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At least 721 records · Page 40Linked to original sources
PubMed1990

Sympathetic reactivity of cerebral arteries in developing fetal lamb and adult sheep.

The response of cerebral arteries to norepinephrine was examined in vivo in six dated preterm fetal (94-121 days gestation), eight term fetal (127-141 days gestation), five newborn (7-14 days), and five adult sheep, anesthetized and equipped with a closed cranial window. Norepinephrine (10(-8)-10(-4) M in cerebrospinal fluid) caused a dose-dependent decrease in pial arteriolar diameter in fetal and newborn lambs; however, preterm fetuses were 7- and 14-fold more sensitive to norepinephrine than term fetuses and newborn lambs, respectively. The effective concentration of norepinephrine inducing a 15% decrease in diameter (EC15) was 4.6 +/- 1.8, 33 +/- 11, and 64 +/- 23 microM, for the respective ages. Adult cerebral arterioles did not contract to norepinephrine. In preterm and term fetuses, the contractile response to norepinephrine was blocked by alpha 1-antagonist, prazosin (3 mg iv), and was enhanced by cocaine (10(-5) M; EC15 = 0.086 +/- 0.04 and 1.84 +/- 1.20 microM, respectively) indicating that alpha 1-adrenoceptors mediate the response and that the decrease in sensitivity is not caused by development of neuronal uptake processes. In seven fetuses (111-141 days; mean 123 days gestation), electrical stimulation of the superior cervical sympathetic ganglion constricted pial arterioles by 21 +/- 5%; this contractile response was also blocked by prazosin. The cerebral arterioles of the fetus in utero possess a functional sympathetic innervation capable of influencing cerebrovascular resistance. There is a loss of responsiveness of cerebral arterioles to norepinephrine during fetal and postnatal development, suggesting that the contribution of neuroadrenergic mechanisms to cerebrovascular regulation may be relatively unique to the immature brain.

Aging↗
PubMed1997

Vitamin and mineral transfer during fetal development and the early postnatal period in pigs.

There are periods during pregnancy when sows may have a temporally high requirement for certain vitamins and minerals. Proteins transferring retinol and Fe to the developing pig fetus have been discovered, whereas transport mechanisms for other vitamins and minerals are probably present but have not yet been identified. Sow body tissues can serve as a reservoir for many micronutrients, but it is not known whether these reserves can supply an adequate quantity during critical fetal developmental periods. There is a low placental transfer of vitamin E to the fetus even if the dietary concentration fed to a gestating animal is high, but colostrum and milk concentrations can be increased when the nutrient is fed to sows. If the dam's diet contains inadequate Ca or P, the concentration of these elements in the developing fetus and milk will not be affected. Consequently, sow bone demineralization will occur under conditions of dietary inadequacy of Ca and P. Other nutrients can be depleted from sow tissue reservoirs over several parities (e.g., Se), resulting in low quantities being provided in the milk for nursing pigs. Scientific information involving adequate vitamin and mineral nutrition for female pigs to improve conception rate and embryonal survival that will result in optimum fetal and postnatal pig development can be considered to be in its infancy.

Animal Nutritional Physiological Phenomena↗
PubMed2002

Fibrillin-1 and fibrillin-2 in human embryonic and early fetal development.

The extracellular glycoproteins fibrillin-1 and fibrillin-2 are major components of connective tissue microfibrils. Mutations in the fibrillin-1 and fibrillin-2 genes are responsible for the phenotypical manifestations of Marfan syndrome and congenital contractural arachnodactyly respectively, which emphasizes their essential roles in developmental processes of various tissues. Consistent with this last notion, organ culture experiments have indirectly suggested morphogenic roles for fibrillins in lung and kidney development. In order to contribute to the understanding of the roles of fibrillins in developmental and morphogenetic events, we have investigated the distribution of fibrillin-1 and fibrillin-2 in human embryonic and early fetal tissues between the 5th and the 12th gestational week, i.e. at the beginning of organogenesis. Fibrillin-1 and fibrillin-2 were localized immunohistochemically using specific monoclonal antibodies, mAb 69 and mAb 48, respectively. Both fibrillins are widely distributed in various human anlagen, from early developmental stages. In most embryonic and early fetal human organs such as skin, lung, heart, aorta, central nervous system anlage, nerves, and ganglia, fibrillin-1 and fibrillin-2 follow the same temporo-spatial pattern of distribution. However, in other organs such as kidney, liver, rib anlagen, notochord fibrillin-1 and fibrillin-2 are distributed differentially. The present paper is focused on this aspect. These results suggest different roles for fibrillin-1 and -2 in the development of these structures.

Embryo, Mammalian↗
PubMed1998

[Early fetal development of the small intestine mucosa in cattle (Bos primigenius taurus)].

The development of the bovine small intestine was examined in 24 embryos and fetuses by light microscopic, scanning and transmission electron microscopic methods. Special reference was paid to the genesis of the epithelium and particularly of the villi intestinales. The primitive intestine consists of one layer of epithelial cells surrounded by mesenchym and tunica serosa. The fetal intestine (up to the 24th week of gestation) shows all the morphologic structures of the adult. In small intestine the development of cryptae and villi intestinales starts before the 7th week of gestation and progresses with a proximo-distal gradient. Epithelial proliferation that gives rise to primary epithelial villi makes epithelium become temporarily stratified. Finger-like secondary villi develop by proliferation of the mesenchym. In addition to this process mucosal folds occur in duodenum giving rise to villi by segmentation. At the same time the differentiation of epithelium starts. The fetal small intestine, like many other fetal tissues displays masses of glycogen.

Animals↗
PubMed1998

Immunocytochemical study of the maxilla and maxillary sinus during human fetal development.

We quantitatively examined the distribution of the proliferating cell nuclear antigen (PCNA), which is associated with cell division, and of components of the ECMs (collagen types I and III, tenascin and osteonectin) in the immature zones at three sites: palatine, inferior and vertical surface region of the fetal human maxilla as well as the maxillary sinus (MS) at 12, 16, 20, 24, and 28 weeks gestation. The percentage of PCNA-positive cells was the highest at 16 weeks in the immature zones of maxilla. Tenascin and fibrillar collagens (collagen types I and III) were especially present in the cellular zone linked to the bone and cartilage matrices of the immature zones of the maxillary bone at 20-24 weeks gestation. The osteonectin was detected on the maxillary bone from 24 weeks. These distributions of ECMs revealed the specific and contrasting profiles of development in the human maxillary bone and might reflect the formation of paranasal sinus as MS.

Cell Count↗
PubMed1995

Inhibin and activin in embryonic and fetal development in ruminants.

Inhibin, activin and follistatin are protein hormones with diverse physiological roles. The involvement of inhibin in the regulation of pituitary FSH production and secretion in adult males and non-pregnant females is well established. However, it is unlikely that inhibin plays a similar role in pregnancy in ruminants. Inhibin and activin molecules show a high degree of structural similarity to potent growth and differentiation factors of the transforming growth factor beta (TGF-beta) superfamily of peptides and their localization in a range of embryonic and fetal tissues indicates that they may thus play a role in development. Furthermore, the demonstration that follistatin is also present in a number of embryonic and fetal tissues and fluids has further implications for the actions of activin to which it binds. The role of inhibin, activin and follistatin in early development has yet to be established since gene knockout experiments have so far proved inconclusive. During mid- and late gestation, high concentrations of inhibin are found in the testes and plasma of male fetuses of sheep and cattle. Inhibin may play a role in regulating pituitary FSH release in late pregnancy, but the very high concentrations of this hormone in ovine fetal testes and in male fetal plasma compared with that observed in the fetal ovary and female fetal plasma has yet to be explained. The recent observation of high concentrations of inhibin, activin and follistatin in amniotic fluid surrounding the fetus is intriguing. Excretion via urine or lung liquid is partly responsible for the presence of these proteins in amniotic fluid. The fetal membranes and the placenta are also possible sources. It remains to be established whether these proteins constitute an inactive pool of secreted hormone or whether they have other actions in this fetal compartment.

Activins↗
PubMed2003

Dynorphin and the hypothalamo-pituitary-adrenal axis during fetal development.

Although dynorphin has long been considered an endogenous opioid peptide with high affinity for the kappa-opioid receptor, its biological function remains uncertain. The high concentration of dynorphin peptides and kappa-opioid receptors in the hypothalamus suggest a possible role for dynorphin in neuroendocrine regulation. This review will summarize evidence that support a role for dynorphin in regulation of the developing hypothalamo-pituitary-adrenal (HPA) axis. Dynorphin can exert dual actions on adrenocorticotropin (ACTH) release: (i) via activation of hypothalamic kappa-opioid receptors leading to release of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), and (ii) via a non-opioid mechanism that involves N-methyl-D-aspartate (NMDA) receptors and prostaglandins, and which is not dependent on CRH or AVP. The primary site of action of dynorphin and NMDA appears to be the fetal hypothalamus or a supra-hypothalamic site. The non-opioid mechanism does not mature until a few days prior to parturition and is active for only the brief perinatal period. In contrast, the opioid mechanism behaves as a constitutive system with sustained activity from prenatal to postnatal life. It is likely that the two mechanisms may respond to different stress stimuli and play a different role during development.

Animals↗
PubMed1997

Early fetal development of lung vasculature.

Despite its relevance to a variety of congenital anomalies, the earliest stages of lung vascular development are poorly understood. In other organs, two processes have been identified: vasculogenesis, the development of blood lakes in mesenchyme, and angiogenesis, the branching of new vessels from preexisting ones. In the present study we established the events in the development of the lung's vasculature in Swiss-Weber mouse fetuses between 9 and 20 days gestation, using light microscopy (LM), transmission electron microscopy (TEM), barium-gelatin angiograms, and scanning electron microscopy (SEM) of Mercox (methyl methacrylate) vascular casts. Three features were identified: (1) central sprouting or angiogenesis for up to approximately seven generations (counting the artery to each lung as first generation); (2) the formation of peripheral lakes by vasculogenesis; and (3) the development of communications between the central and peripheral systems. At 9 days gestation, intercellular spaces were apparent in the lung mesenchyme; these were formed by discharge of vesicles from mesenchymal cells, which then regrouped to provide "endothelial" cells lining the spaces. The isolated lakes coalesced to form sinusoidal spaces of irregular profile. At 12 days gestation, the earliest time at which were able to make a cast, sprouting of arteries and veins from the central pulmonary vascular trunks was apparent. Between 13 and 14 days gestation the earliest connection between the peripheral and central spaces was identified. Such connections became more numerous and dense by term. Similar images seen on examination of human fetal lung sections by LM indicated that similar processes occur in the vascular development of the human lung.

Animals↗
PubMed2003

Transcription factor 3',5'-cyclic adenosine 5'-monophosphate-responsive element-binding protein (CREB) is decreased during human adrenal cortex tumorigenesis and fetal development.

Various cellular and molecular alterations of the cAMP pathway have been observed in adrenal Cushing syndrome. We recently reported the loss of cAMP-responsive element-binding protein (CREB) expression in the adrenocortical cancer cell line H295R. CREB is the major nuclear target of the cAMP pathway. This study therefore aimed to analyze the status of the CREB protein in various types of human adrenocortical tumors and normal fetal adrenal cortex. CREB protein status was studied by Western blotting in adrenocortical adenomas (AAs, n = 27) and adrenocortical carcinomas (ACs, n = 24). A decrease of CREB protein was noticed in the majority of the adrenocortical tumors. The dramatic decrease in CREB protein levels was more pronounced in ACs than in AAs. Levels of the phosphorylated form of CREB were also low in adrenocortical tumors, with a greater decrease in ACs than in AAs. EMSAs also showed decreases in the amounts of CREB- containing complexes in nuclear extracts from adrenocortical tumors. The secretory status of adenomas was strongly correlated with CREB levels, significantly lower in nonfunctioning AAs (n = 9) than in functioning AAs (n = 9). CREB levels, determined by Western blotting and immunohistochemistry, were very low in the fetal zone of human fetal adrenal cortex, whereas they were normal in the definitive zone. In tumors, adrenocortical cells in several zones were weakly immunohistochemically stained for CREB, whereas CREB was uniformly detected in nonendocrine cell nuclei (e.g. vascular cells, fibroblasts). These results suggest that the absence of CREB may be linked to the development of a highly aggressive tumor with a dedifferentiated benign (nonfunctioning AA) or malignant (AC) phenotype. These findings highlight the similarities between the normal human fetal adrenal gland and adrenal cancers previously observed in terms of parallelism in IGF-II production.

Adolescent↗
PubMed2003

Alpha-2 adrenergic receptors stimulate actin organization in developing fetal rat cardiac myocytes.

Expression of alpha(2)-adrenergic receptors (alpha(2)-AR) is very high in fetal rat heart although numbers decline with increasing gestational age. The current experiments were designed to identify the subtypes of alpha(2)-AR expressed and the function of these receptors in fetal cardiac myocytes. Expression of alpha(2)A and alpha(2)C, but not alpha(2)B, was confirmed in the myocyte population by indirect immunofluorescence microscopy with subtype-specific antibodies and by Western blot. Both dexmedetomidine, an alpha(2)-selective agonist, and norepinephrine, increased actin cytoskeleton organization and this increase was blocked by the alpha(2)-selective antagonist, atipamezole. Furthermore, dexmedetomidine inhibited isoproterenol-stimulated cAMP accumulation in isolated fetal rat heart and this was blocked by rauwolscine. Therefore, functional alpha(2)A and alpha(2)B subtypes are present in the fetal rat heart where they may have a role in cardiac development.

Actins↗
PubMed1982

Pregnancy and fetal development in hamsters treated with prostaglandin F2 alpha.

The influence of PGF2 alpha on pregnancy and fetal outcome was investigated in the hamster. Following subcutaneous treatment with 50, 100, 200, 400, and 800 micrograms PGF2 alpha prenatal loss was significantly increased only at the highest dose level. The offspring of the treated animals were all alive and normal. Fetal weight was not affected. However, following intravenous injection of 100 and 200 micrograms PGF2 alpha there was a significant reduction in fetal weight, and at the 400 micrograms dose level an increase in fetal indicate that PGF2 alpha is not teratogenic in hamsters despite the apparent greater sensitivity of the hamster embryo to prostaglandin.

Animals↗
PubMed1990

Blood coagulation factors in human embryonic-fetal development: preferential expression of the FVII/tissue factor pathway.

The expression of a number of blood coagulation factors (F) (FX, FIX, FVIII, FVII, alpha-, beta-, gamma-fibrinogen chains, protein C, and antithrombin III [AT III]) was analyzed at RNA and protein level in 5- to 10-week-old human embryos and fetuses. FX, FIX, and FVII were also analyzed at protein level. Total and poly(A)+ RNA, extracted from embryonic-fetal (FL) and adult liver (AL), were analyzed by dot and Northern blot hybridization with specific cDNA probes. The results indicate that: (1) the size of the messenger RNAs of these factors is equivalent in FL and AL; (2) in the 5- to 10-week period, their abundance in FL increases from 30% to 50% of the adult level except for FIX (from 2% to 10%) and FX (always 100% of the adult value). Western blot analysis of FIX, FX, and FVII in 5- to 10-week soluble liver proteins and 6- to 8-week plasma showed a low level of FIX versus a higher concentration of both FVII and FX, when compared with corresponding adult values, ie, a liver protein level of 10% versus 100% and a plasma concentration level of 10% versus 40%. Although little is known so far on the activity and the functional role of the clotting factors in early human ontogenic development, these studies suggest an activation of FX via the FVII/tissue factor activity rather than the FIXa/FVIIIa phospholipid complex in human embryonic and early fetal life.

Blood Coagulation Factors↗
PubMed2002

Formation of ovarian follicles during fetal development in sheep.

The origin of follicle (i.e., pregranulosa) cells that become the somatic component of primordial follicles is obscure. In addition, information regarding the structural changes that accompany the concomitant regression of ovigerous cords and the appearance of primordial follicles is lacking. In the present study, ovine ovaries collected at frequent time intervals between Day 38 and Day 100 of fetal life were examined by light and electron microscopy. To gain new information regarding the origin of follicular cells, incorporation of 5-bromo-2'-deoxyuridine was used to identify proliferating cells at selected stages of development. Based on the location and identity of proliferating cells, apoptotic cells, and sequential changes in histoarchitecture, we hypothesize 1) that most (i.e., >95%) of the granulosal cells in newly formed primordial follicles originate from the ovarian surface epithelium; 2) that the sequential events leading to follicle formation take place entirely within ovigerous cords, with the first follicles forming at the interface of the cortex and medulla; and 3) that the loss (i.e., >75%) of germ cells, but not of somatic cells, within the ovigerous cords is a means by which each surviving oocyte gains additional pregranulosal cells before follicle formation. Conceptual models detailing the chronology of developmental events involved in the formation of primordial follicles in sheep are discussed.

Animals↗
PubMed1992

Fetal development of delta-sleep-inducing-peptide-like immunoreactivity in hypothalamus of guinea pig with special regard to the prenatal colocalization with gonadotropin-releasing-hormone-like immunoreactivity.

Delta-sleep-inducing peptide (DSIP) colocalizes within gonadotropin-releasing-hormone (GnRH)-containing neurons in adult hypothalamus and could play a role in the regulation of hypothalamic-pituitary axis in adults. To support the possibility that DSIP also participates in fetal neuroendocrine events and to demonstrate the ontogenic evidence of coexisting neuropeptides, we have performed a detailed immunocytochemical study of DSIP- and GnRH-immunoreactivity in fetal hypothalamus of guinea pig. Using indirect immunofluorescent and sequential double-immunolabeling (elution-restaining) techniques, the results indicated that DSIP immunoreactivity was initially detected at the 38th day of gestation. In contrast to the first appearance of GnRH immunoreactivity at day 28, therefore, a 10-day delay was found. Such a delay remains as yet unexplained. From its first occurrence, DSIP immunoreactivity was always labeled with GnRH, whereas some of GnRH-immunoreactive structures did not display a DSIP immunoreactivity. But with the growth of fetus, especially before and after birth, a complete overlap between DSIP and GnRH immunoreactivity was observed throughout various regions of hypothalamus. Attention was also focused on prenatal morphological development of DSIP/GnRH- and GnRH-immunolabeled neurons. Initially, labeled neurons were visualized as uni- or bipolar types. Thereafter, their smooth and irregular subtypes could be distinguished. During later fetal age, relatively mature features were evident such as the increase of multipolar and irregularly labeled neurons. Taken together, these data provide, for the first time, anatomical evidence that DSIP exists in fetal hypothalamus and that, like GnRH, it could regulate the hypothalamic-pituitary axis during ontogenesis.

Animals↗