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PubMed1994

Long-run migration incentives and migration effects: the case of different fertility rates.

"In this paper the direction of the long-run migration incentive in the presence of closed borders and the long-run welfare effects of a regime change from 'autarky' to 'free permanent migration' are studied. A difference in birth-country specific fertility rates is treated as the final cause for the creation of migration incentives in a two-country model where the standard overlapping-generations framework is used.... Opening the borders for permanent migration can always lead to the equalization of labour force growth rates. A continuum of such equilibria with migration does exist, but the application of the concept of migration-stability, introduced in this paper, gives reason to the suspicion that free migration can also lead to a collapse of the emigration country's economy." (SUMMARY IN GER)

Demography↗
PubMed1995

[Theories on migration and migration policy].

"In its first part the article gives a short historical overview of theories on migration.... The author tries to clarify the term[s]...'migration policy' and...'migration' itself and assesses the usefulness of various migration typologies. The final chapter analyses determinants and trends of migration policies in Europe in the 1990s: the continuing pressures for migration in developing countries, the end of numerous barriers to emigration, the revival of nationalistic concepts of immigration and exclusionary tendencies founded on culturalistic arguments, the process of harmonizing control mechanisms in the European Union, and the influence of international human rights declarations on the formulation of migration policies." (SUMMARY IN ENG AND FRE)

Classification↗
PubMed1993

Involvement of protein kinase C in nuclear migration during compaction and the mechanism of the migration: analyses in two-cell mouse embryos.

Compaction and nuclear migration occur in mouse embryos at the late eight-cell stage. It has been reported that activators of protein kinase C (PKC) increase adhesion of cells at the two-cell, four-cell, and uncompacted eight-cell stage. We report here that nuclear migration followed the increased adhesion of cells in such embryos when they were treated with PKC activators. These cellular events resembled those in normal embryos at the late eight-cell stage and were blocked by sphingosine, a PKC inhibitor. The responses were proportional to the dose of the PKC activator. Molecular analogues of the PKC activators, which do not affect PKC, did not induce these events. These results suggest an important role for PKC in initiation of nuclear migration as well as in compaction. Experiments were also conducted to identify the source of the mechanical force that moves the nucleus. Nuclear migration was suppressed in embryos pretreated with colchicine. Calmodulin is known to have effects on Ca(2+)-induced assembly and disassembly of microtubules. The calmodulin antagonists W-7 and W-5 suppressed nuclear migration. These results suggest that microtubules are essential for the migration and that nuclei are migrated via the Ca(2+)-induced, calmodulin-mediated assembly and disassembly of the microtubule networks. Together, these results obtained with PKC activators/inhibitor, colchicine, and calmodulin antagonists suggest that nuclear migration is mediated by increases in PKC activity, requires intact microtubules, and is accompanied by PKC-dependent increases in cell-cell adhesion.

Animals↗
PubMed2005

Steroid receptor coactivator-3, a homolog of Taiman that controls cell migration in the Drosophila ovary, regulates migration of human ovarian cancer cells.

Border cell migration is a process that occurs during Drosophila ovarian development in which cells derived from a simple epithelium migrate and invade neighboring tissue. This process resembles the behavior of cancerous cells that derive from the simple epithelium of the human ovary. One important regulator of border cell migration is Taiman, a homolog of steroid receptor coactivator-3 (SRC-3). Because increasing evidence indicates that similarities exist between the molecular control of migration of border cells and of cancer cells, we investigated whether SRC-3 controls ovarian cancer cell migration. Little or no SRC-3 expression was detected in normal ovarian surface epithelium, ovarian cysts and borderline ovarian tumors that lack stromal invasion. In contrast, SRC-3 was abundantly expressed in high-grade ovarian carcinomas. Inhibiting SRC-3 expression in ovarian cancer cells markedly reduced cell spreading and migration, and altered intracellular localization of focal adhesion kinase. This inhibitory effect on cell migration was independent of the estrogen receptor (ER) status of the cells. These studies reveal a novel role for SRC-3 in ovarian cancer progression by promoting cell migration, independently of its role in estrogen receptor signaling.

Acetyltransferases↗
PubMed2006

Defects in tangential neuronal migration of pontine nuclei neurons in the Largemyd mouse are associated with stalled migration in the ventrolateral hindbrain.

The LARGE gene encodes a putative glycosyltransferase that is required for normal glycosylation of dystroglycan, and defects in LARGE can cause abnormal neuronal migration in congenital muscular dystrophy (CMD). Previous studies have focused on radial migration, which is disrupted at least in part due to breaks in the basal lamina. Through analysis of precerebellar nuclei development in the Large(myd) mouse hindbrain, we show that tangential migration of a subgroup of hindbrain neurons may also be disrupted. Within the precerebellar nuclei, the pontine nuclei (PN) are severely disrupted, whereas the inferior olive (IO), external cuneate nuclei (ECN) and lateral reticular nuclei (LRN) appear unaffected. Large and dystroglycan are widely expressed in the hindbrain, including in the pontine neurons migrating in the anterior extramural migratory stream (AES). BrdU labeling and immunohistochemical studies suggest normal numbers of neurons begin their journey towards the ventral midline in the AES in the Large(myd) mouse. However, migration stalls and PN neurons fail to reach the midline, surviving as ectopic clusters of cells located under the pial surface dorsally and laterally to where they normally would finish their migration near the ventral midline. Stalling of PN neurons at this location is also observed in other migration disorders in mice. These observations suggest that glycan-dependent dystroglycan interactions are required for PN neurons to correctly respond to signals at this important migrational checkpoint.

Amino Acids↗
PubMed2002

Neutrophil transepithelial migration: evidence for sequential, contact-dependent signaling events and enhanced paracellular permeability independent of transjunctional migration.

Active migration of polymorphonuclear leukocytes (PMN) through the intestinal crypt epithelium is a hallmark of inflammatory bowel disease and correlates with patient symptoms. Previous in vitro studies have shown that PMN transepithelial migration results in increased epithelial permeability. In this study, we modeled PMN transepithelial migration across T84 monolayers and demonstrated that enhanced paracellular permeability to small solutes occurred in the absence of transepithelial migration but required both PMN contact with the epithelial cell basolateral membrane and a transepithelial chemotactic gradient. Early events that occurred before PMN entering the paracellular space included increased permeability to small solutes (<500 Da), enhanced phosphorylation of regulatory myosin L chain, and other as yet undefined proteins at the level of the tight junction. No redistribution or loss of tight junction proteins was detected in these monolayers. Late events, occurring during actual PMN transepithelial migration, included redistribution of epithelial serine-phosphorylated proteins from the cytoplasm to the nucleus in cells adjacent to migrating PMN. Changes in phosphorylation of multiple proteins were observed in whole cell lysates prepared from PMN-stimulated epithelial cells. We propose that regulation of PMN transepithelial migration is mediated, in part, by sequential signaling events between migrating PMN and the epithelium.

Actomyosin↗
PubMed1992

Migration stock and the issue of competing and complementary flows in United States interstate migration.

"The purpose of this paper is to study the determinants of interstate migration in the United States from 1965-1970 when a new change in direction of migration has started, and to examine the flow creation or flow diversion that results from migration to some appealing regions. Several related variables have been selected and tested for gross interstate migration flows. The results show that overall both push and pull factors have not been important.... Distance was not found to act as a significant deterrence to migration, whereas population density of origin and destination was significant. Previous migration was found to have a very strong effect on migration. The results of the study also suggested that there has been a major change in the location of growth areas in the United States during 1955-1970."

Americas↗
PubMed1982

Net migration by commercial air: a lower bound on total net migration to the United States.

"This article presents evidence that net migration to the United States by commercial air alone was between 400 and 500 thousand a year over the period 1969 to 1978. This evidence is drawn from data gathered by the U.S. Department of Transportation in cooperation with the Immigration and Naturalization Service, by the International Air Transport Association, and individually by 20 major international airports in the United States. Net migration by commercial air may be used as a lower bound to total net migration to the United States. The latter would include, in addition to net migration by commercial air, net migration by land, by sea, and by clandestine and noncommercial (military- and government-chartered) air." The author concludes that "total net migration to the United States exceeds by a significant margin estimates of total net migration published by the U.S. Bureau of the Census, which have averaged around 370 thousand over this same period, as well as recent estimates published in the demographic literature of between 500 and 600 thousand per year." A critique by Jennifer Marks (pp. 351-5) and a reply by Vining (pp. 357-60) are also included.

Americas↗
PubMed1990

Scottish emigration in the 1980s: a migration channels approach to the study of skilled international migration.

"British emigration is now dominated by skilled transient movements rather than traditional settler emigration movements. This switch requires new frameworks for migration analysis. A migration channels approach is advocated with attention focused on the roles of the internal labour markets of multi-national companies, international recruitment agencies and international skill transfers by small- and intermediate-sized companies in moulding contemporary skilled migration. The migration processes which have emerged in relation to the operation of these three channels can be differentiated in terms of migrant characteristics, the status of migration contracts and patterns of movement. The regional dimension is highlighted in this article by contrasting the experience of recent Scottish emigration with that of the South-East of England. Three data sources (the International Passenger Survey, the results of a survey questionnaire, and company case study material) are employed to illustrate the nature of Britain's main migration channels. It is argued that the three channels are responsible for a selective structuring of the British migration system."

Demography↗
PubMed1976

[Migration inhibition of mononuclear cells in idiopathic adrenal insufficiency. Inhibition of migration of mononuclear cells with adrenal microsomes and blocking of the reaction by adrenal antibodies (author's transl)].

In 19 patients with idiopathic adrenal insufficiency and in 19 controls, cellular (as measured by the migration inhibition test) and humoral (by means of immunoflourescence) immune reaction to adrenal antigens were investigated. Significant inhibition of migration was observed in 12 patients with adrenal microsomes; migration of mononuclear cells was however within normal range in 18 out of 19 controls. Adrenal antibodies could be detected in 11 (53%) of the patients. In a further series of investigations adrenal microsomes have been preincubated with specific antibody and used in migration inhibition tests. The migration indices observed with microsomes were compared to those obtained with microsomes preincubated with adrenal antibody. Migration inhibition with microsomes could be blocked by antibody in almost all antibody-positive patients. No uniform trend on the migration of mononuclear cells was found in the antibody-negative patients. A blocking of the cellular immune reaction by specific antibody seems likely. Possible mechanisms which could lead to such phenomena as well as the biologic significance of adrenal antibodies are discussed.

Adrenal Glands↗
PubMed1990

The relative impact of migration type on the reversal of black out-migration from the South.

"In this article historical patterns and recent trends in black migration in the United States are examined. The purpose of the article is two-fold: (1) to examine historical changes in the volume and rates of migration between the southern region and nonsouthern regions; and (2) to determine the relative impact of migration types on the South's changeover to net in-migration during the 1975-1980 migration interval.... The single most important factor influencing the turnaround was a decrease in the number of southern-born blacks migrating out of the region. This finding is contrary to much current speculation about the role of return migrants in influencing the South's changeover to net in-migration for the black population."

Black or African American↗
PubMedDate not supplied

Stimulation of vascular smooth muscle cell migration by macrophage migration inhibitory factor.

Macrophage migration inhibitory factor (MIF) is a well known proinflammatory factor that influences the migration and proliferation of various cell types, predominantly monocytes and macrophages. Recent evidence suggests an important role for MIF in the progression of atherosclerosis and restenosis. For this reason, we studied the effect of MIF on platelet-derived growth factor-BB (PDGF-BB)-induced migration and PDGF receptor protein expression in vascular smooth muscle cells (VSMCs). Furthermore, the possibility of MIF influencing the migration of VSMCs was investigated. Our results show that short-term incubation of MIF is able to enhance PDGF-BB-induced migration. Long-term incubation decreases PDGF-BB-induced migration, but preserves a short-term stimulatory effect. These effects are not regulated at the level of PDGF receptor protein expression. MIF also acts as a chemoattractant for VSMCs, with a maximum response at 15 ng/ml. In contrast, the proliferation of VSMCs was unaffected by MIF. We conclude that MIF has a biphasic effect on VSMC migration. It remains unclear whether this effect is direct or involves the secretion of unidentified promigratory factors. Exogenous MIF does not stimulate VSMC proliferation; however, a role for MIF in proliferation cannot be fully ruled out. In view of the known key contributions of macrophage-derived MIF and VSMCs, the observed effects may well play a role in the progression of atherosclerosis and restenosis.

Animals↗
PubMed1977

Leukocyte migration agarose test for the assessment of human neutrophil chemotaxis. I. Effects of environmental factors on neutrophil migration under agarose.

To apply the leukocyte migration agarose test (LMAT) to the in vitro assessment of human neutrophil chemotaxis, effects of different culture conditions on neutrophil migration under agarose were studied. Presence of either serum or human serum albumin (HSA) in the culture medium was necessary for detectable neutrophil migration. HSA was preferred since heat-stabile chemotactic agents were found to be generated from fresh serum in the presence of agarose. Additional CO2 in the assay milieu could be replaced by decreasing the NaHCO3 concentration of the culture medium. Both the directed and the spontaneous migration rates of neutrophil leukocytes increased when the concentration of agarose was decreased. Area and distance of migration and cumulative cell count of migrated neutrophil leukocytes were suitable for quantitating the neutrophil migration rate.

Adult↗
PubMed1980

Cyclic AMP levels in migrating and non-migrating newt epidermal cells.

Cyclic AMP (cAMP) levels were measured in 8-hour migrating wound epithelial and non-migrating epithelial cells of the newt. Tissues were collected in vivo and in vitro with and without epidermal-dermal separation by collagenase. Regardless of manner of collection and treatment, cAMP levels were always significantly higher in the migrating cells. Levels were also measured in 28-hour and 36-hour wound epithelia. There was a progressive decline in levels in wound epithelia between 8, 28, and 36 hours, suggesting that levels were in the process of returning to normal. When cells were treated with a dose of cAMP and theo-phylline previously shown to inhibit migration, levels of cAMP were much higher than any migrating epithelium. The fact that cAMP inhibits migration, yet migrating cells have higher cAMP levels, seems contradictory at first, but possible explanations are advanced to account for the apparent discrepancy.

Animals↗
PubMed1976

The sealed capillary migration technique and thymocyte migration in vitro.

The in vitro migration of thymocytes in sealed capillary tubes was influenced by cell number, temperature, cell viability and oxygen supply. Migration was successively slower over a 24 h period. There was no major influence of gravity or the degree of initial packing of the cells by centrifugation. Migration was inhibited by cytochalasin B, although the cells escaped from this effect after 8 h. A transient stimulatory effect on migration was seen after addition of serum or supernatants from cultured thymocytes. There was no effect of isoproterenol, theophylline or carbacholine. A paradoxic effect was obtained with high doses of some metabolic inhibitors, which produced increased migration in spite of cell death. The technique may be used for studies on lymphocyte migration in vitro, but care must be taken to exclude a toxic influence of added substances, and expected effects should preferably be looked for early after onset of migration, since cell viability is gradually decreased.

Animals↗
PubMed1999

Migration of Langerhans cells in an in vitro organ culture system: IL-6 and TNF-alpha are partially responsible for migration into the epidermis.

Although it is well established that epidermal Langerhans cells (LC) originate from bone marrow, little is known about the mechanism of this migration into the epidermis from bone marrow. In order to clarify the mechanism of this migration, we constructed an in vitro model. LC were depleted by daily topical application of clobetazole propionate (CP) solution onto the ear of Balb/c mice. Seven days later, ear skin was cut off, separated and co-cultured dermal-side-up with syngeneic (Balb/c), semisyngeneic ((C3H x Balb/c)F1), or allogeneic (C3H) epidermal cells (EC) for 3 days. We found (1) that a marked migration of donor LC into the recipient epidermis was observed in the LC-depleted skin, (2) that only syngeneic LC actively migrated into the recipient epidermis; however, the migration of semisyngeneic and allogeneic LC was detected at very low levels, (3) that the migratory capacity of donor LC was directly proved by a biolabeling technique using donor EC labeled with PKH-26, and (4) that anti-IL-6 and anti-TNF-alpha antibodies inhibited the migration of donor LC into the recipient epidermis. These data demonstrate that the resident LC have the potential to traffic through the dermis into the epidermis in a highly syngeneic-specific fashion, and that IL-6 and TNF-alpha are partially responsible for promoting this migration.

Animals↗
PubMed2002

Migration of LHRH neurons into the spinal cord: evidence for axon-dependent migration from the transplanted chick olfactory placode.

In the chick embryo, luteinizing hormone-releasing hormone (LHRH) neurons originate in the olfactory placode and migrate along the olfactory nerve to the forebrain. In previous studies, we demonstrated that LHRH neurons followed the trigeminal nerve when the olfactory nerve was physically interrupted. To examine whether LHRH neurons possess the capacity to migrate along the different type of axons, the olfactory placode was transplanted into the base of the forelimb. Three to five days after the transplantation, LHRH neurons were detectable in the spinal nerve, the dorsal root ganglion, the sympathetic ganglion and the spinal cord. Double or triple labelling studies for LHRH, somatostatin and/or axonin-1 showed that LHRH neurons entered the spinal nerve in contact with the olfactory axons, which are specifically immunoreactive to somatostatin. Migrating LHRH neurons continued to associate closely with the olfactory axons in the spinal nerve. However, some LHRH neurons often migrated along with the axonin-1 positive spinal sensory axons, maintaining a distance from the olfactory axons. Furthermore, a few LHRH neurons were observed in the ventral root and the ventral funiculus independent of olfactory axons. As LHRH neurons were observed in the motor component of the spinal nerve, it is probable that LHRH neurons also invaded the spinal cord using the motor axons as a guiding substrate for their migration. These results suggest that the migration mode of LHRH neurons is axon dependent in the peripheral region, however, chemical identity with regard to axonal substrate choice for migration was not specified in the present study.

Animals↗
PubMed2004

Cell migration: mechanisms of rear detachment and the formation of migration tracks.

Cell migration is central to many biological and pathological processes, including embryogenesis, tissue repair and regeneration as well as cancer and the inflammatory response. In general, cell migration can be usefully conceptualized as a cyclic process. The initial response of a cell to a migration-promoting agent is to polarize and extend protrusions in the direction of migration. These protrusions can be large, broad lamellipodia or spike-like filopodia, are usually driven by actin polymerization, and are stabilized by adhering to the extracellular matrix (ECM) via transmembrane receptors of the integrin family linked to the actin cytoskeleton. These adhesions serve as traction sites for migration as the cell moves forward over them, and they must be disassembled at the cell rear, allowing it to detach. The mechanisms of rear detachment and the regulatory processes involved are not well understood. The disassembly of adhesions that is required for detachment depends on a coordinated interaction of actin and actin-binding proteins, signaling molecules and effector enzymes including proteases, kinases and phosphatases. Originally, the biochemically regulated processes leading to rear detachment of migrating cells were thought not to be necessarily accompanied by any loss of cell material. However, it has been shown that during rear detachment long tubular extensions, the retracting fibers, are formed and that "membrane ripping" occurs at the cell rear. By this process, a major fraction of integrin-containing cellular material is left behind forming characteristic migration tracks that exactly mark the way a cell has taken.

Animals↗