Side Effects of Being Blue: Influence of Sad Mood on Visual Statistical Learning

It is well established that mood influences many cognitive processes, such as learning and executive functions. Although statistical learning is assumed to be part of our daily life, as mood does, the influence of mood on statistical learning has never been investigated before. In the present study, a sad vs. neutral mood was induced to the participants through the listening of stories while they were exposed to a stream of visual shapes made up of the repeated presentation of four triplets, namely sequences of three shapes presented in a fixed order. Given that the inter-stimulus interval was held constant within and between triplets, the only cues available for triplet segmentation were the transitional probabilities between shapes. Direct and indirect measures of learning taken either immediately or 20 minutes after the exposure/mood induction phase revealed that participants learned the statistical regularities between shapes. Interestingly, although participants from the sad and neutral groups performed similarly in these tasks, subjective measures (confidence judgments taken after each trial) revealed that participants who experienced the sad mood induction showed increased conscious access to their statistical knowledge. These effects were not modulated by the time delay between the exposure/mood induction and the test phases. These results are discussed within the scope of the robustness principle and the influence of negative affects on processing style.     

Autoinhibition of the platelet-derived growth factor beta-receptor tyrosine kinase by its C-terminal tail

In this report, we investigated the role of the C-terminal tail of the platelet-derived growth factor (PDGF) beta-receptor in the control of the receptor kinase activity. Using a panel of PDGF beta-receptor mutants with progressive C-terminal truncations, we observed that deletion of the last 46 residues, which contain a proline- and glutamic acid-rich motif, increased the autoactivation velocity in vitro and the V(max) of the phosphotransfer reaction, in the absence of ligand, as compared with wild-type receptors. By contrast, the kinase activity of mutant and wild-type receptors that were pre-activated by treatment with PDGF was comparable. Using a conformation-sensitive antibody, we found that truncated receptors presented an active conformation even in the absence of PDGF. A soluble peptide containing the Pro/Glu-rich motif specifically inhibited the PDGF beta-receptor kinase activity. Whereas deletion of this motif was not enough to confer ligand-independent transforming ability to the receptor, it dramatically enhanced the effect of the weakly activating D850N mutation in a focus formation assay. These findings indicate that allosteric inhibition of the PDGF beta-receptor by its C-terminal tail is one of the mechanisms involved in keeping the receptor inactive in the absence of ligand.     

Effects of leucine-enkephalin and methionine-enkephalin on prolactin and gonadotropin secretion and synthesis in vitro

In vivo, Enkephalins, stimulate PRL, inhibit LH and are inactive on FSH. However, in monolayer pituitary cell cultures, PRL, LH and FSH secretions and synthesis are not modified by Met-Enk. (5 microgram/ml) or Leu-Enk. (5 and 10 microgram/ml). But the simultaneous presence of LHRH and Enk. induces an increase in LH secretion and synthesis without modifying FSH and PRL. In conclusion 1) Enk do not act by themself at the pituitary level but 2) they are able to modify the responses induced by hypothalamic hormones.     

Les traitements médicaux de l’oligoasthénozoospermie idiopathique

In number cases, couple infertility results of an oligoasthenozoospermia without any recognized etiology. Various medical therapies have been proposed in the literature to increase sperm count and their mobility. Some studies demonstrate an improvement of spermatic parameters without taking physiological variations into consideration and without comparing the results with those obtained in patients treated with a placebo. For others, the final aim of the treatment is not specified, that means to get a pregnancy by the couples. In this review of literature, only randomized studies giving the pregnancy rate, were taken into account. Various hormones of the hypothalamo-hypophyso-testicular axe have been used. GnRH and its analogs, gonadothropins and their purified forms, antiestrogens, androgens and aromataze inhibitors. Among these molecules, positive effects have been sporadically observed. Mesterolone stimulated spermatogenesis in one on five studies. Testosterone undecanoate and FSH have a benefic effect onin vitro fertilization. Two antiestrogens have been tested for a couple of years. Clomiphene and tamoxifen induce a sifnificant increase in the pregnancy rates with however, some paradoxical effects. Other non hormonal molecules have also been studied. The oldest studied medication is kallicrein, a glycoprotein implicated in the release of kinins from kininogens. Contradictory results have been obtained with this therapy. Pentoxifyllin, a phosphodiesterase inhibitor is active on spermatozoa mobilityin vitro, but its activityin vivo is not demostrated. Other medicators as arginin, carnitin, mast cell blockers, α-blockers, vitamins etc have also been tested. Publications are sporadic and any conclusion can be drawn. In conclusion, idiopathic oligoasthenozoospermia seems still unamenable to treat. Choice of a therapy is empirical and must be leaved for trying a medically assisted treatment     

Increased conjugation of catecholamines during normal pregnancy

Urinary elimination of conjugated catecholamines (adrenaline and noradrenaline) is increased during normal pregnancy (60.5 % in the normal ; 70 % in the pregnants).     

Identification in human seminal fluid of an inhibin-like factor which selectively regulates FSH secretion.

Human seminal plasma obtained by centrifugation of human semen contains a factor capable of selectively inhibiting the secretion of FSH both in vivo (reduction of the levels of FSH in rats 24 h after castration) and in vitro (reduction of the FSH released by LH-RH in rat pituitary cell culture). This effect is not due to testosterone, oestradiol-17 beta or progesterone present in the active fractions. The factor has the characteristics of a protein in that its biological activity is destroyed by heat and trypsin digestion. It does not resemble androgen-binding protein. The biological action is not completely specific for FSH as inhibition of LH can be seen with doses usually higher than those which produce inhibition of FSH alone. There is no effect on TSH or prolactin levels in vitro. The factor clearly acts on the release and synthesis of gonadotrophins by gonadotrophs but an effect on the hypothalamus is not excluded. This factor fits the definition of inhibin.