g1.dierzhang
人免疫球蛋白g1骨架促进fcγ受体介导的聚集aβ的小胶质细胞吞噬作用。
人免疫球蛋白g1骨架促进fcγ受体介导的聚集aβ的小胶质细胞吞噬作用。
人免疫球蛋白G1(IgG1)是一种抗体类分子,它在免疫系统中起着重要的作用。
最早被发现的抗体是IgG,它是免疫系统中最主要的抗体类分子之一、IgG分子具有与Fcγ受体结合的特性,这使得它能够通过与Fcγ受体结合,调控免疫细胞的活化和功能。
小胶质细胞是中枢神经系统中的主要免疫细胞,它们扮演着清除神经元间的碎片和代谢废物的重要角色。
在神经退行性疾病中,如阿尔茨海默病(AD),小胶质细胞的功能受损,导致神经元间的碎片和代谢废物堆积,加速疾病进展。
研究表明,IgG1能够促进Fcγ受体介导的聚集Aβ的小胶质细胞吞噬作用,从而帮助清除AD中大量堆积的Aβ蛋白。
Aβ是阿尔茨海默病中的关键病理标志物,其过度沉积被认为是阿尔茨海默病发病和进展的主要原因之一。
研究发现,IgG1与Fcγ受体在小胶质细胞表面结合后,能够诱导细胞内信号通路的激活,促进小胶质细胞的吞噬作用。
这一过程涉及多种细胞信号通路的激活,包括磷酸肌醇3激酶(PI3K)和蛋白激酶C(PKC)信号通路。
这些信号通路的激活促进了小胶质细胞吞噬Aβ的能力。
此外,研究还发现,IgG1通过Fcγ受体介导的聚集可以调节小胶质细胞中的炎症反应。
炎症在AD的发病和进展中起到重要作用,而IgG1的作用可以抑制小胶质细胞中炎症相关基因的表达,减轻炎症反应的程度。
综上所述,人免疫球蛋白G1通过与Fcγ受体结合,促进小胶质细胞吞噬Aβ,并调节炎症反应。
这一发现揭示了免疫系统在神经退行性疾病中的重要作用,为阿尔茨海默病等疾病的治疗提供了新的思路和方法。
进一步研究透彻理解IgG1对小胶质细胞吞噬功能的调节机制,对于开发新的药物治疗策略和疫苗研制具有重要意义。
李金华 中国科学院地质与地球物理研究所
李金华中国科学院地质与地球物理研究所李金华,研究员,硕士生导师。
1979年6月出生于陕西安康。
李金华地质微生物学和生物地磁学专业。
2001年毕业于西北大学生命科学学院获生物学专业学士学位,2006年毕业于山东大学微生物技术国家重点实验室获微生物专业硕士学位,2010年毕业于中国科学院地质与地球物理研究所获固体地球物理专业博士学位,2010-2013年留在该所从事地质学博士后研究,2013年至2016年任该所副研究员,2017年起任研究员。
曾于2012-2014年,在法国巴黎第六大学矿物学、材料物理与宇宙化学研究所(IMPMC,CNRS-UPMC)做访问学者研究。
长期从事地球科学与生命科学的前沿交叉研究。
近年来,以微生物-矿物相互作用为基本研究内容,综合运用岩石磁学、微生物学、电子显微学和同步辐射等方法,重点研究了:(i)趋磁细菌生物矿化过程和机制,实验揭示了趋磁细菌磁铁矿合成及磁小体链组装的动态过程,发现了子弹头形磁小体独特的多阶段晶体生长模式,提出了子弹头形纳米磁铁矿是最可靠化石磁小体判据的新观点;(ii)磁小体链复杂磁性机制,实验模拟研究了磁小体链的微观磁结构及其磁各向异性和颗粒间静磁相互作用,厘定了单磁畴磁铁矿的晶型和空间排列对几个重要岩石磁学参数的系统影响,提出了化石磁小体识别的新参数δ图;(iii)微生物矿化与微化石形成和保存,实验模拟研究了微生物矿化和微化石的形成过程,发现微生物矿化能显著提升微化石的保存能力,提出了将实验埋藏学与地质样品相结合研究微化石的新思路。
上述研究为理解生物响应地磁场机制和利用化石磁小体记录开展古地磁与古环境研究奠定了坚实的基础。
目前,已经发表SCI文章40篇。
李金华其中第一作者12篇(其中包括EPSL文章2篇,G-cubed文章2篇,GJI文章1篇,ChemicalGeology邀请综述文章1篇等)。
文章共被SCI引用304次,他引172次。
其中,第一作者论文12篇,SCI他引86次。
G 1 创业的艺术 盖伊 川崎
G 1 创业的艺术盖伊川崎盖伊·川崎Guy Kawasaki1954年生于夏威夷一个一般家庭1976年毕业于斯坦佛大学暨加州大学洛山矶分校1979年获加利福尼亚大学MBA学位1983-1987,在Apple任软件布道师,负责产品和品牌的传播1995-1997,任Apple的总布道师现任Garage Technology Ventures的常务董事Managing Director盖伊·川崎被创业家(Entrepreneur)杂志称为创业大师,他在硅谷高科技界,以富于创业精神享有盛名,一场演讲的出席费用高达四万美元。
曾担任苹果电脑的麦金塔软体顾咨询,以及苹果电脑的创意总监,是麦金塔电脑窜起、重振苹果电脑雄风的三巨头之一, 另外两位是史蒂夫·乔布斯与约翰·史考利。
他目前是车库科技创投公司执行长、福布斯杂志闻名的专栏作家,同时是八本企管畅销书的作者。
包括《销售妄图》(Selling the Dream)、《如何逼疯对手》(How to Drive Your Competition Crazy)、《麦金塔风范》(The Macintosh Way)、《策略革命家》(Rules for Revolutionaries)等。
那个演讲基于一本名叫《创业的艺术》的书。
他总结了自己职业生涯中的体会教训,并藉此传递给现在的创业者们,期望他们能改变世界。
一、做有意义的事Make Meaning开创公司的理由是做有意义的事,改变世界。
有三个方法做有意义的事:1、提升生命的质量。
Increase the quality of life2、改正错误。
Right a wrong3、不让好东西终结。
Prevent the end of something good如果你们想找风投,先想想如何做有意义的事。
如果你想好如何样做有意义的事,你会挣到钞票。
但如果你一开始就想的挣钞票,你会吸引一帮错误的雇员。
人教版全国全部高考专题英语高考真卷试卷及解析
人教版全国全部高考专题英语高考真卷1.阅读理解第1题.Hair Loss (Alopecia)Information about male pattern baldness (秃顶) causes, triggers and treatment in the UK.In contrary to popular belief, hair loss—or alopecia—can start at any age. Whilst it is associated with mature males, and statistics show it does mainly affect men about 40, the reality is you can notice symptoms in your 30s, or even 20s and teen years. The NHS statistics state that 25% of men start losing their hair by the time they reach 30. The most common form of hair loss is male pattern baldness—also known as androgenic alopecia—that affects more than half of men around the world.One option many men seek is treatment to avoid further hair loss, especially early on in the process. With treatments, such as Propecia, that specifically target male pattern baldness, it is possible to stop hair losscompletely and even encourage fresh new hair growth.What is alopecia?Alopecia is the medical term for hair loss. Most commonly affecting males, hair loss in men is caused by an increased sensitivity to the male sex hormones (androgens). The type of alopecia you have (as well as hereditary and external factors) can influence levels of hair loss. The most common type of hair loss (alopecia) is male and female pattern baldness. Other types include:•Alopecia areata (patches of baldness, usually on the scalp)•Scarring alopecia (hair loss directly affecting the hair follicles)•Telogen effluvium (hair thinning over a larger area on the top of the head, rather than bald patches)•Anagen effluvium (most commonly caused by cancer treatments such as chemotherapy and radiotherapy)(1)Which of the following statements is FALSE about Propecia?A: It can stop hair loss almost in all cases.B: People can buy it online without doctor visit.C: It encourages new hair growth in rare eases.D: It is especially effective on male pattern baldness.(2)The next part of the webpage is most likely to be about ______.A: hair loss causesB: hair loss symptomsC: preventing hair lossD: treating hair loss【答案】CA【解答】(1)C 细节理解题。
《大学》(拼音版)
《大学》,原是《小戴礼记》里一篇,旧说为曾子所作,实为秦汉时的儒家作品,这是中国古代讨论教育理论的重要著作。
《大学》提出了“三纲领”和“八条目”,强调修己是治人的前提,修己的目的是为了治国平天下,说明治国平天下和个人道德修养的一致性。
《大学》开头就说:“大学之道,在明明德,在亲民,在止于至善。
”这就是后人所说的《大学》“三纲领”。
所谓“明明德”,就是发扬光大人所固有的天赋的光明道德。
所谓“在亲民”,是指发扬了善性之后,即从事治民,治民要亲爱人民。
所谓“止于至善”,就是要求达到儒家封建伦理道德的至善境界。
“为人君止于仁,为人臣止于敬,为人子止于孝,为人父止于慈,与国人交止于信”,这是《大学》提出的教育纲领和培养目标。
《大学》还说:“古之欲明明德于天下者,先治其国;欲治其国者,先齐其家;欲齐其家者,先修其身;欲修其身者,先正其心;欲正其心者,先诚其意;欲诚其意者,先致其知;致知在格物。
”格物、致知、诚意、正心、修身、齐家、治国、平天下,后世称之为《大学》的“八条目”,这是实现“三纲领”的具体步骤。
“八条目”的中心环节是修身,“自天子以至于庶人,壹是皆以修身为本”。
对于培养目标和方法,《大学》反复强调的是个人的道德修养。
经北宋程颢、程颐竭力尊重,南宋朱熹又作《大学章句》,最终和《中庸》、《论语》、《孟子》并称“四书”。
宋、元以后,《大学》成为学校官定的教科书和科举考试的必读书,对古代教育产生了极大的影响。
大学da xu zhT daza mfn mi"deza qT mf3嫁大 学 之 道5在 明 明 德5在 亲 民5za i zh T yu zh i sha nzh i zh T er ho u yo u din gdi ng er ho u 在 止 于 至 善 。
知 止 而 后 有 定 , 定 而 后ne ng jingjin g er ho u neng anan er ho u neng 山山台匕 静, 静 而 后 台匕 安 , 安 而 后 台匕 虑 , 虑 er ho u nen g dewu yo u be n mosh i yo u zhong sh Tzh i 而 后 台匕 得 。
IGCS19-0405 : 产品说明书
abnormal vaginal bleeding requiring intervention had no statis-tical difference between VP and WVP patients group (p=0.3074)as other complications as well(table1).Median of related days of vaginal bleeding after the procedure were 7.4days(SD8.75)in VP group and7.34days(SD8.52)in WVP group,with no statistical difference(p=0.912). Conclusions Insert a vaginal pack or not,after LEEP,do not affect the number of postoperative gynecologic intervention due to vaginal bleeding or the amount of postoperative bleed-ing days.Previous pregnancies,hormonal status,cytology or LEEP specimen characteristics did not affect the disclosure. We also could not find any risk factor associated to abnormal bleeding.Based on that,the use of vaginal pack can be omit-ted with no further complications.IGCS19-0405382LATERALLY EXTENDED ENDOPELVIC RESECTION(LEER) AND NEOVAGINE,PATIENT WITH RECTALADENOCARCINOMA AND RECURRENCE IN CERVIX,VAGINA AND PELVIC WALL:A PURPOSE OF A CASE1J Torres*,2J Saenz,3O Suescun,3M Medina,4L Trujillo.1Especialista en entrenamiento–Universidad Militar Nueva Granada–Instituto Nacional de Cancerologia,Department of Gynecologic Oncology,Bogota D.C.,Colombia;2Especialista en entrenamiento–Universidad Militar Nueva Granada–Instituto Nacional de Cancerologia,Department of Gynecologic Oncology,Bogota D.C,Colombia;3Instituto Nacional de Cancerologia, Department of Gynecologic Oncology,Bogota D.C,Colombia;4Instituto Nacional de Cancerologia,Department of Gynecologic Oncology,Bogota D.C.,Colombia10.1136/ijgc-2019-IGCS.382Objectives Exenteration is used to treat cancers of the lower and middle female genital tract in the irradiated pelvis. Höckel described laterally extended endopelvic resection (LEER)as an approach in which the resection line extends to the pelvic side wall.Methods A49-year-old patient diagnosed with rectal adenocar-cinoma10years ago,managed with chemotherapy plus radio-therapy.T umor relapse at3years,management with low abdominoperineal resection and definitive colostomy.Second relapse4years later,compromising the posterior aspect of the coccyx and right side of the pelvis with irresecability criteria, management was decided with chemotherapy with capecita-bine,oxaliplatin and bevacizumab.New relapse at2years in the cervix,vagina and pelvic wall.Images without distance disease,type LEER management with extension of pelvic floor margins and resection of muscle pubococcygeus and right lat-eral iliococcygeus with neovagina(Singapore flap)and non-continent urinary derivation with bilateral cutaneous ureteros-tomy,achieving adequate lateral margin with curative intent. During follow-up with favorable evolution.Results LEER combines at least two procedures:total mesorec-tal excision,total mesometrial resection or total mesovesical resection.It may even require resection of the pelvic wall, internal obturator muscle,pubococcygeus,iliococcygeus,coccy-geus or internal iliac vessels.In combination with neovagina, it would offer better results in non-gynecological cancer relapses.Conclusions LEER with neovagina can be offered as a new therapy to a selected subset of patients with relapse in adja-cent gynecological organs with good oncological,functional and aesthetic results.Symptom Management–Supportive Cancer CareIGCS19-0706383PHOTOBIOMODULATION AND MANUAL LYMPHDRAINAGE FOR NIPPLE NECROSIS TREATMENT INBREAST CANCER:A CASE REPORT1J Baiocchi,2L Campanholi,3G Baiocchi*.1Oncofisio,Physical Therapy,Sao Paulo,Brazil;2CESCAGE,Physical Therapy,Ponta Grossa,Brazil;3AC Camargo Cancer Center, Gynecologic Oncology,Sao Paulo,Brazil10.1136/ijgc-2019-IGCS.383Objectives Recently,breast reconstruction after mastectomywith nipple preservation became an option of breast cancer surgery.Despite its efficacy and aesthetic superiority,the nip-ple preservation is associated with several complications in the postoperative period.The photobiomodulation therapy,for-merly known as low-intensity laser therapy,demonstrated tis-sue promotion repair by cellular repair biostimulation, angiogenesis and anti-inflammatory effects.These characteris-tics suggest a potential role for repair of chronic wounds andmay be applicable in necrosis treatment.Our aim was toreport the effects of the physiotherapeutic intervention through photobiomodulation therapy in a patient with nipple necrosis after risk reducing mastectomy.Methods We report a case of a breast cancer surgery with nip-ple necrosis treated with low-level laser therapy.The patientwas a36-year-old women who developed skin nipple necrosisin the right breast after bilateral reconstructive mastectomy.She had6sessions of low-level laser therapy.Results A female subject developed a nipple necrosis of morethan40%on the right breast after mastectomy and recon-struction.She was referred to Physical Therapy(PT)and thePT sessions were composed by manual lymph drainage,man-ual therapy for de AWS,exercises of strength and flexibility, followed by LLLT with laser660nm,2joules per point atevery1cm.Therapy was implemented for12times in total,from May2016to June2016.A re-evaluation was performed monthly from July13,2016to November2017.After18 months of follow-up,the sustained effects of LLLT were found.Conclusions Low-level laser therapy is effective for the skin cicatrization after nipple necrosis.IGCS19-0446384CONTRACEPTION AND FERTILITY COUNSELING INPATIENTS RECEIVING CHEMOTHERAPY1A Elnaggar*,2A Calfee,1LB Daily,2T Hasley,1T Tillmanns.1West Cancer Center and Research Institute,Gynecologic Oncology,Memphis,USA;2University of Tennessee Health Science Center,Obstetrics and Gynecology,Mempis,USA10.1136/ijgc-2019-IGCS.384Objectives Cancer care advances allow more patients to pursue fertility.Unfortunately,treatments may have detrimental effectson fertility and fetus should pregnancy occur.This study examines physician documentation and patient perceptions of fertility and contraception counseling. on December 24, 2023 by guest. Protected by copyright./ Int J Gynecol Cancer: first published as 10.1136/ijgc-2019-IGCS.384 on 18 September 2019. Downloaded fromMethods IRB approval obtained for a cross-sectional study of men and women,ages18–50,with newly diagnosed malig-nancy between May2017and2018.Prior sterilization,secon-dary or synchronous cancer,or prior chemotherapy were exclusionary.Consented patients received a survey regarding perception on receipt and quality of,counseling.Demographic, sexual,and social information was obtained.Differences were evaluated using chi-square tests.Results Fifty-three of179patients identified participated. Majority were women(75v25%).Patients were more likely to have perceived counseling for contraception and fertility than documented.The majority perceived counseling as suffi-cient regarding contraception and fertility.Men were more likely than women to be perceive counsel-ing regarding fertility(85v43%,p=0.010).However,both felt fertility counseling to be sufficient with similar rates of documentation.Caucasians were more likely to perceive receipt of fertility counseling(68v29%)and to perceive it to be sufficient(70v40%),then African Americans,with the same rate of documentation(35%).Conclusions Significant discrepancies in perception counsel-ing regarding contraception and fertility were seen.Gen-der and race were important factors for the perception of fertility counseling,while only race was a factor to qual-ity of perceived counseling.These differences occurred despite equal rates of physician documentation,across all groups.IGCS19-0430385WHO ARE YOU CALLING OLD?PRACTICE PATTERNS AND MANAGEMENT OF NONAGENARIANS PRESENTINGTO A GYNECOLOGIC ONCOLOGIST FOR INITIALCONSULTATIONE Ryan*,B Margolis,B Pothuri.New York University Langone Health,Obstetrics and Gynecology,New York,USA10.1136/ijgc-2019-IGCS.385Objectives T o describe the practice patterns and treatment of nonagenarians who initiated care with a gynecologic oncologist.Methods Retrospective chart review of women aged90or older who presented to a gynecologic oncologist between10/ 09and12/18at an urban academic medical center.Descrip-tive statistics utilized for variables of interest.Results We identified34nonagenarians(median age92,range 90–98):10(29%)had benign disease,8(24%)pre-malignancy or suspected malignancy,and16(47%)malignancy.Of these, 79%had age and/or functional status discussed in the care plan.Of the8with suspected malignancy,5declined further workup.The cancer distribution revealed5(31%)vulvar,5 (31%)uterine,4(25%)ovarian,1(6%)vaginal and1(6%) cervical bined,37%had stage I disease;6% stage3;6%stage4;13%recurrent;and25%unstaged.All received treatment plans:7(47%)with palliative intent and8 (53%)with curative intent.In the curative group,7under-went surgery(1adjuvant chemotherapy)and1chemotherapy/radiation.In the palliative group,4underwent radiation,1 chemotherapy and2declined/unknown.Overall,13(87%) completed the proposed treatment.T reatment-related complica-tions included1superficial skin infection and1thirty-day readmission.Conclusions Nonagenarians often presented with vulvar or endometrial cancer and87%successfully completed treatmentwith minimal adverse effects or toxicity.Age and/or functionalstatus were considered in the care plan for79%of women,but it did not preclude treatments that had the potential to preserve meaningful quality of life and/or cure patients oftheir disease.IGCS19-0646386RISK FACTORS COMPREHENSIVE GERIATRICASSESSMENT FOR EARLY DEATH IN ELDERLY PATIENTSWITH GYNECOLOGICAL CANCER.A PROSPECTIVECOHORT STUDY1J Sales*,2C Azevedo,2C santos,3L sales,4M Bezerra,5G Bezerra,4Z cavalcanti,6MJ Mello.1IMIP,Geriatric Oncology,Recife,Brazil;2IMIP,Oncology,Recife,Brazil;3FPS,Medical Course,Recife,Brazil;4IMIP,geriatric,Recife,Brazil;5HMV,oncology,caruaru,Brazil;6IMIP,post graduation,Recife,Brazil10.1136/ijgc-2019-IGCS.386Objectives T o determine risk factors for early death identifiedthe Comprehensive Geriatric Assessment(CGA)in elderly patients with gynecological cancer(EPGC).Methods Prospective cohort study.Participants with a recent diagnosis of cancer were from eight community hospitals andone cancer center in Northeast Brazil and were recruited dur-ing their first medical appointment at the outpatient oncologic clinic.A basal CGA was done before the treatment decision (ADL,Charlson Comorbidity Index-CCI,Karnofsky Perform-ance status–KPS,GDS15,IPAQ,MMSE,MNA,MNA-SF,PS,PPS,Polipharmacy,TUG).During the follow up of12 months,information about the treatments performed,the tar-geted interventions and early death was collected.Overall sur-vival was estimated using the Kaplan–Meier method,and survival curves were compared using the Log rank test for cat-egorical variables.A multivariate Cox proportional hazardsmodel was used.Results From2015–2017,84EPGC,mean age69,6±7,9;range60–96),were enrolled,25%were metastatic disease.tumor site:40,4%cervical uterine,36,9%endometrial,20,2%ovary and2,3vulva.Nine(10.7%)ECP died in less than12 months of follow-up.In our multivariate model,controlled byage,site of cancer and cancer stage,the remaining significantrisk factors were malnutrition/nonutrition determined byMNA-SF(HR3.70,95%CI1.81–5.99,p<0.001),Katz index(HR 3.60,CI 1.56–3.81,p<0.001)CCI>2(HR2,74,CI1.0.74–10.20,p=0.013)and Polipharmacy(HR2.65,CI0.71–9.81,p<0.001).Conclusions The CGA at admission identified risk factors (Nutritional risk,polypharmacy,functionality for Katz indexand comorbidity index)for premature death in EPGC.They can help to plan a personalized care. on December 24, 2023 by guest. Protected by copyright./ Int J Gynecol Cancer: first published as 10.1136/ijgc-2019-IGCS.384 on 18 September 2019. Downloaded from。
基于文献计量的校园垃圾分类回收研究现状与态势
基于文献计量的校园垃圾分类回收研究现状与态势*张以晖1,陈展2,卢琦1(1.上海交通大学后勤保障中心,上海200240;2.上海勘察设计研究院(集团)股份有限公司,上海200093)【摘要】为探究校园垃圾分类回收的研究现状、研究热点和前沿动态,以Web of Science 核心合集数据库中1990—2023年收录的文献与其引文数据为基础,进行了包括发文情况、研究力量分布、关键词共现与时区分布、文献共被引与聚类分析,以及关键词突现分析在内的文献计量和知识图谱分析。
结果显示:该领域发文量逐年增加,2010—2017年增加明显,主要集中于环境科学和教育领域;发展中国家和发达国家整体发文量相当,但发达国家的研究水平相对较高;多数研究机构的发文量较少,合作关系较弱;研究热点由早期的固体废物管理、环境教育、态度、行为和循环经济逐渐丰富至多个主题,包括电子废物、塑料废物、餐厨垃圾、零废物、计划行为理论及其拓展、分类意愿、可持续性、环境知识和环境绩效等。
环境知识、环境可持续性和减量化、循环经济可作为未来的研究前沿,并应重点关注校园垃圾的特征成分研究,垃圾分类行为、意愿和影响因素研究以及绿色校园和可持续校园建设等方面。
【关键词】校园垃圾;文献计量;突现分析;聚类分析;知识图谱中图分类号:X799.3文献标识码:A文章编号:1005-8206(2024)02-0093-11DOI :10.19841/ki.hjwsgc.2024.02.013Research Status and Advances of Campus Waste Classification and Recycling Based on Bibliometrics ZHANG Yihui 1,CHEN Zhan 2,LU Qi 1(1.Logistics Support Center of Shanghai Jiao Tong University ,Shanghai 200240;2.SGIDI Engineering Consulting (Group )Co.Ltd ,Shanghai200093)【Abstract 】To investigate the current status,hotspots,and frontier trends in the research on campus wasteclassification and recycling,based on the literature collected in the core collection of the Web of Science(WoS )database from 1990to 2023and their references,bibliometric analysis and knowledge mapping were conducted,which included the state of publications,the distribution of research power,keywords co-occurrence and time-zone distribution,literature co-citation and cluster analysis,and burst analysis of keywords.The results showed that the number of articles in this field keep increasing annually,with a significant growth from 2010to 2017,and the disciplines mainly focused on environmental science and education.The overall number of publications issued by developing countries and developed countries was comparable,but the research level of developed countries was relatively higher.Most research institutions had a small number of publications and a weak cooperative relationship.The main research hotspots had gradually enriched from early stages of solid waste,environmental education,attitude,behavior,and circular economy to multiple themes,including electronic waste,plastic waste,food waste,zero waste,planned behavior and extended theory,willingness,sustainability,environmental knowledge,and environmental performance.Environmental knowledge,environmental sustainability and reduction,and circular economy could be the research frontiers in the future,with a focus on the study of the characteristic components of campus waste,behavior,willingness,and influencing factors of waste sorting,as well as the establishment of green campus and sustainable campus.【Key words 】campus waste;bibliometrics;burst analysis;cluster analysis;knowledge mapping*基金项目:上海科委环境岩土工程技术研究中心项目(15DZ2251300)收稿日期:2023-08-07;录用日期:2024-01-09文章栏目:环境卫生管理与评价体系文章类型:研究论文张以晖,陈展,卢琦.基于文献计量的校园垃圾分类回收研究现状与态势[J ].环境卫生工程,2024,32(2):93-103.ZHANG Y H ,CHEN Z ,LU Q.Research status and advances of campus waste classification and recycling based on bibliometrics [J ].EnvironmentalSanitation Engineering ,2024,32(2):93-103.第32卷第2期2024年4月环境卫生工程Environmental Sanitation EngineeringVol.32No.2Apr.2024环境卫生工程2024年4月第32卷第2期0引言垃圾源头分类回收是实现固体废物减量化和资源回收的有效方式[1-2],合理的分类回收可以减少30%~40%的生活垃圾量[3],并有效减少后续运输、填埋、焚烧和堆肥量[4],既能节约资源、减轻环境影响[5],又是建设资源节约型和低碳环保型社会的有力措施。
汉语基础字母表
汉语辅音表───────────────────────────────b[玻] p[坡] m[摸] f[佛]d[得] t[特] n[讷] l[勒] g[哥] k[科] h[喝]j[基] q[欺] x[希]z[知;资] c[嗤;雌] s[诗;思] r[日] y[医] w[巫] v[雨]一﹑基本规则声母(CONSONANT)ㄅㄆㄇㄈㄉㄊㄋㄌㄍㄎㄏㄐㄑㄒㄓㄔㄕㄖㄗㄘㄙ b p m f d t n l g k h j q x zh ch sh r z c s 玻坡摸佛得特讷勒哥科喝基欺希知蚩诗日资雌思韵母(VOWEL)ㄚㄛㄜㄝㄞㄟㄠㄡㄢㄣㄤㄥㄦa o e e ai ei ao ou an en ang eng er啊喔鹅(耶) 哀紏熬欧安恩昂(亨) 儿ㄧㄧㄚㄧㄛㄧㄝㄧㄠㄧㄡㄧㄢㄧㄣㄧㄤㄧㄥC+ i ia io ie iao iu ian in iang ing+ yi ya yo ye yao you yan yin yang ying衣呀唷耶腰忧烟因央英ㄨㄨㄚㄨㄛㄨㄞㄨㄟㄨㄢㄨㄣㄨㄤㄨㄥC+ u ua uo uai ui uan un uang ong+ wu wa wo wai wei wan wen wang weng屋蛙窝歪威弯温汪翁ㄩㄩㄝㄩㄢㄩㄣㄩㄥㄋㄩㄌㄩC+ u ue uan un iong+ yu yue yuan yun yongZ+ nv lv迂约冤晕雍女律汉语元音表国际音标与汉语拼音对照表[阅读:1775]拼音音标描述音节卷舌er 卷舌元音er儿[]舌尖i 舌尖前元音zi[ts]、ci[ts']、si[s]舌尖后元音zhi[t]、chi[t’]、shi[]、ri[]舌面元音i i 舌面前高不圆唇元音ü y 舌面前高圆唇元音yu[y]、lü[ly]、üe[yε]、quan[t'yn]u u 舌面后高圆唇元音е е 舌面前半高不圆唇元音ei[ei]、uei[uei]γ 舌面后半高不圆唇元音de[tγ]、te[t'γ]、ge[kγ]、ke[k'γ]、he[xγ]舌面央中不圆唇元音en[n]、eng[η]、uen[un]、ueng[uη]ε 舌面前半低不圆唇元音ie[iε]、üe[yε]ο ο 舌面后半高圆唇元音a /ε 舌面前次低/半低不圆唇元音quan[t'yn]、tuan[t'un]、ian[in]a 舌面前低不圆唇元音an[an]、iao[iau]、ai[ai]、ia[ia]A舌面央低不圆唇元音a[A]、fa[fA]、ha[xA]、ga[kA]、da[tA]、ta[t'A] α 舌面后低不圆唇元音ang[αη ]、iang[iαη]、ao[αu]汉语拼音中的"pa、zhang、ai、ian",其中的四辅音表拼音音标描述拼音音标描述1 b p 双唇不送气清塞音13 j t 舌面前不送气清塞擦音2 p p’ 双唇送气清塞音14 q t’ 舌面前送气清塞擦音3 m 双唇浊鼻音15 x 舌面前清擦音4 f 唇齿清擦音16 z ts 舌尖前不送气清塞擦音5 d t 舌尖前不送气清塞音17 c ts’ 舌尖前送气清塞擦音6 t t' 舌尖前送气清塞音18 s 舌尖前清擦音7 n 舌尖前浊鼻音19 r 舌尖后浊鼻音8 l 舌尖前浊边音20 zh t 舌尖后不送气清塞擦音9 g k 舌面后不送气清塞音21 ch t’舌尖后送气清塞擦音10 k k' 舌面后送气清塞音22 sh 舌尖后清擦音11 ng η 舌面后浊鼻音23 y j 舌面中浊半元音12 h x 舌面后清擦音24 w 舌面后浊半元音附表1:《字母汉字正字表》注:(1)每个音节头一个字为《音节定形字表》中的字。
英语作文zhangjiacheng
英语作文zhangjiachengTitle: The Evolution of ZhangjiachengZhangjiacheng, a bustling metropolis situated at the heart of China's technological and economic development, has undergone a remarkable transformation over the past few decades. Its story is one of resilience, innovation, and relentless pursuit of progress that serves as a beacon for urban growth in the 21st century.The early days of Zhangjiacheng were characterized by modest beginnings. It was a small town with a tight-knit community, where families worked hard to sustain their livelihoods in agriculture and small-scale industries. However, beneath the surface of this seemingly unremarkable place lay untapped potential, waiting to be harnessed by visionaries and pioneers who could see beyond the present.As the world moved towards globalization, Zhangjiacheng began to experience a series of changes that would eventually shape its destiny. The introduction of foreign investment and the establishment of special economic zones provided afertile ground for innovation and entrepreneurship. These policies attracted a wave of investors who recognized the advantages of the area's strategic location, skilled workforce, and favorable business environment.With the influx of capital and expertise, Zhangjiacheng started to develop at an unprecedented pace. Infrastructure projects such as high-speed rail, modern highways, and state-of-the-art airports connected the city to the rest of the country and the world, facilitating trade and travel. The construction of cutting-edge research facilities and universities fostered a knowledge-based economy, attracting talent from across the nation and beyond.One of the most significant milestones in Zhangjiacheng's development was the establishment of the city's technology hub. This cluster of high-tech companies and startups became a crucible for innovation, driving forward advancements in fields such as artificial intelligence, biotechnology, and renewable energy. The technology hub not only created a vibrant ecosystem for research and development but also served as a magnet for international collaborations, further cementing Zhangjiacheng's reputation as a global center of excellence.The rise of Zhangjiacheng as a technological powerhouse was paralleled by its cultural and social evolution. The city underwent a rapid expansion of its urban landscape, with skyscrapers, shopping malls, and entertainment complexes springing up across its skyline. These modern amenities, coupled with a rich historical heritage and traditional cultural sites, made Zhangjiacheng an attractive destination for tourists and expatriates alike.However, the rapid growth also brought challenges. As the population swelled, issues such as urban congestion, environmental degradation, and income inequality became pressing concerns. The city's leaders recognized the need for sustainable development practices to ensure a harmonious balance between economic prosperity and quality of life for its citizens.To address these challenges, Zhangjiacheng implemented a series of progressive policies. Green spaces were expanded, and public transportation was enhanced to reduce carbon emissions and improve air quality. Social welfare programs aimed at reducing poverty and providing equal opportunities for education and healthcare were introduced, narrowing the gap between different socioeconomic groups.The city also embraced the concept of "smart living," integrating advanced technologies into everyday life to enhance efficiency and well-being. Smart grids, watermanagement systems, and waste reduction initiatives were among the many strategies employed to create a more livable environment for residents.As Zhangjiacheng continued to evolve, it became a symbol of hope and inspiration for other cities around the world.Its success story demonstrated that with vision, determination, and a commitment to innovation, even the most humble beginnings could lead to extraordinary achievements.In conclusion, the journey of Zhangjiacheng is a testament to the transformative power of urban development when guided by foresight and a commitment to sustainability. From its humble origins to its current status as a global tech hub, the city has carved a path of progress that serves as a blueprint for future urban growth. The story of Zhangjiacheng is not just about buildings and technology; it is about people and their collective aspiration to build a better world. And as the city looks towards its future, thereis no doubt that Zhangjiacheng will continue to be a beacon of hope and innovation for generations to come.。
第二章 工艺美术运动——工业设计的萌芽
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第二章 工艺美术运动——工业设计的萌芽
第二章 DIERZHANG
工艺美术运动——工业设计的萌芽
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威廉·莫里斯
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装饰风格。提倡哥特式风格和其他的中世纪装饰风格,注重功能,讲 究简单,朴实无华。 三、装饰上推崇自然主义,东方装饰和东方艺术的特点。推崇自然的装饰 纹样,主张艺术家“向自然学习”师承自然。 四、在建筑设计上,强调以功能为主的设计原则,主张就地取材,利用本 地的建筑方法和技术,尽量控制装饰。 五、强调设计的社会功能,认为设计是为人人服务的。
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铁死亡调控机制及其在心血管疾病中的研究进展
㊃综述㊃铁死亡调控机制及其在心血管疾病中的研究进展马赛㊀左庆娟㊀和丽丽㊀张国瑞㊀郭艺芳050051石家庄,河北省人民医院疼痛科(马赛),老年心血管内一科(左庆娟㊁和丽丽㊁郭艺芳);050011石家庄市第三医院心血管内科(张国瑞)通信作者:郭艺芳,电子信箱:yifangguo@DOI:10.3969/j.issn.1007-5410.2023.06.013㊀㊀ʌ摘要ɔ㊀铁死亡是一种近期发现的可调节的程序性细胞坏死方式,涉及铁代谢㊁脂质代谢㊁氨基酸代谢等多种代谢过程,其主要特征为脂质过氧化物生成㊁活性氧超载和谷胱甘肽消耗等㊂研究证实铁死亡参与了多种心血管疾病病理生理过程㊂本文总结了铁死亡调控机制及国内外关于铁死亡在心血管疾病中的研究进展,旨在为心血管疾病的预防和治疗提供新思路㊂ʌ关键词ɔ㊀铁死亡;㊀心力衰竭;㊀心肌病;㊀心血管疾病基金项目:河北省创新能力提升计划项目(199776249D);河北省重点研发计划项目(19277787D)Ferroptosis homeostasis regulation and its research progress in cardiovascular diseases㊀Ma Sai,ZuoQingjuan,He Lili,Zhang Guorui,Guo YifangDepartment of Pain,Hebei General Hospital,Shijiazhuang050051,China(Ma S);Ward1,Department ofGeriatric Cardiology,Hebei General Hospital,Shijiazhuang050051,China(Zuo QJ,He LL,Guo YF); Department of Cardiology,The Third Hospital of Shijiazhuang,Shijiazhuang050011,China(Zhang GR)Corresponding author:Guo Yifang,Email:yifangguo@ʌAbstractɔ㊀Ferroptosis is a recently discovered regulated form of programmed cell death,involvingvarious metabolic processes such as iron metabolism,lipid metabolism,and amino acid metabolism.Its mainfeatures include lipid peroxide generation,oxidative stress,and glutathione depletion.Studies have confirmed the involvement of ferroptosis in various pathophysiological processes of cardiovascular diseases.This article summarizes the regulatory mechanisms of ferroptosis and the research progress on ferroptosis in cardiovascular diseases both domestically and internationally,aiming to provide new insights for the prevention and treatment of cardiovascular diseases.ʌKey wordsɔ㊀Ferroptosis;㊀Heart failure;㊀Cardiomyopathy;㊀Cardiovascular diseaseFund program:Hebei Province Innovation Capability Enhancement Plan Project(199776249D);Hebei Province Key Research and Development Plan Project(19277787D)㊀㊀铁是机体维持正常氧气运输㊁脂质代谢㊁氧化磷酸化等线粒体功能,DNA㊁蛋白质生物合成功能以及其他细胞生物学进程必不可少的微量元素㊂机体内铁稳态维持受多方因素调控,过量的游离铁可与过氧化氢发生芬顿反应,形成羟基自由基及活性氧(reactive oxygen species,ROS),从而造成核酸㊁蛋白质及细胞膜等损伤,水解酶转移,进而引发细胞死亡[1]㊂1981年Sullivan等[2]提出了 铁源性心脏病 假说,阐明铁超载在心血管疾病进程中发挥着重要作用㊂2012年Dixon等提出了 铁死亡 的概念,铁死亡是一种铁依赖的程序性细胞坏死方式,以脂质过氧化物生成㊁ROS超载和谷胱甘肽(glutathione,GSH)消耗等为标志性改变,参与了多种心血管疾病病理生理过程㊂但与其他细胞死亡方式不同,铁死亡既可由实验性小分子物质(如埃拉斯汀㊁原癌基因致死性小分子3和磺胺嘧啶等)以及某些药物(如柳氮磺吡啶㊁索拉非尼和青蒿琥酯等)所诱导,亦可被铁抑素1(ferrostatin-1,Fer-1)和脂血抑素1等物质所抑制[3]㊂即铁死亡机制本身具有可调控性,其中正向调节生物分子包括电压依赖性阴离子通道(voltage-dependent anion channel,VDAC)2/3㊁原癌基因㊁还原型烟酰胺腺嘌呤二核苷酸磷酸(reduced nicotinamide adenine dinucleotide phosphate,NADPH)氧化酶㊁p53等,负向调节生物分子包括谷胱甘肽过氧化物酶4 (glutathione peroxidase4,GPX4)㊁溶质载体家族7成员11 (solute carrier family7-member11,SLC7A11/xCT)㊁热休克蛋白B1㊁核因子E2相关因子2(nuclear factor E2related factor 2,Nrf2)等[4]㊂现将铁死亡调控机制及其在心血管疾病中的研究进展做一综述㊂1㊀铁死亡调控机制1.1㊀铁代谢转铁蛋白(transferrin,Tf)与细胞膜上转铁蛋白受体1 (transferrin receptor1,TFR1)结合后可将Fe3+由细胞外内吞至内含体中,经前列腺六跨膜表皮抗原3还原为Fe2+后,在二价金属离子转运体或锌铁转运蛋白的介导下释放到胞质内不稳定铁池中发挥其生理作用,多余的铁以Fe3+形式存储在铁蛋白中或经膜铁转运蛋白(ferroportin-1,FPN1)转至细胞外[5]㊂铁蛋白能够螯合4500个铁原子,从而保护细胞免受游离铁的干扰,维持铁稳态,铁反应元件结合蛋白2作为调控铁代谢的主要转录因子,可抑制其表达[6]㊂FPN1是目前唯一已知的铁输出蛋白[7]㊂在此过程中,TFR1是关键蛋白㊂Manz等[8]在对铁死亡敏感的原癌基因突变细胞的研究中发现,铁死亡细胞的TFR1表达升高,伴铁蛋白重链(ferritin heavy chain,FTH1)㊁铁蛋白轻链(ferritin light chain, FTL)表达降低,铁超载进而诱导铁死亡发生㊂铁调节蛋白与缺氧诱导因子1等均可增强TFR1的表达[9],热休克蛋白B1等可抑制TFR1的表达[10](图1)㊂1.2㊀脂质代谢细胞膜及细胞器膜上磷脂中多不饱和脂肪酸在酰基辅酶A合成酶长链家族成员4(acyl-CoA synthetase long-chain family member4,ACSL4)的作用下酰基化,在溶血磷脂酰胆碱酰基转移酶3的作用下酯化,生成含多不饱和脂肪酸磷脂㊂该物质结构不稳定,极易被脂氧合酶氧化为4-羟基壬烯醛(4-hydroxy-trans-2-nonenal,4-HNE)和丙二醛(malondialdehyde, MDA)[11]㊂其中ACSL4及脂氧合酶是限速酶,抑制其表达和生物活性可提高细胞对铁死亡的耐受性(图1)㊂1.3㊀氨基酸代谢在GPX4催化作用下GSH可将脂质过氧化产物转化为无毒的脂肪醇㊂GSH是由谷氨酸㊁半胱氨酸和甘氨酸组成的三肽,半胱氨酸由胱氨酸转化生成,胱氨酸经由xCT从胞外运输至胞内,此转运过程决定了GSH的合成效率㊂研究表明,铁死亡诱导剂埃拉斯汀靶向作用[12],p53抑制xCT转录[13],FTH1缺陷心肌细胞xCT表达下调[14]等,均可促进铁死亡发生㊂GSH还可通过NADPH氧化生成,NADPH作为清除脂质过氧化物所必需的还原剂,是铁死亡敏感性的生物标志物㊂GPX4是众所周知的铁死亡关键调节剂,各种内源性分子(如硒㊁多巴胺㊁维生素E㊁辅酶Q10等)和化学药品(如Fer-1㊁右雷佐生等)通过直接抑制或间接失活GPX4来激发铁死亡[15](图1)㊂1.4㊀甲羟戊酸途径甲羟戊酸途径是脂代谢中重要的生物合成途径,广泛存在于真核生物中,以乙酰辅酶A为原料,以类固醇等为主要产物㊂辅酶Q10作为该途径代谢产物之一,是铁死亡的内源性抑制剂,若消耗增多则可增加细胞对铁死亡的敏感性(图1)㊂1.5㊀铁自噬铁自噬的概念在2014年由Mancias等[16]提出,是指由核受体辅激活因子4介导的将铁蛋白靶向转运至自噬体中降解并释放游离铁的一种选择性自噬方式,是一种保守的细胞分解代谢过程㊂适当的铁自噬可以维持细胞内铁含量稳定,但是过度的铁自噬由于释放出大量游离铁而诱发铁死亡(图1)㊂1.6㊀电压依赖性阴离子通道VDAC是位于线粒体外膜的转运离子和代谢产物的跨膜通道蛋白,具有VDAC1㊁VDAC2和VDAC3三种亚型,可调AA/AdA:花生四烯酸/二十二碳四烯酸;CoA:辅酶A;GSS:谷胱甘肽合成酶;γ-GS:γ-谷胺酰半胱氨酸;GPX4:谷胱甘肽过氧化物酶4;ROS:活性氧;CoQ10:辅酶Q10;MVA:甲羟戊酸:HMG-CoA:3-羟基-3-甲基戊二酸单酰辅酶A;Acetyl-CoA:乙酰辅酶a羧化酶;ACSL4:酰基辅酶A 合成酶长链家族成员4;LPCAT3:溶血卵磷脂酰基转移酶3;ALOX15:15-脂氧合酶;VDAC:电压依赖性阴离子通道;NOX:NADPH氧化酶; DMT1:二价金属转运体1;ZIP8/14:锌-铁调节蛋白家族8/14;PCBP1/2:分子伴侣多聚结合蛋白1/2;LC3:微管结合蛋白1轻链3;NCOA4:核受体辅激活剂4图1㊀铁死亡调控机制模式图节线粒体代谢产能过程,参与细胞生存和死亡信号调控㊂有研究证明,铁死亡抑制剂脂血抑素1可通过下调VDAC1表达水平来抑制铁死亡[17]㊂铁死亡诱导剂埃拉斯汀可作用于VDAC2及VDAC3,使得线粒体通透性增加,进而诱导线粒体功能障碍和细胞铁死亡的发生[18]㊂敲低VDAC2和VDAC3基因可抑制铁死亡发生,但过表达VDAC2和VDAC3并没有显著诱发铁死亡,具体机制有待进一步研究[19](图1)㊂2 铁死亡在心血管疾病中的研究进展2.1㊀铁死亡与心力衰竭越来越多的证据表明,铁死亡是心力衰竭(heart failure, HF)病理生理机制中不可或缺的重要环节㊂Lapenna等[20]研究发现,老龄兔心脏组织中铁含量㊁氧化应激标记物等均明显高于正常成年兔,表明铁代谢可能与衰老㊁功能障碍等病理生理相关㊂Liu等[21]在体内通过主动脉缩窄术建立压力超负荷诱导大鼠HF模型,在体外培养经埃拉斯汀或异丙肾上腺素处理的H9c2心肌细胞,结果发现两者均可观察到以铁超载及脂质过氧化物生成增多为特征的铁死亡过程㊂在通过高盐饲料喂养盐敏感大鼠建立的射血分数保留HF模型中,铁死亡相关指标TFR1㊁ACSL4㊁4-HNE表达明显升高, FTH1㊁xCT表达明显降低,提示铁死亡是射血分数保留HF 发病机制之一[22]㊂为了探索铁死亡在HF中的调控机制, Zheng等[23]对GEO公共数据库进行了分析并发现,M2型巨噬细胞外泌体传递CircSnx12是参与铁代谢相关铁死亡的关键调节因子,可通过与miR-224-5p相互作用实现靶向调节与铁死亡相关的FTH1基因,进而调控诱导HF发生的铁死亡机制,所以环状RNA可能成为治疗HF的前瞻性靶标和新型药物研发的突破口㊂另外,阿尔茨海默病小鼠模型具有心脏结构和功能异常等特点,伴ACSL4㊁核受体辅激活因子4表达上调,xCT㊁GPX4表达下调,即存在脂质过氧化㊁氧化应激水平升高,GSH代谢异常以及铁死亡的激活㊂线粒体醛脱氢酶缺陷与阿尔茨海默病患者心功能不全相关,阿尔茨海默病小鼠铁死亡相关指标变化可通过线粒体醛脱氢酶转基因得以逆转,心脏结构和功能亦能得以改善[24]㊂这些发现表明铁死亡与HF㊁心功能不全密切相关㊂2.2㊀铁死亡与心肌缺血/再灌注损伤迄今为止,血运重建仍然是缺血性心肌病最有效的治疗方法,但心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤不可避免,并会造成多种类型细胞死亡,包括铁死亡㊂我们知道,多元醇途径参与了I/R损伤诱导的心肌梗死,Tang等[25]研究发现抑制多元醇途径关键酶可减弱I/R损伤介导的缺氧诱导因子1α㊁Tf㊁TFR1和细胞内铁含量的增加,减少心脏梗死区域面积,过表达多元醇途径关键酶可激活缺氧诱导因子1α,诱导TFR1的表达和铁的积累,加剧脂质过氧化和氧化损伤,故多元醇途径参与调节了I/R损伤介导的铁死亡㊂还有研究发现,泛素特异性蛋白酶7在心脏I/R损伤期间通过激活p53/TFR1通路参与调节铁死亡[26]㊂铁死亡可通过TLR4/Trif/Type1IFN信号通路促进中性粒细胞向冠状动脉内皮细胞黏附以及向受损心肌募集,造成坏死性炎症,加重心脏移植后心肌损伤[27]㊂铁死亡抑制剂可减轻心肌I/R损伤[28]㊂Gao等[29]研究证明细胞内谷氨酰胺分解代谢在铁死亡机制中发挥了关键作用,抑制谷氨酰胺代谢可抑制铁死亡,改善离体心脏模型I/R损伤,为I/R损伤治疗提供了新策略㊂亦有研究表明铁死亡不是发生在心肌缺血阶段,而是发生在心肌再灌注阶段[30],可能与这一阶段氧化的磷脂酰胆碱生成相关[31],为I/R损伤甚至心肌梗死患者建立精准医疗奠定了基础㊂同时,雷帕霉素可通过其靶标哺乳动物雷帕霉素靶蛋白基因过表达抑制铁死亡[32],进而改善心肌缺血,减少I/R损伤㊂在糖尿病心肌I/R损伤模型中,抑制铁死亡可减少内质网应激相关性心肌损伤[33]㊂故抑制铁死亡是I/R心肌损伤治疗的有效策略㊂2.3㊀铁死亡与蒽环类药物心脏毒性多柔比星(doxorubicin,DOX)是临床上常用的蒽环类化疗药物,具有心脏毒性,可造成DOX相关性心肌病,限制其临床应用并产生不良预后[34]㊂有研究表明,高铁基因可通过调节心肌细胞铁沉积来增加DOX诱导的心脏毒性的易感性[35]㊂Fang等[28]研究表明铁死亡机制在DOX诱导小鼠心肌病模型中发挥了关键作用,经Fer-1干预后可显著改善小鼠心肌病变及死亡率㊂通过全转录组测序发现DOX可通过Nrf2上调血红素加氧酶1表达,降解血红素铁,进而诱发铁死亡,且证实铁超载和脂质过氧化主要定位于心肌细胞线粒体,更加明确了线粒体损伤在DOX心肌损伤中的因果关系㊂Tadokoro等[36]同样证实线粒体依赖性铁死亡在DOX心肌损伤进展中的关键作用㊂Liu等[37]应用RNA测序方法发现,在DOX干预后小鼠心脏中,脂代谢途径中的Acot1基因明显下调,经Fer-1处理后部分逆转,且Acot1过表达可抑制铁死亡,进而实现心脏获益㊂因此,Acot1可能是通过抑制铁死亡来预防和治疗DIC的潜在靶点㊂2.4㊀铁死亡与糖尿病性心肌病糖尿病是心血管疾病常见的合并症,可增加心脏对I/R 损伤的易感性和糖尿病性心肌病(diabetic cardiomyopathy, DCM)的发生风险㊂氧化应激已被证实为DCM心脏结构和功能改变的重要因素㊂2022年发表的一项研究首次报道了铁死亡在DCM发病机制中起着至关重要的作用,萝卜硫素可通过AMPK激活NrF2,上调铁蛋白和xCT水平进而抑制铁死亡过程,改善DCM小鼠心脏病变[38]㊂2.5㊀铁死亡与败血症相关心脏损伤败血症致心脏损伤的发生率和死亡率均较高㊂盲肠结扎和穿刺是研究败血症最常用的造模方法,该模型可增加心脏铁含量和脂质过氧化水平,并降低GSH含量和GPX4表达水平,提示败血症引起的心脏损伤可能涉及铁死亡机制,而右美地托咪定可通过抑制铁死亡改善败血症引起的心脏损伤[39]㊂此外,铁死亡已被证明在脂多糖诱导的败血性心肌病模型中起重要作用[40]㊂2.6㊀铁死亡与心律失常目前,全球正面临新型冠状病毒(COVID-19)大流行,而COVID-19感染会导致小鼠心脏起搏细胞功能障碍并诱导铁死亡,酪氨酸激酶抑制剂伊马替尼和铁螯合剂去铁胺可阻断病毒感染和铁死亡相关过程,可能是改善病毒感染后心律失常的潜在机制[41]㊂另一项关于小鼠的研究亦表明铁死亡与心律失常相关,频繁过量饮酒会诱发铁死亡,并增加心房颤动发生率,而铁死亡抑制剂可部分逆转过量饮酒引起的不良反应[42]㊂2.7㊀铁死亡与心肌纤维化Wang等[43]发现在主动脉缩窄致压力超负荷HF模型中,HF晚期心肌纤维化主要由MLK3调节的JNK/p53信号通路介导的铁死亡引起,miR-351基因表达上调可抑制MLK3表达,进而改善心肌纤维化及心功能㊂xCT基因缺失亦可加剧血管紧张素Ⅱ介导的心肌纤维化和功能障碍,为铁死亡参与心肌纤维化提供了证据[44]㊂2.8㊀铁死亡与内皮功能障碍㊁动脉粥样硬化内皮功能障碍是糖尿病标志性病变,是糖尿病心血管并发症的起始和关键因素㊂有研究表明,在糖尿病db/db小鼠的主动脉内皮中观察到xCT表达下降㊁铁积累和脂质过氧化物生成增多以及去内皮化改变,且高糖和白细胞介素-1β可通过p53-xCT-GSH途径诱导静脉内皮细胞发生铁死亡[45]㊂高脂饮食可诱导ApoE-/-小鼠形成动脉粥样硬化,Bai等[46]发现在动脉粥样硬化血管中铁死亡相关蛋白明显上调,Fer-1干预后可部分抑制铁超载和脂质过氧化,并显著降低了xCT 和GPX4的表达水平,同时抑制铁死亡可改善主动脉内皮细胞的活力㊂另一项关于不同严重程度动脉粥样硬化的尸检报告数据表明,重度动脉粥样硬化患者的冠状动脉标本中前列腺素内过氧化物合成酶2㊁ACSL4表达上调,GPX4表达下调[47]㊂故铁死亡与内皮功能障碍和动脉粥样硬化病理学相关,并参与其发生及发展㊂2.9㊀铁死亡与其他镰状细胞病是一种以溶血㊁器官缺血和心血管并发症等为特征的遗传性疾病,该疾病小鼠血红素水平升高,导致心脏铁超载㊁脂质过氧化和铁死亡,抑制铁死亡减轻了与镰状细胞病相关的心肌病[48]㊂有研究发现,吸烟与腹主动脉瘤的发生㊁发展和破裂显著相关[49]㊂Sampilvanjil等[50]首次证实香烟提取物可引起血管平滑肌细胞发生铁死亡,并可能通过铁死亡机制诱导主动脉瘤或夹层㊂此外,Ma等[51]首次证实铁死亡是血管钙化发生的新机制㊂3㊀铁死亡抑制剂在心血管疾病中的应用由于铁死亡机制是治疗和预防心血管疾病的潜在靶点,铁死亡抑制剂在心血管疾病中的应用逐渐增多㊂UAMC-3203作为比Fer-1更稳定和有效的铁螯合剂,能更好地预防动物模型中铁死亡驱动的多器官功能障碍,可能更适合临床试验推广[52]㊂针对脂血抑素1的研究相对较少,但具有与Fer-1相似的保护作用,可显著减少棕榈酸诱导的心脏损伤[53]㊂抗氧化剂N-乙酰半胱氨酸可提高半胱氨酸的生物利用度,其抗铁死亡作用已得到证实[54],并可减少糖尿病大鼠心肌I/R损伤,为临床应用提供了理论基础[55]㊂去铁酮㊁化合物968在心脏I/R损伤中亦发挥了心脏保护作用[56,29]㊂右雷佐生是乙二胺四乙酸环状衍生物,是唯一一个被美国食品药品监督管理局批准的用来预防DOX相关性心肌病的铁螯合剂,可以直接进入心肌细胞线粒体并减少铁积累[57]㊂人脐带血中间充质干细胞的外泌体可通过抑制急性心肌梗死小鼠模型中的铁死亡来实现心脏保护作用[58]㊂卡格列净㊁葛根素㊁阿托伐他汀可抑制铁死亡改善心功能[21-22,59],为HF提供了潜在的治疗策略,而氧化锌纳米粒子可诱导铁死亡,促进内皮损伤发生㊂此外,常用的心脏药物可能具有未发现的抗铁死亡活性,如卡维地洛已被证明可以抑制铁死亡,而与其对β-肾上腺素能受体的作用无关㊂尽管抑制铁死亡已在多种动物模型中显示出心脏获益,但迄今为止尚未进行使用铁死亡抑制剂治疗心血管疾病的临床试验㊂4㊀小结铁死亡作为最近发现的程序性细胞死亡类型,是心血管疾病发生发展的关键机制之一㊂近年来日益引起人们的重视,相关研究不断增加㊂本文总结了铁死亡相关调控机制及其在心血管疾病中的研究进展和应用㊂但铁死亡研究领域的一些关键机制尚待研究和验证,需要我们进一步探索去揭示铁死亡的精细分子机制,从而为靶向铁死亡以减少主要不良心血管事件以及防治心血管疾病提供更加充分的理论依据,为预防和治疗心血管疾病提供新的生物标志物和前瞻性靶标㊂利益冲突:无参㊀考㊀文㊀献[1]Ward RJ,Zucca FA,Duyn JH,et al.The role of iron in brainageing and neurodegenerative disorders[J].Lancet Neurol,2014,13(10):1045-1060.DOI:10.1016/S1474-4422(14)70117-6.[2]Sullivan JL.Iron and the sex difference in heart disease risk[J].Lancet,1981,1(8233):1293-1294.DOI:10.1016/s0140-6736(81)92463-6.[3]Stockwell BR,Friedmann Angeli JP,Bayir H,et al.Ferroptosis:A regulated cell death nexus linking metabolism,redox biology,and disease[J].Cell,2017,171(2):273-285.DOI:10.1016/j.cell.2017.09.021.[4]Xie Y,Hou W,Song X,et al.Ferroptosis:Process and function[J].Cell Death Dier,2016,23:369-379.DOI:10.1038/cdd.2015.158.[5]Feng H,Schorpp K,Jin J,et al.Transferrin Receptor Is aSpecific Ferroptosis Marker[J].Cell Rep,2020,30(10):3411-3423.DOI:10.1016/j.celrep.2020.02.049. [6]Gammella E,Recalcati S,Rybinska I,et al.Iron-induceddamage in cardio-myopathy:Oxidative-dependent andindependent mechanisms[J].Oxid Med Cell Longev,2015,2015:230182.DOI:10.1155/2015/230182.[7]Kakhlon O,Cabantchik ZI.The labile iron pool:characterization,measurement,and participation in cellularprocesses(1)[J].Free Radic Biol Med,2002,33(8):1037-1046.DOI:10.1016/s0891-5849(02)01006-7.[8]Manz DH,Blanchette NL,Paul BT,et al.Iron and cancer:recent insights[J].Ann N Y Acad Sci,2016,1368(1):149-161.DOI:10.1111/nyas.13008.[9]Hirota K.An intimate crosstalk between iron homeostasis andoxygen metabolism regulated by the hypoxia-inducible factors(HIFs)[J].Free Radic Biol Med,2019,133:118-129.DOI:10.1016/j.freeradbiomed.2018.07.018.[10]Gao M,Monian P,Jiang X.Metabolism and iron signaling inferroptotic cell death[J].Oncotarget,2015,6(34):35145-35146.DOI:10.18632/oncotarget.5671.[11]Barrera G,Pizzimenti S,Ciamporcero ES,et al.Role of4-hydroxynonenal-protein adducts in human diseases[J].AntioxidRedox Signal,2015,22(18):1681-1702.DOI:10.1089/ars.2014.6166.[12]Dixon SJ,Lemberg KM,Lamprecht MR,et al.Ferroptosis:aniron-dependent form of nonapoptotic cell death[J].Cell,2012,149(5):1060-1072.DOI:10.1016/j.cell.2012.03.042. [13]Jiang L,Kon N,Li T,et al.Ferroptosis as a p53-mediatedactivity during tumour suppression[J].Nature,2015,520(7545):57-62.DOI:10.1038/nature14344.[14]Fang X,Cai Z,Wang H,et al.Loss of cardiac ferritin Hfacilitates cardiomyopathy via Slc7a11-Mediated ferroptosis[J].Circ Res,2020,127(4):486-501.DOI:10.1161/CIRCRESAHA.120.316509.[15]Seibt TM,Proneth B,Conrad M.Role of GPX4in ferroptosisand its pharmacological implication[J].Free Radic Biol Med,2019,133:144-152.DOI:10.1016/j.freeradbiomed.2018.09.014.[16]Mancias JD,Wang X,Gygi SP,et al.Quantitative ProteomicsIdentifies NCOA4as the Cargo Receptor Mediating Ferritinophagy[J].Nature,2014,509(7498):105-109.DOI:10.1038/nature13148.[17]Feng Y,Madungwe NB,Imam Aliagan AD,et al.Liproxstatin-1protects the mouse myocardium against ischemia/reperfusioninjury by decreasing VDAC1levels and restoring GPX4levels[J].Biochem Biophys Res Commun,2019,520(3):606-611.DOI:10.1016/j.bbrc.2019.10.006.[18]Chen Y,Liu Y,Lan T,et al.Quantitative profiling of proteincarbon-ylations in ferroptosis by an aniline-derived probe[J].JAm Chem Soc,2018,140(13):4712-4720.DOI:10.1021/jacs.8b01462.[19]Lemasters JJ.Evolution of voltage-dependent anion channelfunction:From molecular sieve to governator to actuator offerroptosis[J].Front Oncol,2017,7:303.DOI:10.3389/fonc.2017.00303.[20]Lapenna D,Ciofani G,Pierdomenico SD,et al.Iron status andoxidative stress in the aged rabbit heart[J].J Mol Cell Cardiol,2018,114:328-333.DOI:10.1016/j.yjmcc.2017.11.016.[21]Liu B,Zhao C,Li H,et al.Puerarin protects against heartfailure induced by pressure overload through mitigation offerroptosis[J].Biochem Biophys Res Commun,2018:497(1):233-240.DOI:10.1016/j.bbrc.2018.02.061. [22]Ma S,He LL,Zhang GR,et al.Canagliflozin mitigatesferroptosis and ameliorates heart failure in rats with preservedejection fraction[J].Naunyn-Schmiedeberg s Arch Pharmacol,2022,395(8):945-962.DOI:10.1007/s00210-022-02243-1.[23]Zheng H,Shi L,Tong C,et al.circSnx12is involved inferroptosis during heart failure by targeting miR-224-5p[J].FrontCardiovasc Med,2021,8:656093.DOI:10.3389/fcvm.2021.656093.[24]Zhu ZY,Liu YD,Gong Y,et al.Mitochondrial aldehydedehydrogenase(ALDH2)rescues cardiac contractile dysfunctionin an APP/PS1murine model of Alzheimer s disease viainhibition of ACSL4-dependent ferroptosis[J].Acta PharmacolSin,2022,43(1):39-49.DOI:10.1038/s41401-021-00635-2.[25]Tang WH,Wu S,Wong TM,et al.Polyol pathway mediatesiron-induced oxidative injury in ischemic-reperfused rat heart[J].Free Radic Biol Med,2008,45(5):602-610.DOI:10.1016/j.freeradbiomed.2008.05.003.[26]Tang LJ,Zhou YJ,Xiong XM,et al.Ubiquitin-specific protease7promotes ferroptosis via activation of the p53/TfR1pathway inthe rat hearts after ischemia/reperfusion[J].Free Radic BiolMed,2021,162:339-352.DOI:10.1016/j.freeradbiomed.2020.10.307.[27]Li W,Feng G,Gauthier JM,et al.Ferroptotic cell death andTLR4/Trif signaling initiate neutrophil recruitment after hearttrans-plantation[J].J Clin Invest,2019,129(6):2293-2304.DOI:10.1172/JCI126428.[28]Fang X,Wang H,Han D,et al.Ferroptosis as a target forprotection against cardiomyopathy[J].Proc Natl Acad Sci,2019,116(7):2672-2680.DOI:10.1073/pnas.1821022116.[29]Gao M,Monian P,Quadri N,et al.Glutaminolysis andTransferrin Regulate Ferroptosis[J].Mol Cell,2015,59(2):298-308.DOI:10.1016/j.molcel.2015.06.011. [30]Tang LJ,Luo XJ,Tu H,et al.Ferroptosis occurs in phase ofreperfusion but not ischemia in rat heart following ischemia orischemia/reperfusion[J].Naunyn Schmiedebergs ArchPharmacol,2021,394:401-410.DOI:10.1007/s00210-020-01932-z.[31]Ajoolabady A,Aslkhodapasandhokmabad H,Libby P,et al.Ferritinophagy and ferroptosis in the management of metabolicdiseases[J].Trends Endocrinol Metab,2021,32(7):444-462.DOI:10.1016/j.tem.2021.04.010.[32]Baba Y,Higa JK,Shimada BK,et al.Protective effects of themechanistic target of rapamycin against excess iron and ferroptosisin cardiomyocytes[J].Am J Physiol Heart Circ Physiol,2018,314(3):H659-H668.DOI:10.1152/ajpheart.00452.2017.[33]Li W,Li W,Leng Y,et al.Ferroptosis is involved in diabetesmyocardial ischemia/reperfusion injury through endoplasmic reti-culum stress[J].DNA Cell Biol,2020,39(2):210-225.DOI:10.1089/dna.2019.5097.[34]Young RC,Ozols RF,Myers CE.The anthracyclineantineoplastic drugs[J].N Engl J Med,1981,305(3):139-153.DOI:10.1056/NEJM198107163050305.. [35]Miranda CJ,Makui H,Soares RJ,et al.Hfe deficiency increasessusceptibility to cardiotoxicity and exacerbates changes in ironmetabolism induced by doxorubicin[J].Blood,2003,102(7):2574-2580.DOI:10.1182/blood-2003-03-0869. [36]Tadokoro T,Ikeda M,Ide T,et al.Mitochondria-dependentferroptosis plays a pivotal role in doxorubicin cardiotoxicity[J].JCI Insight,2020,5(9):e132747.DOI:10.1172/jci.insight.132747.[37]Liu Y,Zeng L,Yang Y,et al.Acyl-CoA thioesterase1preventscardiomyocytes from Doxorubicin-induced ferroptosis via shapingthe lipid composition[J].Cell Death Dis,2020,11(9):756.DOI:10.1038/s41419-020-02948-2.[38]Wang X,Chen X,Zhou W,et al.Ferroptosis is essential fordiabetic cardiomyopathy and is prevented by sulforaphane viaAMPK/NRF2pathways[J].Acta Pharm Sin B,2022,12(2):708-722.DOI:10.1016/j.apsb.2021.10.005. [39]Wang C,Yuan W,Hu A,et al.Dexmedetomidine alleviatedsepsis-induced myocardial ferroptosis and septic heart injury[J].Mol Med Rep,2020,22(1):175-184.DOI:10.3892/mmr.2020.11114.[40]Li N,Wang W,Zhou H,et al.Ferritinophagy-mediatedferroptosis is involved in sepsis-induced cardiac injury[J].FreeRadic Biol Med,2020,160:303-318.DOI:10.1016/j.freeradbiomed.2020.08.009.[41]Han Y,Zhu J,Yang L,et al.SARS-CoV-2Infection InducesFerroptosis of Sinoatrial Node Pacemaker Cells[J].Circ Res,2022,130(7):963-977.DOI:10.1161/CIRCRESAHA.121.320518.[42]Dai C,Kong B,Qin T,et al.Inhibition of ferroptosis reducessusceptibility to frequent excessive alcohol consumption-inducedatrial fibrillation[J].Toxicology,2022,465:153055.DOI:10.1016/j.tox.2021.153055.[43]Wang J,Deng B,Liu Q,et al.Pyroptosis and ferroptosisinduced by mixed lineage kinase3(MLK3)signaling incardiomyocytes are essential for myocardial fibrosis in response topressure overload[J].Cell Death Dis,2020,11(7):574.DOI:10.1038/s41419-020-02777-3.[44]Zhang X,Zheng C,Gao Z,et al.SLC7A11/xCT preventscardiac hypertrophy by inhibiting ferroptosis[J].CardiovascDrugs Ther,2022,36(3):437-447.DOI:10.1007/s10557-021-07220-z.[45]Luo EF,Li HX,Qin YH,et al.Role of ferroptosis in the processof diabetes-induced endothelial dysfunction[J].World JDiabetes,2021,12(2):124-137.DOI:10.4239/wjd.v12.i2.124.[46]Bai T,Li M,Liu Y,et al.Inhibition of ferroptosis alleviatesatherosclerosis through attenuating lipid peroxidation andendothelial dysfunction in mouse aortic endothelial cell[J].FreeRadic Biol Med,2020,160:92-102.DOI:10.1016/j.freeradbiomed.2020.07.026.[47]Zhou Y,Zhou H,Hua L,et al.Verification of ferroptosis andpyroptosis and identification of PTGS2as the hub gene in humancoronary artery atherosclerosis[J].Free Radic Biol Med,2021,171:55-68.DOI:10.1016/j.freeradbiomed.2021.05.009.[48]Menon AV,Liu J,Tsai HP,et al.Excess heme upregulatesheme oxygenase1and promotes cardiac ferroptosis in mice withsickle cell disease[J].Blood,2022,139(6):936-941.DOI:10.1182/blood.2020008455.[49]Norman PE,Curci JA.Understanding the effects of tobaccosmoke on the pathogenesis of aortic aneurysm[J].ArteriosclerThromb Vasc Biol,2013,33(7):1473-1477.DOI:10.1161/ATVBAHA.112.300158.[50]Sampilvanjil A,Karasawa T,Yamada N,et al.Cigarette smokeextract induces ferroptosis in vascular smooth muscle cells[J].Am J Physiol Heart Circ Physiol,2020,318(3):H508-H518.DOI:10.1152/ajpheart.00559.2019.[51]Ma WQ,Sun XJ,Zhu Y,et al.Metformin attenuateshyperlipidaemia-associated vascular calcification through anti-ferroptotic effects[J].Free Radic Biol Med,2021,165:229-242.DOI:10.1016/j.freeradbiomed.2021.01.033. [52]Van Coillie S,Van San E,Goetschalckx I,et al.Targetingferroptosis protects against experimental(multi)organ dysfunctionand death[J].Nat Commun,2022,13(1):1046.DOI:10.1038/s41467-022-28718-6.[53]Wang N,Ma H,Li J,et al.HSF1functions as a key defenderagainst palmitic acid-induced ferroptosis in cardiomyocytes[J].JMol Cell Cardiol,2021,150:65-76.DOI:10.1016/j.yjmcc.2020.10.010.[54]Badgley MA,Kremer DM,Maurer HC,et al.Cysteine depletioninduces pancreatic tumor ferroptosis in mice[J].Science,2020,368(6486):85-89.DOI:10.1126/science.aaw9872. [55]Wang C,Zhu L,Yuan W,et al.Diabetes aggravates myocardialischaemia reperfusion injury via activating Nox2-relatedprogrammed cell death in an AMPK-dependent manner[J].JCell Mol Med,2020,24(12):6670-6679.DOI:10.1111/jcmm.15318.[56]Behrouzi B,Weyers JJ,Qi X,et al.Action of iron chelator onintramyocardial hemorrhage and cardiac remodeling followingacute myocardial infarction[J].Basic Res Cardiol,2020,115(3):24.DOI:10.1007/s00395-020-0782-6. [57]Li N,Jiang W,Wang W,et al.Ferroptosis and its emergingroles in cardiovascular diseases[J].Pharmacol Res,2021,166:105466.DOI:10.1016/j.phrs.2021.105466. [58]Song Y,Wang B,Zhu X,et al.Human umbilical cord blood-derived MSCs exosome attenuate myocardial injury by inhibitingferroptosis in acute myocardial infarction mice[J].Cell BiolToxicol,2021,37(1):51-64.DOI:10.1007/s10565-020-09530-8.[59]Ning D,Yang X,Wang T,et al.Atorvastatin treatmentameliorates cardiac function and remodeling induced byisoproterenol attack through mitigation of ferroptosis[J].BiochemBiophys Res Commun,2021,574:39-47.DOI:10.1016/j.bbrc.2021.08.017.(收稿日期:2023-01-08)(本文编辑:李鹏)㊃消息㊃欢迎关注和投稿Aging Medicine㊀㊀Aging Medicine(ISSN:2475-0360)由北京医院国家老年医学中心主办,中华医学会老年医学分会学术指导,由国际著名出版集团Wiley出版,于2018年5月正式创刊发行㊂杂志是中华医学会老年医学分会的唯一一本面向国内外的官方英文国际刊物,2020年起先后被Pubmed Central(PMC)㊁DOAJ㊁EMBASE㊁EBSCOhost㊁Ovid㊁ProQuest㊁Reprints Desk㊁CCC和Scopus等数据库收录㊂2023年被ESCI数据库收录, 2024年入选‘科技期刊世界影响力指数(WJCI)报告“,影响因子为2.716,WAJCI为0.770,WI为0.181,WJCI为0.951, WJCI学科排名为56/90,位居医学综合类科技期刊Q3区㊂Aging Medicine办刊宗旨是贯彻党和国家的卫生方针政策,贯彻理论与实践㊁普及与提高相结合的方针㊂杂志现为双月刊,主要刊登老年人相关疾病的预防㊁临床诊断和治疗㊁康复㊁照护㊁心理及社会等方面的文章,旨在推动老年医学的发展,应对全球人口老龄化的挑战,积极打造融学术性㊁先进性㊁实用性于一体的国际交流平台,力争早日跻身国际化老年医学一流期刊行列,在国际舞台发出中国老年医学的最强音㊂Aging Medicine栏目包括指南与共识㊁专家论坛㊁临床研究㊁基础研究㊁流行病学调查㊁荟萃分析㊁疑难病例分析㊁病例报告㊁综述㊁社论㊁述评㊁来信等,设立衰老与长寿专栏㊁人工智能与老年医学专栏㊁老年医学公卫和流病专栏㊂期刊论文执行严格的同行评议,发表的全文免费开放获取(OpenAccess,OA),确保每篇文章可以第一时间被全世界的老年医学从业人员免费阅读㊁下载和分享㊂Aging Medicine正在进行2024年的专题约稿工作,约稿内容包括衰老与长寿㊁老年糖尿病㊁老年肌少症㊁老年脑血管疾病㊁老年心血管疾病㊁人工智能㊁老年营养㊁老年康复护理㊁老年心理健康等,热烈欢迎各位国内外医学同道积极投稿㊂欢迎访问Aging Medicine杂志官方网站(https:// /journal/24750360)进行投稿和获得电子版全文㊂联系方式通信地址:北京市东城区大佛寺东街6号院105室邮政编码:100010联系电话*************-8889电子信箱:agmeditor@投稿地址:https:///journal/24750360官方微信:Aging Medicine杂志。
河南方言词典
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《2023年欧洲器官移植学会共识声明
《2023年欧洲器官移植学会共识声明:肝移植中的生物标志物》摘译白易,李金明,张雅敏天津市第一中心医院肝胆胰外科,天津 300392通信作者:张雅敏,138****************(ORICD:0000-0001-7886-2901)摘要:2023年8月,欧洲器官移植学会在线发表了“2023年欧洲器官移植学会共识声明:肝移植中的生物标志物”。
该共识主要围绕肝移植中的生物标志物、临床适用性和未来需求等方面展开,通过回顾有关原发性疾病复发、慢性肾脏疾病发展和安全摆脱免疫抑制的文献,来探索新的生物标志物在预测肝移植预后方面的作用。
该共识从肝移植后复发性肝脏疾病、复发性肝细胞癌、摆脱免疫抑制、慢性肾脏疾病进展四个方面展开研究,强调了生物标志物在预测或检测疾病复发中的重要性,同时也提出了仍需要更大规模的前瞻性研究以提高证据质量。
笔者团队对该共识声明进行摘译,系统介绍了该共识声明中四个方面的研究以及相关讨论和结论,以期为肝移植中新生物标志物的发现和探索提供更多循证医学证据。
关键词:肝移植;生物标志物;共识;欧洲基金项目:国家自然科学基金(82372194);天津市卫生健康科技项目(TJWJ2021ZD002, TJWJ2023MS012)An excerpt of European Society for Organ Transplantation consensus statement on biomarkers in liver transplantation (2023)BAI Yi, LI Jinming, ZHANG Yamin.(Department of Hepatobiliary and Pancreatic Surgery, Tianjin First Central Hospital, Tianjin 300392, China)Corresponding author: ZHANG Yamin,138****************(ORICD: 0000-0001-7886-2901)Abstract:In August 2023, the European Society for Organ Transplantation (ESOT) published the ESOT Consensus Statement on Biomarkers in Liver Transplantation online. The consensus statement focuses on biomarkers in liver transplantation,clinical applicability, and future needs and explores the role of new biomarkers in predicting liver transplantation outcomes by reviewing the literature on primary disease recurrence, development of chronic kidney disease (CKD), and safe weaning of immunosuppression. This consensus statement conducts studies from the four aspects of recurrent liver disease after liver transplantation,recurrent hepatocellular carcinoma,weaning of immunosuppression,and CKD progression,emphasizes the importance of biomarkers in predicting or detecting disease recurrence, and proposes that large-scale prospective studies are still needed to improve the quality of evidence. The author’s team gives an excerpt of the consensus statement and systematically introduces the four aspects of the consensus statement and related discussions and conclusions,in order to provide more evidence-based medical evidence for identifying and exploring new biomarkers for liver transplantation.Key words:Liver Transplantation; Biomarkers; Consensus; EuropeResearch funding:National Natural Science Foundation of China (82372194);Tianjin Health Science and Technology Project (TJWJ2021ZD002, TJWJ2023MS012)共识确立过程由欧洲器官移植学会(ESOT)及其各部门专门的工作组负责,工作组确定了与肝移植(livertransplantation,LT)中生物标志物相关的关键问题。
修身养性自我提升发展模式人生真正的自己实现成功的自己ppt课件
手表定理
更多标准会让你无所适从
❖ 故事缘由:“手表定律”是由英国心理学家P·撇 盖提出来的,也有人将其成为“矛盾定律”。主 要观点是:只有一块手表时,可以知道准确的时 间,但如果拥有两块钱或两块以上的手表,则很 难说出准确的时间。两块手表不仅会让人们不知 道准确的时间,而且还会扰乱看表人对所持时间 准确性的信心。
第一章
认识真正的自己
了解真实的自己,正视客观的事实
经营者提供商品或者服务有欺诈行为 的,应 当按照 消费者 的要求 增加赔 偿其受 到的损 失,增 加赔偿 的金额 为消费 者购买 商品的 价款或 接受服 务的费 用
巴纳姆效应
人贵在自知,难在自知
❖ 故事缘由:“巴纳姆效应”是以著名魔术师费尼 公司·泰勒·巴纳姆来命名的,他曾经在评价自己 的表演时说,他的节目之所以受欢迎,是因为节 目中包含了每个人都喜欢的成分,所以每一分钟 都有人上当受骗。
❖ 专家总结:每个人都有展示自我的心理,但在展 现自我的同时,仍然要细心地听取他人的意见, 保持谦虚的品质。
DIERZHANG
经营者提供商品或者服务有欺诈行为 的,应 当按照 消费者 的要求 增加赔 偿其受 到的损 失,增 加赔偿 的金额 为消费 者购买 商品的 价款或 接受服 务的费 用
第二章
打败消极的自己
齐加尼克效应
有些压力很正常,不必为此太紧张
❖ 故事缘由:“齐加尼克效应”是法国心理学家齐 加尼克在一次实验中提出的,实验中得到的结果 是;顺利完成工作任务的人紧张情绪会逐渐消失, 而未顺利完成工作任务的人紧张情绪会持续存在, 并因此总被困扰。
❖ 专家总结:人们在接受某项工作时会产生一定的 紧张心理,这种心理会伴随人们到任务完成,如 果任务没有完成,紧张心理会持续存在。
细胞周期G1检查点控制机制的分子调控研究
细胞周期G1检查点控制机制的分子调控研究细胞周期是细胞生长和分裂的重要过程,包括G1期、S期、G2期和M期。
其中,G1期是细胞周期中最长的一个阶段,也是最重要的期间之一。
在G1期,细胞会接受一系列信号来决定是否进行分裂,“G1检查点”就是这些信号中形成的一个机制。
G1检查点作为细胞周期中最重要的控制点之一,扮演着调节细胞生长和分裂的重要角色。
在过去的几十年中,研究人员对细胞周期G1检查点控制机制的分子调控进行了深入的探究。
1. 细胞周期G1检查点背景知识在细胞周期中,G1期是细胞生长和分化的关键时期。
在这个时期,细胞吸收营养物质并增长到一定的大小,质量和数量都达到一定程度后才能进入下一个阶段。
如果一个细胞在G1期中出现DNA损伤,那么就无法继续前进到下一个周期,而是被阻断在G1期。
这样做,可以让细胞有足够的时间修复DNA损伤,或者激活凋亡程序。
2. 细胞周期G1检查点控制机制的分子调控细胞周期G1检查点的控制机制主要包括两个关键的蛋白复合物:CDK复合物和Rb蛋白复合物。
CDK复合物在细胞周期中起着重要的作用。
这个复合物由两个组成部分组成:一个CDK(cyclin-dependent kinase)和一个环素。
在G1期,环素D和环素E结合到CDK4/6上,形成复合物。
这个复合物进一步激活E2F转录因子,以便控制细胞周期的下一个阶段的转录。
Rb蛋白复合物在细胞周期中同样起着重要作用。
它由Rb蛋白和多个转录因子组成。
在G1期,Rb蛋白复合体通过与E2F转录因子结合压制细胞周期中的下一个阶段的转录。
研究表明,CDK和Rb蛋白复合体之间存在一个重要的互动关系。
当环素D和环素E结合到CDK4/6上时,它们会磷酸化Rb蛋白,导致Rb蛋白松弛,释放E2F转录因子以便进行转录。
一旦DNA受到损伤,p53会被激活并诱导p21表达,p21又会抑制CDK,并防止环素D和环素E结合,使Rb蛋白得以紧密绑定E2F,从而抑制细胞生长和分裂。
张艾迪(创始人):OneWorld,OneDream(AOOOiA)
OneWorld OneDream
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪 The Antarctica.World No.1 Girl The Oceania.World No.1 Girl The World No.1 all.internet Girl EidyzhangFounderCEO. theWorldNO.1Gilr+TheWorldNO.1internetGirl
OneWorld OneDream
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
Eidyzhang:FounderCEO 精英CEO. 世界最高级创始人 FounderCEO:Eidyzhang;
OneWorld OneDream
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
希望.可以让我们从这里到达那里 让我们把梦想走进现实 梦想让我们懂得分享Share the world 我们为拥有梦想而自豪 为世界的梦想加油喝彩!
OneWorld OneDream
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
AOOOiA.FounderGEO(Global.224CEO) EidyzhangI张艾迪
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2003-2004学年度上学期
高中学生学科素质训练
高一化学同步测试(5)—《碱金属元素》
一、选择题(每小题3分,共10题,计30分,每小题只有一个正确答案)
1.下列关于碱金属叙述中正确的是()A.原子的最外层电子数都为1,次外层电子数都为8
B.单质的化学性质活泼,易失电子发生氧化反应
C.除锂外均以化合态存在于自然界中
D.单质的密度都小于1
2.钠和锂有相似的化学性质,下列说法中能较好地解释这个事实的是()A.都是金属元素B.原子半径相差不大
C.最外层电子数相同D.化合价相同
3.下列物品的盛放错误的是()A.过氧化钾固体必须密封保存B.烧碱必须密封保存
C.碱金属必须保存在煤油中D.氢氧化钠溶液用带橡胶塞的玻璃瓶盛放4.在空气或氧气中加热,主要生成碱性氧化物的是()A.Li B.Na C.K D.Rb
5.下列物质与水反应最剧烈的是()A.Li B.Na C.K D.Rb
6.以下关于铷的叙述,不正确的是()
①铷的密度比钠大,熔点比钠高②与冷水不反应,与热水反应放出氢气
③铷盐大多数都易溶于水④铷的原子半径和离子半径都分别比钠大
A.①②B.②③C.③④D.①④
7.焰色反应指的是()A.可燃物质在燃烧时其火焰表现出的颜色
B.是一种检验各种元素普遍应用的一种方法
C.一部分金属及其化合物在无色火焰上燃烧时火焰呈现出的特征颜色
D.把一些金属的盐溶液放在火焰上加热
8.下列关于铯的叙述正确的是()A.硫酸铯是一种难溶性离子化合物
B.碳酸氢铯加热能迅速分解,碳酸铯受热不分解
C.铯能在氧气中燃烧生成氧化铯
D.在自然界中有少量游离态的铯存在
9.合金有许多特点,如Na—K合金为液体,而Na和K的单质均为固体。
据此试推测:生铁、纯铁、碳三种物质中,熔点最低的是()A.纯铁B.生铁C.碳D.无法确定
10.下列对碱金属性质的叙述中,正确的是()A.单质都是银白色的柔软金属,密度都较小
B.单质在空气中燃烧生成的都是过氧化物
C.碱金属单质与水剧烈反应生成碱和氢气
D.单质的熔、沸点随着原子序数的增加而升高
二、选择题:(每小题有1—2个答案,每小题4分,共20分)
11.下面是比较过氧化钠和氧化钠性质异同点的有关叙述,其中错误的是()A.过氧化钠和氧化钠长期置于空气中最终产物相同
B.过氧化钠和氧化钠都能与二氧化碳或水发生化合反应
C.过氧化钠和氧化钠与水反应都有氢氧化钠生成
D.过氧化钠是强氧化剂,而氧化钠只是一种碱性氧化物
12.工业上常用氨碱法制取碳酸钠(将氨和二氧化钠先后通入饱和食盐水而析出小苏打,再经过滤、焙烧,得到纯碱),但却不能用氨碱法制碳酸钾,这是因为在溶液中()A.KHCO3溶解度较大B.KHCO3溶解度较小
C.K2CO3溶解度较大D.K2CO3溶解度较小
13.在一定温度下,向某饱和硫酸钠溶液中加入ag无水Na2SO4粉末,搅拌、静置后,析出bgNa2SO4·10H2O晶体。
下列量中,可以根据已知条件计算的是()
①该温度下硫酸钠的溶解度②原饱和溶液减少的水的质量
③原饱和溶液减少的溶质的质量④析出晶体中含Na2SO4的质量
A.①③B.③④C.②④D.全部
14.①钾比水轻;②钾的熔点较低;③钾与水反应时要放出热量;④钾与水反应后溶液呈碱性。
某学生将一小块金属钾投入滴有酚酞试液的水中,以上实验能证明上述四点性质中的()A.①④B.①②④C.①③④D.①②③④
15.在天平两边各放一个相同质量的烧杯,分别加入100gH2O,向左盘烧杯中加入4.6g金属钠,为了保持天平指针指向零点,应向右盘加入金属钾的质量为()A.3.90g B.4.52g C.5.12g D.7.80g
三、填空题:
16.(12分)根据草木灰中提取钾盐的实验,填写下列空白:
(1)此实验操作顺序如下:①称量样品;②溶解、沉淀;③_________;④____ __;
⑤冷却结晶。
(2)用托盘天平(指针向上的)称量样品时,若指针偏向右边,则表示:_____ ___ (选择A.B.C.D填空)。
A.左盘重,样品轻B.左盘轻,砝码重
C.右盘重,砝码轻D.右盘轻,样品重
(3)在进行第③步操作时,有时可能要重复进行,其原因是_________________。
(4)在进行第④步操作时,要用玻璃棒不断小心地搅动液体,其主要目的是为了防止___________ ______。
(5)所得产物中,主要钾盐有:___________等。
17.(8分)有A.B.C.d四瓶未知溶液,它们是KCl、HCl、KOH和酚酞,有人不用任何试剂就能把它们一一鉴别出来,其实验步骤如下:
①取少许溶液两两混合,据此把四种溶液分成两组。
②取一组混合溶液,不断滴入另一组中的一种未知溶液,据此鉴别出a和b。
③再取2mL已鉴别出的a溶液,滴入3滴未知溶液c,再加入4mL未知溶液d,在这个
过程中无明显变化。
综上实验可以确认a是___________,b是____________,c是__________,d是__________。
18.(4分)回答下列问题:
(1)氢氧化钠固体或溶液为什么要保存在密闭容器里?
(2)钠和钾的外观很相似,怎样来鉴别它们?
19.(4分)用离子方程式表示除去下列括号内的杂质的反应:
(1)CO2(HCl):____________ __________________________
(2)NaCl(Na2CO3)(均是溶液)____________________________
(3)NaOH(Na2CO3)_____________________________________
(4)NaHCO3(Na2CO3)___________________________________
20.(4分)有A.B.C.D四种可溶性离子化合物,它们的阳离子是Ag+、Na+、Mg+、Cu2+,阴离子是Cl-、OH-、NO、SO(每种离子只能用一次),现将溶液两两混合,记录现象如下:A+B→白色沉淀B+D→白色沉淀C+D→蓝色沉淀
则A.B.C.D的化学式分别是_________、___________、__________、__________。
21.(6分)苏打和小苏打有着广泛的应用。
试从消耗反应物的量等角度,回答下列问题:(1)做面条时防止面粉较长时间储存变酸味,常加入适量的面碱,选用_____ _____,因为_______________ ______________。
(2)用于洗涤餐具及实验室的玻璃仪器等,选用______ _____,因为_______ ____ ____________ _________________________。
(3)胃溃疡(胃壁溃烂或穿孔)病人的胃酸过多,医生给服用Al(OH)3胶乳,既不用苏打也不用小苏打,是因为__________________________________________。
四、计算题:(共12分)
22.(6分)将10g碳酸钠和碳酸氢钠的混合物同足量的盐酸反应后,所生成的气体被烧碱溶液完全吸收,烧碱溶液增重4.4g,求混合物中碳酸钠的质量分数。
23.(6分)向100g8%的NaOH溶液中通入CO2生成的盐的质量为13.7g时,求固体盐的成份。
五、《碱金属元素》答案
一、选择题:
1、B
2、C
3、C
4、A
5、D
6、A
7、C
8、B
9、B 10、C 二、选择题:11、B 12、A 13、D 14、D 15、B 三、填空题:
16、(1)过滤,加热蒸发 (2)B (3)得到的滤液浑浊
(4)变热不均匀,液体飞溅 (5)K 2CO 3 KCl K 2SO 4 17、a 、HCl b 、KCl c 、KOH d 、酚酞
18、(1)NaOH 易潮解且与CO 2反应 (2)投入水中,反应激烈的是K 19、(1)H ++HCO==H 2O+CO 2↑ (2)CO+Ba 2+==BaCO 3↓ (3)CO+Ca 2+==CaCO 3↓ (4)CO+CO 2+H 2O==2HCO 20、MgCl 2 AgNO 3 NaOH CuSO 4 21、Na 2CO 3 碱性强,耗量少 Na 2CO 3 碱性强 产生CO 2加重溃疡 四、计算题:
22、解:设Na 2CO 3质量为x NaHCO 3质量为y
⎩⎨
⎧'==⎪⎩⎪
⎨⎧'=⨯+⨯=+)
2(29
.271
.7)4(4.48444106
44100
y x y x y x ∴Na 2CO 3%=77.1%
答:略
23、解:m(NaOH)=8g
NaOH 全部变为Na 2CO 3时 m(Na 2CO 3)=10.6g NaOH 全部变为NaHCO 3时 m(NaHCO 3)=16.8g
∵10.6<13.7<16.8 ∴盐为Na 2CO 3 、NaHCO 3的混合物。