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Getting the right diagnosis is a key aspect of health care - it provides an explanation of a patient's health problem and informs subsequent health care decisions. The diagnostic process is a complex, collaborative activity that involves clinical reasoning and information gathering to determine a patient's health problem. According to Improving Diagnosis in Health Care, diagnostic errors-inaccurate or delayed diagnoses-persist throughout all settings of care and continue to harm an unacceptable number of patients. It is likely that most people will experience at least one diagnostic error in their lifetime, sometimes with devastating consequences. Diagnostic errors may cause harm to patients by preventing or delaying appropriate treatment, providing unnecessary or harmful treatment, or resulting in psychological or financial repercussions. The committee concluded that improving the diagnostic process is not only possible, but also represents a moral, professional, and public health imperative. Improving Diagnosis in Health Care, a continuation of the landmark Institute of Medicine reports To Err Is Human (2000) and Crossing the Quality Chasm (2001), finds that diagnosis-and, in particular, the occurrence of diagnostic errorsâ€"has been largely unappreciated in efforts to improve the quality and safety of health care. Without a dedicated focus on improving diagnosis, diagnostic errors will likely worsen as the delivery of health care and the diagnostic process continue to increase in complexity. Just as the diagnostic process is a collaborative activity, improving diagnosis will require collaboration and a widespread commitment to change among health care professionals, health care organizations, patients and their families, researchers, and policy makers. The recommendations of Improving Diagnosis in Health Care contribute to the growing momentum for change in this crucial area of health care quality and safety.
This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.
Advances and Avenues in the Development of Novel Carriers for Bioactives and Biological Agents provides sound data on the utility of biological and plant-based drugs and describes challenges faced in all aspects offering indispensable strategies to use in the development of bioactive medicines. Bioactive based medications are commonly used throughout the world and have been recognized by physicians and patients for their therapeutic efficacy. Bioactive formulations, including their subordinates and analogs, address 50% of all medicines in clinical practice. Novel bioactive medicine transporters can cure many disorders by both spatial and transitory approaches and have various justifications in medicinal potential. This book presents information on the utility of natural, plant, animal and bioengineered bioactive materials. It is a fundamental source of information and data for pharmacognosists, pharmaceutical analysts, drug transport scientists and pharmacologists working in bioactive medications. Advances information on various bioactive based medications, their sources, clinical consequences and transport strategies Illustrates diverse transport systems for bioactives and derivatives, novel techniques for formulations, targeting strategies and fundamental qualities of developed bioactive carriers, and their safety concerns and standardization Discusses distinctive transport systems, stability, upgraded dissolvability, and enhanced bioavailability of bioactives
This monograph offers a cross-system exchange and cross-modality investigation into brain-heart interplay. Brain-Heart Interplay (BHI) is a highly interdisciplinary scientific topic, which spreads from the physiology of the Central/Autonomous Nervous Systems, especially Central Autonomic Network, to advanced signal processing and modeling for its activity quantification. Motivated by clinical evidence and supported by recent findings in neurophysiology, this monograph first explores the definition of basic Brain-Heart Interplay quantifiers, and then moves onto advanced methods for the assessment of health and disease states. Non-invasive use of brain monitoring techniques, including electroencephalogram and function Magnetic Resonance Imaging, will be described together with heartbeat dynamics monitoring through pulseoximeter and ECG signals. The audience of this book comprises especially of biomedical engineers and medical doctors with expertise in statistics and/or signal processing. Researchers in the fields of cardiology, neurology, psychiatry, and neuroscience in general may be interested as well.
Muscle: Fundamental Biology and Mechanisms of Disease will be the first reference covering cardiac, skeletal, and smooth muscle in fundamental, basic science, translational biology, disease mechanism, and therapeutics. Currently there are no publications covering the science behind the medicine, as the majority of books are 90% clinical and 10% science. Muscle: Fundamental Biology and Mechanisms of Disease will discuss myocyte biology, also known as muscle cell biology, providing information about the science behind clinical work and therapeutics with a 90% science and 10% clinical focus. A needed resource for researchers, clinical professionals, postdocs, and graduate students, this publication will further discuss basic biology development and physiology, how processes go awry in disease states, and how the defective pathways are targeted for therapy. This book will assist both the new and experienced clinician's and researcher's need for science translation of background research into clinical applications, bridging the gap between research and clinical knowledge.
Vols. for 1963- include as pt. 2 of the Jan. issue: Medical subject headings.
The calcium-calmodulin dependent protein kinases (CaMKs) are a broadly expressed family of calcium-sensitive intracellular kinases, which are responsible for transducing cytosolic calcium signals into phosphorylation-based regulation of proteins and physiological functions. As the multifunctional member of the family, CaMKII has become the most prominent for its roles in the central nervous system and heart, where it controls a diverse range of calcium-dependent processes; from learning and memory at the neuronal synapse, to cellular growth and death in the myocardium. In the heart, CaMKII directly regulates many of the most important ion channels and calcium handling proteins, and controls the expression of an ever-increasing number of transcripts and their downstream products. Functionally, these actions are thought to orchestrate many of the electrophysiologic and contractile adaptations to common cardiac stressors, such as rapid pacing, chronic adrenergic stimulation, and oxidative challenge. In the context of disease, CaMKII has been shown to contribute to a remarkably wide variety of cardiac pathologies, of which heart failure (HF) is the most conspicuous. Hyperactivity of CaMKII is an established contributor to pathological cardiac remodeling, and is widely thought to directly promote arrhythmia and contractile dysfunction during HF. Moreover, several non-failing arrhythmia-susceptible phenotypes, which result from specific genetic channelopathies, functionally mimic constitutive channel phosphorylation by CaMKII. Because CaMKII contributes to both the acute and chronic manifestations of major cardiac diseases, but may be only minimally required for homeostasis in the absence of chronic stress, it has come to be one of the most promising therapeutic drug targets in cardiac biology. Thus, development of more specific and deliverable small molecule antagonists remains a key priority for the field. Here we provide a selection of articles to summarize the state of our knowledge regarding CaMKII in cardiac health and disease, with a particular view to highlighting recent developments in CaMKII activation, and new targets in CaMKII-mediated control of myocyte physiology.