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Exosome-mediated horizontal and vertical transmission of subgroup J avian leukosis virus (ALV-J) in poultry flocks can lead to growth inhibition and severe immunosuppression. However, there are few reports on the early infection of chicken embryonic stem cells (cESCs) with ALV-J. In this study, we confirmed that early infection with ALV-J can accelerate the differentiation of cESCs and promote the secretion of exosomes. To investigate the modulation strategy of ALV-J in cESCs, circRNA sequencing was performed for further analysis. A total of 305 differentially expressed circRNAs (DECs) were obtained, including 71 upregulated DECs. Circ-CCDC7 was found to be the most upregulated DEC and was assessed by qRT-PCR, with the result consistent with the result of circRNA-seq. Based on qRT-PCR, gga-miR-6568-3p was found to be the target of the top 3 DECs, including circ-CCDC7, and the stem cell marker gene Pax7 was identified as the target gene of gga-miR-6568-3p. This study demonstrated that exosomal circ-CCDC7/gga-miR-6568-3p/Pax7 accelerates the differentiation of cESCs after early infection with ALV-J.

Hyperuricemic C. eleganswere obtained after normal worms were treated by xanthine (0.25 mg/mL, 18 h). For hyperuricemic worms, there was a statistically significant increase in the uric acid level (p < 0.001) and a lower drug damage (p > 0.05). Moreover, the model was proved to keep a high uric acid level for up to 12 h. After given allopurinol (0.25 mg/mL, 12 h), the uric acid of hyperuricemic C. eleganshad a significant reduction by 15%. Furthermore, xanthine oxidase activity in hyperuricemic C. elegansshowed a statistically significant increase (p < 0.001), which resulted in a raised uric acid content. A high uric acid model with low drug damage and high efficiency and stability was established in C. elegansafter simply xanthine treatment.

The functional role of colonic epithelium in the pathogenesis of ulcerative colitis (UC) remains unclear. Here, we reveal a novel mechanism by which colonic epithelia recruit T helper-17 (Th17) cells during the onset of UC. mTOR complex 1 (mTORC1) was hyper-activated in colonic epithelia of UC mice. While colonic epithelial TSC1 (mTORC1 negative regulator) disruption induced constitutive mTORC1 activation in the colon epithelia and aggravated UC, RPTOR (essential mTORC1 component) depletion inactivated mTORC1 and ameliorated UC. TSC1 deficiency enhanced, whereas RPTOR ablation reduced the expression of cyclooxygenase 2 (COX-2), interleukin-1 (IL-1), IL-6, and IL-23, as well as Th17 infiltration in the colon. Importantly, inhibition of COX-2 reversed the elevation in the expression of these proinflammatory mediators induced by TSC1 deficiency, and subsequently reduced the symptoms and pathological characteristics of UC in mouse models. Mechanistically, mTORC1 activates COX-2 transcription via phosphorylating STAT3 and enhancing it’s binding to the COX-2 promoter. Consistently, enhanced mTORC1 activity and COX2 expression, as well as strong positive correlation between each other, were observed in colonic epithelial tissues of UC patients. Collectively, our study demonstrates an essential role of epithelial mTORC1 in UC pathogenesis and establishes a novel link between colonic epithelium, Th17 responses, and UC development.

The functional role of colonic epithelium in the pathogenesis of ulcerative colitis (UC) remains unclear. Here, we reveal a novel mechanism by which colonic epithelia recruit T helper-17 (Th17) cells during the onset of UC. mTOR complex 1 (mTORC1) was hyper-activated in colonic epithelia of UC mice. While colonic epithelial TSC1 (mTORC1 negative regulator) disruption induced constitutive mTORC1 activation in the colon epithelia and aggravated UC, RPTOR (essential mTORC1 component) depletion inactivated mTORC1 and ameliorated UC. TSC1 deficiency enhanced, whereas RPTOR ablation reduced the expression of cyclooxygenase 2 (COX-2), interleukin-1 (IL-1), IL-6, and IL-23, as well as Th17 infiltration in the colon. Importantly, inhibition of COX-2 reversed the elevation in the expression of these proinflammatory mediators induced by TSC1 deficiency, and subsequently reduced the symptoms and pathological characteristics of UC in mouse models. Mechanistically, mTORC1 activates COX-2 transcription via phosphorylating STAT3 and enhancing it's binding to the COX-2 promoter. Consistently, enhanced mTORC1 activity and COX2 expression, as well as strong positive correlation between each other, were observed in colonic epithelial tissues of UC patients. Collectively, our study demonstrates an essential role of epithelial mTORC1 in UC pathogenesis and establishes a novel link between colonic epithelium, Th17 responses, and UC development.

Solid wood materials and wood–plastic composites as two kinds of lightweight materials are attracting great interest from academia and industry due to their green and recycling nature. However, the relatively lower specific strength limits their wider applications. In particular, solid wood is vulnerable to moisture and decay fungi in nature, resulting in its poor durability for effectively long-term utilization. Inspired from the porous structure of wood, we propose a new design to build a wood-based nanocomposite with higher specific strength and satisfactory durability by in situ generation of organic–inorganic hybrid polymer within wood via a sol–gel method. The derived composite has 50–1200% improvement of impact toughness, 56–192% improvement of tensile strength, and 110–291% improvement of flexural strength over those of typical wood–plastic composites, respectively; and even 34% improvement of specific tensile strength than that of 36A steel; 208% enhancement of hardness; and 156% enhancement of compression strength than those of compared solid wood, respectively; as well as significantly improved dimensional stability and decay resistance over those of untreated natural wood. Such materials could be potentially utilized as lightweight and high-strength materials for applications in construction and automotive industries. This method could be extended to constitute other inorganic nanomaterials for novel organic–inorganic hybrid polymer within wood.

Anaerobic digestion of Chinese cabbage waste was investigated through a pilot-scale two-stage digester at a mesophilic temperature of 37°C. In the acidification digester, the main product was acetic acid, with the maximum concentration of 4289mg·L−1on the fourth day, accounting for 50.32% of total volatile fatty acids. The oxidation reduction potential (ORP) and NH4+-N level decreased gradually with hydraulic retention time (HRT) of acidification. In the second digestion phase, the maximum methanogenic bacterial concentration reached 9.6×1010ml−1at the organic loading rate (OLR) of 3.5–4 kgVS·m−3, with corresponding HRT of 12–16days. Accordingly, the optimal biogas production was 0.62m3·(kgVS)−1, with methane content of 65%–68%. ORP and NH4+-N levels in the methanizer remained between −500 and −560mV and 2000–4500mg·L−1, respectively. Methanococcusand Methanosarcinaserved as the main methanogens in the anaerobic digester.

Obestatin, originally identified and purified from rat stomach extracts, was reported to bind to orphan G protein-coupled receptor, GPR39, and inhibit appetite and gastric motility. This study was conducted to investigate the effects of porcine obestatin on proliferation, differentiation and apoptosis of porcine preadipocytes isolated from subcutaneous fat of piglets. At indicated times of culture, morphology of preadipocytes and accumulated lipid droplets within the cells were identified by invert microscope. After treating with obestatin (0, 0.1, 1, 10 and 100nM), cell proliferation was measured by MTT method and protein expression of CCAAT/enhancer binding protein-α (C/EBPα), peroxisome proliferator-activated receptor-γ (PPARγ), Caspase-7 and Caspase-9 was determined by Western Blot, mRNA expression of GPR39 and Caspase-3 was analyzed by RT-PCR, and the activity of Caspase-3 was measured by spectrophotometric method. The results showed that obestatin had no effect on GPR39 expression, while promotes the optical density (OD) value of cells, enhanced protein expression of PPARγ and C/EBPa, decreased mRNA expression and activity of Caspase-3, and inhibited protein expression of Caspase-7 and Caspase-9 in a dose-dependent manner. These results suggested that obestatin enhance proliferation and differentiation of preadipocytes promoting PPARγ and C/EBPa expression, and inhibiting preadipocyte apoptosis by decreasing expression of Caspase-3, Caspase-7 and Caspase-9.

Autophagy plays an important role in cellular responses to pathogens. However, the impact of the autophagy machinery on classical swine fever virus (CSFV) infection is not yet confirmed. In this study, we showed that CSFV infection significantly increases the number of autophagy-like vesicles in the cytoplasm of host cells at the ultrastructural level. We also found the formation of 2 ubiquitin-like conjugation systems upon virus infection, including LC3-I/LC3-II conversion and ATG12–ATG5 conjugation, which are considered important indicators of autophagy. Meanwhile, high expression of ATG5 and BECN1 was detected in CSFV-infected cells; conversely, degradation of SQSTM1 was observed by immunoblotting, suggesting that CSFV infection triggered a complete autophagic response, most likely by the NS5A protein. Furthermore, by confocal immunofluorescence analysis, we discovered that both envelope protein E2 and nonstructural protein NS5A colocalized with LC3 and CD63 during CSFV infection. Examination by immunoelectron microscopy further confirmed the colocalization of both E2 and NS5A proteins with autophagosome-like vesicles, indicating that CSFV utilizes the membranes of these vesicles for replication. Finally, we demonstrated that alteration of cellular autophagy by autophagy regulators and shRNAs affects progeny virus production. Collectively, these findings provide strong evidence that CSFV infection needs an autophagy pathway to enhance viral replication and maturity in host cells.

AbstractThis paper is part of Chapter One "The Origin of Art and Artistic Thinking" in the book An Introduction to the Logic of NarrativeArt. But before discussing artistic thinking, we find it necessary to investigate the origin of thinking and its relation with symbols. Since it's impossible for us to go back to the ancient times, what we can do is to examine the occurrence of thinking and symbols and their relation by means of studying babies' and aborigines' thinking methods and animals' cognition of symbols. The developmental process of thinking proves that thinking is undoubtedly prior to each conscious action. It's not the case that labor creates human beings or language, but that labor, language and writing mark the developmental level of thinking. It also proves that the two-way motion ("concrete to abstract ←→ abstract to concrete") of thinking occurs at all times. Human modes of thinking experience a gradual evolutionary process from primitive thinking to mythological thinking and then to abstract thinking. And mythological thinking is retained in artistic creation and becomes various figures of speech which are still in use now.

We show that for certain complex parameters $ {\lambda _1},\ldots,{\lambda _{n - 1}}$ $ {\lambda _n}$

$\displaystyle {e^{{\lambda _1}{e^{^{{.^{{.^{{.^{{{^{{\lambda _{n - 1}}}}^{{e^\lambda }^{_{{n^z}}}}}}}}}}}}}}}}$ is the whole plane $ \mathbb{C}$ the set of $ n$ $ ({\lambda _1},\ldots,{\lambda _n}),{\lambda _1},\ldots,{\lambda _n} \in \mathbb{R}$

$\displaystyle {e^{{\lambda _1}{e^{^{{.^{{.^{{.^{{{^{{\lambda _{n - 1}}}}^{{e^\lambda }^{_{{n^z}}}}}}}}}}}}}}}} - z= 0$ has exact two real solutions. In fact, one of them is an attracting fixed point of

$\displaystyle {e^{{\lambda _1}{e^{^{{.^{{.^{{.^{{{^{{\lambda _{n - 1}}}}^{{e^\lambda }^{_{{n^z}}}}}}}}}}}}}}}},$ which is denoted by $ q$ $ ({\lambda _1},\ldots,{\lambda _n})\, \in \Lambda $

$\displaystyle {e^{{\lambda _1}{e^{^{{.^{{.^{{.^{{{^{{\lambda _{n - 1}}}}^{{e^\lambda }^{_{{n^z}}}}}}}}}}}}}}}}$ is the complement of the basin of attraction of . The ideas used in this note may also be applicable to more general functions.

•EZH2 is considered as a direct target of miR-506-3p.•MiR-506-3p overexpression decreased the level of β-catenin.•MiR-506-3p increases response to PARP inhibitors and cisplatin in serous ovarian cancer by targeting EZH2/β-catenin pathway.