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BEGIN:VEVENT

CATEGORIES:Medicine
CATEGORIES:Natural Sciences
CATEGORIES:Lectures/Conferences
CATEGORIES:Utilities
CATEGORIES:Lecture/Talk
CATEGORIES:Panel/Seminar/Colloquium
CATEGORIES:Main
CONTACT;X-BEDEWORK-UID=2c918084-67810a22-0167-8547cfec-000013b9:Gerondelis
 \, Kristen
CREATED:20191010T220826Z
DESCRIPTION:The diagnosis and treatment of gliomas continue to pose a sign
 ificant challenge for oncologists who not only have to contend with manag
 ing acute neurological symptoms\, but also the almost inevitable developm
 ent of resistance to treatment. Indeed\, the last 25 years have produced 
 minimal advancements in treatment efficacy\, even though significant effo
 rts and resources have been invested in the quest for breakthroughs. This
  effort has not been restricted only to clinicians or oncologists\, with 
 mathematical modeling also playing an increasingly important role. The wo
 rk presented seeks to focus our attention back to the most fundamental qu
 estion: why are gliomas fatal? Biologically\, it is known that glioma let
 hality is driven by a fast growth that increases intracranial pressure re
 sulting in lethal neurological damage\, which current treatments fail to 
 prevent due to tumor cell resistance to treatments such as chemotherapy. 
 The work comprises two main parts: (1) in silico optimization of treatmen
 t strategies using chemotherapy coupled with novel cell-repair inhibitors
  currently in various stages of the clinical trial\; and (2) a study of t
 umor-induced intracranial pressure and edema in gliomas of grade I-IV. Bo
 th approaches come together as a first step towards a better understandin
 g of the poor survival rates of patients afflicted with gliomas. They rai
 se new questions about what characterizes the malignancy of primary brain
  tumors and how clinicians can fight it...
DURATION:PT1H
DTSTAMP:20191010T222403Z
DTSTART;TZID=America/New_York:20191011T133000
LAST-MODIFIED:20191010T222403Z
LOCATION;X-BEDEWORK-UID=18832edc-1b27e154-011b-283f5122-00000081:Physics 2
 35
STATUS:CONFIRMED
SUMMARY:Gliomas Diagnosis\, Progress\, and Treatment: A Mathematical Appro
 ach
UID:CAL-2c918083-6dac0dd2-016d-b7b7505f-000070a1demobedework@mysite.edu
URL:https://math.duke.edu/events/96546-gliomas-diagnosis-progress-and-trea
 tment-mathematical-approach
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Main:/user/public-user/Utili
 ties/Main
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Lecture_Talk:/user/public-us
 er/Lectures_Conferences/Lecture_Talk
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Panel_Seminar_Colloquium:/us
 er/public-user/Lectures_Conferences/Panel_Seminar_Colloquium
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Medicine:/user/public-user/T
 opics/Medicine
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Natural Sciences:/user/publi
 c-user/Topics/Natural Sciences
X-BEDEWORK-SPEAKER:Inmaculada Sorribes (Duke University\, Mathematics)
X-BEDEWORK-DUKE-SERIES:Mathematical Biology Seminar
X-BEDEWORK-SUBMITTEDBY:kg182 for Mathematics (agrp__ArtsandSciences_Mathem
 atics)
X-BEDEWORK-IMAGE-X1:0
X-BEDEWORK-IMAGE-Y1:-0.3333333333333144
X-BEDEWORK-IMAGE-X2:530
X-BEDEWORK-IMAGE-Y2:353
X-BEDEWORK-IMAGE-CROP-WIDTH:530
X-BEDEWORK-IMAGE-CROP-HEIGHT:353.3333333333333
X-BEDEWORK-IMAGE-ALT-TEXT:Duke Math
X-BEDEWORK-IMAGE:/public/Images/Duke Math Logo JPG Duke Events Image_20191
 010062403PM.jpg
X-BEDEWORK-THUMB-IMAGE:/public/Images/Duke Math Logo JPG Duke Events Image
 _20191010062403PM-thumb.png
END:VEVENT
BEGIN:VEVENT

CATEGORIES:Natural Sciences
CATEGORIES:Lectures/Conferences
CATEGORIES:Utilities
CATEGORIES:Lecture/Talk
CATEGORIES:Panel/Seminar/Colloquium
CATEGORIES:Main
CONTACT;X-BEDEWORK-UID=2c918084-67810a22-0167-8547cfec-000013b9:Gerondelis
 \, Kristen
CREATED:20191010T221830Z
DESCRIPTION:The Langlands program is a far-reaching collection of conjectu
 res that relate different areas of mathematics including number theory an
 d representation theory. A fundamental problem on the representation theo
 ry side of the Langlands program is the construction of all (irreducible\
 , smooth\, complex) representations of certain matrix groups\, called p-a
 dic groups. In my talk I will introduce p-adic groups and provide an over
 view of our understanding of their representations\, with an emphasis on 
 recent progress. I will also briefly discuss applications to other areas\
 , e.g. to automorphic forms and the global Langlands program. Reception t
 o follow at 4:30pm.
DURATION:PT1H
DTSTAMP:20191010T221830Z
DTSTART;TZID=America/New_York:20191018T120000
LAST-MODIFIED:20191010T221830Z
LOCATION;X-BEDEWORK-UID=18832edc-1b27e154-011b-283f5122-00000081:Physics 2
 35
STATUS:CONFIRMED
SUMMARY:Representations of p-adic groups Lecture 2
UID:CAL-2c918083-6dac0dd2-016d-b7c086ca-0000714cdemobedework@mysite.edu
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Main:/user/public-user/Utili
 ties/Main
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Lecture_Talk:/user/public-us
 er/Lectures_Conferences/Lecture_Talk
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Panel_Seminar_Colloquium:/us
 er/public-user/Lectures_Conferences/Panel_Seminar_Colloquium
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Natural Sciences:/user/publi
 c-user/Topics/Natural Sciences
X-BEDEWORK-SPEAKER:Jessica Fintzen (University of Cambridge)
X-BEDEWORK-DUKE-SERIES:Frontiers in Mathematics Seminar
X-BEDEWORK-IMAGE-X1:0
X-BEDEWORK-IMAGE-Y1:-0.3333333333333144
X-BEDEWORK-IMAGE-X2:530
X-BEDEWORK-IMAGE-Y2:353
X-BEDEWORK-IMAGE-CROP-WIDTH:530
X-BEDEWORK-IMAGE-CROP-HEIGHT:353.3333333333333
X-BEDEWORK-IMAGE-ALT-TEXT:Jessica Fintzen
X-BEDEWORK-SUBMITTEDBY:kg182 for Mathematics (agrp__ArtsandSciences_Mathem
 atics)
X-BEDEWORK-IMAGE:/public/Images/Duke Events Calendar Fintzen_2019101006183
 0PM.jpg
X-BEDEWORK-THUMB-IMAGE:/public/Images/Duke Events Calendar Fintzen_2019101
 0061830PM-thumb.png
END:VEVENT
BEGIN:VEVENT

CATEGORIES:Medicine
CATEGORIES:Natural Sciences
CATEGORIES:Lectures/Conferences
CATEGORIES:Utilities
CATEGORIES:Lecture/Talk
CATEGORIES:Panel/Seminar/Colloquium
CATEGORIES:Main
CONTACT;X-BEDEWORK-UID=2c918084-67810a22-0167-8547cfec-000013b9:Gerondelis
 \, Kristen
CREATED:20191010T221627Z
DESCRIPTION:Early embryogenesis of most metazoans is characterized by rapi
 d and synchronous cleavage divisions. While diffusion is too slow for syn
 chronization of mitosis across large spatial scales\, traveling waves rep
 resent a possible process of synchronization. I will discuss our recent w
 ork dissecting the molecular and physical mechanisms for the generation o
 f traveling waves of activity of Cdk1\, the master regulator of the cell 
 cycle. I will show that the in vivo dynamics of Cdk1 are captured by a tr
 ansiently bistable reaction-diffusion model\, where time-dependent reacti
 on terms account for the growing level of cyclins and Cdk1 activation acr
 oss the cell cycle. I will discuss two distinct regimes. The first one is
  observed in mutants of the mitotic switch. There\, waves are triggered b
 y the classical mechanism of a stable state invading a metastable one. Co
 nversely\, waves in wild type reflect a transient phase that preserves th
 e Cdk1 spatial gradients while the overall level of Cdk1 activity is swep
 t upward by the time-dependent reaction terms. This unique mechanism gene
 rates a wave-like spreading (sweep-waves) that differs from bistable wave
 s for its dependence on dynamic parameters and its faster speed. I will a
 lso discuss how the integration of biochemical and mechanical processes i
 s required for the early establishment of synchronization of the cell cyc
 le.
DURATION:PT1H
DTSTAMP:20191010T221627Z
DTSTART;TZID=America/New_York:20191018T133000
LAST-MODIFIED:20191010T221627Z
LOCATION;X-BEDEWORK-UID=18832edc-1b27e154-011b-283f5122-00000081:Physics 2
 35
STATUS:CONFIRMED
SUMMARY:Cell cycle synchronization in early Drosophila embryos
UID:CAL-2c918083-6dac0dd2-016d-b7bea607-00007105demobedework@mysite.edu
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Main:/user/public-user/Utili
 ties/Main
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Lecture_Talk:/user/public-us
 er/Lectures_Conferences/Lecture_Talk
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Panel_Seminar_Colloquium:/us
 er/public-user/Lectures_Conferences/Panel_Seminar_Colloquium
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Medicine:/user/public-user/T
 opics/Medicine
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Natural Sciences:/user/publi
 c-user/Topics/Natural Sciences
X-BEDEWORK-SPEAKER:Stefano Di Talia (Duke University\, Cell Biology)
X-BEDEWORK-DUKE-SERIES:Mathematical Biology Seminar
X-BEDEWORK-SUBMITTEDBY:kg182 for Mathematics (agrp__ArtsandSciences_Mathem
 atics)
END:VEVENT
BEGIN:VEVENT

CATEGORIES:Medicine
CATEGORIES:Natural Sciences
CATEGORIES:Lectures/Conferences
CATEGORIES:Utilities
CATEGORIES:Lecture/Talk
CATEGORIES:Panel/Seminar/Colloquium
CATEGORIES:Main
CONTACT;X-BEDEWORK-UID=2c918084-67810a22-0167-8547cfec-000013b9:Gerondelis
 \, Kristen
CREATED:20191022T165202Z
DESCRIPTION:Recent debate on tumor heterogeneity has largely centered on t
 he presence (or absence) of subclonal selection. While neutral and Darwin
 ian models of tumor evolution have both been shown to recapitulate bulk s
 equencing data\, multi-region sequencing has produced evidence supporting
  the hypothesis that early Darwinian selection precedes late neutral evol
 ution after malignant transformation. Transitioning modes of evolution (D
 arwinian to neutral) may be the outcome of cellular architecture dictatin
 g spatial constraints for growth. Using a classic\, well-studied computat
 ional model of tumor evolution (a passenger-driver mutation model) we sys
 tematically alter spatial constraints and cell mixing rates to show how t
 issue structure influences functional (driver) mutations and genetic hete
 rogeneity over time. This novel model extension represents biologically r
 ealistic scale (1e6 - 1e7 cells) in a biologically realistic setting (3-d
 imensional breast ductal network derived from imaging data) of premaligna
 ncy. The branching topology of ductal networks at tumor initiation determ
 ines two important evolutionary accelerants: spatial constraints and cell
 ular dispersal. This model approach explores a key mechanism behind both 
 inter-patient and intratumoral tumor heterogeneity: competition for space
 . Initial spatial constraints determine the emergent mode of evolution (D
 arwinian to neutral) without a change in cell-specific mutation rate or f
 itness effects.
DURATION:PT1H
DTSTAMP:20191022T175444Z
DTSTART;TZID=America/New_York:20191025T133000
LAST-MODIFIED:20191022T175444Z
LOCATION;X-BEDEWORK-UID=18832edc-1b27e154-011b-283f5122-00000081:Physics 2
 35
STATUS:CONFIRMED
SUMMARY:Tissue structure accelerates evolution: premalignant sweeps preced
 e neutral expansion
UID:CAL-2c918085-6de22ea0-016d-f461f3af-00007f60demobedework@mysite.edu
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Main:/user/public-user/Utili
 ties/Main
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Lecture_Talk:/user/public-us
 er/Lectures_Conferences/Lecture_Talk
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Panel_Seminar_Colloquium:/us
 er/public-user/Lectures_Conferences/Panel_Seminar_Colloquium
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Natural Sciences:/user/publi
 c-user/Topics/Natural Sciences
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Medicine:/user/public-user/T
 opics/Medicine
X-BEDEWORK-SPEAKER:Jeffrey West (H. Lee Moffitt Cancer Center & Research I
 nstitute)
X-BEDEWORK-DUKE-SERIES:Mathematical Biology Seminar
X-BEDEWORK-SUBMITTEDBY:kg182 for Mathematics (agrp__ArtsandSciences_Mathem
 atics)
X-BEDEWORK-IMAGE-X1:0
X-BEDEWORK-IMAGE-Y1:-0.3333333333333144
X-BEDEWORK-IMAGE-X2:530
X-BEDEWORK-IMAGE-Y2:353
X-BEDEWORK-IMAGE-CROP-WIDTH:530
X-BEDEWORK-IMAGE-CROP-HEIGHT:353.3333333333333
X-BEDEWORK-IMAGE-ALT-TEXT:Duke Math Bio Seminar
X-BEDEWORK-IMAGE:/public/Images/Math Bio image calendar_20191022015444PM.j
 pg
X-BEDEWORK-THUMB-IMAGE:/public/Images/Math Bio image calendar_201910220154
 44PM-thumb.png
END:VEVENT
BEGIN:VEVENT

CATEGORIES:Medicine
CATEGORIES:Natural Sciences
CATEGORIES:Lectures/Conferences
CATEGORIES:Utilities
CATEGORIES:Lecture/Talk
CATEGORIES:Panel/Seminar/Colloquium
CATEGORIES:Main
CONTACT;X-BEDEWORK-UID=2c918084-67810a22-0167-8547cfec-000013b9:Gerondelis
 \, Kristen
CREATED:20191022T165501Z
DESCRIPTION:Concurrent use of a diuretic\, a renin-angiotensin system (RAS
 ) inhibitor\,\nand a nonsteroidal anti-inflammatory drug (NSAID) signific
 antly increases\nthe risk of acute kidney injury (AKI). This phenomenon i
 s known as 'triple\nwhammy'. Diuretics and RAS inhibitors\, such as an an
 giotensin converting\nenzyme inhibitor (ACEI) or angiotensin receptor blo
 cker (ARB)\, are often\nprescribed in tandem for the treatment of hyperte
 nsion\, whereas some NSAIDs\,\nsuch as ibuprofen\, are available over the
  counter. As such\, concurrent\ntreatment with all three drugs is not unc
 ommon. The goals of this study are\nto better understand the mechanisms u
 nderlying the development of triple\nwhammy AKI and to identify physiolog
 ical factors that may increase an\nindividual's susceptibility. To accomp
 lish these goals\, we utilize\ncomputational models of long-term blood pr
 essure regulation. We found that\nindividual variation in water intake or
  the myogenic response as well as\nhigh dosages of these drugs may predis
 pose triple whammy patients to develop AKI. The computational models used
 \ninclude variables describing the heart and circulation\, kidney functio
 n\,\nsodium and water reabsorption in the nephron and the RAS\, and are\n
 parameterized separately for men and women.
DURATION:PT1H
DTSTAMP:20191022T175542Z
DTSTART;TZID=America/New_York:20191025T153000
LAST-MODIFIED:20191022T175542Z
LOCATION;X-BEDEWORK-UID=18832edc-1b27e154-011b-283f5122-00000081:Physics 2
 35
STATUS:CONFIRMED
SUMMARY:Determining Risk Factors for Triple Whammy Acute Kidney Injury: Se
 x-specific Modeling and Analysis
UID:CAL-2c918085-6de22ea0-016d-f464adf9-00007f62demobedework@mysite.edu
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Main:/user/public-user/Utili
 ties/Main
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Lecture_Talk:/user/public-us
 er/Lectures_Conferences/Lecture_Talk
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Panel_Seminar_Colloquium:/us
 er/public-user/Lectures_Conferences/Panel_Seminar_Colloquium
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Medicine:/user/public-user/T
 opics/Medicine
X-BEDEWORK-ALIAS;X-BEDEWORK-PARAM-DISPLAYNAME=Natural Sciences:/user/publi
 c-user/Topics/Natural Sciences
X-BEDEWORK-SPEAKER:Jessica Leete (Duke University)
X-BEDEWORK-DUKE-SERIES:Graduate/faculty Seminar\, special SIAM-AWM Graduat
 e Student Talk
X-BEDEWORK-SUBMITTEDBY:kg182 for Mathematics (agrp__ArtsandSciences_Mathem
 atics)
X-BEDEWORK-IMAGE-X1:0
X-BEDEWORK-IMAGE-Y1:-0.3333333333333144
X-BEDEWORK-IMAGE-X2:530
X-BEDEWORK-IMAGE-Y2:353
X-BEDEWORK-IMAGE-CROP-WIDTH:530
X-BEDEWORK-IMAGE-CROP-HEIGHT:353.3333333333333
X-BEDEWORK-IMAGE-ALT-TEXT:Duke Math Seminar
X-BEDEWORK-IMAGE:/public/Images/Duke Math image calendar_20191022015542PM.
 jpg
X-BEDEWORK-THUMB-IMAGE:/public/Images/Duke Math image calendar_20191022015
 542PM-thumb.png
END:VEVENT
BEGIN:VEVENT

CATEGORIES:Medicine
CATEGORIES:Natural Sciences
CATEGORIES:Lectures/Conferences
CATEGORIES:Utilities
CATEGORIES:Lecture/Talk
CATEGORIES:Panel/Seminar/Colloquium
CATEGORIES:Main
CONTACT;X-BEDEWORK-UID=2c918084-67810a22-0167-8547cfec-000013b9:Gerondelis
 \, Kristen
CREATED:20191024T173336Z
DESCRIPTION:Tumor recurrence following therapy is the leading cause of dea
 th in many cancer types\, including some of the most common epithelial tu
 mors such as breast and prostate cancer. Many breast tumors recur more th
 an 5 years after initial surgery and treatment\, and recurrences as long 
 as 20 years following therapy have been documented. This has led to the s
 uggestion that a population of tumor cells - referred to as minimal resid
 ual disease - can survive treatment and persist in a dormant\, clinically
  undetectable state for years or even decades. These dormant residual cel
 ls are the likely reservoir for disease recurrence. Because recurrent bre
 ast cancer is generally incurable\, developing strategies to forestall re
 currence by therapeutically targeting residual cells during the dormant s
 tage is of paramount importance. While recent work in this area has focus
 ed on specific pathways that promote the survival and recurrence of dorma
 nt cells\, several fundamental questions about dormancy have not yet been
  addressed: How does the clonal composition of tumors change during dorma
 ncy and recurrence? Is tumor recurrence driven by the selection of a subs
 et of dormant residual cells? Do dormant tumor cells undergo adaptive cha
 nges that allow them to recur? Because primary breast tumors are be heter
 ogeneous\, harboring different subclones of (epi)genetically distinct cel
 ls\, it is likely that dormancy and recurrence are accompanied by profoun
 d changes in the...(see website for rest of abstract).
DURATION:PT1H
DTSTAMP:20191024T173539Z
DTSTART;TZID=America/New_York:20191101T133000
LAST-MODIFIED:20191024T173539Z
LOCATION;X-BEDEWORK-UID=18832edc-1b27e154-011b-283f5122-00000081:Physics 2
 35
STATUS:CONFIRMED
SUMMARY:Adaptation and selection during residual disease and tumor recurre
 nce
UID:CAL-2c918085-6de22ea0-016d-fed4ba20-000052f6demobedework@mysite.edu
URL:https://math.duke.edu/events/96752-adaptation-and-selection-during-res
 idual-disease-and-tumor-recurrence
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X-BEDEWORK-SPEAKER:James Alvarez (Duke University\, Pharmacology and Cance
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X-BEDEWORK-DUKE-SERIES:Mathematical Biology Seminar
X-BEDEWORK-SUBMITTEDBY:kg182 for Mathematics (agrp__ArtsandSciences_Mathem
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