Notes

Band-selective Holstein polaron within Luttinger liquefied content A0.3MoO3 (A = K, Rb).
The eRNA-expressing MYC superenhancers were located downstream of the MYC gene in KSHV-infected PELs and played a key role in MYC expression. RNAi-mediated depletion or dCas9-KRAB CRISPR inhibition of eRNA expression significantly reduced MYC mRNA level in PELs, as did the treatment of an epigenomic drug that globally blocks superenhancer function. Finally, while cellular IRF4 acted upon eRNA expression and superenhancer function for MYC expression during latency, KSHV viral IRF4 repressed cellular IRF4 expression, decreasing MYC expression and thereby, facilitating lytic replication. These results indicate that KSHV acts as an epigenomic driver that modifies host epigenomic status upon reactivation by effectively regulating host enhancer function.Theoretical and experimental observations that catalysis enhances the diffusion of enzymes have generated exciting implications about nanoscale energy flow, molecular chemotaxis, and self-powered nanomachines. However, contradictory claims on the origin, magnitude, and consequence of this phenomenon continue to arise. To date, experimental observations of catalysis-enhanced enzyme diffusion have relied almost exclusively on fluorescence correlation spectroscopy (FCS), a technique that provides only indirect, ensemble-averaged measurements of diffusion behavior. Here, using an anti-Brownian electrokinetic (ABEL) trap and in-solution single-particle tracking, we show that catalysis does not increase the diffusion of alkaline phosphatase (ALP) at the single-molecule level, in sharp contrast to the ∼20% enhancement seen in parallel FCS experiments using p-nitrophenyl phosphate (pNPP) as substrate. Combining comprehensive FCS controls, ABEL trap, surface-based single-molecule fluorescence, and Monte Carlo simulations, we establish that pNPP-induced dye blinking at the ∼10-ms timescale is responsible for the apparent diffusion enhancement seen in FCS. Our observations urge a crucial revisit of various experimental findings and theoretical models--including those of our own--in the field, and indicate that in-solution single-particle tracking and ABEL trap are more reliable means to investigate diffusion phenomena at the nanoscale.The Late Devonian was a protracted period of low speciation resulting in biodiversity decline, culminating in extinction events near the Devonian-Carboniferous boundary. Recent evidence indicates that the final extinction event may have coincided with a dramatic drop in stratospheric ozone, possibly due to a global temperature rise. 4-Phenylbutyric acid ic50 Here we study an alternative possible cause for the postulated ozone drop a nearby supernova explosion that could inflict damage by accelerating cosmic rays that can deliver ionizing radiation for up to [Formula see text] ky. We therefore propose that the end-Devonian extinctions were triggered by supernova explosions at [Formula see text], somewhat beyond the "kill distance" that would have precipitated a full mass extinction. Such nearby supernovae are likely due to core collapses of massive stars; these are concentrated in the thin Galactic disk where the Sun resides. Detecting either of the long-lived radioisotopes [Formula see text] or [Formula see text] in one or more end-Devonian extinction strata would confirm a supernova origin, point to the core-collapse explosion of a massive star, and probe supernova nucleosynthesis. Other possible tests of the supernova hypothesis are discussed.We present results of a radiant cooling system that made the hot and humid tropical climate of Singapore feel cool and comfortable. Thermal radiation exchange between occupants and surfaces in the built environment can augment thermal comfort. The lack of widespread commercial adoption of radiant-cooling technologies is due to two widely held views 1) The low temperature required for radiant cooling in humid environments will form condensation; and 2) cold surfaces will still cool adjacent air via convection, limiting overall radiant-cooling effectiveness. This work directly challenges these views and provides proof-of-concept solutions examined for a transient thermal-comfort scenario. We constructed a demonstrative outdoor radiant-cooling pavilion in Singapore that used an infrared-transparent, low-density polyethylene membrane to provide radiant cooling at temperatures below the dew point. Test subjects who experienced the pavilion (n = 37) reported a "satisfactory" thermal sensation 79% of the time, despite experiencing 29.6 ± 0.9 °C air at 66.5 ± 5% relative humidity and with low air movement of 0.26 ± 0.18 m⋅s-1 Comfort was achieved with a coincident mean radiant temperature of 23.9 ± 0.8 °C, requiring a chilled water-supply temperature of 17.0 ± 1.8 °C. The pavilion operated successfully without any observed condensation on exposed surfaces, despite an observed dew-point temperature of 23.7 ± 0.7 °C. The coldest conditions observed without condensation used a chilled water-supply temperature 12.7 °C below the dew point, which resulted in a mean radiant temperature 3.6 °C below the dew point.The D1 reaction center protein of photosystem II (PSII) is subject to light-induced damage. Degradation of damaged D1 and its replacement by nascent D1 are at the heart of a PSII repair cycle, without which photosynthesis is inhibited. In mature plant chloroplasts, light stimulates the recruitment of ribosomes specifically to psbA mRNA to provide nascent D1 for PSII repair and also triggers a global increase in translation elongation rate. The light-induced signals that initiate these responses are unclear. We present action spectrum and genetic data indicating that the light-induced recruitment of ribosomes to psbA mRNA is triggered by D1 photodamage, whereas the global stimulation of translation elongation is triggered by photosynthetic electron transport. Furthermore, mutants lacking HCF136, which mediates an early step in D1 assembly, exhibit constitutively high psbA ribosome occupancy in the dark and differ in this way from mutants lacking PSII for other reasons. These results, together with the recent elucidation of a thylakoid membrane complex that functions in PSII assembly, PSII repair, and psbA translation, suggest an autoregulatory mechanism in which the light-induced degradation of D1 relieves repressive interactions between D1 and translational activators in the complex. We suggest that the presence of D1 in this complex coordinates D1 synthesis with the need for nascent D1 during both PSII biogenesis and PSII repair in plant chloroplasts.
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