A Crucial Event in the Development of the Rules of Socioanalysis: The Printing Shop Intervention

According to the authors, clinical intervention cannot be properly conducted without an appropriate technical tool. Socioanalysis has been founded on the need for clinical intervention: the satisfactory integration of diagnosis, change and evaluation. The present article returns to an early case of intervention (1958), where the elements of this integration in Socioanalysis were technically marked out for the first time. This occured in two stages. A round of interviews, completed by a survey questionnaire, was conducted at a printing shop. The results were made available and discussed with the participants. A co-investigation was undertaken by the members of the shop and the intervention team, which involved use of a socioanalytic technique still in the process of development. During this work, the members of the shop gradually worked out their own diagnosis, which had the effect of modifying their perceptions of each other, of identifying the stakes of interdependence, and of imagining new ways of managing their shop. The recognition of this capacity of self-diagnosis, taking into account the conditions of its emergence and efficacy, led the authors to focus their efforts on the construction of an integrated tool of investigation and intervention. The consequences of adopting this method are analyzed here. Some features of the subsequent development of the socioanalytic technique are also mentioned

Sex determination mechanism in the hymenopteran parasitoid Aphidius rhopalosiphi De Stefani-Peres (Braconidae : Aphidiinae)

Three main sex-determining mechanisms have been proposed for Hymenoptera : genetic balance, single locus (sl-CSD) and multilocus (ml-CSD) complementary sex determination. In the last two cases, sex is not determined by the number of chromosome sets but by heterozygosity at one or several loci. Individuals are male when hemizygous (haploid) or homozygous (diploid) at all sex-determining loci. Usually, this results in haploids developing as males and diploids as females, although diploid males can also appear, particularly under conditions of inbreeding. Aphidius rhopalosiphi (Aphidiineae : Hymenoptera Braconidae) is a cereal aphid parasitoid that can potentially be used as a biological control agent. Phylogenetic studies suggested that, within parasitoid wasps, the sl-CSD is present in both the Ichneumonoidea superfamily and the Braconidae family. Here, we directly test the sl-CSD model in A. rhopalosiphi by inducing diploid male production by brother-sister mating in laboratory-selected isofemale lines. Ploidy levels were analyzed with two complementary methods : DNA flow cytometry and DNA microsatellite markers. We observed a significantly male-biased sex ratio after sib mating, but no diploid males were detected by DNA analysis. The difference between the observed and expected sex ratio suggests that a sl-CSD model with two alleles may be applicable, which would imply that most diploid males are unviable in A. rhopalosiphi. Consequences of diploid male production are discussed in terms of the evolutionary biology of Hymenoptera and aphid biological control

A parallel optical interconnect link with on-chip optical access

This paper describes a complete technology family for parallel optical interconnect systems. Key features are the two-dimensional on-chip optical access and the development of a complete optical pathway. This covers both chip-to-chip links on a single boards, chip-to-chip links over an optical backpanel, and even system-to-system interconnects. Therefore it is a scalable technology. The design of all parts of the link, and the integration of parallel optical interconnect systems in the design flow of electronic systems is presented in this paper

Signal transduction in the human thyrocyte and its perversion in thyroid tumors.

The study of normal signal transduction pathways regulating the proliferation and differentiation of a cell type allows to predict and to understand the perversions of these pathways which lead to tumorigenesis. In the case of the human thyroid cell, three cascades are mostly involved in tumorigenesis: The pathways and genetic events affecting them are described. Caveats in the use of models and the interpretation of results are formulated and the still pending questions are outlined.JOURNAL ARTICLESCOPUS: re.jinfo:eu-repo/semantics/publishe

cAMP-Dependent Activation of Mammalian Target of Rapamycin (mTOR) in Thyroid Cells. Implication in Mitogenesis and Activation of CDK4.

How cAMP-dependent protein kinases [protein kinase A (PKA)] transduce the mitogenic stimulus elicited by TSH in thyroid cells to late activation of cyclin D3-cyclin-dependent kinase 4 (CDK4) remains enigmatic. Here we show in PC Cl3 rat thyroid cells that TSH/cAMP, like insulin, activates the mammalian target of rapamycin (mTOR)-raptor complex (mTORC1) leading to phosphorylation of S6K1 and 4E-BP1. mTORC1-dependent S6K1 phosphorylation in response to both insulin and cAMP required amino acids, whereas inhibition of AMP-activated protein kinase and glycogen synthase kinase 3 enhanced insulin but not cAMP effects. Unlike insulin, TSH/cAMP did not activate protein kinase B or induce tuberous sclerosis complex 2 phosphorylation at T1462 and Y1571. However, like insulin, TSH/cAMP produced a stable increase in mTORC1 kinase activity that was associated with augmented 4E-BP1 binding to raptor. This could be caused in part by T246 phosphorylation of PRAS40, which was found as an in vitro substrate of PKA. Both in PC Cl3 cells and primary dog thyrocytes, rapamycin inhibited DNA synthesis and retinoblastoma protein phosphorylation induced by TSH and insulin. Although rapamycin reduced cyclin D3 accumulation, the abundance of cyclin D3-CDK4 complexes was not affected. However, rapamycin inhibited the activity of these complexes by decreasing the TSH and insulin-mediated stimulation of activating T172 phosphorylation of CDK4. We propose that mTORC1 activation by TSH, at least in part through PKA-dependent phosphorylation of PRAS40, crucially contributes to mediate cAMP-dependent mitogenesis by regulating CDK4 T172-phosphorylation.JOURNAL ARTICLESCOPUS: ar.jinfo:eu-repo/semantics/publishe

Cyclic AMP Inhibits the Proliferation of Thyroid Carcinoma Cell Lines through Regulation of CDK4 Phosphorylation

How cyclic AMP (cAMP) could positively or negatively regulate G1 phase progression in different cell types or in cancer cells versus normal differentiated counterparts has remained an intriguing question for decades. At variance with the cAMP-dependent mitogenesis of normal thyroid epithelial cells, we show here that cAMP and cAMP-dependent protein kinase activation inhibit S-phase entry in four thyroid carcinoma cell lines that harbor a permanent activation of the Raf/ERK pathway by different oncogenes. Only in Ret/PTC1-positive TPC-1 cells did cAMP markedly inhibit the Raf/ERK cascade, leading to mTOR pathway inhibition, repression of cyclin D1 and p21 and p27 accumulation. p27 knockdown did not prevent the DNA synthesis inhibition. In the other cells, cAMP little affected these signaling cascades and levels of cyclins D or CDK inhibitors. However, cAMP differentially inhibited the pRb-kinase activity and T172-phosphorylation of CDK4 complexed to cyclin D1 or cyclin D3, whereas CDK-activating kinase activity remained unaffected. At variance with current conceptions, our studies in thyroid carcinoma cell lines and previously in normal thyrocytes identify the activating phosphorylation of CDK4 as a common target of opposite cell cycle regulations by cAMP, irrespective of its impact on classical mitogenic signaling cascades and expression of CDK4 regulatory partners

Neural mechanisms underlying the effects of emotional arousal on memory

Emotional events (e.g., seeing a snake while hiking) typically stay in the memory longer and in more detail than neutral ones (e.g., seeing a bird while hik-ing). This emotion-induced memory enhancement has been attributed to the amyg-dala’s modulation on other brain regions, such as the medial temporal lobe and visual cortices. In line with this amygdala modulation hypothesis, previous brain imaging research revealed enhanced amygdala activity when encoding and retriev-ing emotional stimuli compared with non-emotional stimuli. However, emotion does not always enhance memory. Indeed, researchers have long been aware that emotion sometimes enhances and sometimes impairs memory. Yet, the underlying mechanisms of the opposing effects of emotion are relatively unknown. For example, if the amygdala’s modulation on other brain regions is critical in the emotion- memory interaction, how does it result in the enhancement effects for some aspects, while impairing other aspects of memory? In this chapter, we argue an alternative possibility: that norepinephrine released by the locus coeruleus under arousal plays a critical role in the complex effects of emotion on memory