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1
Curtin, Nicola J., and Ricky A. Sharma, eds. PARP Inhibitors for Cancer Therapy. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14151-0.
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Curtin, Nicola J., and Ricky A. Sharma. PARP Inhibitors for Cancer Therapy. Humana, 2018.
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PARP as a Therapeutic Target (Handbooks in Pharmacology and Toxicology). CRC, 2002.
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Inhibitors of the Ras Superfamily G-Proteins, Part B. Elsevier Science & Technology, 2013.
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Tamanoi, Fuyuhiko. Inhibitors of the Ras Superfamily G-Proteins, Part A. Elsevier Science & Technology Books, 2013.
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Shokat, Kevan M. Protein Kinase Inhibitors in Research and Medicine, Part B. Elsevier Science & Technology Books, 2013.
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Inhibitors of the Ras Superfamily G-proteins, Part A. Elsevier, 2013. http://dx.doi.org/10.1016/c2012-0-03660-5.
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Inhibitors of the Ras superfamily G-proteins, Part B. Elsevier, 2013. http://dx.doi.org/10.1016/c2012-0-03661-7.
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Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: ‘small molecule’ molecularly targeted agents. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0008.
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The psychiatric consequences of a range of small-molecule, molecularly targeted systemic treatments for cancer are reviewed. Psychopathology may arise from the endocrine complications of VEGFR/multiple TK inhibitors. The mechanisms by which PI3K/AKT inhibition and proteasome inhibition can provoke anxiety and depressive phenomena in animals and humans are discussed. PARP-1 inhibition impairs memory acquisition in animal models and is neuroprotective. PARP-2 inhibitors display anti-neuroinflammatory properties in mice. The cognitive enhancing, mood stabilizing, and neuroprotective effects of HDAC inhibitors are considered.
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Protein Phosphorylation Part B: Analysis of Protein Phosphorylation, Protein Kinase Inhibitors, and Protein Phosphatases. Elsevier, 1991. http://dx.doi.org/10.1016/s0076-6879(00)x0218-2.
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Bhole, Malini. Complement deficiencies. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0299.
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The complement system comprises a group of heat-labile proteins which form part of the innate immune system. The main physiological functions of the complement system include defence against pyogenic bacterial infections, clearance of immune complexes and products of inflammatory damage, and acting as a bridge between the innate and adaptive immune system. The complement system is regulated by various complement inhibitors (regulatory proteins) that are present in both the classical pathway and the alternate pathway and which regulate and prevent spontaneous activation of the complement system, thereby preventing complement-mediated damage to tissues under normal circumstances. This chapter addresses the clinical features, diagnosis, and management of inherited and acquired deficiencies of complement proteins or inhibitors.
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(Editor), John N. Abelson, Melvin I. Simon (Editor), Tony Hunter (Editor), and Bartholomew M. Sefton (Editor), eds. Methods in Enzymology, Volume 201: Protein Phosphorylation, Part B: Analysis of Protein Phosphorylation, Protein Kinase Inhibitors, and Protein (Methods in Enzymology). Academic Press, 1991.
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Wohl, David A., and Jeffrey T. Kirchner. Cardiovascular Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0041.
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There is a growing body of evidence that HIV-infected persons are at increased risk for cardiovascular disease (CVD) and associated complications, including myocardial infarction and stroke. Autopsy studies have noted premature atherosclerosis in HIV-infected adults, and epidemiological studies demonstrate higher rates of CVD among HIV-infected compared to HIV-uninfected patients. These findings are in part due to chronic inflammation and immune activation associated with HIV infection. Traditional CVD risk factors, including hypertension, hyperlipidemia, and cigarette smoking, also play keys roles. There is additional evidence from observational cohort studies that some antiretroviral drugs, including protease inhibitors and nucleoside reverse transcriptase inhibitors, may increase the risk of myocardial infarction. Treatment interventions to reduce the risk of CVD include diet, exercise, smoking cessation, lipid-lowering agents, and antihypertensive medications. For select patients, changing antiretroviral therapy to improve lipid profiles may be appropriate but should not compromise virologic or immunologic control.
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Chinthapalli, Krishna. Pharmacological treatment of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0008.
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Pharmacological treatment of Alzheimer’s disease is an important part of management of the condition. There are only four drugs available for treatment of the disease and none halt the disease process, however they have a benefit on cognition, behaviour, activities of daily living, and global function. Acetylcholinesterase inhibitors are thought to work by enhancing cholinergic transmission in the brain and are particularly effective in mild and moderate AD, with recent evidence suggesting donepezil is also effective in severe AD. Memantine is the only glutamate antagonist that is available for AD and is limited for use in moderate or severe AD. The choice of drug depends on route of administration, adverse effects, and medical comorbidities. There is intense research on alternative treatments especially those that may stop the underlying disease process.
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Mukherji, Deborah, Aurelius Omlin, Carmel Pezaro, and Johann De Bono. Novel therapies and emerging strategies for the treatment of patients with castration-resistant prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0069.
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Castration-resistant prostate cancer (CRPC) represents a final stage of this malignancy for many men and is defined as the progression of prostate cancer despite castrate levels of testosterone. CRPC may present as a rising PSA, the development of new metastases, or worsening of known metastases. Recent advances have resulted in five new treatments for CRPC: the immunotherapy sipuleucel-T; the cytotoxic cabazitaxel; the androgen biosynthesis inhibitor abiraterone acetate; the radioisotope radium-223; and the antiandrogen enzalutamide. These have all improved overall survival in randomized phase III studies for patients with metastatic CRPC. Furthermore, multiple agents and combinations are currently in late-stage clinical testing. Men with advanced prostate cancer represent an important population for clinical and translational research and clinical trial participation should be considered as part of standard care.
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Deramecourt, Vincent, Florence Lebert, and Florence Pasquier. Frontotemporal dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0036.
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Frontotemporal dementia (FTD) is the second most common form of dementia in persons younger than 65 years after Alzheimer’s disease. The FTD spectrum is characterized by clinical, molecular and genetic heterogeneity. Core features of FTD are behavioural and language manifestations and the clinical spectrum of FTD currently includes a behavioural variant, progressive nonfluent aphasia and semantic dementia. The most common behavioural features are disinhibition, apathy, loss of empathy, hyperorality and perseveration. Neuroimaging usually demonstrates focal atrophy and hypometabolism in the anterior part of the frontal and temporal lobes. A careful history and neuropsychological examination, and judicious use of neuroimaging, can help distinguish FTD from other common forms of dementia, especially Alzheimer’s disease, vascular dementia, and dementia with Lewy bodies. Although no specific pharmacological treatments for FTD exists, symptom management with serotonin reuptake inhibitors and non pharmacological interventions have been shown to be beneficial.
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Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.
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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.
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Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. What are axial spondyloarthritis and ankylosing spondylitis? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0001.
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Ankylosing spondylitis (AS) is a chronic inflammatory arthritis affecting mainly the sacroiliac joints and spine, resulting in pain, stiffness, and reduced movement. AS has a major negative impact on patients’ quality of life. AS is part of a larger group of related spondyloarthritis (SpA) conditions and patients with AS often have extra-articular manifestations of these conditions. Over the past decade, there have been major advances in the understanding of the genetics and pathophysiology of the disease. Advances in imaging have allowed patients to be diagnosed without having to develop the radiographic structural damage that characterize AS, resulting in the concept of axial spondyloarthritis (axSpA). Together with the development of highly effective TNF inhibitors, these advances have transformed the management and outlook of patients with this condition. It is hoped that further advances in diagnosis, assessment and treatment of axSpA will lead to further progress in future.
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Ferro, Charles J., and Khai Ping Ng. Recommendations for management of high renal risk chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0099.
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Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.
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Mele, Alfred R., ed. Surrounding Self-Control. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780197500941.001.0001.
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This book is one of the fruits of the Philosophy and Science of Self-Control project, a three-year project designed to explore the topic of self-control from a variety of angles: neuroscience; social, cognitive, and developmental psychology; decision theory; and philosophy. The book is divided into four main parts: “What is self-control and how does it work?”; “Temptation and goal pursuit”; “Self-control, morality, and law”; and “Extending self-control.” Part I explores conceptual and empirical questions about the nature of self-control and how self-control functions. Questions featured here include the following: How is self-control related to willpower and ego depletion? What are the cultural and developmental origins of beliefs about self-control? Does self-control entail competition between or coordination of elements of the mind? Is self-control a set of skills? What is inhibitory control and how does it work? How are attempts at self-control hindered or helped by emotions? How are self-control and decision-making related? A sampling of questions tackled in Parts II, III, and IV includes the following: How do one’s beliefs about one’s own ability to deal with temptation influence one’s behavior? What does the ability to avoid temptation depend on? How is self-control related to moral concerns and beliefs? How should juvenile responsibility be understood, and how should the juvenile justice system be reformed? How does the framing of possible outcomes bear on success at self-control? How are self-control and empathy related? Can an account of self-control help us understand moral responsibility and free will?
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Hammond, Christopher J., Marc N. Potenza, and Linda C. Mayes. Development of Impulse Control, Inhibition, and Self-Regulatory Behaviors in Normative Populations across the Lifespan. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0082.
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Impulsivity represents a complex multidimensional construct that may change across the lifespan and is associated with numerous neuropsychiatric disorders including substance use disorders, conduct disorder/antisocial personality disorder, and traumatic brain injury. Multiple psychological theories have considered impulsivity and the development of impulse control, inhibition, and self-regulatory behaviors during childhood. Some psychoanalytic theorists have viewed impulse control and self-regulatory behaviors as developing ego functions emerging in the context of id-based impulses and inhibitory pressures from the superego. Object relationists added to this framework but placed more emphasis on mother–child dyadic relationships and the process of separation and individuation within the infant. Cognitive and developmental theorists have viewed impulse control and self-regulation as a series of additive cognitive functions emerging at different temporal points during childhood and with an emphasis on attentional systems and the ability to inhibit a prepotent response. Commonalities exist across all of these developmental theories, and they all are consistent with the idea that the development of impulse control appears cumulative and emergent in early life, with the age range of 24–36 months being a formative period. Impulsivity is part of normal development in the healthy child, and emerging empirical data on normative populations (as measured by neuropsychological testing batteries, self-report measures, and behavioral observation) suggest that impulse control, self-regulation, and other impulsivity-related phenomena may follow different temporal trajectories, with impulsivity decreasing linearly over time and sensation seeking and reward responsiveness following an inverted U-shaped trajectory across the lifespan. These different trajectories coincide with developmental brain changes, including early maturation of subcortical regions in relation to the later maturation of the frontal lobes, and may underlie the frequent risk-taking behavior often observed during adolescence.
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Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0057.
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Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet's syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
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Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0057_update_001.
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Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet’s syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
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Pavón Oro, Alequis Tomás. Efecto proapoptótico y antimetastásico en líneas tumorales humanas colorrectales de una proteína secretada por la bacteria Rizosférica Antártica Bacillus sp. K2I17. Universidad Autónoma de Chile, 2019. http://dx.doi.org/10.32457/20.500.12728/87432019dcbm4.
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El cáncer es la segunda causa de muerte en el mundo, y específicamente en Chile el cáncer colorrectal es el único que presenta un aumento sostenido de la mortalidad en la última década. La búsqueda de nuevos agentes quimioterapeúticos anticancerígenos ha propuesto a los microorganismos extremófilos como una fuente potencial para obtener moléculas citotóxicas, que induzcan apoptosis en las células tumorales. Las condiciones extremas del continente antártico y las presiones selectivas por el espacio y los nutrientes que se producen entre los microorganismos del rizobioma de la planta Deschampsia antarctica Desv sugirieron como hipótesis que las bacterias rizosféricas aisladas en la Antártica secretan al sobrenadante de cultivo moléculas bioactivas que inhiben la invasión y proliferación de líneas tumorales humanas de origen colorrectal mediante un mecanismo apoptótico. En este sentido, el objetivo general del trabajo fue identificar y caracterizar a moléculas bioactivas con acción antinvasiva y antiproliferativa, además, determinar el mecanismo inhibitorio de la proliferación en líneas tumorales humanas de origen colorrectal. Los resultados del primer objetivo específico demostraron que los sobrenadantes de cultivo de los aislados rizosféricos antárticos K2 y MI disminuyeron la viabilidad de la línea celular de adenocarcinoma colorrectal LoVo en el ensayo de reducción metabólica del MTT. Además, como los sobrenadantes no tuvieron efecto en la viabilidad de las bacterias E. coli y Staphylococcus aureus, y tampoco en los hongos unicelulares Candida albicans y Saccharomyces cerevisiae, el resultado indicó que la actividad antiproliferativa fue selectiva hacia la línea celular LoVo.