were loaded with the fluorescent dyes fura-2 or BCECF in order to measure intracellular concentrations of calcium and hydrogen ions respectively. Both the parasitophorous vacuole calcium concentration and pH values resembled those of the host cell cytoplasm in infected cells. Calcein entered the parasitophorous vacuole but not other host cell vacuoles or parasite stages within the parasitophorous vacuole. The lack of a pH or calcium concentration gradient across the parasitophorous vacuole membrane and the permeability of this membrane to a large anion such as calcein suggest that the vacuole membrane surrounding E. hellem resembles that surrounding some other intracellular parasites such as Toxoplasma gondii. A potential role is discussed for the parasitophorous vacuole calcium concentration in germination in situ.
Microsporidia of the genus Encephalitozoon infect mammalian cells and have become a source of morbidity and mortality in immunocompromised humans. Encephalitozoon microsporidia develop and mature within parasitophorous vacuoles, enlarging the vacuole over time until it eventually occupies most of the cytoplasm of the host cell. The ability of the host cell to accommodate such a large burden for several days suggests that the parasite subverts normal host cell processes to ensure optimal environmental conditions for its growth and development. Since this environment would be threatened if cell division of the host cell occurred, we have formulated the hypothesis that infection with Encephalitozoon microsporidia induces an arrest in the cell cycle of the host cell. In support of this hypothesis, we have found that mitotic index and DNA duplication are reduced in infected cells as compared to uninfected cells. The number of host cell nuclei in S phase is increased. The levels of cyclin D1 and the percentage of cells in G1 are reduced; however, the levels of cyclin B1 are elevated even though the percentage of cells in G2/M is decreased. These results suggest that host cells infected with Encephalitozoon microsporidia are blocked at multiple points in the cell cycle.
The literature regarding Binswanger's disease is reviewed. Emphasis is placed on reviewing the neuropsychological literature related to Binswanger's disease. In addition, a retrospective analysis was carried out among four groups of subjects (N = 61) who were divided according to the presence or absence of dementia and deep white-matter alterations. A main effect for deep white-matter alterations was found for almost all measures of diastolic and systolic blood pressure. Among the two nondemented groups there was an effect of deep white matter alteration on neuropsychological functioning. Subjects with deep white matter changes performed worse on tests of immediate and delayed recall of a prose passage. Among the two demented groups there were no differences on any of the neuropsychological measures, although subjects with deep white matter alterations exhibited a higher incidence of focal neurologic signs and stroke. We conclude that Binswanger's disease is probably more prevalent than currently appreciated. Also, among clinically nondemented individuals periventricular white-matter alterations may be associated with subtle but definable neuropsychological deficits, and these individuals may be at risk for developing a dementing illness.
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