Relevant bibliographies by topics / Macrophag

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Macrophag'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Macrophag"

1

Poetri, Okti Nadia, Retno D. Soejoedono, Agustin Indrawati, and I. Wayan T. Wibawan. "PERAN ANTIBODI KUNING TELUR (IgY) SEBAGAI OPSONIN UNTUK PENCEGAHAN SERANGAN MUTAN STREPTOCOCCUS SEROTIPE D (STREPTOCOCCUS SOBRINUS)." Berkala Penelitian Hayati 13, no. 2 (June 30, 2008): 129–34. http://dx.doi.org/10.23869/bphjbr.13.2.20086.

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The aim of this study was to explore the role of serotype d Mutan Streptococcus (Streptococcus sobrinus) spesific immunoglobulin Y (IgY-Ss) as opsonin against the same strain. The eggs were collected from Single Comb Brown Leghorn which has been immunized with Streptococcus sobrinus. Agar gel precipitation test was applied to detect IgY-Ss in serum and egg. Egg containing IgY-Ss was collected and extracted by PEG-Amonium sulphate and purified using fast protein liquid chromatography. The purity of IgY-Ss was determined by UV spectrophotometer. Molecular weight was established by SDS-PAGE (sodium dedocyl sulphate-poly acrilamide gel electrophoresis). Biological activities of IgY-Ss as opsonin was determined by phagocytosis assay. Phagositic activity of macrophages was not increased by preincubation of both S. sobrinus (107 CFU/ml) and 100 μg of IgY-S, however the phagositic capacity was increased from 1.6 bacterial cell/ macrophag to 5.17 bacterial cell/ macrophag. These finding suggest that IgY-Ss obtained from hens immunized with S. sobrinus provide an alternative to prevent S. sobrinus infection.
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2

Saidah, Makfiyah, Beta Widya Oktiani, and Irham Taufiqurrahman. "THE EFFECT OF FLAVONOID PROPOLIS KELULUT (Trigona spp) EXTRACT ON MACROPHAGE CELL NUMBER IN PERIODONTITIS (IN VIVO STUDY IN MALE WISTAR RATE (Rattus novergicus) GINGIVA)." Dentino : Jurnal Kedokteran Gigi 5, no. 1 (March 12, 2020): 28. http://dx.doi.org/10.20527/dentino.v5i1.8117.

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Background : Periodontitis is a condition where there is an increase in the number of inflammatory cells, namely macrophages in periodontal tissue. Macrophag cell is 12-15μm in oval shape cell with purplish blue cytoplasm and this cell’s function is to phagocytes bacteria and infiltrate gingival tissue. Propolis kelulut contains flavonoid that have an anti-inflammatory effect by suppressing the signal pathway p38 MAPK, JNK 1/2 and NF-kB that it can reduce the number of macrophage cells in inflammatory periodontal tissues. Objective: The purpose of this study was to determine the effect of 0.5 mg dose flavonoid propolis extract on the number of macrophage cells in gingiva wistar rats that have been made into a periodontitis condition. Method: This study used a pure experimental method with a post test only with control group design. There were 9 treatment groups, including flavonoid propolis extract on 1,3,5 days, ibuprofen gel on 1,3,5 days and negative control on 1,3 dan 5 days. Results: There was an effect of giving 0.5 mg flavonoids propolis kelulut extract to the number of macrophage cells in periodontitis. Conclusion: Flavonoid propolis kelulut extract has an effect in increasing the number of macrophage cells on day 3 and decreasing the number of macrophage cells on the 5th day.
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HAMADA, MASAFUMI, EIKO SONOTAKE, SHIGERU YAMAMOTO, and SATORU MORIGUCHI. "Conagenin Derived from Streptomyces roseosporus Enhances Macrophag Functions." Journal of Antibiotics 52, no. 6 (1999): 548–51. http://dx.doi.org/10.7164/antibiotics.52.548.

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4

Műzes, Györgyi, Hajnal Székely, and Zsolt Tulassay. "Whipple’s disease: current problems." Orvosi Hetilap 148, no. 26 (July 1, 2007): 1225–30. http://dx.doi.org/10.1556/oh.2007.28144.

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A Whipple-kór bakteriális fertőzés okozta, ritkán előforduló, számos szerv érintettségével, így változatos klinikummal társuló, alattomos kezdetű, relapsusokkal kísért idült lefolyású, kezelés nélkül fatális gyulladásos betegség. A kórkép gyanúját a jellegzetes (de nem specifikus) tüneti triász (fogyás, krónikus hasmenés, arthralgia) megjelenése sugallhatja. Elhúzódó, intermittáló jellegű láz és lymphadenopathia társulásakor fennállásának különösen nagy a valószínűsége. A Whipple-kór vonatkozásában meghatározó jelentőségű volt az egyedi tulajdonságokkal bíró kórokozó, a Tropheryma whipplei felismerése. A bakteriális fertőzés vélhetően gyakori, betegség viszont csak a hajlamosító immunológiai tényező(k) megléte esetén alakul ki. Tekintettel az alapvetően a macrophagokban perzisztáló és szaporodó baktériumokra, főként a mononuclearis-phagocyta rendszer kóros funkciója tételezhető fel. (A Whipple-kór elsősorban macrophag betegségként értelmezhető.) A klinikai kép sokszínű. Bár a Whipple-kórt eredetileg a gastrointestinalis rendszer megbetegedésének vélték, ma szisztémás betegségnek tekintik. A fertőzés gyanújakor az elsőként választandó vizsgálat a gasztroszkópia: jellegzetes esetben a postbulbaris duodenum és a jejunum területén az erythemas, erodált, sérülékeny nyálkahártyán szétszórt halványsárgás plaque-ok mutatkoznak. A szövettani mintákban előtérben áll a kifejezett macrophag infiltráció (a baktérium intracelluláris inváziójával). A betegség igazolásának klasszikus eszköze a vékonybél-biopsziás minták PAS-festése, valamint a kórokozó PCR-ral történő igazolása. A megfelelő antibiotikum kiválasztása és a terápia időtartama napjainkban is nagyrészt empirikus.
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Vokhmintseva, L. V., N. N. Mayanskaya, S. S. Rymar′, P. A. Zheleznyi, A. P. Nadeyev, and V. V. Vanyunina. "Peculiarities of functional neutrophil activity in rats having periodontitis in thesetting of toxic hepatitis." Bulletin of Siberian Medicine 6, no. 2 (June 30, 2007): 11–16. http://dx.doi.org/10.20538/1682-0363-2007-2-11-16.

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Experimental toxic hepatitis was induced by single administration of Acetaminophen ( paracetamol) in a dose of 1000 mg per 1 kg of body mass in Wistar rats. Inflammation pathology was modeled by wounding the upper maxilla gingiva in toxic hepatitis rats on the 6-th day. Intact rats were controls. On the 1-st and 7-th day, ratio of neutrophil-macrophag was determined in smears of the upper maxillas gingival, oxygen-dependent functional activity of neutrophils was assessed based upon HST-test, functional activity reserves were assessed by the stimulation index. On the 7-th and 13-th day, alaninaminotransferase and aspartataminotransferase activity, level of general and indirect bilirubin, general blood protein were assessed in blood serum of these rats. Toxic hepatitis was established to be accomplished by increased biocidity of phagocytes, decreased functional reserves of neutrophils and their migration into the parodontium. In experimental inflammation, suppurative processes in parodontium tissues are revealed in toxic hepatitis rats by 1.5 times less than in controls due to lower biocide activity of phagocyte cells and increased migration of macrophages.
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Rodriguez, Eric, Frederic Boudard, Michele Mallié, Jean-Marie Bastide, and Madeleine Bastide. "Murine macrophage elastolytic activity induced by Aspergillus fumigatus strains in vitro: evidence of the expression of two macrophage-induced protease genes." Canadian Journal of Microbiology 43, no. 7 (July 1, 1997): 649–57. http://dx.doi.org/10.1139/m97-092.

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The interaction between Aspergillus fumigatus conidia and murine macrophages of various origins was investigated. Cocultures were carried out between A. fumigatus strains and freshly isolated murine pulmonary alveolar macrophages or two murine macrophage cell-lines: murine alveolar cell-line MALU and murine astrocytoma cell-line J774. By measuring the variation of elastolytic activity in the coculture supernatants with two elastin substrates, we demonstrated that either viable or fixed A. fumigatus or C. albicans yeasts or nonspecific particles induced significant macrophage elastolytic activity. The effect of A. fumigatus supernatant or the purified A. fumigatus galactomannan suggested also the possible involvement of this polysaccharide in macrophage-protease gene expression, release, and activity in invasive aspergillosis. The effect of inhibitory compounds demonstrated the potential implication of a macrophagic metalloprotease and a macrophagic cysteine protease. RNA analysis allowed us to demonstrate the induction of expression of two macrophagic protease genes in stimulated macrophages. Two distinctive mechanisms appeared to be implicated in macrophage protease induction: nonspecific phagocytosis in the earliest times of the coculture and (or) specific galactomannan recognition after its gradual release by the mycelium.Key words: Aspergillus fumigatus, macrophages, proteases, invasive aspergillosis, galactomannan.
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Karatieieva, S. "THE CHANGES OF WOUND MACROPHAGES IN PATIENTS WITH DIABETES." Clinical anatomy and operative surgery 19, no. 3 (November 26, 2020): 48–52. http://dx.doi.org/10.24061/1727-0847.19.3.2020.40.

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Purulent-necrotic lesions of the extremities require amputation in 30-50% of cases. Among all cases of lower extremity amputations 50-70% are due to diabetes. Moreover, 5 out of 6 amputations, not related to the traumatic injury of the limb, are performed in patients with diabetes. The mortality rate among patients with diabetes, who undergo amputation varies from 28 to 40%, and 5-year surveillance is only 10-25%. The study of ultrastructural changes of macrophages on the 3rd day of treatment revealed masses of chaotically located fibrillar structures in the cytoplasm of macrophages that occasionally had an increased electron density. This phenomenon was observed in the purulent-necrotic areas of soft tissues of patients from the main group, compared to the control group. In all cases, mitochondria were enlarged in size, swollen, with a light matrix and contained a reduced amount of cristae. The cristae were deformed and shortened. Swollen matrix in mitochondria led to the formation of vacuoles on their place containing fine-grained contents. The nucleus had a usual form and size with the presence of single invaginations. Chromatin was predominantly concentrated in the form of solid electron-dense masses or evenly distributed throughout the nucleus. There were nuclei with partial chromatin dispersion. The contents of the nuclei included granular, fibrillar, and fine vacuolar material. The nuclear membrane folding did not fluctuate significantly. The folds did not cover the whole surface of the nucleus. In some areas invaginates were represented by the continuation of perinuclear space only. The nuclear envelop pores, which connect the contents of the cytoplasm and nucleoplasm, have been observed. The cytoplasm between the zones of the plate complex was occupied by small mitochondria, single polysomal rosettes, and cisternae of granular endoplasmic reticulum, which was represented by extended intracellular channels and vacuolar formations. The smooth endoplasmic reticulum was predominantly located in the central part. The surface of macrophages in the process of their differentiation from monocytes was relatively plane. Occasionally there occurred small processes or pseudopodia. The number of pinocytic vesicles surrounded by a border was reduced in poorly differentiated cells. Ozone therapy stimulates the functional activity of wound macrophages, as it causes destructive changes in these cells without necrotic lesions. Intravenous introduction of ozonized saline con-tributes to the elimination of wound macrophag-es, mainly through genetically programmed cell death (apoptosis), which plays a significant role in the regulatory mechanisms of the inflammato-ry process.
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Vuarchey, Clément, Sushil Kumar, and Reto Schwendener. "Albumin coated liposomes: a novel platform for macrophage specific drug delivery." Nanotechnology Development 1, no. 1 (July 19, 2011): 2. http://dx.doi.org/10.4081/nd.2011.e2.

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Here we report a new and efficient approach of macrophage specific drug delivery by coating liposomes with albumin. Activated albumin was reacted with liposomes containing polyethylene glycol (PEG) as hydrophilic spacers to create a flexible layer of covalently bound albumin molecules on the liposome surface. Albumin coated liposomes were taken up faster and more efficiently than uncoated liposomes by murine macrophages. Liposome uptake was significantly higher in macropha - ges as compared to other cell types tested (endothelial cells, fibroblasts, tumor cells), suggesting specificity for macrophages. In vivo, splenic macrophages phagocytosed BSA coated liposomes (BSA-L) at faster rates compared to conventional liposomes (L) and PEG liposomes (PEG-L). To prove the effectiveness of this new macrophage specific drug carrier, the bisphosphonates clodronate and zoledronate were encapsulated in BSA-L and compared with conventional liposomes. <em>In vitro</em>, treatment of macrophages with clodronate or zoledronate in BSA-L led to cytotoxic activity within a very short time and to up to 50-fold reduced IC50 concentrations. <em>In vivo</em>, clodronate encapsulated in BSA-L depleted splenic macrophages at a 5-fold lower concentration as conventional clodronate-liposomes. Our results highlight the pharmaceutical benefits of albumin-coated liposomes for macrophage specific drug delivery.
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Liu, Shuangqing, Huilei Zhang, Yanan Li, Yana Zhang, Yangyang Bian, Yanqiong Zeng, Xiaohan Yao, et al. "S100A4 enhances protumor macrophage polarization by control of PPAR-γ-dependent induction of fatty acid oxidation." Journal for ImmunoTherapy of Cancer 9, no. 6 (June 2021): e002548. http://dx.doi.org/10.1136/jitc-2021-002548.

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BackgroundThe peroxisome proliferator-activated receptor γ (PPAR-γ)-dependent upregulation of fatty acid oxidation (FAO) mediates protumor (also known as M2-like) polarization of tumor-associated macrophages (TAMs). However, upstream factors determining PPAR-γ upregulation in TAM protumor polarization are not fully identified. S100A4 plays crucial roles in promotion of cancer malignancy and mitochondrial metabolism. The fact that macrophage-derived S100A4 is major source of extracellular S100A4 suggests that macrophages contain a high abundance of intracellular S100A4. However, whether intracellular S100A4 in macrophages also contributes to cancer malignancy by enabling TAMs to acquire M2-like protumor activity remains unknown.MethodsGrowth of tumor cells was evaluated in murine tumor models. TAMs were isolated from the tumor grafts in whole-body S100A4-knockout (KO), macrophage-specific S100A4-KO and transgenic S100A4WT−EGFP mice (expressing enhanced green fluorescent protein (EGFP) under the control of the S100A4 promoter). In vitro induction of macrophage M2 polarization was conducted by interleukin 4 (IL-4) stimulation. RNA-sequencing, real-time quantitative PCR, flow cytometry, western blotting, immunofluorescence staining and mass spectrometry were used to determine macrophage phenotype. Exogenous and endogenous FAO, FA uptake and measurement of lipid content were used to analyze macrophage metabolism.ResultsTAMs contain two subsets based on whether they express S100A4 or not and that S100A4+ subsets display protumor phenotypes. S100A4 can be induced by IL-4, an M2 activator of macrophage polarization. Mechanistically, S100A4 controls the upregulation of PPAR-γ, a transcription factor required for FAO induction during TAM protumor polarization. In S100A4+ TAMs, PPAR-γ mainly upregulates CD36, a FA transporter, to enhance FA absorption as well as FAO. In contrast, S100A4-deficient TAMs exhibited decreased protumor activity because of failure in PPAR-γ upregulation-dependent FAO induction.ConclusionsWe find that macrophagic S100A4 enhances protumor macrophage polarization as a determinant of PPAR-γ-dependent FAO induction. Accordingly, our findings provide an insight into the general mechanisms of TAM polarization toward protumor phenotypes. Therefore, our results strongly suggest that targeting macrophagic S100A4 may be a potential strategy to prevent TAMs from re-differentiation toward a protumor phenotype.
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Hansen, F., L. Stenbygaard, and T. Skovsgaard. "Reduction by granulocyte-macrophag colonystimulating factor (GM-CSF) of hematologic toxicity induced by high-dose chemotherapy in patients with metastatic breast cancer." European Journal of Cancer 29 (January 1993): S53. http://dx.doi.org/10.1016/0959-8049(93)90886-k.

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Dissertations / Theses on the topic "Macrophag"

1

Brown, Bronnwyn Elizabeth. "The role of glycation and glycoxidation of low-density lipoproteins in foam cell formation." University of Sydney. Central Clinical School, 2005. http://hdl.handle.net/2123/682.

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People with diabetes suffer from an increased incidence of atherosclerosis, possibly due to the hyperglycaemia associated with this disease. Glucose may covalently modify proteins via glycation and glycoxidation reactions. Reactive aldehydes (e.g. methylglyoxal and glycolaldehyde) generated from these glycation and glycoxidation reactions, lipid peroxidation and other metabolic pathways may also modify proteins in glycation and glycoxidation reactions. These reactions can result in the formation of advanced glycation end-products, which are increased in diabetes and associated complications such as atherosclerosis. Low-density lipoproteins (LDLs) are the main source of lipid in atherosclerotic plaques, and the lipid-laden foam cells contained within. Modification of the single protein in LDL, apolipoprotein B-100 (apo B) by glucose and aldehydes may result in recognition of these altered LDL particles by macrophage scavenger receptors and cellular accumulation of cholesteryl esters; such accumulation is characteristic of atherosclerotic foam cells. The extent and nature of the modifications of LDLs that give rise to this behaviour have been poorly characterised, especially in regards to modification/oxidation of protein versus lipid components induced by glucose and low-molecular-mass aldehydes. Therefore the aims of this project were to: 1) characterise LDL modification by glucose, methylglyoxal and glycolaldehyde; 2) examine the effect of these modified LDLs on arterial cells by monitoring cellular viability, proliferation and cholesterol and cholesteryl ester levels; and 3) examine macrophage handling of apo B from these modified LDLs. Glycolaldehyde induced more rapid and more extensive changes to LDL than methylglyoxal, which was significantly more modified than LDL exposed to glucose, in the presence or absence of Cu2+. LDL was modified by glycolaldehyde and methylglyoxal in a time- and concentration-dependent manner. These aldehyde-modified LDLs were significantly more negatively charged relative (determined by changes in relative electrophoretic mobility), more aggregated (by SDS-PAGE) and lost more Arg, Lys and Trp residues (assessed by fluorescence-based assays) than glucose-modified and control LDLs. Glucose-modified LDL had more modest increases in net negative charge, aggregation and only significantly lost Arg residues. Under the conditions examined none of the modified LDLs contained significant levels of the protein oxidation products DOPA and o-tyrosine, the lipid oxidation products 7-ketocholesterol and cholesteryl ester hydro(pero)oxides, nor marked depletion of the major antioxidant α-tocopherol or significant radical formation (EPR spectroscopy). Therefore these LDLs were glycated, but not (glyc)oxidised, and so allowed the cellular uptake of glycated LDL, rather than glycoxidised LDL, to be examined. These glycated LDLs had no effect on the cellular viability (assessed by LDH release), cell protein (BCA assay), and cholesterol and cholesteryl ester levels (quantified by reverse-phase HPLC) of endothelial and smooth muscle cells. The glycated LDLs also had no effects on human and mouse macrophage viability, protein and free cholesterol levels. However, exposure of macrophages to some of the glycated LDLs resulted in significant accumulation of cholesteryl esters and apo B. The greatest cellular accumulation of cholesteryl esters was in cells exposed to glycolaldehyde-modified LDL, which occurred in a time- and concentration-dependent manner. Less cholesteryl ester accumulation was observed in cells exposed to methylglyoxal-modified LDL, but some conditions resulted in significantly more cellular cholesteryl esters as compared to control LDLs, unlike glucose-modified LDL. Macrophages endocytosed significantly more apo B from glycolaldehyde-modified LDL labelled with 125I on the apo B, than methylglyoxal-modified 125I-LDL. Apo B from methylglyoxal-modified 125I-LDL was also endocytosed and degraded in greater amounts than control 125I-LDLs, unlike glucose-modified 125I-LDLs. The glycation of LDL by some low-molecular-mass aldehydes have been shown to result in model foam cell formation as characterised by cholesteryl ester and apo B accumulation. This accumulation correlated with increases in net negative charge, aggregation and loss of Lys and Trp residues of the apo B in glycated LDL particles. However, the differences in cellular uptake of glycolaldehyde- versus methylglyoxal-modified LDL were not completely resolved and it is postulated that this may arise from the extent or type of products formed on key amino acid residues, resulting in differential uptake by macrophage scavenger receptors, rather than loss of particular amino acids per se. Therefore these studies provide a potential mechanism to explain the increased atherosclerosis in people with diabetes, and a suitable model to examine the potential inhibition of the effects of glycated LDLs. This could provide potential therapeutic interventions to reduce diabetes-induced atherosclerosis.
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2

Brown, Bronnwyn Elizabeth. "The role of glycation and glycoxidation of low-density lipoproteins in foam cell formation." Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/682.

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People with diabetes suffer from an increased incidence of atherosclerosis, possibly due to the hyperglycaemia associated with this disease. Glucose may covalently modify proteins via glycation and glycoxidation reactions. Reactive aldehydes (e.g. methylglyoxal and glycolaldehyde) generated from these glycation and glycoxidation reactions, lipid peroxidation and other metabolic pathways may also modify proteins in glycation and glycoxidation reactions. These reactions can result in the formation of advanced glycation end-products, which are increased in diabetes and associated complications such as atherosclerosis. Low-density lipoproteins (LDLs) are the main source of lipid in atherosclerotic plaques, and the lipid-laden foam cells contained within. Modification of the single protein in LDL, apolipoprotein B-100 (apo B) by glucose and aldehydes may result in recognition of these altered LDL particles by macrophage scavenger receptors and cellular accumulation of cholesteryl esters; such accumulation is characteristic of atherosclerotic foam cells. The extent and nature of the modifications of LDLs that give rise to this behaviour have been poorly characterised, especially in regards to modification/oxidation of protein versus lipid components induced by glucose and low-molecular-mass aldehydes. Therefore the aims of this project were to: 1) characterise LDL modification by glucose, methylglyoxal and glycolaldehyde; 2) examine the effect of these modified LDLs on arterial cells by monitoring cellular viability, proliferation and cholesterol and cholesteryl ester levels; and 3) examine macrophage handling of apo B from these modified LDLs. Glycolaldehyde induced more rapid and more extensive changes to LDL than methylglyoxal, which was significantly more modified than LDL exposed to glucose, in the presence or absence of Cu2+. LDL was modified by glycolaldehyde and methylglyoxal in a time- and concentration-dependent manner. These aldehyde-modified LDLs were significantly more negatively charged relative (determined by changes in relative electrophoretic mobility), more aggregated (by SDS-PAGE) and lost more Arg, Lys and Trp residues (assessed by fluorescence-based assays) than glucose-modified and control LDLs. Glucose-modified LDL had more modest increases in net negative charge, aggregation and only significantly lost Arg residues. Under the conditions examined none of the modified LDLs contained significant levels of the protein oxidation products DOPA and o-tyrosine, the lipid oxidation products 7-ketocholesterol and cholesteryl ester hydro(pero)oxides, nor marked depletion of the major antioxidant α-tocopherol or significant radical formation (EPR spectroscopy). Therefore these LDLs were glycated, but not (glyc)oxidised, and so allowed the cellular uptake of glycated LDL, rather than glycoxidised LDL, to be examined. These glycated LDLs had no effect on the cellular viability (assessed by LDH release), cell protein (BCA assay), and cholesterol and cholesteryl ester levels (quantified by reverse-phase HPLC) of endothelial and smooth muscle cells. The glycated LDLs also had no effects on human and mouse macrophage viability, protein and free cholesterol levels. However, exposure of macrophages to some of the glycated LDLs resulted in significant accumulation of cholesteryl esters and apo B. The greatest cellular accumulation of cholesteryl esters was in cells exposed to glycolaldehyde-modified LDL, which occurred in a time- and concentration-dependent manner. Less cholesteryl ester accumulation was observed in cells exposed to methylglyoxal-modified LDL, but some conditions resulted in significantly more cellular cholesteryl esters as compared to control LDLs, unlike glucose-modified LDL. Macrophages endocytosed significantly more apo B from glycolaldehyde-modified LDL labelled with 125I on the apo B, than methylglyoxal-modified 125I-LDL. Apo B from methylglyoxal-modified 125I-LDL was also endocytosed and degraded in greater amounts than control 125I-LDLs, unlike glucose-modified 125I-LDLs. The glycation of LDL by some low-molecular-mass aldehydes have been shown to result in model foam cell formation as characterised by cholesteryl ester and apo B accumulation. This accumulation correlated with increases in net negative charge, aggregation and loss of Lys and Trp residues of the apo B in glycated LDL particles. However, the differences in cellular uptake of glycolaldehyde- versus methylglyoxal-modified LDL were not completely resolved and it is postulated that this may arise from the extent or type of products formed on key amino acid residues, resulting in differential uptake by macrophage scavenger receptors, rather than loss of particular amino acids per se. Therefore these studies provide a potential mechanism to explain the increased atherosclerosis in people with diabetes, and a suitable model to examine the potential inhibition of the effects of glycated LDLs. This could provide potential therapeutic interventions to reduce diabetes-induced atherosclerosis.
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3

Svensson, Ulf. "Macrophage activation by bacteria signalling to prostaglandin and cytokine responses /." Lund : Dept. of Medical & Physiological Chemistry, Lund University, 1994. http://books.google.com/books?id=sAhrAAAAMAAJ.

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4

Higuera, González Laura 1993. "Novel transcription regulators of tissue macrophages and alternative macrophage polarization." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/672702.

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Macrophages play crucial roles in the defense of the organism against a wide range of pathogens. Macrophages can rapidly adapt to perturbations in the microenvironment due to the existence of a network of transcription factors that modulates their responses. While transcription factors that regulate macrophage identity have been widely described in the past decades, the role of transcription regulators that fine-tune tissue macrophage responses in homeostasis and infection is starting to be elucidated. Our group has previously identified transcription regulators of pro-inflammatory macrophage responses, and in the present work we have explored the function of novel transcription mechanisms that participate in the regulation of the homeostatic distribution of tissue macrophages and in anti-inflammatory macrophage responses. We have studied ontogenically different macrophage populations inhabiting different tissues and have characterized their transcription regulation. We have also compared the anti-inflammatory response of tissue macrophages and identified a specific transcriptional control of anti-inflammatory gene expression that depends on their ontogeny.
Los macrófagos juegan un papel muy importante en la defensa del organismo frente a una amplia variedad de patógenos. Los macrófagos se adaptan rápidamente a las perturbaciones en el microambiente gracias a que existe una compleja red de factores de transcripción que modulan sus respuestas. En los últimos años se han identificado factores de transcripción que regulan la identidad de los macrófagos, sin embargo, apenas se está comenzando a conocer la importancia de otros factores de transcripción que permiten adaptar la respuesta de los macrófagos, tanto en condiciones homeostáticas como frente a infecciones. Anteriormente nuestro grupo identificó reguladores transcripcionales de las respuestas pro-inflamatorias de los macrófagos, y en este trabajo hemos explorado la función de nuevos mecanismos reguladores que participan en la regulación de la distribución de los macrófagos en homeostasis, así como en las respuestas anti-inflamatorias de los macrófagos. Hemos estudiado poblaciones de macrófagos con diferentes ontogenias que habitan dentro de los tejidos y hemos caracterizado su regulación transcripcional. Además, hemos comparado la respuesta anti-inflamatoria de los diferentes macrófagos tisulares y así hemos identificado que existe un mecanismo transcripcional específico que controla la expresión de genes anti-inflamatorios según el origen del macrófago.
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5

Tabata, Yasuhiko. "Macrophage phagocytosis of polymer microspheres and antitumor activation of macrophages." Kyoto University, 1987. http://hdl.handle.net/2433/74704.

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6

Raborn, Erinn Shenee. "Cannabinoid Modulation of Chemotaxis of Macrophages and Macrophage-like Cells." VCU Scholars Compass, 2007. http://hdl.handle.net/10156/1333.

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7

Grand-Perret, Thierry A. R. "Induction d'une activité anti-tumorale chez les macrophages péritonéaux murins." Paris 11, 1986. http://www.theses.fr/1986PA112301.

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Di, Maggio Paula. "Dietary lipids and inflammation : chylomicron remnants suppress pro-inflammatory pathways and activate antioxidant defence mechanisms in human macrophages." Thesis, Royal Veterinary College (University of London), 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618287.

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Georges, George Tharwat. "Novel Characteristics of Murine Bone Marrow-Derived Macrophages and Human Macrophage-Like Cells." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/932.

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These studies provide evidence for novel properties of macrophages derived from bone marrow stem cells. In study 1, treatment of activated mouse bone marrow-derived macrophages (BMM) with either catecholamine synthesis inhibitors (α-methyl-para-tyrosine and fusaric acid) or the β2 adrenergic receptor antagonist ICI 118,551 demonstrated that BMM produce catecholamines. The catecholamines modulated macrophage cytokine production through autocrine actions on adrenergic receptors. In study II, undifferentiated human bone marrow cells were incubated in 30% mouse L929 fibroblast conditioned medium and generated adherent cells within three days. The cells were clearly identifiable as macrophages based on surface proteins and phagocytic activity but produced only low levels of the cytokines tumor necrosis factor-α and interleukin-lβ. Cytokine production did not increase in response to the bacterial endotoxin lipopolysaccharide (LPS). Generation of these macrophage-like cells was not repeatable with other samples of human bone marrow, but the cells continue to proliferate in cell culture and will be investigated further in future studies.
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Adler, Heiko. "Fetal bovine bone marrow-derived macrophages : a model for studying basic aspects of macrophage biology and pathogen-macrophage interaction in cattle /." [S.l.] : [s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Books on the topic "Macrophag"

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E, Lewis Claire, and McGee J. O'D, eds. The Macrophage. Oxford: IRL Press at Oxford University Press, 1992.

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Kloc, Malgorzata, ed. Macrophages. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54090-0.

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Rousselet, Germain, ed. Macrophages. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3.

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Röszer, Tamás. The M2 Macrophage. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50480-9.

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1943-, Zwilling Bruce S., and Eisenstein Toby K, eds. Macrophage-pathogen interactions. New York: M. Dekker, 1994.

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Herbein, Georges. HIV and the macrophage. Kerala, India: Transworld Research Network, 2007.

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Gupta, Swati, and Yashwant V. Pathak, eds. Macrophage Targeted Delivery Systems. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-84164-5.

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Russell, Stephen W., and Siamon Gordon, eds. Macrophage Biology and Activation. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77377-8.

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Harris, James, and Eric F. Morand, eds. Macrophage Migration Inhibitory Factor. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-4939-9936-1.

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1929-, Staub Norman C., ed. The Pulmonary intravascular macrophage. Mount Kisco, NY: Futura Pub. Co., 1989.

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Book chapters on the topic "Macrophag"

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Brown, E. J. "Integrins of Macrophages and Macrophage-Like Cells." In Handbook of Experimental Pharmacology, 111–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55742-2_7.

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Kelly, Aoife, Aleksander M. Grabiec, and Mark A. Travis. "Culture of Human Monocyte-Derived Macrophages." In Macrophages, 1–11. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_1.

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Ian Cumming, R., and Yen-Rei A. Yu. "Phenotyping Tumor-Associated Macrophages." In Macrophages, 99–109. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_10.

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Dalby, Elizabeth. "Activating Murine Macrophages In Vitro." In Macrophages, 111–17. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_11.

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Huang, Xuan, Yong Li, Mingui Fu, and Hong-Bo Xin. "Polarizing Macrophages In Vitro." In Macrophages, 119–26. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_12.

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Roback, Linda, and Lisa P. Daley-Bauer. "Viral Replication Assay in Bone Marrow-Derived Macrophages." In Macrophages, 127–34. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_13.

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Aribi, Mourad. "Macrophage Bactericidal Assays." In Macrophages, 135–49. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_14.

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Montaño, Fernando, Sergio Grinstein, and Roni Levin. "Quantitative Phagocytosis Assays in Primary and Cultured Macrophages." In Macrophages, 151–63. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_15.

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Mularski, Anna, Florence Marie-Anaïs, Julie Mazzolini, and Florence Niedergang. "Observing Frustrated Phagocytosis and Phagosome Formation and Closure Using Total Internal Reflection Fluorescence Microscopy (TIRFM)." In Macrophages, 165–75. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_16.

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Rousselet, Germain. "Chromatin Immunoprecipitation in Macrophages." In Macrophages, 177–86. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_17.

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Conference papers on the topic "Macrophag"

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van Dam-Mieras, M. C. E., A. D. Muller, and G. Hornstra. "DIETARY LIPIDS, INFECTION AND MACROPHAGE PROCOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643398.

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It is generally accepted that the type of dietary fat influences arterial thrombosis and atherosclerosis. Although it is still largely unknown how the dietary lipid composition influences the process of atherogenesis, it is evident that several cell types are involved. Morphological evidence for the involvement of monocyte/macropages has been given.We described before that the dietary lipid composition has striking effects on the procoagulant activity of macrophages. When macrophages were isolated from the spleens of healthy rats the procoagulant activity slightly decreased during the first few hours after isolation, and reached a plateau value after 4 hours. When, however, macrophages were obtained from animals infected with a pneumona virus (PVM) different results were obtained:Experiments carried out with peripheral blood monocytes showed close resemblance to those described in the table.These results show that:- moncytes/macrophages isolated from PVM-infected animals increase their procoagulant activity during in vitro culture- the differences in macrophage procoagulant activity found in cells obtained from healthy animals fed diets containing different lipids no longer were found in PVM-infected animalsThis would implicate that the infection process has a more profound influence on macrophage procoagulant activity that the composition of the diet
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Reinhard, Björn M., Hongyun Wang, and Linxi Wu. "Monitoring Cellular Trafficking of Nanoparticle Cargo in Murine Macrophages Through Plasmon Coupling Microscopy." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93078.

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A detailed analysis of silver nanoparticle (NP) uptake and trafficking in the murine macrophage cell line J774A.1 through spectral analysis of the resonance wavelength of the metal NP cargo is presented. The NP spectra reveal a strong phenotypic variability in the NP uptake and processing on the single cell level. Cells containing non- or low-agglomerated NPs are found to coexist with cells containing NPs of varying degrees of NP agglomeration, clearly indicated by a spectral red-shift in the resonance wavelength. Pharmacological inhibition studies indicate that the observed differences in the intracellular NP organization result from coexisting actin- and clathrin-dependent endocytosis mechanisms. Correlation with fluorescence macrophage maturity markers shows that differentiated J774A.1 macrophages preferentially contain compact NP agglomerates, whereas monocyte-like macrophages contain non-agglomerated NPs.
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Mahgoub, Yasmine, Rida Arif, and Susu Zughaier. "Pyocyanin pigment from Pseudomonas aeruginosa modulates innate immune defenses in macrophages." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0137.

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Background: Pseudomonas aeruginosa is a well-known opportunistic pathogen. The gram-negative bacillus, commonly associated with hospital-acquired infections, utilizes the host’s impaired immune responses to establish infection. Of its many virulence factors, pyocyanin is essential for P. aeruginosa to establish its full infectivity. Macrophages act as sentinels of the innate immune system, as well as play other roles in homeostasis, tissue remodeling, and bridging between the innate and adaptive immune systems. Aim: This study aimed to investigate the effects of pyocyanin on macrophage innate immune defenses by assessing the function of macrophages treated with pyocyanin and TLR ligands. Phagocytosis of opsonized zymosan, LPS-induced nitric oxide release and cytokine release were used as measures of functional responses. Results: This study found that pyocyanin inhibited phagocytosis-induced ROS release in a dose-dependent manner and reduced nitric oxide release from macrophages induced with P. aeruginosa LPS. In addition, pyocyanin modulated cytokines and chemokines release from macrophages exposed to P. aeruginosa LPS in a dose-dependent manner. Pyocyanin significantly enhanced IL-1β release as well as several chemokines. Therefore, pyocyanin facilitates Pseudomonas aeruginosa to persevere in the immunocompromised host through modulating macrophage’s innate immune defenses. Conclusion: Pyocyanin inhibits macrophage functional defense responses to facilitate Pseudomonas aeruginosa infection.
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McGee, Maria, and Henry Rothberger. "MECHANISMS OF PROCOAGULANT GENERATION BY ALVEOLAR MACROPHAGES DURING MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643168.

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During maturation in vivo and in vitro alveolar macrophages generate procoagulant(s) capable of activating the extrinsic pathway. It is generally agreed that at least part of the activity is due to TF (tissue factor). However, whether or not macrophages also generate functional factor VII or X is controversial. To characterize procoagulant activity increases, we measured kinetic parameters defining interactions between components of the TF-VII complex on membranes of alveolar macrophages either freshly isolated or cultured in serum free medium. In incubation mixtures with fixed concentrations of macrophages and added factor VII, the rate of factor Xa formation (measured by S-2222 hydrolysis) approached a maximum as factor X concentration was increased. Estimated concentrations of factor X yielding 1/2 maximal activation rates, (apparent Km) were 127.1±26 nM and 99.7±34 nM for fresh and cultured cells, respectively. Vmax (maximal velocities) were 1.21±0.24 and 8.9±5 nM Xa/min/106 cells. When concentrations of added factor X were kept constant, the rate of factor X activation increased as the added factor VII concentration was increased. For fresh and cultured cells, the respective apparent Kd were 1.810.7 and 1.410.25 nM. Maximal rates observed with X concentration fixed at 108 nM were 0.46±10.06 and 5.7±1.6 nM Xa/min/106 cells. In the absence of either added factor X or added factor VII, no factor Xa generation was detected in fresh or cultured cells, during 10-20 min incubation periods used for kinetic studies. The observed increase in Vmax without changes in apparent Km and Kd indicate that gains in procoagulant activity during macrophage maturation are due to increases in the number of functional binding sites for factor VII, without significant generation of functional vitamin K dependent factors (VII and X) by the cells. The data also indicate that maturation does not alter the rate behaviour of the TF-VII enzymatic complex on macrophage membranes. Mechanisms of complex assembly that we observed on macrophage membranes are similar to those described for the TF-VII complex assembly on purified systems.
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Adany, R., A. Kiss, J. Kappelmayer, R. J. Ablin, and L. Muszbek. "EXPRESSION OF FACTOR XIII SUBUNIT A IN DIFFERENT TYPES OF HUMAN MACROPHAGES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644651.

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In addition to plasma the presence of subunit a of blood coagulation Factor XIII (FXIIl) has been verified in platelets and megakariocytes. Most recently, we demonstrated that human peripheral blood monocytes also contain FXIII subunit a. The present study was designed 1/ to determine the stage in the maturation sequence of bone marrow monocytopoesis in which FXIII appears 2/ to establish if FXIII is retained during differentiation into macrophages 3/ to assess how general is the presence of FXIII subunit a in different types of macrophages. FXIII subunit a was immunomorphologically detected in bone marrow smears, in cytospin preparations of cells from serous cavities (pleural, peritoneal, pericardial and synovial spaces), and paraformaldehyde-fixed paraffin-embedded or frozen sections of different organs where classical types of macrophages have been described earlier (liver, lung, thymus, skin, connective tissue, prostate and developing bone) . Cells containing FXIII subunit a were intensively characterized by immunofluorescent and enzymecytochemical techniques in double and treble labeling systems. Its presence was clearly demonstrated in promonocytes of bone marrow, and in all probability, it is present in monoblasts, as well. FXIII was also found in macrophages from different serous cavities and in embryonic osteoclasts. Cells containing FXIII subunit a of connective tissue were found to be tissue histiocytes, and not fibroblasts as previously thought. Kupffer cells of the liver and Langerhans cells of the epidermis were negative supporting theories that these cells are not members of monocyte-derived macrophage cell population. Immunomorphological detection of FXIII subunit a seems to be a useful marker for labeling the continuum of monocyte/macrophage cell line from the earliest ftrais in the bone marrow to the mature forms of macrophages and might be a valuable tool in the cytological diagnosis of malignant disorders of this cell line.
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Gijsen, Frank, Anna Ten Have, Jolanda Wentzel, and Antonius Van Der Steen. "Temperature Measurement of Advanced Murine Atherosclerotic Plaques." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176307.

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Ischaemic heart disease is most frequently caused by coronary atherosclerosis, of which the vulnerable plaque is one of the developmental stages. Rupture of a vulnerable plaque with superimposed thrombosis frequently leads to acute coronary syndromes. The major components of a vulnerable plaque are a lipid-rich, atheromatous core, and a thin fibrous cap with macrophage and macrophage infiltration (Schaar et al., 2004). After the first paper suggesting the possibility of thermographic detection of vulnerable plaques (Casscells et al., 1996), intracoronary thermography as a vulnerable plaque detection technique has been investigated. Increased metabolic activity of macrophages is suggested as the main reasons for the increased temperatures (ten Have et al., 2005).
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Muszbek, L., and R. Adány. "CELLULAR DISTIBUTION OF FACTOR XIII IN HUMAN UTERUS AND PLACENTA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644648.

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As spontaneous abortion is a frequent finding in females with Factor XIII (FXIIl) deficiency it has been presumed that the plasmatic or cellular form of this clotting factor is essential to normal fetus development. In this context it is of special interestthat FXIII subunit a has been demonstrated in the homoge-nate of human uterus and placenta by activity measurements and immunobiochemical methods. However, no information on its cellular distribution has beenpublished, so far. In the present study first FXIII subunit a was detected in paraformaldehyde-fixed, paraffin-embedded sections by immunoperoxidase technique. FXIII containing cells were localized in the connective tissue of uterus and in the mesenchyme of placental chorionic villi. Though in a single report FXIII containing connective tissue cells were interpreted as fibroblasts (Fear et al., J.Clin.Pathoi.,37,560, 1984) the mononuclear, multipolar, stellate morphological appearance of these cells suggested that they rather belong to the monocyte/macrophage cell line. To characterize them the immuno-fluorescent detection of FXIII subunit a was combined by the visualization of different marker antigens for tissue macrophages (RFDT, Leu M3, HLA-DR) and fibroblasts (IIG10) on frozen sections. The coexpression of FXIII subunit a with RFD7 and Leu M3 macrophage markers, butnot with fibroblast membrane antigen IIG10 clearly proves that FXIII containing cells both in the uterusand in the placenta are tissue macrophages. HLA-DR was strongly expressed in cells positive for FXIII subunit a. in the uterus, but not or only very weakly in the placental mesenchyme, which might be due to the relative absence of extrinsic antigens during fetal development. The morphological findings on the presence of FXIII subunit a in placental macrophages were further strengthened by immunobiochemical experiments. FXIII subunit a, but not b content of isolated placental macrophages was also verified by immunoblotting, while fibroblasts were shown to be exemptof this factor. The results well agree with our previous findings demonstrating FXIII subunit a in humanmonocytes and peritoneal macrophages (Muszbek et al., Thrombos. Res. ,37, 401,1985; Adány et al. , Eur.J.Cell Biol.,38,171,1985).
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DUBOR, F., A. M. DOSNE, and L. CHEDID. "Effect of dexamethasone and endothelial cell supernatant on u-PA produced by human promyelocyte cells treated with phorbol myristate acetate (PMA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643191.

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After treatment with PMA the human promyelocytic HL60 cells were induced to differentiate into a monocyte-macrophage population and to produce a high amount of plasminogen activator in the supernatant. This response was detected from 0,5 ng/ml of PMA and culminated at 5 ng. The plasminogen activator appeared of urokinase-type as showed by fibrinenzymographic analysis : the enzymatic profile of cell supernatant showed 2 lysis band (Mr 33.000 and 55.000) corresponding to those of urokinase of low and high mol. weight. Dexamethasone (100 pM) suppressed the production of this macrophage u-PA without evidence of plasminogen activator inhibitor (PAI) generation in the supernatant : free PAI was not detected in urokinase inhibition assays ; complexes of u-PA-PAI were not observed in fibrinoenzymographic studies. Supernatant of human endothelial cells added to HL60 cell supernatant neutralized the two molecular species of macrophage u-PA and gave rise to complexes (Mr 110.000 and 84.000) detected by fibrinoenzymography. These results suggested different possible levels for controlling u-PA of inflammatory macrophages including interaction with endothelial cells secretion since endothelial PAI is increased by some inflammatory monokine and also by dexamethasone, it appears that endothelium could have a regulatory role on inflammatory fibrinolysis.
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Belchamber, K., and E. Sapey. "S51 Hungry hungry macrophages: how multiple prey affects macrophage phagocytosis." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.56.

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Adày, R., A. Szegedi, Z. Nemes, and L. Muszbek. "EXTRAVASAL FIBRIN STABILIZATION BY FACTOR XIII IN LYMPH NODES WITH HODGKIN’S DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643667.

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The formation of extravasal fibrin deposits in various tumors has been recognized a long time ago and it has been implicated in various aspects of tumor growth. However, no adequate information is available on the nature of intratumoral fibrin. In this study we attempted to find out if fibrin deposit in human lymph nodes with Hodgkin’s disease is stabilized and made resistant to fibrinolysis by factor XIII /FXIII/ of blood coagulation. The two main tasks for FXIII in fibrin stabilization is to attach a^antiplas-min the main phyiological inhibitor of fibrinolysis to fibrin strands and crosslink fibrin chains. By double immunofluorescent labeling for fibrin and α2-antiplasmin a complete colocalization of the two antigens could be observed. A part of fibrin strands also stained for α2-antiplasmin-plasmin-complex-neoantigen revealing that α2-antiplasmin covalently linked to fibrin inhibited intratumoral fibrinolysis. The finding that immunolabeling for fibrin was preserved following the treatment of sections by concentrated urea solution clearly demonstrates that fibrin chains became crosslinked by FXIII. These results were further supported by SDS PAGE analysis of intratumoral fibrin deposits. There are two theoretical possibilities for the appearance of FXIII in the interstitial space: 1/ plasmatic FXIII can get acrossthe vessel wall when increased permeability is induced 2/ FXIII can be produced and released by certain cells of the tumorous tissue. We explored the secondpossibility by various immunomorphological and enzymcytochemical techniques. Alarge number of FXIII positive cells were detected by immunoperoxidase technique in the follicular and interfollicular region of malignant, but not in normal lymph nodes. These relatively large, multipolar, mononuclear cells possesseda macrophage-like appearance and showedANAE-positivity,i.e.,they belong to thegroup of tumor associated macrophages. FXIII containing cells were labeled by monoclonal anti-Leu M3 (a monocyte/macrophage marker), but not by anti-HLA-DR.They were often found in the immediate vicinity of malignant Hodgkin’s cells and also showed an intimate relationshipwith extravasal fibrin formation.lt is suggested that FXIII secreted byintactor released from damaged macrophages might be involved in the stabilization offibrin in the tumor stroma or around tumor cells.
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Reports on the topic "Macrophag"

1

Hanna, Philip C. Macrophage Responses to B. Anthracis. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada456287.

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Peterson, Scott N. Macrophage Responses to B. Anthracis. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada428855.

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Broaddus, V. C. Role of Macrophage-induced Inflammation in Mesothelioma. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada582550.

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Abrass, Itamar B., and Christine K. Abrass. Influence of Stress-Induced Catecholamines on Macrophage Phagocytosis. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/ada206608.

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Blystone, Robert V. Image Analysis of Viral-Expressing Mouse Macrophage Cells. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada238230.

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Havell, Edward A. Actions of Interferons on Macrophages. Fort Belvoir, VA: Defense Technical Information Center, June 1985. http://dx.doi.org/10.21236/ada157006.

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Groopman, Jerome E. Pathobiology of HTLV-III/LAV In Human Monocyte-Macrophage. Fort Belvoir, VA: Defense Technical Information Center, April 1990. http://dx.doi.org/10.21236/ada221724.

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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

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Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.
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Laouar, A., C. B. H. Chubb, F. Collart, and E. Huberman. Human macrophage differentiation involves an interaction between integrins and fibronectin. Office of Scientific and Technical Information (OSTI), November 1996. http://dx.doi.org/10.2172/495739.

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Laouar, A., C. B. H. Chubb, F. Collart, and E. Huberman. Human macrophage differentiation involves an interaction between integrins and fibronectin. Office of Scientific and Technical Information (OSTI), March 1997. http://dx.doi.org/10.2172/515532.

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