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myocarditis/tyrosine
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Extensive tyrosine nitration in human myocardial inflammation: evidence for the presence of peroxynitrite.
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OBJECTIVE
Production of nitric oxide via the cytokine-mediated activation of myocardial inducible nitric oxide synthase decreases myocardial contractility. Whether myocardial dysfunction is mediated directly by nitric oxide or indirectly through the formation of secondary reaction products, such as
Phaeochromocytoma with myocarditis managed with alpha-methyl-p-tyrosine.
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A case of bilateral phaeochromocytoma with catecholamine-induced myocarditis is described. The two operations needed allowed comparison of the use of alpha-methyl-p-tyrosine alone and in conjunction with adrenergic blocks in the management of the patient. The combination of both drugs was
Tyrosine Kinase Inhibitor-Induced Acute Myocarditis, Myositis, and Cardiogenic Shock.
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Fatal autoimmune myocarditis with anti-PD-L1 and tyrosine kinase inhibitor therapy for renal cell cancer.
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Vaccination with Flt3L-induced CD8α+ dendritic cells prevents CD4+ T helper cell-mediated experimental autoimmune myocarditis.
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Experimental autoimmune myocarditis (EAM) represents a CD4(+) T helper (Th) cell-mediated mouse model of inflammatory heart disease. Interferon (IFN)-γ, typically produced by Th1 cells, reduces EAM severity in myosin heavy-chain-(MyHC)-α peptide/Complete Freund adjuvant-immunized mice. Thus,
Activation of STAT1 transcription factor precedes up-regulation of coxsackievirus-adenovirus receptor during viral myocarditis.
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The coxsackievirus-adenovirus receptor (CAR) was originally described as a transmembrane protein involved in viral infection and was later found to be required for normal heart development. However, the role of CAR in virus-induced myocarditis has not been investigated so far. The purpose of this
A mechanism of immunoreceptor tyrosine-based activation motif (ITAM)-like sequences in the capsid protein VP2 in viral growth and pathogenesis of Coxsackievirus B3.
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Coxsackievirus B3 (CVB3) is an RNA virus that mainly causes myocarditis. We have reported previously that immunoreceptor tyrosine-based activation motif (ITAM)-like sequences are contained in the capsid protein VP2 of CVB3. The substitution of two tyrosines for phenylalanines in the ITAM-like region
Attenuation of coxsackievirus B3 by VP2 mutation and its application as a vaccine against virus-induced myocarditis and pancreatitis.
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Coxsackievirus B3 (CVB3) is a common agent of viral myocarditis, a major cause of sudden cardiac death, and ultimately dilated cardiomyopathy. However, there is no vaccine in clinical use. In this study, we identified the conserved amino acid sequences in the C-terminal region of the VP2 of the
A closer look at immune-mediated myocarditis in the era of combined checkpoint blockade and targeted therapies.
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Immune checkpoint inhibitors (ICI) and tyrosine kinase inhibitors (TKI) have transformed the management of many malignancies. Although rare, immune-mediated myocarditis presents unique clinical challenges due to heterogenous presentation, potential life-threatening consequences, and the
T-cell protein tyrosine phosphatase deletion results in progressive systemic inflammatory disease.
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The deregulation of the immune response is a critical component in inflammatory disease. Recent in vitro data show that T-cell protein tyrosine phosphatase (TC-PTP) is a negative regulator of cytokine signaling. Furthermore, tc-ptp(-/-) mice display immune defects and die within 5 weeks of birth. We
Eosinophilic Myocarditis.
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Persistent eosinophilia can cause cardiac tissue damage, typically in the form of eosinophilic myocarditis, whether the underlying cause is reactive, a clonal myeloid disorder, or idiopathic hypereosinophilic syndrome (HES). Eosinophilic myocarditis ranges from mild localized disease to multifocal
Global metabolomic profiling of acute myocarditis caused by Trypanosoma cruzi infection.
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Chagas disease is caused by Trypanosoma cruzi infection, being cardiomyopathy the more frequent manifestation. New chemotherapeutic drugs are needed but there are no good biomarkers for monitoring treatment efficacy. There is growing evidence linking immune response and metabolism in inflammatory
The tyrosine kinase p56lck is essential in coxsackievirus B3-mediated heart disease.
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Infections are thought to be important in the pathogenesis of many heart diseases. Coxsackievirus B3 (CVB3) has been linked to chronic dilated cardiomyopathy, a common cause of progressive heart disease, heart failure and sudden death. We show here that the sarcoma (Src) family kinase Lck (p56lck)
Precision Cardio-Oncology: a Systems-Based Perspective on Cardiotoxicity of Tyrosine Kinase Inhibitors and Immune Checkpoint Inhibitors.
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Cancer therapies have been evolving from conventional chemotherapeutics to targeted agents. This has fulfilled the hope of greater efficacy but unfortunately not of greater safety. In fact, a broad spectrum of toxicities can be seen with targeted therapies, including cardiovascular toxicities. Among
Molecular mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and signal transduction pathways.
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Angiotensin II (Ang II), the effector peptide of the renin-angiotensin system (RAS), regulates volume and electrolyte homeostasis and is involved in cardiac and vascular cellular growth in humans and other species. This system, which has been conserved throughout evolution, plays an important role
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