Determination of potential dermal exposure rates of phosphorus flame retardants via the direct contact with a car seat using artificial skin.

Dermal exposure to phosphorus flame retardants (PFRs) has received much attention as a major alternative exposure route in recent years. However, the information regarding dermal exposure via direct contact with a product is limited. In addition, in the commonly used dermal permeability test, the target substance is dissolved in a solvent, which is unrealistic.

Prediction-Related Frontal-Temporal Network for Omission Mismatch Activity in the Macaque Monkey.

Sensory prediction is considered an important element of mismatch negativity (MMN) whose reduction is well known in patients with schizophrenia. Omission MMN is a variant of the MMN which is elicited by the absence of a tone previously sequentially presented. Omission MMN can eliminate the effects of sound differences in typical oddball paradigms and affords the opportunity to identify prediction-related signals in the brain.

Effects of supplemental β-carotene on colostral immunoglobulin and plasma β-carotene and immunoglobulin in Japanese Black cows.

Data from 26 Japanese Black cows were collected to clarify the effects of supplemental β-carotene on colostral immunoglobulin (Ig) and plasma β-carotene and Ig in the cows. Cows were assigned to control or β-carotene groups from 21 days before the expected calving date to 60 days after parturition. Supplemental β-carotene was provided at 500 mg/day in the β-carotene group.

Rasd1 is an estrogen-responsive immediate early gene and modulates expression of late genes in rat anterior pituitary cells.

Dexamethasone-induced Ras-related protein 1 (Rasd1) is a member of the Ras superfamily of monomeric G proteins that have a regulatory function in signal transduction. Here we investigated the role of Rasd1 in regulating estrogen-induced gene expression in primary cultures of rat anterior pituitary cells. Rasd1 mRNA expression in anterior pituitary cells decreased after treatment with forskolin or serum and increased after treatment with 17β-estradiol (E2).

Activation of G protein-coupled estrogen receptor 1 mimics, but does not mediate, the anti-proliferative action of estradiol on pituitary lactotrophs in primary culture.

Estrogen binds to nuclear estrogen receptors (ERs) to modulate transcription of target genes in estrogen-responsive cells. However, recent studies have shown that estrogen also binds to cytoplasmic membrane ERs to modulate protein kinase signaling cascades, leading to non-genomic actions. We investigated whether either nuclear or membrane ERs, including G protein-coupled estrogen receptor 1 (Gper1), mediate the inhibitory action of estrogen on insulin-like growth factor-1 (IGF-1)-induced proliferation of pituitary lactotrophs in primary culture.

Differences between rat strains in the development of PRL-secreting pituitary tumors with long-term estrogen treatment: In vitro insulin-like growth factor-1-induced lactotroph proliferation and gene expression are affected in Wistar-Kyoto rats with low estrogen-susceptibility.

There are differences in the susceptibility of rat strains to pituitary growth and lactotroph proliferation caused by long-term treatment with estrogens. To investigate the pituitary mechanism for this strain difference in estrogen-induced lactotroph proliferation, we compared the abilities of 17-β estradiol (E2) and insulin-like growth factor-1 (IGF-1) to modulate lactotroph proliferation and gene expression in vitro in Wistar and Wistar-Kyoto (WKY) rats. These two strains of rats have a high and very low susceptibility to estrogen, respectively.

Activation of D2 dopamine receptors inhibits estrogen response element-mediated estrogen receptor transactivation in rat pituitary lactotrophs.

Estrogen and dopamine are major opposing regulators of the endocrine functions of pituitary lactotrophs. Dopamine inhibits estrogen-induced changes in the synthesis and secretion of prolactin, and lactotroph proliferation. We studied the mechanism of the inhibitory effects of dopaminergic stimulation on estrogen-induced functional changes of rat lactotrophs in primary culture.

Inhibition of Bcl3 gene expression mediates the anti-proliferative action of estrogen in pituitary lactotrophs in primary culture.

In addition to their well-known stimulatory action, estrogens have an anti-proliferative effect. The present study was undertaken to investigate the mechanism by which 17β-estradiol (E2) inhibits insulin-like growth factor-1 (IGF-1)-induced proliferation in vitro in the rat pituitary lactotroph, a typical estrogen-responsive cell. E2 treatment of pituitary cells did not change levels of IGF-1-induced phosphorylation of proliferation-related protein kinases such as Erk1/2 and Akt.

cAMP response element-binding protein (CREB) is required for epidermal growth factor (EGF)-induced cell proliferation and serum response element activation in neural stem cells isolated from the forebrain subventricular zone of adult mice.

Neurogenesis, which occurs not only in the developing brain but also in restricted regions in the adult brain including the forebrain subventricular zone (SVZ), is regulated by a variety of environmental factors, extracellular signals, and intracellular signal transduction pathways. We investigated whether the transcription factor cAMP response element (CRE)-binding protein (CREB) is involved in the regulation of cell proliferation of neural stem cells (NSCs) isolated from the SVZ of adult mice. Treatment of NSCs with the protein kinase A (PKA) inhibitors H89 and KT5720 inhibited epidermal growth factor (EGF)-stimulated NSC proliferation.

The cAMP response element-binding protein in the bed nucleus of the stria terminalis modulates the formalin-induced pain behavior in the female rat.

Abstract Differences in male and female responses to pain are widely recognized in many species, including humans, but the cerebral mechanisms that generate these responses are unknown. Using the formalin test, we confirmed that proestrus female rats showed nociceptive behavior, modulated by estrogen that was distinct from male rats, particularly during the interphase period. We then explored the brain areas, which were involved in the female pattern of nociceptive behavior.

Absence of ligand-independent transcriptional activation of the estrogen receptor via the estrogen response element in pituitary lactotrophs in primary culture.

The estrogen receptor (ER) is a ligand-activated transcription factor that enhances gene expression by binding to specific regulatory DNA sequences called estrogen response elements (EREs). In some cell lines, the ER is also activated in a ligand-independent manner by multiple signaling pathways. In this study, we developed a novel adenovirus-mediated assay for promoter activation, termed LASETA, which we then used to examine whether ligand-independent activation of the ER occurred in normal pituitary lactotrophs in primary culture.

Involvement of 20alpha-hydroxysteroid dehydrogenase in the maintenance of pregnancy in mice.

The enzyme 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) catabolizes progesterone into a biologically inactive steroid, 20alpha-dihydroprogesterone (20alpha-OHP). In the corpora lutea of rats and mice, 20alpha-HSD is considered to be involved in functional luteolysis. It is also distributed in other tissues including the placenta, endometrial epithelia and fetal skin, although the roles it plays in these tissues remain to be elucidated.

Adenovirus vectors differentially modulate proliferation of pituitary lactotrophs in primary culture in a mitogen and infection time-dependent manner.

Adenoviruses are powerful, widely utilized vectors for gene transfer. Limitations to their application, however, have not been well described. We used rat pituitary lactotrophs in primary culture as a model for studying how adenovirus vector infection modulates mitogen-induced proliferation and the activities of mitogen signaling pathways.

Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture.

Hypothalamic hormones, including dopamine, regulate critical functions of pituitary cells via the cAMP-protein kinase A (PKA) pathway. The PKA-downstream transcription factor cAMP response element (CRE)-binding protein (CREB) is an integrating molecule that is also activated by many other protein kinase pathways. We investigated the involvement of CREB in the regulation of cell proliferation and the PRL promoter of rat lactotrophs in primary cell culture.

Estrogen actions on lactotroph proliferation are independent of a paracrine interaction with other pituitary cell types: a study using lactotroph-enriched cells.

The mitogenic action of estrogen on estrogen-responsive tissues is suggested to be mediated by paracrine growth factors secreted from neighboring estrogen receptor-positive cells. Using pituitary lactotrophs in primary culture, on which estrogen exerts both mitogenic and antimitogenic actions in a cell context-dependent manner, we investigated whether a paracrine cell-to-cell interaction with other pituitary cell types was required for estrogen action. In pituitary cells, enriched for lactotrophs by 85% using differential sedimentation on a discontinuous Percoll gradient, 17beta-estradiol (E2) showed an antimitogenic action on lactotrophs in the presence of IGF-I, which was similar to that in control unenriched cells.

Reproductive phenotypes in mice with targeted disruption of the 20alpha-hydroxysteroid dehydrogenase gene.

In the corpus luteum of rats and mice, 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) catalyzes the conversion of progesterone to a biologically inactive metabolite, 20alpha-dihydroprogesterone (20alpha-OHP). The reduction of progesterone by 20alpha-HSD is believed to be important for functional luteolysis in these rodent species. In addition to the corpus luteum, expression of 20alpha-HSD has been demonstrated in tissues such as the placenta, endometrial epithelia, and fetal skin, although the roles it plays in the latter tissues remain to be determined.

Pup removal suppresses estrogen-induced surges of LH secretion and activation of GnRH neurons in lactating rats.

During lactation, the suckling stimulus exerts profound influences on neuroendocrine regulation in nursing rats. We examined the acute effect of pup removal on the estrogen-induced surge of LH secretion in ovariectomized lactating rats. Lactating and nonlactating cyclic female rats were given an estradiol-containing capsule after ovariectomy, and blood samples were collected through an indwelling catheter for serum LH determinations.

Expression and possible role of 20alpha-hydroxysteroid dehydrogenase in the placenta of the goat.

20Alpha-hydroxysteroid dehydrogenase (20alpha-HSD) catalyzes the conversion of progesterone to its inactive form 20alpha-dihydroprogesterone (20alpha-OHP). 20Alpha-HSD is expressed in the murine placenta, suggesting a role, yet unidentified, played by this enzyme during the course of pregnancy. To elucidate the possible roles of 20alpha-HSD during pregnancy, 20alpha-HSD gene expression in the placenta was examined by Northern blot analysis, and progestin (progesterone and 20alpha-OHP) concentrations in the maternal and fetal sera and the amniotic fluid were measured by radioimmunoassay in pregnant Shiba goats.

Molecular cloning of goat 20alpha-hydroxysteroid dehydrogenase cDNA.

20Alpha-hydroxysteroid dehydrogenase (20alpha-HSD), which catalyzes the conversion of progesterone to its inactive form 20alpha-dihydroprogesterone, is expressed in murine placenta and has been suggested to play roles in maintaining pregnancy. To understand the role of 20alpha-HSD during pregnancy in the goat, as a first step, cloning and sequencing of 20alpha-HSD cDNA were performed. The full nucleotide sequence of 20alpha-HSD cDNA was determined on samples obtained from the corpus luteum at the luteal phase of the estrous cycle and the placenta in late pregnancy by RT-PCR and 3' and 5' RACE systems.

Characterization and functional analysis of the 5'-flanking region of the mouse 20alpha-hydroxysteroid dehydrogenase gene.

20alpha-Hydroxysteroid dehydrogenase (20alpha-HSD), which metabolizes progesterone to an inactive steroid in the corpus luteum of mice and rats but not of humans, is thought to play a crucial role in shortening the oestrous cycles in these rodent species. We determined the nucleotide sequence of the 5'-flanking region of the mouse 20alpha-HSD gene, and examined its promoter activity using a rat luteinized granulosa cell culture. A reporter assay, using reporter constructs of various lengths of the 5'-flanking region, revealed that the region between -83 and 60 bp upstream of the transcription start site was essential for transcriptional activity.

Cloning and chromosomal localization of mouse 20alpha-hydroxysteroid dehydrogenase gene.

20alpha-hydroxysteroid dehydrogenase (20alpha-HSD), a member of the aldo-keto reductase (AKR) superfamily, metabolizes progesterone to its inactive form, 20alpha-dihydroprogesterone (20alpha-OHP). 20alpha-HSD is associated with functional luteolysis and plays a significant role in the reproductive system of rodents. Here we report cloning and determination of the chromosomal location of the mouse 20alpha-HSD gene.