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Biomedical subjects

M Vogel

Publications and source records attributed to M Vogel.

461 records · Page 26Linked to original sources
PubMedDate not supplied

[A kyematopathologic study of perinatal deaths].

On the basis of macro- and microscopic findings of the organs and placentas of 574 perinatally deceased children questionnaires were conceived. They should complement already running peri- and neonatal surveys. In considering also clinical data a primary cause of death was attempted to define with each of 326 cases of whom 51% had died before birth, 4% sub partu, and 44% during the first week of life. Among primary causes of death anoxia/asphyxia (66%), gross malformations (16%), and infections (15%) were most frequent. There were many small-for-dates among stillborns (59%) and early neonatal deaths (44%). In 89% of the neonatal deaths (less than 37 weeks of gestation) microscopic placental insufficiency was found. Most probably the spectrum of causes of death is different now. However, the impact of prenatal growth retardation on mortality and morbidity seems to persist. We recommend to include the weight-gestational age relationship in vital statistics.

Asphyxia Neonatorum↗
PubMedDate not supplied

[Immunohistochemical localization of pregnancy-specific beta 1-globulin in placentas at various ages].

In the study reported here the dispersion of pregnancy-specific beta 1-globulin (SP1) in placentas from the 6th to the 40th week of pregnancy was determined by means of the peroxidase-anti-peroxidase method; cytophotometric quantification of the stain reaction was also carried out. SP1 was only identified in syncytiotrophoblasts. Cytotrophoblasts, villous stroma and vascular endothelia were free of SP1. Within the syncytiotrophoblast SP1 was found in particularly large quantities in proliferation buds. Weaker reactions were obtained in the following order for: nucleated villous epithelium, non-nucleated epithelial squama, including the syncytiocapillary membranes, epithelial nodules with nuclear pyknosis and regressively changed villous epithelium associated with stromal fibrosis. Spectrophotometry of the extinction at the wave-length of the DAB-peroxidase product revealed, in relation to the age of the placenta, a relatively uniform intensity of reaction during the entire duration of pregnancy, with only a moderate rise up to the 24th week and a slight decrease until term.

Beta-Globulins↗
PubMedDate not supplied

[Immunohistochemical localization of human chorionic gonadotropin and human placental lactogen in placentas of various ages].

By means of the peroxidase-anti-peroxidase reaction it was possible to identify HCG and HPL in placentas between the 6th and 40th weeks in the syncytiotrophoblast, though not in the cytotrophoblast, the villous stroma or in vascular endothelia. A cytophotometric extinction measurement at 425 nm revealed a strong reaction intensity for HCG during the first trimester, a reduction to half this value in the second and further reduction in term placentas. In the 6th and 10th weeks of pregnancy only low quantities of HPL were demonstrable; the amount increased in the second trimester, attaining a maximum in the 24th week. In the third trimester the reaction intensity also decreased for HPL. Irrespective of the gestational age the identification decreased in the syncytiotrophoblast for both hormones in the following order; proliferation buds, necleated portions of epithelium, non-nucleated epithelial squamae, syncytiocapillary membranes, epithelium in cases with fibrosis of the villous stroma, epithelial nodes with nuclear pyknosis.

Chorionic Gonadotropin↗
PubMedDate not supplied

Alpha-smooth muscle actin distribution in the pulmonary vasculature comparing hypoplastic and normal fetal lungs.

We investigated the intra-acinar pulmonary vascular muscularization in the developing human fetal lung between the 17th and 24th gestational weeks, that is, during the canalicular phase of lung development. Fifteen hypoplastic and 25 normal developed lungs were included in this study using monoclonal alpha-smooth muscle (sm) actin antibodies for smooth muscle detection. Computer-aided image analysis was performed for morphometrical measurements and statistical evaluation. Alpha-sm-actin-immunoreactive intra-acinar vessels down to a luminal diameter of less than 10 microns were detected in hypoplastic as well as in normally developed lungs. Crucial differences presented as follows: significantly higher density of intra-acinar vessels, especially due to alpha-sm-actin-negative vessels less than 30 microns in luminal diameter, in the control group; significantly higher alpha-sm-actin immunore-activity per section unit as well as per vessel in the hypoplastic lung group. As suggested by others, alpha-sm-actin-positive cells of the intra-acinar vessel wall in the developing human lung were demonstrated to be smooth muscle cells, their immediate precursors, and pericytes. We conclude that the increased alpha-sm-actin immunoreactivity represents muscularization of the vessel wall in functional terms and may be regarded as one structural cause among others for the establishment of persistent fetal circulation in hypoplastic lungs.

Actins↗