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Apoptosis. --- Cell Death. --- Cell death. --- Cellules --- Apoptose --- Mort
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Apoptosis, or cell death, can be pathological, a sign of disease and damage, or physiological, a process essential for normal health. This book, with contributions from experts in the field, provides a timely compilation of reviews of mechanisms of apoptosis. The book is organized into three convenient sections. The first section explores the different processes of cell death and how they relate to one another. The second section focuses on organ-specific apoptosis-related diseases. The third section explores cell death in non-mammalian organisms, such as plants. This comprehensive text is a must-read for all researchers and scholars interested in apoptosis.
Apoptosis. --- Apoptosis --- Cell Death. --- Apoptose --- physiology. --- Cell death
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The ovary is a suitable organ for studying the processes of cell death. Cell death was first described in the rabbit ovary (Graaffian follicles), the phenomenon being called ‘chromatolysis’. To date, it is recognized that various forms of cell death (programmed cell death, apoptosis and autophagy) are essential components of ovarian development and function. Programmed cell death is responsable for the ovarian endowment of primordial follicles around birth; in the prepuberal and adult period, apoptosis is a basic mechanism by which oocytes are eliminated by cancer therapies and environmental toxicants; in the ovarian cycle, follicular atresia and luteal regression involve follicular cell apoptosis. Finally, abnormalities in cell death processes may lead to ovarian disease such as cancer and chemoresistance. In this book, after an introductory description of various forms of cell death and of the ovary development and function in mammals, the processes of cell death in ovarian somatic cells and oocytes are described at cytological, physiological and molecular levels and analyzed in the embryonic, prepuberal and adult ovary. A complex array of molecular pathways triggered by extrinsic and intrinsic signals able tor induce or suppress cell death in the same cell, according to cell type and ovary developmental stage, emerges. Physiological interactions with the axis hypothalamus-hypophysis as well as ovarian internal functional signal are also critically reviewed to explain the abortive development of follicles before the beginning of the ovarian cycle. The book conveys information useful to the updating of biologists and physicians who are interested to the ovary biology and functions. Hopefully it should provide also clues for stimulating novel experiments in the study of cell death in the mammalian ovary still at an early stage.
Apoptosis. --- Cell Death. --- Neoplasm. --- Cell death --- Ovaries --- Mammals --- Vertebrates --- Cell Physiological Processes --- Adnexa Uteri --- Gonads --- Ovum --- Germ Cells --- Genitalia --- Cell Physiological Phenomena --- Genitalia, Female --- Endocrine Glands --- Chordata --- Urogenital System --- Endocrine System --- Phenomena and Processes --- Animals --- Cells --- Anatomy --- Eukaryota --- Organisms --- Ovary --- Oocytes --- Cell Death --- Biology --- Health & Biological Sciences --- Cytology --- Physiology --- Cell death. --- Ovaries. --- Cell degeneration --- Medicine. --- Reproductive medicine. --- Biomedicine. --- Biomedicine general. --- Reproductive Medicine. --- Adnexa uteri --- Death (Biology) --- Human reproduction --- Human reproductive health --- Human reproductive medicine --- Reproductive medicine --- Health --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Health aspects --- Health Workforce --- Biomedicine, general.
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From humble beginnings over 25 years ago as a lipid kinase activity associated with certain oncoproteins, PI3K (phosphoinositide 3-kinase) has been catapulted to the forefront of drug development in cancer, immunity and thrombosis, with the first clinical trials of PI3K pathway inhibitors now in progress. Here the authors give a brief overview of some key discoveries in the PI3K area and their impact, and include thoughts on the current state of the field, and where it could go from here.
Phosphoinositides. --- Cell proliferation. --- Cell death. --- Apoptosis. --- Cell renewal --- Cellular proliferation --- Phosphatidylinositides --- Phosphatidylinositol phosphates --- Medicine. --- Cancer research. --- Biomedicine. --- Cancer Research. --- Cancer research --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Cell death --- Cell degeneration --- Cells --- Death (Biology) --- Cell cycle --- Cell division --- Cell populations --- Phospholipids --- Inositol --- Growth --- Oncology. --- Tumors
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The biennial TNF-family conferences have been held over the past 20 years, from the time that TNF was cloned. These meetings have followed the enormous progress in this field. Much is now known about the members of the TNF ligand and receptor families, their signaling proteins, mechanisms of action and cellular functions. This volume is the proceedings of the 12th TNF International Conference, held in April 2009. This conference focuses on the physiological, pathophysiological, and medical significance of these important regulators. Sessions at the meeting specifically address their involvement in immunity, development, apoptosis, autoimmunity, cancer, and infection, the normal function and pathology of the neuronal system, as well as major unresolved questions about their mechanisms of action.
Cell death -- Congresses. --- Cytokines -- Congresses. --- Tumor necrosis factor -- Congresses. --- Tumor necrosis factors -- Congresses. --- Tumor necrosis factor --- Intercellular Signaling Peptides and Proteins --- Publication Formats --- Cell Physiological Processes --- Publication Characteristics --- Proteins --- Peptides --- Biological Factors --- Cell Physiological Phenomena --- Amino Acids, Peptides, and Proteins --- Chemicals and Drugs --- Phenomena and Processes --- Cell Death --- Tumor Necrosis Factors --- Cytokines --- Congresses --- Biology --- Health & Biological Sciences --- Microbiology & Immunology --- Cachectin --- Lymphotoxin --- TNF (Immunology) --- Medicine. --- Immunology. --- Microbiology. --- Biomedicine. --- Biomedicine general. --- Microbial biology --- Microorganisms --- Immunobiology --- Life sciences --- Serology --- Clinical sciences --- Medical profession --- Human biology --- Medical sciences --- Pathology --- Physicians --- Glycoproteins --- Growth factors --- Macrophages --- Health Workforce --- Biomedicine, general.
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From humble beginnings over 25 years ago as a lipid kinase activity associated with certain oncoproteins, PI3K (phosphoinositide 3-kinase) has been catapulted to the forefront of drug development in cancer, immunity and thrombosis, with the first clinical trials of PI3K pathway inhibitors now in progress. Here the authors give a brief overview of some key discoveries in the PI3K area and their impact, and include thoughts on the current state of the field, and where it could go from here.
Phosphoinositides. --- Cell proliferation. --- Cell death. --- Apoptosis. --- Phosphatidylinositides --- Phosphatidylinositol phosphates --- Cell renewal --- Cellular proliferation --- Medicine. --- Cancer research. --- Human physiology. --- Molecular biology. --- Biomedicine. --- Cancer Research. --- Human Physiology. --- Molecular Medicine. --- Molecular biochemistry --- Molecular biophysics --- Biochemistry --- Biophysics --- Biomolecules --- Systems biology --- Human biology --- Medical sciences --- Physiology --- Human body --- Cancer research --- Clinical sciences --- Medical profession --- Life sciences --- Pathology --- Physicians --- Cell death --- Cell degeneration --- Cells --- Death (Biology) --- Cell cycle --- Cell division --- Cell populations --- Phospholipids --- Inositol --- Growth --- Oncology. --- Tumors --- Health Workforce --- Cancer. --- Medicine --- Biology --- Cancer Biology. --- Biomedical Research. --- Research. --- Biological research --- Biomedical research --- Cancers --- Carcinoma --- Malignancy (Cancer) --- Malignant tumors
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The term “heavy metals” is used as a group name of toxic metals and metalloids (semimetals) causing contaminations and ecotoxicity. In strict chemical sense the density of heavy metals is higher than 5 g/cm3. From biological point of view as microelements they can be divided into two major groups. a. For their physiological function organisms and cells require essential microelements such as iron, chromium (III), cobalt, copper, manganese, molidenium, zinc. b. The other group of heavy metals is toxic to the health or environment. Of highest concern are the emissions of As, Cd, Co, Cu, Hg, Mn, Ni, Pb, Sn, Tl. The toxicity of heavy metals is well known at organismal level, while less attention has been paid to their cellular effects. This book describes the toxicity of heavy metals on microorganisms, yeast, plant and animal cells. Other chapters of the book deal with their genotoxic, mutagenic and carcinogenic effects. The toxicity of several metals touch upon the aspects of environmental hazard, ecosystems and human health. Among the cellular responses of heavy metals irregularities in cellular mecha nisms such as gene expression, protein folding, stress signalling pathways are among the most important ones. The final chapters deal with biosensors and removal of heavy metals. As everybody is eating, drinking and exposed to heavy metals on a daily basis, the spirit of the book will attract a wide audience.
Cell physiology. --- Heavy metals -- Physiological effect. --- Heavy metals -- Toxicology. --- Metals -- Analysis. --- Heavy metals --- Cell physiology --- Metals --- Phenomena and Processes --- Elements --- Inorganic Chemicals --- Chemicals and Drugs --- Cell Physiological Phenomena --- Metals, Heavy --- Public Health --- Health & Biological Sciences --- Toxicology & Public Health --- Toxicology --- Physiological effect --- Analysis --- Cytochemistry. --- Physiological effect. --- Metabolism. --- Toxicology. --- Cell chemistry --- Metallic elements --- Medicine. --- Inorganic chemistry. --- Cell biology. --- Apoptosis. --- Oxidative stress. --- Ecotoxicology. --- Biomedicine. --- Biomedicine general. --- Cell Biology. --- Oxidative Stress. --- Inorganic Chemistry. --- Biochemistry --- Cytology --- Chemical elements --- Ores --- Metallurgy --- Metals as antiseptics --- Cytology. --- Environmental toxicology. --- Chemistry, inorganic. --- Inorganic chemistry --- Chemistry --- Inorganic compounds --- Ecotoxicology --- Pollutants --- Pollution --- Environmental health --- Cell biology --- Cellular biology --- Biology --- Cells --- Cytologists --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Health Workforce --- Biomedicine, general. --- Cell death --- Oxidation-reduction reaction --- Stress (Physiology)
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The two greatest medical fears of the aging population are cancer and Alzheimer’s disease. Despite dramatic advances in understanding the molecular etiology of these disorders, therapeutic options for many patients with advanced disease have changed little and outcomes remain dismal. Paradoxically, recent findings suggest that some of the same molecules and biochemical processes underlying cancer may also participate in neurodegeneration. Therefore, it would be very useful to bring together experts from the fields of cancer research and neurodegeneration for discussions of the latest advances and ideas, with a particular emphasis on areas of overlap, to stimulate transdisciplinary interactions with the hope of accelerating progress. Cancer arises as a consequence of a breakdown in the genetic and epigenetic processes governing cell proliferation and cell death. Alterations in several classes of signaling molecules, both oncogenes and tumor suppressor genes, lead to uncontrolled cell growth. Over the past two decades, details of the intricate signaling pathways, from cell surface receptors through protein kinase cascades, transcription factors and modulators of chromatin, as well as the DNA damage response pathways linked to cell cycle control that guard the genome, have been uncovered. In some instances, key regulatory proteins have provided novel targets for development of small molecule inhibitors that are currently being tested in the clinic. The development of the nervous system relies on many of the signaling pathways and growth control processes that go awry in cancer. However, in mature neurons, the very same signaling proteins participate in transduction cascades linking short-term stimuli, elicited by synaptic stimulation, to long-term alterations in neuronal circuits through the regulation of gene expression and chromatin structure. These long-term adaptive modifications lead to changes in synaptic structure and function that contribute to learning and memory. The persistence of growth regulatory molecules in postmitotic neurons provides an opportunity for their contribution to pathophysiological processes resulting in neuronal loss. Recently, evidence has accumulated suggesting an association of cell cycle proteins and signal transduction proteins with neurodegeneration. Indeed, inhibitors of histone deacetylation have shown promise both as anti-cancer agents and in the prevention of neuronal loss.
Cancer. --- Central Nervous System -- Drug effects. --- Central Nervous System -- Metabolism. --- Hormones -- Metabolism. --- Hormones -- Physiology. --- Neoplasms. --- Nervous system -- Degeneration -- Endocrine aspects. --- Dementia --- Tauopathies --- Physiological Processes --- Cell Growth Processes --- Pathologic Processes --- Diseases --- Cell Physiological Processes --- Physiological Phenomena --- Cell Physiological Phenomena --- Pathological Conditions, Signs and Symptoms --- Brain Diseases --- Delirium, Dementia, Amnestic, Cognitive Disorders --- Neurodegenerative Diseases --- Growth --- Central Nervous System Diseases --- Nervous System Diseases --- Mental Disorders --- Growth and Development --- Phenomena and Processes --- Psychiatry and Psychology --- Alzheimer Disease --- Nerve Degeneration --- Cell Proliferation --- Homeostasis --- Cell Death --- Neoplasms --- Medicine --- Health & Biological Sciences --- Neurology --- Nervous system --- Alzheimer's disease. --- Degeneration. --- Medicine. --- Cancer research. --- Neurosciences. --- Biomedicine. --- Cancer Research. --- Alzheimer disease --- Alzheimer's dementia --- Basal ganglia --- Presenile dementia --- Senile dementia --- Degeneration, Nerve --- Nerve degeneration --- Nervous system degeneration --- Neurodegenerative disease --- Neurodegenerative diseases --- Neurodegenerative disorders --- Neuron degeneration --- Nissl degeneration --- Retrograde degeneration --- Wallerian degeneration --- Degeneration (Pathology) --- Degeneration and regeneration --- Oncology. --- Tumors --- Neural sciences --- Neurological sciences --- Neuroscience --- Medical sciences --- Cancer research
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Multiple Myeloma (MM) is the second most common type of blood cancer, resulting from an overproduction of cancerous infection-fighting white blood cells, known as plasma cells. Plasma cells are a crucial part of the immune system responsible for the production of antibodies. Bortezomib is a promising anticancer drug targeting the proteasome. This proteasome inhibitor induces cell stress and apoptosis in the cancer cells. While multiple mechanisms are likely to be involved, proteasome inhibition may prevent the degradation of pro-apoptotic factors, permitting activation of programmed cell death in neoplastic cells dependent upon the suppression of proapoptotic pathways. This monograph on bortezomib is a valuable source of information for researchers and clinicians from the fields of oncology and pharmacology, working either in academia or the pharmaceutical industry.
Antineoplastic agents. --- Multiple myeloma -- Chemotherapy. --- Multiple myeloma -- Treatment. --- Multiple myeloma --- Antineoplastic agents --- Hemostatic Disorders --- Boron Compounds --- Heterocyclic Compounds, 1-Ring --- Paraproteinemias --- Acids, Noncarboxylic --- Lymphoproliferative Disorders --- Peptide Hydrolases --- Therapeutics --- Therapeutic Uses --- Neoplasms, Plasma Cell --- Enzyme Inhibitors --- Multienzyme Complexes --- Enzymes --- Hydrolases --- Blood Protein Disorders --- Organic Chemicals --- Heterocyclic Compounds --- Acids --- Immunoproliferative Disorders --- Pharmacologic Actions --- Hemorrhagic Disorders --- Multiprotein Complexes --- Vascular Diseases --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Inorganic Chemicals --- Molecular Mechanisms of Pharmacological Action --- Neoplasms by Histologic Type --- Boronic Acids --- Multiple Myeloma --- Antineoplastic Agents --- Drug Therapy --- Proteasome Endopeptidase Complex --- Protease Inhibitors --- Pyrazines --- Chemicals and Drugs --- Immune System Diseases --- Hematologic Diseases --- Macromolecular Substances --- Chemical Actions and Uses --- Cardiovascular Diseases --- Neoplasms --- Enzymes and Coenzymes --- Diseases --- Hemic and Lymphatic Diseases --- Medicine --- Health & Biological Sciences --- Oncology --- Treatment --- Chemotherapy --- Treatment. --- Chemotherapy. --- Anticancer agents --- Antineoplastic drugs --- Antineoplastics --- Antitumor agents --- Antitumor drugs --- Cytotoxic drugs --- Inhibitors, Neoplasm --- Neoplasm inhibitors --- Kahler's disease --- Plasma cell myeloma --- Medicine. --- Cancer research. --- Pharmacology. --- Oncology. --- Apoptosis. --- Medicine & Public Health. --- Cancer Research. --- Pharmacology/Toxicology. --- Drugs --- Cancer --- B cells --- Monoclonal gammopathies --- Plasmacytoma --- Tumors --- Oncology . --- Toxicology. --- Cytology. --- Cell biology --- Cellular biology --- Biology --- Cells --- Cytologists --- Chemicals --- Pharmacology --- Poisoning --- Poisons --- Toxicology --- Cell death --- Drug effects --- Medical pharmacology --- Medical sciences --- Pharmacy --- Cancer research --- Physiological effect
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