PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MIGS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1999

The glucose repressor CRE1 from Sclerotinia sclerotiorum is functionally related to CREA from Aspergillus nidulans but not to the Mig proteins from Saccharomyces cerevisiae.

We isolated the putative glucose repressor gene cre1 from the phytopathogenic fungus Sclerotinia sclerotiorum. cre1 encodes a 429 amino acid protein 59% similar to the carbon catabolite repressor CREA from Aspergillus nidulans. In addition to the overall amino acid sequence relatedness between CRE1 and CREA proteins, cre1 can functionally complement the A. nidulans creAd30 mutation as assessed by repression of the alcohol dehydrogenase I gene expression. The CREI region carrying the two zinc fingers is also very similar to the DNA binding domains of the Saccharomyces cerevisiae glucose repressors Mig1p and Mig2p. Despite the presence in the CRE1 protein of several motifs involved in the regulation of Miglp activity, cre1 cannot complement mig deficiencies in S. cerevisiae. These data suggest that glucose repression pathways may have evolved differently in yeasts and filamentous fungi.

Amino Acid Sequence↗
PubMed2000

Peroxisome proliferator-activated receptor-gamma activators inhibit IFN-gamma-induced expression of the T cell-active CXC chemokines IP-10, Mig, and I-TAC in human endothelial cells.

Peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the nuclear hormone receptor superfamily originally shown to play an important role in adipocyte differentiation and glucose homeostasis, is now known to regulate inflammatory responses. Given the importance of endothelial cell (EC)-derived chemokines in regulating leukocyte function and trafficking, we studied the effects of PPARgamma ligands on the expression of chemokines induced in ECs by the Th1 cytokine IFN-gamma. Treatment of ECs with PPARgamma activators significantly inhibited IFN-gamma-induced mRNA and protein expression of the CXC chemokines IFN-inducible protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC), whereas expression of the CC chemokine monocyte chemoattractant protein-1 was not altered. PPARgamma activators decreased IFN-inducible protein of 10 kDa promoter activity and inhibited protein binding to the two NF-kappaB sites but not to the IFN-stimulated response element ISRE site. Furthermore, PPARgamma ligands inhibited the release of chemotactic activity for CXC chemokine receptor 3 (CXCR3)-transfected lymphocytes from IFN-gamma-stimulated ECs. These data suggest that anti-diabetic PPARgamma activators might attenuate the recruitment of activated T cells at sites of Th1-mediated inflammation.

Chemokine CXCL10↗
PubMed1999

[Interferon alfa-2b treatment of adult patients during early chronic phase of Ph1-positive chronic myeloid leukemia (initial report on a cooperative study, protocol CML-MIG-97)].

AIM: Evaluation of clinical effectiveness of two regimens of induction therapy of an early chronic stage of Ph'-positive chronic myeloid leukemia including interferon-alpha 2b (intron-A, "Schering Plough") in a cooperative randomised trial on the protocol CML MIG-97. MATERIALS AND METHODS: 42 patients with chronic myeloid leukemia were treated either with intron-A in standard doses (5 IU/m2/day) alone or in combination with monthly 10-day courses of low-dose cytosine-arabinoside (10 mg/m2/twice a day). The effect was assessed by the international criteria of a complete and partial hematologic remission and the cytogenetic response. RESULTS: Intron-A therapy in standard doses produced a pronounced cytogenetic response in 28.6% of the patients. In low-dose interferon-alpha-2b (reaferon and intron-A, 1-3 IU/m2/day) in combination with various regimens of chemotherapy only minimal cytogenetic response was achieved. CONCLUSION: A pronounced cytogenetic response in early chronic stage of CML to standard doses of intron A holds promise in prolongation of CML patients survival and design of new effective therapy programs.

Adjuvants, Immunologic↗
PubMed2001

Effect of process parameters upon the dopamine and lipid peroxidation activity of selected MIG welding fumes as a marker of potential neurotoxicity.

There is growing concern over the neurotoxic effects of chronic occupational exposure to metal fume produced by welding. Elevated iron and manganese levels in the brain have been linked to an increase in lipid peroxidation, dopamine depletion and predisposition to the development of a Parkinson's type condition in advanced cases. Chemical and toxicological analysis of selected welding fumes, generated by model processes, were used in order to evaluate their potential to release solutes that promote oxidation of dopamine and peroxidation of brain lipids in cell free assays. This study compared the effect of shield gas, electrode type and voltage/currect upon the dopamine and brain lipid peroxidation potential of selected welding fume, obtained from metal inert gas (MIG) welding systems. Overall, fume extracts were found to enhance dopamine oxidation and inhibit lipid peroxidation. Significant differences were also found in the oxidising potential of fume generated under differing process conditions; it may therefore be possible to determine the potential neurotoxicity of fumes using this system.

Animals↗
PubMed1985

B cell activation. VI. Effects of exogenous diglyceride and modulators of phospholipid metabolism suggest a central role for diacylglycerol generation in transmembrane signaling by mIg.

Previous evidence indicates that in vitro activators of protein kinase C, such as phorbol myristate acetate (PMA), are able to induce early activation events in murine B cells, including membrane depolarization and increased I-A antigen expression. These same events are induced by specific antigen and anti-receptor antibody. This evidence suggests that protein kinase C activation may be an important intermediary event in mIg-mediated transmembrane signaling. Previously, investigators have suggested that protein kinase C activation is regulated by a novel second messenger, diacylglycerol (DG), and DG is generated by phosphatidylinositol (PI) hydrolysis after receptor-ligand interaction in many systems. In view of this concept, we examined the effects of nonspecific activators and inhibitors of DG production and DG itself on membrane potential and levels of I-A antigen expression in murine B cells. Our results indicate that exposure to DG, or induction of DG production by treatment of B cells with exogenous phospholipase C, results in depolarization and increased I-A antigen expression similar to that induced by anti-receptor antibody and specific antigen. Furthermore, we demonstrate that depolarization and increased I-A expression induced by anti-receptor antibody is blocked under conditions in which DG production is inhibited. As expected, based on its direct activation of protein kinase C, PMA stimulation is unaffected by this inhibition. These results support our earlier hypothesis that occupancy of antigen receptors on B cells is linked to subsequent activation events by PI hydrolysis, DG generation, and protein kinase C activation.

Animals↗
PubMed2001

A screen of mammalian antibodies on snapper (Pagrus auratus, Sparidae) peripheral blood leukocytes reveals cross reactivity of an anti-human CD3 antibody with a population of mIg(-) cells.

Detailed immunological studies of the teleosts have been hampered by a lack of antibodies against cell-specific markers. Furthermore, where antibodies have been raised, in many instances they have been found to be species-specific. In comparison, many monoclonal and polyclonal antibodies exist with specificities for mammalian proteins and glycoproteins that effectively differentiate leukocyte sub-populations. In this study, we have tested a panel of 54 commercial antibodies against human and murine cell surface receptors for their ability to bind leukocytes isolated from the peripheral blood of snapper (Pagrus auratus). From this panel, one antibody, A452, which is specific for the intracytoplasmic tail of the epsilon (epsilon) chain of the T cell receptor-associated CD3 complex (CD3epsilon) bound to a subpopulation of peripheral blood leukocytes. Mutually exclusive counterstaining was observed when this antibody was used in conjunction with a monoclonal anti-snapper immunoglobulin antibody. This suggests that A452 may be binding to putative snapper T cells.

Animals↗
PubMed1996

MIG ACCESS: a population-based, nationwide, comparative survey of access to care in migraine in France.

A national control-matched survey was conducted in France to evaluate the access of migraineurs to health care. A validated IHS criteria-based diagnostic procedure for screening was conducted in adults drawn from a sample of 6,000 households. A group of 650 subjects fulfilling the IHS criteria for migraine were matched by sex, age and activity status with a group of non-headache, non-migraine controls. Response rates were 87% and 82% for the migraineurs and the controls, respectively. The comparability of the groups was demonstrated by the absence of statistical differences between either respondents versus non-respondents or migraineurs versus controls for sex, age and occupation. The 3-month prevalence of migraine was estimated at 13% (95% CI: 12-14). The health care consumption of migraineurs was not higher than that of the controls. Migraineurs rarely consult for headaches and seem to content themselves with their routine analgesic treatment. They believe, however, that improvement in their condition is possible and discuss this with their physicians. This ambivalent attitude mainly reflects a fatalistic outlet which may constitute the major obstacle of an improved management of migraine.

Adolescent↗
PubMed1999

Incremental absenteeism due to headaches in migraine: results from the Mig-Access French national cohort.

OBJECTIVE: To assess the costs of headache-related absenteeism of community-dwelling migraineurs, and to compare the amount of absenteeism between migraineurs aged 18 and older and age, sex, and occupation-matched nonheadache-prone subjects. DESIGN: Follow-up over a 3-month period. SAMPLES: 385 migraineurs and 313 nonheadache subjects representative of the setting. METHODS: Every day, the participants recorded the presence of headache, if any, and the work situation (unemployment, holiday, weekend, medical reason, nonmedical reason). Sickness-related absenteeism was the number of workdays missed or interrupted for medical reasons. Headache-related absenteeism was the sickness-related absenteeism during workdays with headaches. The annual headache-related absenteeism costs in France were extrapolated from these data in accordance with the mean income per occupational category. The incremental absenteeism and related costs were the difference between the two samples. RESULTS: Of working migraineurs, 20% had at least one period of absenteeism. During the 3 months, they missed or interrupted on average 1.4 days for medical reasons, 0.25 of which for headaches. Sickness-related absenteeism was statistically higher in migraineurs than in nonheadache-prone subjects. This difference was due to a higher absenteeism for comorbidity reasons, not for headache reasons, representing 20% of all sickness-related absenteeism. Migraineurs avoided sick leave for headache reasons. As an incremental total, 1.68 days or approximately 0.7% of the annual number of working days are lost on average per individual with migraine. The annual incremental headache-related absenteeism cost was 5.22 billions, i.e. 1,551 FF (US$240) per migraineur.

Absenteeism↗
PubMed2003

An alternatively spliced variant of CXCR3 mediates the inhibition of endothelial cell growth induced by IP-10, Mig, and I-TAC, and acts as functional receptor for platelet factor 4.

The chemokines CXCL9/Mig, CXCL10/IP-10, and CXCL11/I-TAC regulate lymphocyte chemotaxis, mediate vascular pericyte proliferation, and act as angiostatic agents, thus inhibiting tumor growth. These multiple activities are apparently mediated by a unique G protein-coupled receptor, termed CXCR3. The chemokine CXCL4/PF4 shares several activities with CXCL9, CXCL10, and CXCL11, including a powerful angiostatic effect, but its specific receptor is still unknown. Here, we describe a distinct, previously unrecognized receptor named CXCR3-B, derived from an alternative splicing of the CXCR3 gene that mediates the angiostatic activity of CXCR3 ligands and also acts as functional receptor for CXCL4. Human microvascular endothelial cell line-1 (HMEC-1), transfected with either the known CXCR3 (renamed CXCR3-A) or CXCR3-B, bound CXCL9, CXCL10, and CXCL11, whereas CXCL4 showed high affinity only for CXCR3-B. Overexpression of CXCR3-A induced an increase of survival, whereas overexpression of CXCR3-B dramatically reduced DNA synthesis and up-regulated apoptotic HMEC-1 death through activation of distinct signal transduction pathways. Remarkably, primary cultures of human microvascular endothelial cells, whose growth is inhibited by CXCL9, CXCL10, CXCL11, and CXCL4, expressed CXCR3-B, but not CXCR3-A. Finally, monoclonal antibodies raised to selectively recognize CXCR3-B reacted with endothelial cells from neoplastic tissues, providing evidence that CXCR3-B is also expressed in vivo and may account for the angiostatic effects of CXC chemokines.

Alternative Splicing↗
PubMed1996

IFN-gamma is a potent inducer of Ig secretion by sort-purified murine B cells activated through the mIg, but not the CD40, signaling pathway.

IFN-gamma has been shown to either stimulate or inhibit Ig secretion. No studies have yet addressed the basis for these seemingly conflicting properties nor whether IFN-gamma acted directly at the level of the B cell to mediate its effects. Thus, we studied the ability of IFN-gamma to regulate Ig secretion in sort-purified, resting murine B cells that were >99% Ig+, activated either through membrane Ig using unconjugated or dextran-conjugated anti-IgD antibodies (alphadelta-dex) or through CD40 using soluble or membrane CD40 ligand (CD40L). B cells activated with alphadelta-dex proliferated but do not secrete Ig, even in the presence of IL-1 + IL-2. We demonstrate that IFN-gamma only when added subsequent to B cell stimulation with alphadelta-dex, but not unconjugated anti-IfD antibody, plus IL-1 + IL-2 induces up to 100-fold enhancements in Ig secretion and in the numbers of Ig-secreting cells. The predominant Ig isotype secreted is IgM, with IgG3 and IgG2a comprising the majority of non-IgM antibody. IFN-gamma must act in concert with IL-2 for stimulation of Ig secretion. Further, IFN-gamma synergizes with IL-3 + granulocyte-macrophage colony stimulating factor for induction of Ig synthesis. IFN-gamma also enhances IgA syntheses by transforming growth factor-beta-induced membrane IgA+ cells. By contrast, 125IIFN-gamma fails to stimulate Ig secretion in B cells activated with CD40L in the presence or absence of IL-1 + IL-2 or IL-4. However, the combination of CD40L and alphabeta-dex is strongly synergistic for IFN-gamma-induced Ig secretion. Thus, these data establish that IFN-gamma can act directly on the B cell to induce Ig synthesis without the participation of any other cell and demonstrates that the mode of activation of the B cell plays an important role in directing the action of IFN-gamma.

Animals↗