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Determinant Role (determinant + role)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

The Insulin-like Growth Factor System: a Key Determinant Role in the Growth and Selection of Ovarian Follicles?

REPRODUCTION IN DOMESTIC ANIMALS, Issue 4 2003
A Comparative Species Study
Contents The aim of the present paper is to make a comparative study of the expression of the elements of the insulin-like growth factor (IGF) system in different mammalian species and thus illuminate their potential role in the process of ovarian folliculogenesis in mammals. In most mammalian species, IGFs and IGFBPs (in particular IGFBP-2 and IGFBP-4) are considered, respectively, as stimulators and inhibitors of follicular growth and maturation. In mammalian species, IGFs might play a key role in sensitizing ovarian granulosa cells to FSH action during terminal follicular growth. Concentrations of IGFBP-2 and IGFBP-4 in follicular fluid strongly decrease and increase during follicular growth and atresia, respectively, leading to an increase and a decrease in IGF bioavailability, respectively. The decrease in these IGFBPs is because of a decrease in mRNA expression (IGFBP-2) and an increase in proteolytic degradation by PAPP-A in follicular fluid (IGFBP-2, IGFBP-4 and IGFBP-5), and likely participates in the selection of dominant follicles. In contrast, levels and/or sites of expression of IGF-I, IGF-II, IGFBP-4, IGFBP-5 and type II receptor in follicular cells strongly differ between mammalian species, suggesting that these phenomena might play species-specific or secondary roles in ovarian folliculogenesis. [source]

Role of sperm ,v,3 integrin in mouse fertilization

DEVELOPMENTAL DYNAMICS, Issue 3 2010
Céline Chalas Boissonnas
Abstract Oocyte integrins have been described as essential for fertilization. But this concept has been challenged by deletion experiments. Recently, we have shown that sperm integrin ,6,1 plays a determinant role in mouse gamete interaction. In this study, we demonstrate the presence of ,v,3 integrin by Western blot and immunofluorescence on the sperm membrane. Oocytes and/or sperm preincubations with anti-,v or anti-,3 antibodies were performed before in vitro fertilization on cumulus-intact and zona-free egg assays. We observed inhibitory effects on the fusion process mostly by means of sperm function. An antibody directed against vitronectin inhibited gametes fusion, whereas the presence of exogenous vitronectin increased its efficiency. We suggest that vitronectin (on multimeric forms) can play a first nonspecific link corresponding to loosely bound spermatozoa to oocyte and that this link could be mediated by means of oocyte proteoglycans or integrins, and sperm ,v,3 integrin. Developmental Dynamics 239:773,783, 2010. © 2010 Wiley-Liss, Inc. [source]

Vasopressin modulates lateral septal network activity via two distinct electrophysiological mechanisms

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2007
G. Allaman-Exertier
Abstract The lateral septal area is rich in vasopressin V1A receptors and is densely innervated by vasopressinergic axons, originating mainly from the bed nucleus of the stria terminalis and the amygdala. Genetic and behavioral studies provide evidence that activation of vasopressin receptors in this area plays a determinant role in promoting social recognition. What could be the neuronal mechanism underlying this effect? Using rat brain slices and whole-cell recordings, we found that lateral septal neurons are under the influence of a basal GABAergic inhibitory input. Vasopressin, acting via V1A but not V1B receptors, greatly enhanced this input in nearly all neurons. The peptide had no effect on miniature inhibitory postsynaptic currents, indicating that it acted on receptors located in the somatodendritic membrane, rather than on axon terminals, of GABAergic interneurons. Cell-attached recordings showed that vasopressin can cause a direct excitation of a subpopulation of lateral septal neurons by acting via V1A but not V1B receptors. The presence in the lateral septum of V1A but not of V1B receptors was confirmed by competition binding studies using light microscopic autoradiography. In conclusion, vasopressin appears to act in the lateral septum in a dual mode: (i) by causing a direct excitation of a subpopulation of neurons, and (ii) by causing an indirect inhibition of virtually all lateral septal neurons. This modulation by vasopressin of the lateral septal circuitry may be part of the neuronal mechanism by which the peptide, acting via V1A receptors, promotes social recognition. [source]

Primary hemophagocytic syndromes point to a direct link between lymphocyte cytotoxicity and homeostasis

IMMUNOLOGICAL REVIEWS, Issue 1 2005
Gael Ménasché
Summary:, Hemophagocytic syndrome (HS) is a severe and often fatal syndrome resulting from potent and uncontrolled activation and proliferation of T-lymphocytes, leading to excessive macrophage activation and multiple deleterious effects. The onset of HS characterizes several inherited disorders in humans. In each condition, the molecular defect impairs the granule-dependent cytotoxic activity of lymphocytes, thus highlighting the determinant role of this function in driving the immune system to a state of equilibrium following infection. It has also been shown that some of the proteins required for lytic granule secretion are required for melanocyte function, leading to associated hypopigmentation in these conditions. This review focuses on several effectors of this secretory pathway, recently identified, because their defects cause these disorders, and discusses their role and molecular interactions in granule-dependent cytotoxic activity. [source]

MHC studies in nonmodel vertebrates: what have we learned about natural selection in 15 years?

JOURNAL OF EVOLUTIONARY BIOLOGY, Issue 3 2003
L. Bernatchez
Abstract Elucidating how natural selection promotes local adaptation in interaction with migration, genetic drift and mutation is a central aim of evolutionary biology. While several conceptual and practical limitations are still restraining our ability to study these processes at the DNA level, genes of the major histocompatibility complex (MHC) offer several assets that make them unique candidates for this purpose. Yet, it is unclear what general conclusions can be drawn after 15 years of empirical research that documented MHC diversity in the wild. The general objective of this review is to complement earlier literature syntheses on this topic by focusing on MHC studies other than humans and mice. This review first revealed a strong taxonomic bias, whereby many more studies of MHC diversity in natural populations have dealt with mammals than all other vertebrate classes combined. Secondly, it confirmed that positive selection has a determinant role in shaping patterns of nucleotide diversity in MHC genes in all vertebrates studied. Yet, future tests of positive selection would greatly benefit from making better use of the increasing number of models potentially offering more statistical rigour and higher resolution in detecting the effect and form of selection. Thirdly, studies that compared patterns of MHC diversity within and among natural populations with neutral expectations have reported higher population differentiation at MHC than expected either under neutrality or simple models of balancing selection. Fourthly, several studies showed that MHC-dependent mate preference and kin recognition may provide selective factors maintaining polymorphism in wild outbred populations. However, they also showed that such reproductive mechanisms are complex and context-based. Fifthly, several studies provided evidence that MHC may significantly influence fitness, either by affecting reproductive success or progeny survival to pathogens infections. Overall, the evidence is compelling that the MHC currently represents the best system available in vertebrates to investigate how natural selection can promote local adaptation at the gene level despite the counteracting actions of migration and genetic drift. We conclude this review by proposing several directions where future research is needed. [source]

Possible involvement of endothelium-derived hyperpolarizing factor (EDHF) in the depressor responses to platelet activating factor (PAF) in rats

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2000
Yoshio Tanaka
In anaesthetized rats, platelet activating factor (PAF; 1 ,g kg,1) decreased mean arterial blood pressure by around 60 mmHg (n=18). This depressor response was completely blocked by the PAF antagonist, CV-6209 (1 mg kg,1), indicating the role of PAF-specific receptor in the response. NG -nitro- L -arginine methyl ester (L -NAME; 50 mg kg,1), an NO synthase inhibitor, profoundly elevated systemic blood pressure (n=19), indicating an important role of NO in the basal blood pressure regulation. The depressor response to PAF (1 ,g kg,1) normalized against that to sodium nitroprusside (SNP) (10 ,g kg,1) was not substantially different between rats treated without and with L -NAME (n=4). In contrast, the depressor effect of acetylcholine (0.03,1.0 ,g kg,1) normalized against that of SNP (10 ,g kg,1) was significantly attenuated by L -NAME (n=5). Charybdotoxin (0.4 mg kg,1) plus apamin (0.2 mg kg,1) significantly attenuated the depressor response to PAF (1 ,g kg,1) (n=5) without affecting the blood pressure change due to SNP (1 mg kg,1) (n=3). Charybdotoxin (0.4 mg kg,1) (n=4) or apamin (0.2 mg kg,1) (n=4) alone did not affect the PAF-induced depressor response. These findings suggest that EDHF may make a significant contribution to the depressor response to PAF in rats. Although NO plays the determinant role in the basal blood pressure regulation, its contribution to PAF-produced depressor response seems to be less as compared with that to the depressor response to acetylcholine. British Journal of Pharmacology (2000) 131, 1113,1120; doi:10.1038/sj.bjp.0703681 [source]