BOTRYOID POLLEN 1 regulates ROS-triggered PCD and pollen wall development by controlling UDP-sugar homeostasis in rice.

Uridine diphosphate (UDP)-sugars are important metabolites involved in the biosynthesis of polysaccharides and may be important signaling molecules. UDP-glucose 4-epimerase (UGE) catalyzes the interconversion between UDP-Glc and UDP-Gal, whose biological function in rice (Oryza sativa) fertility is poorly understood. Here, we identify and characterize the botryoid pollen 1 (bp1) mutant and show that BP1 encodes a UGE that regulates UDP-sugar homeostasis, thereby controlling the development of rice anthers. The loss of BP1 function led to massive accumulation of UDP-Glc and imbalance of other UDP-sugars. We determined that the higher levels of UDP-Glc and its derivatives in bp1 may induce the expression of NADPH oxidase genes, resulting in a premature accumulation of reactive oxygen species (ROS), thereby advancing programmed cell death (PCD) of anther walls but delaying the end of tapetal degradation. The accumulation of UDP-Glc as metabolites resulted in an abnormal degradation of callose, producing an adhesive microspore. Furthermore, the UDP-sugar metabolism pathway is not only involved in the formation of intine but also in the formation of the initial framework for extine. Our results reveal how UDP-sugars regulate anther development and provide new clues for cellular ROS accumulation and PCD triggered by UDP-Glc as a signaling molecule.

A broad-spectrum macrocyclic peptide inhibitor of the SARS-CoV-2 spike protein.

The ongoing COVID-19 pandemic has had great societal and health consequences. Despite the availability of vaccines, infection rates remain high due to immune evasive Omicron sublineages. Broad-spectrum antivirals are needed to safeguard against emerging variants and future pandemics. We used messenger RNA (mRNA) display under a reprogrammed genetic code to find a spike-targeting macrocyclic peptide that inhibits SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) Wuhan strain infection and pseudoviruses containing spike proteins of SARS-CoV-2 variants or related sarbecoviruses. Structural and bioinformatic analyses reveal a conserved binding pocket between the receptor-binding domain, N-terminal domain, and S2 region, distal to the angiotensin-converting enzyme 2 receptor-interaction site. Our data reveal a hitherto unexplored site of vulnerability in sarbecoviruses that peptides and potentially other drug-like molecules can target.

An E3 ubiquitin ligase CSIT2 controls critical sterility-inducing temperature of thermo-sensitive genic male sterile rice.

Thermo-sensitive genic male sterile (TGMS) lines are the core of two-line hybrid rice (Oryza sativa). However, elevated or unstable critical sterility-inducing temperatures (CSITs) of TGMS lines are bottlenecks that restrict the development of two-line hybrid rice. However, the genes and molecular mechanisms controlling CSIT remain unknown. Here, we report the CRITICAL STERILITY-INDUCING TEMPERATURE 2 (CSIT2) that encodes a really interesting new gene (RING) type E3 ligase, controlling the CSIT of thermo-sensitive male sterility 5 (tms5)-based TGMS lines through ribosome-associated protein quality control (RQC). CSIT2 binds to the large and small ribosomal subunits and ubiquitinates 80S ribosomes for dissociation, and may also ubiquitinate misfolded proteins for degradation. Mutation of CSIT2 inhibits the possible damage to ubiquitin system and protein translation, which allows more proteins such as catalases to accumulate for anther development and inhibits abnormal accumulation of reactive oxygen species (ROS) and premature programmed cell death (PCD) in anthers, partly rescuing male sterility and raised the CSIT of tms5-based TGMS lines. These findings reveal a mechanism controlling CSIT and provide a strategy for solving the elevated or unstable CSITs of tms5-based TGMS lines in two-line hybrid rice.

Effects of purple cabbage anthocyanin extract on the gluten characteristics and the gluten network evolution of high-gluten dough.

BACKGROUND: Anthocyanins are polyphenolic pigments that have hypoglycemic, antioxidation, anti-aging, and other effects. Research has shown that polyphenols can optimize the processing of dough and improve the texture and nutritional characteristics of dough products. The formation of gluten networks is decisive for the quality of flour products. The effects of purple cabbage anthocyanin (PCA) extract on the structure, microscopic morphology, and network formation of gluten protein were studied, and the types of cross-linking between PCA and gluten protein are discussed. RESULTS: The results show that PCA extract increased the free sulfhydryl (SH) group content and the free amino group of gluten proteins, stimulated an increase in the ß-sheet ratio and the decrease of α-helix ratio, and increased the gluten index significantly (P < 0.05). The PCA extract also induced gluten protein aggregation, increased the height of protein molecular chains, and stimulated the formation of gluten networks. When PCA extract concentrations were 4 g kg-1 and 8 g kg-1, the gluten network was more homogeneous, continuous, and dense. CONCLUSION: Appropriate anthocyanins have a positive effect on the properties of gluten and promote the formation of gluten networks. Excessive anthocyanins destroy gluten protein interaction and harm gluten cross-linking. This study may provide a useful source of data for the production of functional flour products rich in anthocyanins. © 2024 Society of Chemical Industry.

An Efficient, Site-Selective and Spontaneous Peptide Macrocyclisation During in†vitro Translation.

Macrocyclisation provides a means of stabilising the conformation of peptides, often resulting in improved stability, selectivity, affinity, and cell permeability. In this work, a new approach to peptide macrocyclisation is reported, using a cyanobenzothiazole-containing amino acid that can be incorporated into peptides by both in vitro translation and solid phase peptide synthesis, meaning it should be applicable to peptide discovery by mRNA display. This cyclisation proceeds rapidly, with minimal by-products, is selective over other amino acids including non N-terminal cysteines, and is compatible with further peptide elaboration exploiting such an additional cysteine in bicyclisation and derivatisation reactions. Molecular dynamics simulations show that the new cyclisation group is likely to influence the peptide conformation as compared to previous thioether-based approaches, through rigidity and intramolecular aromatic interactions, illustrating their complementarity.

Erythropoietin promotes energy metabolism to improve LPS-induced injury in HK-2 cells via SIRT1/PGC1-α pathway.

Acute kidney injury (AKI) is one of frequent complications of sepsis with high mortality. Mitochondria is the center of energy metabolism participating in the pathogenesis of sepsis-associated AKI, and SIRT1/PGC1-α signaling pathway plays a crucial role in the modulation of energy metabolism. Erythropoietin (EPO) exerts protective functions on chronic kidney disease. We aimed to assess the effects of EPO on cell damage and energy metabolism in a cell model of septic AKI. Renal tubular epithelial cells HK-2 were treated with LPS and human recombinant erythropoietin (rhEPO). Cell viability was detected by CCK-8 and mitochondrial membrane potential was determined using JC-1 fluorescent probe. Then the content of ATP, ADP and NADPH, as well as lactic acid, were measured for the assessment of energy metabolism. Oxidative stress was evaluated by detecting the levels of ROS, MDA, SOD and GSH. Pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1ß, were measured with ELISA. Moreover, qRT-PCR and western blot were performed to detect mRNA and protein expressions. shSIRT1 was used to knockdown SIRT1, while EX527 and SR-18292 were applied to inhibit SIRT1 and PGC1-α, respectively, to investigate the regulatory mechanism of rhEPO on inflammatory injury and energy metabolism. In LPS-exposed HK-2 cells, rhEPO attenuated cell damage, inflammation and abnormal energy metabolism, as indicated by the elevated cell viability, the inhibited oxidative stress, cell apoptosis and inflammation, as well as the increased mitochondrial membrane potential and energy metabolism. However, these protective effects induced by rhEPO were reversed after SIRT1 or PGC1-α inhibition. EPO activated SIRT1/PGC1-α pathway to alleviate LPS-induced abnormal energy metabolism and cell damage in HK-2 cells. Our study suggested that rhEPO played a renoprotective role through SIRT1/PGC1-α pathway, which supported its therapeutic potential in septic AKI.

Phosphine addition to dehydroalanine for peptide modification.

Thiols are a functional group commonly used for selective reactions in a biochemical setting because of their high nucleophilicity. Phosphorus nucleophiles can undergo some similar reactions to thiols, but remain underexploited in this setting. In this work we show that phosphine nucleophiles react cleanly and quickly with a dehydroalanine electrophile, itself generated from cysteine, to give a stable adduct in a peptide context. NMR reveals the product to be a phosphonium ion and indicates some backbone conformational constraint, possibly arising from transient carbonyl coordination. The reaction proceeded quickly, with a pseudo-first order rate constant of 0.126 min-1 at 1 mM peptide (80% conversion in 10 min), and with no detectable side products on the peptide. A broad peptide sequence scope and water-soluble phosphines with alkyl as well as aromatic groups were all shown to react efficiently. Phosphine addition proved to be efficient on nisin as a model Dha-containing biologically-derived peptide and on an mRNA-displayed peptide, as well as on TCEP-modified agarose for peptide capture from solution. This reaction thus presents a promising approach for modification of peptides for cargo attachment or altered physical properties in peptide discovery.

Discovery of Potent Cyclic Sulfopeptide Chemokine Inhibitors via Reprogrammed Genetic Code mRNA Display.

Targeting chemokine signaling is an attractive avenue for the treatment of inflammatory disorders. Tyrosine sulfation is an important post-translational modification (PTM) that enhances chemokine-receptor binding and is also utilized by a number of pathogenic organisms to improve the binding affinity of immune-suppressive chemokine binding proteins (CKBPs). Here we report the display selection of tyrosine-sulfated cyclic peptides using a reprogrammed genetic code to discover high-affinity ligands for the chemokine CCL11 (eotaxin-1). The selected cyclic sulfopeptides possess high affinity for the target chemokine (as well as one or more of the related family members CCL2, CCL7 and CCL24) and inhibit CCL11 activation of CC chemokine receptor 3 (CCR3). This work demonstrates the utility of exploiting native PTMs as binding motifs for the generation of new leads for medicinal chemistry.

Suppression of Formylation Provides an Alternative Approach to Vacant Codon Creation in Bacterial In Vitro Translation.

Genetic code reprogramming is a powerful approach to controlled protein modification. A remaining challenge, however, is the generation of vacant codons. We targeted the initiation machinery of E. coli, showing that restriction of the formyl donor or inhibition of the formyl transferase during in vitro translation is sufficient to prevent formylation of the acylated initiating tRNA and thereby create a vacant initiation codon that can be reprogrammed by exogenously charged tRNA. Our approach conveniently generates peptides and proteins tagged N-terminally with non-canonical functional groups at up to 99 % reprogramming efficiency, in combination with decoding the AUG elongation codons either with native methionine or with further reprogramming with azide- and alkyne-containing cognates. We further show macrocyclization and intermolecular modifications with these click handles, thus emphasizing the applicability of our method to current challenges in peptide and protein chemistry.

rhEPO inhibited cell apoptosis to alleviate acute kidney injury in sepsis by AMPK/SIRT1 activated autophagy.

BACKGROUND: Nowadays, people diagnosed sepsis may develop acute kidney injury (AKI), resulting heavy burden of health care. Recombinant human erythroprotein (rhEPO) has been suggested to have multifunction and may be used in the prevention or treatment of AKI, and its underlying mechanism remains largely unknown. METHODS: In our study, cell model induced by LPS-activated cell apoptosis in vitro and AKI animal model caused by lipopolysaccharide (LPS) injection in vivo. MTT assay and Flow Cytometry were conducted to analyze cell viability and apoptosis, respectively. Western bot was used to analyze expressions of apoptosis and autophagy associated proteins, and effects on AMPK/SIRT1 pathway. RESULTS: Our results suggested that rhEPO inhibited LPS-induced cell apoptosis in HK-2 and HEK-293. Moreover, we found that rhEPO activated autophagy to prevented cell apoptosis, changing the expression level of autophagy associated proteins such as LC3-I/LC3-II and P62, and AMPK/SIRT1 pathway was involved in its regulation. Additionally, both EX527 (SIRT1 inhibitor) and Compound C (AMPK inhibitor) blocked the autophagy effects caused by rhEPO and thus reversed the anti-apoptotic effects of rhEPO. Furthermore, our data demonstrated that rhEPO inhibited LPS-induced kidney tubular injury and decreased the expression level of apoptotic proteins by altering the expression level of autophagy related proteins and AMPK/SIRT1 pathway related proteins in vitro. CONCLUSION: Collectively, rhEPO suppressed LPS-induced cell apoptosis via AMPK/SIRT1 pathway mediated autophagy, and modulating their levels may serve as potential way in preventing AKI.

Identification and characterization of the rice pre-harvest sprouting mutants involved in molybdenum cofactor biosynthesis.

In cereal crops, ABA deficiency during seed maturation phase causes pre-harvest sprouting (PHS), and molybdenum cofactor (MoCo) is required for ABA biosynthesis. Here, two rice PHS mutants F254 and F5-1 were characterized. In addition to the PHS, these mutants showed pleiotropic phenotypes such as twisting and slender leaves, and then died when the seedling developed to four or five leaves. Map-based cloning showed that OsCNX6 and OsCNX1 encoding homologs of MoaE and MoeA were responsible for F254 and F5-1 mutants, respectively. Genetic complementation indicated that OsCNX6 not only rescued the PHS and seedling lethal phenotype of the cnx6 mutant, but also recovered the MoCo-dependent enzyme activities such as xanthine dehydrogenase (XDH), aldehyde oxidase (AO), nitrate reductase (NR) and sulfite oxidase (SO). Expression pattern showed that OsCNX6 was richly expressed in seed during embryo maturation by quantitative reverse transcriptase PCR and RNA in situ hybridization. Furthermore, the OsCNX6 overexpression plants can significantly enhance the MoCo-dependent enzyme activities, and improved the osmotic and salt stress tolerance without unfavorable phenotypes. Collectively, these data indicated that OsCNX6 participated in MoCo biosynthesis, and is essential for rice development, especially for seed dormancy and germination, and OsCNX6 could be an effective target for improving abiotic stress tolerance in rice.

Exenatide Inhibits the KCa3.1 Channels of Aortic Vascular Smooth Muscle in Diabetic Rats.

BACKGROUND: KCa3.1 ion channels play an important role during atherosclerosis. We aimed to investigate the effect of exenatide on KCa3.1 expression in aortic vascular smooth muscle cells (VSMCs) of diabetic rats. METHODS: Sprague-Dawley rats were randomly divided into normal control (NC), diabetes model (DM), and exenatide treatment (ET) groups. Hematoxylin and eosin and α-actin immunohistochemical staining were used to detect changes in rat aortic vascular smooth muscle. Quantitative RT-PCR and Western blot analysis were used to detect changes in KCa3.1 mRNA and protein levels, respectively. RESULTS: Aortic tissue staining in the DM group revealed an absence of smooth or integrated endothelium, increased smooth muscle cell proliferation in the media, smooth muscle hyperplasia, disorganized smooth muscle cells, and an increased number of collagen fibers, relative to the NC and ET groups. KCa3.1 mRNA expression was higher in the DM group than in the NC and ET groups. Similarly, the KCa3.1 protein level was higher in the DM group than in the NC and ET groups. The KCa3.1 protein level did not significantly differ between the ET and NC groups. CONCLUSIONS: Exenatide could inhibit the expression of the KCa3.1 channel in VSMCs of diabetic rats.

TOPK Inhibition Enhances the Sensitivity of Colorectal Cancer Cells to Radiotherapy by Reducing the DNA Damage Response.

OBJECTIVE: Abnormal expression of T-lymphokine-activated killer cell-originated protein kinase (TOPK) was reported to be closely related to the resistance of prostate cancer to radiotherapy and to targeted drug resistance in lung cancer. However, the role of TOPK inhibition in enhancing radiosensitivity of colorectal cancer (CRC) cells is unclear. This study aimed to evaluate the radiosensitization of TOPK knockdown in CRC cells. METHODS: The expression of TOPK was detected in CRC tissues by immunohistochemistry, and the effect of TOPK knockdown was detected in CRC cells by Western blotting. CCK-8 and clonogenic assays were used to detect the growth and clonogenic ability of CRC cells after TOPK knockdown combined with radiotherapy in CRC cells. Furthermore, proteomic analysis showed that the phosphorylation of TOPK downstream proteins changed after radiotherapy. DNA damage was detected by the comet assay. Changes in the DNA damage response signaling pathway were analyzed by Western blotting, and apoptosis was detected by flow cytometry. RESULTS: The expression of TOPK was significantly greater in CRC tissues at grades 2-4 than in those at grade 1. After irradiation, CRC cells with genetically silenced TOPK had shorter comet tails and reduced expression levels of DNA damage response-associated proteins, including phospho-cyclin-dependent kinase 1 (p-CDK1), phospho-ataxia telangiectasia-mutated (p-ATM), poly ADP-ribose polymerase (PARP), and meiotic recombination 11 homolog 1 (MRE11). CONCLUSIONS: TOPK was overexpressed in patients with moderately to poorly differentiated CRC. Moreover, TOPK knockdown significantly enhanced the radiosensitivity of CRC cells by reducing the DNA damage response.

Peroxiredoxin 6 alleviates high glucose-induced inflammation and apoptosis in HK-2 cells by inhibiting TLR4/NF-κB signaling.

Background: This research sought to elucidate the effects of peroxiredoxin 6 (PRDX6) on the biological processes in diabetic nephropathy (DN) and to identify the underlying regulatory mechanism related to toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling. Methods: To induce an in vitro DN cellular model, human kidney 2 (HK-2) cells were treated with high glucose (HG). The mitochondrial membrane potential, adenosine triphosphate level, reactive oxygen species generation, and oxidative stress of the cells were then evaluated. After the PRDX6 level had been determined, the effects of its overexpression on the mitochondrial membrane potential, adenosine triphosphate level, reactive oxygen species generation, and oxidative stress of the cells were assessed. Next, cytochrome c expression, cell viability, cell apoptosis, the inflammatory level, and the TLR4/NF-κB signaling-related factors were assessed. After the addition of the TLR4 activator CRX-527 or the NF-κB activator phorbol 12-myristate 13-acetate (PMA), cell viability, cell apoptosis and the inflammatory level were evaluated again. Results: The results revealed that HG exposure triggered mitochondrial dysfunction and oxidative stress and decreased PRDX6 expression in the HK-2 cells. PRDX6 elevation exacerbated cell viability while alleviating mitochondrial membrane potential loss, oxidative stress, apoptosis, and inflammation in the HG-treated HK-2 cells. Further, PRDX6 inhibited HG-induced TLR4/NF-κB activation. The administration of CRX-527 or PMA reversed the effects of PRDX6 on the cell viability, apoptosis, and inflammation of the HG-exposed HK-2 cells. Conclusions: To conclude, PRDX6 appears to protect HG-exposed HK-2 cells against inflammation and apoptosis by inhibiting TLR4/NF-κB signaling.

Selective thiazoline peptide cyclisation compatible with mRNA display and efficient synthesis.

Peptide display technologies are a powerful method for discovery of new bioactive sequences, but linear sequences are often very unstable in a biological setting. Macrocyclisation of such peptides is beneficial for target affinity, selectivity, stability, and cell permeability. However, macrocyclisation of a linear hit is unreliable and requires extensive structural knowledge. Genetically encoding macrocyclisation during the discovery process is a better approach, and so there is a need for diverse cyclisation options that can be deployed in the context of peptide display techniques such as mRNA display. In this work we show that meta-cyanopyridylalanine (mCNP) can be ribosomally incorporated into peptides, forming a macrocycle in a spontaneous and selective reaction with an N-terminal cysteine generated from bypassing the initiation codon in translation. This reactive amino acid can also be easily incorporated into peptides during standard Fmoc solid phase peptide synthesis, which can otherwise be a bottleneck in transferring from peptide discovery to peptide testing and application. We demonstrate the potential of this new method by discovery of macrocyclic peptides targeting influenza haemagglutinin, and molecular dynamics simulation indicates the mCNP cross-link stabilises a beta sheet structure in a representative of the most abundant cluster of active hits. Cyclisation by mCNP is also shown to be compatible with thioether macrocyclisation at a second cysteine to form bicycles of different architectures, provided that cysteine placement reinforces selectivity, with this bicyclisation happening spontaneously and in a controlled manner during peptide translation. Our new approach generates macrocycles with a more rigid cross-link and with better control of regiochemistry when additional cysteines are present, opening these up for further exploitation in chemical modification of in vitro translated peptides, and so is a valuable addition to the peptide discovery toolbox.

The E3 ubiquitin ligase CSIT1 regulates critical sterility-inducing temperature by ribosome-associated quality control to safeguard two-line hybrid breeding in rice.

Two-line hybrid breeding can fully utilize heterosis in crops. In thermo-sensitive genic male sterile (TGMS) lines, low critical sterility-inducing temperature (CSIT) is vital to safeguard the production of two-line hybrid seeds in rice (Oryza sativa), but the molecular mechanism determining CSIT is unclear. Here, we report the cloning of CSIT1, which encodes an E3 ubiquitin ligase, and show that CSIT1 modulates the CSIT of thermo-sensitive genic male sterility 5 (tms5)-based TGMS lines through ribosome-associated quality control (RQC). Biochemical assays demonstrated that CSIT1 binds to the 80S ribosomes and ubiquitinates abnormal nascent polypeptides for degradation in the RQC process. Loss of CSIT1 function inhibits the possible damage of tms5 to the ubiquitination system and protein translation, resulting in enhanced accumulation of anther-related proteins such as catalase to suppress abnormal accumulation of reactive oxygen species and premature programmed cell death in the tapetum, thereby leading to a much higher CSIT in the tms5-based TGMS lines. Taken together, our findings reveal a regulatory mechanism of CSIT, providing new insights into RQC and potential targets for future two-line hybrid breeding.

Personalized Smart Clothing Design Based on Multimodal Visual Data Detection.

In the traditional clothing customization system, only the designer participates in the clothing design, and the style is single. In the face of numerous styles, the user just repeatedly arranges and combines the styles, but does not realize the user's innovative design. In this paper, we propose a novel multitask deep convolutional neural network training method for task-by-task transfer learning, and learn deep image features for image retrieval tasks on noisy user click data. Image retrieval model based on image-text multimodal correlation features: this paper uses image-text multimodal correlation features to calculate the correlation between query keywords and images, and calculates the correlation between images and images. In this paper, the method of automatic generation of clothing style is researched, and parameterized coding is designed for it. Taking the typical style of suits as the initial population, through the human-computer interaction interface, the scoring value is assigned to the fitness value to carry out the evolution process. The binary string of the suit style generated by the genetic algorithm is decoded through the decoding algorithm and rules, decoded into a visual style diagram of the style of the suit style, and the style diagram of the suit style is automatically drawn. From the perspective of clothing design, this paper summarizes the general design methods of outdoor sports smart clothing, follows the integration of people-clothing-environment, and proposes a wearer-centered design concept to deeply explore the rationality of outdoor sports smart clothing design methods. This paper further solves the key problems in the design process, and takes the fashion of clothing as the core principle to design the structure of clothing modeling. The fabric selection of suits is based on the principle of clothing comfort. The key is to realize the outdoor sports monitoring function of suits through sensing technology. The design uses Arduino as an electronic prototype platform, so as to detect the heart rate of the human body during exercise and the microclimate temperature under the clothes. This kind of suit with monitoring function is ultimately a combination of sensing device and clothing. It not only has monitoring function, but also has the aesthetic concept of clothing design and conforms to the performance of human body structure, which will provide reference and reference for the design of outdoor sports smart clothing.

Clinical Significance of miR-21-5p in Predicting Occurrence and Progression of Uremic Vascular Calcification in Patients with End-Stage Renal Disease.

PURPOSE: Vascular calcification (VC) is a common complication of end-stage renal disease (ESRD). This study aimed to examine changes in the expression of miR-21-5p in ESRD patients with VC and to explore its clinical value in predicting the occurrence and progression of uremic VC. MATERIALS AND METHODS: 120 ESRD patients were divided into patients without VC group (n=38) and patients with VC group (n=82). All patients were followed up for 2 years to evaluate VC progression. qRT-PCR was used to detect serum miR-21-5p levels. Receiver operating characteristic curves were constructed to assess diagnostic value. Kaplan-Meier and log-rank methods were utilized to calculate associations between VC progression and risk factors. RESULTS: Serum miR-21-5p levels were significantly higher in ESRD patients with VC than in those without VC and increased progressively with increasing disease severity. Serum miR-21-5p levels were able to distinguish patients with VC from those without VC, with an area under the curve value of 0.883, a sensitivity of 81.7%, and a specificity of 84.2%. After 2 years of follow-up, miR-21-5p expression had increased in patients with worse VC severity, compared with those with stable VC severity. Patients with high miR-21-5p levels were more likely to develop more severe VC, indicating an association between miR-21-5p and VC progression (log-rank p=0.002). Multivariable Cox regression analysis suggested that serum miR-21-5p is an independent predictive factor of VC progression in ESRD patients (hazard ratio=2.064, 95% confidence interval=1.225-3.478, p=0.006). CONCLUSION: miR-21-5p is overexpressed in the serum of ESRD patients with VC. Our results suggest that overexpression of miR-21-5p is closely associated with VC progression.

The effects of biochar soil amendment on rice growth may vary greatly with rice genotypes.

While plant growth promotion with increased nutrient uptake had been well addressed for biochar soil amendment in agriculture, there was limited knowledge on the variation of such effects with crop genotypes. In a rice field experiment without and with biochar soil amendment at 20 t ha-1, 19 mutants of a rice cultivar Wuyunjing 7 (Oryza sativa L.) were tested for plant growth in split plots respectively. At harvest, the biomass of grain, stem and leaves were measured and soil and plant samples were collected for measuring N, P and K nutrients. Across the 19 mutants, relative change with biochar soil amendment varied in a range of -41.6% to +35.6% for biomass production and agronomic traits, and -87.0% to +117% for nutrient accumulation. For the nutrients content, the relative change for N was seen in a narrow range of -29.4% to +16.6%, being similar among grain, leaf and shoot samples while that for P in a wide range of -109% to +105%. With factor analysis, variation of biomass and nutrient uptake was least explained with biochar effect (up to 7.0%) but largely by genotype effect (mostly by 40-70%). However, the genotype × biochar interaction effect could also explain 10-40% of the total variations though the interaction explained 40-70% of leaf P variation. Therefore, mutant and mutant × biochar interactions dominated the agronomic variation of rice production of the Wuyunjing 7 cultivar. Furthermore, across the traits analyzed, genotype effects were shown very significantly but negatively correlated to biochar effects. In other words, biochar soil amendment provided little growth or nutrient enhancement for those mutants bred for high efficiency. Hence, genotype selection should be considered in optimizing prioritizing biochar application in crop production. Of course, variation of biochar effect with crop genotypes deserved further plant physio-ecological studies.

Biochar-based fertiliser enhances nutrient uptake and transport in rice seedlings.

Biochar-based compound fertilisers (BCF) are gaining increasing attention as they are cost-effectiveness and improve soil fertility and crop yield. However, little is known about the mechanisms by which micron-size BCF particles enhance crop growth. In the present study, Wuyunjing7 rice seedlings were exposed to micron-size particles of wheat straw-based BCF (mBCF) diffused through a 25-µm nylon mesh. The control was fertilised with urea, diammonium phosphate, and potassium chloride to ensure that both treatments received comparables level of N, P, and K. The effects of mBCF on rice seedling growth were evaluated by determining the changes in nitrogen uptake and utilisation via nitrogen content measurements, short-term 15N-NH4+ influx assays, and analyses of transcript-level nutrient transporter gene expression. The shoot biomass of rice seedling treated with mBCF at the rate of 5 mg/ g soil was 33% greater than that for the control. Root and shoot 15N accumulation rates were 44% and 14% higher, respectively, in the mBCF-treated than the control. The mBCF-treated rice seedlings had higher phosphorus, potassium, and iron content than the control. Moreover, the treatments significantly differed in terms of their nutrient transporter gene expression levels. Spectroscopy and microscopy were used to visualise nutrient distributions across transverse root sections. There were relatively higher iron oxide nanoparticle and silicon-based compound concentrations in the roots of the mBCF-treated rice seedlings than in those of the control. The foregoing difference might account for the fact that the growth of the mBCF-treated rice was superior to that of the control. We demonstrated that the mBCF treatment created a more negative electrical potential at the root epidermal cell layer (~ - 160 mV) than the root surface. This potential difference may have been the driving force for mineral nutrient absorption.