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"Human evolution Health aspects."
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Ingenious : the unintended cost of human innovation
Evolution is the process by which species adapt over time to their environments. The tricky part about human evolution is that, as technology builders, we have the power to alter our environments--and even build new, unprecedented conditions in which to immerse ourselves. This is an extraordinary mastery of nature. Not only can we keep the ruthless process of natural selection at bay; we can force nature to bend to us. But the effects of upending the evolutionary process are not as simple as they may seem. Gluckman and Hanson, both leaders in the exciting new field of evolutionary medicine, explore how, even as our ingenious innovations allow us to thrive, they create unforeseen consequences that demand further ingenuity. We've made the environments around us more food-rich, for example--but at the cost of rampant obesity. We've learned to wipe out the pathogens that most commonly make us ill, but in doing so encouraged the rise of antibiotic-resistant superbugs that our bodies are desperately unable to fend off. We have created new information and communication environs that stimulate our intellectual curiosity and challenge our abstract thinking capacities. The downsides are new forms of social dysfunction and sources of psychological stress. Ironically, in many ways, our efforts to be more comfortable have led to dire consequences for our health. Every time we transform our world, we are confronted by a world that challenges us anew. Ingenious opens our eyes to the dangers we face and offers solutions we cannot ignore.-- Provided by publisher
Book
Debility and the moral imagination in Botswana
In the rush to development in Botswana, and Africa more generally,
changes in work, diet, and medical care have resulted in escalating experiences of
chronic illness, debilitating disease, and accident. Debility and the Moral
Imagination in Botswana documents how transformations wrought by colonialism,
independence, industrialization, and development have effected changes in bodily
life and perceptions of health, illness, and debility. In this intimate and powerful
book, Julie Livingston explores the lives of debilitated persons, their caregivers,
the medical and social networks of caring, and methods that communities have adopted
for promoting well-being. Livingston traces how Tswana medical thought and practice
have become intertwined with Western bio-medical ideas and techniques. By focusing
on experiences and meanings of illness and bodily misfortune, Livingston sheds light
on the complexities of the current HIV/AIDS epidemic and places it in context with a
long and complex history of impairment and debility. This book presents practical
and thoughtful responses to physical misfortune and offers an understanding of the
complex dynamic between social change and suffering.
eBook
Too much of a good thing : how four key survival traits are now killing us
\"Over the past 200 years, human life-expectancy has approximately doubled. Yet we face soaring worldwide rates of obesity, diabetes, high blood pressure, mental illness, heart disease, and stroke. In his ... new book, Dr. Lee Goldman presents a radical explanation: the key protective traits that once ensured our species' survival are now the leading global causes of illness and death. Our capacity to store food, for example, lures us into overeating, and a clotting system designed to protect us from bleeding to death now directly contributes to heart attacks and strokes.\"--Amazon.com.
Book
Human immune diversity: from evolution to modernity
The extreme diversity of the human immune system, forged and maintained throughout evolutionary history, provides a potent defense against opportunistic pathogens. At the same time, this immune variation is the substrate upon which a plethora of immune-associated diseases develop. Genetic analysis suggests that thousands of individually weak loci together drive up to half of the observed immune variation. Intense selection maintains this genetic diversity, even selecting for the introgressed Neanderthal or Denisovan alleles that have reintroduced variation lost during the out-of-Africa migration. Variations in age, sex, diet, environmental exposure, and microbiome each potentially explain the residual variation, with proof-of-concept studies demonstrating both plausible mechanisms and correlative associations. The confounding interaction of many of these variables currently makes it difficult to assign definitive contributions. Here, we review the current state of play in the field, identify the key unknowns in the causality of immune variation, and identify the multidisciplinary pathways toward an improved understanding.
The extreme diversity of the human immune system, forged and maintained throughout evolutionary history, provides a potent defense against opportunistic pathogens. Liston and colleagues review the current state of play in the field, identify the key unknowns in the causality of immune variation and identify the multidisciplinary pathways toward an improved understanding.
Journal Article
Spatiotemporal trajectory of life expectancy and its disparity in China 2000–2030: modelling and prediction
Background
Life expectancy (LE) is one of crucial metrics of human evolution. However, the evolutionary trajectories of LE in different regions of China and the regional inequalities expected in 2030 are still unclear yet.
Methods
This study collected provincial LE data and relevant explanatory variables for the years of 2000, 2010, 2020 in China. The Geotree method was employed to reconstruct the evolution trajectories of LE, while a multilevel model was used to predict LEs at the provincial levels in the country for the year 2030.
Results
The LE in China exhibited significant geographical pattern, decreasing from the east to the west of the country. LE increases with socio-economic development but is constrained by the natural environment. The physical limitation to LE is significant in western China but are being alleviated with the development of socio-economic conditions. LE will increase in all provinces by 2030, with the overall LE in China reaching 80.05 years (95% confidence interval: 78.93 ~ 81.28), and regional inequalities will diminish.
Conclusions
LE is increasing with the improvement of socioeconomic condition over time; the constraints imposed by the natural environment on LE are being overridden with the improvement of socio-economic conditions.
Journal Article
Primate change : how the world we made is remaking us
PRIMATE CHANGE is a wide-ranging, polemical look at how and why the human body has changed since humankind first got up on two feet. Spanning the entirety of human history - from primate to transhuman - Vybarr Cregan-Reid's book investigates where we came from, who we are today and how modern technology will change us beyond recognition. In the last two hundred years, humans have made such a tremendous impact on the world that our geological epoch is about to be declared the 'Anthropocene', or the Age of Man. But while we have been busy changing the shape of the world we inhabit, the ways of living that we have been building have, as if under the cover of darkness, been transforming our bodies and altering the expression of our DNA, too. PRIMATE CHANGE beautifully unscrambles the complex architecture of our modern human bodies, built over millions of years and only starting to give up on us now.
Book
Pan-cancer analysis of whole genomes
Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale
1
–
3
. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the
TERT
promoter
4
; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation
5
,
6
; analyses timings and patterns of tumour evolution
7
; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity
8
,
9
; and evaluates a range of more-specialized features of cancer genomes
8
,
10
–
18
.
The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 cancer whole genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
Journal Article
The weight of nature : how a changing climate changes our brains
\"For readers of Kolbert's Under a White Sky and Merlin Sheldrake's Entangled Life, to all those who love science books about the brain The effects of climate change on our brains are a public health crisis that has gone largely unreported. Based on six years of research, award-winning journalist and trained neuroscientist Clayton Page Aldern synthesizes the emerging neuroscience, psychology, and behavioral economics of climate change and brain health. A masterpiece of deeply reported, superb literary journalism, this book shows readers how a changing environment is changing us, today, from the inside out. Aldern calls it the weight of nature. Newly named mental conditions include: climate grief, ecoanxiety, environmental melancholia, pre-traumatic stress disorder. High-schoolers are preparing for a chaotic climate with the same combination of urgency, fear, and resignation they reserve for active-shooter drills. But mostly, as Aldern richly details, we don't realize what global warming is doing to our brains. More heat means it is harder to think straight and solve problems. It influences serotonin release, which in turn increases the chance of impulsive violence. Air pollution from wildfires and smokestacks affects everything from sleeplessness to baseball umpires' error rates. Immigration judges are more likely to reject asylum applications on hotter days. And these kinds of effects are not easily medicated, since certain drugs we might look to just aren't as effective at higher temperatures. Heatwaves and hurricanes can wear on memory, language, and pain systems. Wildfires seed PTSD. And climate-fueled ecosystem changes extend the reach of brain-disease carriers like the mosquitos of cerebral-malaria fame, brain-eating amoebae, and the bats that brought us the mental fog of long Covid. From farms in the San Joaquin Valley and public schools across the US to communities in Norway's arctic, Micronesian islands, and the French Alps, this is a disturbing, unprecedented portrait of a global crisis we thought we understood\"-- Provided by publisher.
Book
Genomic characterization of metastatic breast cancers
Metastasis is the main cause of death for patients with breast cancer. Many studies have characterized the genomic landscape of breast cancer during its early stages. However, there is evidence that genomic alterations are acquired during the evolution of cancers from their early to late stages, and that the genomic landscape of early cancers is not representative of that of lethal cancers
1
–
7
. Here we investigated the landscape of somatic alterations in 617 metastatic breast cancers. Nine driver genes (
TP53
,
ESR1
,
GATA3
,
KMT2C
,
NCOR1
,
AKT1
,
NF1
,
RIC8A
and
RB1
) were more frequently mutated in metastatic breast cancers that expressed hormone receptors (oestrogen and/or progesterone receptors; HR
+
) but did not have high levels of HER2 (HER2
−
;
n
= 381), when compared to early breast cancers from The Cancer Genome Atlas. In addition, 18 amplicons were more frequently observed in HR
+
/HER2
−
metastatic breast cancers. These cancers showed an increase in mutational signatures S2, S3, S10, S13 and S17. Among the gene alterations that were enriched in HR
+
/HER2
−
metastatic breast cancers, mutations in
TP53
,
RB1
and
NF1
, together with S10, S13 and S17, were associated with poor outcome. Metastatic triple-negative breast cancers showed an increase in the frequency of somatic biallelic loss-of-function mutations in genes related to homologous recombination DNA repair, compared to early triple-negative breast cancers (7% versus 2%). Finally, metastatic breast cancers showed an increase in mutational burden and clonal diversity compared to early breast cancers. Thus, the genomic landscape of metastatic breast cancer is enriched in clinically relevant genomic alterations and is more complex than that of early breast cancer. The identification of genomic alterations associated with poor outcome will allow earlier and better selection of patients who require the use of treatments that are still in clinical trials. The genetic complexity observed in advanced breast cancer suggests that such treatments should be introduced as early as possible in the disease course.
Patient data from six clinical trials are used to compare the genomic landscapes of breast cancer metastases with those of primary tumours, revealing an increase in mutational burden and clonal diversity.
Journal Article