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  • 1
    Article
    Article
    2020
    ISSN: 1748-1708 
    Language: English
    In: Acta Physiologica, 2020-01, Vol.228 (1), p.e13393-n/a
    Subject(s): Gene Expression Regulation ; Humans ; Nephrotic syndrome ; Nephrotic Syndrome - metabolism ; Sodium ; Sodium - metabolism ; Urokinase-Type Plasminogen Activator - metabolism
    ISSN: 1748-1708
    E-ISSN: 1748-1716
    Source: Hellenic Academic Libraries Link
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: SPORTDiscus with Full Text
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  • 2
    Article
    Article
    2018
    ISSN: 0036-8075 
    Language: English
    In: Science (American Association for the Advancement of Science), 2018-10-26, Vol.362 (6413), p.398-399
    Description: The arterial baroreceptor reflex is the most important mechanism for minimizing short-term arterial blood pressure fluctuations (1). In situations of sudden blood pressure drops, the baroreceptor reflex accelerates heart rate, increases cardiac contractility, and induces vasoconstriction. Conversely, sudden increases in blood pressure trigger the opposite response. The autonomic nervous system mediates these physiological reactions. Patients with baroreceptor reflex malfunctions typically suffer from orthostatic hypotension, a severe decrease in blood pressure that occurs when standing up, which leads to dizziness or even fainting (2). However, how blood pressure changes are converted into electrical signals for neurotransmission has remained a puzzle. On page 464 of this issue, Zeng et al. (3) show that the mechanosensitive ion channels PIEZO1 and PIEZO2 are transducers of blood pressure in the sensory neurons of the autonomic nervous system that trigger the baroreceptor reflex. Identifying the molecular players of this response may help clarify the role of arterial baroreceptors in maintaining normotension and help develop new drugs for the treatment of heart failure.
    Subject(s): Autonomic nervous system ; Baroreceptors ; Blood ; Blood Pressure ; Blood Pressure Determination ; Heart diseases ; Heart rate ; Hypotension ; Ion channels ; Malfunctions ; Mechanotransduction ; Mechanotransduction, Cellular ; Muscle contraction ; Nervous system ; Neurotransmission ; Sensory neurons ; Stress, Mechanical ; Transducers ; Variations ; Vasoconstriction
    ISSN: 0036-8075
    E-ISSN: 1095-9203
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: Get It Now
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  • 3
    Language: English
    In: British journal of pharmacology, 2019-06, Vol.176 (12), p.1853-1863
    Description: Traditionally, arterial hypertension and subsequent end‐organ damage have been attributed to haemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign microorganisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Over the past few years, important findings have revolutionized hypertension research. Firstly, in 2007, a seminal paper showed that adaptive immunity is involved in the pathogenesis of hypertension. Secondly, salt storage in the skin and its consequences for cardiovascular physiology were discovered. Thirdly, after the discovery that salt promotes the differentiation of CD4+ T cells into TH17 cells, it was demonstrated that salt directly changes several cells of the innate and adaptive immune system and aggravates autoimmune disease but may improve antimicrobial defence. Herein, we will review pathways of activation of immune cells by salt in hypertension as the framework for understanding the multiple roles of salt and immunity in arterial hypertension and autoimmune disease. Linked Articles This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc
    Subject(s): Adaptive immunity ; Animals ; Autoimmune diseases ; Blood Pressure - drug effects ; Blood Pressure - immunology ; CD4 antigen ; Cell activation ; Cell differentiation ; Helper cells ; Hemodynamics ; Humans ; Hypertension ; Hypertension - chemically induced ; Hypertension - immunology ; Immune system ; Inflammation ; Inflammation - chemically induced ; Inflammation - immunology ; Injury prevention ; Interleukin-17 - antagonists & inhibitors ; Interleukin-17 - immunology ; Life Sciences & Biomedicine ; Lymphocytes ; Lymphocytes T ; Microorganisms ; Pathogenesis ; Pharmacology & Pharmacy ; Review ; Salts ; Science & Technology ; Skin ; Sodium Chloride, Dietary - administration & dosage ; Sodium Chloride, Dietary - adverse effects ; T cells ; Themed Section
    ISSN: 0007-1188
    E-ISSN: 1476-5381
    Source: Academic Search Ultimate
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: Wiley Online Library All Journals
    Source: PubMed Central
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  • 4
    Language: English
    In: Scientific reports, 2018-02-02, Vol.8 (1), p.2312-10
    Description: In cardiovascular research, several mouse strains with differing genetic backgrounds are used to investigate mechanisms leading to and sustaining ventricular arrhythmias. The genetic background has been shown to affect the studied phenotype in other research fields. Surprisingly little is known about potential strain-specific susceptibilities towards ventricular arrhythmias in vivo. Here, we hypothesized that inter-strain differences reported in the responsiveness of the β-adrenergic pathway, which is relevant for the development of arrhythmias, translate into a strain-specific vulnerability. To test this hypothesis, we characterized responses to β-adrenergic blockade (metoprolol) and β-adrenergic stimulation (isoproterenol) in 4 mouse strains commonly employed in cardiovascular research (Balb/c, BS, C57Bl/6 and FVB) using telemetric ECG recordings. We report pronounced differences in the electrical vulnerability following isoproterenol: Balb/c mice developed the highest number and the most complex arrhythmias while BS mice were protected. Balb/c mice, therefore, seem to be the background of choice for experiments requiring the occurrence of arrhythmias while BS mice may give insight into electrical stability. Arrhythmias did not correlate with the basal β-adrenergic tone, with the response to β-adrenergic stimulation or with the absolute heart rates during β-adrenergic stimulation. Thus, genetic factors dominate the susceptibility to ventricular arrhythmias in this model of β-adrenergic stimulation.
    Subject(s): Adrenal glands ; Adrenergic beta-1 Receptor Antagonists - administration & dosage ; Adrenergic beta-Agonists - administration & dosage ; Animal models ; Animals ; Arrhythmias, Cardiac - genetics ; Cardiac arrhythmia ; EKG ; Genetic Background ; Genetic factors ; Genetic Predisposition to Disease ; Isoproterenol ; Isoproterenol - administration & dosage ; Metoprolol ; Metoprolol - administration & dosage ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Muridae ; Phenotypes ; Rodents ; Ventricle
    ISSN: 2045-2322
    E-ISSN: 2045-2322
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 5
    Language: English
    In: Cell and tissue research, 2021-01-04, Vol.385 (2), p.393-404
    Description: Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including monocyte/macrophages and dendritic cells can promote blood pressure elevation via effects mostly on kidney and vascular function. Moreover, convincing evidence shows that T and B cells from the adaptive immune system are involved in hypertension and hypertensive end-organ damage. Skin monocyte/macrophages, regulatory T cells, natural killer T cells, and myeloid-derived suppressor cells have been shown to exert blood pressure controlling effects. Sodium intake is undoubtedly indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake. Modulation of the immune response can reduce severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The purpose of this review is to briefly summarize recent advances in immunity and hypertension as well as hypertensive end-organ damage.
    Subject(s): Analysis ; Animal models ; Animals ; B cells ; Biomedical and Life Sciences ; Biomedicine ; Blood pressure ; Dendritic cells ; Human Genetics ; Humans ; Hypertension ; Hypertension - physiopathology ; Immune system ; Immunomodulation ; Immunoregulation ; Inflammation ; Inflammation - immunology ; Innate immunity ; Kidneys ; Lymphocytes B ; Lymphocytes T ; Macrophages ; Microbiomes ; Molecular Medicine ; Monocytes ; Natural killer cells ; Proteomics ; Review ; Skin ; Suppressor cells ; T cells
    ISSN: 0302-766X
    E-ISSN: 1432-0878
    Source: Alma/SFX Local Collection
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  • 6
    Language: English
    In: American journal of physiology. Heart and circulatory physiology, 2017-03-01, Vol.312 (3), p.H349-H354
    Description: The self-amplifying cascade of messenger and effector molecules of the complement system serves as a powerful danger-sensing system that protects the host from a hostile microbial environment, while maintaining proper tissue and organ function through effective clearance of altered or dying cells. As an important effector arm of innate immunity, it also plays important roles in the regulation of adaptive immunity. Innate and adaptive immune responses have been identified as crucial players in the pathogenesis of arterial hypertension and hypertensive end organ damage. In line with this view, complement activation may drive the pathology of hypertension and hypertensive injury through its impact on innate and adaptive immune responses. It is well known that complement activation can cause tissue inflammation and injury and complement-inhibitory drugs are effective treatments for several inflammatory diseases. In addition to these proinflammatory properties, complement cleavage fragments of C3 and C5 can exert anti-inflammatory effects that dampen the inflammatory response to injury. Recent experimental data strongly support a role for complement in arterial hypertension. The remarkably similar clinical and histopathological features of malignant nephrosclerosis and atypical hemolytic uremic syndrome, which is driven by complement activation, suggest a role for complement also in the development of malignant nephrosclerosis. Herein, we will review canonical and noncanonical pathways of complement activation as the framework to understand the multiple roles of complement in arterial hypertension and hypertensive end organ damage.
    Subject(s): Adaptive Immunity ; Animals ; Complement System Proteins - metabolism ; Histopathology ; Humans ; Hypertension ; Hypertension - complications ; Hypertension - physiopathology ; Immunity, Innate ; Inflammatory diseases ; Medical immunity ; Pathogenesis ; Physiology
    ISSN: 0363-6135
    E-ISSN: 1522-1539
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
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  • 7
    Language: English
    In: Scientific reports, 2019-07-08, Vol.9 (1), p.9831-12
    Description: Human iPSC-derived engineered heart tissue (hEHT) has been used to remuscularize injured hearts in a guinea pig infarction model. While beneficial effects on cardiac remodeling have been demonstrated, the arrhythmogenic potential of hEHTs is a major concern. We investigated whether hiPSC-derived hEHTs increase the incidence of ventricular arrhythmias. HEHTs were created from human iPSC-derived cardiomyocytes and endothelial cells. Left-ventricular cryo-injury was induced in guinea pigs (n = 37) and telemetry sensors for continuous ECG monitoring were implanted. 7 days following the cryo-injury, hEHTs or cell-free constructs were transplanted into the surviving animals (n = 15 and n = 9). ECGs were recorded over the following 28 days. 10 hEHT animals and 8 control animals survived the observation period and were included in the final analysis. After implantation of hEHTs or cell-free constructs, ventricular arrhythmias (premature ventricular contractions, couplets, triplets and non-sustained ventricular tachycardia) were observed in animals of both groups. The fraction of animals with the respective arrhythmias as well as the rate of arrhythmic events did not differ between groups. Following hEHT implantation, no clinically relevant sustained ventricular tachycardia or ventricular fibrillation was detected. Our telemetric data provides first evidence for the electrical safety of human iPSC-derived EHTs in this experimental model, thereby supporting further development of this approach.
    Subject(s): Animals ; Arrhythmias, Cardiac - diagnosis ; Cardiac arrhythmia ; Cardiac regeneration ; Cardiomyocytes ; Cell Differentiation ; Disease Models, Animal ; EKG ; Electrocardiography ; Endothelial cells ; Fibrillation ; Freezing - adverse effects ; Guinea Pigs ; Heart ; Humans ; Induced Pluripotent Stem Cells - cytology ; Infarction ; Multidisciplinary Sciences ; Myocardial Infarction - complications ; Myocardial Infarction - etiology ; Myocardial Infarction - therapy ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - transplantation ; Regeneration ; Science & Technology ; Science & Technology - Other Topics ; Tachycardia ; Telemetry ; Tissue Engineering ; Ventricle
    ISSN: 2045-2322
    E-ISSN: 2045-2322
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 8
    Language: English
    In: The Journal of physiology, 2014-03-01, Vol.592 (5), p.1139-1157
    Description: Key points The adrenal hormone aldosterone can stimulate K+ secretion during hyperkalaemia and Na+ reabsorption during hypovolaemia in the kidney. Angiotensin II is thought to switch the physiological mode of action from K+ excretion towards Na+ retention, but how the regulation is achieved when angiotensin II levels are suppressed by high Na+ intake remains unknown. We report that both dietary K+ depletion and dietary K+ loading provoke renal Na+ retention and increase blood pressure in Na+ replete mice, but these occur through different renal kinase signalling and Na+ transport pathways. An angiotensin II‐ and aldosterone‐independent activation of the sodium‐chloride cotransporter NCC contributes to the blood pressure increase induced by K+ depletion, whereas the hypertensive response to K+ loading is dependent on neither aldosterone nor Na+ transport via the epithelial sodium channel ENaC. These findings imply a major impact of K+ homeostasis on renal Na+ handling in the Na+ replete state and suggest a mechanism for the hypertensive effect of the Western diet (high Na+ and low K+) in humans. A network of kinases, including WNKs, SPAK and Sgk1, is critical for the independent regulation of K+ and Na+ transport in the distal nephron. Angiotensin II is thought to act as a key hormone in orchestrating these kinases to switch from K+ secretion during hyperkalaemia to Na+ reabsorption during intravascular volume depletion, thus keeping disturbances in electrolyte and blood pressure homeostasis at a minimum. It remains unclear, however, how K+ and Na+ transport are regulated during a high Na+ intake, which is associated with suppressed angiotensin II levels and a high distal tubular Na+ load. We therefore investigated the integrated blood pressure, renal, hormonal and gene and protein expression responses to large changes of K+ intake in Na+ replete mice. Both low and high K+ intake increased blood pressure and caused Na+ retention. Low K+ intake was accompanied by an upregulation of the sodium‐chloride cotransporter (NCC) and its activating kinase SPAK, and inhibition of NCC normalized blood pressure. Renal responses were unaffected by angiotensin AT1 receptor antagonism, indicating that low K+ intake activates the distal nephron by an angiotensin‐independent mode of action. High K+ intake was associated with elevated plasma aldosterone concentrations and an upregulation of the epithelial sodium channel (ENaC) and its activating kinase Sgk1. Surprisingly, high K+ intake increased blood pressure even during ENaC or mineralocorticoid receptor antagonism, suggesting the contribution of aldosterone‐independent mechanisms. These findings show that in a Na+ replete state, changes in K+ intake induce specific molecular and functional adaptations in the distal nephron that cause a functional coupling of renal K+ and Na+ handling, resulting in Na+ retention and high blood pressure when K+ intake is either restricted or excessively increased.
    Subject(s): Aldosterone - metabolism ; Angiotensin ; Animals ; Blood Pressure ; Corticosteroids ; Homeostasis ; Hyperkalemia - physiopathology ; Hypertension ; Hypertension, Renal - physiopathology ; Integrative ; Kidney - physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Physiological aspects ; Potassium - metabolism ; Potassium, Dietary - metabolism ; Retention ; Sodium ; Sodium - metabolism ; Sodium, Dietary - metabolism
    ISSN: 0022-3751
    E-ISSN: 1469-7793
    Source: Hellenic Academic Libraries Link
    Source: Wiley Online Library All Backfiles
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 9
    Language: English
    In: British journal of pharmacology, 2019-06, Vol.176 (12), p.2002-2014
    Description: Background and Purpose The adaptive immune response and IL‐17A contribute to renal damage in several experimental models of renal injury. Experimental Approach To evaluate the role of the adaptive immune response, 5/6 nephrectomy was performed in wildtype DBA/1J mice and in recombination‐activating gene‐1 (RAG‐1) deficient mice that lack B and T‐cells. To assess the role of IL‐17A, we carried out 5/6 nephrectomy in IL‐17A deficient mice. Flow cytometric analysis, immunohistochemistry and RT‐PCR were used. Key Results Infiltration of CD3+ T‐cells in the remnant kidney was increased after 5/6 nephrectomy in wildtype mice, along with a robust induction of IL‐17A production in CD4+ T and γδ T‐cells. After 5/6 nephrectomy, wildtype mice developed albuminuria in the nephrotic range over 10 weeks. This was accompanied by severe glomerular sclerosis and tubulointerstitial injury, and as well as renal mRNA expression of markers of inflammation and fibrosis (the chemokine CCL2, plasminogen activator inhibitor‐1; PAI‐1 and neutrophil gelatinase‐associated lipocalin; NGAL). Unexpectedly, RAG‐1 deficient mice and IL‐17A deficient mice developed renal injury, similar to that in wildtype mice. No differences were found for albuminuria, glomerular sclerosis, tubulointerstitial injury and mRNA expression of CCL2, PAI‐1 and NGAL. Mortality did not differ between the three groups. Conclusions and Implications Numbers of CD3+ T‐cells and IL‐17A+ lymphocytes infiltrating the kidney were increased after 5/6 nephrectomy. In contrast to other experimental models of renal injury, genetic deficiency of the adaptive immune system or of IL‐17A did not attenuate induction or progression of chronic kidney disease after 5/6 nephrectomy. Linked Articles This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc
    Subject(s): Adaptive immunity ; Adaptive Immunity - immunology ; Analysis ; Animals ; CD3 antigen ; CD4 antigen ; Chemokines ; Chronic kidney failure ; Damage assessment ; Fibrosis ; Flow cytometry ; Gelatinase ; Gene expression ; Hypertension ; Immune response ; Immune system ; Immunohistochemistry ; Injuries ; Interferon ; Interleukin-17 - deficiency ; Interleukin-17 - immunology ; Kidney diseases ; Kidneys ; Life Sciences & Biomedicine ; Lipocalin ; Lymphocytes ; Lymphocytes B ; Male ; Mice ; Mice, Inbred DBA ; Mice, Knockout ; Monocyte chemoattractant protein 1 ; Nephrectomy ; Pharmacology & Pharmacy ; Plasminogen activator inhibitors ; Recombination ; Renal Insufficiency, Chronic - immunology ; Renal Insufficiency, Chronic - surgery ; Research Paper ; Research Papers ; RNA ; Science & Technology ; Sclerosis ; T cells ; Themed Section
    ISSN: 0007-1188
    E-ISSN: 1476-5381
    Source: Academic Search Ultimate
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: Wiley Online Library All Journals
    Source: PubMed Central
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  • 10
    Language: English
    In: PloS one, 2019-04-12, Vol.14 (4), p.e0214513-e0214513
    Description: Background Unloading of failing hearts by left ventricular assist devices induces an extensive cardiac remodeling which may lead to a reversal of the initial phenotype-or to its deterioration. The mechanisms underlying these processes are unclear. Hypothesis Heterotopic heart transplantion (hHTX) is an accepted model for the study of mechanical unloading in rodents. The wide variety of genetically modified strains in mice provides an unique opportunity to examine remodeling pathways. However, the procedure is technically demanding and has not been extensively used in this area. To support investigators adopting this method, we present our experience establishing the abdominal hHTX in mice and describe refinements to the technique. Methods In this model, the transplanted heart is vascularised but implanted in series, and therefore does not contribute to systemic circulation and results in a complete mechanical unloading of the donor heart. Training followed a systematic program using a combination of literature, video tutorials, cadaveric training, direct observation and training in live animals. Results Successful transplantation was defined as a recipient surviving 〉 24 hours with a palpable, beating apex in the transplanted heart and was achieved after 20 transplants in live animals. A success rate of 90% was reached after 60 transplants. Operative time was shown to decrease in correlation with increasing number of procedures from 200 minutes to 45 minutes after 60 operations. Cold/warm ischemia time improved from 45/100 to 10/20 minutes. Key factors for success and trouble shootings were identified. Conclusion Abdominal hHTX in the mouse may enable future examination of specific pathways in unloading induced myocardial remodeling. Establishment of the technique, however, is challenging. Structured training programs utilising a variety of training methods can help to expedite the process. Postoperative management, including daily scoring increases animal wellbeing and helps to predict survival.
    Subject(s): Abdomen ; Animal models ; Animals ; Aorta - anatomy & histology ; Aorta - surgery ; Aorta, Abdominal - diagnostic imaging ; Biology and Life Sciences ; Cadaver ; Cadavers ; Care and treatment ; Cold Ischemia ; Coronary vessels ; Disease Models, Animal ; Female ; Genetic modification ; Genetically modified mice ; Heart ; Heart - physiopathology ; Heart attack ; Heart Failure - physiopathology ; Heart Failure - surgery ; Heart surgery ; Heart transplantation ; Heart Transplantation - methods ; Heart Ventricles - anatomy & histology ; Heart-Assist Devices ; Intraoperative Period ; Ischemia ; Learning Curve ; Male ; Mechanical unloading ; Medicine and Health Sciences ; Mice ; Models ; Multidisciplinary Sciences ; Myocardial Contraction ; Myocardium - pathology ; Pathways ; Perioperative Period ; Phenotype ; Phenotypes ; Physical Sciences ; Physiology ; Postoperative Period ; Pulmonary arteries ; Pulmonary Artery - anatomy & histology ; Research and Analysis Methods ; Rodents ; Science & Technology ; Science & Technology - Other Topics ; Stress, Mechanical ; Training ; Transplantation ; Transplantation, Heterotopic - methods ; Transplants ; Transplants & implants ; Treatment Outcome ; Unloading ; Usage ; Vena Cava, Inferior - anatomy & histology ; Ventricle ; Ventricular assist devices ; Ventricular Function, Left ; Ventricular Remodeling ; Warm Ischemia
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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