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Results for “elevational migration”

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PubMed1979

Effects of ascorbate on leucocytes: Part I. Effects of ascorbate on neutrophil motility and intracellular cyclic nucleotide levels in vitro.

A preliminary series of experiments indicated that ascorbic acid and calcium and sodium ascorbate in the absence of serum had no stimulatory effect on neutrophil motility. However, when neutrophils were pre-incubated with ascorbate at concentrations between 5 X 10(-2)M and 1 X 10(-1)M in the presence of fresh normal autologous serum (5% final concentration) considerable stimulation of random motility and migration towards the leuco-attractants C5a and casein was observed. The serum factor required for ascorbate-mediated enhanced locomotion was heat unstable and was probably not serum albumin since no stimulation of cell migration was observed when serum was replaced with varying amounts of human serum albumin. Calcium ascorbate was the most potent stimulant of neutrophil motility. Concentrations of calcium and sodium ascorbate which increased migration promoted elevation of intracellular cyclic guanosine monophosphate (cGMP) levels, but not of adenosine monophosphate (cAMP). These same concentrations also caused increased glyclytic activity. It is suggested that the enhanced neutrophil motility mediated by ascorbic acid and calcium and sodium ascorbate in the presence of serum may be due to increased cGMP and/or glycolysis.

Ascorbic Acid↗
PubMed2002

Metalloprotease inhibitor blocks angiotensin II-induced migration through inhibition of epidermal growth factor receptor transactivation.

In vascular smooth muscle cells (VSMCs), angiotensin II (AngII) induces transactivation of the EGF receptor (EGFR) which involves a metalloprotease that stimulates processing of heparin-binding EGF from its precursor. However, the identity and pharmacological sensitivity of the metalloprotease remain unclear. Here, we screened the effects of several metalloprotease inhibitors on AngII-induced EGFR transactivation in VSMCs. We found that an N-phenylsulfonyl-hydroxamic acid derivative [2R-[(4-biphenylsulfonyl)amino]-N-hydroxy-3-phenylpropinamide] (BiPS), previously known as matrix metalloprotease (MMP)-2/9 inhibitor, markedly inhibited AngII-induced EGFR transactivation, whereas the MMP-2 or -9 inhibition by other MMP inhibitors failed to block the transactivation. BiPS markedly inhibited AngII-induced ERK activation and protein synthesis without affecting AngII-induced intracellular Ca2+ elevation. VSMC migration induced by AngII was also inhibited not only by an EGFR inhibitor but also by BiPS. Thus, BiPS is a specific candidate to block AngII-induced EGFR transactivation and subsequent growth and migration of VSMCs, suggesting its potency to prevent vascular remodeling.

Angiotensin II↗
PubMed2006

Alkaline comet assay study with breast cancer patients: evaluation of baseline and chemotherapy-induced DNA damage in non-target cells.

The sensitivity of the alkaline comet assay for the evaluation of baseline and treatment-induced DNA damage in white blood cells of breast cancer patients receiving adjuvant chemotherapy according to three conventional anthracycline- and cyclophosphamide-containing protocols was investigated. Additionally, baseline DNA damage in cancer patients was compared with the levels of DNA damage recorded in healthy women. Altogether 30 patients with diagnosed breast cancer and 30 female blood donors with no known familial history of breast cancer participated in the study. Alkaline comet assay was performed according to standard protocol and DNA migration in peripheral blood leukocytes was measured by a computer-based image analysis system. For each subject the frequency of "damaged" cells, i.e., long-tailed nuclei (LTN) with tail length exceeding 95th percentile for the considered parameter among controls, is also reported. Breast cancer patients had significantly increased background levels of DNA damage in their peripheral blood leukocytes as compared to healthy women. Prior to the chemotherapy, a majority of patients showed a statistically significant increase in the number of LTN compared to healthy blood donors. Marked interindividual variations in baseline DNA damage among patients were recorded, some of them related to the disease stage and status. The present study confirmed the alkaline comet assay as a sensitive technique able to detect significantly elevated DNA migration in blood cells of patients already one hour after completion of the first cycle of chemotherapy. Administration of antineoplastic drugs in three chemotherapy protocols studied induced a similar increase of primary DNA damage in nontarget cells. The evaluation of the LTN frequencies indicates the best response to the protocol containing cyclophosphamide, methotrexate and 5-fluorouracil (CMF). Our results point to the significance of simultaneous evaluation of DNA migration and frequency of LTN in the same subject and approved the use of alkaline comet assay as a suitable method for the routine detection of critical DNA lesions produced after administration of antineoplastic drugs in the clinical settings.

Adult↗
PubMed1997

Nitric oxide mediates hyperglycemia-induced defective migration in cultured endothelial cells.

PURPOSE: To examine the effects of elevated glucose on the migration and proliferation of vascular endothelial cells in an in vitro wound model and to investigate whether nitric oxide (NO) mediates the effects of elevated glucose. METHODS: Migration was investigated in monolayers of bovine aortic endothelial cells wounded by scraping and measuring the distance, the number of cells migrating, and the area covered by the migrating cells in the presence of various concentrations of glucose. The effects of NO were evaluated by adding to the cultures NG-monomethyl arginine (NMMA), an inhibitor of NO synthase, or S-nitrosylated penicillamine, which is a slow-release agent of NO. Proliferation was investigated in the presence of various concentrations of serum, glucose, or both. RESULTS: Elevated glucose levels (16.5 and 27.7 mmol/L) inhibited endothelial cell migration in a dose-dependent manner compared with cells cultured in the presence of 5.5 mmol/L glucose. Inhibition of migration was also observed when wounded mono-layers cultured in 5.5 mmol/L glucose were treated with S-nitrosylated penicillamine, which generates NO. Inhibition of NO synthase by NMMA prevented the inhibition of migration observed in media containing 27.7 mmol/L glucose. Elevated glucose levels did not affect cell proliferation except in the presence of 20% fetal bovine serum. CONCLUSIONS: An elevated glucose level inhibits endothelial cell migration in an in vitro wound model, and the inhibition appears to be mediated by increased levels of NO.

Animals↗
PubMed2002

Elevated levels of serum macrophage migration inhibitory factor in patients with pulmonary tuberculosis.

Macrophage migration inhibitory factor (MIF) was originally described as a T-cell-derived cytokine that inhibits the random migration of macrophages and promotes the delayed-type hypersensitivity reaction. MIF plays an important role in the regulation of the Th1/Th2 balance in inflammatory response. This study investigated serum levels of circulating MIF in patients with pulmonary tuberculosis. The levels of MIF in sera were measured by enzyme-linked immunosorbent assay in 34 patients with pulmonary tuberculosis (16 males and 18 females) and 30 healthy controls (15 males and 15 females). The mean levels of circulating MIF values were significantly higher in those with pulmonary tuberculosis (19.84 +/- 11.27 ng/ml; P < 0.0001) than in the healthy controls (4.38 +/- 1.34 ng/ml). Circulating MIF values significantly correlated with circulating interferon-gamma values (r = 0.537, P < 0.0001). Thus, MIF may play an important role in immune responses to human infection with Mycobacterium tuberculosis.

Adult↗
PubMed1992

Antitumor effect of RBS (rice bran saccharide) on ENNG-induced carcinogenesis.

We examined whether orally administered RBS (rice bran saccharide), prepared from rice bran by hot water extraction, increases immunocompetence, inhibits gastrointestinal carcinogenesis with N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) or shows an antitumor effect. After the administration of RBS, phytohemagglutinin (PHA)- and pokeweed mitogen (PWM)-stimulated blastogenesis of lymphocytes derived from the mesenteric lymph nodes and peripheral blood was enhanced, and the helper/suppressor T-cell ratio was elevated, and migration activity of peritoneal macrophages was also increased in rats treated continuously with ENNG. ENNG-induced gastrointestinal carcinomas were observed in 43% of those administered RBS (ENNG-RBS) as compared with 88% in the control (ENNG) and 94% in the prednisolone (PRD) group (ENNG-PRD). The 12-month survival rate of rats bearing gastrointestinal cancer was 58% in the ENNG-RBS group as compared with 25% in the ENNG group and 15% in the ENNG-PRD group. RBS prevented the reduction in immunocompetence in the course of carcinogenesis, suppressed carcinogenesis, and prolonged the survival of rats with gastrointestinal cancer. Antitumor activities of RBS are thought to be a kind of host mediated action. The growth inhibition ratio of transplantable ENNG-induced cancer in Wistar rats was 42.1% in the RBS and 51.8% in the 5-FU group. Since little is known about the potent antitumor activity of alpha-glucan, it would be interesting to consider the relationship between the structure and the biological activities of polysaccharides.

Adjuvants, Immunologic↗
PubMed2004

Heparin-binding EGF-like growth factor regulates human extravillous cytotrophoblast development during conversion to the invasive phenotype.

Cytotrophoblasts of the anchoring villi convert during human placentation from a transporting epithelium to an invasive, extravillous phenotype that expresses a distinct repertoire of adhesion molecules. Developing extravillous trophoblasts accumulate heparin-binding EGF-like growth factor (HB-EGF), a multifunctional cytokine, which binds HER1 and HER4 of the human EGF receptor (HER/ErbB) family. HB-EGF is downregulated in placentae of women with preeclampsia, a disorder associated with deficient trophoblast invasion, raising important questions about its physiological impact on cytotrophoblasts. Addition of HB-EGF during explant culture of first-trimester chorionic villi enhanced extravillous trophoblast differentiation and invasive activity. Using a first-trimester human cytotrophoblast line, the potential for autocrine and paracrine regulation of the developing trophoblast was established based on the expression of all four HER isoforms, as well as HB-EGF and related growth factors. HB-EGF did not alter proliferation, but initiated extravillous differentiation, with decreased alpha6 integrin expression, increased alpha1, and elevated cell migration. Function-blocking antibodies against EGF family members reduced basal cell motility and antibody inhibition of either HER1 or HER4 ligation prevented HB-EGF-induced integrin switching. We conclude that HER-mediated autocrine and paracrine signaling by HB-EGF or other EGF family members induces cytotrophoblast differentiation to an invasive phenotype.

Animals↗
PubMed1978

Blood pressure and rural--urban migration in Iran.

To find the possible association between rural-urban migration and elevation of blood pressure a cross-sectional study was carried out with 379 subjects 40--59 years of age in rural areas of East Azarbaijan, northwest Iran. Another cross-sectional study was carried out in Teheran City in which 403 migrants from the same rural areas and also 357 non-migrant urban residents of the same age group from both sexes were examined. Comparison of the three groups showed that, in all age and sex groups, migrants had higher systolic and diastolic blood pressure than did the people in the rural areas of origin. The blood pressure levels of migrants and non-migrants in the city were not much different from each other. The effect of other variables on the levels of blood pressure was investigated. Age, sex and body build (as measured by ponderal index) were also associated with blood pressure. None of these factors however explained the differences in blood pressure levels between rural-urban migrants and people in the rural areas of origin.

Adult↗
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↗
PubMed2006

Focal arterial inflammation is augmented in mice with a deficiency of the protein C gene.

Increased risk of thrombosis, with propitious conditions for fibrin deposition, along with upregulation of inflammation, are important factors that enhance plaque formation in atherosclerosis. Evidence supporting the role of anticoagulant protein C (PC) as an inflammatory agent has emerged, supplementing its well-known function as an anticoagulant. Thus, we sought to examine whether a PC deficiency would lead to an enhanced response to an acute arterial hyperplasic challenge. The presentation of early arterial inflammation was studied using a copper/silicone arterial cuff model of accelerated focal neointimal remodeling in mice with a heterozygous total deficiency of PC (PC+/-). Increased inflammation, cell proliferation, cell migration, fibrin elevation, and tissue necrosis were observed in the treated arteries of PC+/- mice, as compared to arteries of equally challenged age- and gender-matched WT mice. These results indicate that PC+/- mice subjected to this challenge displayed enhanced focal arterial inflammation and thrombosis, leading to larger neointimas and subsequent localized occlusion, as compared to their WT counterparts.

Animals↗
PubMed2006

Plectin-controlled keratin cytoarchitecture affects MAP kinases involved in cellular stress response and migration.

Plectin is a major intermediate filament (IF)-based cytolinker protein that stabilizes cells and tissues mechanically, regulates actin filament dynamics, and serves as a scaffolding platform for signaling molecules. In this study, we show that plectin deficiency is a cause of aberrant keratin cytoskeleton organization caused by a lack of orthogonal IF cross-linking. Keratin networks in plectin-deficient cells were more susceptible to osmotic shock-induced retraction from peripheral areas, and their okadaic acid-induced disruption (paralleled by stress-activated MAP kinase p38 activation) proceeded faster. Basal activities of the MAP kinase Erk1/2 and of the membrane-associated upstream protein kinases c-Src and PKCdelta were significantly elevated, and increased migration rates, as assessed by in vitro wound-closure assays and time-lapse microscopy, were observed. Forced expression of RACK1, which is the plectin-binding receptor protein for activated PKCdelta, in wild-type keratinocytes elevated their migration potential close to that of plectin-null cells. These data establish a link between cytolinker-controlled cytoarchitecture/scaffolding functions of keratin IFs and specific MAP kinase cascades mediating distinct cellular responses.

Animals↗
PubMedDate not supplied

Baseline and stress-induced plasma corticosterone during long-distance migration in the bar-tailed godwit, Limosa lapponica.

The specific roles of corticosterone in promotion of avian migration remain unclear even though this glucocorticosteroid is elevated in many migrating bird species. In general, glucocorticosteroids promote metabolic homeostasis and may elicit effects on feeding and locomotion. Because the migratory stages of refueling and flight are characterized by distinct behaviors and physiology, the determination of corticosterone levels during each stage should help identify potential processes in which corticosterone is involved. We measured baseline levels of corticosterone in bar-tailed godwits (Limosa lapponica) during two distinct stages of migration: (1) immediately after arrival at a false stopover site just short of the Wadden Sea and (2) throughout the subsequent 4-wk refueling period on the Wadden Sea. Plasma corticosterone was higher in arriving than in refueling birds. In addition, corticosterone increased with size-corrected body mass during the refueling phase, suggesting that corticosterone rises as birds prepare to reinitiate flight. Therefore, elevated corticosterone appears associated with migratory flight and may participate in processes characterizing this stage. We also performed a capture stress protocol in all birds and found that corticosterone increased in both arriving and refueling godwits. Therefore, the normal course of migration may be typified by corticosterone concentrations that are lower than those associated with stressful and life-threatening episodes.

Animals↗
PubMed1993

Leu-enkephalin modulates the migration inhibition of mouse splenocytes induced by cAMP-elevating agents.

The ability of Leu-enkephalin (LENK) to alter random migration of mouse spleen cells was tested in vitro and in vivo. Incubation of the cells with LENK (10(-14) M-10(-7) M) for 1 h at 37 degrees C suppressed the migration. The dose-response was irregular, showing two peaks in the physiological concentration range: 10(-10) M, and 10(-13)-10(-14) M. Intraperitoneal (i.p.) injection of LENK (7.5 mg/kg body wt) depressed the migratory capacity of the splenocytes harvested 2 and 24 h later. In contrast to the inhibitory effect of LENK on the migration of native cells, its effect on cells pretreated with the cAMP-elevating agents theophylline, 3-isobutyl-1-methyl-xanthine (IBMX) and forskolin was predominantly a stimulatory one. The addition of LENK resulted in attenuation or even full reversion of the migration-inhibition caused by those agents. Occasionally, potentiation of the suppression was also observed. There was no discrimination between the phosphodiesterase (PDE) inhibitors IBMX and theophylline, and the adenylate cyclase activator forskolin. Specificity of LENK effects was tested by using naloxone (10(-6) M), an opioid-receptor antagonist. Migration-inhibition induced by LENK was reversed in about two-thirds of the experiments. In contrast, migration-inhibition induced by cAMP-elevating agents, could not be reversed by naloxone. Naloxone itself was not inert, usually suppressing the locomotor ability of splenocytes. The data suggest that LENK-induced modulation of cell migration is (at least partly) mediated via opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed2004

Levels of fecal corticosterone in sandhill cranes during a human-led migration.

Fourteen captive-reared greater sandhill cranes (Grus canadensis tabida) were conditioned to follow ultralight aircraft to promote migration between Wisconsin and Florida (USA) after release. Fecal samples were collected throughout the training period in Wisconsin and during a l977-km human-led migration to Florida to determine fecal corticosterone (FC) concentrations by radioimmunnoassay. The mean (+/-SE) FC concentration during the training period was 109.5 +/- 7.5 ng/g and was representative of baseline levels recorded previously from sandhill cranes. Fecal corticosterone concentrations increased in early migration compared to concentrations I mo prior to departure (P < 0.01) but were not different from baseline concentrations at tile end of the 6-wk migration period. The variability of FC concentrations in individual samples was greater throughout the migration than the training period. Increases in FC during migration were modest and generally consistent with normal corticosterone elevations observed in migrating birds.

Animal Migration↗
PubMed1985

Migration of the elderly from high altitudes in Colorado.

The reason for the reported decline in the proportion of elderly (greater than 60 years) persons at high (greater than 2,456 m) compared with low altitude (less than 1,376 m) in Colorado was unknown. We hypothesized that adverse effects of high altitude on the elderly, particularly those with heart and lung diseases, prompted their migration to lower elevations. Colorado census data indicated that selective out-migration occurred from high to low altitude among the elderly. Interviews (n = 833) in high- and low-altitude Colorado towns revealed that the elderly were unique in that they moved down for reasons of poor health and that for the majority (81%) ill health meant heart and lung diseases. Elderly migrants from high altitude reported heart and lung diseases more frequently than those remaining and cited improvement in symptoms at low altitude. We suggest that symptoms of heart and lung disease are exacerbated with advancing age at high altitude and influence choice of residence.

Aged↗