[Migration and health. A literature review. I. Studies of effects. Summary and theoretical observations based on a selection from the general literature on migration].
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Acculturation↗
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[Use of 131I labeling for studying the distribution and migration of spermatozoa in the genital tract of female sheep following artificial insemination. 1. Gamma camera studies of the course of migration].
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Animals↗
Route of lymphocyte migration in pigs. II. Migration to the intestinal lamina propria of antigen-specific cells generated in response to intestinal immunization in the pig.
Intestinal lymph-duct cannulae were established in normal and mesenteric lymphadenectomized (MLNx) pigs for the 6-day duration of a local intestinal immune response to a protein antigen (ovalbumin). The daily output of anti-ovalbumin-containing cells (AOCC) in intestinal lymph and the numbers of AOCC in the intestinal lamina propria at the end of the experiment were recorded. Very few AOCC were recovered in the intestinal lymph of normal pigs whereas in MLNx pigs large numbers were recovered reaching a peak output on day 4. However, there were significantly more AOCC detected in the jejunal lamina propria of normal pigs than MLNx pigs despite continuous drainage of intestinal lymph throughout the response. The absence of AOCC from efferent intestinal lymph of normal pigs, the failure of chronic intestinal-lymph drainage to abrogate the AOCC response in the intestine of these pigs and the reversal of these findings in MLNx pigs indicate that, in contrast to other species, lymphoblasts are diverted from porcine intestinal lymph, and probably enter the blood circulation at the level of the mesenteric lymph node (MLN).
Animals↗
Migrating glioma cells activate the PI3-K pathway and display decreased susceptibility to apoptosis.
Glioma cells that migrate out of the main tumor mass into normal brain tissue contribute to the failure of most gliomas to respond to treatment. Treatments that target migratory glioma cells may enhance the therapeutic response. Multiple lines of evidence suggest that suppression of apoptosis accompanies activation of the migratory phenotype. Here, we determine whether migration and apoptosis are consistently linked in glioma cells and whether manipulation of migration influences cytotoxic therapy-induced apoptosis. Camptothecin and Trail-induced apoptosis were decreased 2-5-fold in actively migrating glioma cells relative to migration-restricted cells. Consistent with a mechanistic link between migration and apoptosis, the dose-response for stimulation of migration on laminin was inversely proportional to apoptosis induction. Treatment of glioma cells with migration inhibitors alone had little effect on basal rates of apoptosis and had little effect on Trail-induced or camptothecin-induced apoptosis in migration-restricted cells. By contrast, migration inhibitors increased camptothecin and Trail-induced apoptosis in actively migrating glioma cells. Migrating glioma cells have increased amounts of phosphorylated Akt and its downstream substrate glycogen synthase kinase-3 relative to migration restricted cells. Treatment of migrating cells with a specific inhibitor of phosphoinositide 3-kinase (PI3-K), LY294002, blocked the phosphorylation of Akt and increased the sensitivity to apoptosis. LY294002 had no effect on the migration of restricted cells. This suggests that migrating glioma cells activate the PI3-K survival pathway, protecting migrating cells from apoptosis. Taken together, these data provide support for a link between migration and apoptosis in glioma cells. In addition, evidence indicates that treatment with migration inhibitors, while not affecting apoptosis-induction in migration-restricted cells, can sensitize migrating glioma cells to cytotoxic agents.
Animals↗
Stent graft migration after endovascular aneurysm repair: importance of proximal fixation.
OBJECTIVE: We reviewed the incidence of stent-graft migration after endovascular aneurysm repair in a prospective multicenter trial and identified factors that may predispose to such migration. METHODS: All patients who received treatment during the course of the multicenter AneuRx clinical trial were reviewed for evidence of stent-graft migration over 5 years, from 1996 to 2001. Post-deployment distance from the renal arteries to the proximal end of the stent graft and the proximal fixation length (length of the infrarenal neck covered by the stent graft) were determined in patients for whom pre-procedure and post-procedure computed tomography scans were measured in an independent core laboratory. RESULTS: Stent-graft migration was reported in 94 of 1119 patients, with mean time after device implantation of 30 +/- 11 months. Freedom from migration was 98.6% at 1 year, 93.4% at 2 years, and 81.2% at 3 years (Kaplan-Meier method). Subset (n = 387) analysis revealed that initial device deployment was lower in 47 patients with migration, as evidenced by a greater renal artery to stent-graft distance (1.1 +/- 0.7 cm), compared with 340 patients without migration (0.8 +/- 0.6 cm; P =.006) on post-implantation computed tomography scan. Proximal fixation length was shorter in patients with migration (1.6 +/- 1.4 cm) compared with patients without migration (2.3 +/- 1.4 cm; P =.005). There was significant variation in migration rate among clinical sites (P <.001), ranging from 0% to 30% (median, 8%), with a greater than twofold difference in migration rate between the lowest quartile (6%) and the highest quartile (15%) clinical sites. Univariate and multivariate analysis revealed that renal artery to stent-graft distance (P =.001) and proximal fixation length (P =.005) were significant predictors of migration, and that each millimeter increase in distance below the renal arteries increased risk for subsequent migration by 5.8% and each millimeter increase in proximal fixation length decreased risk for migration by 2.5%. Pre-implantation aortic neck length, neck diameter, degree of device oversizing, correct versus incorrect oversizing, device type (stiff vs flexible), placement of proximal extender cuffs at the original procedure, and post-procedure endoleak were not significant predictors of migration. Migration was treated with placement of extender modules in 23 patients and surgical conversion in 7 patients; 64 patients (68%) with migration have required no treatment. CONCLUSIONS: Stent-graft migration among patients treated in the AneuRx clinical trial appears to be largely related to low initial deployment of the device, below the renal arteries, and short proximal fixation length. Significant variation in migration rate among clinical sites highlights the importance of the technical aspects of stent-graft deployment. Advances in intraoperative imaging and deployment techniques that have been made since completion of the clinical trial facilitate precision of device placement below the renal arteries and should increase proximal fixation length. Whether this, together with increased iliac fixation length, will result in lower risk for migration remains to be determined in long-term follow-up studies.
Aged↗
[Migration of shoulder prosthesis as a consequence of hemi- or total arthroplasty].
BACKGROUND: Migration after shoulder arthroplasty can induce muscular dysbalance and instability of the shoulder joint. The aim of this study was to analyse the frequency, causes and consequences of secondary migration after shoulder arthroplasty. METHODS: 107 shoulder arthroplasties in patients with primary osteoarthritis (OA, n = 83) or avascular necrosis of the humeral head (AVN, n = 24), were followed clinically and radiographically over a period of 1 to 10 years. RESULTS: 17 Patients (16 %) developed secondary migration of the prosthesis. These were determined after a mean period of 33 months after shoulder arthroplasty. Patients with secondary migration of the prosthesis showed a worse function with a mean Constant score (CS) of 52.3 points in comparison to the patient group without migrated shoulder arthroplasties (62 points) (p = 0.038). In patients with total shoulder arthroplasty (TSA, n = 75), migration was observed in 13 % of cases during follow-up. Lucent lines at the glenoid were found in radiographs in 55 % of migrated shoulders and in 52 % of non-migrated shoulders (p = 0.633). The Constant score showed no significant difference between the groups (non-migrated shoulders 63 points, migrated shoulders 61 points, p > 0.5). Migration was seen in 22 % (7/32 patients) after hemiarthroplasty, however, no significant difference could be found between the respective Constant scores for migrated (47.7 points) or non-migrated (55.1 points) shoulders (p = 0.447). In patients with OA there was no significant difference in Constant score between migrated and non-migrated shoulders (p = 0.331), whereas patients with AVN showed significantly worse function after migrated shoulder arthroplasty (p = 0.007). CONCLUSION: Migration after total shoulder arthroplasty leads in the medium term neither to an increased frequency of lucent lines at the glenoid nor to a worsening of the functional score in comparison to non-migrated prosthesis. In patients with AVN, migration is accompanied by a worsening of the functional score and can consequently be regarded as a negative prognostic factor.
Arthroplasty, Replacement↗
The importance of iliac fixation in prevention of stent graft migration.
OBJECTIVE: Secure proximal fixation of endografts to the infrarenal aortic neck is known to be important in the short- and long-term success of endovascular aneurysm repair. We sought to determine the relative importance of distal iliac fixation in preventing endograft migration and adverse clinical events after endovascular aneurysm repair. METHODS: We reviewed the outcome of 173 patients treated from 1996 to 2003 at Stanford University Medical Center with an externally supported stent graft. Quantitative image analysis of the postimplantation computed tomography scan was performed to determine the proximal aortic and distal iliac fixation lengths and the proximity the distal end of the stent graft to the iliac bifurcation. Subsequent follow-up computed tomography scans were reviewed for evidence of stent graft migration. Patients were grouped according to good (>15 mm), intermediate, or bad (<10 mm) aortic fixation and good (iliac fixation length > or =25 mm and iliac limbs <10 mm from iliac bifurcation), intermediate, or bad (<25-mm fixation length) iliac fixation. RESULTS: Stent graft migration of 10 mm or more was seen in 17 patients (10%) during the 23 +/- 19-month follow-up period. Patients with no migration had a greater iliac fixation length (30 +/- 12 mm) than those with migration (22 +/- 8 mm; P = .01), and the distal ends of the iliac limbs were closer to the iliac bifurcation (15 +/- 12 mm) than in patients with migration (25 +/- 10 mm; P < .001). Patients with no migration also had a greater proximal aortic fixation length (23 +/- 12 mm) than migration patients (13 +/- 7 mm; P = .001). There were no migrations among patients with good iliac fixation whether aortic fixation was good, intermediate, or bad (0/63; 0%). Among patients with bad/intermediate iliac and good aortic fixation, there were 5 (9%) of 58 patients had migrations. Patients with both bad/intermediate iliac and bad/intermediate aortic fixation had the highest migration rate (12/52; 23%). Cox proportional hazards regression modeling revealed that the significant factors predicting migration were poor proximity of the distal end of the iliac limbs to the iliac bifurcation (odds ratio 17.2; P = .01) and aortic fixation length (odds ratio 2.0; p = 0.007 for each centimeter). Iliac extender modules were placed in 9 patients with bad iliac fixation and migration, with no further migration during a mean follow-up of 12 months. Patients with good iliac and aortic fixation and no endoleak on the initial postprocedure computed tomography scan (n = 43) had no migrations, secondary procedures, or adverse clinical events over a 2-year follow-up period. CONCLUSIONS: Iliac fixation, along with proximal aortic fixation, is an important factor in preventing the migration of stent grafts that have longitudinal columnar support. Patients with good iliac fixation did not experience migration even in the presence of suboptimal proximal aortic fixation. Close proximity of the distal end of the stent graft to the iliac bifurcation seems to provide stability against migration.
Aged↗
Migration of Implanon.
OBJECTIVE: To determine whether or not migration of the Implanon rod does occur if correctly positioned and, if indeed migration does occur, to measure the degree of such migration. METHODS: A prospective study of 100 women who requested and had Implanon rods inserted by one fully trained health care professional holding the Faculty of Family Planning and Reproductive Health Care Letter of Competence in Subdermal Contraceptive Implant Techniques. Measurements were made from the insertion site to the distal end of the rods at 3 and 12 months post-insertion. RESULTS: Of the 100 women studied, 95 were seen for follow-up at 3 months. There was no migration of Implanon in 58 (61%) patients. Of the remaining 37 (39%) patients where migration had occurred, 34 showed migration caudally and only three demonstrated cranial migration. With regard to the degree of migration, all but one case showed this to be less than 2 cm either cranially or caudally. At 1-year follow-up 87 patients were seen. No migration was noted in 39 (45%) patients. In the remaining 48 (55%) patients where migration had occurred, 44 showed migration caudally and only four demonstrated cranial migration, which in one case was over 2 cm. With regard to the degree of migration, all but one case showed this to be less than 2 cm either cranially or caudally. The measurement in the single case showing migration over 2 cm at 3 months remained the same at the 1-year follow-up. CONCLUSIONS: These results show that up to 1 year after insertion of Implanon significant migration of the rod does not occur. The degree of migration noted in all cases except one was less than 2 cm. Where migration was noted, in the majority of cases this occurred caudally towards the insertion site. There were no cases of deep migration.
Adolescent↗
Mid- and long-term device migration after endovascular abdominal aortic aneurysm repair: a comparison of AneuRx and Zenith endografts.
BACKGROUND: Freedom from migration is key to the durability of endovascular aneurysm repair (EVAR). This study evaluates the mid- and long-term incidence of migration with two different endografts. METHODS: Between September 1997 and June 2004, 235 patients were scheduled for EVAR with an AneuRx (Medtronic/AVE Inc.) or Zenith (Cook) endograft. Patients with fusiform, infrarenal aneurysms and a minimum 12 months of follow-up were analyzed, for a final cohort of 130 patients. Migration was assessed on axial computed tomography (CT) (2.5 to 3 mm cuts) as the distance from the most caudal renal artery to the first slice containing endograft (AneuRx) or to the top of the bare suprarenal stent (Zenith). Aortic neck diameters were measured at the most caudal renal artery. The initial postoperative CT scan was the baseline. Migration was defined by caudal movement of the endograft at two thresholds, > or =5 mm and > or =10 mm, or any migration with a related clinical event. RESULTS: Life-table analysis demonstrated AneuRx freedom from migration (> or =10 mm or clinical event) was 96.1%, 89.5%, 78.0%, and 72.0% at 1, 2, 3, and 4 years, respectively. Zenith freedom from migration was 100%, 97.6%, 97.6%, and 97.6% at 1, 2, 3, and 4 years, respectively (P = .01, log-rank test). The stricter 5-mm migration threshold found 67.4% of AneuRx and 90.1% of Zenith patients free from migration at 4 years of follow-up. Twelve out of 14 (85.7%) AneuRx patients (12/14) with migration (> or =10 mm or clinical event) underwent 14 related secondary procedures (13 endovascular, 1 open conversion). The single Zenith patient with migration (> or =10 mm) has not required adjuvant treatment. Mean follow-up was 39.0 +/- 2.3 months (AneuRx) and 30.8 +/- 1.9 months (Zenith, P = .01). Patients with and without migration did not differ in age, gender ratio, aneurysm diameter, and neck diameter. However, initial neck length was shorter in patients with migration (22.1 +/- 2.1 mm vs 31.2 +/- 1.2 mm, P = .02). A subset of patients (21.6%) experienced significant (defined as > or =3 mm) maximum aortic neck dilation. Of the AneuRx patients, > or =3 mm aortic neck dilation affected 30.8% of migrators vs 13.0% of nonmigrators (P = .20). CONCLUSIONS: Endograft migration is a time-dependent phenomenon affected by both device choice and aortic neck length. A great majority of patients (85.7%) with migration of the AneuRx device ultimately required treatment. A minority of patients experienced aortic neck dilation that could be considered clinically significant. Careful surveillance for migration is an essential component of long-term follow-up after EVAR.
Aged↗
Pathologic migration of anterior teeth in patients with moderate to severe periodontitis.
The purpose of this study was to determine the prevalence of pathologic migration of anterior teeth in patients with moderate to severe periodontitis. The correlation between pathologic migration of anterior teeth and attachment loss (AL) was investigated, and an attempt was made to identify the most common early form of pathologic migration. Prevalence of tooth migration was studied in a group of 343 patients with moderate to severe periodontitis before treatment. The presence of pathologic migration was determined from the chief complaint and patient awareness o tooth movement in the last 5 years. Forty-four patients (age range 18 to 69; mean = 48.75) with 75 pairs of migrated and non-migrated teeth were studied further to determine if there is a correlation between severity of periodontal AL and pathologic migration. Migrated teeth were compared to control contralateral teeth that did not have migration. In addition, tooth mobility of the anterior teeth on 36 of the 44 patients was measured using the mobility meter. It was anticipated that tooth mobility would follow the same pattern as AL in relation to pathologic migration. The type and severity of displacement was recorded for each tooth affected by migration. The types of pathologic migration recorded were diastema, extrusion, rotation, facial flaring, and drifting into edentulous spaces. Pathologic migration prevalence was 30.03% +/- 2.5 (103/343 subjects). The mean AL of migrated teeth (4.79 +/- 0.28 mm) was significantly greater (P < 0.0001) than control teeth (3.21 +/- 0.18 mm). The numeric values (called PTV) of migrated teeth (17.6 +/- 1.5) were significantly greater (P < 0.0001) than control teeth (9.4 +/- 1.1). It was difficult to identify a primary form of displacement, as most patients demonstrated a combination of movements. The percentage of the 44 patients who presented with a specific type of movement was: facial flaring (90.9 +/- 4.4%), diastema (88.6 +/- 4.8%), rotation (72.7 +/- 6.8%), extrusion (68.2 +/- 7.1%), and tipping (13.6 +/- 5.2%). The results of this study confirms clinical impressions that periodontal disease destruction of the attachment apparatus plays a major role in the etiology of pathologic migration.
Adolescent↗
Platelet-derived growth factor-BB, insulin-like growth factor-I, and phorbol ester activate different signaling pathways for stimulation of vascular smooth muscle cell migration.
Vascular smooth muscle cell (VSMC) migration is an important process in the development of vascular occlusive disease. To investigate mitogen regulation of VSMC migration, a cell-layer-scrape assay was used to measure migration 20 h after stimulation of VSMC with platelet-derived growth factor-BB (PDGF-BB), insulin-like growth factor I (IGF-I), or phorbol 12-myristate 13-acetate (PMA). The contributions of cell proliferation were eliminated by treatment of VSMC with hydroxyurea, which suppressed DNA synthesis.PDGF-BB stimulated VSMC migration 2.5-fold, while PMA and IGF-I stimulated migration 1.7- and 1.5-fold, respectively. The importance of protein kinase C (PKC), ERK, and phosphoinositide-3' kinase (PI3 kinase) in mitogen-stimulated migration was investigated, using specific inhibitors of these signaling molecules. PDGF-BB-stimulated migration was inhibited by the general PKC inhibitor RO 31-8220 (40%), the MEK inhibitor PD98059 (31%), and the PI3 kinase inhibitor wortmannin (22%) but not by PMA-induced downregulation of conventional and novel PKC isoforms. IGF-I-stimulated migration was inhibited by RO 31-8220 (34%) and wortmannin (37%) but was much less affected by PD98059 (19%) or PKC downregulation (10%). PMA-stimulated migration was inhibited by RO 31-8220 (53%), PD98059 (50%), wortmannin (45%), and PKC downregulation (47%). Western analysis confirmed that ERK was strongly activated by PDGF-BB and PMA but not by IGF-I. To examine potential in vivo negative regulators of VSMC migration, we analyzed the ability of heparin, an analogue of heparan sulfate, and TGFbeta to attenuate mitogen-stimulated migration. Heparin but not TGFbeta inhibited VSMC migration stimulated by all three mitogens. Delayed-addition experiments showed that RO 31-8220 retained substantial inhibitory activity even if added 3 h after PMA or IGF-I stimulation and 5 h after PDGF-BB addition, suggesting that sustained PKC activation is important for migration. The MEK inhibitor retained some effectiveness for 5 h after PDGF-BB stimulation but only 1 h after PMA addition. Western analysis showed ERK activation was transient after PMA treatment but sustained for 6 h after PDGF-BB treatment. Heparin strongly inhibited migration even if added 5-7 h after mitogen stimulation, suggesting that heparin may inhibit both short- and long-term signals necessary for migration. The present studies indicate that PMA and IGF-I activate a limited number of second messengers resulting in moderate stimulation of migration; in contrast PDGF-BB stimulates multiple signaling pathways resulting in strong stimulation of migration and lessened sensitivity to inhibitory signals.
Animals↗
Insulinlike growth factor-I-mediated migration and invasion of human colon carcinoma cells requires activation of c-Met and urokinase plasminogen activator receptor.
OBJECTIVE: To determine whether insulinlike growth factor-I (IGF-I) and hepatocyte growth factor (HGF) cooperate to induce migration and invasion of human colorectal carcinoma (CRC) cells and whether the effects of IGF-I and/or HGF are mediated through activation of the urokinase plasminogen activator (uPA)/uPA receptor (uPAR) system, a central mediator of tumor-cell migration and invasion. SUMMARY BACKGROUND DATA: CRC cells must invade through the basement membrane of the colon and migrate to form metastases. CRC cells are known to overexpress IGF-I receptor (IGF-IR), c-Met, and uPAR, 3 cell-surface receptors known to mediate cell migration and invasion. We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasion in CRC cells and that this signaling is dependent on uPAR. METHODS: KM12L4 human CRC cells were treated with IGF-I, HGF, or IGF-I + HGF in transwell migration and invasion chambers; cells that had migrated or invaded were counted. To determine the role of c-Met in IGF-I-induced migration and invasion, c-Met was inhibited by infection of cells with an adenovirus containing a c-Met ribozyme; transwell assays were then repeated. To determine the role of the uPA/uPAR system in IGF-I-induced CRC cell migration and invasion, transwell assays were repeated after pretreating cells with the uPA inhibitor amiloride or with neutralizing antibodies to uPA and uPAR. RESULTS: IGF-I and HGF, alone or in combination, increased cell migration and invasion. The c-Met ribozyme inhibited IGF-I- and HGF-mediated migration and invasion, indicating that c-Met is essential for these processes. uPA and uPAR inhibition blocked IGF-I- and HGF-mediated migration and invasion, suggesting that uPAR is downstream of IGF/IGF-IR and HGF/c-Met in the signaling pathways that mediate cell migration and invasion. CONCLUSIONS: IGF-I and HGF cooperate to induce migration and invasion of CRC cells, and c-Met and uPA/uPAR are required for IGF-I-mediated migration and invasion. In our in vitro model of CRC migration and invasion, uPA and uPAR appear to be downstream of IGF-IR and c-Met and are required for migration and invasion. Elucidation of the pathways that contribute to tumor progression and metastasis should provide a foundation for the rational development and use of targeted therapies for CRC.
Cell Line, Tumor↗
Autocrine fibronectin-induced migration of human colonic fibroblasts.
OBJECTIVES: A central event during wound repair is the migration of activated fibroblasts to the wound area. Thus far, the mechanisms inducing migration of colonic lamina propria fibroblasts (CLPF) have not been studied in detail. Previously, we have shown that CLPF secrete factors that are essential to their ability to migrate in response to different growth factors. METHODS: Primary human CLPF were obtained from endoscopic biopsies or surgical specimens taken from normal mucosa areas of patients undergoing surveillance colonoscopy or surgery for colorectal carcinoma. Migration assays of CLPF were performed in the modified 48-well Boyden chamber. RESULTS: Conditioned medium of CLPF collected after 24-h stimulated migration of CLPF (22 +/- 2 cells/ hpf). Filtration of conditioned medium through a 300-kDa filter reduced the migration-inducing potential in subsequent migration assays to 2 +/- 1 cells/hpf, filtration through a 100-kDa filter abolished migration of CLPF completely, indicating that large molecules such as extracellular matrix components could be responsible for the induction of CLPF migration. Enzyme-linked immunosorbent assays revealed the presence of fibronectin in conditioned medium (17.3 microg/ml). Immunoprecipitation of fibronectin in conditioned medium of CLPF reduced the migration-inducing potential by 63%. Addition of fibronectin to fibronectin-depleted conditioned medium reconstituted the migration. Dose-response assays with fibronectin (1-100 microg/ml) diluted in nonconditioned medium induced migration of CLPF in a dose-dependent manner. Maximum migration was induced with 25 microg/ml fibronectin (37 +/- 5 cells/hpf). CONCLUSION: Fibronectin is an autocrine and paracrine factor essential for intestinal fibroblast migration. Fibronectin induces migration of intestinal fibroblasts and is essential for their ability to migrate in response to different growth factors. A detailed understanding of the regulation of the migration of intestinal fibroblasts is necessary to gain further insights in the pathophysiology of stricture and fistula formation.
Autocrine Communication↗
Conceptualising Irish rural youth migration: a biographical approach.
This paper explores the usefulness of a biographical approach in studying Irish rural youth migration. There have been calls recently for an approach to migration study that involves conceptualizing migration as part of individual biographies as well as social structures. However, there is little research that explicitly adopts a biographical approach. This paper presents the theoretical underpinnings, methodological issues and findings of a recent study that was guided by the principles of a biographical approach to migration. The study was an exploration of life-path formation among Irish rural youth from the 1970s to the 1990s. The paper focuses on the three key elements of a biographical approach to migration, and relates them to Irish rural youth migration. Firstly, migration is considered as part of an individual's biography, and the methodological implications of this are explored. Secondly, it is argued, drawing on the research in Ireland, that migration decision-making is a multilayered process. In the case of Irish rural youth migration, a biographical approach highlights the complexity of migration decision-making, revealing the tensions and struggles that lie behind each move, and thus raises questions over the tendency towards simplification of the migration process. Finally, it is argued that migration is a cultural phenomenon, but that this assertion needs careful qualification. This paper problematizes the role of culture in migration processes by untangling the systems of competing discourses of migration that underlie societal norms regarding migration, thereby challenging the view of migration as "normal" for particular societies or cultures.
Adolescent↗
Implications of radioactive seed migration to the lungs after prostate brachytherapy.
OBJECTIVES: To review the incidence and the impact of pulmonary seed migration after prostate brachytherapy on lung function. Isolated reports of seed migration to the lungs after prostate brachytherapy have been published; however, the clinical consequences of this pulmonary migration have not been adequately evaluated. METHODS: We performed a retrospective review of patients undergoing prostate brachytherapy from 1998 to 2000. Pulmonary imaging with chest x-ray was performed 15 to 90 days (median 45) after the procedure. The chest radiographs were reviewed by a single radiologist (V.S.D.), and patients with seed migration to the lungs were evaluated by a single pulmonologist (A.M.H.) using a questionnaire, chest radiography, and pulmonary function tests. Computed tomography of the prostate after seed implantation was performed to check seed position and dosimetry. Odds ratio, confidence intervals, chi-square tests, and logistic regression analysis were performed to evaluate the relationship between the type and number of seeds used, the incidence of pulmonary migration, and the effects on pulmonary function. RESULTS: A total of 83 patients underwent prostate brachytherapy during the study period and 58 patients underwent chest radiography. Seed migration occurred in 21 (36.2%) of 58 patients (95% confidence interval 23.8% to 48.6%). Thirty-four (0.71%) of 4755 seeds used migrated to the lungs. Nine patients had single seed migration to the right lung and three to the left lung. Nine patients had multiple (maximum of 4) and bilateral seed migration. No consistent relationship was found between seed migration and the type of seeds used (P = 0.24). Borderline statistical significance suggested an increased incidence of seed migration with an increasing number of implanted seeds (P = 0.054). Repeat chest radiography in 21 patients revealed no delayed migration at a median follow-up of 16 months. Clinical and pulmonary function testing revealed no consistent abnormality attributable to seed migration. CONCLUSIONS: Radioactive seed migration occurred in 36.2% of brachytherapy patients who had chest radiographs done in our series. Pulmonary seed migration may be influenced by the number of implanted seeds and does not appear to be influenced by the seed type. Additional study of this observed phenomenon is required. A thorough pulmonary workup failed to reveal any short-term harmful side effects; however, long-term follow-up is needed. Healthcare providers should discuss the possibility of pulmonary seed migration with patients with prostate cancer considering prostate brachytherapy.
Brachytherapy↗
Migration of retinal pigment epithelium cells in vitro is regulated by protein kinase C.
The migration of retinal pigment epithelial (RPE) cells is an important step in various pathologic conditions, including subretinal neovascularization (SRN) and proliferative vitreoretinopathy (PVR). Therefore, elucidation of the mechanism of RPE migration may be useful in devising effective treatment for these disorders. Since protein kinase C (PKC) has been shown to regulate the migration of other cell types, we studied the effects of PKC agonists and antagonists on RPE migration. We used an in vitro wound healing model in which a small area of a confluent monolayer of bovine RPE cells was denuded with a razor blade. The cultures were subsequently incubated with agents known to stimulate [phorbol 12-myristate 13-acetate (PMA)] or inhibit (calphostin C, staurosporine) PKC. After 20 hr, migration was measured as the number of cells that had entered the denuded area. We also measured the translocation of PKC from the cytosol to the membrane in order to determine the activation or inhibition of PKC by PMA and calphostin C in the cells. The phorbol ester PMA stimulated migration by 41%, and calphostin C and staurosporine inhibited migration by 38% and 31%, respectively, in a medium supplemented with 10% serum. To determine the requirement for serum in this modulation, we also measured the effects of PMA and calphostin C on RPE migration in serum-free medium. Under these conditions, basal migration was greatly decreased, but PMA stimulated migration by 177% and calphostin C inhibited migration by 93%. Since PKC modulation is known to induce the proliferation of cells, we also tested the effects of these agents on growth-inhibited migration by pretreating the cells with the antiproliferative drug mitomycin C. We found that modulation of PKC under these conditions equally affected growth-inhibited and growth-dependent migration. Therefore, based on the increase in RPE migration induced by a PKC agonist, and the decrease in migration caused by PKC antagonists, it is suggested that PKC-mediated signal transduction plays a crucial role in RPE cell migration. This knowledge may be useful in devising effective treatments for SRN and PVR.
Alkaloids↗
Transuterine embryo migration in recipient cattle.
Transuterine migration of bovine embryos following fertilization in vivo is apparently rare, but little is known about migration following embryo transfer. We studied heifers receiving either 1 or 2 in vitro produced embryos to determine 1) the incidence of transuterine migration, 2) the timing of migration and 3) the random or systematic occurrence of the event. In 4 experiments, 436 heifers received embryos and 218 of these were pregnant at necroscopy on either Day 14, Day 18, Day 26 or Day 60 of pregnancy. Overall, 43/218 (20%) of the heifers had embryos that had migrated. The frequency of migration was higher in twin (30/68) than in single (13/150) embryo transfers of pregnant recipients (44 vs 9%; P<0.001), and in contralateral (9/15) than in ipsilateral (33/170) transfers (60 vs 19%; P<0.001). Among the heifers that received embryos by ipsilateral transfer, the migration rate was similar to that in heifers pregnant with a singleton after the transfer of either 1 (2/48) or 2 (4/60) embryos (4 vs 7%, NS). The migration rate was highest at Day 26 (12/37) in heifers receiving twin embryos by ipsilateral transfer but was similar at all other stages of pregnancy (15/111, 32 vs 14%; P<0.01). Migration was first observed by Day 14, and it appears that either further migration occurred over the next 12 d or that migration was associated with a higher survival rate from Day 14 to Day 26. The low migration rate evident at Day 60 suggests that migration by Day 26 was associated with increased embryo or fetal death by Day 60. The data suggest that embryo migration is probably independent for each of a pair of surviving embryos. We conclude that in cattle embryo migration is embryo-dependent, but this capability is dormant unless more than 1 embryo is present in a uterine horn or the embryos are transferred to the contralateral uterine horn. The relationship between migration and embryo survival remains unclear.
Animals↗
Control of astrocyte migration in the developing cerebral cortex.
Development of the vertebrate central nervous system is characterized by significant long distance cell migration. While the radial migration of neuronal precursors to their final location is well established the migration of glial cells and their precursors is less well understood. To define the pathways of migration and dissect the cell and molecular mechanisms mediating such migration requires the development of appropriate models. Here we show that purified neonatal astrocytes injected into organotypic slice cultures of developing cerebral cortex migrate in defined patterns depending on where they are placed within the tissue. Injection into gray matter resulted in radially oriented migration either towards the pial or ventricular surface. By contrast injection into developing white matter resulted in largely longitudinal migration along developing axon tracts. While the cytoarchitecture of the tissue influenced the pattern of migration, the extent of migration appeared to be regulated primarily by the age of the host tissue. Homochronic injections performed prior to postnatal day 4 resulted in extensive migration while after day 7 migration was relatively limited. Heterochronic injections indicated that while astrocytes within the 1st postnatal week retained the capacity to migrate extensively, older tissue failed to support extensive migration of either young or old astrocytes. These data suggest the existence of distinct migrational cues in the CNS and that environmental, not cell intrinsic properties primarily regulate astrocyte migration through the developing cortex.
Aging↗