[Analysis of Spatiotemporal Variation and Driving Factors of Water Quality in the Xiangjiang River Basin from 1990 to 2016].

In order to explore the spatiotemporal variation characteristics and driving mechanism of water quality in the Xiangjiang River Basin, the data of 16 water quality parameters at 113 stations over 26 years from 1990 to 2016 in the Xiangjiang River Basin were collected for synthetically assessing the water quality and identifying its main pollutants through the water quality index and other methods. The causal mechanism of water quality, especially the driving effect of water level and land use pattern, was analyzed. The results showed that： ① The overall water quality grade of the Xiangjiang River Basin during the study period was "good." However, the water quality deteriorated first （from 1990 to 2003） and then improved （from 2004 to 2016）. The season variation in water quality was not obvious, but the water quality fluctuation of the wet season was larger. The water pollution load of the main stream decreased successively from the middle reaches, downstream reaches, and upstream reaches. The upstream tributaries had the best water quality, whereas areas with poor water quality were mainly distributed at the mouth of the middle and downstream tributaries, especially in areas where multiple tributaries converged. ② Toxic heavy metals had the characteristics of toxicity, persistence, and bioaccumulation. If they exceeded a certain concentration in water, they were difficult to purify, posing great harm to the natural environment and human health. The toxic metal index （CI1） was the leading factor affecting water quality, in which Hg and Cd were the main parameters affecting the overall water quality of the Xiangjiang River Basin. ③ The water level had a positive impact on the water quality of the Xiangjiang River by diluting environmental parameters. Land type had little effect on heavy metal concentration, whereas forest land could improve water quality. Grassland had a negative correlation with permanganate index over a large scale range （≥ 5 km）. The increase in water bodies, arable land, and impermeable surface areas within the watershed increased the probability of high fecal coliform concentration in the water body. ④ With the increase in buffer distance, the water quality explained by the land use pattern increased. On the scale of 10 km buffer zone in the riparian zone, the explanation degree by land use pattern on water quality was the highest, which was an effective scale for water quality control of the Xiangjiang River. This research showed that the driving factors of heavy metal pollution and other pollution were different, but their regional differences were all obvious in the Xiangjiang River Basin. Therefore, pollution control should be classified and taken according to local conditions.

Unveiling the link: Neonicotinoids and elevated cardiometabolic risks in Chinese rural residents-from a prospective cohort study combing mendelian randomization study.

PURPOSE: This study aimed to evaluate the relationships of separate and mixed exposure of neonicotinoids on cardiometabolic risk at baseline and follow-up and its change over 3 years, and further explore whether inflammatory markers levels and platelet traits (PLT) mediate these relationships. METHODS: In this prospective cohort study from the Henan Rural Cohort Study, 2315 participants were involved at baseline, and 1841 participants completed cardiometabolic risk predictors determinations during the 3-year follow-up. Each neonicotinoid pesticide was normalized to imidacloprid (IMIeq) using the relative potency factor approach. Quantile-based g-computation (Qgcomp) regression was used to evaluate the effect of the mixtures of neonicotinoids mediation analysis was employed to explore whether inflammatory markers levels and platelet traits mediated these relationships. A two-sample mendelian randomization (MR) study was further used to causal association. RESULTS: Qgcomp regression revealed a statistically positive relationship between neonicotinoids mixture exposure and cardiometabolic risk score at baseline and follow-up over 3 years. Both neutrophils/monocytes and PLT were mediators in the relationship between IMIeq and cardiometabolic risk score at baseline and follow-up over 3 years. The causal risk effect of pesticide exposure were 2.50 (0.05, 4.95) and 5.24 (1.28, 9.19) for cardiometabolic risk indicators including insulin resistance and triglyceride, respectively. Nevertheless, there was no correlation discovered between pesticide exposure and other markers of cardiometabolic risk. CONCLUSION: Neonicotinoid insecticides exposure was connected to an increased cardiometabolic risk, especially in individuals with T2DM. Furthermore, inflammatory markers and PLT seem to be two vital mediators of these associations. Additionally, genetic evidence on pesticide exposure and cardiometabolic risk still needs to be validated by multiregional and multiethnic GWAS studies.

Exploring hot topics and evolutionary paths in the Diagnosis-Related Groups (DRGs) field: a comparative study using LDA modeling.

BACKGROUND: This study reviews the research status of Diagnosis-related groups (DRGs) payment system in China and globally by analyzing topical issues in this field and exploring the evolutionary trends of DRGs in different developmental stages. METHODS: Abstracts of relevant literature in the field of DRGs were extracted from the China National Knowledge Infrastructure (CNKI) database and the Web of Science (WoS) core database and used as text data. A probabilistic distribution-based Latent Dirichlet Allocation (LDA) topic model was applied to mine the text topics. Topical issues were determined by topic intensity, and the cosine similarity of the topics in adjacent stages was calculated to analyze the topic evolution trend. RESULTS: A total of 6,758 English articles and 3,321 Chinese articles were included. Foreign research on DRGs focuses on grouping optimization, implementation effects, and influencing factors, whereas research topics in China focus on grouping and payment mechanism establishment, medical cost change evaluation, medical quality control, and performance management reform exploration. CONCLUSIONS: Currently, the field of DRGs in China is developing rapidly and attracting deepening research. However, the implementation depth of research in China remains insufficient compared with the in-depth research conducted abroad.

Characterization of a powdery mildew resistance gene in wheat breeding line Jingzi 102 using BSR-Seq.

Wheat (Triticum aestivum L.) is one of the most important crops worldwide. Powdery mildew caused by Blumeria graminis f. sp. tritici (Bgt) is a destructive disease threatening wheat yield and quality. The utilization of resistant genes and cultivars is considered the most economical, environmentally-friendly, and effective method to control powdery mildew. Wheat breeding line Jingzi 102 was highly resistant to powdery mildew at both seedling and adult plant stages. Genetic analysis of F1, F2, and F2:3 populations of "Jingzi 102 × Shixin 828" showed that the resistance of Jingzi 102 against powdery mildew isolate E09 at the seedling stage was controlled by a single dominant gene, temporarily designated PmJZ. Using bulked segregant RNA-Seq combined with molecular markers analysis, PmJZ was located on the long arm of chromosome 2B and flanked by markers BJK695-1 and CIT02g-20 with the genetic distances of 1.2 and 0.5 cM, respectively, corresponding to the bread wheat genome of Chinese Spring (IWGSC RefSeq v2.1) 703.8-707.6 Mb. PmJZ is most likely different from the documented Pm genes on chromosome 2BL based on their physical positions, molecular markers analysis, and resistance spectrum. Based on the gene annotation information, five genes related to disease resistance could be considered as the candidate genes of PmJZ. To accelerate the application of PmJZ, the flanking markers BJK695-1 and CIT02g-20 can serve for marker-assisted selection of PmJZ in wheat disease resistance breeding.

Fusarium pseudograminearum biomass and toxin accumulation in wheat tissues with and without Fusarium crown rot symptoms.

Fusarium crown rot (FCR) is an important and devastating disease of wheat (Triticum aestivum) caused by the fungus Fusarium pseudograminearum and related pathogens. Using two distinct susceptible cultivars, we investigated the isolation frequencies of F. pseudograminearum and quantified its biomass accumulation and the levels of the associated toxins deoxynivalenol (DON) and DON-3-glucoside (D3G) in inoculated field-grown wheat plants. We detected F. pseudograminearum in stem, peduncle, rachis, and husk tissues, but not in grains, whereas DON and D3G accumulated in stem, rachis, husk, and grain tissues. Disease severity was positively correlated with the frequency of pathogen isolation, F. pseudograminearum biomass, and mycotoxin levels. The amount of F. pseudograminearum biomass and mycotoxin contents in asymptomatic tissue of diseased plants were associated with the distance of the tissue from the diseased internode and the disease severity of the plant. Thus, apparently healthy tissue may harbor F. pseudograminearum and contain associated mycotoxins. This research helps clarify the relationship between F. pseudograminearum occurrence, F. pseudograminearum biomass, and mycotoxin accumulation in tissues of susceptible wheat cultivars with or without disease symptoms, providing information that can lead to more effective control measures.

Propofol alleviates spinal cord ischemia-reperfusion injury by preserving PI3K/AKT/GIT1 axis.

Spinal cord ischemia-reperfusion injury (SCIRI) is a major contributor to neurological damage and mortality associated with spinal cord dysfunction. This study aims to explore the possible mechanism of Propofol and G-protein-coupled receptor-interacting protein 1 (GIT1) in regulating SCIRI in rat models. SCIRI rat models were established and injected with Propofol, over expression of GIT1 (OE-GIT1), or PI3K inhibitor (LY294002). The neurological function was assessed using Tarlov scoring system, and Hematoxylin & Eosin (H&E) staining was applied to observe morphology changes in spinal cord tissues. Cell apoptosis, blood-spinal cord barriers (BSCB) permeability, and inflammatory cytokines were determined by TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, evans blue (EB) staining, and enzyme-linked immuno sorbent assay (ELISA), respectively. Reverse transcription-quantitative polymerase chain reaction and western blot were used to detect the expression levels of GIT1, endothelial nitric oxide synthase (eNOS), PI3K/AKT signal pathway and apoptosis-related proteins. SCIRI rats had decreased expressions of GIT1 and PI3K/AKT-related proteins, whose expressions can be elevated in response to Propofol treatment. LY294002 can also decrease GIT1 expression levels in SCIRI rats. Propofol can attenuate neurological dysfunction induced by SCIRI, decrease spinal cord tissue injury and BSCB permeability in addition to suppressing cell apoptosis and inflammatory cytokines, whereas further treatment by LY294002 can partially reverse the protective effect of Propofol on SCIRI. Propofol can activate PI3K/AKT signal pathway to increase GIT1 expression level, thus attenuating SCIRI in rat models.

Wireless Technologies in Flexible and Wearable Sensing: From Materials Design, System Integration to Applications.

Wireless and wearable sensors attract considerable interest in personalized healthcare by providing a unique approach for remote, noncontact, and continuous monitoring of various health-related signals without interference with daily life. Recent advances in wireless technologies and wearable sensors have promoted practical applications due to their significantly improved characteristics, such as reduction in size and thickness, enhancement in flexibility and stretchability, and improved conformability to the human body. Currently, most researches focus on active materials and structural designs for wearable sensors, with just a few exceptions reflecting on the technologies for wireless data transmission. This review provides a comprehensive overview of the state-of-the-art wireless technologies and related studies on empowering wearable sensors. The emerging functional nanomaterials utilized for designing unique wireless modules are highlighted, which include metals, carbons, and MXenes. Additionally, the review outlines the system-level integration of wireless modules with flexible sensors, spanning from novel design strategies for enhanced conformability to efficient transmitting data wirelessly. Furthermore, the review introduces representative applications for remote and noninvasive monitoring of physiological signals through on-skin and implantable wireless flexible sensing systems. Finally, the challenges, perspectives, and unprecedented opportunities for wireless and wearable sensors are discussed.

New findings on the risk of hypertension from organophosphorus exposure under different glycemic statuses: The key role of lipids?

BACKGROUND AND OBJECTIVE: Considering the widespread use of organophosphorus pesticides (OPs) and the global prevalence of hypertension (HTN), as well as studies indicating that different glycemic statuses may respond differently to the biological effects of OPs. Therefore, this study, based on the Henan rural cohort, aims to investigate the association between OPs exposure and HTN, and further explores whether lipids mediate these associations. METHODS: We measured the plasma levels of OPs in 2730 participants under different glycemic statuses using gas chromatography-triple quadrupole mass spectrometry (GC-MS/MS). A generalized linear model, Quantile g-computation (QGC), adaptive elastic net (AENET), and Bayesian kernel machine regression (BKMR) models were used to assess the impact of OPs exposure on HTN, with least absolute shrinkage and selection operator (LASSO) penalty regression identifying main OPs. Mediation models were used to evaluate the intermediary role of blood lipids in the OPs-HTN relationship. RESULTS: The detection rates for all OPs were high, ranging from 76.35 % to 99.17 %. In the normal glucose tolerance (NGT) population, single exposure models indicated that malathion and phenthoate were associated with an increased incidence of HTN (P-FDR < 0.05), with corresponding odds ratios (ORs) and 95 % confidence intervals (CIs) of 1.624 (1.167,2.260) and 1.290 (1.072,1.553), respectively. QGC demonstrated a positive association between OP mixtures and HTN, with malathion and phenthoate being the primary contributors. Additionally, the AENET model's Exposure Response Score (ERS) suggested that the risk of HTN increases with higher ERS (P < 0.001). Furthermore, BKMR revealed that co-exposure to OPs increases HTN risk, with phenthoate having a significant impact. Furthermore, triglycerides (TG) mediated 6.55 % of the association between phenthoate and HTN. However, no association was observed in the impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM) populations. CONCLUSIONS: Our findings suggest that in the NGT population, OPs may significantly contribute to the development of HTN, proposing TG as a potential novel target for HTN prevention.

Ziyuglycoside II attenuated OVX mice bone loss via inflammatory responses and regulation of gut microbiota and SCFAs.

BACKGROUND AND PURPOSE: Osteoporosis (OP) is a frequent clinical problem for the elderly. Traditional Chinese Medicine (TCM) has achieved beneficial results in the treatment of OP. Ziyuglycoside II (ZGS II) is a major active compound of Sanguisorba officinalis L. that has shown anti-inflammation and antioxidation properties, but little information concerning its anti-OP potential is available. Our research aims to investigate the mechanism of ZGS II in ameliorating bone loss by inflammatory responses and regulation of gut microbiota and short chain fatty acids (SCFAs) in ovariectomized (OVX) mice. METHODS: We predicted the mode of ZGS II action on OP through network pharmacology and molecular docking, and an OVX mouse model was employed to validate its anti-OP efficacy. Then we analyzed its impact on bone microstructure, the levels of inflammatory cytokines and pain mediators in serum, inflammation in colon, intestinal barrier, gut microbiota composition and SCFAs in feces. RESULTS: Network pharmacology identified 55 intersecting targets of ZGS II related to OP. Of these, we predicted IGF1 may be the core target, which was successfully docked with ZGS II and showed excellent binding ability. Our in vivo results showed that ZGS II alleviated bone loss in OVX mice, attenuated systemic inflammation, enhanced intestinal barrier, reduced the pain threshold, modulated the abundance of gut microbiota involving norank_f__Muribaculaceae and Dubosiella, and increased the content of acetic acid and propanoic acid in SCFAs. CONCLUSIONS: Our data indicated that ZGS II attenuated bone loss in OVX mice by relieving inflammation and regulating gut microbiota and SCFAs.

Optogenetic Stimulation of the Cardiac Vagus Nerve to Promote Heart Regenerative Repair after Myocardial Infarction.

Background: It had been shown that selective cardiac vagal activation holds great potential for heart regeneration. Optogenetics has clinical translation potential as a novel means of modulating targeted neurons. This study aimed to investigate whether cardiac vagal activation via optogenetics could improve heart regenerative repair after myocardial infarction (MI) and to identify the underlying mechanism. Methods: We used an adeno-associated virus (AAV) as the vector to deliver ChR2, a light-sensitive protein, to the left nodose ganglion (LNG). To assess the effects of the cardiac vagus nerve on cardiomyocyte (CM) proliferation and myocardial regeneration in vivo, the light-emitting diode illumination (470 nm) was applied for optogenetic stimulation to perform the gain-of-function experiment and the vagotomy was used as a loss-of-function assay. Finally, sequencing data and molecular biology experiments were analyzed to determine the possible mechanisms by which the cardiac vagus nerve affects myocardial regenerative repair after MI. Results: Absence of cardiac surface vagus nerve after MI was more common in adult hearts with low proliferative capacity, causing a poor prognosis. Gain- and loss-of-function experiments further demonstrated that optogenetic stimulation of the cardiac vagus nerve positively regulated cardiomyocyte (CM) proliferation and myocardial regeneration in vivo. More importantly, optogenetic stimulation attenuated ventricular remodeling and improved cardiac function after MI. Further analysis of sequencing results and flow cytometry revealed that cardiac vagal stimulation activated the IL-10/STAT3 pathway and promoted the polarization of cardiac macrophages to the M2 type, resulting in beneficial cardiac regenerative repair after MI. Conclusions: Targeting the cardiac vagus nerve by optogenetic stimulation induced macrophage M2 polarization by activating the IL-10/STAT3 signaling pathway, which obviously optimized the regenerative microenvironment and then improved cardiac function after MI.

The retinal oxygen metabolism and hemodynamics as a substitute for biochemical tests to predict nonproliferative diabetic retinopathy.

Predicting the occurrence of nonproliferative diabetic retinopathy (NPDR) using biochemical parameters is invasive, which limits large-scale clinical application. Noninvasive retinal oxygen metabolism and hemodynamics of 215 eyes from 73 age-matched healthy subjects, 90 diabetic patients without DR, 40 NPDR, and 12 DR with postpanretinal photocoagulation were measured with a custom-built multimodal retinal imaging device. Diabetic patients underwent biochemical examinations. Two logistic regression models were developed to predict NPDR using retinal and biochemical metrics, respectively. The predictive model 1 using retinal metrics incorporated male gender, insulin treatment condition, diastolic duration, resistance index, and oxygen extraction fraction presented a similar predictive power with model 2 using biochemical metrics incorporated diabetic duration, diastolic blood pressure, and glycated hemoglobin A1c (area under curve: 0.73 vs. 0.70; sensitivity: 76% vs. 68%; specificity: 64% vs. 62%). These results suggest that retinal oxygen metabolic and hemodynamic biomarkers may replace biochemical parameters to predict the occurrence of NPDR .

Advances in ionogels for proton-exchange membranes.

To ensure the long-term performance of proton-exchange membrane fuel cells (PEMFCs), proton-exchange membranes (PEMs) have stringent requirements at high temperatures and humidities, as they may lose proton carriers. This issue poses a serious challenge to maintaining their proton conductivity and mechanical performance throughout their service life. Ionogels are ionic liquids (ILs) hybridized with another component (such as organic, inorganic, or organic-inorganic hybrid skeleton). This design is used to maintain the desirable properties of ILs (negligible vapor pressure, thermal stability, and non-flammability), as well as a high ionic conductivity and wide electrochemical stability window with low outflow. Ionogels have opened new routes for designing solid-electrolyte membranes, especially PEMs. This paper reviews recent research progress of ionogels in proton-exchange membranes, focusing on their electrochemical properties and proton transport mechanisms.

Trifluoromethyl Rhodium-Carbynoid in [2+1+2] Cycloadditions.

Trifluoromethyl cationic carbyne (CF3 C+ :) possessing dual carbene-carbocation behavior emulated as trifluoromethyl metal-carbynoid (CF3 C+ =M) has not been explored yet, and its reaction characteristics are unknown. Herein, a novel α-diazotrifluoroethyl sulfonium salt was prepared and used in Rh-catalyzed three-component [2+1+2] cycloadditions for the first time with commercially available N-fused heteroarenes and nitriles, yielding a series of imidazo[1,5-a] N-heterocycles that are of interest in medicinal chemistry, in which the insertion of trifluoromethyl Rh-carbynoid (CF3 C+ =Rh) into C=N bonds of N-fused heteroarenes was involved. This strategy demonstrates synthetic applications in late-stage modification of pharmaceuticals, construction of CD3 -containing N-heterocycles, gram-scale experiments, and synthesis of phosphodiesterase 10A inhibitor analog. These highly valuable and modifiable imidazo[1,5-a] N-heterocycles exhibit good antitumor activity in vitro, thus demonstrating their potential applications in medicinal chemistry.

Two functional CC-NBS-LRR proteins from rye chromosome 6RS confer differential age-related powdery mildew resistance to wheat.

Rye (Secale cereale), a valuable relative of wheat, contains abundant powdery mildew resistance (Pm) genes. Using physical mapping, transcriptome sequencing, barley stripe mosaic virus-induced gene silencing, ethyl methane sulfonate mutagenesis, and stable transformation, we isolated and validated two coiled-coil, nucleotide-binding site and leucine-rich repeat (CC-NBS-LRR) alleles, PmTR1 and PmTR3, located on rye chromosome 6RS from different triticale lines. PmTR1 confers age-related resistance starting from the three-leaf stage, whereas its allele, PmTR3, confers typical all-stage resistance, which may be associated with their differential gene expression patterns. Overexpression in Nicotiana benthamiana showed that the CC, CC-NBS, and CC-LRR fragments of PMTR1 induce cell death, whereas in PMTR3 the CC and full-length fragments perform this function. Luciferase complementation imaging and pull-down assays revealed distinct interaction activities between the CC and NBS fragments. Our study elucidates two novel rye-derived Pm genes and their derivative germplasm resources and provides novel insights into the mechanism of age-related resistance, which can aid the improvement of resistance against wheat powdery mildew.

Decoding the mechanism of Eleutheroside E in treating osteoporosis via network pharmacological analysis and molecular docking of osteoclast-related genes and gut microbiota.

Objective: Eleutheroside E (EE) is an anti-inflammatory natural compound derived from the edible medicinal herb Acanthopanax senticosus. This study aims to investigate the underlying mechanism of the anti-osteoporosis action of EE through network pharmacology, molecular docking and gut microbiota. Materials and methods: Network pharmacology was used to explore the potential core targets and main pathways mediated by EE in osteoporosis (OP) treatment. Molecular docking was exploited to investigate the interactions between the active anti-OP compounds in EE and the potential downstream targets. Following the multi-approach bioinformatics analysis, ovariectomy (OVX) model was also established to investigate the in vivo anti-OP effects of EE. Results: The top 10 core targets in PPI network were TP53, AKT1, JUN, CTNNB1, STAT3, HIF1A, EP300, CREB1, IL1B and ESR1. Molecular docking results that the binding energy of target proteins and the active compounds was approximately between -5.0 and -7.0 kcal/mol, which EE has the lowest docking binding energy with HIF1A. Enrichment analysis of GO and KEGG pathways of target proteins indicated that EE treatment could potentially alter numerous biological processes and cellular pathways. In vivo experiments demonstrated the protective effect of EE treatment against accelerated bone loss, where reduced serum levels of TRAP, CTX, TNF-α, LPS, and IL-6 and increased bone volume and serum levels of P1NP were observed in EE-treated mice. In addition, changes in gut microbiota were spotted by 16S rRNA gene sequencing, showing that EE treatment increased the relative abundance of Lactobacillus and decreased the relative abundance of Clostridiaceae. Conclusion: In summary, these findings suggested that the characteristics of multi-target and multi-pathway of EE against OP. In vivo, EE prevents the onset of OP by regulating gut microbiota and inflammatory response and is therefore a potential OP drug.

Di-(2-ethylhexyl) phthalate aggravates psoriasis-like skin lesions: In vitro and in vivo evaluation.

Di-(2-ethylhexyl) phthalate (DEHP), which is a widely used phthalate (PAE), has recently received public attention owing to it causing health problems. The aim of this study was to elucidate the aggravating effects of DEHP on psoriasis and skin toxicity. Human keratinocyte (HaCaT) cells were treated with gradient concentrations of DEHP, and mice with imiquimod (IMQ)-induced psoriasiform dermatitis were hypodermically injected with 40 µg/kg/day of DEHP for seven consecutive days. The skin condition was assessed based on the psoriasis area and severity index score, which indicated the deterioration of IMQ-induced psoriasis-like skin lesions after DEHP exposure. To further analyze the effect of DEHP on psoriasis, the proliferation, inflammation, and tight junction (TJ) damage were examined, which correlated with the development and severity of psoriasis. The results showed that DEHP promoted proliferation both in vivo and in vitro, which manifested as epidermal thickening; an increase in cell viability; upregulation of Ki67, CDK2, cyclinD1, and proliferating cell nuclear antigen; and downregulation of p21. An excessive inflammatory response is an important factor that exacerbates psoriasis, and our results showed that DEHP can trigger the release of inflammatory cytokines as well as the infiltration of T cells. TJ disorders were found in mice and cells after DEHP treatment. Additionally, p38 mitogen-activated protein kinase (MAPK) was strongly activated during this process, which may have contributed to skin toxicity caused by DEHP. In conclusion, DEHP treatment promotes proliferation, inflammation, TJ disruption, and p38 MAPK activation in HaCaT cells and psoriasis-like skin lesions.

Bioinspired Microadhesives with Greatly Enhanced Reversible Adhesion Fabricated by Synthesized Silicone Elastomer with Increasing Phenyl Contents.

We present a facile chemical method for fabricating bioinspired microadhesives with significant improved reversible adhesion strength. Four kinds of polysiloxane with gradient varying phenyl contents were synthesized and used to fabricate microadhesives. The chemical structures and mechanical properties, as well as surface properties of the four microadhesives, were confirmed and characterized by ATR-FTIR, DSC, XPS, low-field NMR, tensile tests, and SEM, respectively. The macroadhesion test results revealed that phenyl contents showed remarkable and positive impacts on the macroadhesion performance of microadhesives. The pull-off adhesion strength of microadhesives with 90% phenyl content (0.851 N/cm2) was nearly 300% higher than that of pure PDMS (0.309 N/cm2). The macroadhesion mechanism analysis demonstrates that a larger bulk energy dissipation caused by massive π-π interaction, as well as the hydrophobic interaction and van der Waals forces at the interface synergistically resulted in a significant enhancement of the adhesion performance. Our results demonstrate the remarkable impact of chemical structures on the adhesion of microadhesives, and it is conducive to the further improvement of adhesion properties of bioinspired microadhesives.

Development of novel wheat-rye 6RS small fragment translocation lines with powdery mildew resistance and physical mapping of the resistance gene PmW6RS.

KEY MESSAGE: Novel wheat-rye 6RS small fragment translocation lines with powdery mildew resistance were developed, and the resistance gene PmW6RS was physically mapped onto 6RS-0.58-0.66-bin corresponding to 18.38 Mb in Weining rye. Rye (Secale cereale L., RR) contains valuable genes for wheat improvement. However, most of the rye resistance genes have not been successfully used in wheat cultivars. Identification of new rye resistance genes and transfer of these genes to wheat by developing small fragment translocation lines will make these genes more usable for wheat breeding. In this study, a broad-spectrum powdery mildew resistance gene PmW6RS was localized on rye chromosome arm 6RS using a new set of wheat-rye disomic and telosomic addition lines. To further study and use PmW6RS, 164 wheat-rye 6RS translocation lines were developed by 60Coγ-ray irradiation. Seedling and adult stage powdery mildew resistance analysis showed that 106 of the translocation lines were resistant. A physical map of 6RS was constructed using the 6RS translocation and deletion lines, and PmW6RS was localized in the 6RS-0.58-0.66-bin, flanked by markers X6RS-3 and X6RS-10 corresponding to the physical interval of 50.23-68.61 Mb in Weining rye genome. A total of 23 resistance-related genes were annotated. Nine markers co-segregate with the 6RS-0.58-0.66-bin, which can be used to rapidly trace the 6RS fragment carrying PmW6RS. Small fragment translocation lines with powdery mildew resistance were backcrossed with wheat cultivars, and 39 agronomically acceptable homozygous 6RS small fragment translocation lines were obtained. In conclusion, this study not only provides novel gene source and germplasms for wheat resistance breeding, but also laid a solid foundation for cloning of PmW6RS.

Degradation of plastic wastes to commercial chemicals and monomers under visible light.

Plastics are playing an incrementally extensive and irreplaceable role in human life, but with alarming cyclic unsustainability. Numerous attempts have been undertaken to recycle plastics, among which chemical recycling from waste plastics back to chemicals and monomers has attracted great attention. Herein, the depolymerization of nine types of plastics to commercial chemicals and monomers was achieved under ambient conditions via synergetic integrated uranyl-photocatalysis, which contains a process for converting five kinds of mixed plastics into a value-added product. The degradation processes were depicted in terms of variation in scanning electron microscopy imaging, distinction in the X-ray diffraction pattern, alteration in water contact angle, and dynamic in molecular weight distribution. Single electron transfer, hydrogen atom transfer, and oxygen atom transfer were synergistically involved in uranyl-photocatalysis, which were substantiated by mechanistic studies. Relying on flow system design, the chemical recycling of plastics was feasible for kilogram-scale degradation of post-consumer-waste polyethylene terephthalate bottles to commercial chemicals, displaying a promising practical application potential in the future.

Stiffened fibre-like microenvironment based on patterned equidistant micropillars directs chondrocyte hypertrophy.

Articular cartilage, composed of collagen type II as a major extracellular matrix and chondrocyte as a unique cell type, is a specialized connective tissue without blood vessels, lymphatic vessels and nerves. This distinctive characteristic of articular cartilage determines its very limited ability to repair when damaged. It is well known that physical microenvironmental signals regulate many cell behaviors such as cell morphology, adhesion, proliferation and cell communication even determine chondrocyte fate. Interestingly, with increasing age or progression of joint diseases such as osteoarthritis (OA), the major collagen fibrils in the extracellular matrix of articular cartilage become larger in diameter, leading to stiffening of articular tissue and reducing its resistance to external tension, which in turn aggravates joint damage or progression of joint diseases. Therefore, designing a physical microenvironment closer to the real tissue and thus obtaining data closer to the real cellular behaviour, and then revealing the biological mechanisms of chondrocytes in pathological states is of crucial importance for the treatment of OA disease. Here we fabricated micropillar substrates with the same topology but different stiffnesses to mimic the matrix stiffening that occurs in the transition from normal to diseased cartilage. It was first found that chondrocytes responded to stiffened micropillar substrates by showing a larger cell spreading area, a stronger enhancement of cytoskeleton rearrangement and more stability of focal adhesion plaques. The activation of Erk/MAPK signalling in chondrocytes was detected in response to the stiffened micropillar substrate. Interestingly, a larger nuclear spreading area of chondrocytes at the interface layer between the cells and top surfaces of micropillars was observed in response to the stiffened micropillar substrate. Finally, it was found that the stiffened micropillar substrate promoted chondrocyte hypertrophy. Taken together, these results revealed the cell responses of chondrocytes in terms of cell morphology, cytoskeleton, focal adhesion, nuclei and cell hypertrophy, and may be beneficial for understanding the cellular functional changes affected by the matrix stiffening that occurs during the transition from a normal state to a state of osteoarthritis.