Books on the topic 'High susceptibility'
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1
Dahlin, D. C. Magnetic susceptibility of minerals in high magnetic fields. Washington, DC: U.S. Dept. of the Interior, Bureau of Mines, 1993.
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2
1926-, Roth June, ed. Reversing health risks: How to get out of high-risk category for cancer, heart disease, diabetes, and other health problems. New York: Putnam, 1988.
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Karapetrov, Goran. Flux creep in Bi₂Sr₂CaCu₂O[subscript x] and YBa₂Cu₃O[subscript x] thin films: Magnetization and susceptibility studies. 1996.
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4
Turner, Neil, Teena Tandon, and Rajiv Agarwal. APOL1 and renal disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0341_update_001.
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Although apolipoprotein L1 (APOL1) is not known to be a direct cause of renal disease, it has emerged as a powerful cofactor in several important conditions. APOL1 gene polymorphisms account for the restriction of HIV-associated collapsing focal segmental glomerulosclerosis (FSGS) to those with African ancestry. In Africa, the disease-predisposing alleles seem to have been selected for because they convey resistance to some strains of trypanosomiasis. The same alleles are associated with increased susceptibility to primary FSGS, and are probably able to fully account for the excess of FSGS in black races. Two high-risk alleles have been labelled G1 and G2. To have increased susceptibility, individuals must usually have two copies, that is, it is recessive, but the gene frequency is high in West and Southern Africa and in those descended from those regions. The same alleles convey susceptibility to other more common renal diseases. Numerically the most significant association is with nephropathy previously attributed to hypertension. Recent evidence suggests that the gene may increase rate of progression in renal disease of various types, including diabetes. The mechanism is not known.
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Eyre, Steve, and Jane Worthington. Genetics of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0040.
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A range of epidemiological studies have clearly established that susceptibility to rheumatoid arthritis (RA) is determined by both genetic and environmental factors. Studies over the last five decades have used a variety of approaches to identify the genetic variants associated with disease. HLA DRB1 was the first RA susceptibility locus to be discovered and has the largest effect size. We describe current understanding of the complexities of HLA association for RA. Linkage and small-scale association studies prior to 2007 provided convincing evidence for only one more RA susceptibility locus, PTPN22. Major breakthroughs in high-throughput genotyping and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. This approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 60 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
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Eyre, Steve, Jane Worthington, and Sebastien Viatte. Genetics of rheumatoid arthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0040_update_003.
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A range of epidemiological studies have clearly established that susceptibility to rheumatoid arthritis (RA) is determined by both genetic and environmental factors. Studies over the last five decades have used a variety of approaches to identify the genetic variants associated with disease. HLA DRB1 was the first RA susceptibility locus to be discovered and has the largest effect size. We describe current understanding of the complexities of HLA association for RA. Linkage and small-scale association studies prior to 2007 provided convincing evidence for only one more RA susceptibility locus, PTPN22. Major breakthroughs in high-throughput genotyping, and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. Widespread utilization of this approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 100 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease, and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
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Penney, Kathryn L., Kyriaki Michailidou, Deanna Alexis Carere, Chenan Zhang, Brandon Pierce, Sara Lindström, and Peter Kraft. Genetic Epidemiology of Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0005.
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Chapter 5 reviews epidemiologic studies conducted to identify germline (inherited) susceptibility loci. These studies can involve associations observed within high-risk family pedigrees or in large studies of unrelated individuals. The chapter reviews the methods used to estimate the aggregate contribution of inherited genetic susceptibility and to identify specific genetic loci associated with risk. Although there is considerable variability across cancers, most cancers exhibit familial clustering, driven in part by a small number of known rare variants with large relative risks and a larger number of common variants with modest relative risks. The chapter discusses the implications of these findings for clinical care, public health, and tumor biology. It closes with a discussion of open questions, most notably the puzzle of “missing heritability”: the fact that—despite tremendous advances—multiple lines of evidence suggest that most specific risk variants, both rare and common, have yet to be discovered.
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Macronutrients and fibre requirements during pregnancy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0004.
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In this chapter, the impact of varying intakes of protein, carbohydrate and lipids, which are the key nutrients that contribute to calorie intake, is examined. Fibre is also an important food component that needs to be considered. The maternal macronutrient profile can influence embryonic and fetal development. For instance, both low and excessively high protein intakes during pregnancy are associated with restricted growth, increased adiposity, and impaired glucose tolerance. High-fat maternal diets can significantly increase the susceptibility to diet-induced obesity and percentage total body fat in offspring, although types of fats need to be considered, as intake of polyunsaturated fatty acids is important for fetal development. The type and content of carbohydrate (high- vs low-glycaemic sources) in the maternal diet influences blood glucose concentration, which has a direct effect on fetal glucose levels and metabolism.
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Furst, Eric M., and Todd M. Squires. Interferometric tracking. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199655205.003.0006.
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The purpose of this chapter is to present a survey of passive microrheology techniques that are important complements to more widely used particle tracking and light scattering methods. Such methods include back focal plane interferometry and extensions of particle tracking to measure the rotation of colloidal particles. Methods of passive microrheology using back focal plane interferometry are presented, including the experimental design and detector sensitivity and limits in frequency bandwidth and spatial resolution. The Generalized Stokes Einstein relation is derived from linear response theory of the particle position power spectrum and complex susceptibility. Applications of interoferometric tracking include high frequency microrheology and two-point measurements. Lastly, the chapter includes a discussion of rotational passive microrheology and the rotational GSER.
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Raghavan, Sri. Infection in the Cancer Patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0054.
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Cancer patients have increased susceptibility to a variety of both common and atypical infections due to the steady increase in outpatient chemotherapy regimens, these patients are presenting more often to the emergency department when acutely ill. Already immunocompromised, patients’ chemotherapy regimens lead to neutropenia, deficits in cellular and humoral immunity, and disruption of mucosal barriers that predisposing them to severe disease presentations with high morbidity and mortality rates. There are different subsets of oncologic patients predisposed to specific infections. One of the most common presentations of oncologic chemotherapy patients is neutropenic fever caused by bacterial infection; neutropenic patients are also highly susceptible to fungal infections. Patients with hematologic malignancies, particularly those undergoing chemotherapy or bone marrow transplant, can present with inflammation of the cecum with high risk for bacterial translocation and possible perforation. Patients who have indwelling catheters or mediports are at risk for catheter-associated bloodstream 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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Faraone, Stephen V., Pradeep G. Bhide, and Joseph Biederman. Neurobiology of Attention Deficit Hyperactivity Disorder. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0064.
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Attention deficit hyperactivity disorder (ADHD) is a prevalent, early-onset and persistent disorder of inattention, hyperactivity, and impulsivity. The mechanisms of action of ADHD medications, neuroimaging studies, and studies of monoamine systems and animal models suggest that dysregulation of catecholaminergic neurotransmission in cerebellar-corticostriatal circuits plays a key role in the pathophysiology of ADHD. The efficacy of ADHD medications likely arises from their differing profile of effects on (a) dopaminergic and noradrenergic systems and (b) the localization of these effects in prefrontal cortex and striatum. ADHD has a very high heritability, and although molecular genetic studies have found no causal common DNA variants yet, they have found strong evidence that rare duplications and deletions are risk factors for ADHD. Environmental risk factors, especially those that impact early neurodevelopment (i.e., exposure to cigarette smoking and alcohol during pregnancy), also influence susceptibility to ADHD.
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Weaver, Michael F. Pain and Addiction in Adolescents and Young Adults (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0030.
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Distinguishing between the needs of adults and those of adolescents, this chapter concentrates on practical operational approaches to both addiction and pain in the ephebiatric population. The susceptibility of this group to substance use disorders, and the profound impact on the developing brain and body of substances of misuse, is complicated further by their high level of physical activity and vulnerability to trauma. Data are provided from the Monitoring the Future project to profile the substance use risk of this population; a summary table is included giving the prevalence of various substances of misuse among youths. Unique requirements in their treatment are addressed, with emphasis placed on a network therapy, enlistment of family cooperation, and neighborhood resources. Noting that this is a population for whom physicians may be reluctant to initially consider medication, safety profiles are examined.
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Montironi, Rodolfo, Liang Cheng, Antonio Lopez-Beltran, Roberta Mazzucchelli, Matteo Santoni, and Marina Scarpelli. Prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0060.
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The incidence of prostate cancer (PCa) has risen dramatically in the last years. This event may be partially explained by the employment of digital rectal examination (DRE), serum prostate-specific antigen (PSA), and transrectal ultrasonography. In developed countries, PCa is the most frequent non-skin malignancy in males. It is estimated that one in six males will be diagnosed with PCa during their lifetime, the risk of death due to metastatic PCa being 1 in 30. Multiple factors contribute to the development of PCa, as well as to its progression to an androgen-independent state: dietary factors, inherited susceptibility factors, gene defects, and androgens and their receptors. The chapter will discuss the following topics: high-grade prostatic intraepithelial neoplasia (PIN); atypical small acinar proliferation; morphological criteria for the identification of PCa; reporting of PCa biopsies; prognostic factors in radical prostatectomies (RPs); and specimens.
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Maher, Christopher J., and Elaine R. Mardis. Genomic Landscape of Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0004.
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The study of cancer genomics has advanced rapidly during the last decade due to the development of next generation or massively parallel technology for DNA sequencing. The resulting knowledge is transforming the understanding of both inherited (germline) genetic susceptibility and the somatic changes in tumor tissue that drive abnormal growth and progression. The somatic alterations in tumor tissue vary depending on the type of cancer and its characteristic “genomic landscape.” New technologies have increased the speed and lowered the cost of DNA sequencing and have enabled high-volume characterization of RNA, DNA methylation, DNA-protein complexes, DNA conformation, and a host of other factors that, when altered, can contribute to the development and/or progression of the cancer. Technologic advances have greatly expanded research on somatic changes in tumor tissue, revealing both the singularity of individual cancer genomes and the commonality of genetic alterations that drive cancer in different tissues.
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Thomas, Ranjeny, and Andrew P. Cope. Pathogenesis of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0109.
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In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process at a whole-genome level. Here we describe the key molecular and cellular characteristics of the inflamed synovium and how infiltrating cells get there. With this background, we outline current concepts of the different phases of disease, how the first phase of genetic susceptibility evolves into autoimmunity, triggered by the exposome, prior to the onset of clinically apparent inflammatory disease. We then describe the pathways that actively contribute to this early inflammatory phase and document the key effector cells and molecules of the innate and adaptive immune systems that orchestrate and maintain chronic synovial inflammatory responses. We summarize how this inflammatory milieu translates to cartilage destruction and bone resorption in synovial joints, and conclude by reviewing those factors in inflamed synovium that promote immune homeostasis.
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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.
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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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Thun, Michael J., Martha S. Linet, James R. Cerhan, Christopher A. Haiman, and David Schottenfeld. Introduction. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0001.
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This Introduction provides a broad overview of the scientific advances and crosscutting developments that increasingly influence epidemiologic research on the causes and prevention of cancer. High-throughput technologies have identified the molecular “driver” events in tumor tissue that underlie the multistage development of many types of cancer. These somatic (largely acquired) alterations disrupt normal genetic and epigenetic control over cell maintenance, division and survival. Tumor classification is also changing to reflect the genetic and molecular alterations in tumor tissue, as well as the anatomic, morphologic, and histologic phenotype of the cancer. Genome-wide association studies (GWAS) have identified more than 700 germline (inherited) genetic loci associated with susceptibility to various forms of cancer, although the risk estimates for almost all of these are small to modest and their exact location and function remain to identified. Advances in genomic and other “OMIC” technologies are identifying biomarkers that reflect internal exposures, biological processes and intermediate outcomes in large population studies. While research in many of these areas is still in its infancy, mechanistic and molecular assays are increasingly incorporated into etiologic studies and inferences about causation. Other sections of the book discuss the global public health impact of cancer, the growing list of exposures known to affect cancer risk, the epidemiology of over 30 types of cancer by tissue of origin, and preventive interventions that have dramatically reduced the incidence rates of several major cancers.
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Jordan, Jenna. Leadership Decapitation. Stanford University Press, 2019. http://dx.doi.org/10.11126/stanford/9781503608245.001.0001.
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Does leadership targeting work? This question lies at the heart of studies on the efficacy of counterterrorism policy. This book examines whether killing or arresting terrorists is an effective means by which to weaken and degrade a group’s operational capacity. It aims to identify and explain why decapitation works in some cases and not in others. In order to determine whether decapitation is an effective strategy, this project examines nearly one thousand instances of leadership targeting. A group’s susceptibility to leadership targeting is a function of three factors: organizational structure, communal support, and group type or ideology. Leadership decapitation is unlikely to result in the demise of groups that are highly bureaucratized, have high levels of communal support, or are driven by a religious or separatist ideology. Leaders matter less under these conditions, and their removal can have adverse consequences, such as retaliatory attacks or an overall increase in the frequency of attacks. The data reveals that the largest and oldest organizations are highly resistant to destabilization after targeting. Separatist, religious, and especially Islamist groups are unlikely to weaken after the removal of their leaders. In order to develop counterterrorism policies that will degrade and weaken terrorist organizations, it is essential to identify whether our policies are likely to be effective or to have adverse consequences. The book examines the cases of Hamas, al-Qaeda, Shining Path, and ISIS to understand how organizational structure, local support, and ideology contributes to their resilience in the face of repeated leadership attacks.