414 results on '"Andreas Schober"'
Search Results
402. Alternate coexistence of NADPH-diaphorase with choline acetyltransferase or somatostatin in the rat neostriatum and basal forebrain
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Andreas Schober, Hans Luppa, and Kurt Brauer
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NADPH dehydrogenase ,Medial septal nucleus ,Basal forebrain ,Histology ,Physiology ,Cell Biology ,Biology ,Biochemistry ,Choline acetyltransferase ,Molecular biology ,Pathology and Forensic Medicine ,Ventral pallidum ,medicine.anatomical_structure ,Somatostatin ,nervous system ,Diaphorase ,medicine ,Cholinergic neuron - Abstract
The coexistence of reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) with somatostatin (SOM) and choline acetyltransferase (ChAT) was compared between the rat neostriatum (ST) and basal forebrain complex (BF) . NADPH-d coexists with SOM in ST, but not in the ventral pallidum (VP), in the substantia innominata-nucleus basalis complex (SI-NB) and in the magnocellular preoptic nucleus (NPM) of the BF. In the medial septal nucleus as well as in the vertical and the horizontal limbs of the diagonal band (MS-vDB, hDB) representing the rostral BF and in the SI-NB, a high number of ChAT-positive cells also contain NADPH-d. The NPM shows a smaller number of double-stained cholinergic neurons. The functional significance of the NADPH-d coexistence in BF cholinergic cells is still unknown.
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- 1989
403. Serotoninergic raphe nuclei projection to the basal forebrain in the rat: A combined HRP- and 5-HT-immunohistochemical investigation
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Hans Luppa, Andreas Schober, and Wilfried Schober
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medicine.medical_specialty ,Basal forebrain ,Histology ,Physiology ,Cell Biology ,Biology ,Serotonergic ,Biochemistry ,Pathology and Forensic Medicine ,Endocrinology ,Internal medicine ,medicine ,Immunohistochemistry ,Serotonin ,Raphe nuclei ,5-HT receptor - Published
- 1989
404. Determination of equine serum inhibitors for poliovirus by the gel-adsorption technique
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R. Thomssen, Gerrit Koehne-Barleben, and Andreas Schober
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Hot Temperature ,Globulin ,viruses ,medicine.disease_cause ,Antiviral Agents ,Virus ,Antigen-Antibody Reactions ,chemistry.chemical_compound ,Neutralization Tests ,Virology ,Centrifugation, Density Gradient ,medicine ,Animals ,Centrifugation ,Horses ,Infectivity ,Chromatography ,biology ,Immune Sera ,Poliovirus ,Phosphorus Isotopes ,General Medicine ,Molecular biology ,Papain ,Immunoglobulin M ,chemistry ,Sephadex ,Mutation ,Chromatography, Gel ,biology.protein ,Adsorption ,Antibody - Abstract
Inhibitors found in certain equine sera active against poliovirus type 1 have been determined by the gel-adsorption method using aluminiumhydroxide-gel in the absence of cells. The inhibitor belongs to the 19S-class of macroglobulins (IgM), as revealed by gel-filtration with Sephadex G 200, by DEAE-cellulose-chromatography, and by sucrose density centrifugation. It is bound to the viral surface in-vitro in the absence of tissue cells. The specific complex may be precipitated with anti-equine globulin from rabbits. The inhibitor is destroyed by papain and by 2-mercapto-ethanol. The “residual infectivity” (10–25%) has been found bound to the inhibitor in-vitro. Its behavior in the gel-adsorption system is not altered if the virus-inhibitor complexes have previously been diluted. — Nonsensitive mutants and double mutants have been selected. There must exist at least three different combining sites for equine inhibitors on the surface of poliovirus type 1, strain Mahoney. Equine sera may be grouped according to the specificity of their inhibitory activity. The specific binding capacity is lost if the virus is heated at 50° C for 30 min.
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- 1966
405. In-vitro-Stimulation der Lymphozyten von HB-Antikörper-Trägern durch HB-Antigen (Australia -Antigen)*
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Ulrich H. Koszinowski, Andreas Schober, and Reiner Thomssen
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biology ,medicine.diagnostic_test ,Chemistry ,Stimulation ,Radioimmunoassay ,General Medicine ,Immunoelectrophoresis ,Precipitin ,In vitro ,Antigen ,Macrophage-1 antigen ,Immunology ,biology.protein ,medicine ,Antibody - Published
- 1973
406. Lipoprotein-Derived Lysophosphatidic Acid Promotes Atherosclerosis by Releasing CXCL1 from the Endothelium
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Andreas Schober, Jean Sébastien Saulnier-Blache, Oliver Soehnlein, Markus Reinholz, Ela Karshovska, Christian Weber, Gueler Sevilmis, Brigitta Globke, Jerold Chun, Kathrin Heyll, Zhe Zhou, Pallavi Subramanian, Remco T. A. Megens, Marc A. M. J. van Zandvoort, Pathologie, Fysiologie, Biomedische Technologie, and RS: CARIM School for Cardiovascular Diseases
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Endothelium ,Physiology ,Chemokine CXCL1 ,Hyperlipidemias ,Monocytes ,chemistry.chemical_compound ,Mice ,Apolipoproteins E ,Lysophosphatidic acid ,medicine ,Animals ,RNA, Small Interfering ,Receptors, Lysophosphatidic Acid ,Receptor ,Molecular Biology ,Cells, Cultured ,Mice, Knockout ,Monocyte ,Macrophages ,Cell Biology ,Atherosclerosis ,Cell biology ,CXCL1 ,Lipoproteins, LDL ,Mice, Inbred C57BL ,Lysophosphatidylcholine ,medicine.anatomical_structure ,Carotid Arteries ,chemistry ,Immunology ,Diet, Atherogenic ,lipids (amino acids, peptides, and proteins) ,Endothelium, Vascular ,Autotaxin ,Lysophospholipids ,biological phenomena, cell phenomena, and immunity ,Lipoprotein - Abstract
SummaryOxidatively modified low-density lipoprotein (oxLDL) plays a key role in the initiation of atherosclerosis by increasing monocyte adhesion. The mechanism that is responsible for the oxLDL-induced atherogenic monocyte recruitment in vivo, however, still remains unknown. Oxidation of LDL generates lysophosphatidylcholine, which is the main substrate for the lysophosphatidic acid (LPA) generating enzyme autotaxin. We show that oxLDL requires endothelial LPA receptors and autotaxin to elicit CXCL1-dependent arterial monocyte adhesion. Unsaturated LPA releases endothelial CXCL1, which is subsequently immobilized on the cell surface and mediates LPA-induced monocyte adhesion. Local and systemic application of LPA accelerates the progression of atherosclerosis in mice. Blocking the LPA receptors LPA1 and LPA3 reduced hyperlipidemia-induced arterial leukocyte arrest and atherosclerosis in the presence of functional CXCL1. Thus, atherogenic monocyte recruitment mediated by hyperlipidemia and modified LDL crucially depends on LPA, which triggers endothelial deposition of CXCL1, revealing LPA signaling as a target for cardiovascular disease treatments.
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407. Regulation of GDF-15, a distant TGF-β superfamily member, in a mouse model of cerebral ischemia
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Katharina Schindowski, Oliver Herrmann, Andreas Schober, Klaus Unsicker, Markus Schwaninger, Oliver von Bohlen und Halbach, Dirk A. Ridder, and Jens Strelau
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Male ,Pathology ,medicine.medical_specialty ,Middle Cerebral Artery ,Growth Differentiation Factor 15 ,Histology ,Hippocampus ,Substantia nigra ,Expression ,Biology ,Hippocampal formation ,Brain Ischemia ,Pathology and Forensic Medicine ,Lesion ,Mice ,Neurotrophic factors ,Ischemia ,Transforming Growth Factor beta ,Cortex (anatomy) ,medicine ,Animals ,RNA, Messenger ,Cells, Cultured ,Cerebral Cortex ,Neurons ,Dentate gyrus ,Regular Article ,Cerebral Infarction ,Cell Biology ,GDF-15 knockout ,Up-Regulation ,Mice, Inbred C57BL ,medicine.anatomical_structure ,Growth/differentiation factor-15 ,Gene Expression Regulation ,nervous system ,Models, Animal ,embryonic structures ,biology.protein ,Cortex ,Mouse (adult, male, C57BL/6) ,medicine.symptom ,NeuN ,Occlusion of the middle cerebral artery - Abstract
GDF-15 is a novel distant member of the TGF-β superfamily and is widely distributed in the brain and peripheral nervous system. We have previously reported that GDF-15 is a potent neurotrophic factor for lesioned dopaminergic neurons in the substantia nigra, and that GDF-15-deficient mice show progressive postnatal losses of motor and sensory neurons. We have now investigated the regulation of GDF-15 mRNA and immunoreactivity in the murine hippocampal formation and selected cortical areas following an ischemic lesion by occlusion of the middle cerebral artery (MCAO). MCAO prominently upregulates GDF-15 mRNA in the hippocampus and parietal cortex at 3 h and 24 h after lesion. GDF-15 immunoreactivity, which is hardly detectable in the unlesioned brain, is drastically upregulated in neurons identified by double-staining with NeuN. NeuN staining reveals that most, if not all, neurons in the granular layer of the dentate gyrus and pyramidal layers of the cornu ammonis become GDF-15-immunoreactive. Moderate induction of GDF-15 immunoreactivity has been observed in a small number of microglial cells identified by labeling with tomato lectin, whereas astroglial cells remain GDF-15-negative after MCAO. Comparative analysis of the size of the infarcted area after MCAO in GDF-15 wild-type and knockout mice has failed to reveal significant differences. Together, our data substantiate the notion that GDF-15 is prominently upregulated in the lesioned brain and might be involved in orchestrating post-lesional responses other than the trophic support of neurons.
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408. Inapparent infections in the course of an epidemic of Australia-SH-antigen positive hepatitis
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Reiner Thomssen, Worch R, U. Kaboth, and Andreas Schober
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Hepatitis ,Cross Infection ,Hepatitis B virus ,Immunodiffusion ,business.industry ,Germany, West ,Outbreak ,Jaundice ,Hepatitis A ,medicine.disease ,Complement fixation test ,Virology ,Incubation period ,Disease Outbreaks ,Hepatitis B Antigens ,Antigen ,Pediatrics, Perinatology and Child Health ,Immunology ,medicine ,Humans ,medicine.symptom ,business ,SH antigen ,Transaminases - Abstract
Two forms of infectious jaundice are recognized, serum hepatitis (with a long incubation period), in which Australia-SH antigen can be demonstrated in the patient's serum1,2; and infectious hepatitis (with a short incubation period), in which Australia-SH antigen cannot be demonstrated. Previously studied local outbreaks of infectious hepatitis were all Australia-SH-antigen negative2-7(our observations in three epidemics). It has not been possible in these to assess whether in addition to the apparent forms there have also been inapparent ones without jaundice or elevated serum transaminase levels. Between March 20 and April 30, 1970, 18 pulmonary disease patients in a hospital developed acute hepatitis as shown by high values of transaminases, jaundice, and subjective symptoms. Eleven of these patients (61%) were found positive for Australia-SH antigen tested by immunodiffusion and complement fixation assay (Figure). Since the examination for Australia-SH antigen was not performed until the middle of May 1970, the
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- 1972
409. Hamming chromatography
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Andreas Schwienhorst, Andreas Schober, Rolf G�nther, and Peter F. Stadler
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Chromatography ,Base Sequence ,Organic Chemistry ,Nucleic Acid Hybridization ,General Medicine ,DNA ,Catalysis ,Inorganic Chemistry ,RNA, Transfer, Phe ,Bacteriophage T7 ,Drug Discovery ,DNA, Viral ,Physical and Theoretical Chemistry ,Cloning, Molecular ,Directed Molecular Evolution ,Promoter Regions, Genetic ,Molecular Biology ,Information Systems - Abstract
Selection of molecules with desired properties from random pools of biopolymers has become a powerful tool in biotechnology. On designing an evolution experiment, a certain knowledge of the concomitant fitness landscape is clearly helpful to set up the optimal experimental conditions. The correlation function is a useful means of characterizing a given landscape, since it can be efficiently measured if one has a method of separating a pool of random sequences according to their Hamming distance from a moderately small number of test sequences. In this paper we describe a special type of hybridization chromatography, where a mixture of oligomers (partially) complementary to a given test sequence is hybridized to the test sequence, covalently bound to a matrix. DNA oligomers are eluted in an 'effective temperature gradient' using conditions that minimize the differences of effects of GC versus AT pairs on the melting temperatures. This method should be a means to quickly separate error classes and thus be the crucial step in characterizing fitness landscapes of biopolymers through an experimental approach. It would also be a useful tool to design sequence pools with a bias towards desired mutant spectra.
410. Persistent expression of BMP-4 in embryonic chick adrenal cortical cells and its role in chromaffin cell development
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Andreas Schober, Uwe Ernsberger, Aylin Franke, Oliver von Bohlen und Halbach, Hermann Rohrer, Katrin Huber, Chaya Kalcheim, Klaus Unsicker, Barbara Brühl, and Shlomi Krispin
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medicine.medical_specialty ,endocrine system ,animal structures ,Tyrosine 3-Monooxygenase ,Chromaffin Cells ,Fluorescent Antibody Technique ,Bone Morphogenetic Protein 4 ,CHO Cells ,Chick Embryo ,Biology ,Cell fate determination ,Steroidogenic Factor 1 ,Bone morphogenetic protein ,lcsh:RC346-429 ,Tissue Culture Techniques ,Dorsal aorta ,Cricetulus ,Developmental Neuroscience ,Pregnancy ,Cricetinae ,Internal medicine ,ddc:570 ,Adrenal Glands ,medicine ,Animals ,Bone Morphogenetic Protein Receptors, Type I ,In Situ Hybridization ,lcsh:Neurology. Diseases of the nervous system ,Cell Proliferation ,Neurons ,Catecholaminergic ,Ganglia, Sympathetic ,Reverse Transcriptase Polymerase Chain Reaction ,Cell growth ,Gene Expression Regulation, Developmental ,Neural crest ,Immunohistochemistry ,Cell biology ,Microscopy, Electron ,medicine.anatomical_structure ,Endocrinology ,Bone morphogenetic protein 4 ,Chromaffin cell ,embryonic structures ,Female ,Research Article - Abstract
BackgroundAdrenal chromaffin cells and sympathetic neurons both originate from the neural crest, yet signals that trigger chromaffin development remain elusive. Bone morphogenetic proteins (BMPs) emanating from the dorsal aorta are important signals for the induction of a sympathoadrenal catecholaminergic cell fate.ResultsWe report here that BMP-4 is also expressed by adrenal cortical cells throughout chick embryonic development, suggesting a putative role in chromaffin cell development. Moreover, bone morphogenetic protein receptor IA is expressed by both cortical and chromaffin cells. Inhibiting BMP-4 with noggin prevents the increase in the number of tyrosine hydroxylase positive cells in adrenal explants without affecting cell proliferation. Hence, adrenal BMP-4 is likely to induce tyrosine hydroxylase in sympathoadrenal progenitors. To investigate whether persistent BMP-4 exposure is able to induce chromaffin traits in sympathetic ganglia, we locally grafted BMP-4 overexpressing cells next to sympathetic ganglia. Embryonic day 8 chick sympathetic ganglia, in addition to principal neurons, contain about 25% chromaffin-like cells. Ectopic BMP-4 did not increase this proportion, yet numbers and sizes of 'chromaffin' granules were significantly increased.ConclusionBMP-4 may serve to promote specific chromaffin traits, but is not sufficient to convert sympathetic neurons into a chromaffin phenotype.
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411. Effect of intensive care after cardiac arrest on patient outcome: a database analysis
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Martin Posch, Rene Schmutz, Michael Holzer, Philipp G. H. Metnitz, Helene Hochrieser, and Andreas Schober
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Male ,medicine.medical_specialty ,Critical Care ,Databases, Factual ,Critical Care and Intensive Care Medicine ,law.invention ,Cohort Studies ,law ,Intensive care ,Critical care nursing ,Severity of illness ,medicine ,Humans ,Prospective Studies ,Simplified Acute Physiology Score ,Prospective cohort study ,Aged ,Aged, 80 and over ,business.industry ,Research ,Middle Aged ,Intensive care unit ,Heart Arrest ,Intensive Care Units ,Treatment Outcome ,SAPS II ,Emergency medicine ,Female ,business ,Cohort study - Abstract
Introduction The study aimed to determine the impact of treatment frequency, hospital size, and capability on mortality of patients admitted after cardiac arrest for postresuscitation care to different intensive care units. Methods Prospectively recorded data from 242,588 adults consecutively admitted to 87 Austrian intensive care units over a period of 13 years (1998 to 2010) were analyzed retrospectively. Multivariate analysis was used to assess the effect of the frequency of postresuscitation care on mortality, correcting for baseline parameters, severity of illness, hospital size, and capability to perform coronary angiography and intervention. Results In total, 5,857 patients had had cardiac arrest and were admitted to an intensive care unit. Observed hospital mortality was 56% in the cardiac-arrest cohort (3,302 nonsurvivors). Patients treated in intensive care units with a high frequency of postresuscitation care generally had high severity of illness (median Simplified Acute Physiology Score (SAPS II), 65). Intensive care units with a higher frequency of care showed improved risk-adjusted mortality. The SAPS II adjusted, observed-to-expected mortality ratios (O/E-Ratios) in the three strata (26 resuscitations per ICU per year) were 0.869 (95% confidence interval, 0.844 to 894), 0.876 (0.850 to 0.902), and 0.808 (0.784 to 0.833). Conclusions In this database analysis, a high frequency of post-cardiac arrest care at an intensive care unit seemed to be associated with improved outcome of cardiac-arrest patients. We were able to identify patients who seemed to profit more from high frequency of care, namely, those with an intermediate severity of illness. Considering these findings, cardiac-arrest care centers might be a reasonable step to improve outcome in this specific population of cardiac-arrest patients.
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412. Emergency Cardiopulmonary Bypass for Cardiac Arrest (ECPB4OHCA)
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Andreas Schober, MD
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- 2018
413. Quality of post arrest care does not differ by time of day at a specialized resuscitation center.
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Uray T, Sterz F, Weiser C, Schreiber W, Spiel A, Schober A, Stratil P, and Mayr FB
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- Adult, Aged, Austria epidemiology, Emergency Medical Services standards, Emergency Service, Hospital standards, Humans, Male, Middle Aged, Out-of-Hospital Cardiac Arrest mortality, Registries, Retrospective Studies, Time Factors, Treatment Outcome, Emergency Medical Services statistics & numerical data, Emergency Service, Hospital statistics & numerical data, Out-of-Hospital Cardiac Arrest therapy, Quality of Health Care statistics & numerical data, Resuscitation statistics & numerical data
- Abstract
Previous studies suggest worse outcomes after out-of-hospital cardiac arrest (OHCA) at night. We analyzed whether patients admitted after nontraumatic OHCA to a resuscitation center received the same quality post arrest care at day and night and whether quality of care affected clinical outcomes. We analyzed data of OHCA patients with return of spontaneous circulation admitted to the Vienna general hospital emergency department between January 2006 and May 2013. Data reported include admission time (day defined from 8 AM to 4 PM based on staffing), time to initiation of hypothermia, and door-to-balloon time in patients with ST-elevation myocardial infarction. Survival and cognitive performance at 12 months were assessed. In this retrospective observational study, 1059 patients (74% males, n = 784) with a mean age of 58 ± 16 years were analyzed. The vast majority was treated with induced hypothermia (77% of day vs. 79% of night admissions, P = 0.32) within 1 hour of admission (median time admission to cooling 27 (confidence interval [CI]: 10-60) vs. 23 (CI: 11-59) minutes day vs. night, P = 0.99). In 298 patients with ST-elevation myocardial infarction, median door-to-balloon time did not differ between day and night admissions (82 minutes, CI: 60 to 142 for day vs. 86 minutes, CI: 50 to 135 for night, P = 0.36). At 12 months, survival was recorded in 238 of 490 day and 275 of 569 night admissions (49% vs. 48%, P = 0.94%), and a good neurologic outcome was recorded in 210 of 490 day and 231 of 569 night admissions (43% vs. 41%, P = 0.46). Patients admitted to our department after OHCA were equally likely to receive timely high-quality postresuscitation care irrespective of time of day. Survival and good neurologic outcome at 12 months did not differ between day and night admissions. Our results may support the concept of specialized post arrest care centers.
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- 2015
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414. MicroRNAs and the response to injury in atherosclerosis.
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Natarelli L and Schober A
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- Animals, Atherosclerosis pathology, Cell Proliferation, Endothelial Cells pathology, Humans, Atherosclerosis metabolism, Endothelial Cells metabolism, MicroRNAs metabolism, Models, Cardiovascular, Vascular System Injuries metabolism, Wound Healing physiology
- Abstract
Endothelial cells (ECs) at arterial branching points are physiologically subjected to chronic damage by disturbed blood flow, which triggers a vascular wound healing response. Additional damage by hyperlipidaemia perturbs this delicate balance of endothelial injury and regeneration, and the progressive accumulation of noxious modified lipoproteins leads to macrophage death. Several miRNAs such as miR-92a and miR-712, which modulate EC proliferation and inflammation, are up-regulated by disturbed flow in ECs, and contribute to atherosclerosis. In addition, reduced endothelial levels of miR-126-5p limit the regenerative capacity of ECs, which becomes apparent by insufficient endothelial repair under hyperlipidemic stress. In macrophages, miR-342-5p induces the expression of miR-155 during the progression of atherosclerosis, which promotes inflammatory gene expression and inhibits efferocytosis by targeting Bcl6, thus contributing to necrotic core formation. Deciphering the complex cell- and context-specific effects of miRNAs during vascular wound healing appears essential for the development of miRNA-based therapies of atherosclerosis.
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- 2015
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