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PurposeThis work sheds new light on the roles of gender, age and expatriation type—self-initiated expatriate (SIE) vs. assigned expatriate (AE)—by applying the transactional theory of stress and coping (and a validated measurement tool) to the expatriation experience.Design/methodology/approachBased on quantitative data from 448 expatriates, the authors examined the coping mechanisms (cognitions and actions) employed by senior and younger expatriates, females and males and SIE and AEs when they face hardships while working abroad.FindingsYounger expatriates display less active problem-solving coping, planning, and restraint and consume more alcohol and drugs. Female expatriates express their emotions and use social support more than their male counterparts. SIEs rely on emotional social support more than AEs.Practical implicationsRecognizing that individual repertoires of responses to expatriate challenges are bounded by personal characteristics—such as age, gender, and expatriation type—should improve efforts to support expatriates. This research suggests that expatriate support should be tailored. It offers indications on who needs what.Originality/valueThis work provides a fresh perspective and new insights into classic topics (age, gender, and expatriation type). Individuals react differently abroad. They have different resources and face different demands (to a certain extent) that lead to different coping reactions. Older people manage their emotions better, and female expatriates and SIEs gather and use support; these abilities are assets abroad.

Despite the importance of distance in international business and management research, the theoretical foundation for the concept and the underlying causal mechanisms are subject to shortcomings. We propose reinvigorating the study of distance through a diversity lens. We draw on research on diversity and develop a theoretical framework that distinguishes types of diversity (separation, variety, and disparity) at three levels (institutional, organizational, and individual). We show how this framework allows scholars to extend their analysis of distance, revisit important questions, and explore new issues. We discuss the theoretical and empirical implications of our diversity lens for the international business and management community.

We integrate research on global work demands (Shaffer et al., 2012) with transactional stress theory to examine both the harmful and beneficial effects of three global work demands-international travel, cognitive flexibility, and nonwork disruption-for employees engaged in global work. We propose that global work demands have indirect, and conditional, effects on burnout and work-to-family conflict (WFC), as well as thriving and work-family enrichment, through employees' appraisals that their global work is both hindering and challenging, respectively. We tested the hypotheses with a matched sample of 229 global employees and their spouses. We found that cognitive flexibility demands are related to harmful and beneficial outcomes: It increases WFC through hindrance appraisals of the global work, but also increases thriving through challenge appraisals. In comparison, international travel demands have only beneficial outcomes, such that it positively related to employee thriving through challenge appraisals, but only among employees working in jobs that have fewer nonwork disruption demands. Finally, nonwork disruption demands had only harmful effects in that it positively related to burnout and WFC through hindrance appraisals. Exploratory analyses also revealed that nonwork disruption demands negatively related to employee thriving, through challenge appraisals, when employees experienced

How intertwined are expatriates with their families? And what makes some expatriates better than others at leveraging positive or compensating for negative influences from their family life? Drawing on conservation of resources, crossover and spillover theories, we examine when partner family role adjustment influences expatriates’ family experiences, and how and when these experiences translate into expatriate work role engagement. Using data from 105 expatriate–partner dyads at two time points, we establish the key personal resource of general self-efficacy as a boundary condition for crossover and spillover. We find that expatriates with high self-efficacy experience no crossover between partner family role adjustment and expatriate family role adjustment, and positive spillover between their family role engagement and their work role engagement. By contrast, expatriates with low self-efficacy experience strong crossover between partner family role adjustment and expatriate family role adjustment, and negative spillover between their family role engagement and work role engagement. Our results suggest that the way in which the family domain influences expatriate work role engagement depends on general self-efficacy. We contribute to conservation of resources, crossover and spillover theories, and the work–family interface during expatriation. Our results also pinpoint organizational interventions to improve expatriates’ work role engagement.

Purpose Expatriation is known to be stressful. The purpose of this paper is to examine stress as an antecedent of substance use (SU) during expatriation and related effects on expatriates’ work adjustment. Moreover, the study sheds light on individual-level moderators (i.e. gender and prior international experience) and organizational-level moderators (i.e. organizational social support) that might condition the stress–SU link. Design/methodology/approach This work adopts a quantitative survey approach. It is based on two studies, one of 205 expatriates and one of 96 expatriate–supervisor dyads. The data were collected through personal networks and with the help of multinational companies. Findings This research shows that stress at a medium- to high-level increases SU among male expatriates, but not among female expatriates. Expatriates with substantial prior international experience were identified as being more prone to react to stress by resorting to SU. It also provides evidence that SU to aid coping harms professional adjustment. Moreover, some implications relating to professional adjustment are discussed. Research limitations/implications SU was self-reported; this may have deterred users from accurately reporting their consumption levels. Moreover, convenience samples have been used. Preventive actions limiting SU, such as well-being programs, could be sponsored by local human resource managers in order to limit this phenomenon. Originality/value This work is one of the first to analyze SU among expatriates. It shows that some expatriates are more at risk than others of resorting to such use to cope with the hardships of expatriation.

Drawing on crossover, spillover and conservation of resources theories, we investigate the dynamics of how experiences in the family domain influence the work sphere in the context of expatriation....

Although the original model of expatriate adjustment proposed by Black and colleagues has received substantial empirical support, it has come under increased academic scrutiny, due to both the conceptual overlap among its dimensions and its limited applicability for global professionals who interact with individuals from diverse cultures. Drawing on role theory, we conceptualize and develop a multidimensional scale of the work- and family-role adjustment of global professionals. We assess this scale through five interlocking studies using data from a total of 1231 corporate and self-initiated expatriates, international business travelers, and global domestics. After confirming the scale’s dimensionality, we provide evidence for convergent, discriminant, nomological, and predictive validity. We also demonstrate differences in levels of adjustment and in relationships between work and family demands and resources and their respective forms of adjustment across various types of global professionals. We contribute to international business research, and the organizational behavior and work family literatures, by offering a theoretically based scale that assesses adjustment to both work and family roles for a wide range of global employees. Our scale further lends itself as a diagnostic tool during the selection, training, and support of global professionals and their families.

Owing to the increasing number of studies on expatriates, their partners and families, we are starting to understand the main challenges related to work and personal life interaction involved with international mobility. Moreover, the first edited book on the work-life interface (WLI) in the context of international careers has recently been published (Makela and Suutari 2015). In this chapter, we aim to draw together what is known about the interaction between working life and personal life (including family) in regard to the spheres of different types of internationally mobile professionals. We start from the discussion on negative interactions between these two life spheres. Next, we will complement the picture by discussing the often-forgotten side of these experiences—the positive experiences of international professionals and their families. Given the large amount of transference between the work and non-work spheres of families during international assignments, it is also important to understand the ways in which organisations can help expatriates and their families. We will thus also discuss how firms can manage the WLI issues of their internationally mobile staff.

A focal topic in international business research is the analysis of distance. Despite the importance of the construct of distance, relatively little attention has been paid to its underlying mechan...

This study draws on social learning theory to analyse and compare the effects of pre-departure cross-cultural training (PDCCT) and in-country cross-cultural training (ICCCT) on performance. It focuses on the structural distinction between these two types of training: whether they occur before or during expatriation. Analysis of a sample of 206 expatriates and their firm's annual professional evaluation shows that ICCCT facilitates professional performance, while no impact of PDCCT on performance could be ascertained.

Despite years of intense research, acute ischemic stroke remains a leading cause of death and long-term disabilities worldwide. Although preclinical studies lead to the identification of over 1000 potential neuroprotective compounds, the current treatments for brain ischemia only rely on clot thrombolysis through injection of recombinant-tissue plasminogen activator (r-tPA) or mechanical revascularization, which benefit to less than 10 % of stroke victims due to a narrow therapeutical time window and side effects. Consequently, there is a crucial need for the identification of new molecules and the development of other strategies that could target later phases of the pathophysiological cascade of mechanisms following stroke. Indeed, because stroke initiates a complex series of pathophysiological events evolving both in time and location, putative therapeutic molecules need to be effective on several of the biochemical processes evoked by stroke. Pituitary adenylate cyclase-activating polypeptide (PACAP) has been reported to decrease infarct volume and improve functional recovery in several models of global and focal brain ischemia. The unique particularity of PACAP relies on its ability to act on various pathological processes of cerebral ischemia. PACAP can counteract excitotoxicity, inhibit apoptosis, reduce oxidative stress, modulate inflammation, and promote brain repair mechanisms. Nevertheless, due to several limitations, the pertinence of a potential therapeutical use of PACAP is still under investigation to successfully ensure the bench to bedside continuum.

International audience; Chemotactic migration is a fundamental behavior of cells and its regulation is particularly relevant in physiological processes such as organogenesis and angiogenesis, as well as in pathological processes such as tumor metastasis. The majority of chemotactic stimuli activate cell surface receptors that belong to the G protein-coupled receptor (GPCR) superfamily. Although the autophagy machinery has been shown to play a role in cell migration, its mode of regulation by chemotactic GPCRs remains largely unexplored. We found that ligand-induced activation of 2 chemotactic GPCRs, the chemokine receptor CXCR4 and the urotensin 2 receptor UTS2R, triggers a marked reduction in the biogenesis of autophagosomes, in both HEK-293 and U87 glioblastoma cells. Chemotactic GPCRs exert their anti-autophagic effects through the activation of CAPNs, which prevent the formation of pre-autophagosomal vesicles from the plasma membrane. We further demonstrated that CXCR4- or UTS2R-induced inhibition of autophagy favors the formation of adhesion complexes to the extracellular matrix and is required for chemotactic migration. Altogether, our data reveal a new link between GPCR signaling and the autophagy machinery, and may help to envisage therapeutic strategies in pathological processes such as cancer cell invasion.

It is by now widely recognized that cell membranes show complex patterns of lateral organization. Two mechanisms involving either a lipid-dependent (microdomain model) or cytoskeleton-based (meshwork model) process are thought to be responsible for these plasma membrane organizations. In the present study, fluorescence correlation spectroscopy measurements on various spatial scales were performed in order to directly identify and characterize these two processes in live cells with a high temporal resolution, without any loss of spatial information. Putative raft markers were found to be dynamically compartmented within tens of milliseconds into small microdomains (∅

Background and Purpose— Until now, except thrombolysis, the therapeutical strategies targeting the acute phase of cerebral ischemia have been proven ineffective, and no approach is available to attenuate the delayed cell death mechanisms and the resulting functional deficits in the late phase. Then, we investigated whether a targeted and delayed delivery of pituitary adenylate cyclase–activating polypeptide (PACAP), a peptide known to exert neuroprotective activities, may dampen delayed pathophysiological processes improving functional recovery. Methods— Three days after permanent focal ischemia, PACAP-producing stem cells were transplanted intracerebro ventricularly in nonimmunosuppressed mice. At 7 and 14 days post ischemia, the effects of this stem cell–based targeted delivery of PACAP on functional recovery, volume lesions, and inflammatory processes were analyzed. Results— The delivery of PACAP in the vicinity of the infarct zone 3 days post stroke promotes fast, stable, and efficient functional recovery. This was correlated with a modulation of the postischemic inflammatory response. Transcriptomic and Ingenuity Pathway Analysis–based bioinformatic analyses identified several gene networks, functions, and key transcriptional factors, such as nuclear factor-κB, C/EBP-β, and Notch/RBP-J as PACAP’s potential targets. Such PACAP-dependent immunomodulation was further confirmed by morphometric and phenotypic analyses of microglial cells showing increased number of Arginase-1 + cells in mice treated with PACAP-expressing cells specifically, demonstrating the redirection of the microglial response toward a neuroprotective M2 phenotype. Conclusions— Our results demonstrated that immunomodulatory strategies capable of redirecting the microglial response toward a neuroprotective M2 phenotype in the late phase of brain ischemia could represent attractive options for stroke treatment in a new and unexploited therapeutical window.

The rate of atmospheric vanadium is constantly increasing due to fossil fuel combustion. This environmental pollution favours vanadium exposure in particular to its vanadate form, causing occupational bronchial asthma and bronchitis. Based on the well admitted bronchodilator properties of the pituitary adenylate cyclase-activating polypeptide (PACAP), we investigated the ability of this neuropeptide to reverse the vanadate-induced airway hyperresponsiveness in rats. Exposure to ammonium metavanadate aerosols (5 mg/m3/h) for 15 minutes induced 4 hours later an array of pathophysiological events, including increase of bronchial resistance and histological alterations, activation of proinflammatory alveolar macrophages, and increased oxidative stress status. Powerfully, PACAP inhalation (0.1 mM) for 10 minutes alleviated many of these deleterious effects as demonstrated by a decrease of bronchial resistance and histological restoration. PACAP reduced the level of expression of mRNA encoding inflammatory chemokines (MIP-1α, MIP-2, and KC) and cytokines (IL-1αand TNF-α) in alveolar macrophages and improved the antioxidant status. PACAP reverses the vanadate-induced airway hyperresponsiveness not only through its bronchodilator activity but also by counteracting the proinflammatory and prooxidative effects of the metal. Then, the development of stable analogs of PACAP could represent a promising therapeutic alternative for the treatment of inflammatory respiratory disorders.

Thumbnail image of graphical abstract PC12 cells are used to study the signaling mechanisms underlying the neurotrophic and neuroprotective activities of pituitary adenylate cyclase-activating polypeptide (PACAP) and nerve growth factor (NGF). Previous microarray experiments indicated that serpinb1a was the most induced gene after 6 h of treatment with PACAP or NGF. This study confirmed that serpinb1a is strongly activated by PACAP and NGF in a time-dependent manner with a maximum induction (~ 50-fold over control) observed after 6 h of treatment. Co-incubation with PACAP and NGF resulted in a synergistic up-regulation of serpinb1a expression (200-fold over control), suggesting that PACAP and NGF act through complementary mechanisms. Consistently, PACAP-induced serpinb1a expression was not blocked by TrkA receptor inhibition. Nevertheless, the stimulation of serpinb1a expression by PACAP and NGF was significantly reduced in the presence of extracellular signal-regulated kinase, calcineurin, protein kinase A, p38, and PI3K inhibitors, indicating that the two trophic factors share some common pathways in the regulation of serpinb1a. Finally, functional investigations conducted with siRNA revealed that serpinb1a is not involved in the effects of PACAP and NGF on PC12 cell neuritogenesis, proliferation or body cell volume but mediates their ability to block caspases 3/7 activity and to promote PC12 cell survival. Pituitary adenylate cyclase-activating polypeptide (PACAP) and nerve growth factor (NGF) induce a strong increase in serpinb1 a expression in PC12 cells. Functional investigations revealed that this increase in serpinb1a does not affect cell proliferation or differentiation but inhibits caspase 3 activity and promotes cell survival., link_to_OA_fulltext

While the demand for international professionals willing and able to work in locations where they are needed around the world is high and increasing, the identification of employees with adequate competencies, who are interested in relocating abroad and able to successfully complete an international assignment, is a challenge of strategic importance for international firms. In this article, we discuss the challenges to talent management presented by global careerists, i.e. very experienced international managers with long-term global careers involving various international tasks. We reflect on and cross-analyse observations from a set of studies carried out with such Finnish business professionals. We analyse how multinational corporations (MNCs) can attract, motivate and gain the commitment of global careerists who offer companies the most experienced human resources available in terms of implementing their internationalisation strategies.

International audience

International audience; Pituitary adenylate cyclase-activating polypeptide (PACAP) is a 38-amino acid C-terminally alpha-amidated peptide that was first isolated 20 years ago from an ovine hypothalamic extract on the basis of its ability to stimulate cAMP formation in anterior pituitary cells (Miyata et al., 1989. PACAP belongs to the vasoactive intestinal polypeptide (VIP)-secretin-growth hormone-releasing hormone-glucagon superfamily. The sequence of PACAP has been remarkably well conserved during evolution from protochordates to mammals, suggesting that PACAP is involved in the regulation of important biological functions. PACAP is widely distributed in the brain and peripheral organs, notably in the endocrine pancreas, gonads, respiratory and urogenital tracts. Characterization of the PACAP precursor has revealed the existence of a PACAP-related peptide, the activity of which remains unknown. Two types of PACAP binding sites have been characterized: type I binding sites exhibit a high affinity for PACAP and a much lower affinity for VIP, whereas type II binding sites have similar affinity for PACAP and VIP. Molecular cloning of PACAP receptors has shown the existence of three distinct receptor subtypes: the PACAP-specific PAC1-R, which is coupled to several transduction systems, and the PACAP/VIP-indifferent VPAC1-R and VPAC2-R, which are primarily coupled to adenylyl cyclase. PAC1-Rs are particularly abundant in the brain, the pituitary and the adrenal gland, whereas VPAC receptors are expressed mainly in lung, liver, and testis. The development of transgenic animal models and specific PACAP receptor ligands has strongly contributed to deciphering the various actions of PACAP. Consistent with the wide distribution of PACAP and its receptors, the peptide has now been shown to exert a large array of pharmacological effects and biological functions. The present report reviews the current knowledge concerning the pleiotropic actions of PACAP and discusses its possible use for future therapeutic applications.

International audience; Pituitary adenylate cyclase-activating polypeptide (PACAP), a peptide of the vasoactive intestinal polypep-tide (VIP)-glucagon superfamily, was initially characterized by virtue of its ability to stimulate cAMP formation in cultured rat anterior pituitary cells. Three PACAP receptors have been cloned so far: a PACAP-selective receptor, termed PAC1-R, and two PACAP/VIP common receptors, termed VPAC1-R and VPAC2-R. PACAP and its receptors are widely expressed in the brain and in peripheral organs, notably in the hypothalamus and in endocrine glands. Indeed, there is now clear evidence that PACAP exerts neuroendocrine, paracrine, and autocrine control of the activity of the pituitary, thyroid, testis, ovary, adrenal medulla, adrenal cortex, and endocrine pancreas. These observations suggest that selective PACAP agonists and antagonists could have therapeutic value for the treatment of various endo-crine disorders.

The mechanisms by which Th1 and Th2 cells inter-regulate in vivo are still poorly understood. In this study we examined the plasticity of Th1 cell differentiation and how Th2 cells may down-regulate these responses. We show here that IL-4 affects Th1 cell responses by two developmentally regulated mechanisms. During the commitment phase of naive CD4+ T cells, IL-4 inhibits Th1 cell differentiation and induces a reversion of developing Th1 cells to the Th2 lineage. In contrast, for effector Th1 cells IL-4 does not affect the developmental process, but only the transcription of the IFN-gamma gene. We further show that the difference in IL-4 responsiveness correlates with a loss, in effector Th1 cells, of IL-4-dependent up-regulation of GATA-3 expression despite normal activation of STAT6. Transient inhibition of IFN-gamma production by differentiated effector cells may explain why Th1 and Th2 responses can co-exist in vivo although Th2 effector cells dominate functionally, as observed in some infectious or autoimmune mice models.

Previous research (Shaffer, Kraimer, Chen, & Bolino, 2012) identified three work demands that make global work distinct from "domestic" work: international travel, cognitive flexibility, and nonwor...

Summary: The Cre-loxP system permits the generation of mouse models in which the fate of a cell can be followed through time. Such approach is of great value in immunology because it may allow lineage studies and the dissection of the contribution of specific effector T cells to long-term memory responses or autoimmune responses. An essential component of such a strategy is the development of appropriate reporter strains of mice in which the inducible reporter molecule is not immunogenic and is well expressed at the cell surface of T cells. We describe here a novel reporter strain of mice that is designed to fulfill these criteria and show that this strain permits the monitoring of Cre-mediated recombination in both T cells and NK cells. genesis 32:287–292, 2002. © 2002 Wiley-Liss, Inc.

This study examines the trajectory of cross-cultural adjustment based on the multidimensional and subjective aspects of culture shock. We focus on six intrapersonal diversity factors that affect in...

We draw on social learning theory (Bandura, 1977; Black & Mendenhall, 1990) to analyze and compare the effects of cross-cultural training on performance. We focus on the structural distinction betw...

International audience; In neurological insults, such as cerebral ischemia and traumatic brain injury, complex molecular mechanisms involving inflammation and apoptosis are known to cause severe neuronal cell loss, emphasizing the necessity of developing therapeutic strategies targeting simultaneously these two processes. Over the last decade, numerous in vitro and in vivo studies have demonstrated the unique therapeutical potential of pituitary adenylate cyclase-activating polypeptide (PACAP) for the treatment of neuronal disorders involving apoptotic cell death and neuroinflammation. The neuroprotective activity of PACAP is based on its capacity to reduce the production of deleterious cytokines from activated microglia, to stimulate the release of neuroprotective agents from astrocytes and to inhibit pro-apoptotic intracellular pathways. However, the use of PACAP as a clinically applicable drug is hindered by its peptidic nature. As most natural peptides, native PACAP shows poor metabolic stability, low bioavailability, inadequate distribution and rapid blood clearance. Moreover, injection of PACAP to human can induce peripheral adverse side effects. Therefore, targeted chemical modifications and/or conjugation of PACAP to different macromolecules are required to improve the pharmacokinetic and pharmacological properties of PACAP. This review presents the chemical, biochemical and pharmacological strategies that are currently under development to convert PACAP from a hypophysiotropic neurohormone into a clinically relevant neuroprotective drug.

The mechanisms that regulate CD4+ T cells responses in vivo are still poorly understood. We show here that initial Ag stimulation induces in CD4+ T cells a program of proliferation that can develop, for at least seven cycles of division, in the absence of subsequent Ag or cytokine requirement. Thereafter, proliferation stops but can be reinitiated by novel Ag stimulation. This initial Ag stimulation does not however suffice to induce the differentiation of naive CD4+ T cells into effector Th1 cells which requires multiple contacts with Ag-loaded APC. Thus, recurrent exposure to both Ag and polarizing cytokines appears to be essential for the differentiation of IFN-γ-producing cells. Ag and cytokine availability therefore greatly limits the differentiation, but not the initial proliferation, of CD4+ T cells into IFN-γ-producing cells.