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1
Ong, Debra. Assessment of hypersensitivity syndrome reactions to trimethoprim-sulfamethoxazole and abacavir in HIV-positive individuals using a lymphocyte toxicity assay. Ottawa: National Library of Canada, 2001.
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2
Bernhard, David. Cigarette Smoke Toxicity: Linking Individual Chemicals to Human Diseases. Wiley & Sons, Limited, John, 2011.
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3
Bernhard, David. Cigarette Smoke Toxicity: Linking Individual Chemicals to Human Diseases. Wiley & Sons, Incorporated, John, 2011.
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4
Cigarette Smoke Toxicity Linking Individual Chemicals To Human Diseases. Wiley-VCH Verlag GmbH, 2011.
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5
Individual Susceptibility to Genotoxic Agents in the Human Population. Springer, 2011.
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6
Serres, Frederick J. De. Individual Susceptibility to Genotoxic Agents in the Human Population. Springer, 2012.
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7
Frid, Christopher L. J., and Bryony A. Caswell. Toxicology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198726289.003.0002.
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To determine whether or not a contaminant has the potential to become a pollutant, its biological effects must first be established. The scientific discipline of toxicology considers the measurement of toxins, their mechanisms and the effects they have on the environment, its inhabitants and on human health. This chapter describes how contaminants behave in marine environments, how organisms are exposed to them and how they respond at the molecular, individual, population and ecosystem levels. Marine organisms exhibit a range of different responses and detoxification mechanisms that are used as the basis of approaches for measuring toxicity. The complex interactions of pollutants in the environment, their interactions with other toxicants and the large natural variability in toxic effects between species and individuals make this challenging. However, in order to regulate the production and discharge of pollutants it is critical that the impacts on ecosystems and ecosystem services are understood.
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Scordino, David. Infectious Colitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0031.
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Infectious colitis is diarrhea with evidence of colonic inflammation by visualization (colonoscopy), history (blood or mucus in the stool), or laboratory evidence (high lactoferrin). Infectious colitis is associated with direct bacterial or indirect bacterial toxin invasion of the colonic mucosa, leading to toxicity, volume loss, hemorrhage, and colonic inflammation. The most important treatment is adequate hydration, but treatment also may include loperamide (useful in patients without fever or bloody stools) and antibiotics in individuals with evidence of colitis (although not for mild to moderate diarrhea without colitis). In any individual with diarrhea, address recent travel history, possible immunosuppression, the presence of blood or mucus in the stool, and any history of vomiting or severe abdominal pain. Therapy should be focused on maintaining adequate hydration and not missing potentially dangerous etiologies. Intravenous hydration can be used for those with moderate to severe dehydration with supplemental oral hydration solutions if discharge is possible.
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Forsyth, Duncan. Physical assessment of older patients. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0011.
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Mental health problems may co-exist with or be the presenting feature of other medical illness in older age. All clinicians also need to consider the potential psychological impact of ill-health and its treatments on patients and their carers. This chapter gives a geriatrician’s guide to comprehensive geriatric assessment, identifying physiological changes that occur with ageing and the potential mental health presentations of common medical conditions. The ‘geriatric giants’ of falls, immobility, incontinence, delirium and drug toxicity are put in the context of maintaining higher-order cortical functioning to enable the individual to remain upright, mobile, continent and clear in their thinking. These are considered with admissions avoidance or safe discharge planning in mind.
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Hughes, Alis, and Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.
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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.
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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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Cutter, David, and Martin Scott-Brown. Treatment of cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0325.
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The variety of conditions that are considered to be ‘cancer’ is extremely wide, with marked variation in the management approach from disease to disease. A common feature in the management of malignant conditions, however, is the involvement of a wide range of medical professionals at different stages of the patient pathway. This commonly includes physicians, surgeons, radiologists, pathologists, medical oncologists, radiation oncologists, and specialist nurses, as well as a plethora of other allied disciplines. As such, a practice that has been widely adopted is to work as a multidisciplinary team (MDT), with regular meetings to decide the appropriate treatment for each patient with a cancer diagnosis, on an individual and case-by-case basis. The main treatment modalities for the treatment of cancer are surgery, radiotherapy, and chemotherapy. While these are often combined to form a multimodality therapy, they are all, in isolation, potentially radical (curative) therapies for certain conditions. For example, surgery (in the case of a Stage I colon adenocarcinoma), radiotherapy (in the case of early laryngeal squamous cell carcinoma), and chemotherapy (in the case of acute lymphoblastic leukaemia) are all curative as single-modality treatments. It is commonly the case, however, for a patient to require more than one mode of therapy to achieve the best outcome, for example a combination of surgery, chemotherapy, and radiotherapy for early breast cancer. It can also be the case that two or more different management strategies are thought to give equivalent oncological results, for example surgery or radiotherapy for early prostate cancer. In this situation, the MDT and the patient need to decide on the ‘best’ management plan for the individual, based on their personal and professional opinions and on the differing toxicity profiles of the alternate treatments.
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Srivastava, Siddharth, and Jeffrey Chinsky. Methylmalonic Acidemia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0062.
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Isolated methylmalonic acidemia (MMA) refers to a group of inborn errors of organic acid metabolism caused by impaired conversion of methylmalonyl-CoA to succinyl-CoA. Individuals with MMA experience both acute and chronic neurological complications. The pathophysiology likely reflects impaired energy metabolism in the mitochondria leading to neuronal toxicity in MMA. MMA presents with a spectrum of clinical phenotypes with onset of symptoms anytime from the neonatal period to adulthood. Once there is clinical suspicion for MMA, definitive diagnosis requires biochemical testing. The treatment of MMA centers on acute interventions when affected individuals are ill, as well as preventative measures when they are doing relatively well. Neuroimaging in MMA demonstrates a variety of findings.
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Fuks, Abraham. The Language of Medicine. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190944834.001.0001.
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The words that physicians use with patients have the power to heal or harm. The practice of medicine is shaped by the potent metaphors that are prevalent in clinical care, and military metaphors and the words of war bring with them unfortunate consequences for patients and physicians alike. Physicians who fight disease turn the patient into a passive battlefield. Patients are encouraged to remain stoic, blamed for “failing” chemotherapy and sadly remembered in heroic obituaries of lost battles. The search for disease as enemy shifts the doctor’s gaze to the computer and imaging technologies that render the patient transparent, unseen and unheard. Modern treatments save lives but patients can be the victims of collateral damage and friendly fire. In The Language of Medicine, Abraham Fuks, physician, medical educator and former Dean of Medicine, shows us how words are potent drugs that must be tailored to the individual patient and applied in carefully chosen and measured doses to offer benefits and avoid toxicity. The book shines a light on our culture that deprecates the skill of listening that is, paradoxically, the attribute that patients most desire of their doctors. Societal metronomes beat rapidly and compress clinic visits into stroboscopic encounters that leave patients puzzled, fearful and uncertain. Building on research about physicians in practice, the experiences of patients, stories of medical students as well as the history of medicine, Dr. Fuks promotes an ideal of clinical practice that is achieved by humble physicians who provide time and space for listening, select words with care, and choose metaphors that engender healing.
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Kuypers, Dirk R. J., and Maarten Naesens. Immunosuppression. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.
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Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids and corticosteroids has been fine-tuned over the last decade, based on empirically derived observations as well as on the results of large multicentre randomized clinical studies. Corticosteroid withdrawal and avoidance are feasible, at least in patients with a low immunological risk, but CNI-free protocols have had few long-term successes. Some minimization strategies have increased risk of developing acute rejection or (donor-specific) anti-HLA antibodies, with deleterious effects on the graft. Mammalian target of rapamycin inhibitors (mTORi) have shown limited benefit in early CNI replacement regimens and their long-term use as primary drug is hampered by intolerance. In the setting of particular malignant disease occurring after transplantation, such as squamous cell carcinoma of the skin and Kaposi’s sarcoma, mTORi seem promising. Induction agents (anti-interleukin 2 receptor monoclonal antibodies, antithymocyte globulins) effectively diminish the risk of early immunological graft loss in recipients with moderate to high immunological risk but at the price of more infectious or malignant complications. While personalized transplantation medicine is only in its early stages of development, attempts are made to quantitatively measure the clinical degree of immunosuppression, to tailor immunosuppressive therapy more specifically to the patient’s individual profile, and to monitor graft status by use of invasive (e.g. surveillance renal biopsies) and non-invasive biomarkers. These scientific endeavours are a necessity to further optimize the current immunosuppressive therapy which will remain for some time to come.
16
O’Donoghue, John L. Neurologic Manifestations of Organic Chemicals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0176.
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Organic chemicals can produce many different effects on the nervous system. The nervous system functions are affected by a variety of different organic chemicals. Organic chemicals that induce neurotoxicity may be naturally occurring or synthetic. Those that are naturally occurring products of plants or animals are referred to as “toxins,” whereas those that are synthetic are referred to as “toxicants”; however, publications and regulations sometimes use these terms interchangeably. Underlying these functional changes are cellular and subcellular changes that mediate the clinical and pathological appearance of the neurotoxicity. The ability to make a diagnosis of organic-chemical-induced neurotoxicity is dependent on being able to link a clinical situation with an exposure in a dose-related manner. Treatment and management of organic-chemical-induced neurotoxicity in affected individuals is dependent upon the specific chemical involved and the underlying mechanism by which toxicity occurs.
17
Al-Darraji, Haider A., and Frederick L. Altice. The Perfect Storm. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199374847.003.0008.
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Globally, tuberculosis (TB) is a major cause of morbidity and mortality among people who use drugs (PWUD), particularly those co-infected with HIV. This chapter describes how TB is prevalent in several prison systems by virtue of the concentration of PWUD and people living with HIV. TB is further amplified within this system through overcrowding, poor ventilation, and delayed access to quality prevention and treatment services. In many countries, individuals cycling through prisons are inadequately screened and treated for TB, and affected individuals may have frequent treatment interruptions. For PWUD, relapse to drug use immediately after release from custody can impede continuity of care, which may contribute to the development of drug-resistant TB. Particularly in countries with high incarceration rates, prisons act as amplifiers of TB and drug-resistant TB in the community. The World Health Organization’s recommendations for integration of TB, HIV, and addiction treatment are seldom achieved, especially within prisons. Other factors contributing to poor TB outcomes among PWUD interfacing with prisons include insufficient support to promote medication adherence and co-morbidities, like viral hepatitis that potentiate hepatic toxicity, both of which are prevalent among PWUD.
18
Sullivan, Maria, and Frances Levin, eds. Addiction in the Older Patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199392063.001.0001.
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Addictive disorders in older adults are underdiagnosed and undertreated. An important reason for this lack of recognition of a serious health problem is a paucity of clinical knowledge about how such disorders present in this population. The presentation for alcohol and substance use disorders in the elderly can be confusing, given the metabolic changes and concurrent conditions associated with aging, together with interactions between alcohol and prescribed psychoactive drugs. Further, screening instruments have not been validated for this population. Brief interventions may be effective but should take into account contextual needs such as medical conditions, cognitive decline, and mobility limitations. Treatment strategies, including detoxification regimens, need to be modified for older patients and - in the case of opioid dependence - must address the management of chronic pain in this population. Ironically, benzodiazepines are the most frequently prescribed psychoactive medication in the elderly, despite older individuals' greater sensitivity to side effects and toxicity. Older women are at particularly heightened vulnerability for iatrogenic dependence on sedatives and hypnotics. More clinical research data are needed to inform screening and referral strategies, behavioral therapies, and pharmacological treatment. At the same time, emerging technologies such as communication tools and monitoring devices offer important opportunities to advance addiction treatment and recovery management in older adults. Although research to date has been limited in this population, recent data suggest that treatment outcomes are equal or better to those seen in younger cohorts.
19
Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.
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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.