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PubMed1987

Expression of myosin light chains during fetal development of human skeletal muscle.

The expression of myosin light chains (MLCs) during the development of human skeletal muscle was investigated by using two different two-dimensional electrophoretic techniques. In both electrophoretic systems the predominant light chain 1 (LC1) expressed during the whole fetal period was found to co-migrate with the adult fast LC1 (LC1F). The main LC2 expressed during the whole fetal period was found to be different from the main fast LC2 (LC2F) and slow LC2 (LC2S) usually present in adult muscle, but co-migrated with a minor component often present in adult muscle. This fetal LC2 was phosphorylatable, and the phosphorylated form co-migrated with the main component of LC2F expressed in the adult. The adult fast LC3 appeared as early as week 20 of gestation, whereas the adult slow light chains (LC1S and LC2S) appeared only during the late fetal period. A minor component of LC1, previously described in humans as an 'embryonic LC' (LCemb.) [Strohman, Micou-Eastwood, Glass & Matsuda (1983) Science 221, 955-957], was only expressed in the early fetal period and was found to co-migrate with atrial LC1 (ALC1). We discuss the expression of these specific developmental forms of MLCs co-existing with immature myosin heavy chains during fetal life.

Adult↗
PubMed1996

Embryonic and early fetal development of human taste buds: a transmission electron microscopical study.

BACKGROUND: Taste buds are assemblies of slender epithelial cells that receive chemical stimuli from the outer (oral) environment. In contrast to the large and well documented information on the morphology of taste buds in adult humans and animals, there are only a few reports on fetal ones, and ultrastructural studies of prenatal human taste buds are lacking completely. Therefore, the present investigation has been carried out to study the taste bud primordium, its morphological changes including synaptogenesis, cell differentiation, and taste pore formation from the time of the onset of taste bud formation around the 8th week until the 15th postovulatory week. METHODS: Taste bud primordia of 42 human embryonic/fetal tongues have been examined by means of transmission electron microscopy. RESULTS: Nerve fibers approach the lingual epithelium between the 6th and 7th postovulatory week. They penetrate the basal lamina during the 8th week and form synapses with poorly differentiated, elongated, epithelial cells. By the 12th week, more differentiated cell types are seen: 1) electron-dense cells resembling type III cells of the adult taste bud containing large numbers of dense-cored vesicles (80-150 nm in diameter); 2) electron-dark cells with well developed endoplasmic reticulum and many apical mitochondria, being candidates for type II cells. Basally, these cells have foot-like processes containing dense-cored vesicles (120-200 nm in diameter), but they do not synapse to nerve fibers. Type I cells, characterized by apically located dense secretory granules, are not observed. First shallow grooves above the taste bud primordium are found around the 10th week. Untypically differentiated apical cellular processes extend onto the surface. Most of the taste pores develop around the 14th to 15th week. In the taste pit, mucous material is not present during the first 15 weeks of gestation. Synapses between cells and afferent nerve fibers were found by the 8th week, reaching a maximum around the 12th to 13th week. CONCLUSIONS: The early presence of taste bud cells containing dense-cored vesicles suggests an at least dual function of embryonic/ fetal taste buds: First, from the 8th until the 14th week, non-gustatory, paracrine functions should be considered. After the 14th week of gestation, when typical taste pores are present, the taste buds possibly start their gustatory function. Differentiated marginal cells are possibly involved in the formation of the taste pore. The lack of type I cells producing the mucous material in the taste pit indicates that the taste bud has not achieved a fully developed function until the 15th week of gestation.

Aging↗
PubMed1979

Red cell oxygen affinity, hemoglobin type, 2,3-diphosphoglycerate, and pH as a function of fetal development.

Studies were carried out on fresh cord blood obtained at delivery from nonstressed normal fetuses ranging from 24 to 42 weeks of gestation, to determine the relationship of 2,3-diphosphoglycerate (DPG), the intracellular red cell and extracellular pH, and the proportions of adult and fetal hemoglobin in regulating the position of fetal red cell oxygen affinity in utero. There was a significant positive correlation between P50 and gestational age (r = .62, P less than .001), the linear regression increased from 17.8 to 22.5 mm Hg. There was also a significant positive correlation between P50 and the percentage of adult type hemoglobin (HbA) (r = .67, P less than .001). In contrast gestational age had no effect of 2,3-DPG levels, the mean and SD was 14.86 +/- 2.04 mol/gm of Hb or delta pH between plasma and red cell, the mean was 0.187 +/- SD 0.032. However, there was a significant negative correlation between the intraerythrocyte hydrogen ion concentration and DPG level (r = .5, P less than .025). It is concluded therefore that the decrease in fetal oxygen affinity as gestation progresses is related mainly to the increase in the amount of HbA and the levels of DPG or delta pH between plasma and red cells are not a function of gestational age.

Blood↗
PubMed1975

Ultrastructure of the developing fetal hepatocyte of Macaca arctoides: a proposed model for studies of fetal drug metabolism.

The ultrastructure of the hepatocyte of the fetal stumptail monkey was examined with the aim of defining a possible model for studies of fetal drug metabolism. Hepatocytes from fetuses of 80 and 160 days gestation, as well as from one animal one week of postnatal age, were examined and compared to human fetal hepatocytes at 12 and 16 weeks gestation. Marked variation was observed in the amount of lipid and the distribution of organelles within the cytoplasm of the hepatocyte in the monkey population. These differences were attributed to genetic variation. Two changes were seen which correlated with developmental age. The amount of hemopoietic tissue decreased and the amount of smooth endoplasmic reticulum increased as the animal matured. The problems of genetic variation and the relative number of hepatocytes at different stages of development were discussed relative to the use of this animal as a model for fetal drug metabolism studies. Attention to both of these problems is considered necessary for the interpretation of biochemical data in future studies.

Animals↗
PubMed1976

Bacterial endotoxin and impaired fetal development.

Small doses of E. coli endotoxin given to pregnant mice on the 13th day of pregnancy caused only a mild maternal illness but induced resorption of approximately half the number of fetuses in each mouse. The remaining live fetuses developed normally and showed no evidence of retarded growth or malformations. The weights of their placentas and maternal spleens increased significantly. Endotoxin given on the 6th day of pregnancy caused a small reduction in fetal weights.

Animals↗
PubMedDate not supplied

11 beta-hydroxysteroid dehydrogenase type II in human colon: a new marker of fetal development and differentiation in neoplasms.

The colon plays an important role in water and electrolyte homeostasis and is a major target tissue for aldosterone. 11 beta-Hydroxysteroid dehydrogenase type II enzyme (11 beta HSD2) confers specificity to the non-selective mineralocorticoid receptor by inactivating glucocorticoids, thus allowing binding by mineralocorticoids. Using immunohisto/cytochemistry and Northern blot analysis, we examined 11 beta-HSD2 expression in human fetal colon (23 cases ranging in age from 15 to 40 weeks gestation), neonatal colon (2 cases, 6 and 12 months old), normal adult colon (15), adenoma (35), adenocarcinoma (34) and the human colonic epithelial cell line T84, in the presence or absence of sodium butyrate, to study the correlation between enzyme expression and cellular or neoplastic differentiation. In fetal colon, weak 11 beta-HSD2 immunoreactivity was detectable in superficial epithelium from 25 weeks gestation, but normal adult levels were apparent only after 40 weeks gestation, suggesting that fully developed aldosterone induced electrolyte transport can occur only at late gestational stages. In adult normal colon, superficial absorptive cells at the top of crypts were strongly positive for 11 beta-HSD2, whereas immunoreactivity was weak in adenomas and carcinomas, and the pattern of localization varied among patients. Northern blot analysis performed on 4 cases of adenocarcinoma also demonstrated lower levels of mRNA than autologous non-neoplastic colonic mucosa. In carcinomas, 11 beta-HSD2 immunoreactivity was more frequently detected in differentiated structures, such as those forming glandular or tubular structures. Studies with T84 cells showed that expression of 11 beta-HSD2 was markedly enhanced with the addition of sodium butyrate, a well known inducer of cell differentiation in colonic epithelia. These results suggest that the expression of 11 beta-HSD2 is associated with differentiation or maturation in human colonic epithelia and that the enzyme may serve as a useful marker in development and disease.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1982

Immature B cells in fetal development and immunodeficiency: studies of IgM, IgG, IgA and IgD production in vitro using Epstein-Barr virus activation.

Epstein-Barr virus has been used as a B cell mitogen to explore the parallels between the B cells found in patients with hypogammaglobulinemia and the immature B cells in fetal tissues. Peripheral blood lymphocytes from 29 cases of late onset hypogammaglobulinemia (common variable immunodeficiency) and from 10 cases of X-linked hypogammaglobulinemia were depleted of T lymphocytes and stimulated with virus in vitro. Immunoglobulin production was measured over a 4-week culture period using inhibition radioimmunoassays for IgM, IgG, IgA and IgD. The results were compared with those seen with fetal liver cells, cord blood lymphocytes and adult lymphocytes. Virus-stimulated cells from fetal sources produced small amounts of IgG and IgA relative to IgM, the ratio of IgM to IgG in the second week being in all cases greater than 10. Similar patterns were seen in 25/29 cases of late onset hypogammaglobulinemia, and in the eight cases of X-linked hypogammaglobulinemia that responded in vitro. In contrast, the ratio of IgM to IgG was always less than 8 in cultures of normal adult peripheral blood or bone marrow lymphocytes, and also in cultures from four cases of hypogammaglobulinemia known independently to have abnormal circulating suppressor cells. Eight cases of selective IgA deficiency showed reduced IgA production; six of these showed a normal ratio of IgM to IgG production. Thus, the B lymphocytes which circulate in many patients with hypogammaglobulinemia are functionally immature.

Adult↗
PubMed1980

The effects of betamethasone on fetal development in the rabbit.

Pregnant rabbits were injected with either 0.8 mg of betamethasone or with a comparable volume of saline on days 24 and 25 of gestation and delivered by cesarean section on day 26. There was a significant reduction in the weight of fetuses and in the weights of fetal brain, lungs, liver, and placenta in betamethasone-treated animals. With respect to the fetal brain, the concentration of DNA, the average of cell number, cell size, cell weight, and cell phospholipids were unaffected whereas the concentrations of phospholipids and protein were elevated in the treatment group.

Animals↗
PubMed1976

Prostaglandin biosynthesis and catabolism in the developing fetal sheep brain.

The biosynthesis of prostaglandins E2 and F2alpha as well as the catabolism of [9beta- 3H1]prostaglandin F2alpha by homogenates of whole brain from fetal and neonatal lambs was investigated. The biosynthetic measurements utilized the mass spectrometric deuterium isotope dilution-dual ion monitoring technique (Samulsson, B., Hamberg, M., and Sweeley, C.C. (1970) Anal. Biochem. 38, 301-304; Wolfe, L.S., and Pace-Asciak, C. (1972) in Prostaglandins in Fertility Control (Bergström, S., Green, K., and Samuelsson, B., eds) Vol. 2. pp. 201-207, WHO, Karolinska Institutet, Stockholm), whereas the activity of the catabolizing system was measured by the radiolabel dilution-thin layer chromatographic technique reported previously (Pace-Asciak, C. (1975) J. Biol. Chem. 250, 2795-2800). The structures of all products were confirmed by mass spectrometry. Early fetal brain (gestational age 30 to 32 days) contained the highest activity of NAD-dependent prostaglandin 15-hydroxy dehydrogenase which varied inversely with age of the fetus, dropping to almost undetectable levels by neonatal Day 4. Both prostaglandins E2 and F2alpha, were formed by brain from all ages tested and the total prostaglandins formed rose gradually with age. Thus, the period of maximal prostaglandin catabolism which we term the "critical prostaglandin period" appears in the fetal lamb brain around 30 days gestational age or earlier. These findins together with others previously reported by us in other tissues, support the concept that prostaglandin catabolism might play an important role in protecting the developing organ from possible adverse effects of locally formed or circulating prostaglandins. These adverse effects on the developing brain might relate to the known vasoconstrictor properties of the prostaglandins, as well as to their known effects on the induction of cell differentiation.

Aging↗
PubMed1976

[Investigations on the effect of the combination sulfamoxole/trimethoprim on fertility and fetal development in rats and rabbits (author's tranls)].

The chemotherapeutically active combination of N1-(4,5-dimethyl-2-oxazolyl)-sulfanilamide (sulfamoxole) and 2,4-diamino-5-(3,4,5-trimethoxy-benzyl)-pyrimidine (trimethoprim) in a dose ratio of 5:1 (CN 3123, Nevin, Supristol) was investigated, with respect to teratogenicity, effects on fertility and reproduction and influence on peri- and post-natal development. Experiments with the combination and partly with the single substances were done on Sprague-Dawly and Wistar rats and on rabbits (New Zealand White). With regard to the known effects of trimethoprim in this field--fetal malformations typical of those caused by folic acid antagonists--it was to clarify whether or not potentiation phenomena or new toxic effects occur with the combination. The results were as follows: 1. CN 3123 is teratogenically and fetotoxically active when given in very high doses to pregnant rats and rabbits during the critical phase of organogenesis (day 8-15 of pregnancy in rats, day 8-14 in rabbits). There were malformations, decrease in the number of pups and an increase in the number of absorption sites. Litter size and litter weight were reduced. The malformations observed were cleft palates, rarely cleft lips, micrognathies and shortening of limbs. Doses up to 180 mg/kg CN 3123, corresponding to more than tenfold the daily maintenance dose in man, were without any effects on all parameters observed. Toxic effects were observed in Sprague-Dawley rats at a dose level of 420 mg/kg and in Wistar rats with 600 mg/kg, corresponding to the effects seen following 100 mg/kg of trimethoprim alone. Sulfamoxole in the corresponding dose of 500 mg/kg caused no embryotoxic effects in the rat. In rabbits 600 mg/kg CN 3123 induced no malformations but increased fetal loss. Therefore it can be concluded, that the teratogenic and fetotoxic effects seen with high doses of CN 3123 are due to the amount of trimethoprim in the combination. The observed effects with the combination are quantitatively related to those seen with trimethoprim. 2. CN 3123 in high doses which are teratogenic also provoked a reduction of growth of the animals. Food consumption and weight gain were reduced in dams with 420 and 600 mg/kg CN 3123. In this dose range the pup weights and the weight gain of the offspring of dams with continued dosing during lactation were also reduced. Variation rate including retardations was increased. The depressing effect of CN 3123 in high doses on food consumption and weight gain is known from long-term toxicological studies previously described [7]. 3. CN 3123 even with high doses has no effects on the fertility of male and female rats. The number of corpora lutea and implantations and also the pregnancy rate were unaffected when either the female or the male rats used for mating had been treated. There was also no influence on mating activity of the male animals treated. 4. According to the results of the fertility study with treatment of the male rats for a period of ten weeks or more there were no signs of mutagenic effects due to CN 3123.

Abnormalities, Drug-Induced↗