Learning Degradation-Robust Spatiotemporal Frequency-Transformer for Video Super-Resolution.

Video Super-Resolution (VSR) aims to restore high-resolution (HR) videos from low-resolution (LR) videos. Existing VSR techniques usually recover HR frames by extracting pertinent textures from nearby frames with known degradation processes. Despite significant progress, grand challenges remain to effectively extract and transmit high-quality textures from high-degraded low-quality sequences, such as blur, additive noises, and compression artifacts. This work proposes a novel degradation-robust Frequency-Transformer (FTVSR++) for handling low-quality videos that carry out self-attention in a combined space-time-frequency domain. First, video frames are split into patches and each patch is transformed into spectral maps in which each channel represents a frequency band. It permits a fine-grained self-attention on each frequency band so that real visual texture can be distinguished from artifacts. Second, a novel dual frequency attention (DFA) mechanism is proposed to capture the global and local frequency relations, which can handle different complicated degradation processes in real-world scenarios. Third, we explore different self-attention schemes for video processing in the frequency domain and discover that a "divided attention" which conducts joint space-frequency attention before applying temporal-frequency attention, leads to the best video enhancement quality. Extensive experiments on three widely-used VSR datasets show that FTVSR++ outperforms state-of-the-art methods on different low-quality videos with clear visual margins.

Clostridium prolinivorans sp. nov., a thermophilic bacterium isolated from an anaerobic reactor degrading propionate.

An anaerobic, Gram-stain-positive, spore-forming bacterium, designated strain PYR-10T, was isolated from a mesophilic methanogenic consortium. Cells were 0.7-1.2×6.0-6.3 µm, straight or slightly curved rods, with flagellar motility. Growth was observed in PYG (peptone-yeast glucose) medium at pH 5.5-8.0 (optimum, pH 6.5), 30-55 °C (45 °C) and in NaCl concentrations of 0-15 g l-1 (0 g l-1). Phylogenetic analysis based on the 16S rRNA gene sequence indicated that strain PYR-10T belongs to the genus Clostridium. The strain showed 95.4, 93.7, 93.5 and 93.0 % 16S rRNA gene sequence similarity to Clostridium swellfunianum DSM 27788T, Clostridium pascui DSM 10365T, Clostridium pasteurianum DSM 525T and Clostridium punense DSM 28650T, respectively. The genomic DNA G+C content was 27.7 mol%. The major cellular fatty acids of strain PYR-10T were iso-C15 : 0, C16 : 0, C16 : 0 DMA, anteiso-C15 : 0 and C14 : 0. The main polar lipids were glycolipid, phosphoaminoglycolipid, diphosphatidylglycerol, phosphatidylglycerol, phospholipids, phosphatidylethanolamine and lipids. An unknown menaquinone was detected. 2,6-Diaminopimelic acid was not detected. The whole-cell sugars contained ribose and lower amounts of glucose. Based on the results of phylogenetic, chemotaxonomic and phenotypic analyses, strain PYR-10T represents a novel species of the genus Clostridium, for which the name Clostridium prolinivorans sp. nov. is proposed. The type strain is strain PYR-10T (=JCM 33161T=CCAM 531T=CGMCC 1.5286T).

CRISPR/Cas-mediated genome editing in the rat via direct injection of one-cell embryos.

Conventional embryonic stem cell (ESC)-based gene targeting, zinc-finger nuclease (ZFN) and transcription activator-like effector nuclease (TALEN) technologies are powerful strategies for the generation of genetically modified animals. Recently, the CRISPR/Cas system has emerged as an efficient and convenient alternative to these approaches. We have used the CRISPR/Cas system to generate rat strains that carry mutations in multiple genes through direct injection of RNAs into one-cell embryos, demonstrating the high efficiency of Cas9-mediated gene editing in rats for simultaneous generation of compound gene mutant models. Here we describe a stepwise procedure for the generation of knockout and knock-in rats. This protocol provides guidelines for the selection of genomic targets, synthesis of guide RNAs, design and construction of homologous recombination (HR) template vectors, embryo microinjection, and detection of mutations and insertions in founders or their progeny. The procedure from target design to identification of founders can take as little as 6 weeks, of which <10 d is actual hands-on working time.

High-efficiency and heritable gene targeting in mouse by transcription activator-like effector nucleases.

Transcription activator-like effector nucleases (TALENs) are a powerful new approach for targeted gene disruption in various animal models, but little is known about their activities in Mus musculus, the widely used mammalian model organism. Here, we report that direct injection of in vitro transcribed messenger RNA of TALEN pairs into mouse zygotes induced somatic mutations, which were stably passed to the next generation through germ-line transmission. With one TALEN pair constructed for each of 10 target genes, mutant F0 mice for each gene were obtained with the mutation rate ranged from 13 to 67% and an average of ∼40% of total healthy newborns with no significant differences between C57BL/6 and FVB/N genetic background. One TALEN pair with single mismatch to their intended target sequence in each side failed to yield any mutation. Furthermore, highly efficient germ-line transmission was obtained, as all the F0 founders tested transmitted the mutations to F1 mice. In addition, we also observed that one bi-allele mutant founder of Lepr gene, encoding Leptin receptor, had similar diabetic phenotype as db/db mouse. Together, our results suggest that TALENs are an effective genetic tool for rapid gene disruption with high efficiency and heritability in mouse with distinct genetic background.

Lgr4-mediated Wnt/ß-catenin signaling in peritubular myoid cells is essential for spermatogenesis.

Peritubular myoid cells (PMCs) are myofibroblast-like cells that surround the seminiferous tubules and play essential roles in male fertility. How these cells modulate spermatogenesis and the signaling pathways that are involved are largely unknown. Here we report that Lgr4 is selectively expressed in mouse PMCs in the testes, and loss of Lgr4 leads to germ cells arresting at meiosis I and then undergoing apoptosis. In PMCs of Lgr4 mutant mice, the expression of androgen receptor, alpha-smooth muscle actin and extracellular matrix proteins was dramatically reduced. Malfunctioning PMCs further affected Sertoli cell nuclear localization and functional protein expression in Lgr4(-/-) mice. In addition, Wnt/ß-catenin signaling was activated in wild-type PMCs but attenuated in those of Lgr4(-/-) mice. When Wnt/ß-catenin signaling was reactivated by crossing with Apc(min/+) mice or by Gsk3ß inhibitor treatment, the Lgr4 deficiency phenotype in testis was partially rescued. Together, these data demonstrate that Lgr4 signaling through Wnt/ß-catenin regulates PMCs and is essential for spermatogenesis.

PAK1IP1, a ribosomal stress-induced nucleolar protein, regulates cell proliferation via the p53-MDM2 loop.

Cell growth and proliferation are tightly controlled via the regulation of the p53-MDM2 feedback loop in response to various cellular stresses. In this study, we identified a nucleolar protein called PAK1IP1 as another regulator of this loop. PAK1IP1 was induced when cells were treated with chemicals that disturb ribosome biogenesis. Overexpression of PAK1IP1 inhibited cell proliferation by inducing p53-dependent G1 cell-cycle arrest. PAK1IP1 bound to MDM2 and inhibited its ability to ubiquitinate and to degrade p53, consequently leading to the accumulation of p53 levels. Interestingly, knockdown of PAK1IP1 in cells also inhibited cell proliferation and induced p53-dependent G1 arrest. Deficiency of PAK1IP1 increased free ribosomal protein L5 and L11 which were required for PAK1IP1 depletion-induced p53 activation. Taken together, our results reveal that PAK1IP1 is a new nucleolar protein that is crucial for rRNA processing and plays a regulatory role in cell proliferation via the p53-MDM2 loop.