Animal migration: is there a common migratory syndrome?

Ornithologists, and especially northern hemisphere ornithologists, have traditionally thought of migration as an annual return movement of populations between regular breeding and non-breeding grounds. Problems arise because selection does not ordinarily act on populations and because organisms of many taxa (including birds) are clearly migrants, but fail to undertake movements of the kind described. There are also extensive return movements that are not migratory. I propose that it is more useful to think of migration as a syndrome of behavioral and other traits that function together within individuals, and that such a syndrome provides a common ground across taxa from aphids to albatrosses. Large-scale return movements of populations are one outcome of the syndrome. Similar behavioral and physiological traits serve both to define migration and to provide a test for it. I use two insect (Hemipteran) examples to illustrate migratory syndromes and to demonstrate that, in many migrants, behavior and physiology correlate with life history and morphological traits to form syndromes at two levels. I then compare the two Hemipterans with migration in birds, butterflies, and fish to assess the question of whether there are migratory syndromes in common between these diverse migrants. Syndromes are more similar at the level of behavior than when morphology and life history traits are included. Recognizing syndromes leads to important evolutionary questions concerning migration strategies, trade-offs, the maintenance of genetic variance and the responses of migratory syndromes to both similar and different selective regimes.

Links between migration and the presence of foreign combatants in armed conflict

This article explores the connections between migration and foreign combat, offering an improved definition of „foreign fighters,” and a general concept of foreign combatants’ behaviour as an anomalous form of migration. In contrast with the popular discourse and terrorism-related concerns about present-day Western European foreign fighters in Iraq and Syria (and their return to Europe) and Middle Eastern migrant refugees (and their arrival in Europe), the intention of this article is to offer a conceptually thorough consideration of the causal connections between movements of migration and the presence of foreign combatants in armed conflict, informed by a wide sample of cases. Such an assessment has to take place with a view to all forms of migration (including forced migration), all forms of foreign combat (not only foreign combat on the side of non-state actors as David Malet's oft-cited but overly restrictive definition would imply), and regions of the world beyond the Middle East and Islamic countries. Along these guiding lines, the article points out many comparatively rarely considered cases of foreign combat as well as the underestimated obstacles in the way of fighting abroad. Taking account of the latter allows refutation of a key implication of „new war theory” (its focus on „greed” as a motive of combatants), in light of the continued importance of cultural factors and ideological motives for participation in foreign combat.

Les étrangers aux frontières de la France : étude de récits de migration (1870 à nos jours)

In this dissertation, I examine how migration narratives make an ambiguous contribution to the democratization of French national borders. National borders are essentially spaces of crises from which it is possible to study the constant evolution of national identity. Migration narratives, regardless of their ideological dimension, offer representations of the border and of the foreigner that result from a tension between the difficulty to think identity outside of the national frame and the questioning of such a strong tie between identity and the nation. At the border, identities are fundamentally unstable. The first part is focused on the north-eastern and the southern borders of France at the end of the 19th century. The French nationalist literature at the time, advocating for the return of Alsace-Lorraine to the Republic, is characterized by a tension between nationalism and regionalism. The ideology of latinity constitutes a second major feature of the discourse on French identity. Developed by Louis Bertrand, it claims that France can only be regenerated in Algeria. However, a gap between his fictional works and his essays reveals latinity as hybrid and heterogeneous. Borders are also polysemic, namely, they do have the same meaning for everyone. The second part of the dissertation focuses on the southern border of France from the 30s to the 90s. The study of films and novels demonstrate that former borders are still active, especially colonial borders. Finally, the third part of the dissertation addresses the representation of migrants who were trapped in the north of France, at the border of the Schengen area, from the 90s to 2009. Migration narratives bring attention to the totalitarian tendencies of the state, but they also struggle with the contradictions of the humanitarian discourse and the analogies made with previous immigration waves.

Ankhd1 Silencing Inhibits Stathmin 1 Activity, Cell Proliferation And Migration Of Leukemia Cells.

ANKHD1 is highly expressed in human acute leukemia cells and potentially regulates multiple cellular functions through its ankyrin-repeat domains. In order to identify interaction partners of the ANKHD1 protein and its role in leukemia cells, we performed a yeast two-hybrid system screen and identified SIVA, a cellular protein known to be involved in proapoptotic signaling pathways. The interaction between ANKHD1 and SIVA was confirmed by co-imunoprecipitation assays. Using human leukemia cell models and lentivirus-mediated shRNA approaches, we showed that ANKHD1 and SIVA proteins have opposing effects. While it is known that SIVA silencing promotes Stathmin 1 activation, increased cell migration and xenograft tumor growth, we showed that ANKHD1 silencing leads to Stathmin 1 inactivation, reduced cell migration and xenograft tumor growth, likely through the inhibition of SIVA/Stathmin 1 association. In addition, we observed that ANKHD1 knockdown decreases cell proliferation, without modulating apoptosis of leukemia cells, while SIVA has a proapoptotic function in U937 cells, but does not modulate proliferation in vitro. Results indicate that ANKHD1 binds to SIVA and has an important role in inducing leukemia cell proliferation and migration via the Stathmin 1 pathway. ANKHD1 may be an oncogene and participate in the leukemia cell phenotype.

Imigrantes bolivianos em São Paulo : a Praça Kantuta e o futebol

Universidade Estadual de Campinas . Faculdade de Educação Física

Paracoccidioides brasilinsis-Induced Migration of Dendritic Cells and Subsequent T-Cell Activation in the Lung-Draining Lymph Nodes

Paracoccidioidomycosis is a mycotic disease caused by a dimorphic fungus, Paracoccidioides brasiliensis (Pb), that starts with inhalation of the fungus; thus, lung cells such as DC are part of the first line of defense against this microorganism. Migration of DC to the lymph nodes is the first step in initiating T cell responses. The mechanisms involved in resistance to Pb infection are poorly understood, but it is likely that DC play a pivotal role in the induction of effector T cells that control Pb infection. In this study, we showed that after Pb Infection, an important modification of lung DC receptor expression occurred. We observed an increased expression of CCR7 and CD103 on lung DC after infection, as well as MHC-II. After Pb infection, bone marrow-derived DC as well lung DC, migrate to lymph nodes. Migration of lung DC could represent an important mechanism of pathogenesis during PCM infection. In resume our data showed that Pb induced DC migration. Furthermore, we demonstrated that bone marrow-derived DC stimulated by Pb migrate to the lymph nodes and activate a T helper (Th) response. To the best of our knowledge, this is the first reported data showing that Pb induces migration of DC and activate a T helper (Th) response.

Cross talk Initiated by Endothelial Cells Enhances Migration and Inhibits Anoikis of Squamous Cell Carcinoma Cells through STAT3/Akt/ERK Signaling

It is well known that cancer cells secrete angiogenic factors to recruit and sustain tumor vascular networks. However, little is known about the effect of endothelial cell-secreted factors on the phenotype and behavior of tumor cells. The hypothesis underlying this study is that endothelial cells initiate signaling pathways that enhance tumor cell survival and migration. Here, we observed that soluble mediators from primary human dermal microvascular endothelial cells induce phosphorylation of signal transducer and activator of transcription 3 (STAT3), Akt, and extracellular signal-regulated kinase (ERK) in a panel of head and neck squamous cell carcinoma (HNSCC) cells (OSCC-3, UM-SCC-1, UM-SCC-17B, UM-SCC-74A). Gene expression analysis demonstrated that interleukin-6 (IL-6), interleukin-8 (CXCL8), and epidermal growth factor (EGF) are upregulated in endothelial cells cocultured with HNSCC. Blockade of endothelial cell-derived IL-6, CXCL8, or EGF by gene silencing or neutralizing antibodies inhibited phosphorylation of STAT3, Akt, and ERK in tumor cells, respectively. Notably, activation of STAT3, Akt, and ERK by endothelial cells enhanced migration and inhibited anoikis of tumor cells. We have previously demonstrated that Bcl-2 is upregulated in tumor microvessels in patients with HNSCC. Here, we observed that Bcl-2 signaling induces expression of IL-6, CXCL8, and EGF, providing a mechanism for the upregulation of these cytokines in tumor-associated endothelial cells. This study expands the contribution of endothelial cells to the pathobiology of tumor cells. It unveils a new mechanism in which endothelial cells function as initiators of molecular crosstalks that enhance survival and migration of tumor cells.

Paleoamerican Diet, Migration and Morphology in Brazil: Archaeological Complexity of the Earliest Americans

During the early Holocene two main paleoamerican cultures thrived in Brazil: the Tradicao Nordeste in the semi-desertic Sertao and the Tradicao Itaparica in the high plains of the Planalto Central. Here we report on paleodietary singals of a Paleoamerican found in a third Brazilian ecological setting - a riverine shellmound, or sambaqui, located in the Atlantic forest. Most sambaquis are found along the coast. The peoples associated with them subsisted on marine resources. We are reporting a different situation from the oldest recorded riverine sambaqui, called Capelinha. Capelinha is a relatively small sambaqui established along a river 60 km from the Atlantic Ocean coast. It contained the well-preserved remains of a Paleoamerican known as Luzio dated to 9,945 +/- 235 years ago; the oldest sambaqui dweller so far. Luzio's bones were remarkably well preserved and allowed for stable isotopic analysis of diet. Although artifacts found at this riverine site show connections with the Atlantic coast, we show that he represents a population that was dependent on inland resources as opposed to marine coastal resources. After comparing Luzio's paleodietary data with that of other extant and prehistoric groups, we discuss where his group could have come from, if terrestrial diet persisted in riverine sambaquis and how Luzio fits within the discussion of the replacement of paleamerican by amerindian morphology. This study adds to the evidence that shows a greater complexity in the prehistory of the colonization of and the adaptations to the New World.

High Glucose-Mediated Oxidative Stress Impairs Cell Migration

Deficient wound healing in diabetic patients is very frequent, but the cellular and molecular causes are poorly defined. In this study, we evaluate the hypothesis that high glucose concentrations inhibit cell migration. Using CHO.K1 cells, NIH-3T3 fibroblasts, mouse embryonic fibroblasts and primary skin fibroblasts from control and diabetic rats cultured in 5 mM D-glucose (low glucose, LG), 25 mM D-glucose (high glucose, HG) or 25 mM L-glucose medium (osmotic control - OC), we analyzed the migration speed, protrusion stability, cell polarity, adhesion maturation and the activity of the small Rho GTPase Rac1. We also analyzed the effects of reactive oxygen species by incubating cells with the antioxidant N-Acetyl-Cysteine (NAC). We observed that HG conditions inhibited cell migration when compared to LG or OC. This inhibition resulted from impaired cell polarity, protrusion destabilization and inhibition of adhesion maturation. Conversely, Rac1 activity, which promotes protrusion and blocks adhesion maturation, was increased in HG conditions, thus providing a mechanistic basis for the HG phenotype. Most of the HG effects were partially or completely rescued by treatment with NAC. These findings demonstrate that HG impairs cell migration due to an increase in oxidative stress that causes polarity loss, deficient adhesion and protrusion. These alterations arise, in large part, from increased Rac1 activity and may contribute to the poor wound healing observed in diabetic patients.

Spatiotemporal patterns of macrophage migration inhibitory factor (Mif) expression in the mouse placenta

Background: Macrophage migration inhibitory factor (MIF) has special pro-inflammatory roles, affecting the functions of macrophages and lymphocytes and counter-regulating the effects of glucocorticoids on the immune response. The conspicuous expression of MIF during human implantation and early embryonic development also suggests this factor acts in reproductive functions. The overall goal of this study was to evaluate Mif expression by trophoblast and embryo placental cells during mouse pregnancy. Methods: Mif was immunolocalized at implantation sites on gestation days (gd) 7.5, 10.5, 13.5 and 17.5. Ectoplacental cones and fetal placentas dissected from the maternal tissues were used for Western blotting and qRT-PCR assays on the same gestation days. Results: During the post-implantation period (gd7.5), trophoblast giant cells showed strong Mif reactivity. In later placentation phases (gds 10.5-17.5), Mif appeared to be concentrated in the junctional zone and trophoblast giant cells. Mif protein expression increased significantly from gd7.5 to 10.5 (p = 0.005) and from gd7.5 to 13.5 (p = 0.03), remaining at high concentration as gestation proceeded. Higher mRNA expression was found on gd10.5 and was significantly different from gd13.5 (p = 0.048) and 17.5 (p = 0.009). Conclusions: The up-regulation of Mif on gd10.5 coincides with the stage in which the placenta assumes its three-layered organization (giant cells, spongiotrophoblast and labyrinth zones), fetal blood circulation begins and population of uNK cells reaches high proportions at the maternal counter part of the placenta, suggesting that Mif may play a role in either the placentation or in the adaptation of the differentiated placenta to the uterus or still in gestational immunomodulatory responses. Moreover, it reinforces the possibility of specific activities for Mif at the maternal fetal interface.

Defect-induced effects on carrier migration through one-dimensional poly(para-phenylenevinylene) chains

Defects in one-dimensional (1D) systems can be intrinsically distinct from its three-dimensional counterparts, and polymer films are good candidates for showing both extremes that are difficult to individuate in the experimental data. We study theoretically the impact of simple hydrogen and oxygen defects on the electron transport properties of one-dimensional poly(para-phenylenevinylene) chains through a multiscale technique, starting from classical structural simulations for crystalline films to extensive ab initio calculations within density functional theory for the defects in single crystalline-constrained chains. The most disruptive effect on carrier transport comes from conjugation breaking imposed by the overcoordination of a carbon atom in the vinyl group independently from the chemical nature of the defect. The particular case of the [C=O] (keto-defect) shows in addition unexpected electron-hole separation, suggesting that the experimentally detected photoluminescence bleaching and photoconductivity enhancement could be due to exciton dissociation caused by the 1D characteristics of the defect.

Neospora caninum excreted/secreted antigens trigger CC-chemokine receptor 5-dependent cell migration

Neospora caninum, the causative agent of neosporosis, is an obligate intracellular parasite considered to be a major cause of abortion in cattle throughout the world. Most studies concerning N. caninum have focused on life cycle, seroepidemiology, pathology and vaccination, while data on host-parasite interaction, such as host cell migration, mechanisms of evasion and dissemination of this parasite during the early phase of infection are still poorly understood. Here we show the ability of excreted/secreted antigens from N. caninum (NcESAs) to attract monocytic cells to the site of primary infection in both in vitro and in vivo assays. Molecules from the family of cyclophilins present on the NcESAs were shown to work as chemokine-like proteins and NcESA-induced chemoattraction involved G(i) protein signaling and participation of CC-chemokine receptor 5 (CCR5). Additionally, we demonstrate the ability of NcESAs to enhance the expression of CCR5 on monocytic cells and this increase occurred in parallel with the chemotactic activity of NcESAs by increasing cell migration. These results suggest that during the first days of infection, N. caninum produces molecules capable of inducing monocytic cell migration to the sites of infection, which will consequently enhance initial parasite invasion and proliferation. Altogether, these results help to clarify some key features involved in the process of cell migration and may reveal virulence factors and therapeutic targets to control neosporosis. (C) 2010 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved.

Influence of the slice position on chloride migration tests for concrete in marine conditions

Chloride migration tests are used to measure the concrete capacity to inhibit chloride attack. Many researchers carry out this test in a slice of concrete extracted from the central part of cylindrical specimens, discarding about 75% of the concrete used to mold the specimens. This fact generated the question: would it be possible to extract more slices from a same specimen without losing the confidence in the results? The main purpose of this work is to answer this question. Moreover, another aim of this study was to show the difference of chloride penetration between finished faces and the formwork surfaces of concrete beams and slabs. The results indicated that it is possible to use more slices of a single specimen for a chloride migration test. Moreover, it was demonstrated that there is a significant difference of chloride penetration between the finished surface and the formwork surface of the specimens. (C) 2008 Elsevier Ltd. All rights reserved.

Modelling grain boundary migration during geometric dynamic recrystallization

High-angle grain boundary migration is predicted during geometric dynamic recrystallization (GDRX) by two types of mathematical models. Both models consider the driving pressure due to curvature and a sinusoidal driving pressure owing to subgrain walls connected to the grain boundary. One model is based on the finite difference solution of a kinetic equation, and the other, on a numerical technique in which the boundary is subdivided into linear segments. The models show that an initially flat boundary becomes serrated, with the peak and valley migrating into both adjacent grains, as observed during GDRX. When the sinusoidal driving pressure amplitude is smaller than 2 pi, the boundary stops migrating, reaching an equilibrium shape. Otherwise, when the amplitude is larger than 2 pi, equilibrium is never reached and the boundary migrates indefinitely, which would cause the protrusions of two serrated parallel boundaries to impinge on each other, creating smaller equiaxed grains.

RECK-Mediated Inhibition of Glioma Migration and Invasion

RECK is an anti-tumoral gene whose activity has been associated with its inhibitory effects regulating MMP-2, MMP-9, and MT1-MMP. RECK level decreases as gliobastoma progresses, varying from less invasive grade II gliomas to very invasive human glioblastoma multiforme (GBM). Since RECK expression and glioma invasiveness show an inverse correlation, the aim of the present study is to investigate whether RECK expression would inhibit glioma invasive behavior. We conducted this study to explore forced RECK expression in the highly invasive T98G human GBM cell line. Expression levels as well as protein levels of RECK, MMP-2, MMP-9, and MT1-MMP were assessed by qPCR and immunoblotting in T98G/RECK+ cells. The invasion and migration capacity of RECK+ cells was inhibited in transwell and wound assays. Dramatic cytoskeleton modifications were observed in the T98G/RECK+ cells, when compared to control cells, such as the abundance of stress fibers (contractile actin-myosin II bundles) and alteration of lamellipodia. T98G/RECK+ cells also displayed phosphorylatecl focal adhesion kinase (P-FAK) in mature focal adhesions associated with stress fibers; whereas P-FAK in control cells was mostly associated with immature focal complexes. Interestingly, the RECK protein was predominantly localized at the leading edge of migrating cells, associated with membrane ruffles. Unexpectedly, introduced expression of RECK effectively inhibited the invasive process through rearrangement of actin filaments, promoting a decrease in migratory ability. This work has associated RECK tumor-suppressing activity with the inhibition of motility and invasion in this GBM model, which are two glioma characteristics responsible for the inefficiency of current available treatments. J. Cell. Biochem. 110: 52-61, 2010. (C) 2010 Wiley-Liss. Inc.