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| 1 | Necroptosis, pyroptosis and apoptosis: an intricate game of cell death显示文摘Cell death is a fundamental physiological process in all living organisms.Its roles extend from embryonic development,organ maintenance,and aging to the coordination of immune responses and autoimmunity.In recent years,our understanding of the mechanisms orchestrating cellular death and its consequences on immunity and homeostasis has increased substantially.Different modalities of what has become known as‘programmed cell death’have been described,and some key players in these processes have been identified.We have learned more about the intricacies that fine tune the activity of common players and ultimately shape the different types of cell death.These studies have highlighted the complex mechanisms tipping the balance between different cell fates.Here,we summarize the latest discoveries in the three most well understood modalities of cell death,namely,apoptosis,necroptosis,and pyroptosis,highlighting common and unique pathways and their effect on the surrounding cells and the organism as a whole. | Damien Bertheloot Eicke Latz Bernardo S.Franklin | 2021 | Cellular & Molecular Immunology2021，18，5： | 84 |
| 2 | HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins显示文摘我们的免疫系统为对主人的任何威胁的快速的察觉基于天生、适应的免疫系统的靠近的合作。导出病原体的分子的识别被委托给特定的编码 germline 的发信号受体。一样的受体现在也作为表明例如,列在后面的织物损坏和房间死亡的错放或改变的自我分子的有效察觉者出现了血供应和随后的组织缺氧的混乱。当免除了垂死的房间时,内长的分子的许多类型被显示了挑起如此的无菌的煽动性的状态。然而,叫作 alarmins 的一组蛋白质有是强烈研究的题目的细胞内部、细胞外的功能。确实, alarmins 也能施加有益的房间家务功能,导致织物修理,或挑起有害不受管束的发炎。这组蛋白质包括高活动性的组盒子 1 蛋白质(HMGB1 ) , interleukin (IL )-1α, IL-33 和 Ca 2+-binding S100 蛋白质。这些双功能的蛋白质分享保存规章的机制,例如能分泌的线路, translational 以后修正并且酶的处理,在时空管理他们的细胞外的功能。从间充质的房间的 alarmins 的版本是有免疫力的房间能被组织损坏,和 alarmins 玩警告的高度相关的机制在急性或长期的煽动性的疾病的发展并且在癌症开发的一个关键角色。 | Damien Bertheloot Eicke Latz | 2017 | Cellular & Molecular Immunology2017，14，1： | 40 |
| 3 | Clinically detected gastroenteropancreatic neuroendocrine tumors are on the rise: Epidemiological changes in Germany显示文摘AIM:To study the epidemiologic changes of gastroenteropancreatic neuroendocrine tumors(GEP-NET)in Germany,we analyzed two time periods 1976-1988 and1998-2006.METHODS:We evaluated epidemiological data of GEP-NET from the former East German National Cancer Registry(DDR Krebsregister,1976-1988)and its successor,the Joint Cancer Registry(GKR,1998-2006),which was founded after German reunification.Due to a particularly substantial database the epidemiological data from the federal states of Mecklenburg-Western Pomerania,Saxony,Brandenburg and Thuringia,covering a population of more than 10.8 million people,were analyzed.Survival probabilities were calculated using life table analysis.In addition,GEP-NET patients were evaluated for one or more second(non-GEP-NET)primary malignancies.RESULTS:A total of 2821 GEP neuroendocrine neoplasms were identified in the two registries.The overall incidence increased significantly between 1976 and2006 from 0.31(per 100.000 inhabitants per year)to2.27 for men and from 0.57 to 2.38 for women.In the later period studied(2004-2006),the small intestine was the most common site.Neuroendocrine(NE)neoplasms of the small intestine showed the largest absolute increase in incidence,while rectal NE neoplasms exhibited the greatest relative increase.Only the incidence of appendiceal NET in women showed little change between 1976 and 2006.Overall survival of patients varied for sex,tumor site and the two periods studied but improved significantly over time.Interestingly,about 20%of the GEP-NET patients developed one or more second malignancies.Their most common location was the gastrointestinal tract.GEP-NET patients without second malignancies fared better than those with one or more of them.CONCLUSION:The number of detected GEP-NET increased about 5-fold in Germany between 1976 and2006.At the same time,their anatomic distribution changed,and the survival of GEP-NET patients improved significantly.Second malignancies are common and influence the overall survival of GEP-NET patients.Thus,GEP-NET warrant our attention as well as intensive research on their tumorigenesis. | Hans Scherübl Brigitte Streller Roland Stabenow Hermann Herbst Michael Hopfner Christoph Schwertner Joachim Steinberg Jan Eick Wanda Ring Krishna Tiwari Soren M Zappe | 2013 | World Journal of Gastroenterology2013，19，47： | 16 |
| 4 | Blocking the Metabolism of Starch Breakdown Products in Arabidopsis Leaves Triggers Chloroplast Degradation显示文摘在大多数植物,吸收相片的碳的大部分作为淀粉在日子期间在叶绿体被存储并且在随后的夜里期间重新动员支持新陈代谢。在 Arabidopsis thaliana 堵住淀粉合成或淀粉故障的变化减少植物生长。麦芽糖是在夜里从叶绿体出口的淀粉故障的主要产品。麦芽糖过量 1 异种(mex1 ) 缺乏叶绿体信封麦芽糖 transporter,在叶绿体积累麦芽糖和淀粉的高水平并且发展一特殊但是以前叶子成熟的 unexplained 萎黄病显型。阻止淀粉合成的另外的变化的介绍,或从淀粉的那块麦芽糖生产,也阻止 mex1 的褪绿。相反,在 disproportionating 酶(DPE1 ) 的变化的介绍除了麦芽糖导致 maltotriose 的累积,并且极大地增加褪绿。这些数据建议在麦芽糖累积和叶绿体动态平衡之间的一个连接。显微镜的分析证明在萎黄病 mex1 叶子的叶肉房间比野类型的房间比叶绿体的半数字有少数。传播电子显微镜学在 mex1 和 dpe1/mex1 揭示象 autophagy 一样叶绿体降级两倍异种。Microarray 分析揭示新陈代谢、细胞的过程的实质的 reprogramming,建议那 organellar 蛋白质周转在 mex1 被增加,尽管叶老朽和老朽相关的叶绿素分解代谢没被导致。我们建议麦芽糖和 malto-oligosaccharides 的累积引起叶绿体机能障碍,它可以由经由一种形式发信号后退发信号并且被触发叶绿体降级。 | Michaela Stettler Simona Eicke Tabea Mettler Gaelle Messerli Stefan Hortensteiner Samuel C. Zeeman | 2009 | Molecular Plant2009，2，6： | 9 |
| 5 | Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1显示文摘Periodontal disease is associated with chronic oxidative stress and inflammation. Caffeic acid phenethyl ester(CAPE), which is a potent inducer of heme oxygenase 1(HO1), is a central active component of propolis, and the application of propolis improves periodontal status in diabetic patients. Here, primary murine macrophages were exposed to CAPE. Target gene expression was assessed by whole-genome microarray, RT-PCR and Western blotting. The antioxidative and anti-inflammatory activities of CAPE were examined by exposure of the cells to hydrogen peroxide, saliva and periodontal pathogens. The involvement of HO1 was investigated with the HO1 inhibitor tin protoporphyrin(SnPP) and knockout mice for Nrf2, which is a transcription factor for detoxifying enzymes. CAPE increased HO1 and other heat shock proteins in murine macrophages. A p38 MAPK inhibitor and Nrf2 knockout attenuated CAPE-induced HO1 expression in macrophages. CAPE exerted strong antioxidative activity. Additionally, CAPE reduced the inflammatory response to saliva and periodontal pathogens. Blocking HO1 decreased the antioxidative activity and attenuated the anti-inflammatory activity of CAPE. In conclusion, CAPE exerted its antioxidative effects through the Nrf2-mediated HO1 pathway and its anti-inflammatory effects through NF-κB inhibition. However, preclinical models evaluating the use of CAPE in periodontal inflammation are necessary in future studies. | Alexandra St?hli Ceeneena Ubaidha Maheen Franz Josef Strauss Sigrun Eick Anton Sculean Reinhard Gruber | 2019 | International Journal of Oral Science2019，11，1： | 4 |
| 6 | PKR stirs up inflammasomes显示文摘 | H James Stunden Eicke Latz | 2013 | Cell Research2013，23，2： | 3 |
| 7 | How location and cellular signaling combine to activate the NLRP3 inflammasome显示文摘NOD-,LRR-,and pyrin domain-containing 3(NLRP3)is a cytosolic innate immune sensor of cellular stress signals,triggered by infection and sterile inflammation.Upon detection of an activating stimulus,NLRP3 transitions from an inactive homo-oligomeric multimer into an active multimeric inflammasome,which promotes the helical oligomeric assembly of the adaptor molecule ASC.ASC oligomers provide a platform for caspase-1 activation,leading to the proteolytic cleavage and activation of proinflammatory cytokines in the IL-1 family and gasdermin D,which can induce a lytic form of cell death.Recent studies investigating both the cellular requirement for NLRP3 activation and the structure of NLRP3 have revealed the complex regulation of NLRP3 and the multiple steps involved in its activation.This review presents a perspective on the biochemical and cellular processes controlling the assembly of the NLRP3 inflammasome with particular emphasis on structural regulation and the role of organelles.We also highlight the latest research on metabolic control of this inflammatory pathway and discuss promising clinical targets for intervention. | Anil Akbal Alesja Dernst Marta Lovotti Matthew S.J.Mangan Róisín M.McManus Eicke Latz | 2022 | Cellular & Molecular Immunology2022，19，11： | 2 |
| 8 | Infuence of hormonal contraceptiveson microbial flora of gingival sulcus显示文摘 | Klinger G Eick S Pfister W | 1998 | Contraception1998，57，6： | 1 |
| 9 | Respiratory disease in army recruits: surveillance program overview, 1995-2006 显示文摘 | Lee SE Eick A Cirninera P | 2008 | Am J Prey Med2008，34，5： | 1 |
| 10 | Effect of storage conditions on the properties of cement 显示文摘 | RICHARTZ W EICK H | 1973 | ZKG Int1973，，2： | 1 |
| 11 | Nanosecond Spectroscopic Investigations of Molecular Processes in W/O Microemulsions显示文摘 | H F Eicke P E Zinsli | 1978 | Journal of Colloid and Interface Science1978，65，1： | 1 |
| 12 | Antiproliferative effects of the GnRH antagonist cetrorelix and of GnRH Ⅱ on human endometrial and ovarian cancer cells are not mediated through the GnRH type Ⅰ receptor显示文摘 | Grundker C Schlotawa L Viereck V Eicke N Horst A Kairies B | 2004 | Eur J Endocrinol2004，151，： | 1 |
| 13 | Serial transcranial doppler monitoring after transient ischemic attack显示文摘 | Eicke BM von Lorentz J Paulus W | 1996 | J Neuroimaging1996，6，3： | 1 |
| 14 | Current concepts on adhesion to dentin显示文摘 | Eick JD Gwinnett AJ Pashley DH | 1997 | Crit Rev Oral Biol Med1997，8，3： | 1 |
| 15 | Visualizing network data 显示文摘 | Becker R A Eick S G Wilks A R | 1995 | IEEE Transactions on Visualization and Computer Graphics1995，1，1： | 1 |
| 16 | Enhanced functional expression of transient outward current in hyper2 trophied feline myocytes 显示文摘 | TEN EICK RE ZANG K HARVEY RD | 1993 | Cardiovasc Drugs Ther1993，7，3： | 1 |
| 17 | Further delineation of the continuous human neoplastic enterochromaffin cell line,KRJ-I,and the inhibitory effects of lanreotide and rapamycin 显示文摘 | Kidd M Eick GN Modlin IM | 2007 | J Mol Endocrinol2007，38，： | 1 |
| 18 | Comparison of microbial cultivation and a commercial PCR based method for detection of periodontopathogenic species in subgingival plaque samples显示文摘 | Eick S Pfister W | 2002 | J Clin Periodontol2002，29，7： | 1 |
| 19 | A method to reduce or prevent postoperative sensitivity with posterior composite resin restoration 显示文摘 | Weltch FH Eick JD | 1986 | Quin-tessence Int1986，17，10： | 1 |
| 20 | Information Visualization 显示文摘 | Nahum D Gershon Stephen G Eick | 1997 | IEEE Computer Graphics and Applications1997，，78： | 1 |
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