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  • 1
    Keywords: Cytology. ; Neurosciences. ; Immunology. ; Medicine Research. ; Biology Research. ; Cancer. ; Cell Biology. ; Neuroscience. ; Immunology. ; Biomedical Research. ; Cancer Biology.
    Description / Table of Contents: Part I. Cancer -- Ubiquitin-Regulated Cell Proliferation and Cancer -- Ubiquitin, SUMO, and Nedd8 as Therapeutic Targets in Cancer -- The Proteasome System in Health and Disease -- Proteostasis Dysregulation in Pancreatic Cancer -- Divergent Modulation of Proteostasis in Prostate Cancer -- Resistance to the Proteasome Inhibitors: Lessons from Multiple Myeloma and Mantle Cell Lymphoma -- Part II. Neurodegeneration -- Altered Proteostasis in Neurodegenerative Tauopathies -- The Ubiquitin System in Alzheimer’s Disease -- The Interplay Between Proteostasis Systems and Parkinson’s Disease -- Machado–Joseph Disease: A Stress Combating Deubiquitylating Enzyme Changing Sides -- Part III. Infection, Inflammation and Developmental Disorders -- SUMO and Cytoplasmic RNA Viruses: From Enemies to Best Friends -- The Role of Proteostasis in the Regulation of Cardiac Intercellular Communication -- By the Tips of Your Cilia: Ciliogenesis in the Retina and the Ubiquitin-Proteasome System -- TRIM E3 Ubiquitin Ligases in Rare Genetic Disorders -- Part IV. Diet -- We Are What We Eat: Ubiquitin–Proteasome System (UPS) Modulation Through Dietary Products.
    Abstract: This book, written by members of the European network PROTEOSTASIS, provides an up-to-date review of the research regarding protein homeostasis in health and disease. With new discoveries contributing to the increasing complexity of this topic, the book offers a detailed overview of the pathways regulating protein homeostasis, including autophagy and the ubiquitin protein family. Following a basic introduction, it explains how defects in protein homeostasis contribute to numerous pathologies, including cancer, neurodegeneration, inflammation and a number of rare diseases. In addition, it discusses, the role of protein homeostasis in cellular development and physiology. Highlighting the latest research in the field of protein homeostasis and its implications for various clinically relevant diseases, the book appeals to researchers and clinicians, while also offering a reference guide for scholars who are new to the field.
    Type of Medium: Online Resource
    Pages: XII, 348 p. 42 illus., 24 illus. in color. , online resource.
    Edition: 1st ed. 2020.
    ISBN: 9783030382667
    Series Statement: Advances in Experimental Medicine and Biology, 1233
    DDC: 571.6
    Language: English
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  • 2
    ISSN: 1573-4919
    Keywords: myocardial stunning ; losartan ; enalaprilat ; diastole ; isovolumic relaxation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The aim was to determine whether enalaprilat (0.08 mg/kg/min) or losartan (0.01 mg/kg/min) administration before ischemia can improve postischemic systolic and diastolic dysfunction ('stunned myocardium') and attenuate the ‘hyperfunction’ phase at the beginning of reperfusion. An isolated isovolumic rabbit heart preparation was subjected to 15 min of ischemia followed by 30 min of reperfusion without (group 1) or with pretreatment with enalaprilat (group 2) or losartan (group 3). Left ventricular developed pressure and end-diastolic pressure (diastolic stiffness) were measured and the time constant of isovolumic relaxation (t, Tau) and the ratio between +dP/dt and −dP/dt were calculated. In comparison to the stunned group (group 1) both enalaprilat (group 2) and losartan (group 3) exerted a significant protective effect on postischemic recovery of contractile state and diastolic stiffness. Only enalaprilat attenuated the ‘hypercontractile’ phase. However, both enalaprilat and losartan failed to improve myocardial relaxation. In summary, these data strongly suggest a direct deleterious action of the local renin- angiotensin system on ischemic myocardium and diminution of myocardial stunning with its successful blockade. Although, we can not exclude the possibility that bradykinin has some cardioprotective effect, these data suggest that angiotensin exacerbates myocardial injury.
    Type of Medium: Electronic Resource
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