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"Friedman, J"
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Thermophotovoltaic efficiency of 40
Thermophotovoltaics (TPVs) convert predominantly infrared wavelength light to electricity via the photovoltaic effect, and can enable approaches to energy storage
1
,
2
and conversion
3
–
9
that use higher temperature heat sources than the turbines that are ubiquitous in electricity production today. Since the first demonstration of 29% efficient TPVs (Fig.
1a
) using an integrated back surface reflector and a tungsten emitter at 2,000 °C (ref.
10
), TPV fabrication and performance have improved
11
,
12
. However, despite predictions that TPV efficiencies can exceed 50% (refs.
11
,
13
,
14
), the demonstrated efficiencies are still only as high as 32%, albeit at much lower temperatures below 1,300 °C (refs.
13
–
15
). Here we report the fabrication and measurement of TPV cells with efficiencies of more than 40% and experimentally demonstrate the efficiency of high-bandgap tandem TPV cells. The TPV cells are two-junction devices comprising III–V materials with bandgaps between 1.0 and 1.4 eV that are optimized for emitter temperatures of 1,900–2,400 °C. The cells exploit the concept of band-edge spectral filtering to obtain high efficiency, using highly reflective back surface reflectors to reject unusable sub-bandgap radiation back to the emitter. A 1.4/1.2 eV device reached a maximum efficiency of (41.1 ± 1)% operating at a power density of 2.39 W cm
–2
and an emitter temperature of 2,400 °C. A 1.2/1.0 eV device reached a maximum efficiency of (39.3 ± 1)% operating at a power density of 1.8 W cm
–2
and an emitter temperature of 2,127 °C. These cells can be integrated into a TPV system for thermal energy grid storage to enable dispatchable renewable energy. This creates a pathway for thermal energy grid storage to reach sufficiently high efficiency and sufficiently low cost to enable decarbonization of the electricity grid.
Two-junction TPV cells with efficiencies of more than 40% are reported, using an emitter with a temperature between 1,900 and 2,400 °C, for integration into a TPV system for thermal energy grid storage.
Journal Article
Rivaroxaban versus Enoxaparin for Thromboprophylaxis after Hip Arthroplasty
Rivaroxaban is an orally administered direct inhibitor of factor Xa. As compared with enoxaparin, rivaroxaban was more effective in preventing venous thromboembolism after hip replacement, without a significant increase in major bleeding.
Rivaroxaban is an orally administered direct inhibitor of factor Xa. As compared with enoxaparin, rivaroxaban was more effective in preventing venous thromboembolism after hip replacement, without a significant increase in major bleeding.
Prophylactic anticoagulant therapy is standard practice after total hip or knee arthroplasty, with a minimum recommended duration of 10 days.
1
After total hip arthroplasty, extended prophylaxis for 5 weeks after surgery reduces the incidence of symptomatic and asymptomatic venous thromboembolism more effectively than does short-term prophylaxis.
2
New deep-vein thromboses have been shown to form after the discontinuation of short-term prophylaxis.
3
Several meta-analyses suggest that extended thromboprophylaxis after total hip arthroplasty leads to a reduction in symptomatic venous thromboembolic events, without increasing the risk of major bleeding.
4
–
6
These findings led to a grade 1A recommendation for extended thromboprophylaxis after total . . .
Journal Article
Enhancer–promoter specificity in gene transcription: molecular mechanisms and disease associations
Although often located at a distance from their target gene promoters, enhancers are the primary genomic determinants of temporal and spatial transcriptional specificity in metazoans. Since the discovery of the first enhancer element in simian virus 40, there has been substantial interest in unraveling the mechanism(s) by which enhancers communicate with their partner promoters to ensure proper gene expression. These research efforts have benefited considerably from the application of increasingly sophisticated sequencing- and imaging-based approaches in conjunction with innovative (epi)genome-editing technologies; however, despite various proposed models, the principles of enhancer–promoter interaction have still not been fully elucidated. In this review, we provide an overview of recent progress in the eukaryotic gene transcription field pertaining to enhancer–promoter specificity. A better understanding of the mechanistic basis of lineage- and context-dependent enhancer–promoter engagement, along with the continued identification of functional enhancers, will provide key insights into the spatiotemporal control of gene expression that can reveal therapeutic opportunities for a range of enhancer-related diseases.
Enhancers in focus: insights into spatiotemporal gene expression control
This review summarizes the current understanding of enhancer-promoter interactions (EPIs), a key feature of genome structure, in gene regulation and disease. EPIs are crucial for proper gene activity, and their alteration by mutational events can be pathological, causing, among others, cancer, and neurodevelopmental disorders. The authors provide an overview of various methods used to study 3D genome architecture (the physical structure of chromosomes) and discuss recent insights that these techniques have afforded, especially with regard to the specificity and dynamics of EPIs as well as the underlying molecular mechanisms. The review highlights the broad experimental utility of CRISPR-based strategies and their therapeutic potential for targeting disease-related EPIs. While substantial progress has been made, further elucidation of the physical and functional interplay of enhancers with their cognate promoter(s) will reveal new treatment opportunities for many diseases.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
Journal Article
Phase separation of ligand-activated enhancers licenses cooperative chromosomal enhancer assembly
A crucial feature of differentiated cells is the rapid activation of enhancer-driven transcriptional programs in response to signals. The potential contributions of physicochemical properties of enhancer assembly in signaling events remain poorly understood. Here we report that in human breast cancer cells, the acute 17β-estradiol-dependent activation of functional enhancers requires assembly of an enhancer RNA–dependent ribonucleoprotein (eRNP) complex exhibiting properties of phase-separated condensates. Unexpectedly, while acute ligand-dependent assembly of eRNPs resulted in enhancer activation sensitive to chemical disruption of phase separation, chronically activated enhancers proved resistant to such disruption, with progressive maturation of eRNPs to a more gel-like state. Acute, but not chronic, stimulation resulted in ligand-induced, condensin-dependent changes in spatial chromatin conformation based on homotypic enhancer association, resulting in cooperative enhancer-activation events. Thus, distinct physicochemical properties of eRNP condensates on enhancers serve as determinants of rapid ligand-dependent alterations in chromosomal architecture and cooperative enhancer activation.After acute agonist stimulation, phase-separated complexes form at estrogen-receptor-bound enhancer sites and coalesce into condensates with cooperative enhancer activity. Chronic stimulation causes the condensates to mature into a less dynamic, gel-like state.
Journal Article
Transcriptomic organization of the human brain in post-traumatic stress disorder
Despite extensive study of the neurobiological correlates of post-traumatic stress disorder (PTSD), little is known about its molecular determinants. Here, differential gene expression and network analyses of four prefrontal cortex subregions from postmortem tissue of people with PTSD demonstrate extensive remodeling of the transcriptomic landscape. A highly connected downregulated set of interneuron transcripts is present in the most significant gene network associated with PTSD. Integration of this dataset with genotype data from the largest PTSD genome-wide association study identified the interneuron synaptic gene
ELFN1
as conferring significant genetic liability for PTSD. We also identified marked transcriptomic sexual dimorphism that could contribute to higher rates of PTSD in women. Comparison with a matched major depressive disorder cohort revealed significant divergence between the molecular profiles of individuals with PTSD and major depressive disorder despite their high comorbidity. Our analysis provides convergent systems-level evidence of genomic networks within the prefrontal cortex that contribute to the pathophysiology of PTSD in humans.
A transcriptome-wide characterization of the molecular pathology of post-traumatic stress disorder (PTSD) postmortem brains provides a comprehensive resource for mechanistic insight and therapeutic development.
Journal Article