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PubMed1993

Human cervical mucus: relationship between biochemical characteristics and ability to allow migration of spermatozoa.

Cervical mucus is produced throughout the menstrual cycle. Sperm migration, however, is possible only during the periovulatory period of the cycle. Cervical mucus is also produced during the amenorrhoeic post-partum period. Post-partum mucus is very similar to luteal phase mucus except that it can allow sperm migration. In this study, mucus samples obtained from all these periods were classified according to their capacity to allow sperm migration. The biochemical characteristics of mucus samples that did (peri-ovulatory and 40% of post-partum samples) and did not (luteal and 60% of post-partum samples) allow sperm migration were then compared. Mucus samples with positive sperm migration showed the highest percentage of water and lowest protein and glycoprotein concentration (per ml of mucus). In addition, post-partum mucus samples with positive sperm migration showed lower concentrations of proteins and glycoproteins than post-partum mucus samples that did not allow sperm migration. However, the amount of glycoproteins per mg of protein was similar between post-partum samples that were positive and negative for sperm migration. These data suggest that the carbohydrate composition of the glycoproteins is playing a key role in the ability of cervical mucus to accept spermatozoa.

Body Water↗
PubMed1999

Analysis of in vitro migration patterns of human spermatozoa by a petri dish-based horizontal column.

Spermatozoa are required to travel a considerable distance in vivo to meet the oocyte at the fertilization site. However, none of the existing in vitro tests critically evaluates migration of sperm to assess their potential of reaching the oocyte. On the other hand, an in vivo model is not suitable for this type of study because of ethical and technical constraints. In the present study we utilized a horizontal column technique to analyze sperm migration. Migratory characteristics of fresh, unwashed semen sperm and sperm undergoing various treatments were examined in vitro using a Petri dish-based horizontal fluid column. The procedure involved loading a sperm sample into the column and determining sperm concentration, motility, and viability at different column segments for different migration durations (6, 12, 24, 48, and 72 h). All sperm samples produced an exponential migration pattern in all durations of migration. Propagation along the column edge, tendency to exit from the column, and hiding in the blind pouches were some of the important characteristic features exhibited by the migratory sperm. Variations in migration patterns were documented among semen donors, between fresh and frozen semen, and between washed and unwashed sperm. Prolonged postejaculation time diminished migratory potential. The recovery of sperm in the column end was independent of seminal variables with the exception of oligozoospermia. These observations suggest that the Petri dish-based horizontal column is effective for analyzing sperm migration characteristics for prolonged periods. The potential of this migration assay in predicting the in vivo potential of spermatozoa to reach the fertilization site will be worth exploring.

Humans↗
PubMed1997

Thymosin beta 4 stimulates directional migration of human umbilical vein endothelial cells.

Thymosin beta 4 (T beta 4) is a 4.9 kDa polypeptide that interacts with G-actin and is thought to be an important mediator in cell proliferation, migration, and differentiation. T beta 4 has been identified as a factor involved in the differentiation of human umbilical vein endothelial cells (HUVECs) cultured on Matrigel. Here we have used various in vitro and in vivo migration assays to demonstrate the role of T beta 4 in endothelial cell migration. Our results demonstrate that T beta 4 acts as a chemoattractant for endothelial cells, stimulating the migration of HUVECs in Boyden chambers four- to sixfold over that observed with media alone. Of the primary cell types tested, only human coronary artery cells responded to T beta 4 treatment, suggesting that the migration activity of T beta 4 was endothelial cell-specific. T beta 4 significantly accelerated the rate of migration into the scratch wounded area of a HUVEC monolayer. T beta 4 treatment also increased the production of matrix metalloproteinases that may degrade the basement membrane during angiogenesis. Additional experiments using subcutaneously implanted Matrigel showed that T beta 4 stimulated cell migration in vivo. These results provide the first direct evidence that T beta 4 has chemoattractive activity and promotes angiogenesis by stimulating the migration of endothelial cells.

Cell Movement↗
PubMed2006

Greatly impaired migration of implanted aquaporin-4-deficient astroglial cells in mouse brain toward a site of injury.

We reported previously that astroglia cultured from aquaporin-4-deficient (AQP4-/-) mice migrate more slowly in vitro than those from wild-type (AQP4+/+) mice (J. Cell Sci. 2005;118, 5691-5698). Here, we investigate the migration of fluorescently labeled AQP4+/+ and AQP4-/- astroglia after implantation into mouse brains in which directional movement was stimulated by a planar stab wound 3 mm away from the axis of the injection needle. Two days after cell injection we determined the location, elongation ratio, and orientation of labeled cells. Migration of AQP4+/+ but not AQP4-/- cells toward the stab was greater than away from the stab. AQP4+/+ astroglia moved on average 1.5 mm toward the stab compared with 0.6 mm for AQP4-/- cells. More than 25% of the migrating AQP4+/+ cells but <3% of AQP4-/- cells appeared elongated (axial ratio>2.5). In transwell assays, AQP4+/+ astroglia migrated faster than AQP4-/- cells in a manner dependent on pore size. At 8 h, approximately 50% of AQP4+/+ cells migrated through 8-microm diameter pores, whereas equivalent migration of AQP4-/- cells was found for 12-microm diameter pores. These results provide in vivo evidence for AQP4-dependent astroglial migration and suggest that modulation of AQP4 expression or function might alter glial scarring.

Animals↗
PubMed1997

In vitro transendothelial migration of blood T lymphocytes from HIV-infected individuals.

OBJECTIVE: We hypothesized that differential extravasation of circulating CD4+ or CD8+ T lymphocytes contributes to HIV-associated CD8+ lymphocytic alveolitis. Differences in T-cell transendothelial migration may be intrinsic or emerge at sites where vascular endothelium is activated by overexpression of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. DESIGN: We used an in vitro model of lymphocyte extravasation to assess transendothelial migration of peripheral blood mononuclear cells (PBMC) from HIV-positive individuals. We assayed bronchoalveolar lavage (BAL) fluid from HIV-positive and normal individuals to determine if increased levels of TNF-alpha and IFN-gamma were present in the lungs of HIV-infected individuals. METHODS: Transendothelial migration was assessed by determining the number and flow cytometric phenotype of PBMC adherent to or migrating across unstimulated or TNF-alpha and IFN-gamma-activated endothelial cell monolayers. We measured BAL fluid cytokine concentrations using standard antigen-capture enzyme-linked immunosorbent assays for TNF-alpha and IFN-gamma. RESULTS: T cells migrating across unactivated endothelial cells were significantly enriched for CD4+ T cells. Cytokine activation of endothelial cells allowed significantly greater transendothelial migration of CD8+ T cells compared to unactivated endothelial cells. TNF-alpha was increased in BAL fluid from HIV-positive individuals relative to controls. CONCLUSIONS: These data suggest that, in HIV-positive individuals, CD4+ T cells are migration competent and blood CD8+ T cells do not have enhanced migration competence relative to CD4+ T cells. CD8+ T cell extravasation is aided by TNF-alpha and IFN-gamma-induced endothelial cells activation.

Bronchoalveolar Lavage↗
PubMed2002

Migration of human monocytes in response to procalcitonin.

OBJECTIVE: Circulating serum levels of procalcitonin rise significantly during bacterial infection. Because calcitonin is known to be a monocyte chemoattractant, we investigated whether procalcitonin, a prohormone of calcitonin, also affects leukocyte migration. DESIGN: Prospective, controlled in vitro study. SETTING: University research laboratories. INTERVENTIONS: Forearm venous blood polymorphonuclear neutrophils and monocytes were isolated from healthy human donors. Cell migration was assessed in a blindwell chemotaxis chamber. The distance of migration into filter micropores was measured. To biochemically confirm functional data on cell migration, effects of procalcitonin on cellular levels of cyclic adenosine monophosphate were measured by high-performance liquid chromatography. MEASUREMENTS AND MAIN RESULTS: Both procalcitonin and calcitonin elicited dose-dependent migration of monocytes at concentrations from the femtomolar to the micromolar range. Neutrophils did not migrate toward procalcitonin or calcitonin, nor was their oxygen free radical release affected as measured fluorimetrically. Checkerboard analysis of monocyte locomotion revealed procalcitonin-induced migration as true chemotaxis. Pretreatment of monocytes with procalcitonin or calcitonin rapidly deactivated their migratory response to formyl-Met-Leu-Phe, and both also induced homologous deactivation of migration. Procalcitonin elevated levels of cyclic adenosine monophosphate in monocytes. CONCLUSIONS: In vitro procalcitonin is a monocyte chemoattractant that deactivates chemotaxis in the presence of additional inflammatory mediators. Procalcitonin stimulates cyclic adenosine monophosphate production in monocytes, suggesting that its action may be specific and comparable with calcitonin, which exerts similar functions.

Calcitonin↗
PubMed1998

Altered gene expression in human astrocytoma cells selected for migration: I. Thromboxane synthase.

Human glioma cells from a long-term cell line were selected for their ability to migrate on a glioma-derived extracellular matrix. When tested over 28 serial passages, the migration-selected strain showed a genetically stable, enhanced migration rate compared with the parental cells. Proliferation studies demonstrated that the growth rate of migration-selected cells was slightly arrested. Both the selected strain and the parental culture showed anchorage-independent growth in soft agarose and were tumorigenic in athymic mice. Using molecular genetic strategies' display to isolate genes expressed differentially between the 2 populations, a 300-bp sequence homologous to thromboxane synthase was upregulated in the migration-selected cells relative to the parental cells. Expression levels of thromboxane synthase were highly elevated in the migration-selected cells when assessed by RNAse-protection assay and by flow cytometry. Two specific thromboxane synthase inhibitors, Dazmegrel and Furegrelate, reduced the migration rate of the migration-selected cells to a rate equal to or less than the rate exhibited by the parental cells, respectively. The inhibitors effect on the parental cells was inconsequential. These results suggest that aberrations in the regulation of thromboxane synthase expression or activity may influence the motility of human glioma cells.

Animals↗
PubMed1999

In vitro adhesion and migration of T lymphocytes across monolayers of human brain microvessel endothelial cells: regulation by ICAM-1, VCAM-1, E-selectin and PECAM-1.

Increased lymphocyte traffic across an altered blood-brain barrier (BBB) is a prominent and early event in inflammatory and immune-mediated CNS diseases. The factors that control the entry of lymphocytes into the brain have not been fully elucidated. In this study, primary cultures of human brain microvessel endothelial cells (HBMEC) were used to investigate the role of endothelial cell (EC) adhesion molecules in the adhesion and migration of peripheral blood T lymphocytes across TNF-alpha treated and untreated monolayers. Adhesion of T cells to unstimulated HBMEC was minimal and few of the adherent cells migrated across the monolayers. Treatment of HBMEC with TNF-alpha augmented adhesion by 5-fold. The binding to activated EC was significantly, but not completely, inhibited by monoclonal antibodies (mAbs) to ICAM-1 and VCAM-1, whereas adhesion to unstimulated EC was blocked by mAb to ICAM-1 but not VCAM-1. Transendothelial migration of lymphocytes increased by up to 30-fold following treatment of HBMEC with TNF-alpha. Migration across activated monolayers, but not across untreated EC, was almost completely blocked by Ab to ICAM-1 and significantly inhibited by Abs to PECAM-1 and E-selectin. VCAM-1 was not utilized during transendothelial migration. Ultrastructurally, pseudopodia from lymphocytes contacted finger-like cytoplasmic projections on EC and eventually penetrated the EC cytoplasm at focal points along the apical surface. Migrating lymphocytes moved either through the EC cytoplasm or between adjacent EC across intercellular contacts. The overlying monolayers showed no evidence of disruption and intercellular junctions appeared intact over the migrated T cells. These studies indicate that adhesion and migration of T lymphocytes across the cerebral endothelial barrier are distinct processes that depend upon the activation state of EC and are controlled by diverse receptor-ligand interactions.

Blood-Brain Barrier↗
PubMed1999

PPAR gamma-ligands inhibit migration mediated by multiple chemoattractants in vascular smooth muscle cells.

The purpose of this study was to determine the effect of the peroxisome proliferator-activated receptor gamma-(PPAR gamma) ligands troglitazone (TRO), rosiglitazone (RSG), and 15-deoxy-delta prostaglandin J2 (15d-PGJ2) on vascular smooth muscle cell (VSMC) migration directed by multiple chemoattractants. Involvement of mitogen-activated protein kinase (MAPK) in migration also was examined, because TRO was previously shown to inhibit nuclear events stimulated by this pathway during mitogenic signaling in VSMCs. Migration of rat aortic VSMCs was induced 5.4-fold by PDGF, 4.6-fold by thrombin, and 2.3-fold by insulin-like growth factor I (IGF-I; all values of p < 0.05). The PPAR gamma ligands 15d-PGJ2, RSG, or TRO all inhibited VSMC migration with the following order of potency: 15d-PGJ2 > RSG > TRO. Inhibition of MAPK signaling with PD98059 completely blocked PDGF-, thrombin-, and IGF-I-induced migration. All chemoattractants induced MAPK activation. PPAR gamma ligands did not inhibit MAPK activation, suggesting a nuclear effect of these ligands downstream of MAPK. The importance of nuclear events was confirmed because actinomycin D also blocked migration. We conclude that PPAR gamma ligands are potent inhibitors of VSMC migration pathways, dependent on MAPK and nuclear events. PPAR gamma ligands act downstream of the cytoplasmic activation of MAPK and appear to exert their effects in the nucleus. Because VSMC migration plays an important role in the formation of atherosclerotic lesions and restenosis, PPAR gamma ligands like TRO and RSG, which ameliorate insulin resistance in humans, also may protect the vasculature from diabetes-enhanced injury.

Animals↗
PubMed1996

A magnetic resonance template for normal neuronal migration in the fetus.

OBJECTIVE: Although the features of neuronal migration have been known since the turn of the century, the serial features of neuronal migration as seen with magnetic resonance imaging (MRI) have not been described. Our objective was to provide a template of the normal appearance and the temporal pattern of neuronal migration in the human fetal brain early in the second trimester as seen with MR imaging and to correlate our findings with histological sections and atlases. METHODS: Twenty-eight normal fetal specimens, which ranged from 9 to 24 weeks of gestational age, were imaged with a 1.5 T clinical MRI unit by use of conventional spin echo, fast spin echo, and three-dimensional Fourier transformation spoiled gradient refocussed pulse sequences. RESULTS: The three-dimensional Fourier transformation spoiled gradient refocussed pulse sequence provided the highest resolution images of neuronal migration. At 13 weeks of gestational age, the germinal matrix was identified. A five-layer pattern of the fetal forebrain, which included layers of neuroblast formation and migration, could be identified at 16 to 18 weeks by MRI. The germinal matrix and layers of migrating neurons diminished considerably in size by 21 weeks. Histological studies and correlation with anatomic atlases confirmed the MRI findings. CONCLUSION: Images obtained by use of MRI with standard clinical pulse sequences can document the appearance and the temporal patterns of neuronal migration in postmortem fetal specimens. With the evolution of high-resolution MRI and faster scanning techniques, these findings may serve as a template for the in utero MRI appearance of neuronal migration and thereby compliment the antenatal ultrasonic investigation of congenital anomalies.

Brain↗
PubMed1999

Effects of epidermal growth factor and dibutyryl cyclic adenosine monophosphate on the migration pattern of astrocytes grafted into adult rat brain.

OBJECTIVE: Neonatal rat astrocytes transplanted into host brains migrate in specific patterns, which are determined by the developmental stage of the host brain and the region of implantation. We hypothesized that the differentiation state of the implanted astrocytes could also affect astrocyte migration. METHODS: Astrocytes derived from neonatal rats (1-4 d) were placed in culture and exposed to growth- or differentiation-promoting agents (e.g., epidermal growth factor or dibutyryl cyclic adenosine monophosphate). Treated cells were then injected into different regions of the adult rat brain. At 3, 6, and 9 days after implantation, the extent and pattern of astrocyte migration after injection into the cortex, hippocampus, and corpus callosum were assessed. RESULTS: Astrocytes pretreated with either factor did not migrate during the first 3 days after implantation into the host cortex and hippocampus, whereas untreated cells migrated extensively by Day 3. After 9 days, implanted cells that had been pretreated with dibutyryl cyclic adenosine monophosphate began to demonstrate migratory activity, whereas those exposed to epidermal growth factor remained at the site of implantation. These findings corresponded to the effects of these agents in culture. On the other hand, cells implanted into the corpus callosum migrated in spite of pretreatment. CONCLUSION: Epidermal growth factor and dibutyryl cyclic adenosine monophosphate each altered the cells in culture such that they were inhibited from migrating after transplantation into the host cortex and hippocampus. This finding suggests that the activation of either growth or differentiation cascades partially inhibits the migratory ability in these cells either through effects on their internal migratory potentials or their responsiveness to external migratory signals. In contrast, cells implanted into the corpus callosum migrated in spite of pretreatment, suggesting that this structure may present migratory cues sufficient to override the effects of treatment.

Animals↗
PubMed1993

Effect of cold preservation on lymphocyte migration into peripheral nerve allografts in sheep.

Lymphocyte migration into fresh and preserved peripheral nerve allografts was quantitated to assess the effect of cold preservation and freeze-thawing pretreatment on the local immunological response to nerve allografts. Out-bred ewes received multiple 1.5-cm subcutaneous heterotopic peroneal nerve autografts, fresh allografts, and pretreated allografts, implanted within the same recipient. Lymphocyte migration was studied at 7 days by injecting autologous 111indium-labeled lymphocytes intravenously. After 3 hr of recirculation, lymphocyte migration into graft tissue was quantitated by a gamma counter (epm/g, mean +/- SEM). Lymphocyte traffic into fresh nerve allografts (21,623 +/- 3783) increased an average 9.4-fold over the autograft value (2918 +/- 377, P < 0.04). Histologic studies illustrated a marked lymphocytic infiltrate of CD4+ and CD8+ cells and enhanced class I and II MHC expression in fresh allografts, but not in autografts. Short-term cold preservation, for 6 and 12 hr (5 degrees C), enhanced lymphocyte entry into pretreated allograft tissue. Conversely, cold preservation for longer periods (1 and 3 weeks) dramatically reduced lymphocyte migration to values below corresponding autograft levels (783 +/- 100 and 1,252 +/- 120, respectively, P < 0.01). A comparable reduction in lymphocyte migration into nerve allografts was observed after freeze-thawing pretreatment (P < 0.01). Cold preservation of donor allogeneic lymphocytes inhibited their capacity to induce intradermal host lymphocyte migration, implicating passenger lymphocytes as a potential cold-sensitive allogeneic component of the nerve allograft. Assessment of the local response to ovine peripheral nerve allografts, utilizing radiolabeled autologous lymphocytes, demonstrated that cold preservation and freeze-thawing pretreatment significantly reduced lymphocyte migration into nerve allografts. The mechanism(s) of reduced lymphocyte migration may involve inactivation or death of antigen-presenting cells, including passenger lymphocytes.

Animals↗
PubMed2006

Early migration of the tibial component of the buechel-pappas total ankle prosthesis.

UNLABELLED: Interest in mobile-bearing total ankle arthroplasty has increased in recent years. Clinical studies show favorable but varying results, with survival rates between 70% and 90% at 10-year followup. Design-specific differences in early migration patterns might explain variations in the results and modes of failure. Using radiostereometric analysis (RSA) we prospectively followed 15 RA patients with a cementless mobile-bearing total ankle arthroplasty. The American Orthopaedic Foot and Ankle Society ankle score and radiostereometric radiographs were evaluated immediately postoperatively, 6 weeks postoperatively, 3 months, 6 months, and 12 months postoperatively and yearly thereafter. The postoperative clinical results improved. We observed increased migration of the tibial component during the first 3 months, but this stabilized by the 6 month followup. The mean lateral-medial migration was 0.8 mm, distal-proximal migration was 0.9 mm, and posteroanterior migration was -0.5 mm. The latter implies the total resultant migration was in anterior and valgus tilting of this tibial component. However, migration stabilized at 6 months postoperatively. We believe the surgical technique (anterior cortical window for placement) and the method of tibial fixation likely explain this migration. LEVEL OF EVIDENCE: Therapeutic, Level IV. See Guidelines for Authors for a complete description of levels of evidence.

Ankle Joint↗
PubMed2006

Epithelial migration of the postmyringoplasty tympanic membrane.

OBJECTIVE: To determine whether the postmyringoplasty tympanic membrane (TM) behaves in a similar way compared with a healthy nonoperated eardrum by calculating and comparing the epithelial migration rate and pattern. STUDY DESIGN: Prospective, nonrandomized case-control study. Each subject who has undergone a myringoplasty and with healthy contralateral TM as control is included in this study. SETTING: Otolaryngology outpatient clinic. PATIENTS: A total of 23 subjects with 46 ears have been selected from otolaryngology outpatient clinic of the University Malaya Medical Center after excluding two subjects from this study. The study was conducted from June 2003 to September 2004. INTERVENTION: All the selected subjects' ears were examined under a microscope. Methylene blue ink dot was applied to the epithelium of the TM at the immediate vicinity of the umbo; then, weekly follow-up was performed until the migratory pattern and the rate of epithelial migration was noted. MAIN OUTCOME MEASURE: Direction and rate of epithelial migration in both study and control group were measured and compared. RESULTS: Epithelial migration did occur in postgrafted TM, from the umbo region toward the ear canal wall in a lateral radiating manner. Most of the patients (19 of 23 patients [82.6%]) showed nearly similar migratory pattern (same direction) in both the control and the study ear. None of the 46 ears showed any evidence of epithelial migration in the anteroinferior direction of TM. The rate of migration was slower in the beginning, especially near the umbo region (almost no movement at the first 1 or 2 weeks after ink dot application). For both groups, the rate of migration increased when approaching the periphery or annulus region. There was not much difference in the mean daily migratory rate between the control and the study ear (93.4 microm/d and 91.7 microm/d, respectively). The mean migratory rate was highest in subtotal perforation (97.2 microm/d) and lowest in small perforations (< 20%; 83.6 microm/d). CONCLUSION: There was no difference in epithelial migration rate and pattern between the postmyringoplasty TM and the healthy TM.

Adolescent↗
PubMed2004

Growth factors improve the in vivo migration of human skeletal myoblasts by modulating their endogenous proteolytic activity.

BACKGROUND: A main technological problem related to the clinical application of myoblast transplantation is the poor migration of transplanted cells. In this study, we investigated a new physiologic approach that consists of coinjecting motogenic factors insulin growth factor (IGF)-1 or basic fibroblast growth factor (bFGF) to enhance the migration of human skeletal myoblasts. Among the different ways by which those factors can induce the cell migration processes, we investigated their capacity to enhance cell endogenous proteolytic activity that will help transplanted cells to migrate through the extracellular matrix. METHODS: In vitro, myoblasts were coincubated with bFGF or IGF-1. Growth factors effects on cell migration were evaluated using invasion chambers, and their effects on proteolytic systems were evaluated by zymography, Western blot, and reverse transcription polymerase chain reaction. In vivo, myoblasts were coinjected with growth factors and the intramuscular migration capacity was assessed using the microtube technique. RESULTS: In vitro, the presence of IGF-1 or bFGF significantly enhanced the expression of the gelatinase matrix metalloproteinase-9 and focalized the fibrinolytic system activity at the cell membrane. In vitro and in vivo, both bFGF and IGF-1 showed strong chemokinetic potentials and improved the migration of human myoblasts. Moreover, the implication some proteinases in the in vivo enhanced migration was confirmed using specific inhibitors (BB94 or amiloride). CONCLUSIONS: These results suggest that IGF-1 or bFGF coinjection with human myoblasts increased their proteolytic activities and consequently their migratory capacity. This study may help to develop approaches that will reduce the number of injection sites for the treatment of Duchenne muscular dystrophy patients.

Amiloride↗
PubMed2001

Role of blood shear stress in the regulation of vascular smooth muscle cell migration.

Smooth muscle cell (SMC) migration from the media to the intima of blood vessels contributes to neointimal formation and atherogenesis. Here, we demonstrate how blood shear stress regulates vascular SMC migration in the encapsulating tissue of a micro-cylinder implanted in the center of the rat vena cava with the micro-cylinder perpendicular to blood flow. In this model, the micro-cylinder was exposed to a laminar flow with a known shear stress field in the leading region and a vortex flow in the trailing region. After surgery, the micro-cylinder was encapsulated by a thrombus-like tissue within one day, followed by SMC migration from the vena cava to the encapsulating tissue from day 3 to 20. SMC migration was time-dependent with a peak migration speed at day 5. At each given time (excluding day 1), blood shear stress exerts an inhibitory effect on SMC migration with significantly suppressed SMC migration in the laminar flow region than in the stagnation, separation, and vortex flow regions. SMCs were relatively parallel to the shear stress direction in high shear stress regions, whereas perpendicular to the shear stress direction in low shear stress regions. These results suggest that blood shear stress plays a role in regulating SMC migration and orientation in this model.

Animals↗
PubMed1997

Despite the presence of UVB-induced DNA damage, HLA-DR+ cells from ex vivo UVB-exposed human skin are able to migrate and show no impaired allostimulatory capacity.

In this study, we investigated the effect of ultraviolet B radiation on human Langerhans cell function. Normal human skin was irradiated ex vivo with single doses of ultraviolet B. For assessment of T-cell stimulatory function, cells that spontaneously migrated from epidermal sheets were used, whereas full-thickness skin biopsies were used to investigate alterations in migratory properties. The cells migrating from ultraviolet B-exposed epidermal sheets demonstrated a decrease in the percentage of HLA-DR positive Langerhans cells, as well as a reduced capacity to induce proliferation of allogeneic T cells, when compared with cells migrating from nonexposed sheets. When a correction was made for the decreased number of HLA-DR positive Langerhans cells migrating from ultraviolet B-exposed epidermis, however, it appeared that the capacity to induce T-cell proliferation was identical for Langerhans cells migrating from ultraviolet B-exposed and nonexposed epidermis. The presence of ultraviolet B-induced DNA damage could be demonstrated in the Langerhans cells from ultraviolet B-treated skin, indicating that the cells had received significant doses of ultraviolet B. As regards the effect of ultraviolet B on migratory properties of Langerhans cells, we found not only that reduced numbers of CD1a-positive Langerhans cells migrated from the ultraviolet B-exposed full-thickness skin, but also that there was a reduction in CD1a-positive Langerhans cells in the epidermis. This implies that ultraviolet B induces death of Langerhans cells as well as loss of cell surface molecules rather than altering Langerhans cells migration, whereas the Langerhans cells that were still able to migrate fully retained the capacity to activate allogeneic T cells.

Antigen-Presenting Cells↗
PubMed1976

Migration of Baroda medical graduates, 1949--72.

1. The migration of doctors from Medical College, Baroda, is studied in detail. 2. From 1949 to 1972, 584 doctors migrated to other countries and only twenty-nine doctors have returned so far. The incidence of migration is to the extent of 39-75%. 3. Among those who migrated 77-7% have gone to U.S.A. and 11-7% have gone to the U.K. 4. Ninety-four women graduates out of 241 passed prior to 1971 are abroad.. 5. The majority migrate for better and more comfortable living conditions. A small number migrate for better research facilities and encouragement. Those who are denied the opportunity of a post-graduate training also migrate. 6. Migration of doctors, though universal, is disturbingly high in India and a major cause of concern to the government and the educationist.

Africa↗