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  • Book
    editors, Hanna K. Gaggin, James L. Januzzi, Jr.
    Summary: This comprehensively revised new edition prepares the reader for the cardiology board examination, as well as provide a concise review of the essentials of general cardiology and the less common but clinically relevant topics in a dynamic and time-efficient manner, augmenting existing learning. It uses board-style questions and answers at the end of each topic, enabling readers to test their learning and commit key concepts to long-term memory. Instructive figures and tables are used to consolidate teaching points. This book also contains practical tips from recent board exam takers and other resources in order to make best use of the reader's limited time. In the MGH Cardiology Board Review, the Editors have compiled the expertise of over 60 experienced authors in a succinct volume, applying methods thoroughly tested in Board Review. In addition, two very important sections on ECGs and images are included, contents of which are derived from the board examination answer keys, the very ones that readers are expected to know. Plans on how to best approach board examination preparation and what additional resources to go to are provided. In short, this book has all the strengths to ensure your success on the boards exam. .

    Contents:
    History and Physical Examination
    Acute Coronary Syndrome
    Chronic Coronary Artery Disease
    Systemic Hypertension
    Lipoprotein Disorders
    Diabetes Mellitus and the Metabolic Syndrome
    Exercise Stress Testing and Nuclear Cardiology
    Cardiac Catheterization, Coronary Arteriography and Intravascular Imaging
    Supraventricular Arrhythmias
    Sudden Cardiac Death, Syncope, Ventricular Arrhythmias and Defibrillators
    Bradycardia and Pacemakers/CRT
    Diagnosis and Management of Acute Heart Failure Chronic and End-Stage Heart Failure
    Cardiomyopathies and Myocarditis
    Pericardial Disease
    Pulmonary Hypertension
    Hemodynamics and Right Heart Catheterization
    Aortic and Pulmonic Valvular Heart Disease Mitral and Tricuspid Valvular Heart Disease
    Adult Congenital Heart Disease
    Peripheral Vascular Disease and Venous Thromboembolism
    Diseases of the Aorta.-&n bsp;Cardiac Critical Care and Hypotension
    Perioperative Cardiovascular Management-cardiac and non-cardiac Cardiovascular Disease in Women & Pregnancy
    Cardio-oncology and Tumors of the Heart
    Geriatric Cardiovascular Disease
    Cardiovascular Management and Cardiovascular Screening in Athletes and High Risk Professionals
    Stroke
    Neurological Disease
    Infective Endocarditis and device infections
    Cardiac manifestation of HIV
    Rheumatology
    Endocrine disorders
    Renal disorders
    Injury and poisoning
    Pharmacology
    Heart healthy diet and nutrition
    ACLS
    Basic Statistics
    Electrocardiography
    Cardiac Noninvasive Imaging: Chest Radiography, Cardiovascular Magnetic Resonance and Computed Tomography of the Heart
    Imaging Studies.
    Digital Access Springer 2021
  • Article
    Schendel PF, Defais M, Jeggo P, Samson L, Cairns J.
    J Bacteriol. 1978 Aug;135(2):466-75.
    Mutagenesis by simple alkylating agents is thought to occur by either a lexA+-dependent process called error-prone repair or a lex-independent process often attributed to mispairing during replication. We show here that error-prone repair is responsible for the majority of mutants formed after a large dose of alkylating agent, but it is unlikely that it contributes significantly to mutagenesis during exposure to low concentrations of these chemicals. The mutagenicity of these low doses of alkylating agent is reduced by a repair system constitutively present in lexA+ cells but absent in lexA mutants. This system reduces mutagenesis until a second error-free system, called the adaptive responses, can be induced [P. Jeggo, M. Defais, L. Samson, and P. Schendel, Mol. Gen. Genet, 157:1-9, 1977; L. Samson and J. Cairns, Nature (London) 267:281-283, 1977]. The adaptive response is capable of dealing with a much larger amount of alkylation damage than the constitutive system and, when induced, appears to be able to reduce mutagenesis by both decreasing the number of sites available for mutagenesis and delaying the induction of error-prone repair enzymes. Finally, we discuss a model of chemically induced mutagenesis based on these findings which maintains that the observed mutation frequency is dependent on a "race" between these two error-free systems and the two mutagenic pathways.
    Digital Access Access Options