Books on the topic 'Non genomic effects'
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1
Martin, Wehling, ed. Genomic and non-genomic effects of aldosterone. Boca Raton: CRC Press, 1995.
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2
Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: hormone and cytokine treatments. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0007.
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The antidepressant and neuroprotective effects of oestradiol are described. Psychiatric consequences of oophorectomy, and treatment with tamoxifen and aromatase inhibitors, are then discussed. Androgen-deprivation therapy has temporary effects on cognitive function and mood that reflect the distribution of androgen receptors in the brain. The rapid-onset adverse psychiatric effects of high-dose glucocorticoids are presented (including ‘steroid psychosis’) and a novel, non-genomic molecular mechanism highlighted. In contrast, the depressive effect of chronic glucocorticoid use is then considered.
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Rucker, James J. H., and Peter McGuffin. Copy Number Variation in Neuropsychiatric Disorders. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.005.
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It has long been known that the human genome is subject to deletion and duplication of genetic material by various molecular mechanisms. Until recently, such events were assumed to be relatively rare phenomena. It is now known that submicroscopic deletions or duplications calledcopy number variants(CNVs) are a major source of genomic variation. Rare CNVs (defined as occurring in less than 1 percent of the population) have been implicated in schizophrenia and autism. Measured in terms of odds ratios, individual CNVs have been shown to have large effects, some increasing the risk of disorder several-fold. But they are incompletely penetrant, no one CNV is either necessary or sufficient to cause the disorder. The findings are less clear-cut with bipolar disorder but, here, too, rare CNVs probably play a role. In unipolar depression, initial evidence suggests an overall increase in rare CNVs that disrupt exons, the coding regions of genes.
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Slack, Jonathan. 5. Genes of small effect. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199676507.003.0005.
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‘Genes of small effect’ considers unidentified genes whose variants collectively affect some characteristic of interest. Many aspects of living organisms depend not on the action of a few genes, but on the actions of many, each having a small effect on the overall characteristic. This assumption has been used successfully to inform the breeding of agricultural animals and plants. But some of the concepts have also been very controversial when applied to human beings. The heritability—the proportion of the variance in a population attributable to genetic variation—of human height, serious mental illness, and IQ is considered along with results from genome wide association studies.
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Levinson, Douglas F., and Walter E. Nichols. Genetics of Depression. 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/9780190681425.003.0024.
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Major depressive disorder (MDD) is a common and heterogeneous complex trait. Twin heritability is 35%–40%, perhaps higher in severe/recurrent cases. Adverse life events (particularly during childhood) increase risk. Current evidence suggests some overlap in genetic factors among MDD, bipolar disorder, and schizophrenia. Large genome-wide association studies (GWAS) are now proving successful. Polygenic effects of common SNPs are substantial. Findings implicate genes with effects on synaptic development and function, including two obesity-associated genes (NEGR1 and OLFM4), but not previous “candidate genes.” It can now be expected that larger GWAS samples will produce additional associations that shed new light on MDD genetics.
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Mitchell, Colter. The Genetics of Human Behavior. Edited by Rosemary L. Hopcroft. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190299323.013.43.
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This chapter examines the recent massive expansion of genetic research into human behavior. Based on decades of twin research, there were high expectations of strong genetic effects for almost all behavior. Further work on candidate genes from animal research proved initially exciting. Although that research continues, it now currently receives much less attention, in contrast to whole-genome examinations. This chapter provides insight into the whole-genome era of behavioral research and the extent to which it may or may not be a profitable endeavor. Sociologists are generally unaware of this body of research, but it will likely continue to grow. The methods, strengths, and limitations of genome-wide work are discussed. A discussion of the future of this area and the extent to which this provides any leverage for social research of human behavior concludes the chapter.
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Vermeulen, Roel, Douglas A. Bell, Dean P. Jones, Montserrat Garcia-Closas, Avrum Spira, Teresa W. Wang, Martyn T. Smith, Qing Lan, and Nathaniel Rothman. Application of Biomarkers in Cancer Epidemiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0006.
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Advancements in OMICs are now enabling investigators to explore comprehensively the biological consequences of exogenous and endogenous exposures by detecting molecular signatures of exposure, early signs of adverse biological effects, preclinical disease, and molecularly defined cancer subtypes. These new technologies have proven invaluable for assembling a comprehensive portrait of human exposure, health, and disease. This includes hypothesis-driven biomarkers, as well as platforms that can agnostically analyze entire biologic processes and “compartments,” including the measurement of small molecules (metabolomics), DNA polymorphisms and rarer inherited variants (genomics), methylation and microRNA (epigenomics), chromosome-wide alterations, mRNA (transcriptomics), proteins (proteomics), and the microbiome (microbiomics). Although the implementation of these technologies in epidemiologic studies has already shown great promise, some challenges of particular importance must be addressed. Non-genetic OMIC markers vary over time due to both random variation and physiologic changes. Therefore, there is an urgent need for cohorts to collect repeat biological samples over time.
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Flinter, Frances. Ethical aspects of genetic testing. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0301_update_001.
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The increasing availability of genetic tests is transforming health care. Patients can benefit from earlier, more precise diagnosis and sometimes tailor-made treatment; their relatives can be offered pre-symptomatic, predictive tests and carrier tests. Physicians must balance confidentiality with duty to other individuals, and are responsible for using genetic tests for the benefit of patients in an ethical way. An offer of testing must balance potential additional benefit from potential downsides of testing including psychological effects, risk of error, continuing uncertainty, and cost. The ability to do multiple tests on many genes, even to sequence the whole genome, is rapidly approaching, and mainstreaming of tests means that geneticists are not necessarily involved. Further work and thinking needs to inform medical ethics in this area.
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Dalbeth, Nicola. Clinical features of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0005.
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About 60% of the variance in serum urate levels can be explained by inherited genetic factors, but the extent of the contribution of genetic factors to gout in the presence of hyperuricaemia is not known. Genome-wide association studies in Europeans have identified 28 loci controlling serum urate levels, although the molecular basis of the majority of these genetic associations is currently unknown. The SLC2A9 and ABCG2 renal and gut uric acid transporters have very strong effects on urate levels and the risk of gout. Other uric acid transporters (e.g. SLC22A11/OAT478, SLC22A12/URAT1) and a glycolysis gene (GCKR) are associated with urate levels. Environmental exposures such as sugar-sweetened beverages and alcohol interact with urate-associated genetic variants in an unpredictable fashion. Very little is known about the genetic control of gout in the presence of hyperuricaemia, formation of monosodium urate crystals, and the immune response.
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Lewis, Myles, and Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.
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The advent of genome-wide association studies (GWAS) has been an exciting breakthrough in our understanding of the genetic aetiology of autoimmune diseases. Substantial overlap has been found in susceptibility genes across multiple diseases, from connective tissue diseases and rheumatoid arthritis (RA) to inflammatory bowel disease, coeliac disease, and psoriasis. Major technological advances now permit genotyping of millions of single nucleotide polymorphisms (SNPs). Group analysis of SNPs by haplotypes, aided by completion of the Hapmap project, has improved our ability to pinpoint causal genetic variants. International collaboration to pool large-scale cohorts of patients has enabled GWAS in systemic lupus erythematosus (SLE), systemic sclerosis and Behçet's disease, with studies in progress for ANCA-associated vasculitis. These 'hypothesis-free' studies have revealed many novel disease-associated genes. In both SLE and systemic sclerosis, identified genes map to known pathways including antigen presentation (MHC, TNFSF4), autoreactivity of B and T lymphocytes (BLK, BANK1), type I interferon production (STAT4, IRF5) and the NFκB pathway (TNIP1). In SLE alone, additional genes appear to be involved in dysregulated apoptotic cell clearance (ITGAM, TREX1, C1q, C4) and recognition of immune complexes (FCGR2A, FCGR3B). Future developments include whole-genome sequencing to identify rare variants, and efforts to understand functional consequences of susceptibility genes. Putative environmental triggers for connective tissue diseases include infectious agents, especially Epstein-Barr virus; cigarette smoking; occupational exposure to toxins including silica; and low vitamin D, due to its immunomodulatory effects. Despite numerous studies looking at toxin exposure and connective tissue diseases, conclusive evidence is lacking, due to either rarity of exposure or rarity of disease.
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Pezzini, Alessandro. Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0011.
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Ischaemic stroke is a heterogeneous multifactorial disorder. Although epidemiological data from twin and family studies provide substantial evidence for a genetic basis for stroke, the contribution of genetic factors identified so far is small. Large progress has been made in single-gene disorders associated with ischaemic stroke, particularly at young age. By contrast, little is known about the genes associated with multifactorial stroke. The reported genome-wide association studies of ischaemic stroke have shown that no single common genetic variant imparts major risk, but data on early-onset disease are scarce in this regard. Larger studies with samples numbering in the thousands are ongoing to identify common variants with smaller effects on risk. This approach, in addition with new analytic techniques, will likely contribute to the identification of additional genes, novel pathways, and eventually novel therapeutic approaches to cerebrovascular disorders in the near future. The aims of this review are to summarize data on clinical, genetic, and epidemiologic aspects of monogenic conditions associated with juvenile ischaemic stroke, to discuss recent findings and methodological limitations regarding the genetics of sporadic ischaemic stroke in this age category, and to provide a brief overview of the potential future approaches to stroke genetics.
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Boyer-Kassem, Thomas, Conor Mayo-Wilson, and Michael Weisberg, eds. Scientific Collaboration and Collective Knowledge. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190680534.001.0001.
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Descartes once argued that, with sufficient effort and skill, a single scientist could uncover fundamental truths about our world. Contemporary science proves the limits of this claim. From synthesizing the human genome to predicting the effects of climate change, some current scientific research requires the collaboration of hundreds (if not thousands) of scientists with various specializations. Additionally, the majority of published scientific research is now coauthored, including more than 80% of articles in the natural sciences. Small collaborative teams have become the norm in science. This is the first volume to address critical philosophical questions about how collective scientific research could be organized differently and how it should be organized. For example, should scientists be required to share knowledge with competing research teams? How can universities and grant-giving institutions promote successful collaborations? When hundreds of researchers contribute to a discovery, how should credit be assigned—and can minorities expect a fair share? When collaborative work contains significant errors or fraudulent data, who deserves blame? In this collection of essays, leading philosophers of science address these critical questions, among others. Their work extends current philosophical research on the social structure of science and contributes to the growing, interdisciplinary field of social epistemology. The volume’s strength lies in the diversity of its authors’ methodologies. Employing detailed case studies of scientific practice, mathematical models of scientific communities, and rigorous conceptual analysis, contributors to this volume study scientific groups of all kinds, including small labs, peer-review boards, and large international collaborations like those in climate science and particle physics.
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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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Vaheri, Antti, James N. Mills, Christina F. Spiropoulou, and Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.
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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.
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(Editor), Chandan K. Sen, Lester Packer (Editor), and Patrick A. Baeuerle (Editor), eds. Antioxidant and Redox Regulation of Genes. Academic Press, 2000.
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Packer, Lester, Patrick A. Baeuerle, and Chandan K. Sen. Antioxidant and Redox Regulation of Genes. Elsevier Science & Technology Books, 1999.
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