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PubMed1996

Associations between overseas, intra-urban and internal migration dynamics in Sydney, 1976-91.

"This paper investigates spatial statistical associations between overseas in-migration rates and internal migration loss within Sydney and between housing costs in Sydney and internal migration outflows. The hypothesis was that housing cost changes and overseas migration contributed additively to migration losses from the metropolis. The integration of metropolitan Sydney and Australia into the ¿Pacific rim' economy is examined with reference to wider explanations of house cost changes and migration flows."

Australia↗

PubMed1993

Does migration arbitrage regional labor market differentials?

"This paper examines the determinants of regional migration [in the United States] in the 1980s using a place-to-place migration model in which migration flows depend upon the relative economic opportunities in the origin and destination regions. Using the results of the model, we then examine the potential role for migration in diffusing the economic pressures associated with disparate regional economic growth. Although the results reinforce the notion that divergent regional growth was an impetus to migration in the 1980s, estimates of the employment status of movers suggest that the true effects of migration on unemployment differentials may be quite small."

Americas↗

PubMed1980

Demonstration of a complement-dependent migration inhibitory activity in normal guinea pig serum.

A cell migration inhibitory effect was evidentiated in normal guinea pig serum as compared with heat inactivated serum. Granulocytes when used as target showed a greater sensitivity to this effect than lymphomonocytes or macrophages. The migration inhibitory activity of GPS is abrogated or decreased by using complement destroying agents such as: heating at 56 degrees C for as little as 5 min, absorption on immune complexes in presence of calcium, on zymosan, on Sephadex G-50 or by adding EDTA or heparin to culture medium. The GPS dialysation fractions while exhibiting neither complement haemolytic effect nor migration inhibitory activity when tested alone, restored these functions by recombination. Absorption of GPS on homologous blood cells abrogated the migration inhibitory effect but retained the complement haemolytic function. When GPS absorbed on homologous blood cells mixed 1:5 with heat-inactivated serum (5 min at 56 degrees C), the migration inhibitory activity was regained, suggesting that the complement factors from the first sample were necessary for manifestation for the migration inhibitory activity from the heat-inactivated serum.

Animals↗

PubMed1992

International migration within and from the East and Southeast Asian region: a review essay.

The author reviews the literature on the trends and characteristics of international migration within and from East and Southeast Asia, with a focus on the past 25 years. "Five migration systems are described: settler, student, contract labor, skilled labor, and refugee. Settler migration to the U.S., Canada and Australia has consisted primarily of family members.... Contract labor migration, particularly to the Middle East, has provided jobs, foreign currency through remittances and greater participation of women, but also led to illegal migration, skills drain, and labor abuses. The hierarchy of development has led to intra-regional flows: (1) skilled labor mainly from Japan to other countries in the region, and (2) contract labor and illegal migration from the LDCs to the NIEs [newly industrializing economies] and Japan."

Asia↗

PubMed1978

Some aspects of internal annual migration in India.

Data collected in 1973-1974 during the twenty-eighth round of the National Sample Survey are used to analyze annual internal migration in India. "The analysis reveals that [the in-migration] rate for all-India was estimated at 91 for the rural and 104 for the urban areas per 10,000 population. Out of the total migration intra-state migration was as high as 87 percent and more than 68 percent came from rural areas. The most important flow of migration was rural to rural and next to that was urban to urban followed by rural to urban and urban to rural." Findings are also presented concerning variations among states, rates of urbanization, the age and sex composition of migrants, reasons for migration, the educational level of labor migrants, and changes since the 1963-1964 round of the survey.

Age Distribution↗

PubMed1986

[Migration and the business cycle in the Federal Republic of Germany since the 1960s].

The relationship between migration and economic development in the Federal Republic of Germany is explored. Questions considered include: "How does the economic development change the intensity of migration flows in short and long distance migrations? What kinds of migrations are especially sensitive to economic changes? How do these changes come about?" Migration patterns between West Germany and other European countries are analyzed in comparison with a time series of economic parameters, such as the labor market. Migrations between three West German cities and their surrounding regions are also analyzed in comparison with a different series of parameters, including new housing construction. (SUMMARY IN ENG)

Demography↗

PubMed1991

The determinants of interdistrict labour in-migration in Pakistan, 1971-1980.

"This article begins by reviewing the previous literature pertinent to labour migration within Pakistan. Next, a migration equation at the aggregate level is specified, based on the expected socio-economic determinants of labour migration and data availability. Regression analysis was used to identify and quantify the determinants of interdistrict migration in Pakistan during the period 1971-1980. The results demonstrate that one of the major determinants of migration into a district was the percent of previous migrants in a district's population. Interdistrict migration was also significantly associated with the socio-economic variables of urbanization, population density, and literacy rates. The research presented here provides evidence that the movement of labour between districts in Pakistan is towards locations of superior socio-economic conditions."

Asia↗

PubMed1985

[Female migration and social change in Africa. The case of Kenya].

Causes of the recent increase in female rural-urban migration in Kenya are investigated. "Reasons for this additional migration-wave are to be found in a general weakening of traditional values and authorities, the increasing land shortage and the resulting population pressure in the rural areas, which are factors that do in fact force women to migrate to towns." Comparisons are made with male migration flows. Regional differences in migration patterns are also noted. The author concludes that the increase in female migration is not a result of greater emancipation of women but rather a symptom of increasing poverty among Kenya's female population. (SUMMARY IN ENG)

Africa↗

PubMed1992

[Demographic differences between nonnative groups: the impact of international migration].

The impact of international migration on the composition of the population of the Netherlands is examined. The authors conclude that "the non-native population shows a considerable variety from a demographic point of view. Differences in composition by age and sex can largely be attributed to differences in migration patterns. Both the size and the period of migration flows have had their influence, as well as the type of migration (labour migration, family reunification, etc.). Apart from the direct influence there are also indirect effects because of demographic events that took place after the migration, like births, marriages and deaths." (SUMMARY IN ENG)

Age Distribution↗

PubMed2006

Cellular migration associated with macular hole: a new method for comprehensive bird's-eye analysis of the internal limiting membrane.

OBJECTIVE: To elucidate the pathogenesis of macular hole formation, focusing in particular on the possible role of cellular migration on the cortical vitreous and internal limiting membrane (ILM) around the macular hole. METHODS: To gain a comprehensive overview of the ILM excised in macular hole surgery (n = 36), the ILMs were carefully unfolded and spread out onto glass slides as continuous flat sheets that each contained a macular hole. The specimens were observed by light microscopy and transmission electron microscopy (n = 9), and the cellular distribution was analyzed by scanning electron microscopy in a quantitative manner (n = 27). Immunohistochemistry for glial fibrillary acidic protein and cytokeratin 18 was carried out for cellular characterization. Cellular proliferation was assessed by immunohistochemistry for proliferating cell nuclear antigen and Ki-67. RESULTS: Cellular migration was not apparent around the macular hole in the early stage of development of the macular hole (stage 2, 0 microm). As the macular hole passed through the later stages of development, cellular migration developed around the macular hole (stage 3, 84 microm) and the area of cellular migration gradually enlarged (stage 4, 420 microm). The immunophenotypic analysis showed that these cells were mainly glial fibrillary acidic protein-positive glial cells and cytokeratin 18-positive retinal pigment epithelial cells. The proliferating cell nuclear antigen and Ki-67 immunohistochemistry showed that some of these cells were proliferating on the ILM. CONCLUSIONS: Cellular migration on the ILM is not necessary for the initial formation of a macular break. Cellular migration developed after the macular break occurred, and the migration and proliferation increased gradually from the macular hole. CLINICAL RELEVANCE: This study provides a new method for understanding the ultrastructural analysis of the pathogenesis of the macular hole.

Basement Membrane↗

PubMed1999

Origin and migration of luteinizing hormone-releasing hormone neurons in mammals.

Luteinizing hormone-releasing hormone (LHRH) neurons are unique among hypothalamic neurons in that they originate outside of the central nervous system. In most vertebrates, LHRH-immunoreactive (-ir) neurons are detected in the epithelium of the medial olfactory pit soon after its formation. The LHRH-ir neurons migrate out of the placodal epithelium and into the brain along a migration route that consists of the central processes of the terminal, olfactory, and vomeronasal nerves. LHRH-ir cell migration follows a highly ordered course from the initial appearance of the LHRH-ir cells in the epithelium of the medial olfactory pit, to the crossing of these cells in cords on the nasal septum, to their entrance into the forebrain. Here they separate and follow an arching trajectory to their final destinations in the septal and preoptic areas and in the hypothalamus. Examination of the molecular makeup of the developing migration route reveals the presence of neural cell adhesion molecule (N-CAM) in non-LHRH-ir cells. The N-CAM-ir cells migrate into the nasal mesenchyme, trailed by N-CAM-ir axons of the olfactory, vomeronasal, and terminal nerves. These N-CAM cells and axons link the olfactory epithelia with the developing forebrain and together form scaffolding along which the LHRH-ir cells migrate into the brain. The focus of this review is on the origin and migration of LHRH-ir neurons in mammals, including humans. A discussion of Kallmann's syndrome (hypogonadotropic hypogonadism with anosmia) is included, in which there is an absence of LHRH-ir in the brain but clusters of LHRH-ir cells in the nasal cavity. This "experiment of nature" lends support to the hypothesis that all LHRH-ir cells in humans originate in the olfactory placode.

Animals↗

PubMed1998

Specification and migration of melanoblasts at the vagal level and in hyperpigmented Silkie chickens.

The final pattern of neural crest derivatives used to be believed to be the result of unspecified neural crest cells haphazardly entering migratory paths and then receiving cues unique to that path that direct their differentiation. An alternative model, which we have coined the phenotype-directed model, is that neural crest cells are fate-specified first and then select a migratory pathway based on their developmental specification. Support for this model comes from recent studies demonstrating that, at the thoracic level, neural crest cells are specified as melanocyte precursors (melanoblasts) prior to entering the dorsolateral path, and that only melanoblasts have the ability to migrate dorsolaterally. Here we examine two examples of melanocyte patterning in birds that apparently contradict this model. The first is neural crest at the vagal level, where early crest cells migrate dorsolaterally and enter the branchial arches. Despite the fact that these cells migrate dorsolaterally (suggesting that they are melanoblasts), branchial arch-derived neural crest cells fail to differentiate as melanocytes in vitro. These observations suggest that the branchial arch environment may not support the survival or differentiation of melanogenic neural crest cells. The second example is the hyperpigmented Silkie chickens, which exhibit extensive internal pigmentation. The Silkie defect has been linked to a difference in the neural crest migratory environment that potentially causes (or allows) unspecified neural crest cells to undergo melanogenesis in the ventral path. In both of these situations, it appears that the final distribution of pigment cells is controlled by environmental factors, which would contradict the phenotype-directed model. Here we show that the final pattern of melanocytes at the vagal level and in Silkie chickens reflects the migratory behavior of lineage-specified melanoblasts, as predicted by the phenotype-directed model. At the vagal level, the early, dorsolaterally migrating crest cells that colonize the branchial arches are not melanoblasts and are biased against melanogenesis in vitro. Melanoblasts are not specified until later, just prior to a second wave of dorsolateral migration, and although these cells migrate dorsolaterally they do not invade the branchial arches. In Silkie embryos, melanoblasts are specified late and only invade the dorsolateral path after they have been specified. Unlike quail and White leghorn melanoblasts, however, Silkie melanoblasts also migrate ventrally, but again only after they are specified.

Animals↗

PubMed1999

Thrombospondin-1 and neural crest cell migration.

Using a monoclonal antibody raised against human platelet thrombospondin, we found anti-thrombospondin immunoreactivity in the extracellular matrix of avian embryos, coincident with the ventral pathways followed by trunk neural crest cells. To confirm that the antibody recognized thrombospondin-1 and to determine the tissue of origin of the thrombospondin matrix, a thrombospondin-1 cRNA probe was used for whole mount in situ hybridization. This probe revealed thrombospondin-1 mRNAs in the developing myotome before and during neural crest cell migration. The effect of thrombospondin-1 on neural crest cell migration, morphology, and adhesion was assayed in vitro. Quail trunk neural crest cells cultured on 4 microg/ml of thrombospondin-1 migrate at 1.14 +/- 0.54 microm/min, which is significantly greater than the rate of cell migration on tissue culture plastic. Using a shaker-based adhesion assay, a significantly greater number of neural crest cells remain attached to dishes coated with 4 microg/ml of thrombospondin-1 than to tissue culture plastic alone. The number of neural crest cells that remain attached to 4 microg/ml of thrombospondin-1 is similar to the number that remain attached to dishes coated with 10 microg/ml of fibronectin. These observations indicate that neural crest cells migrate through a thrombospondin-filled extracellular matrix, and that thrombospondin-1 promotes neural crest cell migration and adhesion. Thus, thrombospondin-1 is the first somite-derived extracellular matrix molecule with properties consistent with a role in the promotion of migration into the anterior somite, as opposed to the repulsion of neural crest cells from the posterior half of the somite.

Animals↗

PubMed1999

Urokinase regulates embryonic cardiac cushion cell migration without converting plasminogen.

Urokinase-type plasminogen activator (uPA) activation of plasminogen is an important mediator of cell migration in many cell types. In the developing avian heart, uPA has been implicated as a mediator of atrioventricular (AV) cushion cell migration; however, the role of the plasminogen/plasmin system has not been examined. The purpose of this study was to test the hypothesis that uPA conversion of plasminogen to plasmin mediates AV cushion cell migration in vitro. Stage 17/18 chicken atrioventricular tissue lysates converted plasminogen into plasmin through uPA activity but no tissue-type plasminogen activator activity was detected. Zymograms on living cultured AV explants also activated plasminogen producing plasmin that degraded extracellular protein. The migratory capacity of cushion cells was assessed in the presence or absence of various test reagents known to alter the plasminogen/plasmin system. Addition of either human or chicken plasminogen or aprotinin (an inhibitor of plasmin) had no effect on cell migration. However, an anti-catalytic uPA antibody that blocked AV uPA activity, significantly decreased cell migration at all concentrations tested. These results showed that uPA mediated a portion of cushion cell migration in vitro. Although AV segments activated plasminogen and degraded extracellular proteins, uPA's functional role in cushion cell migration did not involve the plasminogen/plasmin system.

Animals↗

PubMed1996

Dichotomy of astrocytoma migration and proliferation.

Astrocytomas often show high rates of local invasion that lead to local recurrence of the disease. Histologically, the most highly invasive astrocytoma cells are detected in isolation rather than as nests of tumor. Our study attempted to determine whether the migratory response to extracellular substrates influences the proliferative behavior of these highly invasive cells. The preferential and specific migratory response of human astrocytoma cells to extracellular matrix proteins was assessed by a microliter scale migration assay. Growth curve studies on protein ligands permissive (merosin) for cell migration indicated that the lag phase was protracted compared with cells seeded on non-permissive proteins (vitronectin). Once a certain cell density was reached, logarithmic proliferation was indistinguishable on the different proteins. The proliferation index of populations of cells migrating on merosin and vitronectin was measured by both BrdU incorporation and MIB-1 immunocytochemistry labeling. Cells seeded on vitronectin showed higher proliferation throughout the population than cells seeded on merosin. On merosin, the more migratory cells at the periphery were less proliferative than non-migratory cells in the central region of that population. The integrin-associated signal transduction protein, p125FAK, was heavily localized in the membrane of non-migrating cells and largely absent in migrating astrocytoma cells. We conclude that temporally, proliferation and migration are mutually exclusive behaviors. Cell density or non-permissive substrates that inhibit cell motility favor a more proliferative phenotype. Conversely, active migration suppresses cell proliferation.

Astrocytoma↗

PubMed1999

Integrins and E-cadherin cooperate with IGF-I to induce migration of epithelial colonic cells.

Although the detailed mechanisms of cell migration remain largely unknown, it is now clear that growth factors and cell adhesion molecules are crucial for this process. We have shown that type I insulin-like growth factor (IGF-I) promotes migration of human colonic tumour cells. Since morphological analysis suggested an involvement of adhesion molecules, we have now examined the role of integrins (cell-matrix adhesion molecules) and E-cadherin/catenins complex (cell-cell adhesion molecules) in the IGF-I-induced migration. Using a monolayer wounding assay, we have determined that, except for alpha2beta1, all of the integrins expressed in HT29-D4 cells are involved in the induced cell migration. Immunofluorescence studies revealed that upon IGF-I stimulation the integrins reorganized at the leading edge of migrating cells. We also demonstrate that E-cadherin is involved in cell migration. A rapid tyrosine phosphorylation of E-cadherin and beta-catenin was detected upon IGF-I stimulation. Tyrosine phosphorylation was associated with reduced membranous expression of E-cadherin and promotion of cell motility, suggesting a regulation of the E-cadherin/catenins complex. This effect can be reversed by incubating cells with tyrosine kinase inhibitors. Taken together, our results suggest that IGF-I promotes colonic cell migration through reorganization of integrin receptors and through modulation of E-cadherin/catenins complex function.

Antibodies, Monoclonal↗

PubMed1999

Role in neuronal cell migration for high-threshold potassium currents in the chicken hindbrain.

We have investigated the influence of voltage-dependent, potassium conductances on the migration of embryonic neurons, using a culture preparation taken from the acoustico-vestibular anlage long before the onset of electrical excitability and synaptic function. Whole-cell patch clamp recordings from migrating neuroblasts at Hamburger-Hamilton stage 28 (E 5.5) revealed the exclusive expression of voltage-dependent, high-threshold, outward currents, activating at potentials positive to -20 mV. These currents were completely suppressed by the potassium channel blockers, 1.0 mM tetraethylammonium chloride (TEA) or 1.0 mM 4-aminopyridine (4-AP). In control media, the active migration of individual neuroblasts was recorded at 27 +/- 6 microm per hr. Within minutes after adding either drug to the culture, normal migration completely stopped for several hours. Calcium channel blockers, omega-conotoxin (3 microM) or cadmium chloride (100 microM), slowed, but did not halt, migration, while nickel chloride (100 microM) or N-methyl-D-glucamine (1 mM) had no effect. However, within 8 hr after TEA exposure, migratory activity usually returned. This recovery was associated with the appearance of a previously undetected, low-threshold and 4-AP- sensitive potassium conductance. We suggest that high-threshold, TEA/4-AP-sensitive potassium channels may normally support the migration of these neurons, while their chronic blockade can be compensated by the appearance of novel potassium channels. Potassium currents may act in concert with N-type calcium channels to regulate neuronal migration.

4-Aminopyridine↗

PubMed1996

Control of cell adhesion, migration, and orientation on photochemically microprocessed surfaces.

Using surface-photochemistry-driven microprocessing, striped patterns of cell-adhesive and nonadhesive domains were prepared on tissue-culture dishes. The width of striped patterns ranged from 20 to 130 microns. When endothelial cells were cultured on such dimensionally well-defined surfaces, cells adhered, migrated, and proliferated only on cell-adhesive domains. Migration potentials such as tracks of moving cells and migration rates were determined using a time-lapse video recording apparatus under a phase-contrast microscope and a computer-assisted image analyzer. The migration track in the direction of the width of the stripe-pattern was limited to the size of the width, and effective migratory distance over 400 min of observation was considerably reduced, to almost half that for a nontreated surface, whereas migratory rate was not changed by surface processing, irrespective of the stripe-pattern width. After a 2-day culture, oriented patterned cellular sheets were obtained. Cells were elongated and aligned along the axis of the striped pattern. The degrees of orientation and elongation were enhanced with a decrease of the line width. At the narrowest surface domain, cells only migrated back and forth, and eventually they became highly elongated and oriented along the axis of the domain. These results indicated that the adhesion area, migrating direction, and orientation of cells can be controlled by this method with micron-order precision. This method provides quantitative information on the kinetics of the migration process and the morphogenesis of the microprocessed surface.

Animals↗