92 research outputs found
2,2′,2′′,2′′′-[Pyridine-2,6-diylbis(methylenenitrilo)]tetraethanol
In the crystal structure of the title compound C15H27N3O4, the molecule is located on a twofold axis and the asymmetric unit contains one half-molecule, with one N and one C atom lying on the rotation axis. The pyridine ring is the hydrogen-bond acceptor, while two hydroxyl O atoms act as hydrogen-bond donors in intramolecular O—H⋯N and intermolecular O—H⋯N and O—H⋯O hydrogen bonds, thereby forming a closed hydrogen-bonded cage
HOSNeRF: Dynamic Human-Object-Scene Neural Radiance Fields from a Single Video
We introduce HOSNeRF, a novel 360{\deg} free-viewpoint rendering method that
reconstructs neural radiance fields for dynamic human-object-scene from a
single monocular in-the-wild video. Our method enables pausing the video at any
frame and rendering all scene details (dynamic humans, objects, and
backgrounds) from arbitrary viewpoints. The first challenge in this task is the
complex object motions in human-object interactions, which we tackle by
introducing the new object bones into the conventional human skeleton hierarchy
to effectively estimate large object deformations in our dynamic human-object
model. The second challenge is that humans interact with different objects at
different times, for which we introduce two new learnable object state
embeddings that can be used as conditions for learning our human-object
representation and scene representation, respectively. Extensive experiments
show that HOSNeRF significantly outperforms SOTA approaches on two challenging
datasets by a large margin of 40% ~ 50% in terms of LPIPS. The code, data, and
compelling examples of 360{\deg} free-viewpoint renderings from single videos
will be released in https://showlab.github.io/HOSNeRF.Comment: Project page: https://showlab.github.io/HOSNeR
The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function
RNA binding proteins (RBPs) have a broad biological and physiological function and are critical in regulating pre-mRNA posttranscriptional processing, intracellular migration, and mRNA stability. QKI, also known as Quaking, is a member of the signal transduction and activation of RNA (STAR) family, which also belongs to the heterogeneous nuclear ribonucleoprotein K- (hnRNP K-) homology domain protein family. There are three major alternatively spliced isoforms, QKI-5, QKI-6, and QKI-7, differing in carboxy-terminal domains. They share a common RNA binding property, but each isoform can regulate pre-mRNA splicing, transportation or stability differently in a unique cell type-specific manner. Previously, QKI has been known for its important role in contributing to neurological disorders. A series of recent work has further demonstrated that QKI has important roles in much broader biological systems, such as cardiovascular development, monocyte to macrophage differentiation, bone metabolism, and cancer progression. In this mini-review, we will focus on discussing the emerging roles of QKI in regulating cardiac and vascular development and function and its potential link to cardiovascular pathophysiology
BMP10 preserves cardiac function through its dual activation of SMAD-mediated and STAT3-mediated pathways
Bone morphogenetic protein 10 (BMP10) is a cardiac peptide growth factor belonging to the transforming growth factor β superfamily that critically controls cardiovascular development, growth, and maturation. It has been shown that BMP10 elicits its intracellular signaling through a receptor complex of activin receptor-like kinase 1 with morphogenetic protein receptor type II or activin receptor type 2A. Previously, we generated and characterized a transgenic mouse line expressing BMP10 from the α-myosin heavy chain gene promoter and found that these mice have normal cardiac hypertrophic responses to both physiological and pathological stimuli. In this study, we report that these transgenic mice exhibit significantly reduced levels of cardiomyocyte apoptosis and cardiac fibrosis in response to a prolonged administration of the β-adrenoreceptor agonist isoproterenol. We further confirmed this cardioprotective function with a newly generated conditional Bmp10 transgenic mouse line, in which Bmp10 was activated in adult hearts by tamoxifen. Moreover, the intraperitoneal administration of recombinant human BMP10 was found to effectively protect hearts from injury, suggesting potential therapeutic utility of using BMP10 to prevent heart failure. Gene profiling and biochemical analyses indicated that BMP10 activates the SMAD-mediated canonical pathway and, unexpectedly, also the signal transducer and activator of transcription 3 (STAT3)-mediated signaling pathway both in vivo and in vitro Additional findings further supported the notion that BMP10's cardioprotective function likely is due to its dual activation of SMAD- and STAT3-regulated signaling pathways, promoting cardiomyocyte survival and suppressing cardiac fibrosis
Synchronous post-acceleration of laser-driven protons in helical coil targets by controlling the current dispersion
Post-acceleration of protons in helical coil targets driven by intense, ultrashort laser pulses can enhance ion energy by utilizing the transient current from the targets’ self-discharge. The acceleration length of protons can exceed a few millimeters, and the acceleration gradient is of the order of GeV/m. How to ensure the synchronization between the accelerating electric field and the protons is a crucial problem for efficient post-acceleration. In this paper, we study how the electric field mismatch induced by current dispersion affects the synchronous acceleration of protons. We propose a scheme using a two-stage helical coil to control the current dispersion. With optimized parameters, the energy gain of protons is increased by four times. Proton energy is expected to reach 45 MeV using a hundreds-of-terawatts laser, or more than 100 MeV using a petawatt laser, by controlling the current dispersion
QKI is a critical pre-mRNA alternative splicing regulator of cardiac myofibrillogenesis and contractile function
The RNA-binding protein QKI belongs to the hnRNP K-homology domain protein family, a well-known regulator of pre-mRNA alternative splicing and is associated with several neurodevelopmental disorders. Qki is found highly expressed in developing and adult hearts. By employing the human embryonic stem cell (hESC) to cardiomyocyte differentiation system and generating QKI-deficient hESCs (hESCs-QKIdel) using CRISPR/Cas9 gene editing technology, we analyze the physiological role of QKI in cardiomyocyte differentiation, maturation, and contractile function. hESCs-QKIdel largely maintain normal pluripotency and normal differentiation potential for the generation of early cardiogenic progenitors, but they fail to transition into functional cardiomyocytes. In this work, by using a series of transcriptomic, cell and biochemical analyses, and the Qki-deficient mouse model, we demonstrate that QKI is indispensable to cardiac sarcomerogenesis and cardiac function through its regulation of alternative splicing in genes involved in Z-disc formation and contractile physiology, suggesting that QKI is associated with the pathogenesis of certain forms of cardiomyopathies
Pairing symmetry and properties of iron-based high temperature superconductors
Pairing symmetry is important to indentify the pairing mechanism. The
analysis becomes particularly timely and important for the newly discovered
iron-based multi-orbital superconductors. From group theory point of view we
classified all pairing matrices (in the orbital space) that carry irreducible
representations of the system. The quasiparticle gap falls into three
categories: full, nodal and gapless. The nodal-gap states show conventional
Volovik effect even for on-site pairing. The gapless states are odd in orbital
space, have a negative superfluid density and are therefore unstable. In
connection to experiments we proposed possible pairing states and implications
for the pairing mechanism.Comment: 4 pages, 1 table, 2 figures, polished versio
An integrated analysis of mRNA and sRNA transcriptional profiles in tomato root: Insights on tomato wilt disease.
Tomato wilt disease caused by Fusarium oxysporum f. sp. lycopersici (FOL) is a worldwide destructive disease of tomato. As exploring gene expression and function approaches constitute an initial point for investigating pathogen-host interaction, we performed RNA-seq and sRNA-seq analysis to investigate the transcriptome of tomato root under FOL infection. Differentially expressed (DE) protein-coding gene and miRNA gene profiles upon inoculation with FOL were presented at twenty-four hours post-inoculation in four treatments. A total of more than 182.6 million and 132.2 million high quality clean reads were obtained by RNA-seq and sRNA-seq, respectively. A large overlap was found in DE mRNAs between susceptible cultivar Moneymaker and resistant cultivar Motelle. Gene Ontology terms were mainly classified into catalytic activity, metabolic process and binding. Combining with qRT-PCR and Northern blot, we validated the transcriptional profile of five genes and five miRNAs conferred to FOL infection. Our work allowed comprehensive understanding of different transcriptional reaction of genes/miRNAs between the susceptible and resistant cultivars tomato to the FOL challenge, which could offer us with a future direction to generate models of mediated resistance responses
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