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Fabrication of hydrophobic Pd/Al_(2)O_(3)-phosphoric acid via P-O-Al bond for liquid hydrogenation reaction

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Chinese Journal of Chemical Engineering 2023年第1期53卷 232-242页

作者： lu lv Min Zhao Yanan Liu Yufei He Dianqing Li State Key Laboratory of Chemical Resource Engineering Beijing University of Chemical TechnologyBeijing 100029China Beijing Engineering Center for Hierarchical Catalysts Beijing University of Chemical TechnologyBeijing 100029China

Alumina(Al_(2)O_(3))is widely used in the chemical industry as the catalyst and support due to its high specific surface area,abundant pore size distribution and chemical stability.However,the occurrence of hydration in water environment,result in outstanding decrease in specific surface area and collapse of pore structure.In this work,dodecyl phosphoric acid(PA)is used to modify the surface of Al_(2)O_(3)to obtain a series of hydrophobic material(Al_(2)O_(3)-PA).Based on XPS and NMR analysis,PA is chemically bonded on Al_(2)O_(3)to form PAOAAl bond.Furthermore,BET and WCA results display that Al_(2)O_(3)-1PA exhibits excellent the hydrophobicity and hydrothermal stability while maintains the pore structure.Take it as the substrate to support the Pd nanoparticles,the as-prepared Pd/Al_(2)O_(3)-PA shows the superior catalytic performance in the hydrogenation of phenol and anthraquinone relative to Pd/Al_(2)O_(3),indicating the accessibility of Pd sites after PA modification.Especially,the significantly enhanced stability is also obtained in four cycles for aqueous phenol hydrogenation.This can be ascribed that the PA modification inhibits the aggregation of Pd nanoparticles and the products adhesion in the reaction process.The extension of PA coatings to monolithic catalysts could expand their current capabilities in industrial applications and warrants ongoing investigation.

关键词： Alumina modification Hydrophobic catalyst Phenol hydrogenation Anthraquinone hydrogenation Accessible Pd sites

Secure coordinated direct and untrusted relay transmissions via interference engineering

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Science China(Information Sciences) 2022年第8期65卷 213-227页

作者： lu lv Zan LI Haiyang DING Yuchen ZHOU Jian CHEN State Key Laboratory of Integrated Services Networks Xidian University National Mobile Communications Research Laboratory Southeast University School of Information and Communications National University of Defense Technology

This paper investigates the physical layer security issue of the coordinated direct and untrusted relay transmissions, considering both uplink and downlink scenarios. To effectively prevent the untrusted relay from eavesdropping on the confidential information it receives, two novel interference-assisted jamming schemes are proposed, where the inter-user interference and the artificial noise are intelligently engineered to degrade the signal reception quality at the untrusted relay, therefore enhancing the physical layer security for the uplink and downlink coordinated transmission, respectively. For each of the two proposed jamming schemes, a lower bound for the ergodic secrecy sum rate(ESSR) is derived in closed form to evaluate the secrecy performance. To obtain more system design insights, we further provide an asymptotic analysis for the ESSR scaling laws over the regimes of the high signal-to-noise ratio and a large number of antennas at the base-station. We carry out computer simulations to confirm the accuracy of the derived theoretical analysis.Our simulation results show that the proposed jamming schemes achieve a similar asymptotic performance limit to the case of using a trusted relay. Moreover, the proposed jamming schemes guarantee perfect security for both uplink and downlink coordinated transmissions, and yield a significant ESSR improvement compared with three other baseline schemes.

关键词： physical layer security untrusted relay interference exploitation coordinated transmission ergodic secrecy rate

Elucidating cellular interactome of chikungunya virus identifies host dependency factors

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Virologica Sinica 2023年第4期38卷 497-507页

作者： Peiqi Yin Xia Jian Yihan Liu Yuwen Liu lu lv Haoran Cui Leiliang Zhang Department of Clinical Laboratory Medicine The First Affiliated Hospital of Shandong First Medical University&Shandong Provincial Qianfoshan HospitalJinan250013China NHC Key Laboratory of Systems Biology of Pathogens Institute of Pathogen BiologyChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing100176China Department of Pathogen Biology School of Clinical and Basic Medical SciencesShandong First Medical University&Shandong Academy of Medical SciencesJinan250117China Medical Science and Technology Innovation Center Shandong First Medical University&Shandong Academy of Medical SciencesJinan250117China

Chikungunya virus(CHIKV)is a re-emerging mosquito-transmitted RNA virus causing joint and muscle pain.To better understand how CHIKV rewires the host cell and usurps host cell functions,we generated a systematic CHIKV-human protein-protein interaction map and revealed several novel connections that will inform further mechanistic studies.One of these novel interactions,between the viral protein E1 and STIP1 homology and U-box containing protein 1(STUB1),was found to mediate ubiquitination of E1 and degrade E1 through the proteasome.Capsid associated with G3BP1,G3BP2 and AAAþATPase valosin-containing protein(VCP).Furthermore,VCP inhibitors blocked CHIKV infection,suggesting VCP could serve as a therapeutic target.Further work is required to fully understand the functional consequences of these interactions.Given that CHIKV proteins are conserved across alphaviruses,many virus-host protein-protein interactions identified in this study might also exist in other alphaviruses.Construction of interactome of CHIKV provides the basis for further studying the function of alphavirus biology.

关键词： Chikungunya virus(CHIKV) Interactome STIP1 homology and U-box containing protein 1(STUB1) Valosin-containing protein(VCP) Capsid

Prediction of treatment response to antipsychotic drugs for precision medicine approach to schizophrenia:randomized trials and multiomics analysis

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Military Medical Research 2024年第1期11卷 19-33页

作者： Liang-Kun Guo Yi Su Yu-Ya-Nan Zhang Hao Yu Zhe lu Wen-Qiang Li Yong-Feng Yang Xiao Xiao Hao Yan Tian-Lan lu Jun Li Yun-Dan Liao Zhe-Wei Kang Li-Fang Wang Yue Li Ming Li Bing Liu Hai-Liang Huang lu-Xian lv Yin Yao Yun-Long Tan Gerome Breen Ian Everall Hong-Xing Wang Zhuo Huang Dai Zhang Wei-Hua Yue Institute of Mental Health Peking University Sixth HospitalBeijing 100191China National Clinical Research Center for Mental Disorders Peking University Sixth HospitalBeijing 100191China NHC Key Laboratory of Mental Health and Research Unit of Diagnosis and Treatment of Mood Cognitive Disorder(2018RU006) Chinese Academy of Medical SciencesBeijing 100191China Peking University Huilongguan Clinical Medical School Beijing Huilongguan HospitalBeijing 100096China Department of Psychiatry Jining Medical UniversityJining 272067ShandongChina Henan Key Lab of Biological Psychiatry the Second Affiliated Hospital of Xinxiang Medical UniversityXinxiang 435001HenanChina Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province Kunming Institute of ZoologyChinese Academy of SciencesKunming 650223China Institute of Psychiatry Psychology and NeuroscienceKing’s College LondonLondon WC2R 2LSUK State Key Laboratory of Cognitive Neuroscience and Learning Beijing Normal UniversityBeijing 100875China Analytic and Translational Genetics Unit Massachusetts General HospitalBostonMA 02114USA Stanley Center for Psychiatric Research the Broad Institute of MIT and HarvardCambridgeMA 02141USA Department of Medicine Harvard Medical SchoolBostonMA 02115USA Department of Biostatistics and Computational Biology School of Life SciencesFudan UniversityShanghai 200438China Department of Neurology Xuanwu HospitalCapital Medical UniversityBeijing 100053China State Key Laboratory of Natural and Biomimetic Drugs Key Laboratory for Neuroscience for Ministry of EducationSchool of Pharmaceutical SciencesPeking University Health Science CenterBeijing 100191China PKU-IDG/McGovern Institute for Brain Research Peking UniversityBeijing 100871China Chinese Institute for Brain Research Beijing 102206China

Background:Choosing the appropriate antipsychotic drug(APD)treatment for patients with schizophrenia(SCZ)can be challenging,as the treatment response to APD is highly variable and difficult to predict due to the lack of effective biomarkers.Previous studies have indicated the association between treatment response and genetic and epigenetic factors,but no effective biomarkers have been identified.Hence,further research is imperative to enhance precision medicine in SCZ treatment.Methods:Participants with SCZ were recruited from two randomized trials.The discovery cohort was recruited from the CAPOC trial(n=2307)involved 6 weeks of treatment and equally randomized the participants to the Olanzapine,Risperidone,Quetiapine,Aripiprazole,Ziprasidone,and Haloperidol/Perphenazine(subsequently equally assigned to one or the other)groups.The external validation cohort was recruited from the CAPEC trial(n=1379),which involved 8 weeks of treatment and equally randomized the participants to the Olanzapine,Risperidone,and Aripiprazole groups.Additionally,healthy controls(n=275)from the local community were utilized as a genetic/epigenetic reference.The genetic and epigenetic(DNA methylation)risks of SCZ were assessed using the polygenic risk score(PRS)and polymethylation score,respectively.The study also examined the genetic-epigenetic interactions with treatment response through differential methylation analysis,methylation quantitative trait loci,colocalization,and promoteranchored chromatin interaction.Machine learning was used to develop a prediction model for treatment response,which was evaluated for accuracy and clinical benefit using the area under curve(AUC)for classification,R^(2) for regression,and decision curve analysis.Results:Six risk genes for SCZ(LINC01795,DDHD2,SBNO1,KCNG2,SEMA7A,and RUFY1)involved in cortical morphology were identified as having a genetic-epigenetic interaction associated with treatment response.The developed and externally validated prediction model,which incorporated clinical information,

关键词： Schizophrenia Antipsychotic drug Treatment response Prediction model Genetics Epigenetics

Multiomics reveal human umbilical cord mesenchymal stem cells improving acute lung injury via the lung-gut axis

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世界干细胞杂志:英文版(电子版) 2023年第9期15卷 908-930页

作者： lu lv En-Hai Cui Bin Wang Li-Qin Li Feng Hua Hua-Dong lu Na Chen Wen-Yan Chen Department of Respiratory and Critical Care Medicine Huzhou Central HospitalAffiliated Huzhou HospitalZhejiang University School of MedicineHuzhou 313000Zhejiang ProvinceChina Traditional Chinese Medicine Key Laboratory Cultivation Base of Zhejiang Province for the Development and Clinical Transformation of Immunomodulatory Drugs Huzhou 313000Zhejiang ProvinceChina

BACKGROUND Acute lung injury(ALI)and its final severe stage,acute respiratory distress syndrome,are associated with high morbidity and mortality rates in patients due to the lack of effective specific treatments.Gut microbiota homeostasis,including that in ALI,is important for human health.Evidence suggests that the gut microbiota improves lung injury through the lung-gut axis.Human umbilical cord mesenchymal cells(HUC-MSCs)have attractive prospects for ALI treatment.This study hypothesized that HUC-MSCs improve ALI via the lung-gut microflora.AIM To explore the effects of HUC-MSCs on lipopolysaccharide(LPS)-induced ALI in mice and the involvement of the lung-gut axis in this process.METHODS C57BL/6 mice were randomly divided into four groups(18 rats per group):Sham,sham+HUC-MSCs,LPS,and LPS+HUC-MSCs.ALI was induced in mice by intraperitoneal injections of LPS(10 mg/kg).After 6 h,mice were intervened with 0.5 mL phosphate buffered saline(PBS)containing 1×10^(6) HUC-MSCs by intraperitoneal injections.For the negative control,100 mL 0.9%NaCl and 0.5 mL PBS were used.Bronchoalveolar lavage fluid(BALF)was obtained from anesthetized mice,and their blood,lungs,ileum,and feces were obtained by an aseptic technique following CO_(2) euthanasia.Wright’s staining,enzyme-linked immunosorbent assay,hematoxylin-eosin staining,Evans blue dye leakage assay,immunohistochemistry,fluorescence in situ hybridization,western blot,16S rDNA sequencing,and non-targeted metabolomics were used to observe the effect of HUC-MSCs on ALI mice,and the involvement of the lung-gut axis in this process was explored.One-way analysis of variance with post-hoc Tukey’s test,independent-sample Student’s t-test,Wilcoxon rank-sum test,and Pearson correlation analysis were used for statistical analyses.RESULTS HUC-MSCs were observed to improve pulmonary edema and lung and ileal injury,and decrease mononuclear cell and neutrophil counts,protein concentrations in BALF and inflammatory cytokine levels in the serum,lung,and ileum of ALI mice.Especially,HUC-MS

关键词： Acute lung injury Human umbilical cord mesenchymal cells Lipopolysaccharide Microflora Untargeted metabolomics Toll-like receptor 4/nuclear factor kappa-B signaling pathway

Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma

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Journal of Molecular Cell Biology 2023年第7期15卷 15-30页

作者： Honglu Liu Huanyi Fu Chunhong Yu Na Zhang Canhua Huang lu lv Chunhong Hu Fang Chen Zhiqiang Xiao Zhuohua Zhang Huasong lu Kai Yuan Hunan Key Laboratory of Molecular Precision Medicine Department of OncologyXiangya HospitalCentral South UniversityChangsha 410008China Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology Life Sciences InstituteZhejiang UniversityHangzhou 310058China Hunan Key Laboratory of Medical Genetics School of Life SciencesCentral South UniversityChangsha 410008China Department of Oncology The Second Xiangya HospitalCentral South UniversityChangsha 410011China Research Center of Carcinogenesis and Targeted Therapy Xiangya HospitalCentral South UniversityChangsha 410008China National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangsha 410008China The Biobank of Xiangya Hospital Central South UniversityChangsha 410008China

Lesions on the DNA template can impact transcription via distinct regulatory pathways.Ionizing radiation(IR)as the mainstay modality for many malignancies elicits most of the cytotoxicity by inducing a variety of DNA damages in the genome.How the IR treatment alters the transcription cycle and whether it contributes to the development of radioresistance remain poorly understood.Here,we report an increase in the paused RNA polymerase II(RNAPII),as indicated by the phosphorylation at serine 5 residue of its C-terminal domain,in recurrent nasopharyngeal carcinoma(NPC)patient samples after IR treatment and cultured NPC cells developing IR resistance.Reducing the pool of paused RNAPII by either inhibiting TFIIH-associated CDK7 or stimulating the positive transcription elongation factor b,a CDK9-CycT1 heterodimer,attenuates IR resistance of NPC cells.Interestingly,the poly(ADP-ribosyl)ation of CycT1,which disrupts its phase separation,is elevated in the IR-resistant cells.Mutation of the major poly(ADP-ribosyl)ation sites of CycT1 decreases RNAPII pausing and restores IR sensitivity.Genome-wide chromatin immunoprecipitation followed by sequencing analyses reveal that several genes involved in radiation response and cell cycle control are subject to the regulation imposed by the paused RNAPII.Particularly,we identify the NIMA-related kinase NEK7 under such regulation as a new radioresistancefactor,whose downregulation results in the increased chromosome instability,enabling the development of IR resistance.Overall,our results highlight a novel link between the alteration in the transcription cycle and the acquisition of IR resistance,opening up new opportunities to increase the efficacy of radiotherapy and thwart radioresistance in NpC.

关键词： RNA polymerase II transcriptional pausing radioresistance CDK7 NEK7 nasopharyngeal carcinoma

Rif1 interacts with non-canonical polycomb repressive complex PRC1.6 to regulate mouse embryonic stem cells fate potential

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Cell Regeneration 2022年第1期11卷 246-266页

作者： lu Li Pishun Li Jiale Chen Li Li Yunfan Shen Yangzixuan Zhu Jiayi Liu lu lv Song Mao Fang Chen Guang Hu Kai Yuan Hunan Key Laboratory of Molecular Precision Medicine Department of OncologyXiangya HospitalCentral South UniversityChangshaHunanChina Hunan Key Laboratory of Medical Genetics School of Life SciencesCentral South UniversityChangshaHunanChina Changjun High School ChangshaHunanChina Zhounan High School ChangshaHunanChina Epigenetics and Stem Cell Biology Laboratory National Institute of Environ-mental Health SciencesResearch Triangle ParkNC 2779USA National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangshaHunanChina The Biobank of Xiangya Hospital Central South UniversityChangshaHunanChina

Mouse embryonic stem cells(mESCs)cycle in and out of a transient 2-cell(2C)-like totipotent state,driven by a com-plex genetic circuit involves both the coding and repetitive sections of the genome.While a vast array of regulators,including the multi-functional protein Rif1,has been reported to influence the switch of fate potential,how they act in concert to achieve this cellular plasticity remains elusive.Here,by modularizing the known totipotency regulatory factors,we identify an unprecedented functional connection between Rif1 and the non-canonical polycomb repres-sive complex PRC1.6.Downregulation of the expression of either Rif1 or PRC1.6 subunits imposes similar impacts on the transcriptome of mESCs.The LacO-LacI induced ectopic colocalization assay detects a specific interaction between Rif1 and Pcgf6,bolstering the intactness of the PRC1.6 complex.Chromatin immunoprecipitation followed by sequencing(ChIP-seq)analysis further reveals that Rif1 is required for the accurate targeting of Pcgf6 to a group of genomic loci encompassing many genes involved in the regulation of the 2C-like state.Depletion of Rif1 or Pcgf6 not only activates 2C genes such as Zscan4 and Zfp352,but also derepresses a group of the endogenous retroviral element MERVL,a key marker for totipotency.Collectively,our findings discover that Rif1 can serve as a novel auxiliary component in the PRC1.6 complex to restrain the genetic circuit underlying totipotent fate potential,shedding new mechanistic insights into its function in regulating the cellular plasticity of embryonic stem cells.

关键词： 2C-like Totipotency MERVL Rif1 PRC1.6

Rewiring the transcriptional circuitries in cancer by endogenous retroviruses

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Journal of Molecular Cell Biology 2022年第8期14卷 67-68页

作者： Li Li Yinshuang Li lu lv Kai Yuan Hunan Key Laboratory of Molecular Precision Medicine Department of OncologyXiangya HospitalCentral South UniversityChangsha 410000China The Biobank of Xiangya Hospital Central South UniversityChangsha 410000China

With sequence similarities to exogenous retroviruses,the proviral DNA elements named endogenous retroviruses(ERVs)make up∼8% of human genome,threatening genomic stability meanwhile nurturing regulatory innovations.Diverse host epigenetic mechanisms are enlisted to limit the ERVs’activity.However,in certain physiological and pathophysiological processes,distinct ERVs become abnormally activated,rewiring and perplexing the host regulons at different levels(Cosby et al.,2019).

关键词： endogenous al. listed

Protein O-GlcNAcylation homeostasis regulates facultative heterochromatin to fine-tune sog-Dpp signaling during Drosophila early embryogenesis

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Journal of Genetics and Genomics 2023年第12期50卷 948-959页

作者： Yaowen Zhang Haibin Yu Dandan Wang Xiaoyun Lei Yang Meng Na Zhang Fang Chen lu lv Qian Pan Hongtao Qin Zhuohua Zhang Daan M.F.van Aalten Kai Yuan Center for Medical Genetics School of Life Sciences&Hunan Key Laboratory of Molecular Precision MedicineDepartment of OncologyXiangya HospitalCentral South UniversityChangshaHunan 410008China State Key Laboratory of Chemo/Biosensing and Chemometrics College of BiologyHunan UniversityChangshaHunan 410082China National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangshaHunan 410008China Division of Cell and Developmental Biology School of Life SciencesUniversity of DundeeDundee DD15EHUK Department of Molecular Biology and Genetics University of AarhusAarhus 8000Denmark The Biobank of Xiangya Hospital Central South UniversityChangshaHunan 410008China

Protein O-GlcNAcylation is a monosaccharide post-translational modification maintained by two evolutionarily conserved enzymes, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Mutations in human OGT have recently been associated with neurodevelopmental disorders, although the mechanisms linking O-GlcNAc homeostasis to neurodevelopment are not understood. Here, we investigate the effects of perturbing protein O-GlcNAcylation using transgenic Drosophila lines that overexpress a highly active OGA. We reveal that temporal reduction of protein O-GlcNAcylation in early embryos leads to reduced brain size and olfactory learning in adult Drosophila. Downregulation of O-GlcNAcylation induced by the exogenous OGA activity promotes nuclear foci formation of Polycomb-group protein Polyhomeotic and the accumulation of excess K27 trimethylation of histone H3 (H3K27me3) at the mid-blastula transition. These changes interfere with the zygotic expression of several neurodevelopmental genes, particularly short gastrulation (sog), a component of an evolutionarily conserved sog-Decapentaplegic (Dpp) signaling system required for neuroectoderm specification. Our findings highlight the importance of early embryonic O-GlcNAcylation homeostasis for the fidelity of facultative heterochromatin redeployment and initial cell fate commitment of neuronal lineages, suggesting a possible mechanism underpinning OGT-associated intellectual disability.

关键词： Protein O-GlcNAcylation Drosophila Early embryogenesis Polycomb repressive complex Facultative heterochromatin Neurodevelopment sog