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The cytoplasms of most plant cells are connected by membrane-lined cell wall channels, the plasmodesmata (PD). Dynamic regulation of sugar, hormone and protein diffusion through PD is essential for plant development and stress responses. Understanding this regulation requires knowledge of factors and mechanisms that control PD permeability through the modulation of callose levels in the cell wall around PD openings. We investigated PD regulation in leaf epidermis cells in relation to drought stress in Arabidopsis thaliana. Upon finding PD-mediated cell wall permeability decreased by drought stress and the hormone ABA, we tested several PD-associated genes with drought-responsive expression for their involvement in this response. Mutants of NHL12 showed relatively low PD permeability that was unaffected by drought or ABA treatment. Overexpression of NHL12 in Nicotiana benthamiana epidermis cells increased PD permeability. Moreover, we show that NHL12 can potentially interact with the callose synthase-regulator NHL3 and we explored the effect of NHL12 abundance and/or lower interface permeability on ABA signaling genes. Our results indicate that NHL12 is a drought-responsive negative regulator of PD callose levels and, thereby, interface permeability. Results are discussed with regard to PD function during drought stress and the regulation of intercellular transport.

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Regulatory T cells (Tregs) possess unique immunosuppressive activity among CD4-positive T cells. Tregs are ubiquitously present in mammals and function to calm excessive immune responses, thereby suppressing allergies or autoimmune diseases. On the other hand, due to their immunosuppressive function, Tregs are thought to promote cancer progression. The tumor microenvironment (TME) is a multicellular system composed of many cell types, including tumor cells, infiltrating immune cells, and cancer-associated fibroblasts (CAFs). Within this environment, Tregs are recruited by chemokines and metabolic factors and impede effective anti-tumor responses. However, in some cases, their presence can also improve patient's survival rates. Their functional consequences may vary across tumor types, locations, and stages. An in-depth understanding of the precise roles and mechanisms of actions of Treg is crucial for developing effective treatments, emphasizing the need for further investigation and validation. This review aims to provide a comprehensive overview of the complex and multifaceted roles of Tregs within the TME, elucidating cellular communications, signaling pathways, and their impacts on tumor progression and highlighting their potential anti-tumor mechanisms through interactions with functional molecules.

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Antibiotic substitutes have become a research focus due to restrictions on antibiotic usage. Among the antibiotic substitutes on the market, probiotics have been extensively researched and used. However, the mechanism by which probiotics replace antibiotics remains unclear. In this study, we aimed to investigate this mechanism by comparing the effects of probiotics and antibiotics on broiler growth performance and intestinal microbiota composition. Results shown that both probiotics and antibiotics increased daily weight gain and reduced feed conversion rate in broilers. Analysis of ileum and cecum microorganisms via 16S rRNA gene sequencing revealed that both interventions decreased intestinal microbial diversity. Moreover, the abundance of Bacteroides increased in the mature ileum, while that of Erysipelatoclostridium decreased in the cecum in response to both probiotics and antibiotics. The main metabolites of probiotics and antibiotics in the intestine were found to be organic acids, amino acids, and sugars, which might play comparable roles in growth performance. Furthermore, disaccharides and trisaccharides may be essential components in the ileum that enable probiotics to replace antibiotics. These findings provide important insights into the mechanisms underlying the use of probiotics as antibiotic substitutes in broiler breeding.

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Chondrocytes rely heavily on glycolysis to maintain the metabolic homeostasis and cartilage matrix turnover. Glycolysis in chondrocytes is remodeled by diverse biochemical and biomechanical factors due to the sporty joint microenvironment. Transforming growth factor-ß2 (TGF-ß2), one of the most abundant TGF-ß superfamily members in chondrocytes, has increasingly attracted attention in cartilage physiology and pathology. Although previous studies have emphasized the importance of TGF-ß superfamily members on cell metabolism, whether and how TGF-ß2 modulates glycolysis in chondrocytes remains elusive. In the current study, we investigated the effects of TGF-ß2 on glycolysis in chondrocytes and explored the underlying biomechanisms. The results showed that TGF-ß2 could enhance glycolysis in chondrocytes by increasing glucose consumption, up-regulating liver-type ATP-dependent 6-phosphofructokinase (Pfkl) expression, and boosting lactate production. The TGF-ß2 signal entered chondrocytes via TGF-ß receptor type I (TßRI), and activated p-Smad3 signaling to regulate the glycolytic pathway. Subsequent experiments employing specific inhibitors of TßRI and p-Smad3 further substantiated the role of TGF-ß2 in enhancement of glycolysis via TßRI/p-Smad3 axis in chondrocytes. The results provide new understanding of the metabolic homeostasis in chondrocytes induced by TGF-ß superfamily and might shed light on the prevention and treatment of related osteoarticular diseases.

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AIM: To explore the influence of PDGF-AA on cell communication between human dental pulp stem cells (DPSCs) by characterizing gap junction intercellular communication (GJIC) and its potential biomechanical mechanism. METHODOLOGY: Quantitative real-time PCR was used to measure connexin family member expression in DPSCs. Cell migration and CCK-8 assays were utilized to examine the influence of PDGF-AA on DPSC migration and proliferation. A scrape loading/dye transfer assay was applied to evaluate GJIC triggered by PDGF-AA, a PI3K/Akt signalling pathway blocker (LY294002) and a PDGFR-α blocker (AG1296). Western blotting and immunofluorescence were used to test the expression and distribution of the Cx43 and p-Akt proteins in DPSCs. Scanning electron microscopy (SEM) and immunofluorescence were used to observe the morphology of GJIC in DPSCs. RESULTS: PDGF-AA promoted gap junction formation and intercellular communication between human dental pulp stem cells. PDGF-AA upregulates the expression of Cx43 to enhance gap junction formation and intercellular communication. PDGF-AA binds to PDGFR-α and activates PI3K/Akt signalling to regulate cell communication. CONCLUSIONS: This research demonstrated that PDGF-AA can enhance Cx43-mediated GJIC in DPSCs via the PDGFR-α/PI3K/Akt axis, which provides new cues for dental pulp regeneration from the perspective of intercellular communication.

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Objective: To investigate the effects of stromal cell-derived factor 1α (SDF-1α) on the apoptosis and autophagy of chondrocytes and the underlying mechanisms. Methods: Chondrocytes were isolated from the knee joints of neonatal mice. The chondrocytes were then stimulated with 0 (the control group), 50, 100, and 200 ng/mL of SDF-1α. CCK-8 assay was performed to determine the effects of SDF-1α stimulation for 24 h, 48 h, and 72 h on the viability of the chondrocytes. Wound healing assay was conducted to determine the effects of SDF-1α stimulation for 12 h and 24 h on chondrocyte migration. The changes in the expression of Akt signaling pathway proteins in chondrocytes were determined by Western blot assay. Chondrocytes were stimulated with 0 (the control group) and 200 ng/mL of SDF-1α. Flow cytometry was performed to determine the effect of SDF-1α on the apoptosis of chondrocytes. Transmission electron microscope was used to examine the effect of SDF-1α on chondrocyte autophagy. Immunofluorescence staining assays were performed to visualize the differences in p-Akt expression and distribution in chondrocytes treated with SDF-1α. Results: Compared with the control group, findings for the experimental groups showed that SDF-1α at the concentrations of 50, 100, and 200 ng/mL did not decrease chondrocyte activity at any time point (P<0.01) and it consistently promoted chondrocyte migration at 24 h (P<0.05). Western blot results revealed that, in comparison to the control group, SDF-1α at concentrations of 50, 100, and 200 ng/mL significantly up-regulated the protein expression of p-Akt in chondrocytes, while no significant difference in Akt expression was observed. Flow cytometry demonstrated that SDF-1α could inhibit chondrocyte apoptosis (P<0.05) and transmission electron microscopic observation showed that SDF-1α promoted chondrocyte autophagy (P<0.05). Immunofluorescence staining showed that the expression of p-Akt in chondrocytes was concentrated in the perinuclear area of the cells and this expression was further enhanced in the perinuclear area of the chondrocytes after treatment with SDF-1α. Conclusion: SDF-1α inhibits chondrocyte apoptosis and promotes chondrocyte migration and autophagy through activating the Akt signaling pathway.

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Influenza A virus (IAV) infection causes respiratory disease. Recently, infection of IAV H5N1 among mammals are reported in farmed mink. Therefore, to discover antivirals against IAV, we screened a compound library by using the RNA-dependent RNA polymerase (RdRp) assay system derived from H5N1 IAV including a drug-resistant PA mutant (I38T) and a viral polymerase activity enhancing PB2 mutant (T271A). Upon screening, we found vidofludimus can be served as a potential inhibitor for IAV. Vidofludimus an orally active inhibitor for dihydroorotate dehydrogenase (DHODH), a key enzyme for the cellular de novo pyrimidine biosynthesis pathway. We found that vidofludimus exerted antiviral activity against wild-type and drug-resistant mutant IAV, with effective concentrations (EC50 ) of 2.10 and 2.11 µM, respectively. The anti-IAV activity of vidofludimus was canceled by the treatment of uridine or cytidine through pyrimidine salvage synthesis pathway, or orotic acid through pyrimidine de novo synthesis pathway. This indicated that the main target of vidofludimus is DHODH in IAV RdRp expressing cells. We also produced recombinant seasonal IAV H1N1 virion and influenza B virus (IBV) RdRp assay system and confirmed vidofludimus also carried highly antiviral activity against seasonal IAV and IBV. Vidofludimus is a candidate drug for the future threat of IAV H5N1 infection among humans as well as seasonal influenza virus infection.

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KEY MESSAGE: The leaf hyponasty response depends on tip-to-petiole auxin transport. This transport can happen through two parallel pathways: active trans-membrane transport mediated by PIN proteins and passive diffusion through plasmodesmata. A plant's ability to counteract potential shading by neighboring plants depends on transport of the hormone auxin. Neighbor sensing at the leaf tip triggers auxin production. Once this auxin reaches the abaxial petiole epidermis, it causes cell elongation, which leads to leaf hyponasty. Two pathways are known to contribute to this intercellular tip-to-petiole auxin movement: (i) transport facilitated by plasma membrane-localized PIN auxin transporters and (ii) diffusion enabled by plasmodesmata. We tested if these two modes of transport are arranged sequentially or in parallel. Moreover, we investigated if they are functionally linked. Mutants in which one of the two pathways is disrupted indicated that both pathways are necessary for a full hyponasty response. Visualization of PIN3-GFP and PIN7-GFP localization indicated PIN-mediated transport in parallel to plasmodesmata-mediated transport along abaxial midrib epidermis cells. We found plasmodesmata-mediated cell coupling in the pin3pin4pin7 mutant to match wild-type levels, indicating no redundancy between pathways. Similarly, PIN3, PIN4 and PIN7 mRNA levels were unaffected in a mutant with disrupted plasmodesmata pathway. Our results provide mechanistic insight on leaf hyponasty, which might facilitate the manipulation of the shade avoidance response in crops.

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It is well recognized that mitochondrial dynamics plays a vital role in cartilage physiology. Any perturbation in mitochondrial dynamics could cause disorders in cartilage metabolism and even lead to the occurrence of cartilage diseases such as osteoarthritis (OA). TGF-ß3, as an important growth factor that appears in the joints of OA disease, shows its great potential in chondrocyte growth and metabolism. Nevertheless, the role of TGF-ß3 on mitochondrial dynamics is still not well understood. Here we aimed to investigate the effect of TGF-ß3 on mitochondrial dynamics of chondrocytes and reveal its underlying bio-mechanism. By using transmission electron microscopy (TEM) for the number and morphology of mitochondria, western blotting for the protein expressions, immunofluorescence for the cytoplasmic distributions of proteins, and RNA sequencing for the transcriptome changes related to mitochondrial dynamics. We found that TGF-ß3 could increase the number of mitochondria in chondrocytes. TGF-ß3-enhanced mitochondrial number was via promoting the mitochondrial fission. The mitochondrial fission induced by TGF-ß3 was mediated by AMPK signaling. TGF-ß3 activated canonical p-Smad3 signaling and resultantly mediated AMPK-induced mitochondrial fission. Taken together, these results elucidate an understanding of the role of TGF-ß3 on mitochondrial dynamics in chondrocytes and provide potential cues for therapeutic strategies in cartilage injury and OA disease in terms of energy metabolism.

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Fibroblast growth factor 19 (FGF19) has appeared as a new possible avenue in the treatment of skeletal metabolic disorders. However, the role of FGF19 on cell cycle progression in skeletal system is poorly understood. Here we demonstrated that FGF19 had the ability to reduce the proliferation of chondrocytes and cause cell cycle G2 phase arrest through its interaction with ß-Klotho (KLB), an important accessory protein that helps FGF19 link to its receptor. FGF19-mediated cell cycle arrest by regulating the expressions of cdk1/cylinb1, chk1 and gadd45a. We then confirmed that the binding of FGF19 to the membrane receptor FGFR4 was necessary for FGF19-mediated cell cycle arrest, and further proved that FGF19-mediated cell cycle arrest was via activation of p38/MAPK signaling. Through inhibitor experiments, we discovered that inhibition of FGFR4 led to down-regulation of p38 signaling even in the presence of FGF19. Meanwhile, inhibiting p38 signaling reduced the cell cycle arrest of chondrocytes induced by FGF19. Furthermore, blocking p38 signaling facilitated to retain the expression of cdk1 and cyclinb1 that had been reduced in chondrocytes by FGF19 and decreased the expression of chk1 and gadd45a that had been enhanced by FGF19 in chondrocytes. Taking together, this study is the first to demonstrate that FGF19 induces cell cycle arrest at G2 phase via FGFR4-p38/MAPK axis and enlarges our understanding about the role of FGF19 on cell cycle progression in chondrocytes.

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Animal farming copiously generates indoles, which contribute to odor and pose a challenge for deodorization. While biodegradation is widely accepted, there is a lack of suitable indole-degrading bacteria for animal husbandry. In this study, we aimed to construct genetically engineered strains with indole-degrading abilities. Enterococcus hirae GDIAS-5 is a highly efficient indole-degrading bacterium, which functions via a monooxygenase YcnE presumably contributes to indole oxidation. However, the efficiency of engineered Escherichia coli expressing YcnE for indole degradation is lower than that of GDIAS-5. To improve its efficacy, the underlying indole-degradation mechanisms in GDIAS-5 were analyzed. An ido operon that responds to a two-component indole oxygenase system was identified. In vitro experiments showed that the reductase component of YcnE, YdgI, can improve the catalytic efficiency. The reconstruction of the two-component system in E. coli exhibited higher indole removal efficiency than GDIAS-5. Furthermore, isatin, the key intermediate metabolite in indole degradation, might be degraded via a novel isatin-acetaminophen-aminophenol pathway involving an amidase whose coding gene is located near the ido operon. The two-component anaerobic oxidation system, upstream degradation pathway, and engineering strains investigated in this study provide important insights into indole degradation metabolism and offer efficient resources for achieving bacterial odor elimination.

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Thermophotovoltaic (TPV) generators provide continuous and high-efficiency power output by utilizing local thermal emitters to convert energy from various sources to thermal radiation matching the bandgaps of photovoltaic cells. Lack of effective guidelines for thermal emission control at high temperatures, poor thermal stability, and limited fabrication scalability are the three key challenges for the practical deployment of TPV devices. Here we develop a hierarchical sequential-learning optimization framework and experimentally realize a 6″ module-scale polaritonic thermal emitter with bandwidth-controlled thermal emission as well as excellent thermal stability at 1473 K. The 300 nm bandwidth thermal emission is realized by a complex photon polariton based on the superposition of Tamm plasmon polariton and surface plasmon polariton. We experimentally achieve a spectral efficiency of 65.6% (wavelength range of 0.4-8 µm) with statistical deviation less than 4% over the 6″ emitter, demonstrating industrial-level reliability for module-scale TPV applications.

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Cell-based cartilage tissue engineering faces a great challenge in the repair process, partly due to the special physical microenvironment. Human stem cell from apical papilla (hSCAP) shows great potential as seed cells because of its versatile differentiation capacity. However, whether hSCAP has potent chondrogenic differentiation ability in the physical microenvironment of chondroid remains unknown. In this study, we fabricated poly(dimethylsiloxane) (PDMS) substrates with different stiffnesses and investigated the chondrogenic differentiation potential of hSCAPs. First, we found that hSCAPs cultured on soft substrates spread more narrowly accompanied by cortical actin organization, a hallmark of differentiated chondrocytes. On the contrary, stiff substrates were favorable for cell spreading and stress fiber formation. More importantly, the increased chondrogenic differentiation of hSCAPs seeded on soft substrates was confirmed by characterizing increased extracellular proteoglycan aggregation through Alcian blue staining and Safranin O staining and enhanced markers toward chondrogenic differentiation including SRY-box transcription factor 9 (Sox9), type II collagen (Col2), and aggrecan in both normal α-minimum essential medium (αMEM) and specific chondrogenic medium (CM) culture conditions. Then, we investigated the mechanosensing/mechanotransduction governing the chondrogenic differentiation of hSCAPs in response to different stiffnesses and found that stiffness-sensitive integrin ß1 and focal adhesion kinase (FAK) were essential for mechanical signal perception and were oriented at the start of mechanotransduction induced by matrix stiffness. We next showed that the increased nuclear accumulation of Smad3 signaling and target Sox9 facilitated the chondrogenic differentiation of hSCAPs on the soft substrates and further verified the importance of Rho-associated protein kinase (ROCK) signaling in regulating chondrogenic differentiation and its driving factors, Smad3 and Sox9. By using SIS3, the specific inhibitor of p-Smad3, and miRNA targeting Rho-associated protein kinase 1 (ROCK-1), we finally confirmed the importance of ROCK/Smad3/Sox9 axis in the chondrogenic differentiation of hSCAPs in response to substrate stiffness. These results help us to increase the understanding of how microenvironmental stiffness directs chondrogenic differentiation from the aspects of mechanosensing, mechanotransduction, and cell fate decision, which will be of great value in the application of hSCAPs in cartilage tissue engineering.

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SDF-1α, the most common isoform of stromal cell-derived factor 1, has shown vital effects in regulating chondrocyte proliferation, maturation, and chondrogenesis. Autophagy is a highly conserved biological process to help chondrocytes survive in harsh environments. However, the effect of SDF-1α on chondrocyte autophagy is still unknown. This study aims to investigate the effect of SDF-1α on chondrocyte autophagy and the underlying biomechanism. Transmission electron microscope assays and mRFP-GFP-LC3 adenovirus double label transfection assays were performed to detect the autophagic flux of chondrocytes. Western blots and immunofluorescence staining assays were used to detect the expression of autophagy-related proteins in chondrocytes. RNA sequencing and qPCR were conducted to assess changes in autophagy-related mRNA expression. SDF-1α upregulated the number of autophagosomes and autolysosomes in chondrocytes. It also increased the expression of autophagy-related proteins including ULK-1, Beclin-1 and LC3B, and decreased the expression of p62, an autophagy substrate protein. SDF-1α-mediated autophagy of chondrocytes required the participation of receptor CXCR4. Moreover, SDF-1α-enhanced autophagy of chondrocytes was through the inhibition of phosphorylation of mTOR signaling on the upstream of autophagy. Knockdown by siRNA and inhibition by signaling inhibitor further confirmed the importance of the CXCR4/mTOR signaling axis in SDF-1α-induced autophagy of chondrocytes. For the first time, this study elucidated that SDF-1α promotes chondrocyte autophagy through the CXCR4/mTOR signaling axis.

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Gap junctional intercellular communication (GJIC) is indispensable for the maintenance of physiological balance in articular cartilage. Transforming growth factor-ß3 (TGF-ß3), an important growth factor of TGF-ß superfamily, is well recognized to play a unique regulatory role in cartilage development and diseases. However, the role of TGF-ß3 in GJIC in adult chondrocytes remains elusive. This work aims to investigate the effect of TGF-ß3 on gap-junction mediated intercellular communication in chondrocytes. We first showed that TGF-ß3 could enhance the synaptic connections between chondrocytes by scanning electron microscopy (SEM) and promote the cell-to-cell communication in living chondrocytes by scrape loading/dye transfer assay. We then confirmed that TGF-ß3 enhanced cell-to-cell communication via up-regulation of connexin 43 (Cx43). We next found that TGF-ß3-enhanced GJIC required the participation of TGF-beta type I receptor ALK5 and depended on the activation of p-Smad3 signalling. Finally, through inhibitor experiments of SB525334 and SIS3, we demonstrated that TGF-ß3-induced functional GJIC in chondrocytes via the axis of ALK5/p-Smad3 signalling. Taking together, these results demonstrate a strong correlation between TGF-ß3 and GJIC in chondrocytes, which provides a new perspective on the importance of TGF-ß3 on cartilage physiology and pathobiology.

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Replacement of the sluggish anodic reaction in water electrocatalysis by a thermodynamically favorable urea oxidation reaction (UOR) offers the prospect of energy-saving H2 generation, additionally mitigating urea-rich wastewater pollution, whereas the lack of highly efficient and earth-abundant UOR catalysts severely restricts widespread use of this catalytic system. Herein, Mn-doped nickel hydroxide porous nanowire arrays (denoted Mn-Ni(OH)2 PNAs) are rationally developed and evaluated as efficient catalysts for the UOR in an alkaline solution via the in situ electrochemical conversion of NiMn-based metal-organic frameworks. Mn doping can modulate the electronic structural configuration of Ni(OH)2 to significantly increase the electron density and optimize the energy barriers of the CO*/NH2* intermediates of the UOR. Meanwhile, porous nanowire arrays will afford abundant spaces/channels to facilitate active site exposure and electron/mass transfer. As a result, the Mn-Ni(OH)2 PNAs delivered superior UOR performance with a small potential of 1.37 V vs. RHE at 50 mA cm-2, a Tafel slope of 31 mV dec-1, and robust stability. Notably, the overall urea electrolysis system coupled with a commercial Pt/C cathode demonstrated excellent activity (1.40 V at 20 mA cm-2) and durability operation (only 1.40% decay after 48 h).

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Indole is an inter-species and inter-kingdom signaling molecule widespread in the natural world. A large amount of indole in livestock wastes makes it difficult to be degraded, which causes serious malodor. Identifying efficient and eco-friendly ways to eliminate it is an urgent task for the sustainable development of husbandry. While bioconversion is a widely accepted means, the mechanism of indole microbial degradation is little understood, especially under anaerobic conditions. Herein, a new Enterococcus hirae isolate GDIAS-5, effectively degraded 100 mg/L indole within 28 h aerobically or 5 days anaerobically. Three intermediates (oxindole, isatin, and catechol) were identified in indole degradation, and catechol was further degraded by a meta-cleavage catabolic pathway. Two important processes for GDIAS-5 indole utilization were discovered. One is Fe(III) uptake and reduction, which may be a critical process that is coupled with indole oxidation, and the other is the entire pathway directly involved in indole oxidation and metabolism. Furthermore, monooxygenase ycnE responsible for indole oxidation via the indole-oxindole-isatin pathway was identified for the first time. Bioinformatic analyses showed that ycnE from E. hirae formed a phylogenetically separate branch from monooxygenases of other species. These findings provide new targets and strategies for synthetic biological reconstruction of indole-degrading bacteria.

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BACKGROUND: Exercise-induced fatigue (EIF) is a common occurrence in sports competition and training. It may cause trouble to athletes' motor skill execution and cognition. Although traditional Chinese medicine Jianpi therapy has been commonly used for EIF management, relevant evidence on the effectiveness and safety of Jianpi therapy is still unclear. METHODS: Databases including PubMed, Embase, Web of Science, the Cochrane Library, SinoMed, China Science and Technology Journal Database (VIP), China National Knowledge Infrastructure (CNKI), and Wanfang will be searched for relevant randomized controlled trials from databases from 2000 to 2021. Randomized controlled trials related to traditional Chinese medicine Jianpi therapy in the treatment and management of EIF will be included. Systematic review and meta-analysis of the data will be performed in RevMan 5.3 according to the Preferred Reporting Items of Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Two authors independently performed the literature searching, data extraction, and quality evaluation. Risk of bias was assessed using the Cochrane Risk of Bias Tool for randomized clinical trials. RESULTS: This systematic review and meta-analysis will summarize the latest evidence for traditional Chinese medicine Jianpi therapy in EIF. The results will be submitted to a peer-reviewed journal once completed. CONCLUSION: The conclusion of our research will provide evidence to support traditional Chinese medicine Jianpi therapy as an effective intervention for patients with EIF.OSF Registration DOI: 10.17605/OSF.IO/NRKX4.

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BACKGROUND: Traditional Chinese exercises are more and more popular for type 2 diabetes patients for the treatment and rehabilitation; however, the comparative effectiveness and safety remains unclear. Our study aims to compare the pros and cons of these exercise interventions for type 2 diabetes by implementing a network meta-analysis. METHODS: Eight databases will be searched for relevant systematic reviews including SinoMed, VIP, CNKI, Wanfang, PubMed, Embase, Web of Science and the Cochrane Library from inception to Oct 2021. Randomized controlled trials that meeting eligibility in published systematic reviews will be identified. Randomized controlled trial related to Traditional Chinese Exercises or Qigong therapy in the treatment of type 2 diabetes will be included. Two researchers conducted literature screening, data extraction and risk of bias assessment independently. Network meta-analysis of the data was performed by Stata 14.0. The Grades of Recommendations Assessment, Development and Evaluation system will be used to evaluate the rank of evidence. RESULTS: The findings will be reported according to the preferred reporting items for systematic reviews and meta-analyses- network meta-analysis statement. This systematic review and network meta-analysis will summarize the direct and indirect evidence for different kinds of traditional Chinese exercises therapies and to rank these interventions. The results will be submitted to a peer-reviewed journal once completed. CONCLUSION: The network meta-analysis was designed to update and expand on previous research results of clinical trials to better evaluate the effectiveness and safety of different interventions of traditional Chinese exercises for type 2 diabetes patients. OSF REGISTRATION DOI: 10.17605/OSF.IO/MNJD6.

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This study evaluated the ability of Aspergillus niger and Trichoderma koningii to improve the quality of tea dregs (TDs) through solid-state fermentation as well as the value of the fermented tea dregs (FTDs) produced for use as bio-feed additives. After fermentation, FTDs differed in color and structure. Fermentation with A. niger and T. koningii increased the contents of crude protein, crude fiber, neutral detergent fiber, and acid detergent fiber of TDs. Compared to the unfermented group, the contents of reducing sugar, total flavonoids, total polyphenols, and theasaponins were increased in A. niger FTDs, while in T. koningii FTDs caffeine was completely degraded, the theasaponins were lower, and the contents of reducing sugar and caffeine higher. Regarding free amino acids, A. niger FTDs had the highest content of total amino acids, total essential amino acids, total non-essential amino acids, total aromatic amino acids, total branched-chain amino acids, and total non-protein amino acids, and all types of essential amino acids, followed by T. koningii FTDs and the control TDs. Fungal fermentation had similar effects on the content of various hydrolytic amino acids as those on above free amino acids, and increased the content of bitter and umami components. The composition of essential amino acids of TDs or FTDs was similar to that of the standard model, except for sulfur-containing amino acids and isoleucine. Solid-state fermentation with A. niger and T. koningii effectively improved the nutritional value of TDs, increased the contents of functional substances, and improved the flavor of TDs. This study demonstrated a feasible approach to utilize TDs that not only increases animal feed resources, but also reduces the production of resource waste and pollution.

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