[Rectification].
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AIDS Dementia Complex↗
Biomedical subjects
María I Berría
Publications and source records attributed to María I Berría.
Cholinergic modulation of baker's yeast cell phagocytosis by rat astrocytes.
Cholinergic regulation of baker's yeast cell phagocytosis in rat cultured astrocytes was studied. Phagocytic activity was reduced by 1 x 10(-5) M of atropine or pirenzepine, but not by AF-DX116 or 4-DAMP. In addition, carbachol stimulated phagocytosis in a dose-dependent manner. Furthermore, only 1 x 10(-5)M of atropine, pirenzepine and 4-DAMP significantly reduced enhanced activity induced by 1 x 10(-7)M carbachol. It was also observed that L-NMMA, staurosporine, or U-73122, reduced phagocytosis activity while TFP failed to do so. Nitrite levels in astrocyte supernatants increased after baker's yeast cells were incorporated to astrocyte cultures, correlating with enhanced phagocytosis induced by carbachol stimulation, and were reduced by 1 x 10(-5) M of atropine, pirenzepine or aminopiridine, but not by AF-DX116 or 4-DAMP. Enhanced NO production triggered by astrocyte phagocytosis may have pathological consequences.
Acetylcholine↗
A possible case of myelopathy/tropical spastic paraparesis in an Argentinian woman with human T lymphocyte virus type II.
A case of neurological disease featuring human T lymphocyte virus-associated myelopathy/tropical spastic paraparesis (HAM/TSP) was diagnosed by serological (Western blot) and molecular (polymerase chain reaction) criteria as related to human T lymphocyte virus (HTLV)-II infection. This is, to our knowledge, the first case of this kind found in Argentina and is additional evidence that HAM/TSP solely related to HTLV-II infection occurs in HTLV-I-negative subjects.
Adult↗
Junin virus-induced astrocytosis is impaired by iNOS inhibition.
Because Junin virus (JV) experimental encephalitis of mice and rats is characterized by mild histopathological changes that do not seem to justify per se lethality after intracerebral infection, such a murine model seems adequate to investigate the potential role of inducible nitric oxide synthase (iNOS) as a pathogenic factor. Concomitant with a predominant astrocyte reaction, increased immunoperoxidase expression of iNOS, mitochondrial superoxide dismutase (SODm) and glutathione peroxidase (GPX) was disclosed in brain of mice infected with JV strain #44. When specific inhibition of iNOS was achieved by intraperitoneal administration of amino guanidine (AG), significantly greater mortality was observed in treated animals (70% vs. 40%), together with similar infective titers ( approximately 10(7) PFU/g) but lower astrocytosis, as shown by glial fibrillary acidic (GFAP) labeling. As regards SODm and GPX immunochemical expression in neurons, no differences were found between mice with or without AG treatment. The present results suggest that the apparent protective role of nitric oxide (NO), when synthesized by iNOS, is unrelated to reduced viral replication but rather to enhanced astrocyte activation behaving as a beneficial cell response to virus-induced CNS damage.
Animals↗
Immunochemical expression of proliferative cell nuclear antigen in aging cultured astrocytes.
Cell differentiation degree and mitotic activity were sequentially assessed by immunoperoxidase labeling of glial fibrillary acidic protein (GFAP) and proliferative cell nuclear antigen (PCNA), respectively, in rat brain cultured astrocytes maintained up to 60 days in vitro (DIV) of first subculture, or weekly passaged until their 12th subculture. Cell count was performed through a 0.01 mm2 section reticule and morphometric analysis with a stereological grid. The number of double immunoreactive cells peaked by 2 DIV to achieve its lowest value at 60 DIV. At 24 hs of cell seeding of successive passages, such values peaked by the 6th subculture to gradually decrease thereafter. Increasing cell hypertrophy was found during the long-term first subculture but not after passaging. At the end of the observation period, doubly immunolabeled astrocytes were still recorded, thus evidencing retention of proliferative potential despite aging.
Aging↗