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Food Science and human Wellness 2024年第4期13卷 1845-1855页

作者： Jiang Cao Leilei Yu Jianxin Zhao Hao Zhang Wei Chen Yuzheng Xue Qixiao Zhai State key laboratory of Food Science and Technology Jiangnan UniversityWuxi 214122China School of Food Science and Technology Jiangnan UniversityWuxi 214122China National Engineering Research Center for Functional Food Jiangnan UniversityWuxi 214122China Wuxi Translational medicine Research Center and Jiangsu Translational medicine Research Institute Wuxi Branch Wuxi 214122China Department of Gastroenterology Affiliated Hospital of Jiangnan UniversityWuxi 214122China

The high intraspecies heterogeneity of Baciillus coagulans leads to significant phenotypic differences among different strains.Thus,6 B.coagulans strains were tested in the present study using an irritable bowel syndrome(IBS)animal model to determine whether the IBS-alleviating effects of B.coagulans strains are strain-specific.The results of this study showed that the ingestion of B.coagulans GBI-30,6086,and B.coagulans CCFM1041 significantly alleviated IBS symptoms in mice.In contrast,other B.coagulans strains showed no or limited alleviating effects on IBS symptoms.According to our experimental results,the two main common features of these strains were as follows:1)The resistance of vegetative cells to bile salts,and 2)ability to synthesize specific lipids and secondary metabolites.Screening strains based on these two indicators may greatly reduce costs and provide a basis for mining new functional B.coagulans strains.Our results also suggest that administration of B.coagulans could significantly regulate microbiota dysbiosis in animal models.Moreover,the close relationships between the gut microbiota,gut microbiota metabolites,and IBS were further confirmed in this study.

关键词： Baciillus coagulans Irritable bowel syndrome Resistance to bile salts comparative genomic analysis Gut microbiota

Progress in nanoparticle-based regulation of immune cells

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Medical Review 2023年第2期3卷 152-179页

作者： Ya-Nan Fan Gui Zhao Yue Zhang Qian-Ni Ye Yi-Qun Sun Song Shen Yang Liu Cong-Fei Xu Jun Wang School of Biomedical Sciences and Engineering South China University of TechnologyGuangzhou International CampusGuangzhouGuangdong ProvinceChina National Engineering Research Center for Tissue Restoration and Reconstruction South China University of TechnologyGuangzhouGuangdong ProvinceChina key laboratory of Biomedical Materials and Engineering of the Ministry of Education South China University of TechnologyGuangzhouGuangdong ProvinceChina Department of Biomedical Engineering Wake Forest School of MedicineWinston-SalemNCUSA School of Biomedical Sciences and Engineering South China University of TechnologyGuangzhou International CampusGuangzhou 511442Guangdong ProvinceChina National Engineering Research Center for Tissue Restoration and Reconstruction South China University of TechnologyGuangzhou 510006Guangdong ProvinceChina Guangdong Provincial key laboratory of Biomedical Engineering South China University of TechnologyGuangzhou 510006Guangdong ProvinceChina

Immune cells are indispensable defenders of the human body,clearing exogenous pathogens and toxicities or endogenous malignant and aging cells.Immune cell dysfunction can cause an inability to recognize,react,and remove these hazards,resulting in cancers,inflammatory diseases,autoimmune diseases,and infections.Immune cells regulation has shown great promise in treating disease,and immune agonists are usually used to treat cancers and infections caused by immune suppression.In contrast,immunosuppressants are used to treat inflammatory and autoimmune diseases.However,the key to maintaining health is to restore balance to the immune system,as excessive activation or inhibition of immune cells is a common complication of immunotherapy.Nanoparticles are efficient drug delivery systems widely used to deliver small molecule inhibitors,nucleic acid,and proteins.Using nanoparticles for the targeted delivery of drugs to immune cells provides opportunities to regulate immune cell function.In this review,we summarize the current progress of nanoparticle-based strategies for regulating immune function and discuss the prospects of future nanoparticle design to improve immunotherapy.

关键词： biomaterial drug delivery immune cell immunotherapy nanoparticle

hTERT-targeted E.coli purine nucleoside phosphorylase gene/ 6-methylpurine deoxyribose therapy for pancreatic cancer

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Chinese Medical Journal 2007年第15期120卷 1348-1352页

作者： ZHOU Jia-hua TANG Bo LIU Xun-liang HE Dao-wei YANG De-tong Department of Biliary-Pancreatic Surgery First Affiliated Hospital of Nanjing Medical University Nanjing 210029 China National key Opening laboratory of Biology and medicine and Pharmacology Technology Nanjing University Nanjing 210008 China Clinical medicine School of Southeast University Nanjing 210009 China Department of Biliary-Pancreatic Surgery Zhongda Hospital of Southeast University Nanjing 210009 China

Background Pancreatic cancer is one of the most common tumors and has a 5-year survival for all stages of less than 5%. Most patients with pancreatic cancer are diagnosed at an advanced stage and therefore are not candidates for surgical resection. In recent years, investigation into alternative treatment strategies for this aggressive disease has led to advances in the field of gene therapy for pancreatic cancer. E. coil purine nucleoside phosphorylase/6-methylpurine deoxyribose （ePNP/MePdR） is a suicide gene/prodrug system where PNP enzyme cleaves nontoxic MePdR into cytotoxic membrane-permeable compounds 6-methylpurine （MeP） with high bystander activity, hTERT is expressed in cell lines and tissues for telomerase activity. In this study we examined the efficacy of ePNP under the control of hTERT promoter sequences and assessed the selective killing effects of the ePNP/prodrug MePdR system on pancreatic tumors. Methods Recombinant pET-PNP was established. The protein of E. coil PNPase was expressed and an antibody to E. coil PNPase was prepared. Transcriptional activities of hTERT promoter sequences were analyzed using a luciferase reporter gene. A recombinant phTERT-ePNP vector was constructed. The ePNP/MePdR system affects SW1990 human pancreatic cancer cell lines in vitro. Results The hTERT promoter had high transcriptional activity and conferred specificity on cancer cell lines. The antibody to E. coil PNPase was demonstrated to be specific for the ePNP protein. The MePdR treatment induced a high in vitro cytotoxicity on the sole hTERT-ePNP-producing cell lines and affected SW1990 cells in a dose-dependent manner. Conclusions The hTERT promoter control of the ePNP/MePdR system can provide a beneficial anti-tumor treatment in pancreatic cancer cell lines including a good bystander killing effect.

关键词： hTERT promoter Escherichia coli purinenucleoside phosphorylase pancreatic cancer gene therapy

Intracellular accumulation of tau inhibits autophagosome formation by activating TIA1-amino acid-mTORC1 signaling

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Military Medical Research 2023年第2期10卷 175-190页

作者： Meng-Zhu Li En-Jie Liu Qiu-Zhi Zhou Shi-Hong Li Shi-Jie Liu Hai-Tao Yu Qi-Hang Pan Fei Sun Ting He Wei-Jin Wang Dan Ke Yu-Qi Feng Jun Li Jian-Zhi Wang Department of Pathophysiology School of Basic MedicineKey Laboratory of Education Ministry of China/Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Neurosurgery the Central Hospital of WuhanTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430014China Department of Pathology the First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052China Department of Chemistry Wuhan UniversityWuhan 430072China Co-Innovation Center of Neuroregeneration Nantong UniversityNantong 226000JiangsuChina.

Background:Autophagy dysfunction plays a crucial role in tau accumulation and neurodegeneration in Alzheimer’s disease(AD).This study aimed to investigate whether and how the accumulating tau may in turn affect autophagy.Methods:The primary hippocampal neurons,N2a and HEK293T cells with tau overexpression were respectively starved and treated with vinblastine to study the effects of tau on the initiating steps of autophagy,which was analysed by Student’s two-tailed t-test.The rapamycin and concanamycin A were employed to inhibit the mammalian target of rapamycin kinase complex 1(mTORC1)activity and the vacuolar H+-ATPase(v-ATPase)activity,respectively,which were analysed by One-way ANOVA with post hoc tests.The Western blotting,co-immunoprecipitation and immunofuorescence staining were conducted to gain insight into the mechanisms underlying the tau effects of mTORC1 signaling alterations,as analysed by Student’s two-tailed t-test or One-way ANOVA with post hoc tests.The autophagosome formation was detected by immunofuorescence staining and transmission electron microscopy.The amino acids(AA)levels were detected by high performance liquid chromatography(HPLC).Results:We observed that overexpressing human full-length wild-type tau to mimic AD-like tau accumulation induced autophagy deficits.Further studies revealed that the increased tau could bind to the prion-related domain of T cell intracellular antigen 1(PRD-TIA1)and this association significantly increased the intercellular level of amino acids(Leucine,P=0.0038;Glutamic acid,P=0.0348;Alanine,P=0.0037;Glycine,P=0.0104),with concordant upregulation of mTORC1 activity[phosphorylated eukaryotic translation initiation factor 4E-binding protein 1(p-4EBP1),P<0.0001;phosphorylated 70 kD ribosomal protein S6 kinase 1(p-p70S6K1),P=0.0001,phosphorylated unc-51-like autophagyactivating kinase 1(p-ULK1),P=0.0015]and inhibition of autophagosome formation[microtubuleassociated protein light chain 3 II(LC3 II),P=0.0073;LC3 puncta,P<0.0001].As expected,this tau-induced defic

关键词： Tau Autophagy Amino acid pathway Mammalian target of rapamycin kinase complex 1(mTORC1) T cell intracellular antigen 1(TIA1)

Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity

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World Journal of Cardiology 2014年第5期6卷 314-326页

作者： Nicolas Vuilleumier Fabrizio Montecucco Oliver Hartley Department of Genetics and laboratory medicine Geneva University Hospitals 1211 Geneva Switzerland Department of human Protein Sciences Faculty of Medicine 1211 Geneva Switzerland Department of Internal medicine Foundation for Medical Researches Faculty of Medicine Geneva 1211 Switzerland Department of Immunology and Pathology Faculty of Medicine 1211 Geneva Switzerland

Immune-driven inflammation plays an important part inatherogenesis and is therefore believed to be key to thedevelopment of cardiovascular disease(CVD), whichis currently the leading cause of death in the Westernworld. By fulfilling some of the Koch postulates, athero-genesis has even been proposed to be considered as anautoimmune disease, raising the hope that CVD couldbe prevented by immunomodulation. Nevertheless,the role of the immune system and autoimmune reac-tions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenicattributes. Hence, if immunomodulation is to becomea therapeutic option for atherosclerosis and CVD, it willbe crucial to correctly identify patients who might ben-efit from targeted suppression of deleterious autoim-mune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clini-cal, in vitro, and animal studies dedicated to autoan-tibodies against apolipoprotein A-1(anti-apoA-1 IgG), the major proteic fraction of high density lipoprotein. Current clinical studies indicate that high levels of anti-apoA-1 IgG are associated with a worse cardiovascular prognosis. In addition, in vitro and animal studies indi-cate a pro-inflammatory and pro-atherogenic role, sup-porting the hypothesis that these autoantibodies may play a direct causal role in CVD, and furthermore that they could potentially represent a therapeutic target for CVD in the future.

关键词： Autoantibodies Cardiovascular disease Atherosclerosis Apolipoprotein A-1 Autoimmunity Biomarkers

Oxidative stress-triggered Wnt signaling perturbation characterizes the tipping point of lung adeno-to-squamous transdifferentiation

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Signal Transduction and Targeted Therapy 2023年第2期8卷 730-743页

作者： Zhaoyuan Fang Xiangkun Han Yueqing Chen Xinyuan Tong Yun Xue Shun Yao Shijie Tang Yunjian Pan Yihua Sun Xue Wang Yujuan Jin Haiquan Chen Liang Hu Lijian Hui Lin Li Luonan Chen Hongbin Ji State key laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell BiologyCAS Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China University of Chinese Academy of Sciences Beijing 100049China Zhejiang University-University of Edinburgh Institute Zhejiang University School of MedicineHaining 314400China Department of Thoracic Surgery Fudan University Shanghai Cancer CenterShanghaiChina Department of Oncology Shanghai Medical CollegeFudan UniversityShanghaiChina School of Life Science and Technology ShanghaiTech UniversityShanghai 200120China State key laboratory of Molecular Biology Shanghai Institute of Biochemistry and Cell BiologyCAS Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China key laboratory of Systems Health Science of Zhejiang Province School of Life ScienceHangzhou Institute for Advanced StudyUniversity of Chinese Academy of SciencesChinese Academy of SciencesHangzhou 310024China

Lkb1 deficiency confers the Kras-mutant lung cancer with strong plasticity and the potential for adeno-to-squamous transdifferentiation(AST).However,it remains largely unknown how Lkb1 deficiency dynamically regulates AST.Using the classical AST mouse model(Kras LSL-G12D/+;Lkb1flox/flox,KL),we here comprehensively analyze the temporal transcriptomic dynamics of lung tumors at different stages by dynamic network biomarker(DNB)and identify the tipping point at which the Wnt signaling is abruptly suppressed by the excessive accumulation of reactive oxygen species(ROS)through its downstream effector FOXO3A.Bidirectional genetic perturbation of the Wnt pathway using two different Ctnnb1 conditional knockout mouse strains confirms its essential role in the negative regulation of AST.Importantly,pharmacological activation of the Wnt pathway before but not after the tipping point inhibits squamous transdifferentiation,highlighting the irreversibility of AST after crossing the tipping point.Through comparative transcriptomic analyses of mouse and human tumors,we find that the lineage-specific transcription factors(TFs)of adenocarcinoma and squamous cell carcinoma form a“Yin-Yang”counteracting network.Interestingly,inactivation of the Wnt pathway preferentially suppresses the adenomatous lineage TF network and thus disrupts the“Yin-Yang”homeostasis to lean towards the squamous lineage,whereas ectopic expression of NKX2-1,an adenomatous lineage TF,significantly dampens such phenotypic transition accelerated by the Wnt pathway inactivation.The negative correlation between the Wnt pathway and AST is further observed in a large cohort of human lung adenosquamous carcinoma.Collectively,our study identifies the tipping point of AST and highlights an essential role of the ROS-Wnt axis in dynamically orchestrating the homeostasis between adeno-and squamous-specific TF networks at the AST tipping point.

关键词： squamous homeostasis lung

human TRMT1 catalyzes m^(2)G or(m^(2))_(2)G formation on tRNAs in a substrate-dependent manner

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Science China(Life Sciences) 2023年第10期66卷 2295-2309页

作者： Qing-Ping Xiong Jing Li Hao Li Zhi-Xuan Huang Han Dong En-Duo Wang Ru-Juan Liu State key laboratory of Molecular Biology CAS Center for Excellence in Molecular Cell ScienceShanghai Institute of Biochemistry and Cell BiologyChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China

TRMT1 is an N^2-methylguanosine(m^(2)G)and N^2,N^2-methylguanosine((m^(2))_(2)G)methyltransferase that targets G26 of both cytoplasmic and mitochondrial t RNAs.In higher eukaryotes,most cytoplasmic t RNAs with G26 carry(m^(2))_(2)G26,although the majority of mitochondrial G26-containing t RNAs carry m^(2)G26 or G26,suggesting differences in the mechanisms by which TRMT1 catalyzes modification of these t RNAs.Loss-of-function mutations of human TRMT1 result in neurological disorders and completely abrogate t RNA:(m^(2))_(2)G26 formation.However,the mechanism underlying the independent catalytic activity of human TRMT1 and identity of its specific substrate remain elusive,hindering a comprehensive understanding of the pathogenesis of neurological disorders caused by TRMT1 mutations.Here,we showed that human TRMT1 independently catalyzes formation of the t RNA:m^(2)G26 or(m^(2))_(2)G26 modification in a substrate-dependent manner,which explains the distinct distribution of m^(2)G26 and(m^(2))_(2)G26 on cytoplasmic and mitochondrial t RNAs.For human TRMT1-mediated t RNA:(m^(2))_(2)G26 formation,the semi-conserved C11:G24 serves as the determinant,and the U10:A25 or G10:C25 base pair is also required,while the size of the variable loop has no effect.We defined the requirements of this recognition mechanism as the“(m^(2))_(2)G26 criteria”.We found that the(m^(2))_(2)G26 modification occurred in almost all the higher eukaryotic t RNAs conforming to these criteria,suggesting the“(m^(2))_(2)G26 criteria”are applicable to other higher eukaryotic t RNAs.

关键词： RNA modification m^(2)G (m^(2))_(2)G tRNA TRMT1 neurological disease

Magnetic Resonance Imaging of Alzheimer's disease:from Diagnosis to Therapeutic Evaluation

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Chinese Journal of Integrative medicine 2010年第3期16卷 276-282页

作者：顾雪梅姜招峰黄汉昌 Beijing Military General Hospital Beijing key laboratory of Bioactive Substances and Functional Foods Beijing Union University College of Arts and Science Beijing Union University

Alzheimer＇s disease（AD）is a devastating late-life dementia that produces progressive loss of memory and mental faculties in elderly people.It is important to identify the earliest evidence of AD and to monitor the development of this disease for us to make positive response to its management.Magnetic resonance imaging（MRI）is powerful to image the tissue or organ without damnification.MRI can be employed to diagnose the early AD development and monitor the key biomarker development in AD.MRI may be helpful not only in diagnosing early AD,but also in evaluating its development.This article reviews the progress of MRI on the diagnosis and detection of AD,and makes comments on its therapeutic application.

关键词： Alzheimer＇s disease diagnosis magnetic resonance imaging

Hematopoietic stem cell transplantation for children with β-thalassemia major: multicenter experience in China

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World Journal of Pediatrics 2018年第1期14卷 92-99页

作者： Xin-Yu Li Xin Sun Jing Chen Mao-Quan Qin Zuo Luan Yi-Ping Zhu Jian-Pei Fang Guangdong Provincial key laboratory of MalignantTumor Epigenetics and Gene Regulation Medical ResearchCenter(Pediatrics)Medical Research CenterSun Yat-SenMemorial HospitalSun Yat-Sen UniversityGuangzhouChina Department of Hematology Guangzhou Womenand Children’s Medical CenterGuangzhou MedicalUniversityGuangzhouChina Department of Hematology Shanghai Children’s MedicalCenterShanghai Jiaotong University School of MedicineShanghaiChina

Backgroundβ-Thalassemia major (β-TM) has become a public health problem in China's Mainland. Hematopoietic stem cell transplantation (HSCT) has remained the only cure forβ-TM in China's Mainland since 1998. Methods This multicenter retrospective study provides a comprehensive review of the outcomes of 50 pediatric patients withβ-TM who received HSCT between 1998 and 2009 at five centers in China's Mainland. Both related (n = 35) and unrelated donors (n = 15) with complete human leukocyte antigen matches were included. The stem cell sources included bone mar-row (BM), peripheral blood stem cells, umbilical cord blood (UCB) and a combination of BM and UCB or a combination of BM and peripheral blood stem cells from a single sibling donor. Results The probabilities of 5-year overall survival (OS) and thalassemia-free survival (TFS) after the first HSCT were 83.1 and 67.3%, respectively. Graft failure (GF) occurred in 17 patients. Univariate analyses showed that umbilical cord blood transplantation (UCBT) was one of the potential risk factors for decreased OS (P = 0.051), and that UCBT (P = 0.002) was potentially related to TFS. GF incidence was distinct between the UCBT and non-UCBT groups (P = 0.004). Four cases of UCB-BM combined transplantation led to decreased risks of mortality and recurrence. In the UCBT group, related donor transplantation produced more favorable results than unrelated donor transplantation in OS (P = 0.009) but not in TFS (P = 0.217). Conclusions GF was the primary cause of UCBT failure. Though UCBT from related donors was not favorable, the combined transplantation of UCB and BM could improve the prognosis of UCBT.

关键词： β-Thalassemia major Hematopoietic stem cell transplantation Umbilical cord blood