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1
Chen, Hsiao Ying. Molecular studies of a non-histone chromatin protein B2. Ottawa: National Library of Canada, 1990.
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2
Ciavolella, Paul Edward. The purification and characterization of a developmentally regulated myocardial non-histone nuclear protein and the isolation of a cDNA clone of unknown function which is developmentally expressed. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1991.
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3
Davide, Viterbo, ed. Un rabbino tunisino nei ghetti del Regno di Sardegna 1818-1830: Gli ebrei non lo gradiscono ma la corte lo protegge. Firenze: Giuntina, 2006.
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4
Isaac, Bekhor, Mirell Carol J, and Liew C. C, eds. Progress in nonhistone protein research. Boca Raton, Fla: CRC Press, 1985.
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5
Lehn, Donald Andrew. The non-histone chromosomal protein HMG-I(Y) and its interactions with nucleic acids. 1989.
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6
Emery, Alan E. H., and Marcia L. H. Emery. The history of muscular dystrophy: a unique story. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199591473.003.0001.
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Chapter 1 discusses the history of Duchenne muscular dystrophy, a serious condition and the second most common genetic disorder in many countries. Its cause was unknown until relatively recently and there has been no effective treatment. However, the responsible gene and its protein product have now been identified and gene therapy is under serious consideration.
7
Lucchesi, John C. Epigenetics, Nuclear Organization & Gene Function. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.001.0001.
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Epigenetics is the study of heritable changes in gene function that do not involve changes in the DNA sequence. Epigenetic changes, consisting principally of DNA methylation, histone modifications and non-coding RNAs, maintain and modulate the initial impact of regulatory factors that recognize and associate with particular genomic sequences. This book’s primary goal is to establish a framework that can be used to understand the basis of epigenetic regulation and to appreciate both its derivation from genetics and its interdependence with genetic mechanisms. A further aim is to highlight the role played by the three-dimensional organization of the genetic material itself (the complex of DNA, histones and non-histone proteins referred to as chromatin) and its distribution within a functionally compartmentalized nucleus. Dysfunctions at any level of genetic regulation have the potential to result in an increased susceptibility to disease or actually give rise to overt pathologies. As illustrated in this book, research is continuously uncovering the role of epigenetics in a variety of human disorders, providing new avenues for therapeutic interventions and advances in regenerative medicine.
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Egreteau, Pierre-Yves, and Jean-Michel Boles. Assessing nutritional status in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0204.
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Decreased nutrient intake, increased body requirements, and/or altered nutrient utilization are frequently combined in critically-ill patients. The initial nutritional status and the extent of the disease-related catabolism are the main risk factors for nutrition- related complications. Many complications are related to protein energy malnutrition, which is frequent in the ICU setting. Assessing nutritional status pursues several different goals. Nutritional assessment is required for patients presenting with clinical evidence of malnutrition, with chronic diseases, with acute conditions accompanied by a high catabolic rate, and elderly patients. Recording the patient’s history, nutrient intake, and physical examination, and subjective global assessment allows classification of nutritional status. All the traditional markers of malnutrition, anthropometric measurements and plasma proteins, lose their specificity in the sick adult as each may be affected by a number of non-nutritional factors. Muscle function evaluated by hand-grip strength in cooperative patients and serum albumin provide an objective risk assessment. Several nutritional indices have been validated in specific groups of patients to identify patients at risk of nutritionally-mediated complications and, therefore, the need for nutritional support. A strong suspicion remains the best way of uncovering potentially harmful nutritional deficiencies.
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Puntis, John. Food allergy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0019.
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Food allergy is an immune response to food that can be classified as immunoglobulin (Ig)-E and non-IgE mediated. Milk, egg, peanut, tree nuts, and fish are among the most prevalent causes of food allergy. Mild reactions can include itchy rash, watering eyes, and nasal congestion while a severe reaction results in anaphylaxis. A detailed clinical history is essential when making a diagnosis, and skin prick testing and quantitative measurement of food-specific IgE antibodies can be helpful. Cow milk protein allergy causes a plethora of symptoms and frequently resolves spontaneously over the first 2 years of life; diagnosis is based mainly on clinical history. Food challenges have a pivotal role in the diagnosis of food allergy. Introduction of ‘allergic’ foods at 3–6 months alongside continuing breastfeeding may prevent allergy.
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Machado, Pedro M. Inclusion body myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.
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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.
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Chess, Andrew, and Schahram Akbarian. The Human Brain and its Epigenomes. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0003.
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Conventional psychopharmacology elicits an insufficient therapeutic response in more than one half of patients diagnosed with schizophrenia, bipolar disorder, depression, anxiety, or related disorders. This underscores the need to further explore the neurobiology and molecular pathology of mental disorders in order to develop novel treatment strategies of higher efficacy. One promising avenue of research is epigenetics.Deeper understanding of genome organization and function in normal and diseased human brain will require comprehensive charting of neuronal and glial epigenomes. This includes DNA cytosine and adenine methylation, hundred(s) of residue-specific post-translational histone modifications and histone variants, transcription factor occupancies, and chromosomal conformations and loopings. Epigenome mappings provide an important avenue to assign function to many risk-associated DNA variants and mutations that do not affect protein-coding sequences. Powerful novel single cell technologies offer the opportunity to understand genome function in context of the vastly complex cellular heterogeneity and neuroanatomical diversity of the human brain.
12
Muthukumar, Thangamani, Darshana Dadhania, Choli Hartono, and Manikkam Suthanthiran. Immunology, sensitization, and histocompatibility. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0279.
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Allograft rejection of the histo-incompatible allograft involves a highly orchestrated action of multiple cell types and mediators, with lymphocytes responsible for the identification of the foreignness of the allograft. The immune response directed against the donor is primarily, but not exclusively, directed at the donor’s major histocompatibility complex region class I and class II proteins. This chapter describes the immunobiology of the T cell and the role of human leucocyte antigens in clinical transplantation, thus identifying the targets for manipulation of the immune response by immune suppressants and through strategies designed to create a state of tolerance of the allograft.
13
Dean, Michael, and Karobi Moitra. Biology of Neoplasia. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0002.
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The term “cancer” encompasses a large heterogeneous group of diseases that involve uncontrolled cell growth, division, and survival, culminating in local invasion and/or distant metastases. Cancer is fundamentally a genetic disease at the cellular level. Tumors occur because clones of abnormal cells acquire multiple lesions in DNA, nearly always involving mutations, chromosomal rearrangements, and extensive alteration of the epigenome. Up to 10% of cancers also involve inherited germline mutations that are moderately to highly penetrant. Cancers begin as localized growths or premalignant lesions that may regress or disappear spontaneously, or progress to a malignant primary tumor. The somatic changes that drive abnormal growth involve activating mutations of specific oncogenes, inactivation of tumor suppressor genes, and/or disruption of epigenetic controls. The latter can result from methylation or the modification of histones and other proteins that affect the remodeling of chromosomes. Numerous non-inherited factors can cause cancer by accelerating these events.
14
Snell, Jamey, and Thomas J. Mancuso. Cystic Fibrosis. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0023.
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Cystic fibrosis (CF) is an inherited, autosomal recessive, multisystem disease. Dysfunction of the cystic fibrosis transmembrane conductance regulator protein (CFTR) in epithelial cells is the primary defect in CF. Defects in CFTR are the cause for lung disease, exocrine pancreatic insufficiency and failure, male infertility, and liver disease. CF can present with a variety of respiratory and gastrointestinal signs, including meconium ileus in the newborn period, hypernatremic dehydration, pulmonary insufficiency, nasal polyps, and insulin-dependent diabetes mellitus. As affected children grow, dysfunction in CFTR leads to chronic and progressive lung disease, characterized by suppurative infection and the development of bronchiectasis. CFTR dysfunction also affects exocrine function, leading to pancreatic insufficiency, malabsorption, and growth failure. In the past, history and physical exam with sweat chloride testing were the cornerstones of diagnosis. Diagnosis is now made with the newborn screening test for immunoreactive trypsinogen.
15
Chassy, Bruce M. Food Safety. Edited by Ronald J. Herring. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780195397772.013.027.
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Most consumers expect the food they eat to be safe. This concern is not lost on governments around the world, which explains why there are numerous laws and regulations intended to ensure food safety. There are many misconceptions about food safety, such as the belief that organic foods are safer than conventional food products. This article examines food safety, first by considering the factors that explain why genetically modified (GM) crops as well as the foods and feeds produced from them, are assumed to be as safe as any other food. It provides an overview of the history of the use of recombinant DNA in food crops and the production of transgenic crops. It then looks at the scientific food-safety risk assessment of crops produced using biotechnology. It also discusses food safety in relation to proteins in food, as well as food allergy and allergens. Finally, it reviews the results of animal studies designed to demonstrate the safety of GM crops and the politics underlying such studies.
16
Abhishek, Abhishek, and Michael Doherty. Investigations of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0051.
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Joint aspiration and microscopic examination of the aspirated synovial fluid remains the gold standard for the diagnosis of calcium pyrophosphate crystal deposition (CPPD). If synovial fluid aspiration is not feasible, plain radiography and/or ultrasound scanning may be used to detect chondrocalcinosis (CC) which predominantly occurs due to calcium pyrophosphate (CPP) crystals, and this can be used as a diagnostic surrogate for CPPD as suggested by the EULAR Task Force. Acute CPP crystal arthritis often associates with a brisk acute phase response (elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), plasma viscosity) and neutrophilia. A mildly raised CRP and/or ESR may be present in chronic CPP crystal inflammatory arthritis. On the contrary, asymptomatic CC, or CPPD with osteoarthritis does not cause raised acute phase reactants. As CPPD most commonly occurs due to increasing age and osteoarthritis, investigations to screen for underlying metabolic abnormalities should be carried out in those with early-onset CPPD (under 55 years), or in those with florid polyarticular CC. As hyperparathyroidism gets more common with ageing its presence should be specifically sought in all age groups. Tests for other predisposing metabolic conditions should only be carried out in the presence of specific clinical features. Genotyping for mutations, especially in the ANKH gene, may be warranted in those with a family history of premature CPPD and no evidence of inherited metabolic predisposition, but such testing is unavailable to most clinicians.
17
Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.
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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.
18
Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.
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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.
19
Goldin, Paul. The Art of Chinese Philosophy. Princeton University Press, 2020. http://dx.doi.org/10.23943/princeton/9780691200798.001.0001.
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This book provides an unmatched introduction to eight of the most important works of classical Chinese philosophy—the Analects of Confucius, Mozi, Mencius, Laozi, Zhuangzi, Sunzi, Xunzi, and Han Feizi. The book places these works in rich context that explains the origin and meaning of their compelling ideas. Because none of these classics was written in its current form by the author to whom it is attributed, the book begins by asking, “What are we reading?” and showing that understanding the textual history of the works enriches our appreciation of them. A chapter is devoted to each of the eight works, and the chapters are organized into three sections: “Philosophy of Heaven,” which looks at how the Analects, Mozi, and Mencius discuss, often skeptically, Heaven (tian) as a source of philosophical values; “Philosophy of the Way,” which addresses how Laozi, Zhuangzi, and Sunzi introduce the new concept of the Way (dao) to transcend the older paradigms; and “Two Titans at the End of an Age,” which examines how Xunzi and Han Feizi adapt the best ideas of the earlier thinkers for a coming imperial age. In addition, the book presents explanations of the protean and frequently misunderstood concept of qi—and of a crucial characteristic of Chinese philosophy, nondeductive reasoning. The result is an invaluable account of an endlessly fascinating and influential philosophical tradition.
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Lewis, Cara L. Dynamic Form. Cornell University Press, 2020. http://dx.doi.org/10.7591/cornell/9781501749179.001.0001.
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This book traces how intermedial experiments shape modernist texts from 1900 to 1950. Considering literature alongside painting, sculpture, photography, and film, the book examines how these arts inflect narrative movement, contribute to plot events, and configure poetry and memoir. As forms and formal theories cross from one artistic realm to another and back again, modernism shows its obsession with form—and even at times becomes a formalism itself—but as the book states, that form is far more dynamic than we have given it credit for. Form fulfills such various functions that we cannot characterize it as a mere container for content or matter, nor can we consign it to ignominy opposite historicism or political commitment. As a structure or scheme that enables action, form in modernism can be plastic, protean, or even fragile, and works by Henry James, Virginia Woolf, Mina Loy, Evelyn Waugh, and Gertrude Stein demonstrate the range of form's operations. Revising three major formal paradigms—spatial form, pure form, and formlessness—and recasting the history of modernist form, the book proposes an understanding of form as a verbal category, as a kind of doing. It thus opens new possibilities for conversation between modernist studies and formalist studies and simultaneously promotes a capacious rethinking of the convergence between literary modernism and creative work in other media.