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Sima Halevy - One of the best experts on this subject based on the ideXlab platform.

  • in vitro release of interferon gamma and macrophage Migration Inhibition Factor in drug induced urticaria and angioedema
    Acta Dermato-venereologica, 1999
    Co-Authors: Ella Livni, Moshe Lapidoth, Sima Halevy
    Abstract:

    : T-cells are involved in the pathogenesis of cutaneous drug reactions. T-cell phenotype and cytokine release pattern in rivo and in vitro might correlate with the type of immune response involved in cutaneous drug reactions. In vitro release of interferon-gamma and macrophage Migration Inhibition Factor (MIF) from peripheral blood lymphocytes, following in vitro challenge with the suspected unmodified drugs, was studied in 12 patients with drug-induced urticaria and/or angioedema and in two group-matched controls. The occurrence of positive interferon-gamma and MIF responses was significantly higher in patients with drug-induced urticaria and/or angioedema than in controls. The sensitivity and specificity of the interferon-gamma test (50% and 92%, respectively) were similar to that of the MIF test (58% and 96%, respectively). Percentage agreement between both tests was 80.9 (kappa = 0.76). In vitro release of interferon-gamma and MIF in drug-induced urticaria and/or angioedema suggests a drug-specific immune response, and may implicate the drug as a possible inducer of the reaction.

  • the role of macrophage Migration Inhibition Factor in toxic epidermal necrolysis
    International Journal of Dermatology, 1997
    Co-Authors: Sima Halevy, Ella Livni
    Abstract:

    Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A macrophage Migration Inhibition Factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The macrophage Migration Inhibition Factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P<0.05) than that recorded in the controls (0/17). The MIF test results in TEN patients and controls are summarized in Table 1.

  • allergic vasculitis induced by decapeptyl confirmation by macrophage Migration Inhibition Factor mif test
    European Journal of Obstetrics & Gynecology and Reproductive Biology, 1993
    Co-Authors: Boaz Amichai, Marcelo H Grunwald, Sima Halevy
    Abstract:

    Abstract A case of allergic vasculitis of the skin following treatment with Decapeptyl ® ( d -Trp 6 -LHRH) for in vitro fertilization is described. The possible role of an allergic mechanism in this reaction has been suggested by a positive macrophage Migration Inhibition Factor (MIF) test toward the drug.

  • macrophage Migration Inhibition Factor release in lichenoid drug eruptions
    Journal of The American Academy of Dermatology, 1993
    Co-Authors: Sima Halevy, Miriam Sandbank, Ella Livni
    Abstract:

    Lichenoid drug eruption (DE) that can clinically and histologically resemble lichen planus (LP) can be induced by gold, thiazide diuretics, quinidine, and other agents. 1, 2 Lichenoid DE, which in general spares the mucous membranes, may be photodistributed or nonphotodistributed.P Common causes of photodistributed lichenoid DE are thiazide diuretics-" and quinidine.': 5 The mechanism by which drugs induce a lichenoid tissue reaction is unknown. Recent observations support a critical role of helper/inducer T lymphocytes in lichenoid tissue reaction." In isolated cases of lichenoid photosensitive DE induced by hydrochlorothiazide or quinidine, positive macrophage Migration Inhibition Factor (MIF) responses toward the offending drugs were recorded.f5 MIF is a lymphokine released from sensitized T lymphocytes by an appropriate antigen. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in animal models and in humans.71O Furthermore, MIF release has been recently reported to be valuable in the diagnosis of adverse drug reactions, including DE,ll-15 The present study was conducted to evaluate MIF release in patients with lichenoid DE induced by various drugs.

Ella Livni - One of the best experts on this subject based on the ideXlab platform.

  • in vitro release of interferon gamma and macrophage Migration Inhibition Factor in drug induced urticaria and angioedema
    Acta Dermato-venereologica, 1999
    Co-Authors: Ella Livni, Moshe Lapidoth, Sima Halevy
    Abstract:

    : T-cells are involved in the pathogenesis of cutaneous drug reactions. T-cell phenotype and cytokine release pattern in rivo and in vitro might correlate with the type of immune response involved in cutaneous drug reactions. In vitro release of interferon-gamma and macrophage Migration Inhibition Factor (MIF) from peripheral blood lymphocytes, following in vitro challenge with the suspected unmodified drugs, was studied in 12 patients with drug-induced urticaria and/or angioedema and in two group-matched controls. The occurrence of positive interferon-gamma and MIF responses was significantly higher in patients with drug-induced urticaria and/or angioedema than in controls. The sensitivity and specificity of the interferon-gamma test (50% and 92%, respectively) were similar to that of the MIF test (58% and 96%, respectively). Percentage agreement between both tests was 80.9 (kappa = 0.76). In vitro release of interferon-gamma and MIF in drug-induced urticaria and/or angioedema suggests a drug-specific immune response, and may implicate the drug as a possible inducer of the reaction.

  • the role of macrophage Migration Inhibition Factor in toxic epidermal necrolysis
    International Journal of Dermatology, 1997
    Co-Authors: Sima Halevy, Ella Livni
    Abstract:

    Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A macrophage Migration Inhibition Factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The macrophage Migration Inhibition Factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P<0.05) than that recorded in the controls (0/17). The MIF test results in TEN patients and controls are summarized in Table 1.

  • macrophage Migration Inhibition Factor release in lichenoid drug eruptions
    Journal of The American Academy of Dermatology, 1993
    Co-Authors: Sima Halevy, Miriam Sandbank, Ella Livni
    Abstract:

    Lichenoid drug eruption (DE) that can clinically and histologically resemble lichen planus (LP) can be induced by gold, thiazide diuretics, quinidine, and other agents. 1, 2 Lichenoid DE, which in general spares the mucous membranes, may be photodistributed or nonphotodistributed.P Common causes of photodistributed lichenoid DE are thiazide diuretics-" and quinidine.': 5 The mechanism by which drugs induce a lichenoid tissue reaction is unknown. Recent observations support a critical role of helper/inducer T lymphocytes in lichenoid tissue reaction." In isolated cases of lichenoid photosensitive DE induced by hydrochlorothiazide or quinidine, positive macrophage Migration Inhibition Factor (MIF) responses toward the offending drugs were recorded.f5 MIF is a lymphokine released from sensitized T lymphocytes by an appropriate antigen. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in animal models and in humans.71O Furthermore, MIF release has been recently reported to be valuable in the diagnosis of adverse drug reactions, including DE,ll-15 The present study was conducted to evaluate MIF release in patients with lichenoid DE induced by various drugs.

Sanjay Misra - One of the best experts on this subject based on the ideXlab platform.

  • vascular endothelial growth Factor a matrix metalloproteinase 1 and macrophage Migration Inhibition Factor changes in the porcine remnant kidney model evaluation by magnetic resonance imaging
    Journal of Vascular and Interventional Radiology, 2010
    Co-Authors: Sanjay Misra, Khamal D Misra, James F Glockner
    Abstract:

    Purpose To determine the expression of vascular endothelial growth Factor-A (VEGF-A), macrophage Migration Inhibition Factor (MIF), and matrix metalloproteinase-1 (MMP-1) in the porcine remnant kidney model and quantify renal blood flow and volume using phase contrast magnetic resonance (PC MR) imaging with MR angiography. Materials and Methods In 23 pigs, the left renal artery was completely embolized using polyvinyl acrylide (PVA) particles and the right kidney partially embolized (remnant kidney), and six pigs served as controls. The animals were killed early (day 3, 7, and 14, N=3), day 24 (D24, N=5), day 37 (D37, N=3), day 42 (D42, N=9), and day 84 (D84, N=3). MR imaging/PC MR angiography of the kidneys was performed before death. The remnant and control kidneys were harvested for Western blotting of VEGF-A, MMP-1, and MIF. Blood was removed for blood urea nitrogen (BUN) and creatinine before embolization and at time of death. Results The kidney function after the embolization was characterized by chronic renal insufficiency. The renal artery blood flow, volume, and weight of the remnant kidney increased significantly over time when compared with controls. At early time points, there was increased expression of MIF and MMP-1 followed by an increase in the expression of VEGF-A by day 37 ( P Conclusions In this model, renal blood flow and volume increase as the remnant kidney hypertrophies and scars. There is increased expression of MIF, VEGF-A, and MMP-1 in the remnant kidney.

  • expression of hypoxia inducible Factor 1α macrophage Migration Inhibition Factor matrix metalloproteinase 2 and 9 and their inhibitors in hemodialysis grafts and arteriovenous fistulas
    Journal of Vascular and Interventional Radiology, 2008
    Co-Authors: Sanjay Misra, Alex A Fu, Dheeraj K Rajan, Luis A Juncos, Michael A Mckusick, Haraldur Bjarnason, Debabrata Mukhopadhyay
    Abstract:

    Purpose It is well recognized that arteriovenous fistulas (AVFs) used for hemodialysis access have better primary patency rates with less restenosis than polytetrafluoroethylene (PTFE) grafts; however, the mechanism responsible for this is not known. Recent data suggest that hypoxia inducible Factor–1α (HIF-1α) is associated with vascular restenosis, possibly through mechanisms that increase the production of macrophage Migration Inhibition Factor (MIF), matrix metalloproteinase–2 (MMP-2) and MMP-9, and their inhibitors (tissue inhibitor of MMPs; TIMP). The present study tested the hypothesis that there are differences in the expression patterns of HIF-1α, MIF, MMP-2, MMP-9, and TIMPs in specimens removed from patients with AVFs and PTFE grafts. Materials and Methods Whole-vessel tissue samples were obtained from the vein distal to the vein–to–PTFE graft anastomosis and the proximal outflow vein (within 6 cm of the arteriovenous anastomosis) of AVFs from 17 patients who required a surgical revision for thrombosis and stenosis. Nonstenotic veins of four patients undergoing hemodialysis vascular access placement were used as controls. PTFE grafts ( n = 6), AVFs ( n = 6), and control samples ( n = 3) underwent Western blot analysis and zymography. A separate group of five patients with PTFE hemodialysis grafts and one control subject were used for immunohistochemical analysis. Results Specimens from patients with PTFE grafts had significantly higher expression of HIF-1α ( P = .03), MIF ( P = .02), TIMP-1 ( P = .0006), pro–MMP-2 ( P = .02), and pro–MMP-9 ( P = .046) compared with control veins. The expression of only pro–MMP-9 was significantly higher in AVFs compared with control samples ( P = .004). There was a significant increase in the expression of MIF ( P = .007) and TIMP-1 ( P Conclusions There were major differences in the expression patterns of hypoxia (ie, HIF-1α) and proteins regulated by HIF-1α, including MIF, pro–MMP-2, pro–MMP-9, and TIMP-1, in specimens removed from patients with PTFE grafts and AVFs. Understanding the role of HIF-1α and these proteins in hemodialysis access failure can help improve outcomes.

M. Dighero - One of the best experts on this subject based on the ideXlab platform.

  • The Kmif (Kveim-induced macrophage Migration Inhibition Factor) test in sarcoidosis
    2016
    Co-Authors: Jones W. Williams, E. Pioli, D. J. Jones, M. Dighero
    Abstract:

    SYNOPSIS Circulating lymphocytes from 30 patients with sarcoidosis when stimulated in vitro with Kveim-induced macrophage Migration Factor, the Kmif test, produced a guinea-pig macrophage Migration Inhibition Factor in 21 of 30 cases (70%O). In those patients not on steroids the results showed a good correlation with the cutaneous Kveim test. One positive test was found in 16 normal subjects. Our results suggest that the Kmif test may prove a useful rapid alternative to the Kveim test. Despite the recent controversy as to the specificity of the Kveim test in sarcoidosis (Lancet, 1971; British Medical Journal, 1971; Scadding, 1971, 1972), that test remains of considerable value as a diagnostic tool. In consequence, various attempts are being made to develop in-vitro Kveim tests (Bendixen an

Joe G N Garcia - One of the best experts on this subject based on the ideXlab platform.

  • intracellular interaction of myosin light chain kinase with macrophage Migration Inhibition Factor mif in endothelium
    Journal of Cellular Biochemistry, 2005
    Co-Authors: Raj Wadgaonkar, Steven M Dudek, Ari L Zaiman, Laura Linzmcgillem, Alexander D Verin, Saule Nurmukhambetova, Lewis H Romer, Joe G N Garcia
    Abstract:

    The endothelial cell Ca2+/calmodulin (CaM)-dependent myosin light chain kinase isoform (EC MLCK) is a multifunctional contractile effector involved in vascular barrier regulation, leukocyte diapedesis, apoptosis, and angiogenesis. The EC MLCK isoform and its splice variants contain a unique N-terminal sequence not present in the smooth muscle MLCK isoform (SM MLCK), which allows novel upregulation of MLCK activation by signaling cascades including p60src. The yeast two-hybrid assay system using the entire EC MLCK1 N-terminus (922 aa) as bait, identified additional stable MLCK binding partners including the 12 KDa macrophage Migration inhibitory Factor (MIF). This finding was confirmed by cross immunoprecipitation assays under non-denaturing conditions and by GST pull down experiments using GST-N-terminal MLCK (#1–923) and MLCK N-terminal deletion mutants in TNFα- and thrombin-stimulated endothelium. This EC MLCK–MIF interaction was shown biochemically and by immunofluorescent microscopy to be enhanced in TNFα- and thrombin-stimulated endothelium, both of which induce increased MLCK activity. Thrombin induced the colocalization of an epitope-tagged, full-length MIF fusion protein with phosphorylated MLC along peripheral actin stress fibers. Together these studies suggest that the novel interaction between MIF and MLCK may have important implications for the regulation of both non-muscle cytoskeletal dynamics as well as pathobiologic vascular events that involve MLCK. © 2005 Wiley-Liss, Inc.