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At least 775 records · Page 43Linked to original sources
PubMed1984

Diabetes in pregnancy: decreased placental blood flow and disturbed fetal development in the rat.

Placental blood flow was measured with the aid of radioactive microspheres, in normal (N) and manifest diabetic (MD) rats, and related to fetal body growth and incidence of congenital malformations. The total blood flow in the placentae of the MD rats was decreased to about one-half of the normal flow on gestational days 20 and 22. The placentae of the MD offspring were enlarged, whereas the fetuses in this group were smaller than normal. Thus, the placental blood flow per placental weight was drastically decreased in the MD fetuses on both days 20 and 22. In contrast, the placental blood flow per fetal weight was not different in the N and MD groups on gestational day 20 whereas it was decreased in the MD offspring on gestational day 22. Placental blood flow in the malformed fetuses of the MD group did not differ significantly from that in the nonmalformed MD fetuses.

Animals↗
PubMed1981

The fetal development of the luteinizing hormone-releasing hormone (LHRH) neuronal systems of the guinea pig brain.

We have studied the distribution of LHRH-like immunoreactive material in fetal guinea pig brains beginning at day 25 of gestation. Cells and processes were first detected throughout the peripheral, intracranial and central course of the nervus terminalis at 28 (but not 25) days of gestation. The localization of LHRH in this structure preceded its appearance in the hypothalamus and coincided with the initial detection of immunoreactive LH in the pituitary gland. The possible role of the LHRH neuronal network within the nervus terminals in the development of reproductive function is discussed. Comparisons between the brains of littermates of both sexes were made at each age (days 28 through 60 of gestation) to determine possible differences between the sexes in the development of the LHRH neurosecretory systems. No sexually dimorphic features were evident in these systems throughout the prenatal period except at days 40 and 45. At these ages, differences in the number of LHRH neurons in the arcuate nucleus were found between the sexes in some but not all of the brains examined. These differences in LHRH concentrations may reflect the onset of testicular activity as indicated by an increase in serum testosterone levels. Increased serum testosterone concentrations were observed in the male fetuses beginning at 45 days of gestation. However, cell counts made within this nucleus from days 40 through 60 of gestation indicated no comparable sexual dimorphism in the total neuronal population which appeared to be relatively stable throughout this period of brain growth. The number of immunoreactive LHRH neurons visible throughout the brain increased from days 30 through 45 and fewer LHRH cells were seen on days 50 and 60 of gestation, particularly in the arcuate nucleus. The apparent decrease in visible LHRH neurons was concomitant with an increase in number and more extensive distribution of immunoreactive processes throughout the hypothalamus and in certain extrahypothalamic areas of the brain.

Animals↗
PubMed2004

The concentration of elastic fibres in the male urethra during human fetal development.

OBJECTIVE: To describe the distribution of elastic fibres in the developing male urethra and to provide stereological data of the concentration of elastic fibres in the human urethra. MATERIALS AND METHODS: Urethras were obtained from 10 fresh normal human fetuses at 15-36 weeks of gestation. A place-matched spongy urethra of a 27-year-old normal adult man was also analysed. Samples were fixed in Bouin's solution, embedded in paraffin and histologically processed. The elastic system fibres were evaluated by light microscopy using Weigert's resorcin-fuchsin technique after oxidation. Morphometric values were assessed by the point-counting method. The volumetric density (Vv) of elastic fibres was correlated with fetal age. RESULTS: At 15 weeks the elastic fibres were sparse and homogeneously distributed. The size and thickness of elastic fibres increased with age, mainly in the third trimester of gestation. Elastic fibres formed a randomly orientated network in the trabeculae of the corpus spongiosum. The mean (sem) Vv of elastic fibres in the spongy urethra was 5.2 (0.4)% in the fetus at 15 weeks and 14.8 (1.0)% at 36 weeks. In the urethra of the place- matched young man the Vv was 19.0 (1.3)%. The concentration of elastic fibres in the spongy urethra increased significantly with age. CONCLUSION: The high concentration of elastic fibres in the spongy urethra may partly explain its high extensibility. The progressive increase in elastic fibres during development implies functional adaptation of the fetal male urethra.

Elastic Tissue↗
PubMed2003

Downregulation of Bcl-2 proteins in type I spinal muscular atrophy motor neurons during fetal development.

Spinal muscular atrophy (SMA) is an autosomal recessive disorder caused by mutations in the survival motor neuron gene. The degeneration and loss of the anterior horn cells constitute the major neuropathological finding in SMA, although the mechanism and timing of this abnormal motor neuron death remain unknown. It has recently been reported that the fetal SMA spinal cord shows a significant increase in cells with DNA fragmentation, suggesting that the programmed cell death is aberrantly increased in type I SMA during development. We have analyzed 2 antiapoptotic proteins, Bcl-2 and Bcl-X, by Western blot and immunohistochemistry screening for differential expression in control and SMA fetal spinal cords. Expression of these proteins was found in various neuronal populations and structures of the developing spinal cord. At 15 weeks, motor neurons of SMA fetuses showed a marked decrease in the levels of Bcl-2 and a delay in the expression of Bcl-X in comparison with controls. The difference in the pattern and degree of expression is consistent with a role for both proteins in the aberrant programmed cell death observed in type I SMA.

Anterior Horn Cells↗