المؤلفون: Ren, Yan, Zheng, Yang, Wang, Xiaojing, Qu, Shuang, Sun, Lijun, Song, Chenyong, Ding, Jia, Ji, Yuetong, Wang, Guoze, Zhu, Pengfei, Cheng, Likun

المصدر: Frontiers in Microbiology ; volume 15 ; ISSN 1664-302X

مصطلحات موضوعية: Microbiology (medical), Microbiology

الوصف: Rapid and accurate identification of lactic acid bacteria (LAB) species would greatly improve the screening rate for functional LAB. Although many conventional and molecular methods have proven efficient and reliable, LAB identification using these methods has generally been slow and tedious. Single-cell Raman spectroscopy (SCRS) provides the phenotypic profile of a single cell and can be performed by Raman spectroscopy (which directly detects vibrations of chemical bonds through inelastic scattering by a laser light) using an individual live cell. Recently, owing to its affordability, non-invasiveness, and label-free features, the Ramanome has emerged as a potential technique for fast bacterial detection. Here, we established a reference Ramanome database consisting of SCRS data from 1,650 cells from nine LAB species/subspecies and conducted further analysis using machine learning approaches, which have high efficiency and accuracy. We chose the ensemble meta-classifier (EMC), which is suitable for solving multi-classification problems, to perform in-depth mining and analysis of the Ramanome data. To optimize the accuracy and efficiency of the machine learning algorithm, we compared nine classifiers: LDA, SVM, RF, XGBoost, KNN, PLS-DA, CNN, LSTM, and EMC. EMC achieved the highest average prediction accuracy of 97.3% for recognizing LAB at the species/subspecies level. In summary, Ramanomes, with the integration of EMC, have promising potential for fast LAB species/subspecies identification in laboratories and may thus be further developed and sharpened for the direct identification and prediction of LAB species from fermented food.

الإتاحة: https://doi.org/10.3389/fmicb.2024.1361180Test

المؤلفون: Ding, Ming-Chao, Jing, Bo-Ya, Shi, Jin, Yang, Liu, Liu, Xiang-Dong, Wang, Jing-Fu, Qu, Shuang, Liang, Jia-Wu, Tang, Zi-Hao, Zhao, Jin-Long, Tian, Lei

المصدر: Chinese Journal of Traumatology ; ISSN 1008-1275

مصطلحات موضوعية: Orthopedics and Sports Medicine, Surgery

الإتاحة: https://doi.org/10.1016/j.cjtee.2024.03.004Test
https://api.elsevier.com/content/article/PII:S1008127524000300?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1008127524000300?httpAccept=text/plainTest

المؤلفون: Qu, Shuang, Yang, Chen, Sun, Xinlei, Huang, Hai, Li, Jiacheng, Zhu, Yujie, Zhang, Yaliang, Li, Limin, Liang, Hongwei, Zen, Ke

المساهمون: China Postdoctoral Science Foundation, Program for Jiangsu Excellent Scientific and Technological Innovation Team

المصدر: International Journal of Antimicrobial Agents ; volume 63, issue 5, page 107124 ; ISSN 0924-8579

مصطلحات موضوعية: Pharmacology (medical), Infectious Diseases, Microbiology (medical), General Medicine

الإتاحة: https://doi.org/10.1016/j.ijantimicag.2024.107124Test
https://api.elsevier.com/content/article/PII:S0924857924000426?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0924857924000426?httpAccept=text/plainTest

المؤلفون: Xu, Xiaodong, Qu, Shuang, Zhang, Changming, Zhang, Mingchao, Qin, Weisong, Ren, Guisheng, Bao, Hao, Li, Limin, Zen, Ke, Liu, Zhihong

المساهمون: National Key Research and Development Program of China, National Natural Science Foundation of China, China Postdoctoral Science Foundation

المصدر: Advanced Science ; volume 10, issue 25 ; ISSN 2198-3844 2198-3844

الوصف: T cells play an important role in the development of focal segmental glomerulosclerosis (FSGS). The mechanism underlying such T cell‐based kidney disease, however, remains elusive. Here the authors report that activated CD8 T cells elicit renal inflammation and tissue injury via releasing miR‐186‐5p‐enriched exosomes. Continuing the cohort study identifying the correlation of plasma level of miR‐186‐5p with proteinuria in FSGS patients, it is demonstrated that circulating miR‐186‐5p is mainly derived from activated CD8 T cell exosomes. Renal miR‐186‐5p, which is markedly increased in FSGS patients and mice with adriamycin‐induced renal injury, is mainly delivered by CD8 T cell exosomes. Depleting miR‐186‐5p strongly attenuates adriamycin‐induced mouse renal injury. Supporting the function of exosomal miR‐186‐5p as a key circulating pathogenic factor, intravenous injection of miR‐186‐5p or miR‐186‐5p‐containing T cell exosomes results in mouse renal inflammation and tissue injury. Tracing the injected T cell exosomes shows their preferential distribution in mouse renal tubules, not glomerulus. Mechanistically, miR‐186‐5p directly activates renal tubular TLR7/8 signal and initiates tubular cell apoptosis. Mutating the TLR7‐binding sequence on miR‐186‐5p or deleting mouse TLR7 largely abolishes renal tubular injuries induced by miR‐186‐5p or adriamycin. These findings reveal a causative role of exosomal miR‐186‐5p in T cell‐mediated renal dysfunction.

الإتاحة: https://doi.org/10.1002/advs.202301492Test

المؤلفون: Qu,Shuang, Huang,Xiaoli, Guo,Xiaoling, Zheng,Zhihai, Wei,Tiannan, Chen,Biyun

مصطلحات موضوعية: Drug Design, Development and Therapy

الوصف: Shuang Qu,1,* Xiaoli Huang,2,* Xiaoling Guo,3 Zhihai Zheng,1 Tiannan Wei,1 Biyun Chen1 1Department of Hematology, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, People’s Republic of China; 2Department of Clinical Laboratory Medicine, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, People’s Republic of China; 3Translational Medicine Centre, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China*These authors contributed equally to this workCorrespondence: Shuang Qu, Email shuangerqu@163.comBackground: Acute myeloid leukemia (AML) is a highly heterogenous disease with varying clinical outcomes among patients. Epithelial-mesenchymal transition (EMT) is an important mechanism underlying cancer metastasis and chemotherapy resistance. However, few EMT-based signatures have been established to predict AML prognosis and treatment efficacy.Methods: By conducting comparative RNA-seq analysis, we discovered the differential expression of EMT genes between AML patients with relapse and those without relapse. Based on the prognostic analysis of the differentially expressed EMT genes, a metastasis-related EMT signature (MEMTs) was constructed. An analysis was conducted on both TARGET and TCGA cohorts to explore the possible association between MEMTs and prognosis in AML. Three separate chemotherapy treatment cohorts were utilized to assess the predictive efficacy of MEMTs for chemotherapy response. In addition, the potential correlation between MEMTs and the tumor microenvironment was also investigated. Finally, random forest analysis and functional experiments were conducted to verify the key MEMTs gene associated with AML metastasis.Results: Based on expression and prognostic analysis, we constructed MEMTs that include three EMT genes (CDH2, LOX, and COL3A1). Our findings suggested that the MEMTs could act as a prognostic factor for AML patients, and furthermore, it proved to be ...

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العلاقة: https://www.dovepress.com/metastasis-related-epithelial-mesenchymal-transition-signature-predict-peer-reviewed-fulltext-article-DDDTTest

الإتاحة: https://doi.org/10.2147/DDDT.S415521Test
https://www.dovepress.com/metastasis-related-epithelial-mesenchymal-transition-signature-predict-peer-reviewed-fulltext-article-DDDTTest

المؤلفون: Yao, Bing, Xing, Mengying, Meng, Shixin, Li, Shang, Zhou, Jingwan, Zhang, Ming, Yang, Chen, Qu, Shuang, Jin, Yucui, Yuan, Hongyan, Zen, Ke, Ma, Changyan

المساهمون: National Natural Science Foundation of China, Natural Science Foundation of Jiangsu Province

المصدر: Advanced Science ; volume 11, issue 2 ; ISSN 2198-3844 2198-3844

الوصف: Mono‐methylation of histone H3 on Lys 4 (H3K4me1), which is catalyzed by histone‐lysine N‐methyltransferase 2D (KMT2D), serves as an important epigenetic regulator in transcriptional control. In this study, the authors identify early B‐cell factor 2 (EBF2) as a binding protein of H3K4me1. Combining analyses of RNA‐seq and ChIP‐seq data, the authors further identify killin (KLLN) as a transcriptional target of KMT2D and EBF2 in pancreatic ductal adenocarcinoma (PDAC) cells. KMT2D‐dependent H3K4me1 and EBF2 are predominantly over‐lapped proximal to the transcription start site (TSS) of KLLN gene. Comprehensive functional assays show that KMT2D and EBF2 cooperatively inhibit PDAC cells proliferation, migration, and invasion through upregulating KLLN. Such inhibition on PDAC progression is also achieved through increasing H3K4me1 level by GSK‐LSD1, a selective inhibitor of lysine‐specific demethylase 1 (LSD1). Taken together, these findings reveal a new mechanism underlying PDAC progression and provide potential therapeutic targets for PDAC treatment.

الإتاحة: https://doi.org/10.1002/advs.202302037Test

المؤلفون: Liu, Jiachen, Li, Weili, Li, Jianfeng, Song, Eli, Liang, Hongwei, Rong, Weiwei, Jiang, Xinli, Xu, Nuo, Wang, Wei, Qu, Shuang, Gu, Shouyong, Zhang, Yujing, Yu Zhang, Chen‐, Zen, Ke

المساهمون: National Natural Science Foundation of China

المصدر: Advanced Science ; volume 10, issue 24 ; ISSN 2198-3844 2198-3844

الوصف: Extracellular microRNAs (miRNAs) play a critical role in horizontal gene regulation. Uptake of extracellular miRNAs by recipient cells and their intracellular transport, however, remains elusive. Here RNA phase separation is shown as a novel pathway of miRNA uptake. In the presence of serum, synthetic miRNAs rapidly self‐assembly into ≈110 nm discrete nanoparticles, which enable miRNAs’ entry into different cells. Depleting serum cationic proteins prevents the formation of such nanoparticles and thus blocks miRNA uptake. Different from lipofectamine‐mediated miRNA transfection in which majority of miRNAs are accumulated in lysosomes of transfected cells, nanoparticles‐mediated miRNA uptake predominantly delivers miRNAs into mitochondria in a polyribonucleotide nucleotidyltransferase 1(PNPT1)‐dependent manner. Functional assays further show that the internalized miR‐21 via miRNA phase separation enhances mitochondrial translation of cytochrome b (CYB), leading to increase in adenosine triphosphate (ATP) and reactive oxygen species (ROS) reduction in HEK293T cells. The findings thus reveal a previously unrecognized mechanism for uptake and delivery functional extracellular miRNAs into mitochondria.

الإتاحة: https://doi.org/10.1002/advs.202300452Test

المؤلفون: Chen, Shengqun, Chen, Yingfu, Liang, Mei, Qu, Shuang, Shen, Lianwen, Zeng, Yajun, Hou, Na

المساهمون: The National Natural Science Foundation of China, Innovation and Application of Guizhou Walnut Germplasm, Study on the Vitality and Stigma of Guizhou Wuren Walnut Pollen, The Bridging Project for the Enterprises and the Local walnut R&D Groups in Guizhou Province

المصدر: BMC Genomics ; volume 24, issue 1 ; ISSN 1471-2164

مصطلحات موضوعية: Genetics, Biotechnology

الوصف: Background Juglans sigillata L. (walnut) has a high economic value for nuts and wood and has been widely grown and eaten around the world. Light plays an important role in regulating the development of the walnut embryo and promoting nucleolus enlargement, which is one of the factors affecting the yield and quality of walnut. However, little is known about the effect of light on the growth and quality of walnuts. Studies have shown that far red prolonged hypocotyl 3 (FHY3) and far red damaged response (FAR1) play important roles in plant growth, light response, and resistance. Therefore, FHY3/FAR1 genes were identified in walnuts on a genome-wide basis during their growth and development to reveal the potential regulation mechanisms involved in walnut kernel growth and development. Results In the present study, a total of 61 FHY3/FAR1 gene family members in walnuts have been identified, ranging in length from 117 aa to 895 aa. These gene family members have FHY3 or FAR1 conserved domains, which are unevenly distributed on the 15 chromosomes (Chr) of the walnut (except for the Chr16). All 61 FHY3/FAR1 genes were divided into five subclasses (I, II, III, IV, and V) by phylogenetic tree analysis. The results indicated that FHY3/FAR1 genes in the same subclasses with similar structures might be involved in regulating the growth and development of walnut. The gene expression profiles were analyzed in different walnut kernel varieties (Q, T, and F). The result showed that some FHY3/FAR1 genes might be involved in the regulation of walnut kernel ripening and seed coat color formation. Seven genes ( OF07056-RA , OF09665-RA , OF24282-RA , OF26012-RA , OF28029-RA , OF28030-RA , and OF08124-RA ) were predicted to be associated with flavonoid biosynthetic gene regulation cis-acting elements in promoter sequences. RT-PCR was used to verify the expression levels of candidate genes during the development and color change of walnut kernels. In addition, light responsiveness and MeJA responsiveness are important ...

الإتاحة: https://doi.org/10.1186/s12864-023-09629-2Test

المؤلفون: Zhu, Yujie, Zhang, Mingchao, Wang, Weiran, Qu, Shuang, Liu, Minghui, Rong, Weiwei, Yang, Wenwen, Liang, Hongwei, Zeng, Caihong, Zhu, Xiaodong, Li, Limin, Liu, Zhihong, Zen, Ke

المصدر: Nature Communications ; volume 14, issue 1 ; ISSN 2041-1723

مصطلحات موضوعية: General Physics and Astronomy, General Biochemistry, Genetics and Molecular Biology, General Chemistry, Multidisciplinary

الوصف: Renal tubular atrophy is a hallmark of chronic kidney disease. The cause of tubular atrophy, however, remains elusive. Here we report that reduction of renal tubular cell polynucleotide phosphorylase (PNPT1) causes renal tubular translation arrest and atrophy. Analysis of tubular atrophic tissues from renal dysfunction patients and male mice with ischemia-reperfusion injuries (IRI) or unilateral ureteral obstruction (UUO) treatment shows that renal tubular PNPT1 is markedly downregulated under atrophic conditions. PNPT1 reduction leads to leakage of mitochondrial double-stranded RNA (mt-dsRNA) into the cytoplasm where it activates protein kinase R (PKR), followed by phosphorylation of eukaryotic initiation factor 2α (eIF2α) and protein translational termination. Increasing renal PNPT1 expression or inhibiting PKR activity largely rescues IRI- or UUO-induced mouse renal tubular injury. Moreover, tubular-specific PNPT1-knockout mice display Fanconi syndrome-like phenotypes with impaired reabsorption and significant renal tubular injury. Our results reveal that PNPT1 protects renal tubules by blocking the mt-dsRNA-PKR-eIF2α axis.

الإتاحة: https://doi.org/10.1038/s41467-023-36664-0Test
https://www.nature.com/articles/s41467-023-36664-0.pdfTest
https://www.nature.com/articles/s41467-023-36664-0Test

المؤلفون: Zhao, Tingting, Zhan, Dongdong, Qu, Shuang, Jiang, Song, Gan, Wenhua, Qin, Weisong, Zheng, Chunxia, Cheng, Fang, Lu, Yinghui, Liu, Mingwei, Shi, Jinsong, Liang, Hongwei, Wang, Yi, Qin, Jun, Zen, Ke, Liu, Zhihong

المساهمون: National Key Research and Development Program, the Project of Jinling Hospital, the Project of Clinical Research Center for Kidney Diseases of Jiangsu Province, Key R&D Projects of Jiangsu Province, National Natural Science Foundation of China

المصدر: Journal of Translational Medicine ; volume 21, issue 1 ; ISSN 1479-5876

مصطلحات موضوعية: General Biochemistry, Genetics and Molecular Biology, General Medicine

الوصف: Background Diabetic nephropathy (DN) is a complex disease involving the upregulation of many inflammation-related proteins. Alternative polyadenylation (APA), a crucial post-transcriptional regulatory mechanism, has been proven to play vital roles in many inflammatory diseases. However, it is largely unknown whether and how APA exerts function in DN. Methods We performed transcriptomics and proteomics analysis of glomeruli samples isolated from 50 biopsy-proven DN patients and 25 control subjects. DaPars and QAPA algorithms were adopted to identify APA events from RNA-seq data. The qRT-PCR analysis was conducted to verify 3′UTR length alteration. Short and long 3ʹUTRs isoforms were also overexpressed in podocytes under hyperglycemia condition for examining protein expression. Results We detected transcriptome-wide 3′UTR APA events in DN, and found that APA-mediated 3ʹUTR lengthening of genes (APA genes) increased their expression at protein but not mRNA level. Increased protein level of 3′UTR lengthening gene was validated in podocytes under hyperglycemia condition. Pathway enrichment analysis showed that APA genes were enriched in inflammation-related biological processes including endoplasmic reticulum stress pathways, NF-κB signaling and autophagy. Further bioinformatics analysis demonstrated that 3′UTR APA of genes probably altered the binding sites for RNA-binding proteins, thus enhancing protein translation. Conclusion This study revealed for the first time that 3′UTR lengthening of APA genes contributed to the progression of DN by elevating the translation of corresponding proteins, providing new insight and a rich resource for investigating DN mechanisms.

الإتاحة: https://doi.org/10.1186/s12967-023-03934-wTest