Explore the vast range of titles available.

Kiwifruit bacterial canker is a devastating disease threatening kiwifruit production. To clarify the defense mechanism in response to Pseudomonas syringae pv. actinidiae (Psa), we observed phenotypic changes in resistant Huate (HT) and susceptible Hongyang (HY) kiwifruit varieties at 0, 12, 24, 48, 96, and 144 hour after inoculation (hai) with Psa. Brown lesions appeared in the inoculation areas 12 hai in HY shoots, and the lesion length gradually increased from 24 to 144 h. In contrast, no lesions were found in HT shoots at any time points. Furthermore, RNA-seq analysis showed significantly more differentially expressed genes between HT and HY at 12 hai than at any other time point. According to weighted gene co-expression network analysis, five modules were notably differentially expressed between HT and HY; pathway mapping using the Kyoto Encyclopedia of Gene and Genomes database was performed for the five modules. In MEgreenyellow and MEyellow modules, pathways related to\"plant-pathogen interaction\", \"Endocytosis\", \"Glycine, serine and threonine metabolism\", and \"Carbon fixation in photosynthetic organisms\" were enriched, whereas in the MEblack module, pathways related to \"protein processing in endoplasmic reticulum\", \"plant-pathogen interaction\", and \"Glycolysis / Gluconeogenesis\" were enriched. In particular, the Pti1 and RPS2 encoding effector receptors, and the NPR1, TGA, and PR1 genes involved in the salicylic acid signaling pathway were significantly up-regulated in HT compared with HY. This indicates that the effector-triggered immunity response was stronger and that the salicylic acid signaling pathway played a pivotal role in the Psa defense response of HT. In addition, we identified other important genes, involved in phenylpropanoid biosynthesis and Ca2+ internal flow, which were highly expressed in HT. Taken together, these results provide important information to elucidate the defense mechanisms of kiwifruit during Psa infection.

As important regulators, miRNAs could play pivotal roles in regulation of fruit coloring. Actinidia arguta is a newly emerged fruit tree with extensively application prospects. However, miRNAs involved in A. arguta fruit coloring are unknown. In this study, A. arguta fruit were investigated at three developmental stages by small RNAs high-throughput sequencing. A total of 482 conserved miRNAs corresponding to 526 pre-miRNAs and 581 novel miRNAs corresponding to 619 pre-miRNAs were grouped into 46 miRNA families. Target gene prediction and analysis revealed that miR858, a strongly candidate miRNA, was involved in anthocyanin biosynthesis in which contributes to fruit coloring. The anthocyanin level was determined in three A. arguta cultivars by UPLC-MS/MS (ultra-performance liquid chromatography coupled with tandem mass spectrometry). In addition, qPCR (quantitative real-time PCR), cluster analysis were conducted as well as correlation analysis. All results were combined to propose a model in which describes an association of miRNA and anthocyanin biosynthesis in A. arguta. The data presented herein is the first report on miRNA profile analysis in A. arguta, which can provide valuable information for further research into the regulation of the miRNAs in anthocyanin biosynthesis and fruit coloring.

Objective Lung cancer remains the leading cause of cancer-related deaths worldwide, and lymphovascular invasion (LVI) is an important pathological indicator affecting the prognosis of lung cancer patients. Traditional imaging techniques face challenges in effectively and accurately predicting vascular invasion, but integrating clinical indicators with radiomics features is expected to improve the non-invasive preoperative prediction of LVI, providing valuable reference for clinical treatment decisions. This study aimed to investigate the clinical value of predicting LVI in patients with invasive lung adenocarcinoma (LUAD) based on the intratumoral and peritumoral CT radiomics models. Patients and methods The 384 patients with invasive LUAD from Institution 1 were randomly divided into training ( n  = 268) and internal validation ( n  = 116) sets with a ratio of 7:3, and 251 patients from Institution 2 were used as the external validation set. Altogether, 1226 features were extracted from the tumor gross (GT), gross tumor and peritumor (GPT), and peritumor(PT), respectively. Clinical independent predictors for LVI in patients with invasive LUAD were screened using univariate and multivariate logistic regression analysis, a combined model that included clinical predictors and optimal Radscore was constructed, and a nomogram was drawn. All cases were diagnosed using histopathological examination results as the gold standard. Results The GPT model showed better predictive efficacy than the GT and PT models, with the area under the curve (AUC) of 0.83, 0.79, and 0.75 in the training, internal validation, and external validation sets, respectively. In the clinical model, the preoperative carcinoembryonic antigen (CEA) level, tumor diameter, and spiculation were the independent predictors. The combined model containing the independent predictors and the GPT-Radscore significantly predicted LVI in patients with invasive LUAD, with AUCs of 0.84, 0.82, and 0.77 in the three cohorts, respectively. Conclusion The CT scan-based radiomics model which including intratumoral and peritumoral radiomics features could effectively predict LVI in LUAD patients, and the predictive efficacy were further improved by combining clinically independent predictors. This study holded significant clinical importance, as it provided a non-invasive biomarker for the preoperative prediction of LVI status in lung cancer patients, thereby identifying subgroups with poor prognosis. It demonstrated great potential for risk stratification and guiding personalized treatment strategies in clinical practice.

Cold stress poses a serious treat to cultivated kiwifruit since this plant generally has a weak ability to tolerate freezing tolerance temperatures. Surprisingly, however, the underlying mechanism of kiwifruit’s freezing tolerance remains largely unexplored and unknown, especially regarding the key pathways involved in conferring this key tolerance trait. Here, we studied the metabolome and transcriptome profiles of the freezing-tolerant genotype KL ( Actinidia arguta ) and freezing-sensitive genotype RB ( A. arguta ), to identify the main pathways and important metabolites related to their freezing tolerance. A total of 565 metabolites were detected by a wide-targeting metabolomics method. Under (−25°C) cold stress, KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway annotations showed that the flavonoid metabolic pathways were specifically upregulated in KL, which increased its ability to scavenge for reactive oxygen species (ROS). The transcriptome changes identified in KL were accompanied by the specific upregulation of a codeinone reductase gene, a chalcone isomerase gene, and an anthocyanin 5-aromatic acyltransferase gene. Nucleotides metabolism and phenolic acids metabolism pathways were specifically upregulated in RB, which indicated that RB had a higher energy metabolism and weaker dormancy ability. Since the LPCs (LysoPC), LPEs (LysoPE) and free fatty acids were accumulated simultaneously in both genotypes, these could serve as biomarkers of cold-induced frost damages. These key metabolism components evidently participated in the regulation of freezing tolerance of both kiwifruit genotypes. In conclusion, the results of this study demonstrated the inherent differences in the composition and activity of metabolites between KL and RB under cold stress conditions.

Metabolic reprogramming (MR) in cancer (CA) has been a focus of intense research in the recent two decades. This phenomenon has attracted great interest because it offers potential targets for cancer therapy. To capture the intellectual landscape of this field, we conducted a bibliometric analysis to assess the scientific output, major contributors, and trends in the MR/CA research. We performed a systematic search using the Web of Science to retrieve articles published on MR of cancer from 2006 until 2023. The bibliometric tools such as Biblioshiny, VOSviewer, and Microsoft Excel were used to identify the most prolific authors, institutions, citation patterns, and keywords. We also used co-citation analysis to map the conceptual structure of the field and identify influential publications. Furthermore, we examined the literature by analyzing publication years, citations, and research impact factors. A total of 4,465 publications about MR/CA were retrieved. Publications on MR/CA increased rapidly from 2006 to 2023. published the most papers, while had the most citations. Highly cited papers were mainly published in , , , and . China and the United States led the way in publications and contributed the most to MR/CA research. The University of Texas System, Chinese Academy of Sciences, and Fudan University were the most productive institutions. The profitable authors were Deberardinis Ralph J and Chiarugi Paola. The current topics included MR in tumorigenesis and progression of CA, MR of tumor cells and tumor microenvironment, the effect of MR on the CA treatment, the underlying mechanisms of MR (such as gene regulation, epigenetics, extracellular vesicles, and gut microbiota), and the modulation of MR. Some topics such as tumor microenvironment, lipid MR, circular RNA, long noncoding RNA, exosome, prognostic model, and immunotherapy may be the focus of MR/CA research in the next few years. This study evaluated the global scientific output in the field of MR/CA research, analyzing its quantitative characteristics. It identified some significant and distinguished papers and compiled information regarding the current status and evolving trends of MR/CA research.

Background Mood disorders impose substantial physical and psychological burdens globally. Virtual reality (VR)- based psychological interventions have gained attention as a potential approach in this field. However, current research on these interventions for mood disorders remains heterogeneous and lacks a comprehensive synthesis. A scoping review is needed to map the existing evidence, and to identify trends and gaps in this emerging area. Objective This scoping review was to synthesize the existing status of applications about virtual reality-based psychological interventions for mood disorders by examining the characteristics and reported outcomes of included studies. Methods This scoping review was conducted following Arksey and O’Malley’s methodological framework. We performed systematic searches across seven electronic databases and gray literature sources. The search encompassed all available records from database inception to March 2026, focusing on studies that were about VR-based psychological interventions for mood disorders. Results 18 studies were included, finding four types of VR-based psychological interventions, namely cognitive-oriented, experiential-oriented, social situation simulation, and psychoeducational tools. Based on user interaction modes, these interventions were classified into immersive interactive and non-interactive categories. Interventions generally included 1–24 sessions (4–90 min per session, 1–2 sessions weekly), with the most common being 4–12 sessions of 30–50 min each. All studies assessed efficacy, with depressive symptoms and emotion regulation as the most frequent outcomes. 55.6% included feasibility evaluation. User experience feedback highlighted five themes, including interaction design, environmental fidelity, hardware suitability, user experience, and reality transferability. Conclusions This review identified four intervention types by content and therapeutic orientation and two categories by user interaction modes. VR-based psychological interventions for mood disorders remain at an early stage. Future research should develop standardized intervention frameworks and conduct more high-quality trials across diverse populations to confirm their effectiveness. Clinical trial registration Not applicable.

Background Anthocyanin accumulation in plant tissues requires coordinated regulation of both biosynthesis and transport. In Actinidia arguta , these pigments determine visual quality while enhancing nutritional value and antioxidant capacity, yet the mechanisms underlying the coordinated regulation of anthocyanin synthesis and transport remain poorly understood. Results In this study, we identified AaMYB114, an R2R3-MYB transcription factor, from a skin-color-associated co-expression module in Actinidia arguta . Transient overexpression of AaMYB114 in fruit peel significantly enhanced red pigmentation and anthocyanin content. Yeast one-hybrid (Y1H) and dual-luciferase assays demonstrated that AaMYB114 directly binds to and activates the promoters of key biosynthetic genes AaPAL , AaCHI , and AaF3H . Notably, AaMYB114 also directly targets the promoter of AaGST , a glutathione S-transferase essential for anthocyanin transport into the vacuole. Co-overexpression of AaMYB114 and AaGST synergistically intensified red coloration beyond either gene alone, while chemical inhibition of GST activity with ethacrynic acid suppressed pigmentation and attenuated the effect of AaMYB114 overexpression. Conclusions These findings establish AaMYB114 as a dual-function master regulator that simultaneously orchestrates anthocyanin biosynthesis and transport, providing both theoretical insights into pigment regulation and practical targets for molecular breeding of red-skinned kiwifruit cultivars.

Actinidia arguta is the most basal species in a phylogenetically and economically important genus in the family Actinidiaceae. To better understand the molecular basis of the Actinidia arguta chloroplast (cp), we sequenced the complete cp genome from A. arguta using Illumina and PacBio RS II sequencing technologies. The cp genome from A. arguta was 157,611 bp in length and composed of a pair of 24,232 bp inverted repeats (IRs) separated by a 20,463 bp small single copy region (SSC) and an 88,684 bp large single copy region (LSC). Overall, the cp genome contained 113 unique genes. The cp genomes from A. arguta and three other Actinidia species from GenBank were subjected to a comparative analysis. Indel mutation events and high frequencies of base substitution were identified, and the accD and ycf2 genes showed a high degree of variation within Actinidia. Forty-seven simple sequence repeats (SSRs) and 155 repetitive structures were identified, further demonstrating the rapid evolution in Actinidia. The cp genome analysis and the identification of variable loci provide vital information for understanding the evolution and function of the chloroplast and for characterizing Actinidia population genetics.

Background Kiwifruit ( Actinidia Lindl.) is considered an important fruit species worldwide. Due to its temperate origin, this species is highly vulnerable to freezing injury while under low-temperature stress. To obtain further knowledge of the mechanism underlying freezing tolerance, we carried out a hybrid transcriptome analysis of two A. arguta ( Actinidi arguta ) genotypes, KL and RB, whose freezing tolerance is high and low, respectively. Both genotypes were subjected to − 25 °C for 0 h, 1 h, and 4 h. Results SMRT (single-molecule real-time) RNA-seq data were assembled using the de novo method, producing 24,306 unigenes with an N50 value of 1834 bp. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of DEGs showed that they were involved in the ‘starch and sucrose metabolism’, the ‘mitogen-activated protein kinase (MAPK) signaling pathway’, the ‘phosphatidylinositol signaling system’, the ‘inositol phosphate metabolism’, and the ‘plant hormone signal transduction’. In particular, for ‘starch and sucrose metabolism’, we identified 3 key genes involved in cellulose degradation, trehalose synthesis, and starch degradation processes. Moreover, the activities of beta-GC (beta-glucosidase), TPS (trehalose-6-phosphate synthase), and BAM (beta-amylase), encoded by the abovementioned 3 key genes, were enhanced by cold stress. Three transcription factors (TFs) belonging to the AP2/ERF, bHLH (basic helix-loop-helix), and MYB families were involved in the low-temperature response. Furthermore, weighted gene coexpression network analysis (WGCNA) indicated that beta-GC , TPS5 , and BAM3.1 were the key genes involved in the cold response and were highly coexpressed together with the CBF3 , MYC2 , and MYB44 genes. Conclusions Cold stress led various changes in kiwifruit, the ‘phosphatidylinositol signaling system’, ‘inositol phosphate metabolism’, ‘MAPK signaling pathway’, ‘plant hormone signal transduction’, and ‘starch and sucrose metabolism’ processes were significantly affected by low temperature. Moreover, starch and sucrose metabolism may be the key pathway for tolerant kiwifruit to resist low temperature damages. These results increase our understanding of the complex mechanisms involved in the freezing tolerance of kiwifruit under cold stress and reveal a series of candidate genes for use in breeding new cultivars with enhanced freezing tolerance.

Niclosamide, a cell-permeable salicylanilide, was approved by the Food and Drug Administration for its anthelmintic efficiency. A growing body of evidence in recent years suggests that niclosamide exhibits potential tumor-suppressive activity. However, the role and molecular mechanism of niclosamide in pancreatic cancer remain unclear. In this study, niclosamide inhibited proliferation of pancreatic cancer cells (PCCs), induced apoptosis via the mitochondrial-mediated pathway, and suppressed cell migration and invasion by antagonizing epithelial-to-mesenchymal transition. Also, niclosamide inhibited tumor growth and metastasis in pancreatic cancer xenograft mouse models. Mechanistically, niclosamide exerted these therapeutic effects via targeting β-catenin. Niclosamide did not reduce β-catenin mRNA expression in PCCs, but significantly downregulated its protein level. Moreover, niclosamide induced β-catenin phosphorylation and protein degradation. Interestingly, niclosamide also induced GSK-3β phosphorylation, which is involved in the ubiquitination degradation of β-catenin. Pharmacological activation of β-catenin by methyl vanillate and β-catenin overexpression abolished the inhibitory effects of niclosamide. Furthermore, niclosamide potentiated the antitumor effect of the chemotherapy drug gemcitabine and reduced the ability of cancer immune evasion by downregulating the expression levels of PD-L1, which is involved in T cell immunity. Thus, our study indicated that niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability, and suppress pancreatic cancer progression. Niclosamide may be a potential therapeutic candidate for pancreatic cancer.