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Background Intraductal papillary mucinous neoplasm (IPMN) is a cystic tumor of the pancreas arising from abnormal papillary proliferation of ductal epithelial cells, and is a precancerous lesion of pancreatic malignancy. This study aimed to evaluate associations between acute pancreatitis (AP) and histologic subtypes of IPMN. Methods In the clinical study, patients with IPMN confirmed by surgical resection specimens at our institute between 2009 and 2021 were eligible for inclusion. Associations and predictive accuracy of AP on the presence of HGD were determined by logistic regressions. In addition, a systematic review and meta-analysis was conducted through literatures upon search in PubMed, Embase, CENTRAL, China National Knowledge Infrastructure (CKNI), and Wanfang database, up to June, 2023. Pooled effects of the associations between AP and HGD and intestinal epithelial subtype subtype, shown as odds ratios (ORs) with 95% confidence intervals (CIs), were calculated using random effects model. Results The retrospective cohort study included 47 patients (32 males, 15 females) diagnosed with IPMN at our center between 2009 and 2021, including 11 cases with AP (median 62 years) and 36 cases (median 64.5 years) without. Accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of AP in predicting HGD were 78.7%, 57.1%, 82.5%, 36.4%, and 91.7%, respectively. Univariate logistic regression analysis showed that AP group had greater odds of presence of HGD (OR: 6.29,95% CI: 1.14–34.57) than non-AP group. Meta-analysis of five case-control studies in the literature included 930 patients and showed that AP-IPMN patients had higher odds for HGD (OR: 2.13, 95% CI 1.38–3.29) and intestinal epithelial subtype (OR: 5.38, 95% CI: 3.50–8.27) compared to non-AP IPMN. Conclusions AP is predictive of malignancy in patients with IPMN.

Introduction Hepatocellular adenomas (HCAs), with a risk of malignant transformation into hepatocellular carcinoma (HCC), classically develop in young women who are taking oral contraceptives. It is now clear that HCAs may also occur in men. However, it is rarely reported that HCAs with malignant transformation occur in male patients with non‐cirrhotic livers. This study aimed to characterize the malignancy of HCAs occurring in male patients. Methods All patients with HCAs with malignant transformation who underwent hepatectomy at the Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College between January 1, 1999 and December 31, 2011 were enrolled in the study. The clinical characteristics as well as radiologic and pathologic data were reviewed. Results HCAs with malignant transformation were observed in 5 male patients with non‐cirrhotic livers, but not in female patients. The alpha‐fetoprotein (AFP) levels were higher in patients with HCAs with malignant transformation than in patients with HCAs without malignant transformation. The diameters of the tumors with malignant transformation were larger than 5 cm in 3 cases and smaller than 5 cm in 2 cases. The 5 patients were all alive without recurrence by the end of the study period. The disease‐free survival times of the 5 patients were 26, 48, 69, 69, and 92 months. Conclusion Our results indicate that resection would be advised even if the presumptive diagnosis is adenoma smaller than 5 cm in diameter, especially in male patients.

Histone methylation is believed to provide binding sites for specific reader proteins, which translate histone code into biological function. Here we show that a family of acidic domain-containing proteins including nucleophosmin （NPM 1）, pp32, SET/TAF 113, nucleolin （NCL） and upstream binding factor （UBF） are novel H3K4me2-binding proteins. These proteins exhibit a unique pattern of interaction with methylated H3K4, as their binding is stimulated by H3K4me2 and inhibited by H3K4mel and H3K4me3. These proteins contain one or more acidic domains consisting mainly of aspartic and/or glutamic residues that are necessary for preferential binding of H3K4me2. Furthermore, we demonstrate that the acidic domain with sufficient length alone is capable of binding H3K4me2 in vitro and in vivo. NPM1, NCL and UBF require their acidic domains for association with and transcriptional activation ofrDNA genes. Interestingly, by defining acidic domain as a sequence with at least 20 acidic residues in 50 continuous amino acids, we identified 655 acidic domain-containing protein coding genes in the human genome and Gene Ontology （GO） analysis showed that many of the acidic domain proteins have chromatin-related functions. Our data suggest that acidic domain is a novel histone binding motif that can differentially read the status of H3K4 methylation and is broadly present in chromatin-associated proteins.

Electrochemiluminescence (ECL) plays a key role in analysis and sensing because of its high sensitivity and low background. Its wide applications are however limited by a lack of highly tunable ECL luminophores. Here we develop a scalable method to design ECL emitters of covalent organic frameworks (COFs) in aqueous medium by simultaneously restricting the donor and acceptor to the COFs’ tight electron configurations and constructing high-speed charge transport networks through olefin linkages. This design allows efficient intramolecular charge transfer for strong ECL, and no exogenous poisonous co-reactants are needed. Olefin-linked donor-acceptor conjugated COFs, systematically synthesized by combining non-ECL active monomers with C 2v or C 3v symmetry, exhibit strong ECL signals, which can be boosted by increasing the chain length and conjugation of monomers. The present concept demonstrates that the highly efficient COF-based ECL luminophores can be precisely designed, providing a promising direction toward COF-based ECL phosphors. Electrochemiluminescence (ECL) plays a key role in analysis and sensing but its application is limited by a lack of highly tunable luminophores. Here, the authors demonstrate the design of high efficient ECL luminophores of covalent organic frameworks (COFs) in aqueous media by simultaneously restricting the donor and acceptor to the COFs’ electron configurations and constructing charge transport networks through olefin linkages.

Waterlogging is a major abiotic stress limiting barley （Hordeum vulgare L.） yield and its stability in areas with excessive rainfall. Identification of genomic regions influencing the response of yield and its components to waterlogging stress will enhance our understanding of the genetics of waterlogging tolerance and the development of more tolerant barley cultivars. Quantitative trait loci （QTLs） for grain yield and its components were identified using 156 doubled haploid （DH） lines derived from a cross between the cultivars Yerong （waterlogging-tolerant） and Franklin （waterlogging-sensitive） grown under different conditions （waterlogged and well drained）. A total of 31 QTLs were identified for the measured characters from two experiments with two growth environments. The phenotypic variation explained by individual QTLs ranged from 4.74% to 55.34%. Several major QTLs determining kernel weight （KW）, grains per spike （GS）, spikes per plant （SP）, spike length （SL） and grain yield （GY） were detected on the same region of chromosome 2H, indicating close linkage or pleiotropy of the gene（s） controlling these traits. Some different QTLs were identified under waterlogging conditions, and thus different markers may have to be used in selecting cultivars suitable for high rainfall areas.

Al-Si coated ultra-high strength steel（UHSS）has been commonly applied in hot stamping process.The influence of austenitizing temperature on microstructure of Al-Si coating of UHSS during hot stamping process and its tribological behavior against H13 steel under elevated temperature were simulatively investigated.The austenitizing temperature of Al-Si coated UHSS and its microstructual evolution were confirmed and analyzed by differential scanning calorimetry and scanning electron microscopy.A novel approach to tribological testing by replicating hot stamping process temperature history was presented.Results show that the hard and stable phases Fe_2Al_5＋FeAl_2 formed on Al-Si coating surface after exposure to 930°C for 5 min,which was found to be correlated to the tribological behavior of coating.The friction coefficient of coated steel was more stable and higher than that of uncoated one.The main wear mechanism of Al-Si coated UHSS was adhesion wear,while abrasive wear was dominant for the uncoated UHSS.

Summary STAUROSPORINE AND TEMPERATURE SENSITIVE3 (STT3) is a catalytic subunit of oligosaccharyltransferase, which is important for asparagine‐linked glycosylation. Sharp eyespot, caused by the necrotrophic fungal pathogen Rhizoctonia cerealis, is a devastating disease of bread wheat. However, the molecular mechanisms underlying wheat defense against R. cerealis are still largely unclear. In this study, we identified TaSTT3a and TaSTT3b, two STT3 subunit genes from wheat and reported their functional roles in wheat defense against R. cerealis and increasing grain weight. The transcript abundance of TaSTT3b‐2B was associated with the degree of wheat resistance to R. cerealis and induced by both R. cerealis and exogenous jasmonic acid (JA). Overexpression of TaSTT3b‐2B significantly enhanced resistance to R. cerealis, grain weight, and JA content in transgenic wheat subjected to R. cerealis stress, while silencing of TaSTT3b‐2B compromised resistance of wheat to R. cerealis. Transcriptomic analysis showed that TaSTT3b‐2B affected the expression of a series of defense‐related genes and JA biosynthesis–related genes, as well as genes coding starch synthase and sucrose synthase. Application of exogenous JA elevated expression levels of the abovementioned defense‐ and grain weight–related genes, and rescuing the resistance of TaSTT3b‐2B–silenced wheat to R. cerealis, while pretreatment with sodium diethyldithiocarbamate, an inhibitor of JA synthesis, attenuated the TaSTT3b‐2B–mediated resistance to R. cerealis, suggesting that TaSTT3b‐2B played critical roles in regulating R. cerealis resistance and grain weight via JA biosynthesis. Altogether, this study reveals new functional roles of TaSTT3b‐2B in regulating plant innate immunity and grain weight, and illustrates its potential application value for wheat molecular breeding.

BackgroundAdjuvant therapy may improve survival of patients with hepatocellular carcinoma (HCC) after curative resection. This study compared safety and efficacy outcomes between patients at high risk of recurrence who received different types of adjuvant therapy or no such therapy after hepatic resection for HCC.MethodsRecurrence-free survival (RFS), overall survival, and adverse events were compared among patients who received adjuvant immune checkpoint inhibitors (ICIs) alone, ICIs with tyrosine kinase inhibitors (TKIs), or no adjuvant therapy between 13 March 2019 and 19 March 2022. This study was registered on ClinicalTrials.gov (NCT05221398).ResultsOf the 517 patients in final analysis, 432 (83.6%) received no adjuvant therapy, 53 (10.2%) received ICIs alone, and 32 (6.2%) received adjuvant ICIs and TKIs. During median follow-up of 34.0 months (IQR 27.8 to 41.6 months), RFS was significantly longer among patients who received either type of adjuvant therapy (25.2 months, 95%CI 16.4–34.0) than among those who received none (16.1 months, 95%CI 12.9–19.4), and this difference remained significant after propensity score matching (HR 0.52, 95%CI 0.35–0.76, P = 0.004). Overall survival was unaffected by either type of adjuvant therapy, while significant difference was observed between patients who received adjuvant therapy or not after propensity score matching (HR 0.31, 95%CI 0.17–0.59, P = 0.005). The rate of grade 3 or 4 adverse events was similar between the two types of adjuvant therapy.ConclusionsICIs alone or with TKIs may improve RFS of patients at high risk of HCC recurrence after curative resection.

This study employs bioinformatics analysis with the objective of identifying commonly differentially expressed genes (DEGs) in ulcerative colitis (UC) and rheumatoid arthritis (RA), as well as exploring their underlying molecular mechanisms. By doing so, it aims to provide a theoretical basis for investigating the potential associations between these two diseases and developing novel therapeutic strategies. We downloaded multiple gene expression datasets for Rheumatoid Arthritis (RA) and Ulcerative Colitis (UC) from the Gene Expression Omnibus (GEO) database. For RA, GSE77298, GSE12021, and GSE55457 were selected as the training sets, with GSE89408 serving as the validation set. For UC, GSE36807, GSE87473, and GSE92415 were chosen as the training sets, and GSE13367 as the validation set.During data processing, we first merged the RA and UC data from each training set with standardized data, eliminated batch effects, and obtained combined datasets of differentially expressed genes (DEGs). Subsequently, we conducted a cross-analysis of the DEGs from RA and UC to identify commonly up-regulated and down-regulated genes. To gain a deeper understanding of these DEGs, we constructed a protein-protein interaction (PPI) network and identified hub genes.For further analysis of these hub genes, we utilized the GENEMANIA platform to obtain functional annotations and interaction information. Finally, we validated our analysis results using the GSE89408 and GSE13367 datasets. After a thorough analysis of the differentially expressed genes in the cells of patients with rheumatoid arthritis (RA) and ulcerative colitis (UC) we found that genes such as CCR7, CD19, CXCL13, CXCR4, and SELL were significantly up-regulated, suggesting their crucial roles in the pathology of both diseases. This discovery not only underscores the importance of these genes as biomarkers for the differential diagnosis of RA and UC, but also highlights key nodes worthy of further validation. In the future, it may be possible to slow or halt disease progression by modulating the expression of these genes. The results of this study reveal potential common molecular mechanisms underlying rheumatoid arthritis (RA) and ulcerative colitis (UC). The key target genes CCR7, CD19, CXCL13, CXCR4, and SELL highlight common underlying factors associated with both diseases. Further investigation and exploration of these findings can pave the way for new candidate targets and directions in therapeutic research aimed at treating RA and UC. This study emphasizes the importance of utilizing bioinformatics approaches to uncover the mechanisms of complex diseases, providing a promising pathway for the development of more effective and targeted treatments.

The plant pathogen Xanthomonas campestris effector, AvrAC, is shown to have uridine 5′-monophosphate transferase activity, enabling it to interfere with plant immune signalling by using this protein modification. Black-rot pathogen targets plant immunity The bacterium Xanthomonas campestris, which causes black rot disease in many types of brassica, translocates a number of effectors into the host cells to promote infection. This study shows that the X. campestris effector protein AvrAC inhibits plant immunity by specifically targeting BIK1 and RIPK, two receptor-like cytoplasmic kinases known to mediate immune signalling in Arabidopsis . AvrAC acts as a UMP transferase, targeting BIK1 and RIPK at sites where phosphorylation normally occurs. Plant innate immunity is activated on the detection of pathogen-associated molecular patterns (PAMPs) at the cell surface, or of pathogen effector proteins inside the plant cell 1 , 2 , 3 , 4 . Together, PAMP-triggered immunity and effector-triggered immunity constitute powerful defences against various phytopathogens. Pathogenic bacteria inject a variety of effector proteins into the host cell to assist infection or propagation. A number of effector proteins have been shown to inhibit plant immunity 5 , but the biochemical basis remains unknown for the vast majority of these effectors. Here we show that the Xanthomonas campestris pathovar campestris type III effector AvrAC enhances virulence and inhibits plant immunity by specifically targeting Arabidopsis BIK1 and RIPK, two receptor-like cytoplasmic kinases known to mediate immune signalling 6 , 7 , 8 . AvrAC is a uridylyl transferase that adds uridine 5′-monophosphate to and conceals conserved phosphorylation sites in the activation loop of BIK1 and RIPK, reducing their kinase activity and consequently inhibiting downstream signalling.