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result(s) for
"Diamond, M"
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Has Reducing Ship Emissions Brought Forward Global Warming?
2024
Ships brighten low marine clouds from emissions of sulfur and aerosols, resulting in visible “ship tracks”. In 2020, new shipping regulations mandated an ∼80% reduction in the allowed fuel sulfur content. Recent observations indicate that visible ship tracks have decreased. Model simulations indicate that since 2020 shipping regulations have induced a net radiative forcing of +0.12 Wm−2. Analysis of recent temperature anomalies indicates Northern Hemisphere surface temperature anomalies in 2022–2023 are correlated with observed cloud radiative forcing and the cloud radiative forcing is spatially correlated with the simulated radiative forcing from the 2020 shipping emission changes. Shipping emissions changes could be accelerating global warming. To better constrain these estimates, better access to ship position data and understanding of ship aerosol emissions are needed. Understanding the risks and benefits of emissions reductions and the difficultly in robust attribution highlights the large uncertainty in attributing proposed deliberate climate intervention. Plain Language Summary Ships have a unique climate effect due to brightening of low marine clouds, resulting in visible “ship tracks”. These ship tracks are due to clouds interacting with ship emissions, particularly sulfur. Recently, regulations have drastically reduced allowable ship sulfur emissions. This has resulted in a decrease in observable ship tracks. Modeling and observations indicate that the reduction in ship sulfur emissions could have slightly warmed the planet starting in 2020. These changes are remarkably co‐incident with observed patterns of cloud changes and may have accelerated global warming. Key Points Recent regulations on ship sulfur emissions have decreased ship tracks and resulted in +0.12 Wm−2 of radiative forcing Observed cloud anomalies are correlated with observed ocean temperature anomalies and shipping radiative forcing Reduced ship emissions may have accelerated global warming contributing to recent warm Northern Hemisphere surface temperatures
Journal Article
Selenium-Binding Protein 1 in Human Health and Disease
2018
Selenium-binding protein 1 (SBP1) is a highly conserved protein that covalently binds selenium. SBP1 may play important roles in several fundamental physiological functions, including protein degradation, intra-Golgi transport, cell differentiation, cellular motility, redox modulation, and the metabolism of sulfur-containing molecules. SBP1 expression is often reduced in many cancer types compared to the corresponding normal tissues and low levels of SBP1 are frequently associated with poor clinical outcome. In this review, the transcriptional regulation of SBP1, the different physiological roles reported for SBP1, as well as the implications of SBP1 function in cancer and other diseases are presented.
Journal Article
DNA exonuclease Trex1 regulates radiotherapy-induced tumour immunogenicity
2017
Radiotherapy is under investigation for its ability to enhance responses to immunotherapy. However, the mechanisms by which radiation induces anti-tumour T cells remain unclear. We show that the DNA exonuclease Trex1 is induced by radiation doses above 12–18 Gy in different cancer cells, and attenuates their immunogenicity by degrading DNA that accumulates in the cytosol upon radiation. Cytosolic DNA stimulates secretion of interferon-β by cancer cells following activation of the DNA sensor cGAS and its downstream effector STING. Repeated irradiation at doses that do not induce Trex1 amplifies interferon-β production, resulting in recruitment and activation of Batf3-dependent dendritic cells. This effect is essential for priming of CD8
+
T cells that mediate systemic tumour rejection (abscopal effect) in the context of immune checkpoint blockade. Thus, Trex1 is an upstream regulator of radiation-driven anti-tumour immunity. Trex1 induction may guide the selection of radiation dose and fractionation in patients treated with immunotherapy.
Trex1 is an exonuclease that degrades cytosolic DNA and has been associated with modulation of interferon responses in autoimmunity and viral infections. Here, the authors show that Trex1 attenuates the immunogenicity of cancer cells treated with high radiation doses by degrading cytosolic DNA and preventing the activation of interferon response.
Journal Article
The world until yesterday : what can we learn from traditional societies ?
Diamond reveals how tribal societies offer an extraordinary window into how our ancestors lived for millions of years -- until virtually yesterday, in evolutionary terms -- and provide unique, often overlooked insights into human nature.
The neurobiological properties of tianeptine (Stablon): from monoamine hypothesis to glutamatergic modulation
by
Jay, T M
,
Chattarji, S
,
McEwen, B S
in
Animals
,
Anti-Anxiety Agents - pharmacology
,
Antidepressants
2010
Tianeptine is a clinically used antidepressant that has drawn much attention, because this compound challenges traditional monoaminergic hypotheses of depression. It is now acknowledged that the antidepressant actions of tianeptine, together with its remarkable clinical tolerance, can be attributed to its particular neurobiological properties. The involvement of glutamate in the mechanism of action of the antidepressant tianeptine is consistent with a well-developed preclinical literature demonstrating the key function of glutamate in the mechanism of altered neuroplasticity that underlies the symptoms of depression. This article reviews the latest evidence on tianeptine's mechanism of action with a focus on the glutamatergic system, which could provide a key pathway for its antidepressant action. Converging lines of evidences demonstrate actions of tianeptine on the glutamatergic system, and therefore offer new insights into how tianeptine may be useful in the treatment of depressive disorders.
Journal Article
Upheaval : turning points for nations in crisis
\"In his international bestsellers Guns, Germs and Steel and Collapse, Jared Diamond transformed our understanding of what makes civilizations rise and fall. Now, in his third book in this... trilogy, he reveals how successful nations recover from crises while adopting selective changes -- a coping mechanism more commonly associated with individuals recovering from personal crises. Diamond compares how six countries have survived recent upheavals -- ranging from the forced opening of Japan by U.S. Commodore Perry's fleet, to the Soviet Union's attack on Finland, to a murderous coup or countercoup in Chile and Indonesia, to the transformations of Germany and Austria after World War Two. Because Diamond has lived and spoken the language in five of these six countries, he can present gut-wrenching histories experienced firsthand. These nations coped, to varying degrees, through mechanisms such as acknowledgment of responsibility, painfully honest self-appraisal, and learning from models of other nations. Looking to the future, Diamond examines whether the United States, Japan, and the whole world are successfully coping with the grave crises they currently face. Can we learn from lessons of the past? Adding a psychological dimension to the in-depth history, geography, biology, and anthropology that mark all of Diamond's books, Upheaval reveals factors influencing how both whole nations and individual people can respond to big challenges. The result is a book epic in scope, but also his most personal book yet\" -- Provided by publishers.
Selenoproteins of the Human Prostate: Unusual Properties and Role in Cancer Etiology
2019
The prostate is an important organ for the maintenance of sperm health with prostate cancer being a common disease for which there is a critical need to distinguish indolent from aggressive disease. Several selenium-containing proteins have been implicated in prostate cancer risk or outcome due to either enzyme function, the reduced levels of these proteins being associated with cancer recurrence after prostatectomy or their corresponding genes containing single-nucleotide polymorphisms associated with increased risk. Moreover, experimental data obtained from the manipulation of either cultured cells or animal models have indicated that some of these proteins are contributing mechanistically to prostate cancer incidence or progression. Among these are selenocysteine-containing proteins selenoprotein P (SELENOP), glutathione peroxidase (GPX1), and selenoprotein 15 (SELENOF); and the selenium-associated protein selenium-binding protein 1 (SBP1). Genotyping of some of the genes for these proteins has identified functional single-nucleotide polymorphisms that are associated with prostate cancer risk and the direct quantification of these proteins in human prostate tissues has not only revealed associations to clinical outcomes but have also identified unique properties that are different from what is observed in other tissue types. The location of GPX1 in the nucleus and SELENOF in the plasma membrane of prostate epithelial cells indicates that these proteins may have functions in normal prostate tissue that are distinct from that of the other tissue types.
Journal Article