Ascorbic acid biosynthesis in Pacific abalone Haliotis discus hannai Ino and L-gulonolactone oxidase gene loss as an independent event.

Up to now, it has been believed that invertebrates are unable to synthesize ascorbic acid (AA) in vivo. However, in the present study, the full-length CDs (Coding sequence) of L-gulonolactone oxidase (GLO) from Pacific abalone (Haliotis discus hannai Ino) were obtained through molecular cloning. The Pacific abalone GLO contained a FAD-binding domain in the N-termination, and ALO domain and conserved HWAK motif in the C-termination. The GLO gene possesses 12 exons and 11 introns. The Pacific abalone GLO was expressed in various tissues, including the kidney, digestive gland, gill, intestine, muscle and mantle. The GLO activity assay revealed that GLO activity was only detected in the kidney of Pacific abalone. After a 100-day feeding trial, dietary AA levels did not significantly affect the survival, weight gain, daily increment in shell length, and feed conversion ratio of Pacific abalone. The expression of GLO in the kidney was downregulated by dietary AA. These results implied that the ability to synthesize AA in abalone had not been lost. From the evolutionary perspective, the loss of GLO occurred independently as an independent event by matching with the genomes of various species. The positive selection analysis revealed that the GLO gene underwent purifying selective pressure during its evolution. In conclusion, the present study provided direct evidence to prove that the GLO activity and the ability to synthesize AA exist in abalone. The AA synthesis ability in vertebrates might have originated from invertebrates dating back 930.31 million years.

Anti-VEGFR2-Interferon α Promotes the Infiltration of CD8+ T Cells in Colorectal Cancer by Upregulating the Expression of CCL5.

SUMMARY: Immunocytokines are a promising immunotherapeutic approach in cancer therapy. Anti-VEGFR2-interferon α (IFNα) suppressed colorectal cancer (CRC) growth and enhanced CD8+ T-cell infiltration in the tumor microenvironment, exhibiting great clinical translational potential. However, the mechanism of how the anti-VEGFR2-IFNα recruits T cells has not been elucidated. Here, we demonstrated that anti-VEGFR2-IFNα suppressed CRC metastasis and enhanced CD8+ T-cell infiltration. RNA sequencing revealed a transcriptional activation of CCL5 in metastatic CRC cells, which was correlated with T-cell infiltration. IFNα but not anti-VEGFR2 could further upregulate CCL5 in tumors. In immunocompetent mice, both IFNα and anti-VEGFR2-IFNα increased the subset of tumor-infiltrating CD8+ T cells through upregulation of CCL5. Knocking down CCL5 in tumor cells attenuated the infiltration of CD8+ T cells and dampened the antitumor efficacy of anti-VEGFR2-IFNα treatment. We, therefore, propose upregulation of CCL5 is a key to enhance infiltration of CD8+ T cells in metastatic CRC with IFNα and IFNα-based immunocytokine treatments. These findings may help the development of IFNα related immune cytokines for the treatment of less infiltrated tumors.

Mn Single-Atom Nanozyme Functionalized 3D-Printed Bioceramic Scaffolds for Enhanced Antibacterial Activity and Bone Regeneration.

Infective bone defect is increasingly threatening human health. How to achieve the optimal antibacterial activity and regenerative repair of infective bone defect simultaneously is a huge challenge in clinic. Herein, this work reports a rational integration of Mn single-atom nanozyme into the 3D-printed bioceramic scaffolds (Mn/HSAE@BCP scaffolds). The integrated Mn/HSAE@BCP scaffolds can catalyze the conversion of H2O2 to produce hydroxyl radical (•OH) and superoxide anion (O2 •-) through cascade reaction. Besides, the prominent thermal conversion efficiency of Mn/HSAE@BCP scaffolds can be utilized for sonodynamic therapy (SDT). The synergetic strategy of chemodynamic therapy (CDT)/SDT enables the sufficient generation of reactive oxygen species (ROS) to kill Staphylococcus aureus (S. aureus) or Escherichia coli (E. coli). Furthermore, the enhanced antibacterial efficacy of Mn/HSAE@BCP scaffolds is beneficial to upregulate the expression of osteogenesis-related markers (such as collagen 1(COL1), Runt-related transcription factor 2 (Runx2), osteocalcin (OCN), and osteoprotegerin (OPG)) in vitro and further promote bone regeneration in vivo. The results demonstrate the good potential of Mn/HSAE@BCP scaffolds for the enhanced antibacterial activity and bone regeneration, which provide an effective method for the treatment of clinical infective bone defect.

Effects of Ferric Ions on Cellulose Nanocrystalline-Based Chiral Nematic Film and Its Applications.

Chiral nematic materials have been attracting attention in fields of advanced functional applications due to their unique iridescent colors and tunable helical structure. A precisely decreased pitch is of importance for construction and applications of chiral nematic materials; however, it remains a huge challenge. Herein, cellulose nanocrystal (CNC) is selected as a constructed matrix for chiral nematic films, and ferric chloride (FeCl3) is used as a modification agent. We investigate the effects of the ferric ion loads on the helical structure and optical characteristics of iridescent film. Subsequently, the influence of ferric ions on the assembly process of CNC liquid crystal and the regulation of the structure color of self-assembled monolayers are discussed. Therefore, the CNC/FeCl3 chiral nematic films showed a blueshifted structural color from orange to blue, which highlights a simple route to achieve the regulation of decreased pitch. Further, we have applied this CNC/FeCl3 chiral nematic film for benzene gas detection. The sensing performance shows that the CNC/FeCl3 chiral nematic film reacts to benzene gas, which can be merged into the nematic layer of the CNC and trigger the iron ions chelated on the CNC, consequently arousing the redshift of the reflected wavelength and the effective colorimetric transition. This CNC/FeCl3 chiral nematic film is anticipated to boost a new gas sensing mechanism for faster and more effective in-situ qualitative investigations.

Psychometric properties of the Chinese version of the Exercise Self-Efficacy Scale for the Transtheoretical Model: a confirmatory analysis among Chinese children and adolescents.

BACKGROUND: Self-efficacy has been recognized as a critical component in people's participation and maintenance of physical activity. This study aims to validate the Chinese version of the Exercise Self-Efficacy Scale (ESE) among Chinese children and adolescents using confirmatory factor analysis (CFA). METHODS: A cross-sectional study was conducted on two primary and two secondary schools in central China. The ESE scale was translated into Chinese (ESE-C) using the standard forward-backward translation method. Data were analyzed using Mplus 8 for the CFA. RESULTS: The final model showed a satisfactory level of goodness-of-fit (CFI = 0.918; TLI = 0.905; SRMR = 0.043; RMSEA = 0.066), indicating a good construct validity of the ESE-C for children and adolescents in mainland China. Furthermore, the final ESE-C model achieved composite reliability values of 0.963 and average variance extraction values of 0.597, indicating sufficient convergent and discriminant validity. Besides, the Cronbach's alpha value was 0.964, demonstrating excellent internal consistency of the ESE-C scale. CONCLUSION: The ESE-C scale is a valid instrument for assessing exercise self-efficacy among children and adolescents in mainland China.

Enhanced antitumor and anti-metastasis by VEGFR2-targeted doxorubicin immunoliposome synergy with NK cell activation.

Liposomal doxorubicin exhibits stronger drug accumulation at the tumor site due to the Enhanced Permeability and Retention (EPR) effect. However, the prognosis for the patient is poor due to this drug's lack of targeting and tumor metastasis during treatment. Vascular epidermal growth factor receptor (VEGFR2) plays an important role in angiogenesis and cancer metastasis. To enhance antitumor efficacy of PEGylated liposomal doxorubicin, we constructed a VEGFR2-targeted and doxorubicin-loaded immunoliposome (Lipo-DOX-C00) by conjugating a VEGFR2-specific, single chain antibody fragment to DSPE-PEG2000-MAL, and then we inserted the antibody-conjugated polymer into liposomal doxorubicin (Lipo-DOX). The immunoliposome was formed uniformly with high affinity for VEGFR2. In vitro, Lipo-DOX-C00 enhanced doxorubicin internalization into LLC and 4T1 cells compared with non-conjugated, liposomal doxorubicin. In vivo, Lipo-DOX-C00 delivered DOX to tumor tissues effectively, which exhibited an improved antitumor and anti-metastasis efficacy in both LLC subcutaneous tumor models and 4T1 tumor models. In addition, the combined therapy of a VEGFR2-MICA bispecific antibody (JZC01) and Lipo-DOX-C00 achieved enhanced inhibition of cancer growth and metastasis due to activation of the immune system. Our study provides a promising approach to clinical application of liposomal doxorubicin.

Sustainable production of dopamine hydrochloride from softwood lignin.

Dopamine is not only a widely used commodity pharmaceutical for treating neurological diseases but also a highly attractive base for advanced carbon materials. Lignin, the waste from the lignocellulosic biomass industry, is the richest source of renewable aromatics on earth. Efficient production of dopamine direct from lignin is a highly desirable target but extremely challenging. Here, we report an innovative strategy for the sustainable production of dopamine hydrochloride from softwood lignin with a mass yield of 6.4 wt.%. Significantly, the solid dopamine hydrochloride is obtained by a simple filtration process in purity of 98.0%, which avoids the tedious separation and purification steps. The approach begins with the acid-catalyzed depolymerization, followed by deprotection, hydrogen-borrowing amination, and hydrolysis of methoxy group, transforming lignin into dopamine hydrochloride. The technical economic analysis predicts that this process is an economically competitive production process. This study fulfills the unexplored potential of dopamine hydrochloride synthesis from lignin.

Glucagon Promotes Gluconeogenesis through the GCGR/PKA/CREB/PGC-1α Pathway in Hepatocytes of the Japanese Flounder Paralichthys olivaceus.

In order to investigate the mechanism of glucagon regulation of gluconeogenesis, primary hepatocytes of the Japanese flounder (Paralichthys olivaceus) were incubated with synthesized glucagon, and methods based on inhibitors and gene overexpression were employed. The results indicated that glucagon promoted glucose production and increased the mRNA levels of glucagon receptor (gcgr), guanine nucleotide-binding protein Gs α subunit (gnas), adenylate cyclase 2 (adcy2), protein kinase A (pka), cAMP response element-binding protein 1 (creb1), peroxisome proliferator-activated receptor-γ coactivator 1α (pgc-1α), phosphoenolpyruvate carboxykinase 1 (pck1), and glucose-6-phosphatase (g6pc) in the hepatocytes. An inhibitor of GCGR decreased the mRNA expression of gcgr, gnas, adcy2, pka, creb1, pgc-1α, pck1, g6pc, the protein expression of phosphorylated CREB and PGC-1α, and glucose production. The overexpression of gcgr caused the opposite results. An inhibitor of PKA decreased the mRNA expression of pgc-1α, pck1, g6pc, the protein expression of phosphorylated-CREB, and glucose production in hepatocytes. A CREB-targeted inhibitor significantly decreased the stimulation by glucagon of the mRNA expression of creb1, pgc-1α, and gluconeogenic genes, and glucose production decreased accordingly. After incubating the hepatocytes with an inhibitor of PGC-1α, the glucagon-activated mRNA expression of pck1 and g6pc was significantly down-regulated. Together, these results demonstrate that glucagon promotes gluconeogenesis through the GCGR/PKA/CREB/PGC-1α pathway in the Japanese flounder.

Rapid adsorption of directional cellulose nanofibers/3-glycidoxypropyltrimethoxysilane/polyethyleneimine aerogels on microplastics in water.

Currently, cellulose-based aerogel materials are a hot topic owing to their high specific surface area and high porosity, as well as the green, degradable and biocompatible characteristics of cellulosic materials. Modification of cellulose to enhance the adsorption properties of cellulose-based aerogels has important research significance in solving the problem of water body pollution. In this paper, cellulose nanofibers (CNFs) were modified with polyethyleneimine (PEI), and modified aerogels with directional structures were prepared by a simple reaction and freeze-drying method. The adsorption behavior of the aerogel followed the adsorption kinetic models and isotherm models. More significantly, the aerogel could rapidly adsorb microplastics, reaching equilibrium within 20 min. Furthermore, the fluorescence displayed directly expresses the occurrence of the adsorption behavior of the aerogels. Therefore, the modified cellulose nanofiber aerogels were of reference significance for microplastic removal from water bodies.

αVEGFR2-MICA fusion antibodies enhance immunotherapy effect and synergize with PD-1 blockade.

Antiangiogenic therapy has shown significant clinical benefits in gastric cancer (GC) and non-small cell lung cancer (NSCLC). However, their effectiveness is limited by the immunosuppressive tumor microenvironment. The MHC class I chain-related molecules A and B (MICA/B) are expressed in many human cancers, enabling elimination of cancer cells by cytotoxic lymphocytes through natural killer group 2D (NKG2D) receptor activation. To improve antiangiogenic therapy and prolong its efficacy, we generated a bi-specific fusion protein (mAb04-MICA). This was comprised of an antibody targeting VEGFR2 fused to a MICA α1-α2 ectodomain. mAb04-MICA inhibited proliferation of GC and NSCLC cells through specific binding to VEGFR2 and had superior anti-tumor efficacy in both GC and NSCLC-bearing mouse models compared with ramucirumab. Further investigation revealed that the mAb04-MICA promoted NKG2D+ NK cell activation and induced the tumor-associated macrophage (TAM) polarization from M2 type to M1 type both in vitro and in vivo. The polarization of TAMs upon NKG2D and MICA mediated activation has not yet been reported. Moreover, given the up-regulation of PD-L1 in tumors during anti-angiogenesis therapy, anti-PD-1 antibody enhanced the anti-tumoral activity of mAb04-MICA through stimulating infiltration and activation of NKs and CD8+T cells in responding tumors. Our findings demonstrate that dual targeting of angiogenesis and NKG2D, or in combination with the PD-1/PD-L1 blockade, is a promising anti-tumor therapeutic strategy. This is accomplished through maintaining or reinstating tumor immunosurveillance during treatment, which expands the repertoire of anti-angiogenesis-based cancer immunotherapies.

Vitamin D3/VDR inhibits inflammation through NF-κB pathway accompanied by resisting apoptosis and inducing autophagy in abalone Haliotis discus hannai.

Vitamin D3 is believed to be a contributing factor to innate immunity. Vitamin D receptor (VDR) has a positive effect on inhibiting nuclear factor κB (NF-κB)-mediated inflammation. The underlying molecular mechanisms remain unclear, particularly in mollusks. Consequently, this study will investigate the process of vitamin D3/VDR regulating NF-κB pathway and further explore their functions on inflammation, autophagy, and apoptosis in abalone Haliotis discus hannai. Results showed that knockdown of VDR by using siRNA and dsRNA of VDR in vitro and in vivo led to more intense response of NF-κB signaling to lipopolysaccharide and higher level of apoptosis and autophagy. In addition, 1,25(OH)2D3 stimulation after VDR silencing could partially alleviate apoptosis and induce autophagy. Overexpression of VDR restricted the K48-polyubiquitin chain-dependent inhibitor of κB (IκB) ubiquitination and apoptosis-associated speck-like protein containing CARD (ASC) oligomerization. Besides, VDR silencing resulted in increase of ASC speck formation. In further mechanistic studies, we showed that VDR can directly bind to IκB and IKK1 in vitro and in vivo. In the feeding trial, H&E staining, TUNEL, and electron microscope results showed that vitamin D3 deficiency (0 IU/kg) could recruit more basophilic cells and increase more TUNEL-positive apoptotic cells and lipid droplets (LDs) than vitamin D3 supplement (1000 IU/kg and 5000 IU/kg). In summary, abalone VDR plays a negative regulator role in NF-κB-mediated inflammation via interacting with IκB and inhibiting ubiquitin-dependent degradation of IκB. Vitamin D3 in combination with VDR is essential to establish a delicate balance between autophagy and apoptosis in response to inflammation.

Status and Influencing Factors of Physical Exercise among College Students in China: A Systematic Review.

The status of the physical exercise of college students has been a popular topic in China. This study systematically reviewed the exercise status of Chinese college students and its influencing factors. A keyword and reference search were conducted in the Web of Science, PubMed, Cochrane library, and the China National Knowledge Infrastructure. Additionally, Google Scholar was searched to collect literatures related to physical activity of Chinese university students published in Chinese and English from 1 January 2017 to 30 July 2022. Fifteen studies met the selection criteria and were included in the review. The results show that the main motivation for Chinese college students to exercise is to strengthen their bodies, with running and walking ranking first and ball games ranking second in importance. Most of the college students exercised three times a week, which is the recommended minimum, and most of their workouts were of moderate intensity. Additionally, the workouts lasted for 30 min to 60 min. The main factors affecting college students' exercise are lack of time due to academic pressure, facilities constraints, and lack of professional exercise guidance. In conclusion, the physical fitness of university students should not be underestimated, and this study provides additional reference to promote healthier lifestyles among Chinese college students.

Lignocellulose dissociation with biological pretreatment towards the biochemical platform: A review.

Lignocellulose utilization has been gaining great attention worldwide due to its abundance, accessibility, renewability and recyclability. Destruction and dissociation of the cross-linked, hierarchical structure within cellulose hemicellulose and lignin is the key procedure during chemical utilization of lignocellulose. Of the pretreatments, biological treatment, which can effectively target the complex structures, is attractive due to its mild reaction conditions and environmentally friendly characteristics. Herein, we report a comprehensive review of the current biological pretreatments for lignocellulose dissociation and their corresponding degradation mechanisms. Firstly, we analyze the layered, hierarchical structure of cell wall, and the cross-linked network between cellulose, hemicellulose and lignin, then highlight that the cracking of ß-aryl ether is considered the key to lignin degradation because of its dominant position. Secondly, we explore the effect of biological pretreatments, such as fungi, bacteria, microbial consortium, and enzymes, on substrate structure and degradation efficiency. Additionally, combining biological pretreatment with other methods (chemical methods and catalytic materials) may reduce the time necessary for the whole process, which also help to strengthen the lignocellulose dissociation efficiency. Thirdly, we summarize the related applications of lignocellulose, such as fuel production, chemicals platform, and bio-pulping, which could effectively alleviate the energy pressure through bioconversion into high value-added products. Based on reviewing of current progress of lignocellulose pretreatment, the challenges and future prospects are emphasized. Genetic engineering and other technologies to modify strains or enzymes for improved biotransformation efficiency will be the focus of future research.

Biotin alleviates hepatic and intestinal inflammation and apoptosis induced by high dietary carbohydrate in juvenile turbot (Scophthalmus maximus L.).

Excessive dietary carbohydrate commonly impairs the functions of liver and intestine in carnivorous fish. In the present study, a 10-week feeding trial was carried out to explore the regulation of biotin on the hepatic and intestinal inflammation and apoptosis in turbot (Scophthalmus maximus L.) fed with high carbohydrate diets. Three isonitrogenous and isolipidic experimental diets were designed as follows: the CC diet with 18.6% of carbohydrate and 0.04 mg/kg of biotin, the HC diet with 26.9% of carbohydrate and 0.05 mg/kg of biotin, and the HCB diet with 26.9% of carbohydrate and 1.62 mg/kg of biotin. Results showed that high dietary carbohydrate (HC diet) impaired the morphology of liver and intestine, however, inclusion of dietary biotin (HCB diet) normalized their morphology. Inflammation-related gene expression of nuclear factor κB p65 (nf-κb p65), tumor necrosis factor α (tnf-α), interleukin-1ß (il-1ß), il-6 and il-8, and the protein expression of NF-κB p65 in the liver and intestine were significantly up-regulated in the HC group compared to those in the CC group (P < 0.05), the HCB diet decreased their expression compared to the HC group (P < 0.05). The gene expression of il-10 and transforming growth factor-ß (tgf-ß) in the liver and intestine were significantly decreased in the HC group compared to the CC group (P < 0.05), and inclusion of dietary biotin increased the il-10 and tgf-ß expression in the liver and intestine (P < 0.05). Moreover, compared to the CC group, the HC group had a stronger degree of DNA fragmentation and more TUNEL-positive cells in the liver and intestine, and the HCB group had a slighter degree of DNA fragmentation and fewer TUNEL-positive cells compared to the HC group. Meanwhile, the gene expression of B-cell lymphoma protein-2-associated X protein (bax) and executor apoptosis-related cysteine peptidase 3 (caspase-3) were significantly up-regulated and the gene expression of B-cell lymphoma-2 (bcl-2) was significantly down-regulated both in the liver and intestine in the HC group compared with those in the CC group (P < 0.05). Inclusion of dietary biotin significantly decreased the bax and caspase-3 mRNA levels and increased bcl-2 mRNA level in the liver and intestine (P < 0.05). In conclusion, high dietary carbohydrate (26.9% vs 18.6%) induced inflammation and apoptosis in liver and intestine. Supplementation of biotin (1.62 mg/kg vs 0.05 mg/kg) in diet can alleviate the high-dietary-carbohydrate-induced hepatic and intestinal inflammation as well as inhibit apoptosis in turbot. The present study provides basic data for the application of biotin into feed, especially the high-carbohydrate feed for turbot.

Eco-friendly wood-plastic composites from laminate sanding dust and waste poly(propylene) food pails.

Plastic pollution caused by non-degradable petrochemical-based plastics has become a serious environmental problem in China, and the reasonable management of industrial waste and renewable resources remains a huge challenge. Here, we report environment-friendly wood-plastic composites (WPCs), prepared from decorative high-pressure laminate (HPL) sanding dust (filler) and waste thermoplastic food pails (matrix), as well as comprehensively evaluate the processability, mechanical and interfacial properties, indoor safety evaluation. The elemental composition and thermal stability of these two residue materials were suitable for the WPC manufacturing process. The content of HPL sanding dust in WPC was fixed at 60 wt%, and the amount of maleic anhydride grafted polypropylene (MAPP) added was 5 wt%-7 wt%, which maximized the utilization of waste resources, and can obtain impact strength as high as 5-6 kJ/m2, tensile strength of 35-42 MPa and flexural strength as high as 43-46 MPa. The developed WPCs had low formaldehyde emissions (≤1.53 mg/m3) and slightly improved flame retardancy. Finally, their lower cost (5,035 yuan/ton) and higher eco-efficiency (12.81 yuan/kg CO2) characteristics allowed them to be compatible with the current sustainable development requirements. This study provides a novel approach for the utilization of industrial waste and recyclable resources for sustainable replacement of wood-based products.

Taurine alleviates endoplasmic reticulum stress, inflammatory cytokine expression and mitochondrial oxidative stress induced by high glucose in the muscle cells of olive flounder (Paralichthysolivaceus).

The aim of the present study was to evaluate the effects of taurine on endoplasmic reticulum stress, inflammatory cytokine expression and mitochondrial oxidative stress induced by high glucose in primary cultured muscle cells of olive flounder (Paralichthys olivaceus). Three experimental groups were designed as follows: muscle cells of olive flounder incubated with three kinds of medium containing 5 mM glucose (control), 33 mM glucose (HG) or 33 mM glucose + 10 mM taurine (HG + T), respectively. Results showed that taurine addition significantly alleviated the decreased activity of superoxide dismutase (SOD) and the ratio of reduced to oxidized glutathione (GSH/GSSG) induced by high glucose. The increase of cellular reactive oxygen species (ROS), malondialdehyde content and cell apoptosis induced by high glucose were alleviated by taurine. Besides, gene expression of glucose-regulated protein 78, PKR-like ER kinase, tumor necrosis factor-α, interleukin-6, interleukin-1ß, interleukin-8, muscle atrophy F-box protein and muscle RING-finger protein 1 were significantly up-regulated in the HG group, and taurine addition decreased the expression of these genes. High glucose led to the swelling of the endoplasmic reticulum (ER). Meanwhile, the nuclear translocation of nuclear factor κB (NF-κB) and the release of cytochrome C from mitochondria induced by high glucose were suppressed by taurine addition. These results demonstrated that taurine alleviated ERS, inflammation and mitochondrial oxidative stress induced by high glucose in olive flounder muscle cells. The ROS production, NF-κB signaling pathway and mitochondria function were the main targets of the biological effects of taurine under high glucose condition.

High glucose induces apoptosis, glycogen accumulation and suppresses protein synthesis in muscle cells of olive flounder Paralichthys olivaceus.

The effect and the mechanism of high glucose on fish muscle cells are not fully understood. In the present study, muscle cells of olive flounder (Paralichthys olivaceus) were treated with high glucose (33 mM) in vitro. Cells were incubated in three kinds of medium containing 5 mM glucose, 5 mM glucose and 28 mM mannitol (as an isotonic contrast) or 33 mM glucose named the Control group, the Mannitol group and the high glucose (HG) group, respectively. Results showed that high glucose increased the ADP:ATP ratio and the reactive oxygen species (ROS) level, decreased mitochondrial membrane potential (MMP), induced the release of cytochrome C (CytC) and cell apoptosis. High glucose also led to cell glycogen accumulation by increasing the glucose uptake ability and affecting the mRNA expressions of glycogen synthase and glycogen phosphorylase. Meanwhile, it activated AMP-activated protein kinase (AMPK), inhibited the activity of mammalian target of rapamycin (mTOR) signalling pathway and the expressions of myogenic regulatory factors (MRF). The expressions of myostatin-1 (mstn-1) and E3 ubiquitin ligases including muscle RING-finger protein 1 (murf-1) and muscle atrophy F-box protein (mafbx) were also increased by the high glucose treatment. No difference was found between the Mannitol group and the Control group. These results demonstrate that high glucose has the effects of inducing apoptosis, increasing glycogen accumulation and inhibiting protein synthesis on muscle cells of olive flounder. The mitochondria-mediated apoptotic signalling pathway, AMPK and mTOR pathways participated in these biological effects.

Chiral Nematic Coatings Based on Cellulose Nanocrystals as a Multiplexing Platform for Humidity Sensing and Dual Anticounterfeiting.

The need for a precise regulation of the properties of chiral nematic structures in response to external stimuli is addressed. Self-assembled iridescent coatings are produced under the effect of electrostatic interactions between cellulose nanocrystals and poly(acrylic acid), endowing a high anisotropic dissymmetry (>0.3) and sensitivity to environmental humidity (13.1 nm/1% at 68-75% relative humidity, RH). The phenomena associated with shifts in selective light reflection (green to orange) and polarization, facilitate tunable transmitted colors (blue to orange) at given rotation angles (RA). Such properties are conveniently integrated into a "RH-RA-color" ternary code that is introduced as an anticounterfeiting technology, taking advantage of multicolor patterns that conveniently track with changes in RH and RA. The proposed charge-driven assembly opens new opportunities for chiral nematic materials that enable precise optical sensing and information encryption.

Arginine Regulates TOR Signaling Pathway through SLC38A9 in Abalone Haliotis discus hannai.

Arginine plays an important role in the regulation of the target of the rapamycin (TOR) signaling pathway, and Solute Carrier Family 38 Member 9 (SLC38A9) was identified to participate in the amino acid-dependent activation of TOR in humans. However, the regulations of arginine on the TOR signaling pathway in abalone are still unclear. In this study, slc38a9 of abalone was cloned, and the slc38a9 was knocked down and overexpressed to explore its function in the regulation of the TOR signaling pathway. The results showed that knockdown of slc38a9 decreased the expression of tor, ribosomal s6 protein kinase (s6k) and eukaryotic translation initiation factor 4e (eif4e) and inhibited the activation of the TOR signaling pathway by arginine. Overexpression of slc38a9 up-regulated the expression of TOR-related genes. In addition, hemocytes of abalone were treated with 0, 0.2, 0.5, 1, 2 and 4 mmol/L of arginine, and abalones were fed diets with 1.17%, 1.68% and 3.43% of arginine, respectively, for 120 days. Supplementation of arginine (0.5-4 mmol/L) increased the expressions of slc38a9, tor, s6k and eif4e in hemocytes, and abalone fed with 1.68% of dietary arginine showed higher mRNA levels of slc38a9, tor, s6k and eif4e and phosphorylation levels of TOR, S6 and 4E-BP. In conclusion, the TOR signaling pathway of abalone can be regulated by arginine, and SLC38A9 plays an essential role in this regulation.

Ascorbic Acid Regulates the Immunity, Anti-Oxidation and Apoptosis in Abalone Haliotis discus hannai Ino.

The present study was conducted to investigate the roles of ascorbic acid (AA) in immune response, anti-oxidation and apoptosis in abalone (Haliotis discus hannai Ino). Seven semi-purified diets with graded levels of AA (0, 50, 100, 200, 500, 1000 and 5000 mg/kg) were fed to abalone (initial weight: 12.01 ± 0.001 g, initial shell length: 48.44 ± 0.069 mm) for 100 days. The survival, weight gain rate and daily increment in shell length were not affected by dietary AA. The AA content in the gill, muscle and digestive glands of abalone was significantly increased by dietary AA. In terms of immunity, dietary AA significantly improved the total hemocyte count, respiratory burst and phagocytic activity in hemolymph, and lysozyme activity in cell-free hemolymph (CFH). In the digestive gland, the TLR-MyD88-dependent and TLR-MyD88-independent signaling pathways were suppressed by dietary AA supplementation. The mRNA levels of ß-defensin and arginase-I in the digestive gland were significantly increased by dietary AA. In the gill, only the TLR-MyD88-dependent signaling pathway was depressed by dietary AA to reduce inflammation in abalone. The level of mytimacin 6 in the gill was significantly upregulated by dietary AA. After Vibrio parahaemolyticus infection, the TLR signaling pathway in the digestive gland was suppressed by dietary AA, which reduced inflammation in the abalone. In terms of anti-oxidation, superoxide dismutase, glutathione peroxidase and catalase activities, as well as total anti-oxidative capacity and reduced glutathione content in CFH, were all significantly upregulated. The malondialdehyde content was significantly downregulated by dietary AA. The anti-oxidative capacity was improved by triggering the Keap1-Nrf2 pathway in abalone. In terms of apoptosis, dietary AA could enhance the anti-apoptosis ability via the JNK-Bcl-2/Bax signaling cascade in abalone. To conclude, dietary AA was involved in regulating immunity, anti-oxidation and apoptosis in abalone.