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At least 1,225 records · Page 68Linked to original sources
PubMed1997

High-yield expression and purification of recombinant human macrophage migration inhibitory factor.

We have expressed the human macrophage migration inhibitory factor (MIF) in Escherichia coli using the pKP 1500 expression plasmid, which contains the tac promoter and a temperature-sensitive origin of replication, to ensure a high plasmid copy number at elevated temperatures. The recombinant protein accumulated intracellularly in soluble form. We have designed a simple two-step procedure for protein purification by gel filtration on Sephadex G-50 and cation exchange chromatography on CM cellulose columns. This results in significantly improved yields. One gram of recombinant human MIF was isolated from 50 g of E. coli cells (wet weight). The 12.5-kDa protein was shown to be pure by SDS-PAGE, IEF, and HPLC. The identity of the purified protein was verified by N-terminal amino acid sequencing. The purified protein exhibits MIF activity. The near-UV CD and the 1H NMR spectra confirmed its highly ordered, native-like structure. The far-UV CD spectrum revealed that recombinant human MIF contains well-defined secondary structure.

Animals↗
PubMed2001

20th century climate warming and tree-limit rise in the southern Scandes of Sweden.

Climate warming by ca. 0.8 degree C between the late-19th and late-20th century, although with some fluctuations, has forced multispecies elevational tree-limit advance by > 100 m for the principal tree species in the Swedish part of the Scandinavian mountain range. Predominantly, these processes imply growth in height of old-established individuals and less frequently upslope migration of new individuals. After a slight retardation during some cooler decades after 1940, a new active phase of tree-limit advance has occurred with a series of exceptionally mild winters and some warm summers during the 1990s. The magnitude of total 20th century tree-limit rise varies with topoclimate and is mainly confined to wind-sheltered and snow-rich segments of the landscape. Thickening of birch tree stands in the "advance belt" has profoundly altered the general character of the subalpine/low alpine landscape and provides a positive feedback loop for further progressive change and resilience to short-term cooling episodes. All upslope tree-limit shifts and associated landscape transformations during the 20th century have occurred without appreciable time lags, which constitutes knowledge fundamental to the generation of realistic models concerning vegetation responses to potential future warming. The new and elevated pine tree-limit may be the highest during the past 4000 14C years. Thus, it is tentatively inferred that the 20th century climate is unusually warm in a late-Holocene perspective.

Climate↗
PubMed2004

Inhibition of the arachidonic acid metabolism blocks endothelial cell migration and induces apoptosis.

Previous studies have demonstrated that inhibitors of the arachidonic acid metabolism block migration and sensitise human glioma cells to treatment inducing apoptosis. This paradigm may provide a new concept for anti-invasive treatment strategies targeting invasive glioma cells. However, the effect of such treatment on other cellular elements in glial tumours such as endothelial cells is unknown. In this study we have analysed the expression of metabolites of the arachidonic acid pathway in endothelial cells in vitro and in vivo and we have assessed the influence of inhibitors of this pathway on motility, capillary like tube formation, and apoptosis in human endothelial cells. Human endothelial cells (HUVEC) in culture showed expression for thromboxane synthase and both isoforms of cyclo-oxygenase, COX-1 and COX-2. Immunostaining demonstrated low levels of COX-1 expression in capillaries and larger vessels of normal brain and moderately elevated levels of this enzyme in small vessels of brain tumours of various grades. Both thromboxane synthase and COX-2 expression was limited to endothelial cells found in anaplastic gliomas and glioblastomas. Thromboxane synthase inhibitors strongly decreased endothelial cell migration in HUVEC in vitro and capillary like tube formation was strongly inhibited by the compound at a similar dose range. The non-selective cyclo-oxygenase inhibitor ASA and the selective COX-2 inhibitor sulindac only had a minor effect on endothelial cell migration, however, the COX-2 inhibitor sulindac showed a synergistic effect with the thromboxane synthase inhibitor. Thromboxane synthase inhibitors induced apoptosis in endothelial cells as demonstrated by intracellular histone-complexed DNA fragmentation. These data suggest that inhibitors of thromboxane synthase influence migration and apoptosis in both human glioma cells and human endothelial cells. An anti-invasive treatment strategy using this class of compounds may therefore not only sensitise glioma cells to conventional treatments inducing apoptosis but may also be supported by an anti-angiogenic effect.

Apoptosis↗
PubMed1991

The signal transduction pathway involved in the migration induced by a monocyte chemotactic cytokine.

Recombinant monocyte-chemotactic and activating factor (rMCAF; alternative acronyms MCP-1, TDCF, human JE) induced migration of human monocytes across polycarbonate or nitrocellulose filters. Maximal induction of migration was observed at a concentration of 10 ng/ml (10(-9) M). Checkerboard analysis revealed that rMCAF elicited true gradient-dependent chemotactic migration, although a gradient independent chemokinetic effect was observed at low concentrations (1-5 ng/ml). rMCAF caused a rapid (less than 5 s) and transient (approximately 1.5 min) increase of free cytosolic Ca2+ ions, as assessed by the fura-2 probe. No Ca2+ increase was detected in neutrophils or lymphocytes stimulated by rMCAF. Studies conducted in the absence of extracellular Ca2+ or in the presence of Ni2+ (an inhibitor of Ca2+ influx) suggested that the increase of intracellular Ca2+ induced by rMCAF is dependent on the influx of extracellular Ca2+ through plasma membrane channels. Bordetella pertussis toxin inhibited the intracellular Ca2+ elevation and chemotaxis caused by rMCAF. The possible involvement of Ca(2+)-dependent protein kinases in rMCAF signaling pathway(s) was explored using inhibitors. Inhibitors of GMP-dependent kinase and myosin L chain kinase had no effect on rMCAF-induced monocyte migration. In contrast, protein kinase C/cAMP-dependent kinase inhibitors (such as, C-I, H-7, HA-1004, KT5720, and Staurosporine) markedly decreased rMCAF induced chemotaxis suggesting the involvement of a serine/threonine protein kinase, possibly protein kinase C, in rMCAF signaling pathway.

Calcium↗
PubMed1993

Transduced endothelial cells expressing high levels of tissue plasminogen activator have an unaltered phenotype in vitro.

Elevated cellular plasminogen activator activity has been associated with significant alterations in the in vitro phenotype of both malignant cell lines and nonmalignant endothelial cells. To examine the role of elevated cellular plasminogen activator activity in the production of altered endothelial cell behavior, bovine coronary artery endothelial cells were transduced with a retroviral vector expressing large amounts of tissue plasminogen activator. Cells transduced with the tissue plasminogen activator vector were compared with both untransduced cells and cells transduced with a control vector in a series of in vitro assays of cellular attachment, proliferation, migration, and invasion. The morphology of the 2 transduced populations was unchanged. There was a small decrease (5-15%) in the horizontal migration rate of both transduced cell populations, as compared with that of untransduced cells. No significant differences were detected among the three cell populations in any of the other assays. We conclude that expression of high levels of tissue plasminogen activator does not specifically affect endothelial cell phenotype in vitro. These data lend support to the hypothesis that elevated plasminogen activator activity is necessary but not sufficient to produce alterations in endothelial cell behavior.

Animals↗
PubMed2003

[Relationship between macrophage migration inhibitory factor and cardiac function in patients with congestive heart failure].

OBJECTIVE: To examine the level of plasma macrophage migration inhibitory factor (MIF) in patients with congestive heart failure (CHF) and its relationship with cardiac function. METHOD: The levels of MIF were measured in 278 CHF patients and 85 normal subjects using enzyme-linked immuno-sorbent assay (ELISA). RESULTS: Elevated MIF levels were detected in the patients with heart failure, and the elevation was more significant in cases of coronary artery disease in comparison with that identified in cases of dilated cardiomyopathy. CONCLUSION: The overactivation of MIF may be involved in the pathogenesis of heart failure.

Adolescent↗
PubMed1982

[Variant creatine kinase isoenzymes: frequency and clinical significance (author's transl)].

To estimate the incidence of variant creatine kinase (CK)isoenzymes, 1,191 unselected patients were screened by means of CK:CK - MB ratio. When CK - MB was higher than 20% of the total CK in the immunoinhibition test, and a myocardial infarction could be excluded, a CK-isoenzyme electrophoresis was performed. We found macro-CK-BB-emia in 13 patients, but only three of them had elevated total CK activity. All patients but two were at the typical age of over 60 years; two males were 2 and 9 years old. The clinical diagnosis in macro-CK-BB-emia was predominantly cardiocerebrovascular insufficiency due to arteriosclerosis. In 16 other patients, the presence of an isoenzyme migrating cathodically to CK-MM was found. In this group, a malignant metastatic tumor was found in eight cases, the rest predominantly suffered from severe liver disease. Presence of both variant CK isoenzymes may lead to diagnostic or therapeutic errors due to the altered CK:CK-MB ratio. According to our studies, a variant CK isoenzyme occurs in 2.6% of hospitalized patients, but this will lead to problems diagnosing acute myocardial infarction only in the group with elevated total CK (0.42% of our patients).

Aged↗
PubMed1998

Contributions of the epidermal growth factor receptor to keratinocyte motility.

The epidermal growth factor (EGF) receptor plays a central role in numerous aspects of keratinocyte biology. In normal epidermis, the EGF receptor is important for autocrine growth of this renewing tissue, suppression of terminal differentiation, promotion of cell survival, and regulation of cell migration during epidermal morphogenesis and wound healing. In wounded skin, the EGF receptor is transiently up-regulated and is an important contributor to the proliferative and migratory aspects of wound reepithelialization. In keratinocytic carcinomas, aberrant expression or activation of the EGF receptor is common and has been proposed to play a role in tumor progression. Many cellular processes such as altered cell adhesion, expression of matrix degrading proteinases, and cell migration are common to keratinocytes during wound healing and in metastatic tumors. The EGF receptor is able to regulate each of these cellular functions and we propose that transient and dynamic elevation of EGF receptor during wound healing, or constitutive overexpression in tumors, provides an important contribution to the migratory and invasive potential of keratinocytes.

Cell Adhesion↗
PubMed2007

Azathioprine and mesalazine-induced effects on the mucosal flora in patients with IBD colitis.

BACKGROUND: The impact of azathioprine and 5-aminosalicylic acid (5-ASA) on the innate immunity and mucosal flora is unknown. The study investigated the influence of IBD treatment on the concentrations and spatial organization of mucosal bacteria using fluorescence in situ hybridization with 16s r-RNA targeting probes. METHODS: We prospectively investigated colonoscopic biopsies from five groups of 20 subjects each: patients with ulcerative or indeterminate colitis treated with azathioprine (group 1), azathioprine and 5-ASA (group 2), 5-ASA (group 3), untreated IBD (group 4), and healthy controls. RESULTS: The elevated numbers of leukocytes in mucus of IBD patients were reduced nearly to norm in patients treated with azathioprine alone. In contrast, 5-ASA therapy had no influence on mucus leukocyte migration and was associated with the lowest concentrations of mucosal bacteria of all IBD groups. The suppressed migration of leukocytes in azathioprine-treated patients was accompanied by a 28-fold higher concentration of mucosal bacteria when compared with the 5-ASA group or a 1000-fold increase when compared with healthy controls. The percent of the epithelial surface covered with adherent bacteria (P < 0.001) and the amenability of mucosal bacteria (P = 0.01) were also significantly increased in the azathioprine-treated group compared with all other IBD groups. The patients receiving both 5-ASA and azathioprine did not differ statistically from untreated IBD patients either in mucus leukocyte migration or in bacterial concentrations. CONCLUSIONS: Azathioprine and 5-ASA induce opposite effects on the mucus barrier. Concomitant therapy of 5-ASA and azathioprine mutually neutralizes the effects of both on the mucosal flora and the barrier function.

Adult↗
PubMed2001

Protease inhibitors restore radiation-induced apoptosis to Bcl-2-expressing lymphoma cells.

The proteasome pathway is important for the turnover of many regulatory proteins. This pathway has recently become a target for antitumor agents and several research groups have demonstrated that inhibitors with specificities for the proteasome are potent apoptosis-inducing agents. Many mechanisms by which proteasome inhibitors exert their effects have been suggested, including inhibition of NF-kappa B activity and stabilization of the p53 tumor suppressor protein. We investigated the ability of inhibitors with specificities for the proteasome and for another protein degradation enzyme, calpain, to sensitize a murine B-cell lymphoma with constitutive NF-kappa B1 homodimer activity and high expression of Bcl-2 protein to radiation-induced apoptosis. Protease inhibitors tested were calpain inhibitor I, calpain inhibitor II, calpeptin, MG132, and Lactacystin. All five inhibitors induced apoptosis and sensitized cells to radiation despite the maintenance of Bcl-2 protein levels throughout the course of treatment. An electrophoretic migration shift assay for NF-kappa B1 activity provided evidence that reversal of NF-kappa B activity was not required for induction of cell death; however, p53 levels were elevated for all inhibitors tested. HL-60 cells, devoid of p53, could not be sensitized to radiation by MG132 treatment, suggesting that p53 was important for cell death induced by combined treatment with protease inhibitors and radiation. We concluded that protease inhibitors are capable of overcoming the protective effects of Bcl-2 to induce apoptosis and suggest that protease inhibitor treatment, when combined with ionizing radiation, leads to p53-mediated apoptosis.

Animals↗
PubMed1995

Hyalomma truncatum (Acari; Ixodidae): investigations into the scototaxis of unfed adult ticks.

Under controlled test conditions, unfed male and female Hyalomma truncatum ticks exhibited a positive scototaxis to stationary, two-dimensional targets. Upright-positioned rectangles were the most attractive targets. The attractiveness of these targets increased with their size. Significantly more ticks responded scototactically positively to the targets under a luminance contrast ratio of 5:1, as compared with other luminance contrast ratios. Targets with an elevation angle of 13 degrees were occupied more frequently than objects with higher elevation angles. Scototaxis was the same towards a stationary and a sinusoid oscillating target. When an upright-positioned rectangle was combined with a CO2 gradient, the number of ticks that migrated into the CO2 gradient and contacted the target did not increase significantly. The interval between exposure and first locomotion of the ticks, however, was significantly shorter under the influence of a CO2 gradient than in all other experiments without a CO2 gradient. A temperature gradient simulating a natural host (cattle) did not alter the scototaxis. The results of these investigations suggest that the positive scototaxis exhibited by adult H. truncatum ticks is not likely to be part of their appetence behaviour but rather searching behaviour to find adequate protection from harsh climatic conditions.

Animals↗
PubMed2004

[Functional facial analysis after botulin on toxin injection].

As usual, the face at rest is analysed before btx injection. But the interest of the analysis of the face dynamically, in a functional way, with the help of the palpation, is demonstrated. A key point is to decide to favor the high position of the highbrow more than to totally fade the frontal wrinkles. To perform this, a new functional segmentation of the frontalis muscle is described. The role of the procerus muscle as antagonist of the frontalis muscle, inferior medial part, is explained. To elevate the medium third of the eyebrow, the lateral part of the corrugator muscle is injected with a specific technique. This technique decreases the risk of weakening the overlying frontalis muscle and the underlying levator palpebrae muscle. To achieve a higher elevation of the eyebrow tail, and to totally fade the upper and medium crow's foot, different points of injection on the lateral orbital rim are described, without the risk of migration to the oculo motor muscles. Fading the tear trough with the injection of the superior malar part of the orbicularis oculi muscle is explained. Thanks to the use of the functional analysis of the face and to the comprehension of the fabulous possibilities of the botulinum toxin A, it is now justified to switch from a "ready to wear" way of injection to a "haute couture" way, that is to say adapted to each patient.

Botulinum Toxins, Type A↗
PubMed2006

Calponin and caldesmon cellular domains in reacting microvessels following traumatic brain injury.

Calponin (Cp) and caldesmon (Cd) are actin-binding proteins involved in the regulation of smooth muscle (SM) tone during blood vessel contraction. While in vitro studies have reported modifications of these proteins during vessel contractility, their role in vivo remains unclear. Traumatic brain injury (TBI) causes disruption of cerebral microvascular tone, leading to sustained contractility in reacting microvessels and cerebral hypoperfusion. This study aimed to determine the spatial and temporal expressions of Cp and Cd in rat cerebral cortical and hippocampal microvessels post-TBI. Reacting microvessels were analyzed in control, 4, 24, and 48 h post-injury. Single and double immunocytochemical techniques together with semiquantitative analyses revealed a Cp upregulation in SM at all time frames post-TBI; with the protein migrating from SM cytosol to the vicinity of the cell membrane. Similarly, Cd immunoreactivity significantly increased in both SM and endothelial cells (En). However, while Cp and Cd in SM remained elevated, their levels in En returned to normal at 48 h post-TBI. The results suggest that Cp and Cd levels increase while compartmentalizing to specific subcellular domains. These changes are temporally associated with modifications in the cytoskeleton and contractile apparatus of SM and En during blood vessel contractility. Furthermore, these changes may underlie the state of sustained contractility and hypoperfusion observed in reacting microvessels after TBI.

Animals↗
PubMed2002

A new approach to epitope confirmation by sampling effector/memory T cells migrating to the lung.

The identification of T cell epitopes that elicit a weak T cell response is technically challenging due to the relatively low resolution of many available screening assays. Peptide immunization can confirm the immunogenicity of a given peptide, however, this also often induces a low frequency response in lymphoid organs. In this report, we use the murine gammaherpesvirus-68 model system to describe a novel technique to enrich for antigen-experienced T cells in vivo as an aid to epitope mapping. Mice are immunized with peptides containing putative epitopes then effector/memory cells which migrate to the lungs are washed out and tested for specificity using intracellular staining for interferon gamma (IFN-gamma). We show that the lung is a site where there are elevated numbers of antigen-experienced T cells and this can be exploited to confirm otherwise low frequency T cell responses. In addition, we identify two novel T cell epitopes in the ORF65 protein of MHV-68 which will be valuable tools in the dissection of the immune response to this model gammaherpesvirus.

Animals↗
PubMed1997

p62(dok): a constitutively tyrosine-phosphorylated, GAP-associated protein in chronic myelogenous leukemia progenitor cells.

Characteristic of chronic myelogenous leukemia (CML) is the presence of the chimeric p210(bcr-abl) protein possessing elevated protein tyrosine kinase activity relative to normal c-abl tyrosine kinase. Hematopoietic progenitors isolated from CML patients in the chronic phase contain a constitutively tyrosine-phosphorylated protein that migrates at 62 kDa by SDS-PAGE and associates with the p120 ras GTPase-activating protein (GAP). We have purified p62(dok) from a hematopoietic cell line expressing p210(bcr-abl). p62(dok) is a novel protein with features of a signaling molecule. Association of p62(dok) with GAP correlates with its tyrosine phosphorylation. p62(dok) is rapidly tyrosine-phosphorylated upon activation of the c-Kit receptor, implicating it as a component of a signal transduction pathway downstream of receptor tyrosine kinases.

CSK Tyrosine-Protein Kinase↗
PubMed2003

Inbreeding pattern and reproductive success in a rural community from Galicia (Spain).

The present paper is based on information on marital patterns and reproductive performance (reconstituted families) in the rural community of Los Nogales, Galicia, Spain. Biodemographic data were used to analyse temporal changes and structure of consanguinity in the population, as well as consanguinity versus reproductive success. Of 2347 marriages celebrated between 1871 and 1977, 5.15% were between relatives (up to third degree). The population's inbreeding coefficient was above the Spanish average after 1890, and levels were high during the first part of the 20th century. A possible underestimation of inbreeding coefficients is attributed to the elevated frequency of extramarital births occurring in the Los Nogales population (13.47%). The structures of consanguineous matings, expressed as C22/C33 and C33/C44, turned out to be 0.86 and 0.82 respectively. Regarding migration, before 1920 consanguinity increased, but net migration was negative. In the period 1920-1929 consanguinity began to decrease, prior to maximum emigration. As for reproductive success, information from 1503 reconstituted families shows that complete fertility was slightly higher among consanguineous families despite a greater infant mortality. Lower infertility in consanguineous matings, as well as lower age at marriage and first maternity, could explain the above results.

Adolescent↗
PubMed2006

Cell cycle-dependent phosphorylation of the RUNX2 transcription factor by cdc2 regulates endothelial cell proliferation.

RUNX2 is a member of the runt family of DNA-binding transcription factors. RUNX2 mediates endothelial cell migration and invasion during tumor angiogenesis and is expressed in metastatic breast and prostate tumors. Our published studies showed that RUNX2 DNA-binding activity is low during growth arrest, but elevated in proliferating endothelial cells. To investigate its role in cell proliferation and cell cycle regulation, RUNX2 was depleted in human bone marrow endothelial cells using RNA interference. Specific RUNX2 depletion inhibited DNA-binding activity as measured by electrophoretic mobility shift assay resulting in inhibition of cell proliferation. Cells were synchronized at the G(1)/S boundary with excess thymidine or in mitosis (M phase) with nocodazole. Endogenous or ectopic RUNX2 activity was maximal at late G(2) and during M phase. Inhibition of RUNX2 expression by RNA interference delayed entry into and exit out of the G(2)/M phases of the cell cycle. RUNX2 was coimmunoprecipitated with cyclin B1 in mitotic cells, which further supported a role for RUNX2 in cell cycle progression. Moreover, in vitro kinase assays using recombinant cdc2 kinase showed that RUNX2 was phosphorylated at Ser(451). The cdc2 inhibitor roscovitine dose dependently inhibited in vivo RUNX2 DNA-binding activity during mitosis and the RUNX2 mutant S451A exhibited lower DNA-binding activity and reduced stimulation of anchorage-independent growth relative to wild type RUNX2. These results suggest for the first time that RUNX2 phosphorylation by cdc2 may facilitate cell cycle progression possibly through regulation of G(2) and M phases, thus promoting endothelial cell proliferation required for tumor angiogenesis.

Animals↗
PubMed2004

Involvement of nitric oxide in angiogenic activities of vascular endothelial growth factor isoforms.

We compared effects of vascular endothelial growth factor-121 (VEGF121) and vascular endothelial growth factor-165 (VEGF165) on generation of NO in HUVEC and the involvement of NO in VEGF121- and VEGF165-induced angiogenesis. VEGF stimulated synthesis of NO within seconds, reaching peak concentrations of 450 +/- 25 and 180 +/- 15 nmol/l for VEGF121, and VEGF165, respectively. The VEGF121 increased NO production for about 40 s while VEGF165-stimulated NO release lasted only for about 20 s. Accordingly, cGMP elevation was stronger in VEGF121- than in VEGF165-treated cells. The VEGF121 was a very weak mitogen but strong chemoattractant for HUVEC, whereas VEGF165 potently induced both cell proliferation and migration. NO appeared to be involved in the endothelial migration and morphogenesis but not in the proliferation. NO was also a permissive molecule for VEGF121- but not for VEGF165-induced capillary sprouting in spheroid culture. In conclusion, VEGF121 is a stronger stimulator of endothelial nitric oxide synthase (eNOS) activity, and angiogenic potential of VEGF121 is more reliant on NO contribution.

Alternative Splicing↗