Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight 6-week-old piglets were inoculated with a strain of encephalomyocarditis virus (EMCV) isolated from an outbreak which occurred naturally in the Po Valley in 1988. Two non-infected animals, kept in the same cage, were used as controls. Out of the eight inoculated piglets, two died and two were suppressed on the 2nd post infection day (PID), the four remaining were killed on the 5th, 7th, 11th and 15th PIDs. Control animals were killed at the end of the experiment. The pathogenesis of myocarditis has been studied using routine methods (Alcian-PAS, Masson's trichrome, Gomori's for reticulin and Mallory's stain), histochemical techniques (ATPase and NADH-TR reactions) and ultrastructural observations (TEM). All the inoculated piglets showed macro and/or microscopic lesions of lymphocytic myocarditis, only in one case associated with fibrinous exudation. One control piglet also showed myocarditic lesions, probably due to a contact infection. An early myocardial fibrosis was already present on the 5th PID. Ultrastructurally the cardiac muscle cells showed severe myofibrillar losses and other regressive alterations. Only on the 15th PID did we observe calcification of the degenerating myocytes, while ultrastructurally we detected needle-like calcium deposits in the mitochondria from the 5th PID. From the 5th PID in the areas of myocarditis the myocytes showed a reduction and/or absence of ATPase and NADH-TR reactions. On TEM, one or more aggregates of viral particles in crystalline array were detected in the cytoplasm of many endothelial cells.
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PMID:Ultrastructural study of experimental myocarditis induced by cardiovirus (EMCV-M) in swine. 132 99

Toxoplasmosis was diagnosed in a vinaceous Amazon parrot based on histopathology and immunohistochemistry. The bird was prostrate on the bottom of the cage and died. Necropsy revealed edema and congestion of the lungs, cloudy air sacs, and mild hepatomegaly. Histopathology revealed severe pulmonary congestion and edema and interstitial mononuclear cell inflammation associated with many cysts containing bradyzoites of Toxoplasma gondii scattered throughout. The heart had mild multifocal lymphocytic myocarditis and free tachyzoites in the muscle fibers, and the kidneys had mild interstitial nephritis and a few cysts containing bradyzoites of T. gondii. Immunohistochemistry was negative for Sarcocystis falcatula and Neospora caninum and confirmed the protozoa as T. gondii. This is the first description of T. gondii in an endangered species ofa Brazilian psittacine.
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PMID:Fatal toxoplasmosis in a vinaceous Amazon parrot (Amazona vinacea). 2339 56

The recent position paper of the European Society of Cardiology (ESC) on cardiovascular toxicity of cancer treatments has attracted considerable interest by healthcare professionals, since it is the first concrete help in the difficult task of monitoring and approaching cardiovascular side effects of anticancer treatments. The ESC expert opinion was not intended as a clinical practice guideline; however, it reports major cardiovascular complications grouped into nine categories, addressing current clinical strategies for prevention and mitigation. In this point of view, we discuss key challenges emerging from critical appraisal of the ESC position paper: (1) the wide spectrum of cardiovascular toxicities associated with oncological drugs, focusing on targeted agents, (2) managing strategies in patients with cardiac implantable devices, (3) the underappreciated (but emerging) immune-related cardiovascular toxicities of checkpoint inhibitors, which may also result in severe heart failure and fulminant myocarditis, (4) the evolving role of anticoagulation in oncology, and the evidence supporting (or not) the use of direct-acting oral anticoagulants in cancer-associated thrombosis.
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PMID:ESC position paper on cardiovascular toxicity of cancer treatments: challenges and expectations. 2969 20

Progress in cancer therapy over the past decades improved long-term survival but increased cancer therapy-related cardiotoxicity. Many novel treatment options have been implemented with yet incompletely characterized cardiovascular side effects including heart failure, coronary artery disease, arrhythmias, valvular disease, venous thromboembolism and myocarditis. Diagnosis of potential cardiotoxic side effects is essential for an optimal treatment but remains challenging. Cardiac biomarkers troponin and brain natriuretic peptide/N-terminal proBNP (BNP/NT-proBNP) have been extensively studied in heart failure and acute coronary syndromes. Emerging evidence implicates a significant role in the detection of cardiotoxicity and guidance of therapy in cancer patients. Elevated troponin or BNP/NT-proBNP levels were associated with increased all-cause mortality in cancer patients and have been shown to predict manifest heart failure. BNP/NT-proBNP may be useful for the prediction of cancer therapy-related heart failure and response to heart failure therapy in adult and pediatric cancer patients while troponin can indicate acute myocardial infarction in patients with cancer therapy-related risk for coronary artery disease. Furthermore, troponin may be used for the identification of immune checkpoint inhibitor-related myocarditis with very high sensitivity. Finally, even D-dimer levels have been shown to improve risk stratification and diagnosis in cancer-associated venous thromboembolism. This review aims to summarize the current knowledge about biomarkers in cancer therapy-related cardiotoxicity. We also outline possible clinical recommendations for the detection and treatment of subclinical and clinically apparent cardiotoxic effects using biomarkers.
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PMID:Biomarkers for the detection of apparent and subclinical cancer therapy-related cardiotoxicity. 3070 Oct 97

The combined administration of programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) inhibitors might be considered as a treatment for poorly responsive cancer. We report a patient with brain metastatic lung adenocarcinoma in whom fatal myocarditis developed after sequential use of PD-1 and PD-L1 inhibitors. This finding was validated in syngeneic tumor-bearing mice. The mice bearing lung metastases of CT26 colon cancer cells treated with PD-1 and/or PD-L1 inhibitors showed that the combination of anti-PD-1 and anti-PD-L1, either sequentially or simultaneously administered, caused myocarditis lesions with myocyte injury and patchy mononuclear infiltrates in the myocardium. A significant increase of infiltrating neutrophils in myocytes was noted only in mice with sequential blockade, implying a role for the pathogenesis of myocarditis. Among circulating leukocytes, concurrent and subsequent treatment of PD-1 and PD-L1 inhibitors led to sustained suppression of neutrophils. Among tumor-infiltrating leukocytes, combinatorial blockade increased CD8+ T cells and NKG2D+ T cells, and reduced tumor-associated macrophages, neutrophils, and natural killer (NK) cells in the lung metastatic microenvironment. The combinatorial treatments exhibited better control and anti-PD-L1 followed by anti-PD-1 was the most effective. In conclusion, the combinatory use of PD-1 and PD-L1 blockade, either sequentially or concurrently, may cause fulminant cardiotoxicity, although it gives better tumor control, and such usage should be cautionary.
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PMID:Sequential Blockade of PD-1 and PD-L1 Causes Fulminant Cardiotoxicity-From Case Report to Mouse Model Validation. 3102 41