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1
Lee, Amanda Jayne. Potential biomarkers of cancer risk associated with exposure to hexavalent chromium. Birmingham: University of Birmingham, 2003.
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2
Ballachey, Brenda Elizabeth. Biomarkers of damage to sea otters in Prince William Sound, Alaska, following potential exposure to oil spilled from the Exxon Valdez. Anchorage, AK: U.S. Fish and Wildlife Service, Alaska Fish and Wildlife Research Center, 1995.
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3
Ballachey, Brenda Elizabeth. Biomarkers of damage to sea otters in Prince William Sound, Alaska, following potential exposure to oil spilled from the Exxon Valdez. Anchorage, AK: U.S. Fish and Wildlife Service, Alaska Fish and Wildlife Research Center, 1995.
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4
Ballachey, Brenda Elizabeth. Biomarkers of damage to sea otters in Prince William Sound, Alaska, following potential exposure to oil spilled from the Exxon Valdez. Anchorage, AK: U.S. Fish and Wildlife Service, Alaska Fish and Wildlife Research Center, 1995.
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5
Blumenberg, Miroslav, ed. Human Skin Cancer, Potential Biomarkers and Therapeutic Targets. InTech, 2016. http://dx.doi.org/10.5772/61922.
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6
Tenovuo, Olli, Jean-charles Sanchez, Damir Janigro, and Johan Undén, eds. Biomarkers of Brain Damage – A Complex Challenge with Great Potential. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-754-3.
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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Biomarkers and cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0040.
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Biomarkers and cancer defines these markers and outlines their role in diagnosis, prognosis, prediction of response, and response assessment of a variety of cancers. Established biomarkers are reviewed, and the potential for development of new biomarkers offered by the dramatic progress in both the understanding of molecular biology and the development of laboratory techniques is emphasised. The field of signal transduction has already proved fruitful, with identification of markers allowing successful targeted therapy in a range of cancers. Progress is anticipated also in tumour imaging, with developments in both MRI and PET. Areas of clinical interest are summarised for breast, lung, colorectal, renal, and CNS malignancies.
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Nizari, Shereen, Cheryl Hawkes, Anusha Mishra, and Yorito Hattori, eds. The Neurovascular Unit as a Potential Biomarker and Therapeutic Target in Cerebrovascular Disease. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-238-5.
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9
Prowle, John R. Renal injury biomarkers in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0302.
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Acute kidney injury (AKI) is a common complication of critical illness and its occurrence has been independently associated with both short- and longer-term morbidity and mortality. However, conventional diagnosis of AKI, based on rises in serum creatinine, can be delayed and inaccurate, particularly in the context of critical illness. These diagnostic limitations potentially prevent timely intervention and appropriate follow-up of patients experiencing AKI. Recently, a number of novel urinary and serum biomarkers of AKI have been described that may provide earlier and more precise diagnosis. Importantly, a number of these substances are biologically-linked to the pathophysiology of acute tubular injury. However, true validation and widespread clinical uptake of these biomarkers is likely to require demonstration of improved patients’ outcomes as a consequence of biomarker-driven clinical interventions.
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Farooqui, Akhlaq A. Neurochemical Aspects of Alzheimer's Disease: Risk Factors, Pathogenesis, Biomarkers, and Potential Treatment Strategies. Elsevier Science & Technology Books, 2017.
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Farooqui, Akhlaq A. Neurochemical Aspects of Alzheimer's Disease: Risk Factors, Pathogenesis, Biomarkers, and Potential Treatment Strategies. Elsevier Science & Technology Books, 2017.
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12
Tansley, Sarah L., and Neil J. McHugh. Laboratory features—enzymes and biomarkers. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0012.
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This chapter describes the laboratory tests useful in diagnosing and monitoring patients with myositis. It describes creatinine kinase, it’s different isoforms and explains why this muscle enzyme is helpful in the diagnosis and monitoring of patients with inflammatory muscle disease. It also describes other skeletal muscle enzymes that are often elevated in both adult and juvenile onset disease and examines the specificity of troponins for cardiac muscle involvement. The prevalence and clinical utility of myositis specific and associated autoantibodies is explored, and we report the clinical features associated with different autoantibody subgroups, demonstrating how such autoantibodies can divide patients into clinically homogenous subgroups. Finally, evidence for the potential use of other novel biomarkers including cytokines is also explored.
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Oikonomopoulou, Katerina, and Vinod Chandran. Biomarkers of psoriatic arthritis outcomes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0022.
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Psoriatic arthritis is an inflammatory musculoskeletal disease that occurs in patients suffering from psoriasis. The disease manifests with symptoms affecting the skin, peripheral and axial joints, and periarticular structures. Diagnosis and management of psoriatic arthritis is challenging due to its heterogeneous presentation. However, early diagnosis and subsequent appropriate treatment reduces disease activity, prevents joint damage, and improves long-term outcome. It is hoped that biomarkers for disease progression and activity will aid in cost-effective clinical management of patients. Potential biomarkers under investigation for psoriatic arthritis are disease-related components derived from skin and articular tissues, biological fluids, such as blood and synovial fluid, and arthritis-associated cell populations. Imaging including ultrasound and MRI are also being evaluated as biomarkers for diagnosis, activity and outcome. Despite the challenge of bringing these new markers into the clinic, many of these markers hold promise for the future management of patients with psoriatic arthritis.
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Lameire, Norbert. The role of novel biomarkers in acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0223_update_001.
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Although there is a growing literature on the performance of various biomarkers in clinical studies, there is limited information on how these biomarkers would be utilized by clinicians to manage patients with acute kidney injury (AKI). The majority of investigations have focused on the ability of biomarkers to detect early either incipient or established AKI. Other studies have prospectively explored their prognostic performance in predicting either need for renal replacement therapy or intensive care unit (ICU) or hospital mortality or duration of either ICU or hospital stay. A few studies have also investigated their potential in the differential diagnosis between ‘transient AKI’, ‘prerenal AKI’, and established intrinsic AKI, mostly acute tubular necrosis.
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Toussirot, Eric, Katarzyna Bogunia-Kubik, and Philippe Saas, eds. Recent Advances in Potential Biomarkers for Rheumatic Diseases and in Cell-based Therapies in the Management of Inflammatory Rheumatic Diseases. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-426-8.
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Volk, Hans-Dieter, and Levent Akyüz. Immunotherapy in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0055.
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Immunotherapy in critically-ill patients is only feasible at clinical experimental level; no therapy has been approved so far. To develop a potential therapeutic strategy we need to know the pathogen, immune status of the patient, and interaction between the particular pathogen and immune cells to readjust the patient´s individually imbalanced immunological responsiveness. Giving the right treatment at the right time is crucial for a better outcome and the best economic use of resources. The process starts by matching the therapeutic selection to the clinical need. Personalized immunotherapy, highly dependent on the available biomarker, is required. Future studies on new immunotherapeutic approaches in critically-ill patients can only be interpreted in combination with immunological biomarker analyses. Immune modulation is a promising approach despite many disappointing results and there is a clear need for immunological stratification of critically-ill patients for improved efficacy. The search continues for new clinical endpoints in surviving patients with medical and health-economical impact.
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Yoris, Adrián, Adolfo M. García, Paula Celeste Salamone, Lucas Sedeño, Indira García-Cordero, and Agustín Ibáñez. Cardiac interoception in neurological conditions and its relevance for dimensional approaches. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198811930.003.0010.
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Dimensional and transdiagnostic approaches have revealed multiple cognitive/emotional alterations shared by several neuropsychiatric conditions. While this has been shown for externally triggered neurocognitive processes, the disruption of interoception across neurological disorders remains poorly understood. This chapter aims to fill this gap while proposing cardiac interoception as a potential common biomarker across disorders. It focuses on key aspects of interoception, such as the mechanisms underlying different interoceptive dimensions; the relationship among interoception, emotion, and social cognition; and the roles of different interoceptive pathways. It considers behavioral and brain evidence in the context of an experimental and clinical agenda to evaluate the potential role of interoception as a predictor of clinical outcomes, a marker of neurocognitive deficits across diseases, and a general source of insights for breakthroughs in the treatment and prevention of multiple disorders. Finally, future directions to improve the dimensional and transdiagnostic assessment of interoception are outlined.
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Carrión, Victor G., John A. Turner, and Carl F. Weems. Treatment Outcomes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190201968.003.0008.
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The phenomenology of PTSD has been established in the previous chapters to be an already broad domain that encompasses a myriad of interactions between brain systems. As our understanding of the disorder expands and yields new questions, so do the available options for treatment. The current chapter reviews the cognitive and behavioral interventions for PTSD and other anxiety disorders that have demonstrated efficacy in clinical trials, as well as a variety of emerging pharmacological interventions and the preclinical literature that has informed their development. The identification of biomarkers for PTSD is discussed in terms of their potential application as both potential predictors of the development of PTSD and of the outcome of interventions designed to treat it.
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Todder, Doron, Keren Avirame, and Hagit Cohen. Neuromodulation Methods in PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0039.
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This chapter discusses the rationale and methodology for applying techniques of active and passive neuromodulation for treatment-refractory post-traumatic stress disorder (PTSD). Neuromodulation derives from the concept of neuroplasticity, which signifies long-term changes in the effectiveness of connections between distinct parts of the central nervous system. These changes are reflected across multiple levels of the nervous system, going from the cellular level to circuits and large-scale brain networks. It has been long suggested that altered neuroplasticity is a biomarker of neuropsychiatric diseases. With recent advances in neuroscience, research is emerging on evaluating the potential of modulating neural circuits by using innovative technologies, including noninvasive and invasive brain stimulation, EEG-neurofeedback, and fMRI neurofeedback.
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Weaver, Virginia M., Bernard G. Jaar, and Jeffrey J. Fadrowski. Kidney Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0031.
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This chapter describes kidney disorders related to occupational and environmental exposures and addresses prevention and control. Sections address assessment of kidney function, acute kidney injury, and chronic kidney disease (CKD). Kidney disease from acute, high-level exposures as well as lower level exposures in combination with other CKD risk factors are considered. Established nephrotoxicants, including aristolochic acid, arsenic, cadmium, lead, melamine, mercury, silica, and solvents, are discussed. The limited data available on other agents, such as perfluorooctanoic acid and fine particulate matter, are also presented. The potential for kidney function to impact biomarker levels is considered. A final section addresses a current epidemic of CKD of unknown etiology in agricultural workers in specific countries.
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van der Burg, Jorien M. M., N. Ahmad Aziz, and Maria Björkqvist. Peripheral Pathology. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0014.
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Clinicians and researchers have previously focused on the neurologic and psychiatric aspects of Huntington’s disease (HD). However, it is becoming evident that many neurodegenerative disorders are also complicated by pathology in tissues outside the brain. Although many clinical features of HD can be ascribed to neuronal loss and dysfunction, there is accumulating evidence indicating a role for the pathology of non-neuronal tissues in the disease process. Mutant huntingtin is expressed throughout the body and may induce pathology in parallel in both the brain and other organs. Insights into peripheral pathology in HD have the potential of improving knowledge of key pathogenic mechanisms. This chapter describes peripheral manifestations of HD, including weight loss, muscle wasting, and cardiac dysfunction, and discusses how these might constitute targets for drug treatment as well as offering disease modeling systems and potential sources of biomarkers.
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Felger, Jennifer C., Ebrahim Haroon, and Andrew H. Miller. Inflammation and Immune Function in PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0013.
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Numerous reports have described an association between PTSD and alterations in the immune response primarily characterized by increased biomarkers of inflammation, including inflammatory cytokines and acute phase reactants as well as increased inflammatory responses to immune stimuli. When considering systems that evolved to protect and prepare organisms during challenge, it is not surprising that the immune system is affected by exposure to trauma, or to the chronic stress associated with PTSD symptoms. Conversely, inflammatory cytokines have been shown to affect the brain, and may influence neural circuits of fear and anxiety to contribute to PTSD symptoms. This chapter discusses the evolutionary legacy of a primed inflammatory response in the context of trauma and stress, examines the evidence of altered immune function and inflammation in PTSD, explores the potential mechanisms involved, characterizes the consequences on neurocircuitry and health, and discusses potential translational implications.
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Adami, Hans-Olov, David J. Hunter, Pagona Lagiou, and Lorelei Mucci, eds. Textbook of Cancer Epidemiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.001.0001.
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This book offers an overview of the epidemiology and primary prevention for most forms of human cancer. It summarizes concepts and methods of epidemiology, the biology of cancer, cancer genetics, and the emerging potential of biomarkers. It also reviews specific cancer sites in a consistent way, providing clinical and pathological outlines, descriptive epidemiology, and a comprehensive account of traditional and molecular risk factors and their etiological importance. To facilitate reading and use of our Textbook as a reference, we have consistently addressed potential risk factors in the same order throughout all site-specific chapters. Acknowledging that any causal inference has an element of subjectivity, we have also attempted to classify the strength of existing evidence into distinct categories for each cancer site. An epilogue summarizes the major contributions that epidemiology has made in the last few decades to our understanding of the causes of cancer, and speculates about future developments.
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Over 50 Covid-19 Biomarkers Exacerbated by Glucose, and Potentially Improved by Cannabinoids, Curcumin, Vitamin d, and Gaba: Results of an Ongoing Database Search. Lulu Press, Inc., 2022.
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25
Gipson, Tanjala T., Andrea Poretti, Rebecca McClellan, and Michael V. Johnston. Tuberous Sclerosis Complex. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0050.
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Tuberous sclerosis complex (TSC) is a disease, commonly classified as a neurocutaneous disorder, which may result in benign tumors throughout the brain and body, skin lesions, epilepsy, and cognitive/behavioral difficulties. Scientific discovery in TSC has resulted in the availability of treatments designed to target the neurobiological core of TSC in children. However, research is needed to determine if these treatments are effective for multiple aspects of the TSC phenotype in children. Current pediatric research studies have focused on the effects of early treatment of epilepsy as well as identification of potential biomarkers. This chapter reviews the aspects of TSC unique to pediatric patients, the status of current research, and future directions.
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Yilmaz, Ali, and Anca Florian. Myocarditis: imaging techniques. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0367.
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The clinical presentation of myocarditis is multifaceted and electrocardiogram (ECG) changes as well as biomarkers tend to be non-specific. Therefore, the diagnosis of myocarditis can be challenging and should be based on an integrated approach including patient history, physical examination, non-invasive tests such as ECG and serum biomarkers, and non-invasive cardiac imaging. As myocarditis may lead to global ventricular dysfunction, regional wall motion abnormalities, and/or diastolic dysfunction, echocardiography should be routinely performed. However, hallmarks of acute myocarditis comprise structural changes such as cardiomyocyte swelling, an increase in extracellular space and water content, accumulation of inflammatory cells, potential necrosis or apoptosis of cardiomyocytes, and myocardial remodelling with fibrotic tissue replacement that can be depicted by cardiovascular magnetic resonance. Nuclear techniques are still not routinely recommended for the work-up of myocarditis—with the possible exception of suspected sarcoidosis—due to limited data, limited diagnostic specificity, limited availability, and risk from radiation exposure. This chapter focuses on those non-invasive cardiac imaging techniques that are used in daily clinical practice for work-up of suspected myocarditis. However, as research continues and novel imaging techniques become available, it is hoped that even more accurate and timely diagnosis of myocarditis will be possible in the near future.
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Seeck, Margitta, and Donald L. Schomer. Intracranial EEG Monitoring. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0029.
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Intracranial electroencephalography (iEEG) is used to localize the focus of seizures and determine vital adjacent cortex before epilepsy surgery. The two most commonly used electrode types are subdural and depth electrodes. Foramen ovale electrodes are less often used. Combinations of electrode types are possible. The choice depends on the presumed focus site. Careful planning is needed before implantation, taking into account the results of noninvasive studies. While subdural recordings allow better mapping of functional cortex, depth electrodes can reach deep structures. There are no guidelines on how to read ictal intracranial EEG recordings, but a focal onset (<5 contacts) and a high-frequency onset herald a good prognosis. High-frequency oscillations have been described as a potential biomarker of the seizure onset zone. Intracranial recordings provide a focal but magnified view of the brain, which is also exemplified by the use of microelectrodes, which allow the recording of single-unit or multi-unit activity.
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O’Brien, John T., and Louise Grayson. Mild Cognitive Impairment and predementia syndromes. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0032.
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Mild cognitive impairment is a term used to describe a condition or conditions where subjects have recognisable degrees of objective cognitive impairment which fall short of current standardised definitions for either a dementia syndrome in general, or for particular disorders such as Alzheimer’s disease, dementia with Lewy bodies or frontotemporal dementia. This chapter summarises some of the key issues surrounding the historical development of pre-dementia syndromes, considers the conceptual issues related to the use of the term mild cognitive impairment as a diagnosis, summarises what is known regarding epidemiology, clinical features, pathophysiology, prognosis, therapeutics and outlines current clinical practice in the area. The chapter concludes with a review of recent research developments and looks at the new diagnostic criteria, in particular the potential use of biomarkers to allow diagnosis of Alzheimer’s disease (AD) at an early, or mild cognitive impairment, stage.
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Teixeira, Antonio L., and Moises E. Bauer, eds. Immunopsychiatry. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.001.0001.
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In recent years, great attention has been devoted to the understanding of the immune dysfunction that is associated with major psychiatric disorders. In the context of the reconceptualization of the immune system as a homeostatic system, immune cells, molecules and mechanisms are highly promising as new diagnostic and therapeutic targets to reduce the burden of mental/psychiatric disorders. In this regard, immune cells, molecules and mechanisms are highly promising. The literature on immunology of psychiatric disorders is still disperse, and only very few attempts have been done so far to consolidate the current knowledge in this expanding and exciting area. Each chapter will present the available data on the immune/inflammatory dysfunction in psychiatric disorders, indicating the potential use of novel immunological biomarkers or therapeutic targets, as well as discussing the challenges ahead to incorporate this knowledge into the clinical practice.
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Scobie, Antonia, Mark Gilchrist, Laura Whitney, and Matthew Laundy. Managing antimicrobials on the shop floor. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198758792.003.0005.
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Reducing antimicrobial usage is key to stewardship, reducing adverse effects, and potentially stemming the tide of resistance. Establishment of an antimicrobial team on the shop floor to develop and manage a practical programme is discussed. Suggested methods of reducing antimicrobial usage include preventing initiation of unnecessary antimicrobials by the use of evidence-based guidelines and biomarker-directed clinical pathways, restricting durations to the shortest effective course—with automatic stop orders and separate antibiotic prescription charts, parenteral to oral switch programmes and utilization of outpatient parenteral antimicrobial therapy services when available. Finally, cessation of inappropriate treatment and reducing the use of broad-spectrum antimicrobials are essential and can be achieved by restrictive strategies such as pre-authorization and persuasive strategies such as audit and feedback via stewardship ward rounds. Different approaches to implementing audit and feedback within hospitals are covered in detail in this chapter.
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Moulton, Calum D. Novel pharmacological targets. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0013.
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There is a bidirectional relationship between depression and type 2 diabetes (T2D). Patients with comorbid depression and T2D are at high risk of complications and premature mortality. Conventional treatments for depression do not consistently improve diabetes outcomes, despite improving depressive symptoms. Shared mechanisms may underpin both depression and T2D, providing novel pharmacological targets to treat both conditions simultaneously. There are several candidate pathways. For inflammation and vitamin D deficiency, there is good cross-sectional evidence to support an association with depression in T2D. Prospective epidemiological studies are needed to test biological pathways as predictive biomarkers of depression and T2D. Intervention studies are needed to test the modifiability of these pathways. Repurposing of established diabetes treatments may provide a ‘multiple hit’ strategy. The identification and modification of novel biological targets has the potential to treat both depression and T2D, as well as reducing longer term morbidity and mortality.
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Reckman, Yolan J., and Yigal M. Pinto. The role of non-coding RNA/microRNAs in cardiac disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0031.
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In the past two decades, our knowledge about non-coding DNA has increased tremendously. While non-coding DNA was initially discarded as ‘junk DNA’, we are now aware of the important and often crucial roles of RNA transcripts that do not translate into protein. Non-coding RNAs (ncRNAs) play important functions in normal cellular homeostasis and also in many diseases across all organ systems. Among the different ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have been studied the most. In this chapter we discuss the role of miRNAs and lncRNAs in cardiac disease. We present examples of miRNAs with fundamental roles in cardiac development (miR-1), hypertrophy (myomiRs, miR-199, miR-1/133), fibrosis (miR-29, miR-21), myocardial infarction (miR-15, miR17~92), and arrhythmias/conduction (miR-1). We provide examples of lncRNAs related to cardiac hypertrophy (MHRT, CHRF), myocardial infarction (ANRIL, MIAT), and arrhythmias (KCNQ1OT1). We also discuss miRNAs and lncRNAs as potential therapeutic targets or biomarkers in cardiac disease.
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Franceschi, Silvia, Hashem B. El-Serag, David Forman, Robert Newton, and Martyn Plummer. Infectious Agents. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0024.
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Eleven infectious agents (seven viruses, three parasites, and one bacterium) have been classified by the International Agency for Research on Cancer as carcinogenic to humans for one or more cancer sites: hepatitis B virus; hepatitis C virus; thirteen types of human papillomavirus (HPV); human immunodeficiency virus type 1 (HIV-1); human T-cell leukemia virus type 1; Epstein-Barr virus; Kaposi sarcoma herpesvirus; Helicobacter pylori; Opisthorchis viverrini; Clonorchis sinensis; and Schistosoma haematobium. Other infectious agents, such as Merkel cell polyomavirus, Plasmodium falciparum, and cutaneous HPVs, have been classified as “probably carcinogenic” or “possibly carcinogenic.” Accurate biomarkers of chronic infection have been essential for estimating risk and ascribing a causal role to infectious agents in cancer. Of the 14 million cases of cancer estimated to have occurred worldwide in 2012, 2.2 million were caused by infectious agents. Vaccination and screen-and-treat programs have the potential for greatly reducing the burden of cancer caused by infections.
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Haiman, Christopher, and David J. Hunter. Genetic Epidemiology of Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0004.
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This chapter explores the genetic epidemiology of cancer: the identification and quantification of inherited genetic factors, and their potential interaction with the environment, in the etiology of cancer in human populations. It also describes the techniques used to identify genetic variants that contribute to cancer susceptibility. It describes the older research methods for identifying the chromosomal localization of high-risk predisposing genes, such as linkage analysis within pedigrees and allele-sharing methods, as it is important to understand the foundations of the field. It also reviews the epidemiologic study designs that can be helpful in identifying low-risk alleles in candidate gene and genome-wide association studies, as well as gene–environment interactions. Finally, it describes some of the genotyping and sequencing platforms commonly employed for high-throughput genome analysis, and the concept of Mendelian randomization and how it may be useful in the study of biomarkers and environmental causes of cancer.
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K. Gautam, Rupesh, Lokesh Deb, and Kamal Dua, eds. Natural Products for the Management of Arthritic Disorders. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/97898150507761220101.
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Rheumatoid arthritis (RA) is the most common inflammatory complication and affects approximately 1 % of the global population. It affects three times more women than men. RA is an autoimmune disorder elicited by exposure of genetic factors from the host to unknown antigens causing arthritogenic complaints. It also includes the activation of lymphocytes as well as CD4+ helper T cells along with local release of chronic inflammatory mediators and cytokines like tumor necrosis factor (TNF α) and various cytokines like interleukins (IL) that enormously affect the joints. The available allopathic therapies for RA are not a cure for the complications, and antibody therapy and surgical procedures are expensive. However, in the present era, researchers and healthcare professionals have moved toward natural medicines obtained from plants and other natural sources. Research based on developments in phytomedicine has progressed steadily. Evidence has been collected to show the massive therapeutic potential of medicinal plants used in various traditional systems against many pathological complications. Researchers have focused on the therapeutic potential of natural products used for treatment and counteracting various disorders along with their complications having negligible adverse effects. Natural Products for the Management of Arthritic Disorders compiles current knowledge about the bioactive compounds and herbal formulations useful in the treatment of rheumatoid arthritis. 11 chapters explain the role of natural products in the management of rheumatoid arthritis. Topics have been contributed by experts in medicinal chemistry and rheumatology. The book first introduces the reader to rheumatoid arthritis before delving into conventional and alternative therapies for the disease. The editors have also included special topics such as the biomarkers for RA, cytokines and anti-inflammatory mediators, preclinical and clinical studies. The range of topics should provide a comprehensive overview of natural remedies for arthritis and the role of natural products in anti-arthritic drug development. The information will be useful for many readers including medical and pharmacology students, multidisciplinary research scholars, scientists, pharma / herbal / food industrialists, and policy makers.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.
Full textAbstract:
The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.