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Sustained miniaturization, here defined as a drop in body size of at least two orders of magnitude from ancestors to descendants, is a widespread and important phenomenon in animals,1-3 but among dinosaurs, miniaturization occurred only rarely, once in the lineage leading to birds and once in the Alvarezsauroidea,1,3-5 one of the most bizarre theropod groups.1,5-7 Miniaturization and powered flight are intimately linked in avialan theropods,3,5,6,8-11 but the causes and patterns of body size reduction are less clear in the non-volant Alvarezsauroidea.1,5,6,12,13 Here, we present results from analyses on a comprehensive dataset, which not only includes new data from early-branching alvarezsauroids but also considers the ontogenetic effect based on histological data. Our analyses show that alvarezsauroid body mass underwent rapid miniaturization from around 110 to 85 mya and that there was a phylogenetic radiation of small-sized alvarezsauroids in the Late Cretaceous. Our analyses also indicate that growth strategies were highly variable among alvarezsauroids, with significant differences among extremely small taxa. The suggested alvarezsauroid miniaturization and associated phylogenetic radiation are coincident with the emergence of ants and termites, and combining previous functional morphological data, our study suggests that alvarezsauroid miniaturization might have been driven by ecological changes during the Cretaceous Terrestrial Revolution, more specifically by a shift to the myrmecophagous ecological niche.Glucocorticoids (GCs) are widely used as anti-inflammatory drugs, but their long-term use has severe metabolic side effects. Here, by treating multiple individual adipose stem cell-derived adipocytes and induced pluripotent stem cell-derived hepatocytes with the potent GC dexamethasone (Dex), we uncovered cell-type-specific and individual-specific GC-dependent transcriptomes and glucocorticoid receptor (GR) cistromes. Individual-specific GR binding could be traced to single-nucleotide polymorphisms (SNPs) that altered the binding motifs of GR or its cooperating factors. We also discovered another set of genetic variants that modulated Dex response through affecting chromatin accessibility or chromatin architecture. Several SNPs that altered Dex-regulated GR binding and gene expression controlled Dex-driven metabolic perturbations. Remarkably, these genetic variations were highly associated with increases in serum glucose, lipids, and body mass in subjects on GC therapy. Knowledge of the genetic variants that predispose individuals to metabolic side effects allows for a precision medicine approach to the use of clinically relevant GCs.A metabolic imbalance between lipid synthesis and degradation can lead to hepatic lipid accumulation, a characteristic of patients with non-alcoholic fatty liver disease (NAFLD). Here, we report that high-fat-diet-induced sterol regulatory element-binding protein (SREBP)-1c, a key transcription factor that regulates lipid biosynthesis, impairs autophagic lipid catabolism via altered H2S signaling. SREBP-1c reduced cystathionine gamma-lyase (CSE) via miR-216a, which in turn decreased hepatic H2S levels and sulfhydration-dependent activation of Unc-51-like autophagy-activating kinase 1 (ULK1). [https://www.selleckchem.com/products/bicuculline.html Bicuculline research buy] Furthermore, Cys951Ser mutation of ULK1 decreased autolysosome formation and promoted hepatic lipid accumulation in mice, suggesting that the loss of ULK1 sulfhydration was directly associated with the pathogenesis of NAFLD. Moreover, silencing of CSE in SREBP-1c knockout mice increased liver triglycerides, confirming the connection between CSE, autophagy, and SREBP-1c. Overall, our results uncover a 2-fold mechanism for SREBP-1c-driven hepatic lipid accumulation through reciprocal activation and inhibition of hepatic lipid biosynthesis and degradation, respectively.SPT6 is a histone chaperone that tightly binds RNA polymerase II (RNAPII) during transcription elongation. However, its primary role in transcription is uncertain. We used targeted protein degradation to rapidly deplete SPT6 in human cells and analyzed defects in RNAPII behavior by a multi-omics approach and mathematical modeling. Our data indicate that SPT6 is a crucial factor for RNAPII processivity and is therefore required for the productive transcription of protein-coding genes. Unexpectedly, SPT6 also has a vital role in RNAPII termination, as acute depletion induced readthrough transcription for thousands of genes. Long-term depletion of SPT6 induced cryptic intragenic transcription, as observed earlier in yeast. However, this phenotype was not observed upon acute SPT6 depletion and therefore can be attributed to accumulated epigenetic perturbations in the prolonged absence of SPT6. In conclusion, targeted degradation of SPT6 allowed the temporal discrimination of its function as an epigenetic safeguard and RNAPII elongation factor.<br />Global climate change could have potential impact on enterovirus (EV)-induced infectious diseases. However, the environmental factors promoting acute hemorrhagic conjunctivitis (AHC) circulation remain inconclusive. This study aimed to quantify the relationship between the environment and AHC.<br />We retrieved the monthly counts and incidence of AHC, meteorological variables and air quality in mainland China between 2013 and 2018. Exposure risks were evaluated by multivariate distributed lag nonlinear models.<br />A total of 219,599 AHC cases were reported in 31 provinces of China, predominantly in southern and central China, seasonally increased in summer. AHC incidence increased by 7% between 2013 and 2018, from 2.6873 to 2.7570 per 100,000 people. A moderate positive correlation was seen between AHC and monthly mean temperature, relative humidity (RH) and precipitation. Each unit increment was associated with a relative risk for AHC of 1.058at 17°-32°C at lag 0 months, 1.017at 65-71% RH at lag 1.4 months, and 1.039at 400-569mm at lag 2.4 months. By contrast, a negative correlation was seen between monthly ambient NO<br />and AHC.<br />Long-term exposure to higher mean temperature, RH and precipitation were associated with an increased risk of AHC. The general public, especially susceptible populations, should pay close attention to weather changes and take protective measures in advance to any AHC outbreak as the above situations occur.<br />Long-term exposure to higher mean temperature, RH and precipitation were associated with an increased risk of AHC. The general public, especially susceptible populations, should pay close attention to weather changes and take protective measures in advance to any AHC outbreak as the above situations occur.