tbuckley/cabot-search huggingface dataset:
Abstract 12234: Risk Stratification of Heart Failure Patients With Preserved Ejection Fraction by Multiple Echocardiographic Parameters.
Authors: Shintaro Sasaki, Tetsu Watanabe, Harutoshi Tamura, Satoshi Nishiyama, Masahiro Wanezaki, Takanori Arimoto, Hiroki Takahashi, Tetsuro Shishido, Takehiko Miyashita, Takuya Miyamoto, Joji Nitobe, Isao Kubota
Journal: Circulation (2010)
Well-differentiated systemic mastocytosis*1A new disease variant with mature mast cell phenotype and lack of codon 816 c-Kit mutations
Authors: C. Akin, L. Escribano, R. Nuñez, A. Garcia-Montero, M. Angulo, A. Orfao, D.D. Metcalfe
Journal: Journal of Allergy and Clinical Immunology (2004)
Outcomes of Medical vs Invasive Therapy for Elderly Patients With Angina
Authors: David T. Nash
Journal: JAMA (2003)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
338. Therapeutic Levels for α1-Antitrypsin Following Intrapleural Administration of a Non-Human Primate Serotype rh10 AAV Vector Expressing α1-Antitrypsin
Authors: Bishnu P. De, Nabil Wasif, Neil R. Hackett, Guangping Gao, James M. Wilson, Ronald G. Crystal
Journal: Molecular Therapy (2004)

Alpha 1-antitrypsin (α1AT), a serine protease inhibitor synthesized and secreted by the liver, protects the lung from degradation by neutrophil proteases. α1AT deficiency is a common autosomal recessive disorder associated with the accelerated development of emphysema if serum α1AT levels are <11 μM (570 μg/ml). In this study, we test the hypothesis that persistent expression of α1AT at therapeutic levels can be achieved in mice by intrapleural administration of AAV vectors expressing the cDNA for α1AT at vector doses that can be safely scaled up to humans. In initial studies, mice were injected with 1011 genome copies (gc) of an adeno-associated virus seroytpe 2 (AAV2) based vector expressing human cDNA for α1AT from a cytomegalovirus-chicken β-actin hybrid promoter. Serum levels of 80 ± 19 μg/ml (mean ± SD) were achieved 8 wk following intrapleural administration, a route chosen to minimize safety issues while providing proximity to the lung. Since this fell short of the target expression level, an alternate approach was developed using the same vector construct pseudotyped by the capsid of AAVrh.10. AAVrh.10 is derived from rhesus macaque and utilizes cell surface receptor(s) distinct from that of AAV2 and is not recognized by preexisting anti-AAV2 neutralizing antibodies. The AAVrh.10α1AT vector was prepared by triple transfection with a yield of 15,000 ± 5,000 gc/cell and purified by iodixanol gradient and ion exchange chromatography. The AAVrh.10α1AT vector was administered in C57Bl/6 mice (n=4/group) at a dose of 5 × 1010 gc, via intrapleural, intramuscular, and intratracheal route and serum α1AT levels measured by ELISA. At 2 wk post-injection, the level of α1AT in intrapleural injected animals was 200 ± 10 μg/ml, compared to 1.2 ± 0.6 μg/ml for intratracheal injected animals and 60 ± 15 μg/ml for intramuscular injected animals (p < 0.01 all pairwise comparisons). Intrapleural administration of AAVrh.1α1AT vector at a higher dose (1011 gc) showed serum α1AT levels of 2,200 ± 300 μg/ml after 8 wk, higher than the target for therapy. To determine the relative distribution of the vector in lung following intrapleural administration, an AAVrh.10 vector expressing luciferase was injected intrapleurally in C57Bl/6 mice (n = 4/group) and after 8 wk, luciferase activity was measured in tissue homogenates. The luciferase activity in the diaphragm was 7 × 106 RLU/mg, in the left lung 7.5 × 106 RLU/mg, in the right lung 1.7 × 106 RLU/mg whereas in liver and kidney luciferase activities were 0.8 × 106 RLU/mg and 0.02 × 106 RLU/mg, respectively, indicating that diaphragm and lung are the major sites of gene transfer. These data indicate that intrapleural administration of an AAVrh.10 vector may be a more efficient and readily scalable strategy for delivery of α1AT to the lung than by other routes including direct intratracheal administration.
Abstract 15229: Racial Disparity in Blood Pressure Control in VA Patients from 2000 to 2011
Authors: Ross D Fletcher, Richard L Amdur, Raya Kheirbek, Vasilios Papademetriou, Ali Ahmed, Farrokh Alemi, David Maron, Charles Faselis, Ronald E Jones
Journal: Circulation (2014)

The VA Electronic Health Record with reminders effectively manages hypertension and stores data longitudinally. Vital signs from the entire VA were analyzed between 2000 and 2011. Of 7,361,848 patients with 274,162,609 BP measurements; 4,055,558 had elevations >140 systolic or >90 diastolic on three separate days. Analysis was made for age, race, treatment and BMI. Control for Blacks improved from 49.8 in 2000 to 72.5 in 2011, and Whites from 50.6 to 77.0 respectively (Fig. 1). Black/White difference was small when both groups were poorly controlled (2000 - 2001), but as treatment improved, Blacks consistently were less well controlled than Whites. BMI for hypertensive Blacks and Whites remained steady at 29.5 until 2006, then increasing for both, reaching 30.1 in 2011. This increase may explain why controlling hypertension becoming more difficult in 2006. Normotensive Blacks had a BMI of 25.5 in 2000 rising to 27.7 in 2011, while Whites increased from 26.6 to 27.9 respectively (Fig. 2). Drug data became available starting in 2004. Both Blacks and Whites received the same number of anti-hypertensive medicine classes (2.7 ± 1.4, p=0.21). Medicine coverage, where the number of daily doses were compared with frequency of refills, showed no racial difference (81.0% + 16%, p=0.64).   Conclusion:  Blacks and Whites both improved hypertensive control over 11 years with Blacks consistently 5% less well controlled than Whites. The reason for this disparity cannot be explained by differences in BMI, number of medicine classes or less coverage. More intensive treatment, with improved weight control, may be required if Blacks are to achieve BP control equal to Whites.
Abstract IA15: Circulating tumor DNA
Authors: Luis A. Diaz
Journal: Cancer Research (2015)

Abstract The development of noninvasive methods to detect and monitor tumors continues to be a major challenge in oncology. We used digital polymerase chain reaction–based technologies to evaluate the ability of circulating tumor DNA (ctDNA) to detect tumors in 640 patients with various cancer types. We found that ctDNA was detectable in &amp;gt;75% of patients with advanced pancreatic, ovarian, colorectal, bladder, gastroesophageal, breast, melanoma, hepatocellular, and head and neck cancers, but in less than 50% of primary brain, renal, prostate, or thyroid cancers. In patients with localized tumors, ctDNA was detected in 73, 57, 48, and 50% of patients with colorectal cancer, gastroesophageal cancer, pancreatic cancer, and breast adenocarcinoma, respectively. ctDNA was often present in patients without detectable circulating tumor cells, suggesting that these two biomarkers are distinct entities. In a separate panel of 206 patients with metastatic colorectal cancers, we showed that the sensitivity of ctDNA for detection of clinically relevant KRAS gene mutations was 87.2% and its specificity was 99.2%. Finally, we assessed whether ctDNA could provide clues into the mechanisms underlying resistance to epidermal growth factor receptor blockade in 24 patients who objectively responded to therapy but subsequently relapsed. Twenty-three (96%) of these patients developed one or more mutations in genes involved in the mitogen-activated protein kinase pathway. Together, these data suggest that ctDNA is a broadly applicable, sensitive, and specific biomarker that can be used for a variety of clinical and research purposes in patients with multiple different types of cancer. Citation Format: Luis A. Diaz. Circulating tumor DNA. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr IA15.
Abstract 13412: 24-Hour Water-Only Fasting Acutely Reduces Trimethylamine N-Oxide: the FEELGOOD Trial
Authors: Benjamin D Horne, James E Cox, Joseph B Muhlestein, Viet T Le, Amy R Butler, Heidi T May, John F Carlquist, Jeffrey L Anderson
Journal: Circulation (2014)

Background: Routine, periodic fasting is associated with lower risk of diabetes and coronary artery disease (CAD), and may reduce weight and improve metabolic parameters. Multiple related biologica...
The Liver: Biology and Pathobiology.
Authors: Irwin M. Arias
Journal: Annals of Internal Medicine (1983)

INTRODUCTION Organizational PriciplesEmbryonic Development of the Liver THE CELLS Gap and Tight Junctions in Liver:Composition, Regulation, and FunctionMotor MoleculesGene Regulation and In Vivo Function of Liver Transcription FactorsThe Hepatocyte Plasma Membrane:Organization, Differentiation, Biogenesis,and TurnoverHepatocyte Basolateral Membrane Organic Anion TransportersThe Hepatocyte Surface:Dynamic PolarityThe Endoplasmic Reticulum and Golgi Complex in Secretory Membrane TransportMolecular Mechanisms of Hepatocellular Vesicle FormationReceptor-Mediated EndocytosisPeroxisomal Assembly, Biology, and Disease Relationship SECTION A: HEPATOCYTE:METABOLISM Integrated Cell Function:ApoptosisFundamentals of Cellular OsmoregulationRoles of Intracellular Proteolysis in Hepatocyte Cell-Cycle,Aging, and Programmed Cell DeathRegulation of Hepatic Cholesterol HomeostasisLeptin and the LiverHypoxic, Ischemic, and Reperfusion Injury to LiverProtective Mechanisms Against Reactive oxygen SpeciesDisorders of Bilirubin MetabolismThe PorphyriasCopper Metabolism and the LiverThe Liver and Iron SECTION B:BILE SECRETION The Biology of the Bile CanaliculusConjugate Export Pumps of the Multidrug Resistance Protein (MRP) Family in LiverGenetic Defects of Canalicular TransportHormonal Regulation of Bile SecretionNucleotide Transport and Regulation of Bile FormationThe Pathobiology of Biliary Epithelia SECTION C:SINUSOIDAL CELLS Endothelial and Pit CellsHepatic Stellate Cells:Morphology, Function, and Regulation SECTION D:EXTRACELLULAR MATRIX The Extracellular Matrix of the LiverIntegrins INTERRELATED CELL FUNCTIONS Role of Inositol Trisphosphate and Diacylglycerol in the Regulation of Liver FunctionSynthesis of an Signaling Through D-3 PhosphoinositidesInsulin and Other Growth FactorsCyclic AMP Signaling in the Liver:Coupling Transcription to Psysiology and ProliferationCA2+ Signaling in the LiverNitric Oxide in the LiverInterleukin-6 Signaling During the Acute-Phase Response of the LiverInnate Immune Sensing and the Toll-Like ReceptorsLiver RegenerationHepatocyte Growth Factor:Its Role in Hepatic Growth and Pathobiology THE ORGANRELATION TO OTHER ORGANSHepatic EncephalopathyAlterations of the Kidney in Liver Disease PATHOBIOLOGIC ANLYSISMolecular Pathophysiology of Membrane Transport Function in CholestasisThe Biology of Portal Hypertension1-Antitrypsin DeficiencyPathophysiology of Liver FibrosisAlcoholic and Nonalcoholic SteatohepatitisSchistosomiasis:A Model of Immunologically Mediated Liver DiseaseImmune Mechanisms of Viral Clearance, and Disease Pathogenesis During Viral HepatitisEpidemiology, Natural History, and Prevention of Viral HepatitisMolecular Bases of Hepatitis B and Hepatitis C Related Chronic Liver DiseaseMolecular Biology of Hepatitis VirusesLiver Transplantation:Factors Affecting the Balance Between Tolerance and Rejection in Experimental ModelsViral Hepatitis:Antiviral Therapy HORIZONSTissue Engineering of the LiverA Genomic View of Hepatology:Th
THE AMERICAN BOARD OF INTERNAL MEDICINE AS A FACTOR IN SCHOLARSHIP IN AMERICAN MEDICINE
Authors: Ernest E. Irons
Journal: Annals of Internal Medicine (1941)

Article1 August 1941THE AMERICAN BOARD OF INTERNAL MEDICINE AS A FACTOR IN SCHOLARSHIP IN AMERICAN MEDICINEERNEST E. IRONS, M.D., F.A.C.P.ERNEST E. IRONS, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-2-304 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt is now five years since the American Board of Internal Medicine was organized. In this period a total of 2,449 have been certified, 624 of these by examination. It is perhaps salutary again to review the objectives of such certification as the Board conceives them, and to look ahead to anticipate, if possible, some of the requirements of the medical leaders of the coming years. The Board recognizes that it is only one of the agencies concerned in efforts to improve the quality of medical care and scholarship. All those who participate in programs of graduate education, whether in... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Read at the Boston meeting of the American College of Physicians, April 21, 1941. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1941Volume 15, Issue 2Page: 304-308KeywordsGraduate medical educationHealth care quality ePublished: 1 December 2008 Issue Published: 1 August 1941 PDF downloadLoading ...
A memorable patient: Benefits of a cooperative
Authors: A. Williams
Journal: BMJ (2000)

individuals, and therefore not something that organisations can do much about.If, instead, trust is seen as something which grows through repeated episodes of freely entered exchanges then this offers a practical way of promoting cooperation.People can be encouraged to try and try again when they recognise that their futures are linked.In practice, it is the experience of this behaviour that creates an understanding of who is worthy of trust.
Abstract 11267: LX4211, a Dual Inhibitor of Sodium-Glucose Cotransporters 1 and 2, Reduces Systolic Blood Pressure in Patients With Type 2 Diabetes Mellitus and Moderate to Severe Renal Impairment
Authors: Pablo Lapuerta, Paul Strumph, Philip Banks, Ikenna Ogbaa, Brian Zambrowicz, Arthur Sands
Journal: Circulation (2014)

Introduction: Selective sodium-glucose cotransporter 2 (SGLT2) inhibitors target only the kidney, and they have reduced efficacy when patients with type 2 diabetes mellitus (T2DM) have renal impairment (RI). LX4211 blocks sodium and glucose absorption in the gastrointestinal tract by inhibition of SGLT1, and it enhances urinary sodium and glucose excretion in the urine through inhibition of SGLT2. The dual SGLT1/2 action of LX4211 was anticipated to reduce systolic blood pressure (SBP) in addition to improving glucose control in the setting of RI. Methods: This analysis explored the effect of LX4211 on SBP in a clinical trial of patients with T2DM and moderate to severe RI. Patients (N=31) were randomly assigned to be treated with LX4211 (400 mg, N=16) or placebo (N=15) qd for 7 consecutive days. Postprandial glucose levels after a standard high glucose meal served as the primary measure of pharmacodynamic activity. Baseline and Day 8 trough SBP measures were each an average of 3 seated assessments. Results: Mean baseline characteristics included age 66.4 years, estimated glomerular filtration rate (eGFR) 43.4 mL/min/1.73 m 2 , and SBP 130.9 mmHg. Postprandial glucose area under the curve (sampled from pre-dose to 4 hours post meal) was reduced from Baseline to Day 7 by 169.3 mg*hr/dL on LX4211 compared to placebo (p=0.003). Day 8 SBP reductions were 11.4 mmHg on LX4211 and 0.0 mmHg on placebo (p=0.045 for difference between groups). Patients with greater RI (eGFR &lt;45 mL/min/1.73 m2) treated with LX4211 (N=6) had a 10.5 mmHg SBP reduction compared to 0.3 mmHg on placebo (N=9). The difference between seated and standing SBP did not change with LX4211 (0.0 mmHg change, Day 8 vs. Baseline). There were no reports of hypotension, hypovolemia, no serious adverse events, and no patient discontinued due to an adverse event. Mild hypoglycemia was reported in 1 LX4211 patient compared to 2 placebo patients. Conclusions: LX4211 may reduce SBP and enhance glycemic control in T2DM patients with moderate to severe RI.
Abstract 825: Impaired ABCA-1 Mediated Cholesterol Efflux In Hypoxic Macrophages
Authors: Stephanie L Mick, Sajesh Parathath, Vatsala Maitin, Jonathan E Feig, Lisa Grauer, Victor Joaquin, David Habiel, Edward A Fisher
Journal: Circulation (2007)

Atherosclerotic plaques contain large numbers of metabolically active cells that can be deprived of normal oxygen (0 2 ) tension, with levels documented below 10mm Hg (~1% O 2 ) in rabbit and human plaques (vs. normal tissue; 20 –70mmHg, 2.5%–9% O 2 ). Hypoxia has been assumed, but not documented in mouse plaques. Hypoxia stabilizes transcription factor HIF-1α, the master regulator of the cellular response to hypoxia and also involved in reduction-oxidation and inflammatory pathways. Atherosclerotic plaques of apoE knockout mice were immunostained and areas + for HIF-1α as well as two downstream targets (VEGF and Glut-1) were present in increased levels in deeper plaque regions. We next investigated the effect of hypoxia on macrophage function in vitro by incubating murine J774 macrophages in 1% 0 2 in DMEM containing 15% FBS for 24 h and found a 30% increase in cellular total cholesterol (TC) associated with hypoxia. In cells loaded by cyclodextrin-cholesterol, a ~400% increase in TC was observed in hypoxic relative to normoxic cells. Assays using apoAI as a cholesterol acceptor showed that in 1% 0 2 there was a ~90% decrease in ABCA-1 mediated efflux relative to normoxia. In spite of this, ABCA-1 mRNA was increased ~2.5 fold in hypoxic vs. normoxic macrophages. ABCA-1 protein levels by Western analysis remained equal in the 2 conditions. However, by immunofluorescence and confocal microscopy, in sharp distinction to the plasma membrane and cytoplasmic distribution seen in normoxic cells, ABCA-1 localized mainly in a juxtanuclear location in hypoxic macrophages, suggesting impaired trafficking to the membrane. Conclusions: HIF-1α is present in murine plaques, suggesting that they have true hypoxic areas; Hypoxia in vitro promotes macrophage cholesterol accumulation concurrent with ABCA-1 dysfunction; and Hypoxia redistributes ABCA1 from the plasma membrane to the juxtanuclear region.
INHIBITION OF SWEATING BY POLDINE METHOSULPHATE (NACTON)..
Authors: KATHERINE A. GRICE, F. RAY BETTLEY
Journal: British Journal of Dermatology (1966)

Journal Article INHIBITION OF SWEATING BY POLDINE METHOSULPHATE (NACTON).: Its Use For Measuring Insensible Perspiration. Get access KATHERINE A. GRICE, KATHERINE A. GRICE Institute of Clinical Research, The Middlesex Hospital, London, W.I Search for other works by this author on: Oxford Academic Google Scholar F. RAY BETTLEY F. RAY BETTLEY Institute of Clinical Research, The Middlesex Hospital, London, W.I Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 78, Issue 8-9, 1 August 1966, Pages 458–464, https://doi.org/10.1111/j.1365-2133.1966.tb12249.x Published: 01 August 1966
Selective Use of Adjuvant Therapy in the Management of Merkel Cell Carcinoma
Authors: Christopher K. Bichakjian, Kelly L. Harms, Jennifer L. Schwartz
Journal: JAMA Oncology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
922. Deriving Tissues from Embryonic Stem Cells
Authors: George Q. Daley
Journal: Molecular Therapy (2004)

Top of pageAbstract
Differentiation of embryonic stem (ES) cells in vitro yields abundant hematopoietic progenitors, but achieving stable hematopoietic engraftment of irradiated mice has proven difficult, begging the question of whether ES cells give rise to transplantable hematopoietic stem cells (HSCs) in vitro, and limiting the application of ES cells in experimental and therapeutic models. In an effort to characterize factors that differentiate primitive progenitors derived from yolk sac or ES cells into transplantable HSCs, we have examined the effect of conditional expression of several transgenes linked to leukemogenesis, cytokine signaling, or blood formation in model organisms. These genes include the oncoprotein BCR/ABL, the signal transducer STAT5, the bHLH transcription factor SCL, the homeotic selector gene HoxB4 implicated in self-renewal of definitive HSCs, and Cdx4, an upstream regulator of Hox gene expression. BCR/ABL enables engraftment of animals with hematopoietic cells that exhibit multi-lineage differentiation potential, but leukemia invariably develops. STAT5 activation enhances hematopoietic proliferation in vitro but enables only limited, transient multi-lineage engraftment after transplantation of irradiated mice. Induction of SCL appears to enhance hematopoietic commitment during ES differentiation but does not promote hematopoietic engraftment. Expression of HoxB4 in primitive progenitors combined with culture on hematopoietic stroma enables generates transplantable cells with a definitive HSC phenotype. These progenitors engraft lethally irradiated adults and contribute to long-term, multi-lineage hematopoiesis in primary and secondary recipients. Cdx4 further enhances the capacity for HSC generation from ES cells. We have used HoxB4 modification of ES-derived HSCs to enable therapeutic transplantation with products of ES cells, including a proof-of-principle application of therapeutic cloning to treat an immunodeficient Rag2−/− mouse, and efforts are underway in murine models of thalassemia. Our studies in the blood forming system are laying a foundation for similar studies in germ cell development, and to applications with human ES cells.
Abstract 14083: Physiological and Pathological Functions of Nox2 and Nox4 in Myocardial Ischemia/Reperfusion Injury
Authors: Shoji Matsushima, Junya Kuroda, Tetsuro Ago, Peiyong Zhai, Junichi Sadoshima
Journal: Circulation (2011)

INTRODUCTION: NAD(P)H oxidases (Noxes), including Nox2 and Nox4, are major sources of oxidative stress (OS) and critically affect growth/death of cardiomyocytes (CMs) in response to stress, such as...