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1
Kelley, William Donald. One answer to cancer: Reviewed after 32 years, 1967-1999 : with cancer cure suppressed. Winfield, Kan: College of Metabolic Medicine, 1998.
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One answer to cancer: Reviewed after 30 years, 1967-1997 : the metabolic approach to the successful resolution of malignancy. Mineral Wells, TX: Cancer Coalition, 1997.
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Busacca, Maurizio, and Roberto Paladini. Collaboration Age. Venice: Fondazione Università Ca’ Foscari, 2020. http://dx.doi.org/10.30687/978-88-6969-424-0.
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Recently, public policies of urban regeneration have intensified and multiplied. They are being promoted with the aim to start social and economic dynamics within the local context which is subject to intervention. From the empirical analysis, we realise that such activities are mainly implemented by three subjects or by mixed coalitions (public institutions, actors of the third sector and companies). Within them, each player is moved by a multiplicity of interests and goals that go beyond their own nature – public interest, market and mutualism – and tend to redefine themselves, thus becoming hybrid forms of production of value (social, economic, cultural). By studying a number Italian and Catalan cases, this essay deals with the theory that, under specific conditions and configurations, a collaborative direction – of organization, production and design – would give life to successful procedures, even without the identification of a one-best-way. The collaboration is not simply a choice of operation, but a real production method which mobilises social resources to create hybrid solutions – between state, market and society – to complex issues that could not be faced solely with the use of the rationale of action of one among the three actors. In this framework, the systems of relations and interactions between players and shared capital become an essential condition for the success of every initiative of urban redevelopment, or failure thereof. Such initiatives are brought to life by the strategic role of individuals who foster connections as well as the dissemination of non-redundant information between social networks, and collective and individual actors which would otherwise be separated and barely able to communicate and collaborate with each other. In addition to the functions carried out by knowledge brokers, that have been extensively described in organisational studies and economic sociology, the aforementioned figures act as real social enzymes, that is to say, they handle the available information and function as catalysts of social processes of production of knowledge. Moreover, they increase the reaction speed, working on mechanisms which control the spontaneity.
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Deegan, Patrick. Porphyria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0179.
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This chapter discusses six diseases caused by inborn errors of metabolism affecting the biosynthesis of haem. Haem is a tetracyclic metal-binding compound involved in oxygen transport (in haemoglobin and myoglobin) and redox reactions (e.g. in the cytochrome P450 system). Each of these conditions is caused by a single gene defect in one of the enzymes involved in the biosynthesis of haem. Inheritance is usually autosomal dominant with incomplete penetrance. The enzyme defect results in disease, not as a result of deficiency of the reaction product, but as a result of accumulation of precursors. Early, soluble precursors, 5-aminolaevulinic acid, and porphobilinogen (not porphyrins as such) are neurotoxic and, when present in great excess, as occurs when flux through the haem synthetic pathway is increased in response to particular medications or hormones, lead to acute neurovisceral crises. Later cyclical precursors (porphyrins) in the pathway are also water soluble and excreted in urine, but are susceptible to activation by electromagnetic radiation in the visible spectrum and are converted to free-radical metabolites that cause pain, inflammation, and tissue damage in the skin. The final haem precursors (also porphyrins) are hydrophobic and excreted in the bile and faeces and are also activated by light to toxic metabolites.
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A, Ali Elvis, ed. Natural remedies & supplements: The all-in-one guide to herbs, vitamins, minerals, enzymes, amino acids, fats, herbs ... Niagara Falls, NY: AGES Publications, 2000.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0335_update_001.
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Fabry disease is a rare X-linked disorder of glycosphingolipid metabolism caused by a deficiency of the lysosomal acid hydrolase enzyme, alpha-galactosidase A. The resulting accumulation of substrate, mostly globotriaosylceramide, leads to a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. It is one of over 50 lysosomal storage diseases. It is typically diagnosed in young men after many years of ‘acral pain’ syndrome, when the diagnosis is made through identification of characteristic abnormalities of skin, kidney or heart, or of other organs. Renal failure has been a common outcome. Females may also develop manifestations, usually later in life. Renal biopsy shows vacuoles/deposits in podocytes and other renal cell types with progressive scarring. The diagnosis can be made by measuring enzyme levels in men, or by genetic testing. This latter is the more reliable test in women. Fabry disease can now be treated where affordable by regular (every 2 weeks) intravenous infusions of recombinant preparations of the deficient enzyme. These are burdensome and expensive, but are transforming the outlook for the condition.
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Dierdorf, Stephen F. Porphyria. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0026.
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Heme, and iron containing compound that forms the nonprotein portion of hemoglobin, is essential to life. Heme synthesis requires eight enzymatic steps, and a deficiency in any one of the eight enzymes can lead to the accumulation of potentially toxic intermediates. Some forms of porphyria may be asymptomatic until the patient receives a triggering agent, and acute porphyrias can also be difficult to diagnose because of the nonspecific clinical features. The most serious of the clinical manifestations is severe neurologic dysfunction. An attack can be triggered by medications administered during the perioperative period, and failure to act promptly can result in mortality rates as high as 5%.
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Hendriksz, Christian J., and Francois Karstens. Mucopolysaccharidosis in Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0054.
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There are 8 different types of diseases of the mucopolysaccharides, each caused by a deficiency in one of 10 different enzymes involved in the degradation of glycosaminoglycans (GAGs). Partially degraded GAGs accumulate within the lysosomes of many different cell types and lead to clinical symptoms and excretion of large amounts of GAGs in the urine. Heritability is autosomal recessive except for MPS type II, which is X-linked. The disorders are chronic and progressive and, although the specific types all have their individual features, they share an abundance of clinical similarities. All involve the musculoskeletal, the cardiovascular, the pulmonary and the central nervous system.
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Poll-The, Bwee Tien, Ronald J. A. Wanders, and Hans R. Waterham. Peroxisomal Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0062.
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Peroxisomal disorders represent a group of disorders in which there is an impairment in one or more peroxisomal functions. Clinically, a dysfunction of peroxisomes results in most cases in neurologic symptoms of varying extent ranging from severe neurologic symptoms in children to late-onset disease in adults. In most peroxisomal disorders there is ocular and hearing involvement in combination with a multitude of other clinical manifestations. The peroxisomal disorders are subdivided into two major groups: (1) the peroxisome biogenesis disorders (PBDs), and (2) the single peroxisome enzyme deficiencies. The PBD group comprises the Zellweger spectrum disorders (ZSDs) and rhizomelic chondrodysplasia punctate type 1 (RCDP1) whereas the single peroxisomal enzyme deficiency group contains several different disorders including X-linked adrenoleukodystrophy as the most frequent disorder. Laboratory diagnosis of a peroxisomal disorder involves a variety of different biochemical assays in blood and urine, and should be followed up by detailed biochemical and celbiological studies in cultured fibroblasts including complementation analysis. Prenatal diagnosis is possible either by biochemical testing or by molecular analysis.
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Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.
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This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also reviews other clinically available agents as well as HPA axis-modulating compounds, both for treatment and secondary prevention of PTSD. It concludes with the suggestion that clinical selection of one or more of these medications for PTSD should be based on individual patient considerations, including target symptoms, PTSD subtype, post-traumatic interval, comorbidities, genotypes for CYP450 enzymes, and genetic polymorphisms of clinical relevance.
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Anderson, John A., Pierre-Antoine Laloë, and Derek J. Tuffnell. Hypertension in pregnancy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0036.
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The hypertensive disorders of pregnancy encompass a spectrum of disease, including gestational hypertension, haemolysis, elevated liver enzymes, and low platelets (HELLP syndrome), and acute fatty liver of pregnancy through to pre-eclampsia and eclampsia. These conditions can pose significant problems for clinicians and are associated with significant morbidity and mortality for both mother and baby. Pre-eclampsia and eclampsia remain one of the leading causes of maternal death worldwide. The majority of fatalities occur in settings with low healthcare resources. In the developed world, improvements over the last 60 years in antenatal and intrapartum care, along with national surveillance and audit, have led to tenfold and fivefold reductions in absolute mortality and severe morbidity from eclampsia and pre-eclampsia respectively. Conversely, the incidence of pre-eclampsia has been rising in the developed world as the average age of first maternity increases and rates of obesity and other medical conditions rise. It is therefore increasingly likely that hypertension may complicate the obstetric and anaesthetic management of pregnant women.
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Frey, Perry A., and Adrian D. Hegeman. Enzymatic Reaction Mechanisms. Oxford University Press, 2007. http://dx.doi.org/10.1093/oso/9780195122589.001.0001.
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Books dealing with the mechanisms of enzymatic reactions were written a generation ago. They included volumes entitled Bioorganic Mechanisms, I and II by T.C. Bruice and S.J. Benkovic, published in 1965, the volume entitled Catalysis in Chemistry and Enzymology by W.P. Jencks in 1969, and the volume entitled Enzymatic Reaction Mechanisms by C.T. Walsh in 1979. The Walsh book was based on the course taught by W.P. Jencks and R.H. Abeles at Brandeis University in the 1960's and 1970's. By the late 1970's, much more could be included about the structures of enzymes and the kinetics and mechanisms of enzymatic reactions themselves, and less emphasis was placed on chemical models. Walshs book was widely used in courses on enzymatic mechanisms for many years. Much has happened in the field of mechanistic enzymology in the past 15 to 20 years. Walshs book is both out-of-date and out-of-focus in todays world of enzymatic mechanisms. There is no longer a single volume or a small collection of volumes to which students can be directed to obtain a clear understanding of the state of knowledge regarding the chemicals mechanisms by which enzymes catalyze biological reactions. There is no single volume to which medicinal chemists and biotechnologists can refer on the subject of enzymatic mechanisms. Practitioners in the field have recognized a need for a new book on enzymatic mechanisms for more than ten years, and several, including Walsh, have considered undertaking to modernize Walshs book. However, these good intentions have been abandoned for one reason or another. The great size of the knowledge base in mechanistic enzymology has been a deterrent. It seems too large a subject for a single author, and it is difficult for several authors to coordinate their work to mutual satisfaction. This text by Perry A. Frey and Adrian D. Hegeman accomplishes this feat, producing the long-awaited replacement for Walshs classic text.
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Mazur, Allan. Physiology of Face-to-Face Competition. Edited by Rosemary L. Hopcroft. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190299323.013.24.
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Face-to-face competition for rank in human status hierarchies is similar to “dominance competition” in other primate species, particularly the African apes. Each individual has signs or signals showing that it has or ought to have high or low status. Group members may accept these signs at face value, or one individual may challenge another for high rank. Among apes and humans, such dominance contests are usually nonviolent, often taking the form of an exchange of stressful signals. Eventually, one contestant withdraws or concedes the higher rank, thus lowering the stress level. Serious competition with important stakes is influenced by a physiological substrate of the hormones testosterone and cortisol and the enzyme α-amylase. Among humans, language is an important channel for exchanging dominant and deferent signals. Apart from the physiological substrate, instantaneous stress responses underlie status allocation. These mechanisms are illustrated with recent experimental results.
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Cooper, Bruce Andrew. Normal physiology of the renal system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0208.
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Patients with critical illness often have renal dysfunction, either primary or secondary, that can both complicate and prolong their medical management. Therefore, an understanding of normal renal physiology can help recognize the process or processes that caused the renal dysfunction, and determine the most appropriate corrective and supportive care. The kidney has many important roles other than just urine production. The impact of kidney disease is often predictable. The kidney plays a critical role in fluid and electrolyte balance via many specialized transmembrane pathways. The kidney is also involved in the production and modification of two key hormones and one enzyme. Understanding normal renal physiology can help determine clinical management.This chapter summarizes the important aspects of renal physiology relevant to those who work in a critical care environment.
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Roze, Emmanuel, and Frédéric Sedel. Gangliosidoses (GM1 and GM2). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0050.
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GM1 gangliosidosis is due to beta-galactosidase deficiency. The adult-onset form is characterized by progressive generalized dystonia, often associated with akineto-rigid Parkinsonism. Mild skeletal dysplasia and short stature are good diagnostic clues. GM2 gangliosidosis is due to beta-hexosaminidase deficiency. The adult-onset form is characterized by complex neurological disorders, in which features resulting from cerebellar and motor neuron dysfunction are the most frequent. Movement disorders, psychotic symptoms, mild pyramidal signs, axonal polyneuropathy, autonomic dysfunction, and vertical supranuclear palsy can also be observed. Clinical severity and the rate of progression both vary widely from one patient to another. Diagnosis is based on measurements of enzyme activity and molecular analysis. Physiotherapy, speech therapy and management of swallowing are crucial for these patients’ quality of life and prognosis.
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Ng, Dominic S. Familial Lecithin Cholesterol Acyl Transferase Deficiency Syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0034.
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Lecithin cholesterol ester transferase (LCAT) is the sole enzyme in the circulation that mediates the esterification of free cholesterol (FC) to cholesterol ester (CE) in lipoproteins. Mutations in the LCAT gene result in one of two clinical syndromes: complete LCAT deficiency syndrome, and “fish eye disease.” The former is characterized by a broad spectrum of clinical features, including profound high-density lipoprotein (HDL) deficiency, hypertriglyceridemia, corneal opacities, anemia, neuropathies, and nephropathy. In contrast, fish eye disease patients develop severe HDL deficiency and severe corneal opacities, but the nervous system and kidneys are typically unaffected. Whether there is a predisposition to accelerated coronary heart disease with LCAT deficiency remains controversial. Currently, severe corneal opacities may be treated with corneal transplant. Only anecdotal evidence is available for preventive measures of progressive renal complications. LCAT replacement therapies are under investigation.
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Baumann, Nicole, and Jean-Claude Turpin. Metachromatic Leukodystrophy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0052.
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Metachromatic leukodystrophy can be observed in infantile, juvenile, and adult cases. It is due to deficiency of the enzyme sulfatide sulfatase arylsulfase A. The adult form includes two types—one characterized by predominantly central nervous system motor signs (mainly pyramidal and/or cerebellar) and a peripheral neuropathy, and the other presenting with behavioral abnormalities and progressive mental deterioration. Homozygosity for the P426L mutation is very frequent in motor forms of adult MLD and heterozygosity for the I179S is very frequently found in psychiatric forms. Hematopoietic stem cell transplantation or bone marrow transplantation is the only presently available therapy that attempts to treat the primary central nervous system manifestation of MLD, but substantial risk is involved and long-term effects are not clear. Potential therapeutic application of hematopoietic stem cell gene therapy and intracerebral gene transfer (brain gene therapy) are explored in infantile forms of patients with MLD.
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Olkkola, Klaus T., Hugo E. M. Vereecke, and Martin Luginbühl. Drug interactions in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0021.
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When two or more drugs are administered simultaneously, the pharmacological response may be greater or less than the sum of the effects of the individual drugs. One drug may antagonize or potentiate the effects of the other and there may be also qualitative differences in response. Although some drug interactions increase the toxicity or result in loss of therapeutic effect, others are beneficial. Indeed, modern anaesthetic techniques depend on beneficial drug interactions. A sound combination of drugs helps clinicians to increase both the efficacy and safety of drug treatment. Drugs may interact on a pharmaceutical, pharmacodynamic, or pharmacokinetic basis. Many pharmacodynamic interactions are predictable and can be avoided by the use of common sense. However, it is much more difficult to predict the likelihood of pharmacokinetic and pharmaceutical interactions despite good prior knowledge of pharmacokinetics and chemical properties of individual drugs. Pharmaceutical drug interactions usually occur before the drug is given to the patient and they are caused by chemical (such as acid–base, salt formation, oxidation–reduction, hydrolysis, or epimerization) or physical (such as adsorption/absorption or emulsion breaking) reactions. When drugs have a pharmacokinetic interaction, one drug alters the absorption, distribution, or the elimination of the other drug. Many pharmacokinetic drug interactions are due to inhibition or induction of cytochrome P450 enzymes. Pharmacodynamic drug interactions are caused by drugs having an effect on the same receptors or the same physiological system. This chapter gives anaesthetists an overview of clinically relevant perioperative drug interactions.
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Lambert, David G. Mechanisms and determinants of anaesthetic drug action. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0013.
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This chapter is broken into two main sections: a general description of the principles of ligand receptor interaction and a discussion of the main groups of ‘targets’; and explanation of some common pharmacological interactions in anaesthesia, critical care, and pain management. Agonists bind to and activate receptors while antagonists bind to receptors and block the effects of agonists. Antagonists can be competitive (most common) or non-competitive/irreversible. The main classes of drug target are enzymes, carriers, ion channels, and receptors with examples of anaesthetic relevance interacting with all classes. There are many examples in anaesthesia where multiple interacting drugs are co-administered—polypharmacology. To give an example: neuromuscular blockade. Rocuronium is a non-depolarizing neuromuscular blocker acting as a competitive antagonist at the nicotinic acetylcholine receptor. Rocuronium competes with endogenous acetylcholine to shift the concentration–response curve for contraction to the right. The degree of contractility is less for a given concentration of acetylcholine (agonist) in the presence of rocuronium. Using the same principle, the rightward shift can be compensated by increasing the amount of acetylcholine (as long as the amount of rocuronium presented to the receptor as an antagonist remains unchanged, its action can be overcome by increased agonist). Acetylcholine at the effect site is increased by acetylcholinesterase inhibition with neostigmine. One of the side-effects of neostigmine is that it acts as an indirect parasympathomimetic. In the cardiovascular system this would lead to muscarinic receptor-mediated bradycardia; these effects are routinely reversed by the competitive muscarinic antagonist glycopyrrolate.
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Meurig Thomas, John. Architects of Structural Biology. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198854500.001.0001.
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Designed for the non-specialist, the explanations and illustrations used here describe the work, personalities, collaborations, and idiosyncrasies of four of the most distinguished Nobel Laureates of the twentieth century. They exploited a discovery made over a century ago about the nature of X-rays, and thereby created a new branch of science. This enabled them to elucidate, in atomic detail, the structure and mode of action of molecules of the living world: enzymes, vitamins, and viruses, as well as antibiotics. Perutz and Kendrew, from their pioneering work using X-ray diffraction on haemoglobin and myoglobin, the proteins that transport and store oxygen in all animals, led them to establish in 1962 one of the most successful research centres ever—the Laboratory of Molecular Biology (LMB) in Cambridge. Medicines discovered there are used worldwide to treat leukaemia, arthritis, and other diseases. Their work also led to the creation in the United States of the Protein Data Bank that guides scientists in understanding the misfolding of proteins, which cause Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative diseases. This book is first a memoir of these scientists and their contemporaries, many of them friends of the author. Second, it is an insight into the great excitement associated with structural molecular biology, which directly informs our understanding of ourselves. Third, it describes how two renowned research centres in the United Kingdom—the LMB and the Davy-Faraday Research Laboratory—achieved iconic status. It also highlights the importance of the popularization of science, of which Bragg, Perutz, and Kendrew, as well as Dorothy Hodgkin (who solved the structures of penicillin and vitamin B12) were experts.
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Atkins, Peter. Reactions. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199695126.001.0001.
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Illustrated with remarkable new full-color images--indeed, one or more on every page--and written by one of the world's leading authorities on the subject, Reactions offers a compact, pain-free tour of the inner workings of chemistry. Reactions begins with the chemical formula almost everyone knows--the formula for water, H2O--a molecule with an "almost laughably simple chemical composition." But Atkins shows that water is also rather miraculous--it is the only substance whose solid form is less dense than its liquid (hence ice floats in water)--and incredibly central to many chemical reactions, as it is an excellent solvent, being able to dissolve gases and many solids. Moreover, Atkins tells us that water is actually chemically aggressive, and can react with and destroy the compounds dissolved in it, and he shows us what happens at the molecular level when water turns to ice--and when it melts. Moving beyond water, Atkins slowly builds up a toolkit of basic chemical processes, including precipitation (perhaps the simplest of all chemical reactions), combustion, reduction, corrosion, electrolysis, and catalysis. He then shows how these fundamental tools can be brought together in more complex processes such as photosynthesis, radical polymerization, vision, enzyme control, and synthesis. Peter Atkins is the world-renowned author of numerous best-selling chemistry textbooks for students. In this crystal-clear, attractively illustrated, and insightful volume, he provides a fantastic introductory tour--in just a few hundred colorful and lively pages - for anyone with a passing or serious interest in chemistry.
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Donnelly, Catherine, ed. The Oxford Companion to Cheese. Oxford University Press, 2017. http://dx.doi.org/10.1093/acref/9780199330881.001.0001.
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Over 850 entriesThe Oxford Companion to Cheese is the first truly comprehensive reference work dedicated to the exploration of how four basic ingredients—milk, microorganisms, salt, and enzymes—are transformed into the more than fourteen hundred named cheese varieties enjoyed throughout the world. From cottage cheese to Camembert, from Gorgonzola to Gruyère, the Companion examines cheese on the farm, under the microscope, in the shop, and on the plate.More than just a pizza topping or cracker spread, cheese has been the founding capital of a few European banking systems, a religious sacrament, and an inspiration for writers and artists as far back as Homer. The Companion reveals these hidden depths in more than 850 wide-ranging entries. Here you will read about rightly famous cheeses, but also some that are not well known outside of their area of production, such as the traditional Turkish and Iranian cheeses ripened in sheep's or goat's skin. You will learn about animal species whose milk is commonly used (cow, goat, and sheep) and not so commonly used (yak, camel, and reindeer) in cheesemaking, as well as a few highly important breeds within each species (the Nubian goat or Lacaune sheep). You will explore regional cheesemaking traditions that date back millennia, and both ancient and modern cheesemaking technology and equipment. And you will delve into the vibrant interior world of cheese: the blooms, veins, sticky surfaces, gooey interiors, crystals, and yes, for some, the strong olfactory notes, are all due to microbial action and growth.To discuss cheese in its countless forms and contexts, the Companion enlisted 325 authors, including leading cheesemakers, mongers, dairy scientists, microbiologists, anthropologists, historians, journalists, archaeologists, and more, from backgrounds as diverse as cheese itself. This is the definitive guide to one of humankind's greatest discoveries.
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Lynch, Bernadette, and Aine Burns. The patient with scleroderma. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0165.
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Scleroderma is tightness, thickening, and non-pitting induration of skin. Two forms of the skin disease are described. Limited cutaneous systemic sclerosis (lcSSc) which occurs distal to the wrists (or ankles) and/or over the face and neck, often associated with longstanding Raynaud’s phenomenon, and diffuse cutaneous systemic sclerosis (dcSSc) where truncal as well as acral skin involvement occurs as well as tendon friction rubs. In this latter condition the onset of the skin changes occurs within 1 year of onset of Raynaud’s phenomenon; however, the skin involvement may precede onset of vascular symptoms.The skin manifestations are the outward manifestation of a systemic disease, systemic sclerosis. Lung, heart, and gut involvement are frequent. Scleroderma renal crisis, usually presenting as accelerated hypertension and acute kidney injury, is one of the most severe complications of this disease. Autoantibodies against RNA polymerase are associated with scleroderma renal crisis. It occurs in 12% of dcSSc and 2% of lcSSc patients (men and women) and carries a high morbidity and mortality although careful supportive care and blood pressure management using angiotensin converting enzyme inhibitors (ACEI) or angiotensin-II receptor blockers have improved short-term outcomes. In general, beta blockers should be avoided in the early management.Approximately two-thirds of patients require dialysis, of these many recover enough function to come off dialysis. Higher blood pressure and younger age at presentation have a better prognosis. ACEIs should be continued even after dialysis is established as the latter increases the chance of late recovery. Average time to coming off dialysis is 11 months but recovery is uncommon after 24 months. After a crisis renal function continues to improve for several years.
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Gnudi, Luigi, Giorgio Gentile, and Piero Ruggenenti. The patient with diabetes mellitus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0149_update_001.
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About one third of patients with type 1 diabetes develop diabetic nephropathy long-term (usually not before at least 10 years of diabetes), though this proportion is falling as standards of care have risen. Nephropathy is strongly associated with other microvascular complications of diabetes, so that some degree of retinopathy is to be expected, and evidence of neuropathy is common. Patients with type 2 diabetes are equally susceptible, but this is an older group in which vascular disease and other pathologies are also more likely. The rise in type 2 diabetes accounts for diabetes being the most common recorded cause of end stage renal disease (ESRD) in the developed world.Diabetic nephropathy is characterized by a progression through hyperfiltration, microalbuminuria, hypertension, overt proteinuria, nephrotic syndrome, loss of GFR, to ESRD. Risk factors for developing it include genetic factors (though no major single gene effects have been identified), and quality of glycaemic control.The risk of progression can at early stages be reduced by improved glycaemic control, and control of hypertension also slows progression. However angiotensin converting enzyme inhibitors or receptor blockers (ACEi, ARB) are the standard of care for patients with microalbuminuria or overt proteinuria, as they have been shown to reduce the risk of renal endpoints. Combination therapy with both ACEi and ARB together has been associated with a high risk of AKI, hyperkalaemia and other adverse effects so is not generally recommended. Other promising agents in combination are under investigation but none adequately proven at this stage.Patients who reach ESRD have reduced survival on all modalities compared to age-matched patients with other diagnoses. Best rehabilitation and survival for those who are suitable is through renal transplantation, though combined pancreas-renal transplantation may offer still better outcomes for selected patients.