Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The investigation was carried out on 11 sudden infant death (SIDS) cases which were compared with age- and sex-matched controls. Six brain nuclei were selected for evaluation. Using immunohistochemical methods, macrophages were selectively demonstrated by detection of lysozyme; reactive astrocytes, by detection of intracytoplasmic albumin (marker of prior impairment of blood-brain barrier function) or GFAP. No lysozyme-positive cells were demonstrable in the brain stem of any of the examined cases. Although a greater number of reactive, GFAP-expressing astrocytes were found in the SIDS cases, 3 of the 11 SIDS cases (compared to 5 controls) had no reactive astrocytes in any of examined brain nuclei. Reactive astrocytes, however, were identified in more than half the controls. Sections treated with anti-albumin serum were evaluated quantitatively. Total number of non-neuronal cells, relative proportion of astrocytes, and proportion of albumin-positive astrocytes were determined. Paired brain nuclei were counted on both sides of the brain stem. The number of non-neuronal cells, astrocytes, and albumin-positive astrocytes in the SIDS cases did not differ significantly from those in the controls. No statistically relevant difference was established between the right and left parts of the brain stem. The findings were discussed in light of the literature.
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PMID:Reactive astrocytes and macrophages in the brain stem of SIDS victims? Eleven age- and sex-matched SIDS and control cases. 262 Apr 81

The study was based on the hypothesis that cerebellar hypoxia may play a role in sudden infant death syndrome resulting in morphological changes of the cerebellar cortex, especially with respect to Purkinje cell density. In the morphological evaluation of the Purkinje cell layer, special consideration was additionally given to secondary alterations (i.e., macrophage and/or astrocyte reaction). A total of 12 sudden infant death syndrome cases were compared with an age- and sex-matched control group. The Purkinje cell density was evaluated by determining the number of these cells per surface unit on parasagittal sections in both hemispheres. The myelomonocytic and glial reaction was demonstrated by immunohistochemical methods using lysozyme as leukocyte and macrophage markers and glial fibrillary acidic protein as an astrocyte marker. Qualitatively, no alterations resembling a macrophage or glial cell reaction were detected in sudden infant death syndrome. No differences between the right and left cerebellar hemisphere could be established in the victims of sudden infant death syndrome nor in the controls. The number of Purkinje cells per 0.352 mm2 cortex was higher in the younger victims of sudden infant death (younger than 45 weeks of gestation) than in all matched controls. A statistically significant difference in Purkinje cell density, however, could not be established, and, especially, no indications of hypoxia were observed in the cerebellar cortex.
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PMID:Cytological investigations on the cerebellar cortex of sudden infant death victims. 278 51

Sudden Infant Death Syndrome (SIDS) victims have significantly thickened bronchiolar walls with increased mononuclear cells in the adventitia. An immunohistochemical study was performed on 25 SIDS and 18 aged-matched control infants to characterize these cells. The panel of antibodies included alpha-1-antitrypsin, lysozyme, actin, vimentin, Leu M1, NSE, S-100, Leu 6, bombesin, serotonin, anti-substance P, vasoactive intestinal peptide, MAC 387, and Factor XIIIa. The bronchiolar cells stained with S-100 antibody and demonstrated slender processes similar to dendritic cells, such as Langerhans' cells, and interdigitating reticulum cells, present in normal tissues as well as in certain tumors and inflammatory diseases. Manual counting of the S-100 positive cells and fibers revealed both of these to be significantly increased in SIDS infants as compared to age-matched control infants. Morphologically, the bronchiolar dendritic cells closely resembled Langerhans' cells and therefore may have similar immunologic functions, such as antigen presentation and viral and neoantigen immunosurveillance. We hypothesize that the proliferation of these dendritic cells in SIDS victims is a result of exposure to environmental antigens, resulting in a thickening of the bronchiolar walls, narrowing of the lumen, and reduction in airflow, thus causing a chronic or persistent hypoxia.
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PMID:Proliferation of dendritic cells in the bronchioles of sudden infant death syndrome victims. 834 85