PubMed · 15410976
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M H ROEPKE, K G PATERSON, F C DRIVER, L B CLAUSEN, L OLSON, J E WENTWORTH. 1950. The Brucella abortus ring test.. https://pubmed.ncbi.nlm.nih.gov/15410976/
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Miller Dieker syndrome (MDS, type I lissencephaly) is a neuronal migration disorder, which is caused by deletions along the short arm of chromosome 17 (17p13.3). Recent studies would suggest that the cortical lamination in MDS is inverted, based on morphological criteria. The present neuropathological study examines the cerebral cortex from a 33-week old fetus with MDS using both neuronal and laminar-specific markers. These expression studies demonstrate a relatively preserved cortex and cortical lamination, overlying a layer of immature neurons in MDS brain. The findings are consistent with both a migratory and proliferative defect, giving rise to lissencephaly. Moreover, characterization of such rare human malformations of cortical development by immunohistochemical techniques will provide a greater understanding of the underlying mechanisms.
Radial glial (RG) cells have been demonstrated to be a major neural progenitor cell type, but in the human fetal brain, neither their molecular nor their spatiotemporal characteristics are well known. We used glial and neuronal-specific antibodies to determine the antigen characteristics and distribution of RG cells and other neuronal progenitors in the human brain during the first half of intrauterine development. Proliferating RG (4A4+) cells in the ventricular zone (VZ) showed clear caudorostral and ventrodorsal gradients, spreading from the spinal cord to the ventral rhombencephalon, at embryonic stages (4.5-5.5 gestational weeks [gw]). However, in the same embryo, other dividing cells expressed the neuronal marker SMI-31 and were present throughout the entire CNS, including the rostral prosencephalon. At the beginning of cortical neurogenesis (6 gw), proliferating VZ cells labeled either with neuronal markers (SMI-31, MAP2, beta-III-tubulin), double-labeled 4A4(+)/SMI-31+ cells, or cells not labeled with these antibodies, were in close proximity to each other. At midgestation (17-24 gw), RG divisions were less frequent, but were spread throughout the entire cerebral cortex, including the subventricular and intermediate zones and the subpial granular layer. Several subtypes of RG were co-labeled with vimentin and other glial markers (BLBP, GFAP, or GLAST) and quantified in vitro. In conclusion, the diversity of cortical progenitors in the human brain may, in part, explain the unique complexity of the human cerebral cortex.
Microscopic examination of a blood clot expelled by a physically and mentally disabled woman taken to the emergency room because of genital bleeding revealed the presence of chorionic villi encircled by decidua, hemorrhage, and necrosis. In order to identify the father of the product of conception, sections of formalin-fixed, paraffin-embedded abortion material were subjected to laser microdissection: DNA extraction from chorionic villi selectively isolated from the surrounding tissues allowed successful STR-typing of fetal cells, which was otherwise prevented by excess maternal DNA. The large number of homozygous genotypes in the fetal profile suggested incestuous paternity. Analysis of reference DNA samples from male relatives excluded the woman's father, paternal grandfather, and maternal grandfather, whereas the obligate paternal alleles of the fetus were constantly present in the genotypes of the woman's brother, clearly demonstrating brother-sister incest (probability of paternity > 99.99999%).