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A new refiner containing (Ti + V)B2phase was prepared in this study. It consists of a special VB2–TiB2core–shell structure, and the size of most (Ti + V)B2granular phase is between 100 and 500 nm. Considering Al–7Si alloy as the research object, the refining ability of Al–Ti–B, Al–V–B, and Al–(Ti + V)–B was compared under the condition of same content of added B. The grain refiner containing (Ti + V)B2can significantly reduce the grain size of Al–7Si. Al–(Ti + V)–B refines the as-cast grain size from 854.6 ± 28 to 136.93 ± 2.45 μm, which is better than the results obtained for Al–Ti–B- and Al–V–B-based refiners.

Parasitic plants have evolved to be subtly or severely dependent on host plants to complete their life cycle. To provide new insights into the biology of parasitic plants in general, we assembled genomes for members of the sandalwood order Santalales, including a stem hemiparasite (Scurrula) and two highly modified root holoparasites (Balanophora) that possess chimaeric host–parasite tubers. Comprehensive genome comparisons reveal that hemiparasitic Scurrulahas experienced a relatively minor degree of gene loss compared with autotrophic plants, consistent with its moderate degree of parasitism. Nonetheless, patterns of gene loss appear to be substantially divergent across distantly related lineages of hemiparasites. In contrast, Balanophorahas experienced substantial gene loss for the same sets of genes as an independently evolved holoparasite lineage, the endoparasitic Sapria(Malpighiales), and the two holoparasite lineages experienced convergent contraction of large gene families through loss of paralogues. This unprecedented convergence supports the idea that despite their extreme and strikingly divergent life histories and morphology, the evolution of these and other holoparasitic lineages can be shaped by highly predictable modes of genome reduction. We observe substantial evidence of relaxed selection in retained genes for both hemi- and holoparasitic species. Transcriptome data also document unusual and novel interactions between Balanophoraand host plants at the host–parasite tuber interface tissues, with evidence of mRNA exchange, substantial and active hormone exchange and immune responses in parasite and host.

•RUNX1 governs the direct differentiation potential of MK-HSCs into MKs.•RUNX1 binds to and regulates MK developmental genes in MK-HSCs.

Neurofibromatosis type 1 (NF1) patients are predisposed to develop plexiform neurofibromas (PNFs). Three endoplasmic reticulum (ER) stress response pathways restore cellular homeostasis. The unfolded protein response (UPR) sensors contribute to tumor initiation in many cancers. We found that all three UPR pathways were activated in mouse and human PNFs, with protein kinase RNA [PKR]-like ER kinase (PERK) the most highly expressed. We tested if neurofibroma cells adapt to ER stress, leading to their growth. Pharmacological or genetic inhibition of PERK reduced mouse neurofibroma-sphere number, and genetic inhibition in PERK in Schwann cell precursors (SCPs) decreased tumor-like lesion numbers in a cell transplantation model. Further, in a PNF mouse model, deletion of PERK in Schwann cells (SCs) and SCPs reduced tumor size, number, and increased survival. Mechanistically, loss of Nf1activated PERK-eIF2α-ATF4 signaling and increased ATF4 downstream target gene p21 translocation from nucleus to cytoplasm. This nucleus-cytoplasm translocation was mediated by exportin-1. Runx transcriptionally activated ribosome gene expression and increased protein synthesis to allow SCs to adapt to ER stress and tumor formation. We propose that targeting proteostasis might provide cytotoxic and/or potentially durable novel therapy for PNFs.

Abdominal aortic aneurysm (AAA) and atherosclerosis (AS) have considerable similarities in clinical risk factors and molecular pathogenesis. The aim of our study was to investigate the differences between AAA and AS from the perspective of metabolomics, and to explore the potential mechanisms of differential metabolites via integration analysis with transcriptomics. Plasma samples from 32 AAA and 32 AS patients were applied to characterize the metabolite profiles using untargeted liquid chromatography-mass spectrometry (LC-MS). A total of 18 remarkably different metabolites were identified, and a combination of seven metabolites could potentially serve as a biomarker to distinguish AAA and AS, with an area under the curve (AUC) of 0.93. Subsequently, we analyzed both the metabolomics and transcriptomics data and found that seven metabolites, especially 2′-deoxy-d-ribose (2dDR), were significantly correlated with differentially expressed genes. In conclusion, our study presents a comprehensive landscape of plasma metabolites in AAA and AS patients, and provides a research direction for pathogenetic mechanisms in atherosclerotic AAA.

Abstract ID 98867

MicroRNAs (miRs) are small non-coding RNAs that can have large impacts on oncogenic pathways. Possible functions of dysregulated miRs have not been studied in neurofibromatosis type 1 (NF1) plexiform neurofibromas (PNFs). In PNFs, Schwann cells (SCs) have biallelic NF1mutations necessary for tumorigenesis. We analyzed a miR microarray comparing with normal and PNF SCs and identified differences in miR expression, and we validated in mouse PNFs versus normal mouse SCs by qRT-PCR. Among these, miR-155 was a top overexpressed miR, and its expression was regulated by RAS/MAPK signaling. Overexpression of miR-155 increased mature Nf1-/-mouse SC proliferation. In SC precursors, which model tumor-initiating cells, pharmacological and genetic inhibition of miR-155 decreased PNF-derived sphere numbers in vitro, and we identified Maf as a miR-155 target. In vivo, global deletion of miR-155 significantly decreased tumor number and volume, increasing mouse survival. Fluorescent nanoparticles entered PNFs, suggesting that an anti-miR might have therapeutic potential. However, treatment of established PNFs using anti-miR-155 peptide nucleic acid-loaded nanoparticles marginally decreased tumor numbers and did not reduce tumor growth. These results suggest that miR-155 plays a functional role in PNF growth and/or SC proliferation, and that targeting neurofibroma miRs is feasible, and might provide novel therapeutic opportunities.

Leaf herbivory on tea plants (Camellia sinensis) by tea geometrids (Ectropis oblique) severely threaten the yield and quality of tea. In previous work, we found that local defense response was induced in damaged leaves by geometrids at the transcriptome level. Here, we investigated the systemic response triggered in undamaged roots and the potential role of roots in response to leaf herbivory. Comparative transcriptome analysis and carbohydrate dynamics indicated that leaf herbivory activated systemic carbon reallocation to enhance resource investment for local secondary metabolism. The crucial role of jasmonic acid and the involvement of other potential hormone signals for local and systemic signaling networks were supported by phytohormone quantification and dynamic expression analysis of phytohormone-related genes. This work represents a deep understanding of the interaction of tea plants and geometrids from the perspective of systems biology and reveals that tea plants have evolved an intricate root-mediated resource-based resistance strategy to cope with geometrid attack.

Plexiform neurofibroma, a benign peripheral nerve tumor, is associated with the biallelic loss of function of the NF1tumor suppressor in Schwann cells. Here, we show that FLLL32, a small molecule inhibitor of JAK2/STAT3 signaling, reduces neurofibroma growth in mice with conditional, biallelic deletion of Nf1in the Schwann cell lineage. FLLL32 treatment or Stat3deletion in tumor cells reduced inflammatory cytokine expression and tumor macrophage numbers in neurofibroma. Although STAT3 inhibition downregulated the chemokines CCL2 and CCL12, which can signal through CCR2 to recruit macrophages to peripheral nerves, deletion of Ccr2did not improve survival or reduce macrophage numbers in neurofibroma-bearing mice. Interestingly, Iba1+; F4/80+;CD11b+ macrophages accounted for ~20–40% of proliferating cells in untreated tumors. FLLL32 suppressed macrophage proliferation, implicating STAT3-dependent, local proliferation in neurofibroma macrophage accumulation, and decreased Schwann cell proliferation and increased Schwann cell death. The functions of STAT3 signaling in neurofibroma Schwann cells and macrophages, and its relevance as a therapeutic target in neurofibroma, merit further investigation.

Grafting is one of the key technologies to overcome the obstacles of continuous cropping, and improve crop yield and quality. However, the symbiotic incompatibility between rootstock and scion affects the normal growth and development of grafted seedlings after survival. The specific molecular regulation mechanism of graft incompatibility is still largely unclear. In this study, we found that the IAA-miR164a-NAC100L1 module induced callose deposition to mediate the symbiotic incompatibility of cucumber/pumpkin grafted seedlings. The incompatible combination (IG) grafting interface accumulated more callose, and the activity of callose synthase (CmCalS1) and IAA content were significantly higher than in the compatible combination (CG). Treatment with IAA polar transport inhibitor in the root of the IG plants decreased CmCalS activity and callose content. Furthermore, IAA negatively regulated the expression of Cm-miR164a, which directly targeted cleavage of CmNAC100L1. Interestingly, CmNAC100L1 interacted with CmCalS1 to regulate its activity. Further analysis showed that the interaction between CmNAC100L1 and CmCalS1 increased the activity of CmCalS1 in the IG plants but decreased it in the CG plants. Point mutation analysis revealed that threonine at the 57th position of CmCalS1 protein played a critical role to maintain its enzyme activity in the incompatible rootstock. Thus, IAA inhibited the expression of Cm-miR164a to elevate the expression of CmNAC100L1, which promoted CmNAC100L1 interaction with CmCalS1 to enhance CmCalS1 activity, resulting in callose deposition and symbiotic incompatibility of cucumber/pumpkin grafted seedlings.

Background:The COVID‐19 virus not only has significant pathogenicity but also influences the progression of many diseases, altering patient prognosis. Cardiovascular diseases, particularly aortic aneurysms, are among the most life‐threatening conditions. Main Idea:COVID‐19 infection is reported to accelerate the progression of abdominal aortic aneurysms (AAAs) and increase the risk of rupture; however, a comprehensive understanding of the underlying mechanisms remains elusive. This article primarily reviews the relevant foundational research, focusing on disruptions in the renin‐angiotensin‐aldosterone system (RAAS), immune system activation, and coagulation disorders. Furthermore, we summarize related clinical research, including the epidemiology of aortic aneurysms during the pandemic and specific case studies. Conclusion:COVID‐19 infection can influence the onset and progression of aortic aneurysms by affecting the RAAS, triggering inflammation and immune dysregulation in the arterial wall, and inducing a hypercoagulation state. It is crucial to comprehensively understand the impact of pandemic viral infections on aortic diseases at the foundational and clinical levels, thereby identifying potential preventative or therapeutic approaches and preparing for potential future outbreaks.

IMPORTANCE: Triggering the extrinsic apoptotic pathway is an effective way to kill cutaneous T-cell lymphoma (CTCL) cells in vitro and ex vivo. OBJECTIVE: To compare small molecules that induce extrinsic apoptosis in CTCL to identify and analyze compounds that induce high levels of tumor cell death and block tumor cell growth. DESIGN, SETTING, AND PARTICIPANTS: From November 5, 2014, to January 30, 2018, this study performed high-throughput small molecule screening of 1710 compounds followed by detailed analysis of the ability of gentian violet (GV) to promote apoptosis and inhibit proliferation of CTCL cells. EXPOSURES: In vitro and ex vivo analyses using enzyme-linked immunosorbent assays, flow cytometry, and immunoblotting. MAIN OUTCOMES AND MEASURES: Apoptosis, cleaved caspases, extrinsic apoptotic death receptors and ligands, cell proliferation, nuclear factor–κB expression, and other factors. RESULTS: This study used high-throughput screening to detect cleaved caspase 8 induced in CTCL cells by 1710 unique compounds. The nonprescription, topical antimicrobial remedy GV induced more total apoptosis than did nitrogen mustard (mechlorethamine). Furthermore, GV induced 4 to 6 times greater apoptosis in CTCL lines than in normal keratinocytes, suggesting a favorable topical toxicity profile. In addition to increasing caspase 8, GV also upregulated death receptors 4 and 5, tumor necrosis factor (TNF)–related apoptosis-inducing ligand, and Fas ligand but not the Fas receptor, TNF receptor, or TNF-α ligand. These results are consistent with induction of extrinsic apoptosis via the Fas and TNF-related apoptosis-inducing ligand pathways. Increased phosphorylation of phospholipase C–γ1, Ca2+ influx, and reactive oxygen species were also detected, indicating that the mechanism of Fas ligand upregulation involves key elements of the activation-induced cell death pathway. In ex vivo studies, 1-μmol/L GV induced up to 90% CTCL apoptosis in Sézary blood cells. In addition, GV reduced expression of antiapoptotic myeloid cell leukemia 1 and proproliferative nuclear factor–κB components and increased inhibitory κB levels. This finding was associated with cell cycle arrest and reduced CTCL tumor cell proliferation. Furthermore, the CTCL killing associated with GV was augmented when used in combination with methotrexate. CONCLUSIONS AND RELEVANCE: This study found that GV attacked tumor viability and growth in CTCL. Although purple at neutral pH, GV can be rendered colorless by altering its pH. These preclinical findings may help to broaden knowledge of the antineoplastic features of GV and provide a rationale for clinical studies of its use as a novel, inexpensive, topical therapy for CTCL that is available worldwide.

RUNX1 is a RUNT domain core-binding factor indispensable for the establishment of definitive hematopoiesis in vertebrate. In humans, heterozygous RUNX1germline mutations are closely associated with Familial Platelet Disorder with propensity to develop AML (FPD/AML), a rare autosomal dominant disorder characterized by thrombocytopenia, platelet dysfunction, and markedly elevated risk for myelodysplastic syndrome and leukemia. RUNX1 regulates hematopoietic genes directly or indirectly, acting as a context-dependent activator or repressor of gene transcription. Here we have examined how RUNX1 regulates various subpopulations of hematopoietic stem/progenitor cells (HSPCs) to provide important insights into its physiologic and pathogenic roles and mechanisms.We used two complementary mouse models: a conditional RUNX1 knockout mouse, i,e, Mx-Cre;Runx1flox/flox, and a tetracycline-inducible FPD/AML patient derived RUNX1 S291fsX300 mutation knock-in crossed to a MLL-PTD knock-in mouse, i.e. MLL-PTD;RUNX1 S291fsX300. We monitored hematopoiesis and/or disease progression in both models by tracking CBCs in peripheral blood and analyzing bone marrow cells by flow cytometry. The bone marrow samples were sorted by flow cytometry to yield HSPC subpopulations: HSC (LSK CD34-Flt3-), GMP (LK FCRII/III+CD34+), and MEP (LK FCRII/III-CD34-). Cells were analyzed for transcriptome by deep RNA-seq, epigenetics by ATAC-seq, and gene targets by anti-RUNX1 CHIP-seq. Focusing on the HSC, GMP, and MEP subpopulations, we found that RUNX1 deletion in the hematopoietic system causes thrombocytopenia and HSC engraftment defects, and dramatic changes in HSPC subpopulations: RUNX1 deficiency resulted in an increase MegaK-primed HSCs via blocking their direct differentiation to megakaryocytes leading to thrombocytopenia, and caused a marked increase of GMPs and a significant decrease of MEPs. Induction of RUNX1 S291fsX300 mutant in MLL-PTD;RUNX1 S291fsX300 mice mimicked that of RUNX1 deletion, resulting similarly in thrombocytopenia, an expansion of Mega-HSCs, increased GMPs, and decreased MEPs. “Correction” of the RUNX1S291fsX300 mutation by doxycycline withdraw reversed the FPD phenotype as well as the cellular distribution changes in HSCs, GMPs and MEPs. RNA-seq analyses of DEGs found that RUNX1 acts both as an activator and a suppressor in gene transcription in HSPCs. In HSCs, among 1879 DEGs, 608 are upregulated and 1271 are downregulated in Runx1 -/-compared with WT cells. In GMPs, 2042 DEGs were seen, among which 908 are upregulated and 1134 are downregulated whereas in MEPs, 316 transcripts were upregulated and 1214 were downregulated amongst 1530 DEGs in Runx1 -/-cells. Combining the DEGs from RNA-seq with annotated ATAC-seq peaks, we discovered through gene ontology analyses that a set of systemic development genes are commonly regulated by RUNX1 via chromosome accessibility in all HSPC subpopulations, with potentially shared targets such as Jam2, Bcar1, Irf4 Insrr , Cxcl12, Tnfsf4, Rap1gap, Aldh1a1. In contrast, in HSCs, a unique set of hemostasis/platelet regulatory genes such as Itga2b, Gp5, Pdgfband Vwfwere seen as potential targets, consistent with our recent findings ( Blood Adv7:2590). In GMPs, RUNX1 appears to specifically regulate inflammatory and innate immunity genes with potential targets such as Gfi1b, Ets1, Tnfrsf11awhile in MEP, RUNX1 specifically regulates cell motility and migration gene sets affecting targets such as Notch1, Ifitm1, Hoxa7, Cd300a Cxcl10 Fut7, suggesting a role of RUNX1 in modulating MEP movement/location in the bone marrow. RUNX1 CHIP-seq analyses are under way to further clarify the potential targets in each HSPC subpopulation. Our studies indicate that RUNX1 regulates common as well as distinct transcriptional events in various HSPC subpopulations by context-dependent activation and suppression mechanisms. RUNX1 plays a universal role in the systemic developmental program of various HSPC subpopulations but appears to engage in unique lineage specific factors to deliver subpopulation-specific functions such as mega-K cell fate-priming of HSCs, inflammatory program in GMPs, and bone marrow location signals in MEPs. Ongoing analyses of the FPD/AML mouse genomic data in this context are expected to reveal contributions of patient RUNX1 mutations to the disease development.

The yellowing of leaves caused by the decomposition of chlorophyll (Chl) is a characteristic event during senescence, which can be induced by various environmental stresses. However, the molecular mechanisms of high temperature-induced Chl degradation in horticultural plants remain poorly understood. Here, we found that heat stress induced Chl degradation and the expression of ABI5and MYB44in cucumber. Silencing of ABI5compromised heat stress-induced Chl degradation, and the transcription of pheophytinase (PPH) and pheophorbide aoxygenase (PAO), two key genes in Chl catabolic pathway, but silencing of MYB44exhibited the opposite results. Furthermore, ABI5 interacted with MYB44 in vitroand in vivo. ABI5 positively regulated heat stress-induced Chl degradation through two pathways. ABI5 directly bound to PPHand PAOpromoters to promote their expression, leading to accelerating Chl degradation. On the other hand, the interaction between ABI5 and MYB44 reduced the binding of MYB44 to PPHand PAOpromoters and led to the ubiquitination-depended protein degradation of MYB44, thereby alleviating the transcription inhibitory effect of MYB44 on PPHand PAO. Taken together, our findings propose a new regulatory network for ABI5 in regulating heat stress-induced Chl degradation.

To identify genes and signaling pathways that initiate Neurofibromatosis type 1 (NF1) neurofibromas, we used unbiased insertional mutagenesis screening, mouse models, and molecular analyses. We mapped an Nf1-Stat3-Arid1b/β-cateninpathway that becomes active in the context of Nf1loss. Genetic deletion of Stat3in Schwann cell progenitors (SCPs) and Schwann cells (SCs) prevents neurofibroma formation, decreasing SCP self-renewal and β-catenin activity. β-catenin expression rescues effects of Stat3 loss in SCPs. Importantly, P-STAT3 and β-catenin expression correlate in human neurofibromas. Mechanistically, P-Stat3 represses Gsk3βand the SWI/SNF gene Arid1bto increase β-catenin. Knockdown of Arid1bor Gsk3βin Stat3fl/fl;Nf1fl/fl;DhhCreSCPs rescues neurofibroma formation after in vivo transplantation. Stat3 represses Arid1bthrough histone modification in a Brg1-dependent manner, indicating that epigenetic modification plays a role in early tumorigenesis. Our data map a neural tumorigenesis pathway and support testing JAK/STAT and Wnt/β-catenin pathway inhibitors in neurofibroma therapeutic trials.

This article reviews methotrexate and the more potent, related compound, pralatrexate, for the treatment of cutaneous T-cell lymphomas, including mycosis fungoides, Sézary syndrome, and CD30+ lymphoproliferative disorders. Although these folate antagonists are traditionally viewed as antiproliferative cell cycle inhibitors, it is recognized that they inhibit DNA methylation, providing a rationale for their use as epigenetic regulators and cell proliferation inhibitors. The underlying mechanisms are outlined, key supporting data presented, followed by brief mention of recent mathematical modeling supporting the general superiority of combination therapy. Several novel examples involving folate antagonists are proposed.

SGT1 (suppressor of G-two allele of SKP1) is highly conserved among all eukaryotes. In plants, SGT1 interacts with various proteins, including molecular chaperones (HSP70 and HSP90) and certain SCF ubiquitin ligases, and hence SGT1 likely functions in protein folding and stability. Since these protein complexes are involved in many aspects of plant biology, plants with a defective SGT1 display a plethora of phenotypic alterations. In this review we highlight the interaction between SGT1 with other protein complexes and summarize the function of SGT1 in plant defense responses and development, including the recent advancements in the understanding of the role of SGT1 in jasmonic acid (JA) biosynthesis and signaling.

OBJECTIVE To explore the relationships among (Fas) promoter methylation, Fas expression, and apoptotic sensitivity in cutaneous T-cell lymphoma (CTCL). DESIGN Laboratory investigation. SETTING Dermatology research unit of a university medical center. SAMPLES Five CTCL lines and Sézary syndrome blood. INTERVENTIONS Treatment of cells with 5-azacytidine (aza), methotrexate, and interferon alfa-2b. MAIN OUTCOME MEASURES Fas promoter methylation, Fas expression, and sensitivity to Fas-mediated apoptosis. RESULTS Fas promoter methylation correlates inversely with the level of Fas transcript, protein, and apoptotic sensitivity in CTCL. Increased DNA methylation also correlates with decreased NFkB (nuclear factor kappa–light chain enhancer of activated B cells) binding to the Fas promoter. All of these relationships were reversed by the DNA-demethylating agent, 5-aza. We found that methotrexate also functions as a DNA-demethylating agent by depleting methyl donors and, together with interferon alfa-2b, upregulates Fas and enhances sensitivity to Fas-mediated apoptosis. CONCLUSIONS These findings help explain the previously reported impressive responses of patients with advanced CTCL to combination therapy with methotrexate and interferon alfa. They also provide a new rationale for the treatment of CTCL with methotrexate and its use in combination with other agents.Arch Dermatol. 2011;147(4):443-449. Published online December 20, 2010. doi:10.1001/archdermatol.2010.376--

Benign peripheral nerve tumors called neurofibromas are a major source of morbidity for patients with neurofibromatosis type 1. Some neurofibroma Schwann cells aberrantly express the epidermal growth factor receptor (EGFR). In a mouse model in which the CNPase promoter drives expression of human EGFR in Schwann cells, nerves develop hypertrophy, mast cell accumulation, collagen deposition, disruption of axon-glial interactions, characteristics of neurofibroma and are hypoalgesic. Administration of the EGFR antagonist cetuximab (IMC-C225) for 2 weeks beginning at birth in CNPase-hEGFR mice normalized all pathologies at 3 months of age as evaluated by hotplate testing or histology and by electron microscopy. Mast cell chemoattractants brain-derived neurotrophic factor, monocyte chemoattractant protein-1, and transforming growth factor-β1, which may account for mast cell accumulation and fibrosis, were reduced by cetuximab. Later treatment was much less effective. A birth to 2-week pulse of cetuximab blocked hEGFR phosphorylation and Schwann cell proliferation in perinatal mutant nerve, so CNPase-hEGFR Schwann cell numbers correlate with the cetuximab effect. A 250-fold enlarged population of EGFR+/p75+cells was detected in newborn Nf1+/−mouse nerves. These results suggest the existence of an EGFR+cell enriched in the perinatal period capable of driving complex changes characteristic of neurofibroma formation.

In plants and algae, PGR5-dependent cyclic electron flow (CEF) is an important regulator of acclimation to fluctuating environments, but how PGR5 participates in CEF is unclear. In this work, we analyzed two PGR5s in cucumber (Cucumis sativusL.) under different conditions and found that CsPGR5a played the dominant role in PGR5-dependent CEF. The results of yeast two-hybrid, biomolecular fluorescence complementation (BiFC), blue native PAGE, and coimmunoprecipitation (CoIP) assays showed that PGR5a interacted with PetC, Lhcb3, and PsaH. Furthermore, the intensity of the interactions was dynamic during state transitions, and the abundance of PGR5 attached to cyt b6fdecreased during the transition from state 1 to state 2, which revealed that the function of PGR5a is related to the state transition. We proposed that PGR5 is a small mobile protein that functions when attached to protein complexes.

The East Asian monsoon is characterized by warm, humid summer and cool, dry winter that results in seasonal changes in fluvial sediment and organic carbon (OC) discharge. Here, we report measurements of elemental, isotopic, and optical compositions of OC in surface waters and sediments that were collected along the lower Yangtze River, Estuary, and East China Sea continuum in March and July 2019. The principal component analysis separates samples into three groups that correspond to fresh water area, mixing area, and seawater area. The terrigenous signal in the mixing area, indicated by water salinity and δ13C, is stronger in July. The applications of binary mixing models based on water salinity, dissolved OC (DOC) concentration and specific terrigenous fluorescence component suggest: (a) net removal of DOC from waters in July, but net addition of DOC into waters in March, attributed to more extensive degradation and larger deposition of OC in summer; and (b) more conservative behaviors of terrigenous OC compared to marine or mixed OC, suggesting an important role of intrinsic molecular characteristics on the persistence of DOC. The estimated monthly OC burial flux in the estuary and continent shelf is 0.48 × 1012g in July and 0.081 × 1012g of OC in March, equal to 15.5% and 2.6% of the annual OC discharge by the Yangtze River, respectively. Our study suggests that the burial of OC mainly occurs in the summer monsoon due to the larger sediment load of the Yangtze River, prevailing southeastern wind, and intensified Kuroshio Current. Large rivers export an enormous amount of terrigenous sediment and carbon into the ocean. Under the combined influence of rapid climate change and intense human disturbance, the carbon cycling in estuaries and adjacent seas is highly dynamic. Here, we examine elemental, isotopic, and optical characteristics of organic carbon in waters and sediments along the Yangtze River, Estuary, and East China Sea continuum, and compare organic carbon concentration, composition, and deposition between March and July of 2019, corresponding to normal and high‐water discharge, respectively. We have obtained three key findings of the transport, mixing, and deposition processes of organic carbon in this large river‐dominated margin. (a) There is a net removal of organic carbon from waters in July, and net addition of organic carbon into waters in March. (b) Terrigenous dissolved organic carbon is more conservative than aquatic/marine dissolved organic carbon. (c) The organic carbon burial flux in the estuary and shelf sea is 0.48 × 1012g in July, five‐fold greater than that in March (0.081 × 1012g). Thus, the accumulation of organic carbon mainly occurs in the summer monsoon mainly attributed to the larger sediment load of the Yangtze River, prevailing southeastern wind, and intensified Kuroshio Current. Terrigenous dissolved organic carbon (DOC) is more conservative than aquatic/marine DOC during seaward transport and mixing processesThere is net removal of DOC in July and net addition of DOC in March in the Yangtze River estuary and shelfThe OC burial in the Yangtze River estuary and shelf in July is five‐fold greater than that in March Terrigenous dissolved organic carbon (DOC) is more conservative than aquatic/marine DOC during seaward transport and mixing processes There is net removal of DOC in July and net addition of DOC in March in the Yangtze River estuary and shelf The OC burial in the Yangtze River estuary and shelf in July is five‐fold greater than that in March

AbstractChina is the largest provider of teacher education and training in the world. It also sustains the world's largest number of primary and secondary schools. How to improve teacher education development in the light of economic growth is an extremely demanding task for the Chinese Government and educators. Recent years have witnessed a tremendous effort in China to effectively raise the standards of teachers' professional development so as to help students to play their part in developing China's economic prosperity and to enhance its place in the international market place. This article analyses the key issues in the current reform and development in China of teacher professional development. It also describes the major forms and systems of teacher education and training in China.

AbstractThe nature of the relationship between the work environment and people working in it has become a significant issue for educational research. This paper is based upon the outcomes of investigations made in a number of secondary schools in England and Wales in which a Work Environment Scale and follow-up interviews were used. It contains a snapshot of the British way of portraying the secondary school work environment, provides a perspective of its impact on the professional competence of newly qualified teachers (NQTs) and offers a comparison of NQTs' and more experienced teachers' perceptions about the work environments of their workplaces. The interaction between NQTs and their work environments is considered in order to give ideas about what is happening in these schools when NQTs start their professional careers and how their professional competence might be promoted. An outline of the Work Environment Scale is presented with a special emphasis on its application in educational settings and its implications for educational policy on teacher professional development are explored

On the basis of the reference [1], excitation of Cherenkov radiation with arbitrary azimuthal mode number by a thin annular relativistic electron beam in a plasma-filled dielectric-lined slow-wave waveguide is studied in this paper. A determinantal dispersion equation is obtained. This general dispersion equation is valid for arbitrary azimuthal mode number, and the growth rate of the wave is derived from it. Finally, the effects of the background plasma density on the dispersion relation, the background plasma density and the electron beam radius on the growth rate of the wave are presented. Formulas and results offerd in this paper are general, and are of particular value of reference to the beam-wave interaction in azimuthally unsymmetrical slow-wave waveguide.

An axial relativistic electron beam passing through a slow wave structure is unstable to an electromagnetic perturbation whose phase velocity equals the velocity of the beam. This phenomenon of Cherenkov emission is the basis of all traveling wave tubes. In this paper an excitation of Cherenkov radiation by a thin annular relativistic electron beam in a plasma-filled dielectric-lined waveguide is analysed by use of the self-consistent linear theory. The effect of the thin annular electron beam on the beam-wave interaction is completely described by a jump condition. The dispersion equation and the simultaneous condition of the beam-wave interaction are derived. Finally, the growth rate of the wave is obtained, and the effect of the background plasma density and the electron beam radius on the growth rate of the wave are presented.

The effect of three-dimensional perturbed velocity and three-dimensional perturbed current density on the beam-wave interaction of dielectric Cherenkov maser is analysed by use of the self-consistent linear field theory. Three distinct cases are considered. First, the propagation of the electron beam in an annular dielectric liner enclosed by a loss-free conducting wall is investigated. The dispersion equation and the simultaneous condition of the beam-wave interaction are derived. It's clearly shown that the instability of the interaction results from the coupling of the TM mode in the dielectric lined slow-wave waveguide to the beam mode via the electron beam. And the coupling is proportional to the density of the beam. The growth rate of the wave produced by the electron beam are obtained. Then, the case of a relativistic electron beam guided by a longitudinal magnetic field in the same slow-wave structure is examined. The motion of electrons could be approximated to be one-dimensional when the simultaneous condition of the beam-wave interaction of dielectric Cherenkov maser is satisfied. Finally, the effect of the background plasma on the instability of the beam-wave interaction is studied.

A new type of whispering-gallery mode ring dielectric resonators are first proposed. Theoretical analysis and a method for determination of the resonant frequencies is presented by the mode matching method. The numerical results show good agreement with theoretical analysis.

China is the largest provider of vocational training in the world, with its huge labour population creating a great need of training in all forms. On the basis of a general review of the historical development of vocational training in China since 1949, this article provides a brief introduction to the major forms of vocational training carried out throughout China. In particular, it looks at vocational training in the context of current economic reforms, and analyses how vocational training will develop in the face of the opportunities and challenges brought about by the establishment of a market economy.

Almost a decade ago BRI1-associated kinase 1 (BAK1) was identified as a co-receptor of brassinosteroid (BR) insensitive 1 (BRI1), the receptor for BRs, which plays an essential role in transducing BR signaling to regulate plant development. BAK1 is also critical in resistance to various pathogens. BAK1 rapidly binds to certain receptors for pathogen/microbe-associated molecular patterns (PAMPs/MAMPs) after the perception of pathogen elicitors and is required for the full elicitation of pathogen-induced defense responses, such as the activation of the mitogen-activated protein kinase 6 (MPK6) and production of reactive oxygen species. Thus, BAK1 functions in both BR signaling and PAMP-triggered immunity (PTI). Recently BAK1 was also found to play an important role in mediating defense responses against an insect herbivore (Manduca sexta) of Nicotiana attenuata. In this interaction, BAK1 positively modulates wound- or herbivore feeding-induced accumulation of jasmonic acid (JA) and JA-isoleucine (JA-Ile). This mini-review summarizes recent advances in our understanding the functions of BAK1 in resistance to pathogens and herbivores.

Calcium-dependent protein kinases (CDPKs) modulate plant development and growth and are important regulators of biotic and abiotic stress responses. Recently it was found that simultaneously silencing Nicotiana attenuata NaCDPK4and NaCDPK5(IRcdpk4/5 plants) results in accumulation of exceptionally high JA levels after wounding or simulated herbivory treatments, which in turn induced high levels of defense metabolites that slowed the growth of Manduca sexta, a specialist insect herbivore. To investigate the mechanism by which NaCDPK4 and NaCDPK5 regulate JA accumulation, we analyzed the transcript levels of all important enzymes involved in JA biosynthesis, but these genes showed no differences between wild-type and IRcdpk4/5 plants. Moreover, the dynamics of JA were similar between these plants, excluding the possibility of decreased degradation rates in IRcdpk4/5 plants. To gain insight into the mechanism by which NaCDPK4 and NaCDPK5 regulate JA biosynthesis, free fatty acids, including C18:3, and (9S,13S)-12-oxo-phytodienoic acid (OPDA), two important precursors of JA were quantified at different times before and after wounding and simulated herbivore feeding treatments. We show that after these treatments, IRcdpk4/5 plants have decreased levels of C18:3, but have enhanced OPDA and JA levels, suggesting that NaCDPK4 and NaCDPK5 have a role in the early steps of JA biosynthesis. The possible role of NaCDPK4 and NaCDPK5 regulating AOS and AOC enzymatic activity is discussed.