視覺神經(jīng)科學
在神經(jīng)科學的范圍內(nèi),視覺神經(jīng)科學已經(jīng)成為第一個涵蓋從分子和細胞過程到高級生理學和視覺心理物理學的所有實驗方面的真正的跨學科工作之一。在過去的半個世紀中對脊椎動物和無脊椎動物視覺系統(tǒng)的實驗為統(tǒng)計信息和賦予精美特征的神經(jīng)系統(tǒng)的設(shè)計和功能提供了一個通用框架。盡管加州大學洛杉磯分校在視覺科學的每個實驗方面都有優(yōu)勢,但直到去年,視覺神經(jīng)科學從未被用作將視覺科學家聚集在一起的組織結(jié)構(gòu)。視覺神經(jīng)科學親和小組的使命是為參與者提供一個論壇,以便在生物學和心理學的各個層面進行互動,程序:這個親密團體在十月至六月間每月開會。該計劃將重點介紹親和力小組成員實驗室所產(chǎn)生的科學數(shù)據(jù)。將特別強調(diào)高級研究生或博士后研究人員,為他們提供正式的指導和反饋。親和團每季度一次,將邀請來自大學以外的知名演講者參加開放的研討會,并與學員進行交流。
有關(guān)如何加入的信息,請聯(lián)系:James Bisley博士
加州大學洛杉磯分校David Geffen醫(yī)學院
電話:310-267-3
電子郵件:jbisley**[ta]**net.ucla.edu
Alapakkam P.Sampath博士
Department眼科與神經(jīng)生物學
UCLA David Geffen醫(yī)學院
電子郵件:asampath**[ta]**i.ucla.edu
加州大學洛杉磯分校微生物中心
認知加州大學洛杉磯分校微生物中心匯集了來自不同部門和學校的UCLA調(diào)查人員,他們對人類微生物有興趣,代表了從口腔生物學,粘膜炎癥,新陳代表謝,皮膚到腦腸相互作用等廣泛的專業(yè)知識。
該中心的主要目標是為微生物感興趣的研究者提供一個家園,促進跨學科交流。為了實現(xiàn)這一目標,我們計劃開發(fā)技術(shù)使用(例如,生物信息學,16s分析,代表謝組學)的協(xié)調(diào)機會,為跨學科研討會和講座提供論壇,為學生,學員和初級教員提供發(fā)展機會微生物組領(lǐng)域,并確定和促進大型多學科研究項目資助機會的行動。
欲并加入,請聯(lián)系該小組的教職主任
Elaine Hsaio。
ehsiao**[ta]**a.edu
加州大學洛杉磯分校微生物中心
加州大學洛杉磯分校微生物中心匯集了來自不同部門和學校的UCLA調(diào)查人員,他們對人類微生物有興趣,代表了從口腔生物學,粘膜炎癥,新陳代表謝,皮膚到腦腸相互作用等廣泛的專業(yè)知識。
指導委員會
Wenyuan Shi, PhD
Professor and Chairman, Oral Biology, UCLA School of Dentistry Professor, Microbiology and Molecular Genetics, UCLA School of Medicine Founding scientist and chief science officer, C3 Jian Inc
洛杉磯 CA 9***
電話:(310***
傳真:(310***
電子郵件:wenyuan**[ta]**a.edu
Aydogan Ozcan, PhD
Professor, Department of Electrical Engineering and Bioengineering, UCLA; Associate Director, California NanoSystems Institute (CNSI)
66-127D Engr.IV
電話:(310***
電子郵件:ozcan**[ta]**a.edu
網(wǎng)站:奧茲坎研究集團
Jonathan Jacobs, MD, PhD
Assistant Professor-in-Residence, Division of Digestive Diseases,
電話:(310***
電子郵件:JJacobs**[ta]**net.ucla.edu
網(wǎng)站:Jacobs實驗室
Elaine Y.Hsiao, PhD
Assistant Professor, Department of Integrative Biology and Physiology, De Logi Chair in Biological Sciences, Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at UCLA
電子郵件:ehsiao**[ta]**a.edu
網(wǎng)站:Hsiao Lab
Emeran Mayer, MD, PhD
Director,
Center for Health Science***
MC:73
洛杉磯 CA 9
電話:(310***
傳真:(310***
電子郵件:emayer**[ta]**a.edu
網(wǎng)站:加州大學洛杉磯分校Oppenheimer中心的壓力神經(jīng)生物學
Jonathan Braun, MD, PhD
Chair and Professor, Pathology and Laboratory Medicine; Molecular & Medical Pharmacology, UCLA
MC: 17
電話:(310***
傳真:(310***
電子郵件:jbraun**[ta]**net.ucla.edu
網(wǎng)站:UCLA Pathology&Laboratory Medicine
癌癥研究領(lǐng)域
在文獻中存在2個月至11.5個月的等基因Atm缺陷小鼠壽命中巨大的不明原因的實驗室間和實驗室間差異。腸道微生物群在我們的健康中起著關(guān)鍵的作用; 部分原因是這些細菌比我們體內(nèi)的人體細胞多10倍,因為它們具有巨大的代表謝能力。身體特別是免疫系統(tǒng)與腸道微生物之間錯綜復雜的相互作用強烈地明腸道微生物群影響全身穩(wěn)態(tài)。腸道微生物群組成的差異與諸如肥胖癥,糖尿病和行為的疾病有關(guān)。然而,正常的非致病性腸道細菌在致癌作用中的作用目前尚不清楚。
目前的研究項目
Robert Schiestl博士實驗室對Atm缺陷小鼠的腸道細菌性質(zhì)顯著影響遺傳不穩(wěn)定性,壽命和淋巴瘤潛伏期進行了觀察。ATM在DNA雙鏈斷裂修復,檢查點控制和氧化還原平衡中非常重要。Atm - / - 小鼠模擬人類疾病共濟失調(diào)毛細血管擴張癥(AT),其特征是喪失運動技能,免疫系統(tǒng)受損,癌癥風險增加和過早。AT無法治愈。他們將小鼠保持在無菌環(huán)境中,另外通過實驗改變這種微生物群來特別測試腸道微生物群的貢獻。他們明,同基因Atm - / - 小鼠在10%和43%之間的雙基因座處有DNA缺失的顯著變化,此外,Schiestl實驗室從健康有益的微生物群中分離出一種細菌 - 約氏乳桿菌,其自身顯著降低了基因毒性,減少了炎性細胞因子,誘導了抗炎細胞因子,并降低了自然殺傷細胞,細胞毒性T細胞和CD3細胞的流行肝臟和外周血,這些都與炎癥有關(guān)。另外,他們在野生型小鼠中發(fā)現(xiàn)了P53缺陷型小鼠的類似差異,甚至更少。因此,這種影響是非常重要的。他們的發(fā)現(xiàn)提出了一個直到現(xiàn)在未征的實驗變量,這可能具有巨大的影響。首先在AT患者中預防或延緩淋巴瘤,其次為基礎(chǔ)研究,其中Atm和許多其他癌癥傾向性小鼠模型的眾多實驗室間和實驗室間的差異部分或全部由腸道微生物群的差異來解釋。另外,我們的AT小鼠模型對腸炎癥過敏。由于炎癥與諸如心臟病,所有癌癥,神經(jīng)退行性疾病,關(guān)節(jié)炎,哮喘,糖尿病,可燃腸道疾病,克羅恩氏病等的許多疾病有關(guān),所以在該動物模型中鑒定的細菌可以作為益生菌受益,所有這些疾病。
代表性出版物
Yamamoto,LI Maier,AT Dang,D.Berry,J.Liu,PM Ruegger,J.Yang,PA Soto,LL Presley,R.Reliene,AM Westbrook,B.Wei,A.Loy,Cr Chang,J.Braun,J.Borneman,RH Schiestl(2013)腸細菌通過炎癥介導的全身性宿主氧化應激和白細胞基因毒性修飾遺傳易感性小鼠中的淋巴瘤外顯 - Cancer Research 73(14):4222-4232
Westbrook,A。和RH Schiestl(2010)Atm缺陷小鼠現(xiàn)出對硫酸葡聚糖鈉誘導的結(jié)腸炎的敏感性增加,特征在于DNA損傷升高和持續(xù)的免疫激活。Cancer Research 70,1875,
關(guān)鍵人物
Laurent Bentolila博士
Scientific Director, Advanced Light Microscopy/Spectroscopy Lab; Scientific Director, Macro-Scale Imaging Lab; Researcher, California NanoSystems Institute, UCLA
Advanced Light Microscopy/Spectroscopy Laboratory
California NanoSystems Institute
570
Phone: (310)***
E-mail: bento**[ta]**m.ucla.edu
Website: Laboratory
Dr.Bentolila is a senior researcher at the California NanoSystems Institute (CNSI) at the University of California, Los Angeles (UCLA).He is also the Scientific Director of the Advanced Light Microscopy/Spectroscopy Laboratory (ALMS) and the Macro-Scale Imaging Laboratory (MSI) at CNSI.Dr.Bentolila earned his B.S.in Biochemistry and M.S.in Genetics from Paris-XI University, Orsay and Ph.D.in Molecular Genetics and Immunology from the Pasteur Institute, Paris, France.He was a European Molecular Biology Organization Postdoctoral fellow at the University of California, Berkeley before joining the Department of Chemistry and Biochemistry at UCLA in
Dr.Bentolila’s long-standing research interest focuses on the application of novel fluorescent probes and advanced microscopy techniques to biology and medicine.Towards this goal, Dr.Bentolila has developed and assembled a unique collection of custom-made and commercial light microscopes for the application of novel spectroscopic methods and advanced microscopy techniques used for the study of macromolecules, cellular dynamics and nano-scale characterization of biomaterials.His most recent research projects include developing new experimental tools for visualizing and tracking cells, bacteria and parasites within a host.
Dr.Bentolila is the recipient of several awards from the Burroughs Wellcome Fund, the European Molecular Biology Organization and the Roux Foundation.
Relevant Recent Publications
Bentolila LA, Prakash R, Mihic-Probst D, Wadehra M, Kleinman HK, Carmichael TS, Péault B, Barnhill RL and Lugassy C.Imaging of Angiotropism/Vascular Co-Option in a Murine Model of Brain Melanoma.Implications for Melanoma Progression along Extravascular Pathways.2016.Scientific Reports.In press
Chen AL, Kim EW, Toh JY, Vashisht AA, Rashoff AQ, Van C, Huang AS, Moon AS, Bell HN, Bentolila LA, Wohlschlegel JA and Bradley PJ.Novel components of the Toxoplasma inner membrane complex revealed by BioID.2015.mBio 6(1) e0***
Kisalu NK, Langousis GD, Bentolila LA, Ralston KS, Hill KL.Mouse infection and pathogenesis by Trypanosoma brucei motility mutants.Cellular Microbiology.2014.16(6)***
Mitchell-Jordan S,Chen H,Franklin S,Stefani E,Bentolila LA和Vondriska TM。超分辨率STED顯微鏡顯示內(nèi)源性心肌細胞染色質(zhì)的特征。J Mol Cell Cardiol。53(4):552-8
Dino Di Carlo博士
Dino Di Carlo, PhD
Professor, Department of Bioengineering; Member, California NanoSystems Institute, Jonsson Comprehensive Cancer Center
5121E Engineering V
電話:(310***
電子郵件:dicarlo**[ta]**a.edu
Di Carlo實驗室
Dino Di Carlo is a Professor in the Department of Bioengineering at UCLA.Over the last 8 years he pioneered using inertial fluid dynamic effects for the control, separation, and analysis of cells in microfluidic devices.His work now extends into numerous fields of biomedicine and biotechnology including directed cellular evolution of microbes, cell and microbial analysis for rapid diagnostics, new amplified molecular assays, next generation biomaterials, and phenotypic drug screening.He also serves as Director of the Cancer Nanotechnology Program of the Jonsson Comprehensive Cancer Center at UCLA and holds a visiting Professorship at the University of Tokyo.He co-founded and currently advises four companies that are commercializing intellectual property developed in his lab over the last six years (CytoVale, Vortex Biosciences, Tempo Therapeutics, and Ferrologix).He has received numerous honors and awards including the Pioneers of Miniaturization Prize in 2015, Analytical Chemistry Young Innovator Award in 2014, the National Science Foundation (NSF) CAREER award, the U.S.Office of Naval Research (ONR) Young Investigator Award, the Packard Fellowship, the Defense Advanced Research Projects Agency (DARPA) Young Faculty Award, the National Institutes of Health (NIH) Director’s New Innovator Award and the Coulter Translational Research Awa***
出版物:Weaver WM,Milisavljevic V,Miller JF,Di Carlo D.,“Fluid flow induces biofilm formation in Staphylococcus epidermidis polysaccharide intracellular adhesin-positive clinical isolates,”Appl Environ Microbiol。2012年8月; 78(16):5890-6。doi:10.1128 / AEM.01139-12。Epub 2012年6月15日。
Weaver WM,Dharmaraja S,Milisavljevic V,Di Carlo D.,“剪切應力對皮葡萄球菌和人血漿纖維蛋白原分子受體 - 配體相互作用的影響,使用分子案微流體,”Lab Chip。
Aydogan Ozcan,博士
Phone: (310)***
E-mail: ozcan**[ta]**a.edu
Website: The Ozcan Research Group
Dr.Ozcan is the Chancellor’s Professor at UCLA and an HHMI Professor with the Howard Hughes Medical Institute, leading the Bio- and Nano-Photonics Laboratory at UCLA School of Engineering and is also the Associate Director of the California NanoSystems Institute (CNSI).Dr.Ozcan holds 32 issued patents (all of which are licensed) and20 pending patent applications and is also the author of one book and the co-author of more than 400 peer reviewed research articles in major scientific journals and conferences.Dr.Ozcan is a Fellow of SPIE and OSA, and has received major awards including the Presidential Early Career Award for Scientists and Engineers (PECASE), International Commission for Optics (ICO) Prize, SPIE Biophotonics Technology Innovator Award, SPIE Early Career Achievement Award, ARO Young Investigator Award, NSF CAREER Award, NIH Director’s New Innovator Award, ONR Young Investigator Award, IEEE Photonics Society Young Investigator Award and MIT’s TR35 Award for his seminal contributions to near-field and on-chip imaging, and telemedicine based diagnostics.Dr.Ozcan is also the recipient of the National Geographic Emerging Explorer Award, National Academy of Engineering (NAE) The Grainger Foundation Frontiers of Engineering Award, Popular Science Brilliant 10 Award, Gates Foundation Grand Challenges Award, Popular Mechanics Breakthrough Award, Netexplorateur Award, Microscopy Today Innovation Award, and the Wireless Innovation Award organized by the Vodafone Americas Foundation as well as the Okawa Foundation Awa***
出版物:A.Greenbaum,Y.Zhang,A.Feizi,P.Chung,W.Luo,SR Kandukuri,and A.Ozcan,“Wide-field Computational Imaging of Pathology Slides using Lensfree On-Chip Microscopy”,Science Translational Medicine (AAAS)(***
DOI:10.1126 / scitranslmed***
Q.Wei,W.Luo,S.Chiang,T.Kappel,C.Mejia,D.Tseng,R.Chan,E.Yan,H.Qi,F.Shabbir,H.Ozkan,S.Feng and A Ozcan,“移動
電話上單個DNA分子的成像和大小”,ACS Nano(***
DOI:10.1021 / nn505821y
A.Greenbaum,W.Luo,TW。Su,Z.G r cs,L.Xue,SO Isikman,AF Coskun,O.Mudanyali和A.Ozcan,“
在寬場片上顯微鏡的成就和仍然存在的挑戰(zhàn)”,Nature Methods(2012)DOI :10.1038 / nmeth
Robert Schiestl博士
Robert Schiestl, PhD
Professor, Departments of Pathology and Laboratory Medicine, Environmental Health Sciences, Radiation Oncology, Jonsson Comprehensive Cancer Center, UCLA
心血管疾病研究領(lǐng)域
動脈粥樣硬化與冠心病
由于膽固醇,氧化脂質(zhì),白細胞,細胞廢物和鈣在動脈壁內(nèi)積聚的結(jié)果,斑塊的積聚導致動脈粥樣硬化和導致冠心病的大中型動脈的狹窄和心肌梗塞。動脈壁代表謝,脂蛋白,免疫系統(tǒng)和凝血因子在動脈粥樣硬化,動脈狹窄和最終閉塞中起主要作用。遺傳和環(huán)境因素影響不同個體動脈粥樣硬化的發(fā)生率。此外,腸道微生物群現(xiàn)在已經(jīng)與各種動脈粥樣硬化危險因素有關(guān),包括血脂,膽汁酸,胰島素抵抗和炎癥。最近,通過微生物群的作用得到的代表謝物三甲胺-N-氧化物顯示與動脈粥樣硬化密切相關(guān)。參與的實驗室(Jake Lusis,Mohamad Navab,Alan Fogelman)主要對小鼠模型中宿主 - 微生物相互作用的機制研究感興趣。我們還在芬蘭的一個橫斷面人群中進行了大量腸道微生物的流行病學研究。
我們已經(jīng)觀察到,許多抑制炎癥的肽通過在腸的水平上起作用,我們正在探索它們的作用部分是由腸道微生物群的作用所介導的可能性。我們觀察到,在LDL受體無效小鼠中飼喂含有促炎性脂質(zhì)的飲食后,P.Pacteriode和P.Verruccomrobrobia的比例改變,我們的抗炎肽逆轉(zhuǎn)了這種改變。
Navab M,Hough G,Buga GM,Su F,Wagner AC,Meriwether D,Chattopadhyay A,Gao F,Grijalva V,Danciger JS,Van Lenten BJ,Org E,Lusis AJ,Pan C,Anantharamaiah GM,Farias-Eisner R,Smyth SS,Reddy ST,Fogelman AM。轉(zhuǎn)基因
Navab M,Chattopadhyay A,Hough G,Meriwether D,Fogelman SI,Wagner AC,Grijalva V,Su F,Anantharamaiah GM,Hwang LH,Faull KF,Reddy ST,Fogelman AM。腸源性溶血磷脂酸在血脂異常和動脈粥樣硬化中的來源和作用。J Lipid Res。2015年4月; 56(4):871-87。PMCID:PMC4373744。
Jake Lusis, PhD
Professor, Departments of Medicine, Cardiology, Human Genetics, Microbiology, Immunology & Molecular Genetics, UCLA
UCLA Med-Cardio/Microbio
3730 MRL
BOX 95
Los Angeles CA 9***
Phone: (310)***
E-mail: jlusis**[ta]**net.ucla.edu
Website: Lusis Laboratory
My PhD is in biophysics but somehow I ended up doing mouse genetics for my postdoc.I’m still doing mouse genetics, now with a focus on complex genetic traits, particularly those related to cardiovascular and metabolic disorders.With the development of high throughput technologies, such as expression arrays and sequencing, we have found it useful to marry such data with genetic analysis (‘systems genetics’).I also enjoy teaching.
Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS, Dugar B, Feldstein AE, Britt EB, Fu X, Chung YM, Wu Y, Schauer P, Smith JD, Allayee H, Tang WH, DiDonato JA, Lusis AJ, Hazen SL.(2011) Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease.Nature.472:57-63.PMCID:PM***
Bennett BJ, Vallim TQ, Wang Z, Shih DM, Meng Y, Gregory J, Allayee H, Lee R, Graham M, Crooke R, Edwards PA, Hazen S, Lusis AJ.(2013) Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation.Cell Metab.17:49-60.PMCID:PM***
Elin Org,Brian W.Parks,Jong Wha J Joo,Benjamin Emert,William Schwartzman,Eun Yong Kang,Margarete Mehrabian,Calvin Pan,Rob Knight,Robert Gunsalus,Thomas A.Drake,Eleazar Eskin和Aldons J.Lusis。(2015)宿主 - 腸道微生物群相互作用的遺傳和環(huán)境控制。Genome Res。
研究領(lǐng)域認知與心理健康
在美國,將近五分之一的人患有精神疾病,但許多精神疾病的根本原因大部分是未知的,缺乏有效的治療方法。最近的臨床前研究揭示了微生物操作對復雜的高階行為(包括焦慮,社交性,認知和情緒行為)的顯著影響。而且,分子評估揭示了微生物組在調(diào)節(jié)神經(jīng)化學代表謝,全腦基因達,小膠質(zhì)細胞激活和血腦屏障通透性中的關(guān)鍵作用。在這些發(fā)現(xiàn)的推動下,最近對患有精神障礙(包括精神分裂癥和抑郁癥)的患者的檢查揭示了微生物群的生態(tài)失調(diào)。總之,這些發(fā)現(xiàn)提出了微生物組的變化是否有助于,博士的實驗室伊萊恩蕭在加州大學洛杉磯分校正在研究腸道微生物與神經(jīng)系統(tǒng)之間的神經(jīng)發(fā)育障礙和分子信號傳導的癥狀的微生物 - 腸 - 腦效應。蕭博士此前在這方面的工作明,產(chǎn)后修改共棲菌群可改善自閉癥遺傳和環(huán)境危險因素的小鼠模型中的GI和行為癥狀。這項工作是首次證明微生物調(diào)節(jié)定型,感覺運動和交流行為,并進一步揭示微生物介導的神經(jīng)活性代表謝物水平的變化影響行為。Hsiao實驗室進行的一項獨立研究發(fā)現(xiàn),人和小鼠微生物群中的一個特定的細菌聚生體可逆地調(diào)節(jié)宿主5-羥色胺的生物合成并改善小鼠中5-羥色胺相關(guān)疾病的型。
(Yano JM),Yu K,Donaldson G,Shastri G,Ma L,Ann P,Nagler C,Ismagilov RF,Mazmanian SK,Hsiao EY(2015)腸道微生物中的土著細菌調(diào)節(jié)宿主5-羥色胺的生物合成。Cell,161:26***
(2)微生物調(diào)節(jié)與神經(jīng)發(fā)育相關(guān)的行為和生理異常障礙。Cell,155:1451-***
Hsiao EY,McBride SW,Chow J,Mazmanian SK,Patterson PH(2012)在小鼠中建立自閉癥風險因子導致永久性免疫失調(diào)。PNAS 109:***
Elaine Y.Hsiao博士
Dr.Elaine Y.Hsiao is an Assistant Professor in the Department of Integrative Biology & Physiology at UCLA, where she leads a laboratory studying fundamental interactions between the microbiome, brain and behavior, and their applications to neurological disorders.Her studies on the relationships between the microbiota, immune system and nervous system led her to discover that the microbiota can regulate behavioral, metabolic and gastrointestinal abnormalities relevant to autism spectrum disorder (ASD).Her work in this area, and on neuroimmune interactions in autism, has led to several honors, including the National Institutes of Health Director’s Early Independence Award, distinction as Forbes’ 30 Under
醫(yī)學博士Helen Lavretsky
Helen Lavretsky, MD
Professor in Residence, Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA
研究領(lǐng)域結(jié)締組織疾病
涉及結(jié)締組織的自身免疫病癥具有復雜的發(fā)病起因和不同的臨床現(xiàn)。全身性硬化癥或硬皮病)是所有結(jié)締組織疾病中死亡率最高的原因,大多數(shù)系統(tǒng)性硬化癥患者患有嚴重的胃腸道癥狀。雖然系統(tǒng)性硬化癥的胃腸道功能障礙的原因尚不清楚,但是加州大學洛杉磯分校的風濕病專家Elizabeth Volkmann博士最近與病理學和檢驗醫(yī)學系主任Jonathan Braun博士合作,發(fā)現(xiàn)系統(tǒng)性硬化癥患者的腸道微生物群是否有改變。
加州大學洛杉磯分校的胃腸病專家團隊(包括Bennett Roth博士,Terri Getzug博士和Jeffrey Conklin博士,UCLA硬皮病微生物組織倡議組織)也試確定某些微生物物種是否有助于系統(tǒng)性硬化癥的胃腸型。Volkmann博士的研究小組最近證明,與健康對照組相比,系統(tǒng)性硬化癥患者病原微生物(侵入性,促炎性)增加,共生菌(正常,健康)減少。此外,該研究組發(fā)現(xiàn),脆弱類桿菌(一種共生細菌種類)水平較低的系統(tǒng)性硬化癥患者,與該種類較高的患者相比,有較嚴重的胃腸道癥狀。
Jonathan Braun博士
Dr.Jonathan Braun is Professor and Chair of Pathology and Laboratory Medicine, and Professor of Molecular and Medical Pharmacology at the David Geffen School of Medicine, and Chair of Pathology and Laboratory Medicine.A distinguished pathologist and mucosal immunologist , his 30 year career has been devoted to mucosal host-microbial interaction and the immune cell biology of chronic inflammatory disease (IBD and HIV) and lymphoma pathogenesis.With a long-standing commitment to inflammatory bowel disease, in recent years he has focused on the relationship of the intestinal microbiome and function to human genetic disease variation in IBD disease pathogenesis, penetrance, and phenotype.He has innovated in the detection and bioinformatics analysis of microbiome, metabolites, and peptides, through participation in the NIDDK IBD Genetics Consortium and NIH HMP2 projects, and as PI of the CCFA Microbiome Initiative.
Tong M, McHardy I, Ruegger P, Goudarzi M, Kashyap PC, Haritunians T, Li X, Graeber TG, Schwager E, Huttenhower C, Fornace AJ Jr, Sonnenburg JL, McGovern DP, Borneman J, Braun J.Reprograming of gut microbiome energy metabolism by the FUT2 Crohn’s disease risk polymorphism.ISME J.2014 Nov;8(11):2193-206.doi: 10.1038/ismej.2014.64.PMID: ***
McHardy IH, Goudarzi M, Tong M, Ruegger PM, Schwager E, Weger JR, Graeber TG, Sonnenburg JL, Horvath S, Huttenhower C, McGovern DP, Fornace AJ Jr, Borneman J, Braun J.Integrative analysis of the microbiome and metabolome of the human intestinal mucosal surface reveals exquisite inter-relationships.Microbiome.2013 Jun 5;1(1):17.doi: 10.1186/2049-
McHardy IH, Li X, Tong M, Ruegger P, Jacobs J, Borneman J, Anton P, Braun J.HIV Infection is associated with compositional and functional shifts in the rectal mucosal microbiota.Microbiome.2013 Oct 12;1(1):26.doi: 10.1186/2049-
Active Funding in Microbiome-Related Research
Funding Agency/Grant Number: NIH U54 DK10
Title: “Characterizing the gut microbial community for diagnosis and therapy of IBD”
Goals: To identify the relationship of microbial composition, microbial genes, and their metabolite and peptide products in the intestinal mucosa of IBD patients
Funding Agency/Grant Number: CCFA Microbiome Consortium/323814 Crohn’s and Colitis Foundation of America
Title: “Establishing Mechanistically Validated Targets and Lead Molecules for Microbiome-based Therapy in IBD”
Goals: 機械地驗證確定IBD疾病狀態(tài)和活性的候選微生物群及其產(chǎn)品; 確定針對這些經(jīng)過驗證的候選人的主要分子; 并通過縱向多元分析來擴展?jié)撛诘暮蜻x人。
Elizabeth Volkmann,MD,MS
Elizabeth Volkmann, MD, MS
Clinical Instructor, Division of Rheumatology, Department of Medicine, David Geffen School of Medicine at UCLA