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Framing animals as epidemic villains : histories of non-human disease vectors
This book takes a historical and anthropological approach to understanding how non-human hosts and vectors of diseases are understood, at a time when emerging infectious diseases are one of the central concerns of global health. The volume critically examines the ways in which animals have come to be framed as 'epidemic villains' since the turn of the nineteenth century. Providing epistemological and social histories of non-human epidemic blame, as well as ethnographic perspectives on its recent manifestations, the essays explore this cornerstone of modern epidemiology and public health alongside its continuing importance in today's world. Covering diverse regions, the book argues that framing animals as spreaders and reservoirs of infectious diseases - from plague to rabies to Ebola - is an integral aspect not only to scientific breakthroughs but also to the ideological and biopolitical apparatus of modern medicine. As the first book to consider the impact of the image of non-human disease hosts and vectors on medicine and public health, it offers a major contribution to our understanding of human-animal interaction under the shadow of global epidemic threat.
Book
Host–microbe interactions have shaped the genetic architecture of inflammatory bowel disease
A meta-analysis of previous genome-wide association studies of Crohn’s disease and ulcerative colitis, the two most common forms of inflammatory bowel disease, with a combined total of more than 75,000 cases and controls, finds that most loci contribute to both phenotypes and other immune-mediated disorders.
Pathogenesis of inflammatory bowel disease
Genetic studies have implicated unsuspected mechanisms in the pathogenesis of Crohn's disease and ulcerative colitis, two of the most common forms of inflammatory bowel disease. This paper presents a meta-analysis of published genome-wide association studies, together with validation in more than 75,000 cases and controls. In addition to several new associations, the authors find that most loci contribute to both phenotypes, but also to other immune-mediated disorders. The data reveal an overlap between susceptibility loci for inflammatory bowel disease and mycobacterial infection, and between the pathways that govern host responses to mycobacteria and those predisposing to inflammatory bowel disease.
Crohn’s disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations
1
. Genome-wide association studies and subsequent meta-analyses of these two diseases
2
,
3
as separate phenotypes have implicated previously unsuspected mechanisms, such as autophagy
4
, in their pathogenesis and showed that some IBD loci are shared with other inflammatory diseases
5
. Here we expand on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn’s disease and ulcerative colitis genome-wide association scans, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci, that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional (consistently favouring one allele over the course of human history) and balancing (favouring the retention of both alleles within populations) selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.
Journal Article
The new possible : visions of our world beyond crisis
\"In the midst of loss and death and suffering, our charge is to figure out what freedom really means--and how we take steps to get there. The uprising of 2020 marked a new phase in the unfolding Movement for Black Lives. The brutal killings of Ahmaud Arbery, George Floyd, and Breonna Taylor, and countless other injustices large and small, were the match that lit the spark of the largest protest movement in US history, a historic uprising against racism and the politics of disposability that the Covid-19 pandemic lays bare. In this urgent and incisive collection of new interviews bookended by two new essays, Marc Lamont Hill critically examines the \"pre-existing conditions\" that have led us to this moment of crisis and upheaval, guiding us through both the perils and possibilities, and helping us imagine an abolitionist future.\"--Barnesandnoble.com
Book
Genetic studies of body mass index yield new insights for obesity biology
Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (
P
< 5 × 10
−8
), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.
A genome-wide association study and Metabochip meta-analysis of body mass index (BMI) detects 97 BMI-associated loci, of which 56 were novel, and many loci have effects on other metabolic phenotypes; pathway analyses implicate the central nervous system in obesity susceptibility and new pathways such as those related to synaptic function, energy metabolism, lipid biology and adipogenesis.
Genetic correlates of obesity
In the second of two Articles in this issue from the GIANT Consortium, Elizabeth Speliotes and collegues conducted a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), commonly used to define obesity and assess adiposity, to find 97 BMI-associated loci, of which 56 were novel. Many of these loci have significant effects on other metabolic phenotypes. The 97 loci account for about 2.7% of BMI variation, and genome-wide estimates suggest common variation accounts for more than 20% of BMI variation. Pathway analyses implicate the central nervous system in obesity susceptibility including synaptic function, glutamate signaling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.
Journal Article
The genome factor : what the social genomics revolution reveals about ourselves, our history, and the future
\"For a century, social scientists have avoided genetics like the plague. But in the past decade, a small but intrepid group of economists, political scientists, and sociologists have harnessed the genomics revolution to paint a more complete picture of human social life than ever before. The Genome Factor describes the latest astonishing discoveries being made at the scientific frontier where genomics and the social sciences intersect. The Genome Factor reveals that there are real genetic differences by racial ancestry--but ones that don't conform to what we call black, white, or Latino. Genes explain a significant share of who gets ahead in society and who does not, but instead of giving rise to a genotocracy, genes often act as engines of mobility that counter social disadvantage. An increasing number of us are marrying partners with similar education levels as ourselves, but genetically speaking, humans are mixing it up more than ever before with respect to mating and reproduction. These are just a few of the many findings presented in this illuminating and entertaining book, which also tackles controversial topics such as genetically personalized education and the future of reproduction in a world where more and more of us are taking advantage of cheap genotyping services like 23andMe to find out what our genes may hold in store for ourselves and our children. The Genome Factor shows how genomics is transforming the social sciences--and how social scientists are integrating both nature and nurture into a unified, comprehensive understanding of human behavior at both the individual and society-wide levels.\"-- Provided by publisher.
Book
Regulation of pyruvate metabolism and human disease
Pyruvate is a keystone molecule critical for numerous aspects of eukaryotic and human metabolism. Pyruvate is the end-product of glycolysis, is derived from additional sources in the cellular cytoplasm, and is ultimately destined for transport into mitochondria as a master fuel input undergirding citric acid cycle carbon flux. In mitochondria, pyruvate drives ATP production by oxidative phosphorylation and multiple biosynthetic pathways intersecting the citric acid cycle. Mitochondrial pyruvate metabolism is regulated by many enzymes, including the recently discovered mitochondria pyruvate carrier, pyruvate dehydrogenase, and pyruvate carboxylase, to modulate overall pyruvate carbon flux. Mutations in any of the genes encoding for proteins regulating pyruvate metabolism may lead to disease. Numerous cases have been described. Aberrant pyruvate metabolism plays an especially prominent role in cancer, heart failure, and neurodegeneration. Because most major diseases involve aberrant metabolism, understanding and exploiting pyruvate carbon flux may yield novel treatments that enhance human health.
Journal Article
Epigenome-wide association study of body mass index, and the adverse outcomes of adiposity
A large-scale epigenome-wide association study identifies changes in DNA methylation associated with body mass index in blood and adipose tissue, and correlates DNA methylation sites with high risk of incident type 2 diabetes.
Body fat and diabetes risk
Obesity is a major risk factor for type 2 diabetes and related metabolic disorders. Genetic association studies have identified genomic loci associated with obesity, and recent studies have also suggested associations with DNA methylation. These authors report an epigenome-wide association study for body mass index (BMI), identifying an association with DNA methylation at 187 loci in blood and adipose tissue. They find that these methylation changes are secondary to adiposity and are also associated with an increased risk of developing type 2 diabetes, independent of conventional risk factors.
Approximately 1.5 billion people worldwide are overweight or affected by obesity, and are at risk of developing type 2 diabetes, cardiovascular disease and related metabolic and inflammatory disturbances
1
,
2
. Although the mechanisms linking adiposity to associated clinical conditions are poorly understood, recent studies suggest that adiposity may influence DNA methylation
3
,
4
,
5
,
6
, a key regulator of gene expression and molecular phenotype
7
. Here we use epigenome-wide association to show that body mass index (BMI; a key measure of adiposity) is associated with widespread changes in DNA methylation (187 genetic loci with
P
< 1 × 10
−7
, range
P
= 9.2 × 10
−8
to 6.0 × 10
−46
;
n
= 10,261 samples). Genetic association analyses demonstrate that the alterations in DNA methylation are predominantly the consequence of adiposity, rather than the cause. We find that methylation loci are enriched for functional genomic features in multiple tissues (
P
< 0.05), and show that sentinel methylation markers identify gene expression signatures at 38 loci (
P
< 9.0 × 10
−6
, range
P
= 5.5 × 10
−6
to 6.1 × 10
−35
,
n
= 1,785 samples). The methylation loci identify genes involved in lipid and lipoprotein metabolism, substrate transport and inflammatory pathways. Finally, we show that the disturbances in DNA methylation predict future development of type 2 diabetes (relative risk per 1 standard deviation increase in methylation risk score: 2.3 (2.07–2.56);
P
= 1.1 × 10
−54
). Our results provide new insights into the biologic pathways influenced by adiposity, and may enable development of new strategies for prediction and prevention of type 2 diabetes and other adverse clinical consequences of obesity.
Journal Article
Oxidative Stress in Obesity: A Critical Component in Human Diseases
Obesity, a social problem worldwide, is characterized by an increase in body weight that results in excessive fat accumulation. Obesity is a major cause of morbidity and mortality and leads to several diseases, including metabolic syndrome, diabetes mellitus, cardiovascular, fatty liver diseases, and cancer. Growing evidence allows us to understand the critical role of adipose tissue in controlling the physic-pathological mechanisms of obesity and related comorbidities. Recently, adipose tissue, especially in the visceral compartment, has been considered not only as a simple energy depository tissue, but also as an active endocrine organ releasing a variety of biologically active molecules known as adipocytokines or adipokines. Based on the complex interplay between adipokines, obesity is also characterized by chronic low grade inflammation with permanently increased oxidative stress (OS). Over-expression of oxidative stress damages cellular structures together with under-production of anti-oxidant mechanisms, leading to the development of obesity-related complications. The aim of this review is to summarize what is known in the relationship between OS in obesity and obesity-related diseases.
Journal Article