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At least 811 records · Page 45Linked to original sources
PubMed1991

Lymphocyte migration through the wall of postcapillary venules in the fetal development of human palatine tonsil.

Migration of lymphoid cells through the wall of postcapillary venules was studied in the palatine tonsils of five human fetuses. The direction of the migration of lymphoid cells as observed in the early fetal period seems to be mostly from the lumen of the venule into the tonsillar parenchyma. Migration starts with the adherence of the lymphocyte by means of a cytoplasmic projection to the cellular surface of a high-endothelial cell. The projection slips between two neighbouring endothelial cells and extends to settle on the basal membrane of the endothelium. After the disruption of the basal lamina the lymphocyte migrates into the subendothelial connective tissue and further into the extrafollicular tissue of the tonsil. The possibility of transendothelial migration of lymphoid cell through the wall of the postcapillary venule is discussed. Even in case, when the lymphocyte appears to be completely enveloped by the cytoplasm of the endothelial cell it may be in reality the intercellular migration--the lymphoid cell is pressed into the cytoplasm of an endothelial cell.

Cell Movement↗
PubMed1985

[Sonographic diagnosis of fetal development disorders at the 1st Gynecologic Clinic of the Munich University 1984].

The diagnostic accuracy of sonographic screening is demonstrated by the results obtained in 171 pregnant women referred to the Department of Gynaecology of the University of Munich during 1984 for on-target sonography of foetal developmental disturbances. The accuracy was found to be 80%. Examination of pregnant women at risk shows a very low rate of developmental disturbances. The consequences arising from the observed disturbances of development are discussed.

Abortion, Induced↗
PubMed2004

Alpha-synuclein is expressed in different tissues during human fetal development.

Alpha-synuclein is a small presynaptic protein associated with both normal synaptic plasticity and neurodegenerative processes. Its normal cellular function, however, remains unknown. Even though it is highly enriched in the brain, its presence was reported in other human adult tissues. In the present study, we examined tissue expression of alpha-synuclein in human and rat prenatal development. Using Western blot analysis, various peripheral tissues from 15 to 23 gestational weeks, human and E19 rat fetuses, along with human and rat adult tissues, were assayed. alpha-Synuclein expression was observed in all fetal human organs examined. In adult human tissues the high expression of alpha-synuclein was maintained in the brain, whereas in other organs the expression was greatly reduced. In contrast, both in fetal and adult rat tissues, alpha-synuclein was only detected in the brain. In addition to a 19-kDa alpha-synuclein band, 36- and 52-kDa immunoreactive bands were observed in all fetal and adult human organs, with the exception of the brain, but their identity remains to be determined. These findings suggest that apart from its function in development of the nervous system, alpha-synuclein has an important function in peripheral tissues as well during normal human prenatal development.

Adrenal Glands↗
PubMedDate not supplied

Oxonic acid and fetal development: II. Teratogenicity in rats.

Feeding the uricase inhibitor potassium oxonate (KOx) as 3% of the diet to pregnant rats beginning on the 8th day of gestation for either 2 or 3 days caused a time-related increase in fetal resorptions, with the incidence in the experimental group treated for the additional day being 72% higher than the 2-day group. The shorter treatment period permitted more rat fetuses to survive to term; however 9.3% of these showed gross malformations, exencephaly and/or visceral herniation. Thus, KOx is demonstrated to be both embryotoxic and teratologic in the rat.

Animals↗
PubMedDate not supplied

[Fetal development in mild and severe pre-eclampsia: correlation with maternal laboratory parameters and Doppler ultrasound].

During three and a half years we observed 83 single pregnancies all delivered by caesarean section. All of them had a mild (systolic blood pressure > 140, diastolic > 90 and proteinuria > 0.5 g/dl) or a severe preeclampsia (systolic blood pressure > 160, diastolic > 100 and proteinuria > 3.0 g/dl). We found significantly twice as many abnormal uteroplacental blood flow velocities in the severe preeclampsia group than in the mild one. These results draw us to the conclusion that possible pathological changing of the vessels is due to preeclampsia which does not need to correlate with a placental insufficiency and fetal growth retardation. An abnormal uteroplacental blood flow velocity connected with an abnormal umbilical blood flow velocity raises the fetal morbidity and the early childhood morbidity. Fetal outcome in mild compared to severe preeclampsia definitively shows a worse prognosis for those fetuses whose mother developed a prepartal severe preeclampsia. A distinctly increased rate of cerebral haemorrhages, abnormal neurological signs, acute respiratory distress syndromes and bronchopulmonary dysplasia was found. Finally we show an additional risk for fetal outcome in absent or reverse enddiastolic flow velocity (AREDFV) in the severe preeclampsia group. We observed in the AREDFV group with severe preeclampsia in comparison to a group of AREDFV without maternal preeclampsia more than twice as many cerebral haemorrhages, abnormal neurological signs and bronchopulmonary dysplasia.

Adult↗
PubMed2006

Fetal development of membrane water channel proteins aquaporin-1 and aquaporin-4 in the human brain.

Aquaporin-1 and aquaporin-4, water channel membrane proteins reported in both experimental animals and in adult humans, have been detected in different, non-overlapping areas of the central nervous system. This immunohistochemical study describes the developmental expression pattern of the water channel membrane proteins, aquaporin-1 and aquaporin-4, in various structures of human fetal brain over the gestational period of 14-40 weeks. Aquaporin-1 immunostaining was exclusively found in the epithelial cells of the choroid plexus from the 14th gestational week, and the staining pattern altered slightly over time. At week 14, immunostaining appeared only in the apical cell membranes. By the 18th gestational week, the entire plasma membrane of these apical cells was immunopositive, as well as was the cytosol. These changes in immunoreactivity indicate an increasing production of aquaporin-1 in the epithelial cells during the period between the 14th and 24th weeks of gestation. Aquaporin-4 immunostaining was first detected in the archicortex, from gestational week 14 and was detected in the neocortex, 6-7 weeks later. Immunostained structures were always astrocytes, particularly the astrocytic endfeet in the ventricular wall, at the developing ependymal lining, at the pial surface, and around the capillaries. Neuronal labeling was not observed. These results in human fetal brain lend morphological support to the previous findings that aquaporin-1 and aquaporin-4 play different roles in the regulation of the water homeostasis of the brain.

Aquaporin 1↗
PubMed1977

Fetal development in experimental uremia.

Uremic women on hemodialysis with metabolic bone disease (hyperparathyroidism, osteomalacia resulting from defective vitamin D metabolism) and anemia (erythropoietin deficiency) are known to give birth to infants without bone disease or anemia. Therefore, skeletal development (enchondral and desmal bone formation) and hepatic erythropoiesis were evaluated in fetuses of uremic rats. These fetuses failed to show defective mineralisation or evidence of bone disease. Bolus injection of high doses of exogenous PTH into the maternal or fetal organism did not affect fetal bone histology. In addition, no apparent defect of bone mineralisation or bone formation was found in fetuses of ricketic rats. Normal mineralisation in the offspring of uremic rats may be explained by fetal hyperphosphatemia and/or insensitivity of fetal (woven) bone mineralisation to vitamin D. Absence of fetal anemia (normal hematocrits, normal density of hematopoietic cells in the liver) in the presence of maternal anemia is presumably due to the insensitivity of fetal erythropoiesis to erythropoietin.

Animals↗
PubMed2001

Gene expression of leptin and uncoupling proteins: molecular end-points of fetal development.

Uncoupling proteins (UCPs) are considered to be major determinants of energy expenditure in mammals. During development in rodents, the expression of the UCP genes occurs sequentially. UCP2 mRNA is expressed long before birth. UCP1 mRNA expression in brown adipose tissue (BAT) starts in the late fetal period, and the expression of UCP3 mRNA begins immediately after birth in BAT and skeletal muscle. The postnatal induction of UCP1 gene expression is due mainly to cold stimuli, whereas the switch-on of UCP3 mRNA expression after birth requires the stimulus of food intake, specifically of lipids in the mother's milk. However, UCP3 mRNA expression after birth is also highly sensitive to leptin, and administration of a single injection of leptin to neonatal mice that were not allowed to suckle partly mimicked the natural induction of UCP3 gene expression in BAT and skeletal muscle. The speed of the effects of leptin on UCP3 mRNA expression suggests a direct action on skeletal muscle and BAT. The injection of leptin produced minor effects on UCP1 mRNA expression, and no effects were observed on UCP2 mRNA. In summary, leptin appears to contribute to the regulation of UCP3 gene expression in the perinatal period. Whatever the mechanism of action of leptin in BAT and skeletal muscle, it is already functional at birth.

Adipose Tissue, Brown↗