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Transcript of P 12; PAGE 18 · ist (ranitidine ette Criglar teins NSP2 n. Newly /LDs mer rus proteins nes for...
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P-2. Lathrough
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F ABSTRAbetical order
act Title:
melioration of
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n of Krüpple-liling in normal
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me compositiometabolism in
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peptide-2 repstinal stem cell
tal regulator pnvasive pancr
Center s Symposi2015
al NEC by sur
8 suppresses Tγ
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ultures: A new
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24. J
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Tex 6th Fron
Name and InGirish S. HireClinical PostdTexas ChildreKendal HirscProfessor Baylor CollegDiane Leigh HPredoctoral FBaylor CollegJoseph MichaAssistant ProBaylor CollegFaith Dorsey Clinical PostdBaylor CollegLi Jiao, M.D.,Assistant ProBaylor CollegCoreen L JohPostdoctoral Baylor CollegSunkuk KwonAssistant ProUT Health SEric Lloyd, PInstructor Baylor CollegYuan-Hung LGraduate StuBaylor CollegPankajini MalGraduate StuUniversity of Janielle P MayPh.D. CandidBaylor CollegAdrienne McNPostdoctoral Baylor CollegChristina MorPh.D. CandidBaylor CollegDorottya NagPostdoctoral Baylor Colleg
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nstitution: emath, M.D. Mdoctoral Fellowen's Hospital hi, Ph.D.
ge of MedicineHutchinson, B
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ge of MedicineIhekweazu, M
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ge of Medicinellick, B.S., M.Sdent Houston ynard
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5
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5. Unbiased pferential expre
6. Gut dysfunormation betw
7. Norwalk vifecal microbi
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9. Special condiatric recurren
20. Characterisividuals
21. Effects of Litro cell culture
22. Systemicallfate sodium-in
23. Cerebral smbiosis
24. SPDEF inhenin transcript
25. Animal mo
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27. An outbreaum paratuberculo
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Diseases Ce Diseases
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Page:
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41. J
42.
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47.
Tex 6th Fron
Name and InLaura Ortiz Graduate StuBaylor CollegMuralidhar PrAssistant ProTexas ChildreCana Ross, PhPostdoctoral Baylor CollegJeremy SchaeAssistant ProUT Health ScTattym E ShaSenior ScientiBaylor CollegJennifer K. SpInstructor Baylor Colleg
Yuxiang Sun,Assistant ProBaylor Colleg
Mary ElizabetFellow Baylor CollegCatherine ToPostdoctoral Baylor Colleg
Hongtao “AleGI Fellow Baylor Colleg
Yong Ma Research AssDepartment oPharmaceuticCollege of Ph
Yuying Liu, PAssistant ProUT Health Sc
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dent ge of Medicineremkumar, Mfessor en’s Hospital h.D. Associate
ge of Medicinefer, Ph.D. fessor cience Center aiken, Ph.D. ist
ge of Medicinepinler, Ph.D.
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Diseases Ce Diseases
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Lactobacillus reury of antimicro
Infants with shased intestinal
The role of GAinfection
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n resistance
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y mice
Center s Symposi2015
uteri as a biothobial peptides
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t support moueristaltic respoon in response
h celecoxib den 2,4,6-trinitrocolon
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peptide-1 prostrains
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destruction orely-born infstinal hypox
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xperimental bust assessmarious amoun assessmeC was decreP-A appeardministrationwere the lev
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Diseases Ce Diseases
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of all or part fants. Riskxia, and inysaccharide receptor 4 C are lackin
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NEC in thisment of NECunts of SP-Ant of NEC aeased; howered to haven of SP-A (5vels of IL-1βr the initial tEC had littlehreshold levndent. In aal stages of tages of dist
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logy, §Divisioe University
of the bowek factors fontestinal m
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Baokun HeDepartmen3Pediatric RHouston, T
Backgrourole in muarthritis (Rattractive tretinoic-acdifferentiatTherefore, inflammatoprobiotic Linflammatio(NEC), andin inflammain inflammthrough suAims: ToRORγ. Methods: were incub(ratio of 1:CD4 and dependentRORα anddomain (LBand IL-17Adetermine genes, inclby real-timResults: Wof IL17A-pincreased containing treatment differentiatWe observdependentoverexpresConclusioRORα/γ ac
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significantlyion assay. Sved that LRt manner. ssing RORα ons: Probioctivity. LR17
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differentiation
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D4+T cells ws for TH17 L17A-produfect of LR17γ-dependent IL-17 proreal-time PCl differentiat-mediated in
Center s Symposi2015
entiation thr
J. Marc Rho/Immunologer at Housto
(TH17 cells)wel disease very of TH17e function oORγ) are re
duction of Ipeutics to tr. Anti-inflam
shown in 3 mation necroR17938 affece beneficial eon of TH17
n through ta
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A cell-based38 on transcas fused to use RORα o
ment (ROREexpression
4 and TH17 c
tiation in vitron medium
were stimulacell differe
cing TH17 7938 on trant reporter aomoter activCR assays. tion and funnflammatory
um:
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7 cells provif these cellequired for L-17 transceat TH17-memmatory effanimal mod
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argeting ROR
of C57BL/6bsence of LRnd then staid RORα or criptional actthe ligand
or RORγ fullE) into EL4 c
of TH17 sigcells was qua
ro. The percm was signiated in a mentiation. LRcells in the
nscriptional aactivity in avity in EL4
nction via iny diseases.
an
ology, School,
hogenic umatoid des an ls. The the full
cription. ediated fects of dels of rocolitis ponses R17938 ntiation
Rα and
6J mice R17938 ned for RORγ-tivity of binding l length cells to gnature antified
centage ficantly
medium R17938 e TH17 activity.
a dose-4 cells
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The assocnormal intKristin N. B1Graduate OH; 2DepaTX. Backgrouin the crypconfined tpopulationspreviously and for steKRAS andallele amevitro cell cuhypothesizhomeostas Methods: inducible recombinaadministereanalyzed Functional jejunal cryp Results: Icoincided wshowed thExpressionrecombinecounterparformation. confirmed Conclusiodownstreanecessary restore norstudy suggdate it is intestine, btheir integrthe specifipathways w
Tex 6th Fron
ciation of Krtestinal proBell1 and NoProgram in
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nd and Aimpts of Lieberto proliferats is essentshown that
em cell mad HRAS mutliorates the tulture studie
ze that MAPsis.
To determiKlf5-floxed tion of Klf5 ed for five using convstem cell as
pts.
In addition with a loss hat increasn of KRAS ind Klf5 cryprts. Under
However, that stem ce
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but given therative naturec regulatorywithin the int
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ms: In the adkühn. Withinting cells. Htial to suppt Klf5 is reqintenance; htations play tumorigenic
es suggest tPK signaling
ne if Klf5 reallele was
and activaticonsecutive
ventional imssays were
to decreaseof phosphoed Klf5 lean vivo, rescupts failed to
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ell maintenannitor proliferafor Klf5 in dat the mecheir known roe in normal y effects of testine.
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e experimerom these rmal proliferathan stem cgnaling path
Klf5 or the disease, sp
is. Future eow this may
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activated pr
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ative stem axpression ofnce of thesr of the interation to msm by whichole in intestig pathway inMAPK signaproproliferati
g for prolifestitutively aen by Villin-cce on the swestern bl
g three-dime
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ation. Additistic buddingsion of KRAke those Kession of KR
nts suggestexperiments
ration, MAPKcell numbershways for strole of MAP
pecifically caexperimentsy integrate
Center s Symposi2015
rotein kinas
sity of CincinCollege of Me
and progenitof the transcrse stem antestinal epit
maintain inteh this worksnal cancers this contexaling. Givenive nature i
eration withinactive KRAScreER in micsubsequent ot analysis
ensional ente
of the intesy, immunohase of phoonally, enteg structure AS was ab
Klf5 KO enteRAS in these
t that MAPKs indicate, K signaling is. Preliminatem and proPK signalingancer, it is ims will be reqwith other k
um:
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nati, Cincinnedicine, Hou
or cells are ription factornd progenitthelium. Westinal homes remains us. Loss of ont. Furthermn these resun normal in
n the intestS. Simultace. Tamoxifeday. Tissu
s, and RT-eroids derive
stine, loss istological a
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of their wble to rescueroids. RTe mice.
K signaling mthat while is only sufficry results fro
ogenitor cellg is in the mportant to duired to detknown prolif
g in
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located r Klf5 is tor cell e have
eostasis unclear. ne Klf5
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ine, an aneous en was ue was -qPCR. ed from
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Human In
Blutt SE1, SME1,Foulke1. Departm2. DepartmMedicine, BCollege of
A significanpre-clinicalmodels of Clever’s Lastructures,goblet, entagonists. Wmodels of HRVs havesmall animreplicate inrange and
In ordifferentiatbank of Hquantitatedcytometry assay. HRHIEs, conscompared compared compared immunofluoinfected cecauses diachloride chphysiologicinfection asecretion.
Thespathophysinfections pathogen within the prevent/treexamine th
Funding: N(Baylor), a57007689.
Tex 6th Fron
ntestinal En
Saxena K1, Ee-Abel J2, In
ment of Molement of MediBaltimore, MMedicine
nt limitation l models thathe small intab (Hubrech which contteroendocrinWe have chuman rotave been limit
mals. RVs n mice whedo replicate
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ne, and Panharacterizedvirus (HRV) ted as they generally exreas mouse
e in mice. ermine whetdifferentiated) derived fmount of viofluorescencmore cells
arily of immaferentiated H Like HRVerentiated studies valig presence everal mechvity. We invs in HIEs. treatment o
establish Hthe intestinaRV infection
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Zeng X1, Brnjuk O2, Zacgy and Microoenterology onding Auth
nal researchte human phhelium usingHuman inte
rmal compleneth cells) ad these newinfection, ware difficult xhibit host r
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ther RVs exd HIEs fromfrom patienral RNA byce confocal mwithin HIEs ture enterocHIEs that cV, infectionHIEs (13%dated that of virus facto
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roughman J1
chos NC2, Doobiology, BaDivision, Johor: Estes MK
h in the gasthysiology andg advancemestinal enteement of intand are physw, non-transhich kills neto culture in
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xhibit host m several pa
t small intey qRT-PCR, microscopy,than ARV (
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whether HRme-lapse muced lumin
w models tresponse, inw us to addresponses, s
as well as Es provide anfection or d
nts U18-TRnd Howard
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al Model of
1, Crawford Sonowitz M2,
aylor Collegehns HopkinsK, Dept. of M
trointestinal d disease pa
ments in stemroids (HIEs)testinal epitsiologically asformed, 3Darly 500,000n transformection in repanimal RVs
range restratients with estine biops (2) numbe and (3) yie(50% compaem cells, weominately owas also
d to 8%)ed HIEs shasms) and iulating fluid RV or the Rmicroscopy, wnal swelling
to understancluding hosdress new stem cell acto identify aa physiologidrug treatme
R000552, RHughes M
Center s Symposi2015
Gastrointes
SE1, Karandand Estes M
e of Medicines University SMolViro and
tract is the aathology. W
m cell biolog) self-organithelial cell tyactive base
D HIE cultu0 children aned cell lines
plication. Thu(ARV) exhi
iction in HIeither HRVsies or sur
er of infecteld of virus byared to 13%
ere less suscof mature ehigher in d. Electron ow classicanduction of flow throug
RV enterotowe observeindicative
and host phst restrictionquestions activity, cell-cand test newically relevanent.
R01-AI08065Medical Res
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stinal Virus
dikar U1, ConMK1
e, Houston, School of Micro, Baylo
absence of e have estay pioneeredize into villuypes (enterd on responres as pre-nnually. Studs and do nous, HRV doibit a broade
Es, we inocs or ARVs rgical tissueed cells usiny fluorescen
%). Undiffereceptible to in
enterocytes differentiated
microscopal features lipid dropleth increased
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056338 owship
Min-Shan C 1. IntegrativHouston, TCollege of Colorectal the Unitedrepressor iintestinal ecancer, suunknown. that the geGfi1 has a suppressoGfi1 stainiexpressionfocus on econditionalexpressionFuture stuunderstand
Tex 6th Fron
Gfi1 func
Chen1, Noah
ve MolecularTexas, USA,Medicine, H
cancer (CRd States. Thimplicated inepithelium. uch as leukRecent genoene express
role in tumor of CRC tuing comparen of Gfi1 in examining tl deletion of
n of Gfi1 in iudies for ideding of tumo
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Houston, Tex
RC) is the thhe growth fn the differenPrevious stu
kemia and nome-wide as
sion of Gfi1 or developmumorgenesised to normhuman colothe role of Gfi1 in intes
intestinal tumentifying theor progressio
al Center Drontiers in
nflammator
potential tumin colore
1,2
edical Sciencof Medicine, xas, USA
ird most comfactor-indepentiation of seudies suggeneutropeniassociation stis associate
ment in CRCs. In our wo
mal tissue inorectal cells Gfi1 in CR
stinal epithemor may pree molecular on and benef
Digestive n Digestivery Bowel D
11
mor supprectal cancer
ces GraduateSection of G
mmon and tendent 1 (Gecretory precested that g. However, tudies from
ed with less . Therefore, rk, we find
n human coresults in in
RC in ApcMin
lium will resevent tumorfunction of
fit to therape
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essor by indr cells
e Program, Gastroentero
the third leaGfi1) zinc ficursors into gain or loss
the role ofThe Cancertumor aggr we hypothethat maligna
olorectal spncreased apn mouse m
sults in worsrgenesis andf Gfi1 in CReutic strateg
Center s Symposi2015
ducing apop
Baylor Colleology & Hep
ading cause inger is a t goblet and
s of functionf Gfi1 in Cr Genome Aressiveness esize that Gant CRC ce
pecimens. Mpoptosis. Fuodel in vivoe outcome. d prolong ovRC may imies.
um:
ptosis
ege of Medicpatology, Bay
of cancer dtranscriptionPaneth cellsn of Gfi1 le
CRC is still Atlas have re
in CRC, indfi1 acts as a
ells display wMoreover, trauture directioo. We expeIn the contr
verall survivmprove our
cine, ylor
death in n factor s in the eads to
largely evealed dicating a tumor weaker ansient ons will ect that rast, re-val rate. current
Ka Liu1, Ya1Deparmen
Backgroumorphogenpancreatitissuggest thhypothesizCP. Objective:Methods: (BMPR2+/-)TGF-β1 (1measuringmatrix protResults: IGremlin (1FN, BMP2 treatment Gremlin alBMPR2+/- PConclusioBMPR2 is novel medrepression
Tex 6th Fron
anna Cao1,2,
nt of Surgery
nd: Our labnetic proteis (CP). Deat Gremlin i
ze that Grem
: Determine PSCs were
). The cultur ng/ml), or v phospho(ptein, was men wt PSCs2.5- vs 2.9-inhibited TGof TGF-β, lone inducePSCs (p<0.0ons: Gremlin
required fordiator of pan of BMP sign
xas MedicaAnnual Frntiers of In
A Nov
George H.
y, UTHSC-H
boratory hasn (BMP) a
eletion of Gs pro-fibroge
mlin blocks t
the role of Be isolated fred PSCs wvarious com
p)Smad1/5 leasured by im, comparedfold with theGF-β’s effecBMP2+TGF
ed FN by 205). n promotes r Gremlin’s pncreatic fibronaling, leadi
al Center Drontiers in
nflammator
vel Mediator
Greeley, Jr2
H; 2UTMB, TX
s shown thaantagonist, Gremlin in m
enic in CP. he anti-fibro
BMP signalinfrom wild-ty
were treated mbined treatm
evel using mmunofluore to vehicle,
e treatment ct, and GremF-β, Gremlin.3-fold in w
pancreatic pro-fibrogenosis in CP. ng to an inn
Digestive n Digestivery Bowel D
12
r of Chronic
2 and Tien C
X
t pancreaticare elevate
mice attenuaHowever, th
ogenic BMP
ng in Gremlinype (wt) an
with vehiclements. ActivWestern blescence as , BMP2 indof BMP2 vs
mlin blocked n+BMP2+TG
wt PSCs an
fibrosis throic function. TStrategies tovative CP t
Diseases Ce Diseases
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c Pancreatit
C. Ko1,2
c levels of Ged in both ates CP-ind
he underlyinsignaling, le
n-induced pnd BMP rece, Gremlin (vation of BMotting. Fibroa functionaluced pSma
s Gremlin+BBMP2’s effe
GF-β respecd this effec
ough its bloTogether, wto target patherapy.
Center s Symposi2015
tis
Gremlin, an human an
duced fibrosg mechaniseading to pa
ancreatic fibceptor type (500 ng/ml), MP signalingonectin (FN outcome of
ad1/5, whichMP2, p<0.0ect (4.7-, 1.2ctively, p<0ct was atten
ockade of Bwe have idenancreatic Gre
um:
endogenound mouse csis. These m is unknow
ancreatic fibr
brosis. II knockouBMP2 (50
g was assesN), an extraf fibrosis. h was inhib05). TGF-β in2-, 4.8-fold w.05). Furthenuated by 7
BMP signalinntified Gremlemlin may r
s bone chronic results
wn. We rosis in
ut mice ng/ml),
ssed by cellular
ited by nduced with the ermore, 78% in
ng and lin as a release
Stoo
J.L. Cope (M.M. Tham1. DepartmTexas ChilHouston, TChildren’s Houston, TIndies, Mo
Despite ad(LBW) babincrease aassociationcases, redincreased cTo investigutilization aTheir stooincluding toarginine m16S rRNA the OTU asubjects. Three domcharacterizClostridiumsamples, babsorptive abundanceendogenoulikely to hatotal carboor the mixweight, higwith physiodetected asuggest thdominant cin the PLachnospir We demonpotential torepresent arisk for LBW
Tex 6th Fron
ol microbio
(1,2), J.W. Hme (5), A.V. ment of Patho
dren’s MicroTexas, USA;Nutrition Re
TX, USA; 4. na, Kingston
dequate dietabies at high rarginine pron between tduced bioavacatabolism bgate whetheand metaboll microbial otal carbohy
metabolic patgene from s
assignments
minant comzed by increm, respectivebut not exclu
capacity anes of Clostus arginine fave a Bacterohydrate intaxed Bacterogher energy ological meaamong the mhat the convcommunitiesPrevotella-doraceae and
nstrate that to impact arga future treaW babies.
xas MedicaAnnual Frntiers of In
me composmetabolis
Hsu (3), P. DKurpad (4), ology and Imobiome Cent 3. United S
esearch CenSt. John’s Rn, Jamaica
ary intakes orates. Previo
oduction durthe prevalenailability of by arginase,er the gut clism from Amcommunities
ydrate and ethways. 454stool. Sequewere used
mmunity typeased abunely. These d
usively so. Snd a lower tridium showflux. Subjectroides-dominake possiblyoides with C
and total caasurements members ofversion of as. Likewise, ominated cRuminococc
the gut micrginine availa
atment for in
al Center Drontiers in
nflammator
sition and psm in a mul
Dwarkanath (J. Versalovi
mmunology, ter, Departmtates Departer, Departm
Research Ins
of energy anous researchring pregnance of LBWarginine wa possibly byommunities
merican and s, dietary hnergy intake
4 pyrosequeences were to generate
pes were indances of dominant stubjects harbendogenous
wed a mars with greate
nated commy due to highClostridium-darbohydrate
of argininef this multi-narginine to the further c
communitiescaceae.
obiota vary ability in theadequate ar
Digestive n Digestivery Bowel D
13
predicted futi-national c(4), J. M. Kac (1), E.B. HBaylor Colle
ment of Pathortment of Agrment of Pedistitute, Bang
nd protein, Inh has shownncy, Indian
W babies anas not due ty the gut mic
of Indian wJamaican w
abits, and mes, gut absoncing was uassigned to
e functional p
identified agenera Pretates tendedboring Prevos arginine fked increaser body weigunity even w
h gut absorpdominant typ
intake, and flux and thnational cohornithine is
conversion os as they
in conjunctioe human horginine avail
Diseases Ce Diseases
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unction reflecohort of w
arnes (3), C.CHollister (1,2ege of Medicology, Texasriculture, Agatrics, Bayloalore, India;
ndian women that, althou
women dond reduced to inadequatcrobiota. women diffewe recruited metabolic ch
orptive capacused to seqo operationapredictions,
among the votella, Bacd to reflect otella-dominaflux, while cse in both ght and gut awith a conveptive capacitpe occurredlower gut a
he three domhort, predicts likely to bof ornithine ty largely
on with argiost. Modulatiability during
Center s Symposi2015
ect differentwomen
C. Kao (3), R), F. Jahoor cine, Houstos Children’s
gricultural Reor College of 5. Universit
en give birth ugh women o not, and arginine prte dietary in
er in composa multi-natio
haracteristiccity, and theuence the V
al taxonomic which were
stool speccteroides, othe geograpant communcommunities
gut absorpabsorptive c
erse low enety values. P
d in subjectabsorptive caminant fecaions of met
be higher into citruline islack the
nine metaboion of the gg pregnancy
um:
tial arginine
R.A. Luna (1(3)
on, Texas, UHospital,
esearch Statf Medicine, ty of the We
to low birth from other nthere is a
roduction. Inntake but ra
sition and aonal cohort
cs were evae kinetics of sV3V5 region
units (OTUe compared
cimens andr Bacteroidephic origin onities had lows containing ptive capacicapacity werergy intake aPrevotella-dos with loweapacity. Conl communitytagenomic fun the Bactes likely to beFirmicute
olism and hagut microbioy and decrea
e
1,2),
USA; 2.
tion,
st
weight nations strong
n these ather to
arginine (n=27).
aluated, several
n of the s), and among
d were es with of their wer gut higher
ity and re more and low ominant er body ngruent y types unction
eroides-e lower genera
ave the ta may ase the
Impaire
Jeanette CBaylor Col Rotavirus requires thdroplets (Lhours postMature LDintracellulais unknown We recentdispersed appears aNSP5: dNSwith hypeviroplasm frequiremen
We evaluabecause ehyper-phosprior to infInfectious CKI/CKII-insize, impaidemonstra
Our resultsmay lead to
Tex 6th Fron
ed rotaviruspr
Criglar, Sue Clege of Med
(RV) replicahe interactioLDs). RV inf infection (h
D/viroplasmsar membranen.
ly reported tform of NSt ~3 hpi. EaSP2 only asser-phosphoryformation. Snt for cellula
ated the roleeach kinase sphorylationfection and ayield was d
nhibited cellired lipid dro
ated a decrea
s suggest tho the discov
xas MedicaAnnual Frntiers of In
s viroplasmrovides new
Crawford, anicine, Houst
ation occurson of RV nofection indupi). LD/Virop
s enclose thes containin
that two formSP2 (dNSP2ach form ofsociates withylated NSP
Since no RV-r protein kin
s of casein has been im. Cells wereassayed by determined bs showed a
oplet associaase in NSP5
hat both CKIvery of a new
al Center Drontiers in
nflammator
formation w clues into
nd Mary Esteon, TX. 7703
s in cytoplasonstructural ces LD formplasms increhe viral geng RV nonstr
ms of NSP2) appears af NSP2 inteh hypo-phos
P5, suggest-encoded proases in RV
kinase I (CKmplicated ine pre-treateimmunofluo
by fluorescea delay in viation, and litt5 hyper-phos
and CKII hw phosphory
Digestive n Digestivery Bowel D
14
and maturao cellular lip
es. Departm30
smic inclusiproteins NS
mation and ease in size nome replicaructural prot
2 are producat ~2 hpi, aeracts differesphorylated ting a phootein kinasereplication u
KI) and casen NSP5 phod with inhib
orescence ment focus asroplasm formtle or no asssphorylation
ave a role inylation-depen
Diseases Ce Diseases
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ation in protpid droplet f
ment of Molec
ions, called SP2 and NSnascent virointo larger, mation machtein NSP4. H
ced during Rand a viroplaentially with NSP5 while
osphorylatione has yet beeusing target-
ein kinase IIosphorylationbitors to onemicroscopy (ssay. IF demmation, dramsociation wit.
n viroplasm ndent mecha
Center s Symposi2015
tein kinase-formation
cular Virolog
viroplasmsSP5 and cooplasms formature viropinery and aHow RV ind
RV infectionasm-associa specific ph vNSP2 assn-dependenen describedspecific inhi
(CKII) on vn and NSP2e or both ki(IF) and wesmonstrated matically deh NSP4. We
growth andanism of viro
um:
-inhibited c
gy & Microbi
, whose foromponents rm on LDs aplasms by ~5are surroundduces LD for
. A cytoplasated form (vhospho-isofosociates exclnt mechanisd, we assessbitors.
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Carolina G1Skirball InDepartmenMedical Insand MicrobMedicine, H
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In orde
limiting intemononucleand efficienwell as in mwith evidenCX3CR1+ Mmucosal heintestine toresponsesfunction anWe hypothhomeostasdysregulate
To stud
MNPs can in modulatidentify CXresponseslimiting inflpresentatioconditions inflammatomicrobiotainflammatomay promoUnderstandintestinal in
Tex 6th Fron
crobiota con
Galan1, Randnstitute, NYUnt of Medicinstitute, NYUbiome ReseaHouston, TX
testinal immug a symbioti). A growingd the microbal inflammate developmunostimulatoion, a critica
ens while avo
er to prevent estinal inflamear phagocytnt at killing inmouse colitisnce of both pMNPs integrealing. First,o the mesent. Second, si
nd repair bothesize that Csis by limitinged in IBD.
dy the in vivobe selectiveing T cell res
X3CR1+ MNP. They are cammatory im
on by CX3CRwhere the m
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xas MedicaAnnual Frntiers of In
nditions CX
dy S. LongmaU School of Mne, Weill-Cor School of March and MoX, USA
une system c relationsh
g body of evibiota are esstion against ent of inflamory molecule
al question isoiding inflam
and treat IBmmation. Onte (MNP). Cntracellular bs models, bupro- and antrate signals f, recognitionteric lymph ngnals from tth in mice an
CX3CR1+ cellg inflammati
o role of thesely depletedsponses to i
Ps as critical critical both fommune respR1+ cells is cmicrobiota hasponses. Togcells are critisponses. Disatory behavigulation of C and the trea
al Center Drontiers in
nflammator
X3CR1+ monresponses
an2, Dan R LMedicine, Nernell Medica
Medicine, Neolecular Viro
must protecip with an endence demo
sential for huthe microbio
mmatory bowes as pathogs how the intmmatory resp
BD, we must ne critical inteX3CR1+ MNbacteria. Thut their role ii-inflammatofrom the mic
n of the micronode. We hyhe microbiot
nd humans tls respond toion and prom
se cells, we . We used thntestinal antfor limiting tor inducing t
ponses againcritical for pras been pertgether, our fcal for intest
sturbances inor of these c
CX3CR1+ MNatment of IB
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15
onuclear phs in the inte
Littman1,3, Gew York, NY
al College, New York, NYlogy & Micro
ct the host fronormous loaonstrates thauman healthota. Breakdowel diseases gens and catestinal immuponses again
first undersestinal cell pPs isolated is populationn the norma
ory behaviorcrobiota to limobiota limits ypothesize thta induce CXhrough the ro microbiotamoting barrie
generated nhese mice totigens. In thethe inductiontolerance to nst pathogeniming these turbed, CX3Cfindings indictinal homeosn the microbcells leadingPs will open
BD.
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hagocytes testine.
Gretchen E. DY, USA. 2Theew York, NY, USA. 4Alkeobiology Dep
om pathogead of residenat interaction. Thus, a nu
own of these (IBD). As thn trigger influne system nst the micro
tand the celpopulation isfrom humann expands inal intestine ar. We recentlmit intestinaCX3CR1 MN
hat this limitX3CR1+ MNPregulation of
a-derived siger function, a
novel mouseo understande presence n of inflammsoluble prot
ns. We furthT cell respo
CR1+ MNPscate that, in stasis throug
biota, such ag to a loss ofn up new the
Center s Symposi2015
to limit infla
Diehl4 e Jill RobertsY 10021. 3Hoek Center forpartment, Ba
nic microorgnt microorgans between tmber of mec
e mechanismhe microbiotammation amounts protobiota.
lular and mos a CX3CR1 n colon are hn the colon oas well as in ly demonstra
al inflammatioNP migrations microbiotaPs to promof innate lymp
gnals to mainand that thes
e strains, in wd the role CXof the intact atory intestitein antigenser demonstr
onses in vivos promote the
the presencgh promotio
as those thatf intestinal hoerapeutic tar
um:
ammatory T
s Center for oward Hughr Metagenomaylor College
ganisms whinisms (the the immunechanisms lim
ms is thoughta displays th
and disease tective respo
olecular procexpressing
highly phagoof IBD patienIBD is uncleated two waon and promn from the
a directed T ote mucosal phoid cells (ntain intestinse pathways
which CX3CX3CR1+ MNPmicrobiota,
nal T cell s as well as rate that anto. In contraste induction oce of the intan of anti-t occur durinomeostasis.rgets for limit
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David J. DRobert Bry1 Dept. of AChildren’s USA. Obstructivesleep, is a States. OSmost commhypertensiopathologicaWe hypotinflammatby chronicaremotely ccycle in freon a normrats (underwhen rats in systolic p<0.05) of(ampicillin p<0.05), Oin the gut mFecal samevaluate thsignificant (48% vs. 4hypertensiointo normodeveloped a key role f
Tex 6th Fron
e role of the
urgan, PhD1
yan Jr, PhD1
AnesthesioloMicrobiome
e sleep apnsignificant c
SA has beenmon underlyon is likelyal cascade. hesized tha
tion and ultally implantiontrolled by ee-ranging raal chow dierwent surgewere fed a hblood press
f apneas. Inand neomy
OSA-inducedmicrobiome ples from no
he microbiomincrease in
4%; n=4-6, pon we transotensive OS
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1, Eric E. Llo.
ogy, 2 Dept. oCenter, Dep
nea (OSA), clinical probln shown to bying cause
y multifactorThe source at alterationimately hypng an inflataa computer
ats. We havt do not devry without ahigh fat diet sure after 1nterestingly, ycin), resulti hypertensiofollowing higormal chow me diversity n Firmicutes p<0.05). To splanted cecSA rats that on within 7 dmicrobiome i
al Center Drontiers in
nflammator
biome in ob
oyd, PhD1, E
of Pathologypartment of
characterizem affectingbe an indepof resistant
rial, inflammof the inflam
ns to the gpertension.able obstrucr to produce ve previouslyvelop hypertpneas) fed afor 3 weeks (19mmHg; when rats fng in a sig
on was abolgh fat diet, wand high faand compos(49% vs. 8
further demcal contents
had been days of OSA n the develo
Digestive n Digestivery Bowel D
16
bstructive sl
mily B. Holli
and ImmunPathology, T
ed by repeg upwards ofpendent risk t hypertensio
mation is commation assgut microbiAirway obsttion device (60 apneas/
y demonstratension folloa high fat dis prior to apn
n=10-13, pfed a high nificant decished. Thesewhich may bat diet rats wsition. Comp81%; n=4-6onstrate theisolated fro
previously tA (n=4, p<0.0opment of O
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leep apnea
ster, PhD2,3,
nology, BayloTexas Childr
ated closuref 25% of thefactor for sy
on. While onsidered asociated witiome durintructions, sim(OD) in the /hr (10 sec. eated that youowing 4 weeet do not deneas, they e
p<0.05) and fat diet wer
crease in Fie observatio
be required fwere sequenpared to nor, p<0.05) ae importanceom hypertentreated with 05). In conclSA-induced
Center s Symposi2015
induced hy
, Julia L. Co
or College ofren’s Hospita
e of the upe adult popuystemic hypthe etiology
an integral h OSA is nog OSA pro
mulating apntrachea of raeach) duringung healthy
eks of OSA. evelop hypeexhibited a s
2 weeks (2re treated wirmicutes (8ons led us tofor OSA-indunced for the mal chow, hnd decreasee of dysbiossive OSA raoral antibio
usion, these hypertensio
um:
ypertension
pe, PhD2,3, a
f Medicine, 3
al, Houston,
pper airway lation in the
pertension, ay of OSA -incomponent
ot presently oduces low neas, were inats. The ODg 8 hrs of therats (8 weeAdditionallyrtension. Ho
significant ele21mmHg; n=with oral ant1% to 2%,
o examine chuced hyperte16s rRNA g
high fat diet le in Bactero
sis in OSA-inats on high otic. Recipiee data demoon.
n
and
3Texas TX,
during United
and the nduced in the
known. grade
nduced Ds were e sleep
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ent rats onstrate
Melinda En 1. Departm2. Departm Intestinal mand a matrmucin expaberrant exgrowth conwell docummucins. ToMTX-E12 contrast toMUC5ac aClostridiumLactobacillspecies Ctorques, Bbacterial stransmembPeriodic Amonolayerstool mucalterations agents to c
Tex 6th Fron
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ngevik1,2, Be
ment of Pathoment of Patho
mucus, consrix for bacterression andxpression ofnditions durimented, littleo address thwas incuba
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rkley Luk1,2,
ology & Immology, Texas
isting of glycrial adhesion/or mucin gf mucins withing invasion
e is known ahis gap in knted with 16 olon, which
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ns Muc1, 3 Alcian blue
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al Center Drontiers in
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Bhanu Priya
munology, Bas Children's
cosylated mn/colonizatiolycosylation h distinct olig
n and metasabout the intnowledge, th
human gutsecretes M
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17
testinal mu
a Ganesh1,2
aylor CollegeHospital Ho
ucin proteinson under nor
are associagosaccharid
stasis. Althouteraction of he mucus prt microbiota
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uct, Akkermum induced aomicron, A
decreasedssion. Strainges in muc) stains, thted HT29-M
with alter olnation treatmosa.
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, Christina M
e of Medicinouston Texas
s, provides armal homeoated with thede structuresugh tumor-athe gut micrroducing ad species unn, HT29-MTbrane MUC1
mansia mucinrelease of M
A. muciniphi Muc5ac gin-specific acin gene exat detect m
MTX mucus cligosacchariments for en
Center s Symposi2015
9-MTX-E12
Mora1,2, Jame
ne s
a protective static condite developms protects tuassociated mrobiota with enocarcinom
nder anaeroTX cell secr1 and MUCniphila, EnteMUC5ac fromila, L. reute
gene expresalterations wxpression wemucin protecompared wde content.
nhanced acc
um:
cells
es Versalovi
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mucin changcancer-asso
ma cell line obic conditiorete high le
C3. Incubatioerococcus fam goblet celeri, Ruminossion, whilewere observere correlate
eins of HT2with healthy . Bacterial-scess of thera
c1,2
he host tions in er. The
adverse ges are ociated HT-29-
ons. In vels of on with aecium, lls. The
ococcus e these ved for ed with 29-MTX human specific apeutic
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Chunxu GaRasik Shah
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ao1,3, Angelah4, Robert S
ents of Molecents of Pathoent of Patholof GastroenteTX
nd: Suppleng intestinal nderlying ma complete from L-histidamine in alle
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anu Priya G3, Monica Lu
gy & Microbiounology, BaChildren’s HHepatology,
with probion and inflamare unknowcluster whicss TNF prodnflammation.
trinitrobenzestrain 6475d weight los
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ene sulfonic 5 protected ss, ameliorareceiving Lnes IL-6 anolon by posis dependedal microbiomor. Moreoverectal cancesize of coloncontrol miceh lacks the ole of the h
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or College ofe of Medicineuston, TX nt of Medicin
bacillus strasociated cols studies snsible for thctivated THP
acid-induceBalb/c mice
ation of colo. reuteri 64nd IL-1β, asitron emissiod on introdme, consumer, using an aer model, onic tumors ae that receive
histamine phdcA gene a
at hdc+ L. renversion of L(amino acid
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Center s Symposi2015
ated colore
e3, Zhongche3, James Ve
f Medicine, He, Houston,
e, Baylor Co
ains has blonic cancershowed thathe synthesisP-1 cells, ind
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Houston, TXTX
ollege of Me
been effectr in rodent mt L. reuteris and secredicating a po
odel of colitis. Suppresnd reduced
showed decreduced uptphy (PET). an intact hhistidine-conane/dextran stration of L. of 18F-FDG bnly. Meanwhctivity did noion of histam
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m) by the inncer. The eties for thera
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Xuemei Sh
1Children'sMedicine, HUniversity College of
Backgroureprogramcoupled wabout whicadaptationapproved proabsorptpleiotropic and signalprecursorsWe hypothglucose topathway. Tmetabolic modulates Methods: metabolic tracer andinhibitor (3Results: Wfor GLP-2 MS/MS-baaerobic glreprogramidentified tenzyme). G(PKM2, a that GLP-2proliferatiofor couplinfundamentin part by Center.)
Tex 6th Fron
n-like peptid
hi1, Tiago Alv
s Nutrition ReHouston, TXSchool of MMedicine, H
nd: Emergimed for ste
with crypt cech signals dr/regeneratioby the FD
tive, proliferaactions areing in intes
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esearch CenX; 2Departmeedicine, New
Houston, TX.
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P-2 is secretGLP2R actiroliferation if the nutrie
ming and prreprogrammouse jejunalcell prolifera
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e suggests feration; anon after Roabolic reprogon-like pept short bo
rotective, anhrough the ium are pooted from villovation in intby triggering
ent-responsivoliferation, wing of glucol crypts weration in the The mini-gu) and labeleP2R was reqration in an
e revealed to biosyntheon were negged in glycphosphorylathe Warburgetabolic reps. Thus, GLPmming anddaptation/ rewhich supp
Digestive n Digestivery Bowel D
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rd Kibbey2, M
ments of Peocrinology anT; 3Departm
that a) glud b) intestinux-en-Y gasgramming o
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uts were tred with U-13Cquired for th aerobic glythat GLP-2 sis of glutagated by glycolysis via ination and nug effect) in trogrammingP-2 may be
d cell prolifeegenerationports the Te
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Mary Estes3
ediatrics & Mnd Cellular &ent of Virolo
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endocrine L m cells (ISC) glycolysis ans a key instrto determin proliferatio
and culturedi-guts were
eated with GC-d-glucose the optimal gycolysis-dep
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g of glucose the dual (m
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Center s Symposi2015
oliferation i
and Xinfu G
Medicine, Bay& Molecular ogy & Microb
bolism (aeric reprogram
s surgery. Vnd cell prolife
enterotrophCrohn's diseions in the gr (GLP2R), ys expressed
cells. Hyporeprograms
nd activatinructive signane if and hon in human/d in Matrigequantified b
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pendent manC-glucose mhe mini-gutbition. c) Uswith GAPDHocation of ps. Conclusifor biosynth
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n intestinal
Guan1
ylor College Physiology,
biology, Bay
robic glycolyming of gluc
Very little is feration in inhic hormonease. GLP-gut. GLP-2-inyet its direct
in crypt seothesis and s metabolic fg PKM2 sigal for coupliow GLP2R / mouse min
el. Intracellulby U-13C-d-g0 nM) ± glydU for 90~12ouse mini-gunner. b) Usimetabolic fluts. This meing proteom
H (a key glypyruvate kinaons: We coesis to suppd mitogenic)stem cells, ject was sup
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Audrey M. Nilotpal RoChristine A By 2020, pcancer-relarefractory metastatic mutagenespancreatic significantldevelopingprotein p12Misexpressin pancreapathogeneexpressionp120 catecytoplasmipancreatic of p120 camodel of acceleratioKCiMist1p12KCiMist1p12pancreatic pancreatic Lineage trQuantificatcells in KMicroarraysignificant results sugpancreatic
Tex 6th Fron
cytoskeleta
Hendley, Yuoy, Hao Ho, A. Iacobuzio-
pancreatic cated deaths to chemoth
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cancer is esin the Unite
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0 catenin in ppatients ye
creatic cancepancreatic icytoplasm a
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r to ductal reases one ases are sigpied by fibrocy and die aled remarked epithelial/f pancreashowed >126gene expreical role for
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Janivette Aeynolds, MatSteven D. Le
stimated to ced States. nd treatmen
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20
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Center s Symposi2015
lial cell dela
o Zhang, SaMaitra, Michaailey
he 2nd most as continuednts often extransposon a screen to nd tight junus commonncodes the molecules as correlates w20 catenin
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Hiremath, M..D.b, Christin
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on: Esophabeen describological co
s which canal lumen. Altein alterationdetermine r
sophageal tishy children.
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agus is typibed in assocondition cha eventually though somns remain unrelative globssue obtaine
were extractophageal (Pos/hpf with n
R) exhibiting analyzed by MALDI TOF/Tand unsupervsamples.
were compchildren with y food allerg648 proteinsentification bgh confidenoteins were de upregulatetin involved es and >2.1 fbiased protegnature. Withnd may be amodelling. A
al Center Drontiers in
nflammator
f EsophageG
John E WiktoPh.D.c, Melinonrad PazdraPh.D.b,c Carlpatology and
USA b Departch, Galvestonal Branch, G
College of MPediatrics, Ba
cally devoidciation with earacterized result in epe molecularnclear.
bal protein aed from child
ted and seE and DE, r
no histologicp≤0.05 and matrix-assis
TOF). The pvised hierarc
parable for aEE and the
gy. Proteoms, and 91 by MALDI Mnce identificdown-regulad and 8 werin acute allefold in DE bi
eomic analysh western ba major con
Additional stu
Digestive n Digestivery Bowel D
21
eal Eosinop
Galectin-3 orowicz, Ph.da Mata, M.
ak, M.D., Pha M Davis, Md Nutrition, Dtment of Bion, TX 77555
Galveston, TXedicine, Houaylor Colleg
d of eosinopeosinophilic by eosinop
pithelial-mesr mechanism
abundance adren with EE
parated by espectively)
c evidence oratios of ab
sted laser dproteins abuchial cluster
age, gendere median eosmic analysisstatistically
MS, and the 6cations. Eigated in PE. Dre down regergic inflammopsies. sis of EE alot confirma
ntributor to eudies to conf
Diseases Ce Diseases
Diseases in 2
philia Revea
.D.b,c, Kizhak
.S.c, Norma .D.b,c, KalpeM.D. e* Department ochemistry a5 USA c The X 77555 USuston, TX 77e of Medicin
phils. Persisesophagitis
phil driven enchymal tr
ms related to
and redox sE compared
2D-gel ele) biopsies obof inflammatibundance andesorption ioundance wasing. Candida
r, and preses/hpf was 38s of mucossignificant
62 exhibitingght uniqueDE containeulated. Exprmatory resp
and normal ation, Gal-3 aeosinophilic firm these fin
Center s Symposi2015
als Different
ke V SomanQuintanilla,
esh Thakkar,
of Pediatricsand Molecula
UTMB NHLSA d Section 7030 USA e Sne, Houston,
stent esoph(EoE) - an inflammatio
ransition ando EE have b
state (cysteito esophag
ectrophoresisbtained fromion). Normand RoRs≥1.5onization tims analyzed bate proteins
enting sympt8 (range: 17
sa from pat(p≤0.05) p
g protein sco proteins
ed more differession of g
ponses, was
esophagealappears to esophagea
ndings are u
um:
tial Express
n, Ph.D.b,c, CM.D.d , Mar
, M.D.a, Anth
s, Baylor Coar Biology, BI Proteomiof PathologSection of A, TX 77030 U
hageal eosinallergen-meon limited d narrowingbeen identifi
inyl-S-nitroseal tissue ob
s (2DE) from 6 children w
lized spot vo5 were selecme-of-flight tby t-tests, pwere confirm
toms. Food 7-100). Noneients and crotein spots
ores of 56 orwere signi
erentially abalectin-3 (G
s uniquely el
reveals a be associatel inflammatio
underway.
sion of
Christof rian hony P.
ollege
cs gy, Allergy USA
nophilia ediated,
to the g of the ed, the
ylation; btained
om 2-4 with EE olumes cted for tandem rincipal med by
allergy e of the controls s were r higher ficantly
bundant al-3), a levated
distinct ed with on and
Jian Yang1
1USDA/ARHouston, TStation, TX The prevainfluence oalterations honeysuckdetected inRNAs coulsmall RNAhours afteruptake of were of diemice and gwithout diealtered peconsumersincidence oacids are relationshipopen up ne
Tex 6th Fron
Gut dy
1, Lisa M. Fa
RS Children'sTexas 77030X 77845
ailing sciention the health
in intestinalkle (Loniceran the sera ald also be d
As appear inr the honeysgavage fed etary origin.gavage-fed eetary manipurmeability a
s. We propoof exposureabsorbed a
p between ew vistas for
xas MedicaAnnual Frntiers of In
ysfunction pb
armer1, Abia
s Nutrition R0; 2Vegetable
ific view suhy; howeverl permeabilitra japonica) and urine ofetected with
n circulation suckle was exogenous Cisplatin, aexogenous mulations. Mand gut arcose a mode to dietary sand functionhealth and r gene thera
al Center Drontiers in
nflammator
permits the between pla
A. A. Agyek
Research Cee and Fruit I
uggests the r, our data sty may uptak
containing f animals. Ihout gavage after severaremoved froRNAs and
a chemothermiRNAs couicroscopic ihitecture in l where an small RNAs.ning in the nutrition, hepy.
Digestive n Digestivery Bowel D
22
transmissioants and con
kum1, Ismail
nter, Baylor mprovemen
consumptiosuggest that ke and circu
diet, gavan the honeyfeeding. In
al days on thom the diet. digital drop
rapy drug, wuld be detectnvestigationthe cisplatarray of die Establishinconsumer
elp establish
Diseases Ce Diseases
Diseases in 2
on of genetnsumers
Elbaz1, Ken
College of Mnt Center, Te
on of plant-consumers
ulate these Rage fed micysuckle fed n the honeyshe diet and RT-PCR d
plet PCR showas used toted in the se
n and FITC-in mice, buets and diseng conditions
will drastich useful die
Center s Symposi2015
tic Informat
ndal Hirschi1
Medicine, 11exas A&M U
-based dietawith diet or
RNAs. AftercroRNAs (mpopulation,
suckle fed awere no lon
demonstrateowed that th
o induce gutera of the cisDextran ass
ut not in theease states s whereby dally alter o
etary practice
um:
tion
, 2
100 Bates Sniversity, Co
ary RNAs hr substance-r several daymiRNAs) co
plant basedanimals, the nger detecta
ed dose dephe amplifiedt/kidney damsplatin-treatesays demone honeysucmay influen
diet-derived ur concept es, and pot
treet, ollege
has no -related ys on a
ould be d small dietary
able 48 pendent d RNAs mage in ed mice nstrated kle fed nce the nucleic of the
tentially
Norw
HutchinsonFrederick HGraham, D 1Interdepar2Departme3Alkek Cen4Departme5Human G*Currently a The gut mreplication intestinal mchallenge participatedsamples cmicrobiota not associanot associadays post-Among themore stabshedding).Subdoligrashedders. compositiodemonstrapotential forelationshipreplication
Tex 6th Fron
alk virus sh
n, Diane S1,2
H2; Opekun, David Y2,4; At
rtmental Proent of Molecunter for Metaent of Medicienome Sequat University
microbiome cand syste
microbiota, study. The d in an expeollected at drelated to N
ated with suated with thchallenge, th
e 20 infectedble when co Furtherm
anulum variaThe results
on. Howeveated that loor butyrate pp between tin the huma
xas MedicaAnnual Frntiers of In
hedding dur
2,3; Ajami, NaAntone R2,4
tmar, Robert
ogram in Traular Virologyagenomics ane uencing Ceny of Michigan
contributes tmic pathogand the hustudy popu
erimental chadays -7, 2, Norwalk viruusceptibility te presence he microbiomd individualsompared to
more, metaabile, a buty
indicate thaer, microbioong shedderproduction thhe microbio
an host.
al Center Drontiers in
nflammator
ration is ass
adim J2,3; Wo4; Metcalf, Gt L1,2,4; Estes
anslational By and Microband Microbio
nter, at Baylon Medical Sc
to the deveenesis. We
uman host ulation consallenge with4, 8, 21, ans infection. to NV infectof gastroen
me composi, the microb
o pre-challenagenomic syrate producat Norwalk vme stabilityrs maintainhroughout Nme and inte
Digestive n Digestivery Bowel D
23
sociated wi
ong, Matthewinger A5; Mus, Mary K1,2,4
iology and Mbiology me Researc
or College ochool
elopment of e assessed in fecal sa
sisted of 46 Norwalk vir
nd 56 were The pre-chation, and micnteritis or sption of infect
biome of longnge than thsequencing cer, and butvirus infectioy is associ a stable
Norwalk virusestinal health
Diseases Ce Diseases
Diseases in 2
ith stability
w C2,3, Finkbuzny, Donna4; Petrosino,
Molecular Me
ch
of Medicine
gut immunithe interac
amples colle6 geneticallyrus, the protanalyzed to
allenge fecacrobiome coecific symptted and uning shedders (hat of shor
revealed tyrate metab
on is not assiated with microbiomes infection. h may impro
Center s Symposi2015
of the feca
beiner, Staca M5; Gibbs, , Joseph F1,2
edicine
ity and enhaction betwe
ected from y susceptibotypical noroo assess chl microbiom
omposition ptoms. At prenfected indiv(≥ 18 days vrt shedders
increasedbolism pathwsociated withviral shedd
e characteriFurther cha
ove understa
um:
al microbiom
cy R2*; Neill, Richard A5;
2,3
ances entereen noroviruthe Norwalle individuaovirus strain
hanges in the compositiopost-challenge-challenge viduals was viral sheddin
(≤ 14 dayd abundanway genes h fecal microding duratiozed by incracterizationanding of no
me
ric viral us, the k virus
als who n. Fecal he fecal on was ge was and 56 similar.
ng) was ys viral ce of in long obiome
on. We creased n of the orovirus
BS1
HS
Store-o
Budi Utama1
Sue E. CrawMolecular V
Houston, TXSummer Res
Rotavirus (Rlicensed vavivo, and nmechanismof RV infectCa2+ stores RV replicati(NSP4) is amechanismintegrated tforms a Ca(SOCE) andsubsequentdiarrhea. Wbiosensors.expressing luminal Carecombinanfailed to ac(HEK293FTwe found tchannel, mocell line to and blockinmediated Cinflux inhibiUnexpectedreplication express thereplication, NSP4 releaincluding SCaCC chlonorovirusesgastroenterstudied as p
This work wwhich suppo
Tex 6th Fron
operated anmediat
, Nina K. Rawford1, KhalilVirology & MX. 3Biochemissearch Intern
RV) is the leaccines, caunewly devels of RV-indtion is elevaand Ca2+ e
ion and thoua viroporin (vs of how NSto chloride sa2+ channel d voltage-actly activates
We have ge To evaluYFP-tagged2+ that activ
nt NSP4 expctivate YFPT) and humahat RV induost potently measure Cl-
ng Ca2+ entCa2+ entry isitors all redudly, L-type vand we dis
e Cav1.3 VAsuggesting
ases ER Ca2
OCE and Voride secretis) disrupt hitis. If so, potential ant
was supporteorts the Tex
xas MedicaAnnual Frntiers of In
d voltage-ated viropor
amachandra Ettayebi1, Microbiology astry & Cell Bnship Progra
ading causeses >450,00oped humauced changted cytoplasntry throughught to contviral pore-foSP4 viroporisecretion an
to release ctivated (VA
Ca2+-activaenerated a uate effects d stromal intvates SOCEression activ-STIM1 and
an intestinal uced Ca2+ eby the drug
- secretion, try through critical for uced RV yievoltage-activscovered thaACC. Specifi
Cav1.3 is i2+ to activateVACC channion and suost Ca2+ sidrugs targeiviral drugs t
ed in part bas Medical C
al Center Drontiers in
nflammator
activated carin activity t
an1,3, Alicia CMary K. Esteand 2Molecu
Biology, Riceam, Rock Isl
e of viral chil00 deaths wn intestinal es in Ca2+ s
smic Ca2+ ([Ch plasma meribute to sec
orming proten activity disd diarrhea rluminal ER
ACC) Ca2+ cated chloride
series of sof NSP4 o
teraction moE upon ERvated YFP-Sd did not in(Caco2BBe
entry was in 2-APB. Preindicate theOrai1 with Cl- secretioeld, underlin
vated Ca2+ cat human eic VACC bloimportant fo
e STIM1, trignels. This gpports RV gnaling, ma
eting cellularto reduce ga
y NIH grantCenter Dige
Digestive n Digestivery Bowel D
24
alcium chanhrough rele
C. Strtak1,4, Des1, and Joseular Physioloe University, land, IL.
dhood gastrworldwide. O
enteroid msignaling thaCa2+]c) causembrane (PMcretory diarr
ein) and this srupts host Cremained un
R Ca2+ and hannels in t
e channels (stable cell on SOCE,
olecule 1 (YFR Ca2+ storeSTIM1 and encrease [Cae) cell lines snhibited by eliminary rese Anoctamin
2-APB inhn, which is ning the impchannel (VAnterocyte cockers inhibor RV-induceggering Ca2+
global disrupreplication.
aking theser Ca2+ chanastrointestina
s DK093657stive Diseas
Diseases Ce Diseases
Diseases in 2
nnels are acease of ER
Doug Peterseph M. Hyse
ogy & BiophyHouston, TX
roenteritis anOur studies model systemat contributesed by releasM) Ca2+ charhea. We sh function eleCa2+ homeoncharacterizER Ca2+ dethe PM. Ca(CaCCs) to lines that ewe generat
FP-STIM1), e release. elevated [Caa2+]c. Using stably expremultiple blo
sults using a1 (Ano1) C
hibited CaCClikely respoportance of
ACC) blockeell lines an
bited both Ned Ca2+ upt
+ entry througption of Ca2
It is posse pathways nels, such al virus-indu
7, U18-TR00ses Center
Center s Symposi2015
ctivated by rcalcium sto
s1,4, Alexandrer1 ysics, BaylorX. 4Augusta
nd, despite iuse a comb
ms to undee to diarrhease of endopnnels, all of
howed RV nevates [Ca2+
ostasis and hzed. We hypepletion acta2+ entry thrinduce Cl- s
express fluoted a biosean ER transWe found
a2+]c, but a N both huma
essing a GFPockers of tha halide-quenCaCC is stroC activation
onsible for df this procesers also signd human inSP4-inducetake. Our sgh host Ca2
2+ homeostaible other ea general
as Orai1 anuced diarrhea
00552, AI08
um:
rotavirus Nores
ra Chang-G
r College of na College T
implementatbination of irstand the
al disease. Alasmic reticuwhich is esonstructural+]c, but the how these spothesized tivates storerough these secretion thorescent Caensor cell lismembrane that RV inf
NSP4 viropoan embryonP-based Cahe SOCE Onched YFP-
ongly activatn, suggestindiarrhea. SOss for RV renificantly redntestinal ented Ca2+ entrstudies show2+ channels iasis directly enteric virusmechanism
nd Cav1.3, sal disease.
80656, and
SP4-
raham1,
Medicine, TMC
tion of two in vitro, in molecular
A hallmark ulum (ER) sential for protein 4 molecular ignals are hat NSP4
e-operated channels
at causes a2+ or Cl- ine stably sensor of fection or rin mutant
nic kidney a2+ sensor, Orai1 Ca2+ -biosensor ted by RV ng SOCE-OCE Ca2+ eplication. duced RV teroids all ry and RV w that RV in the PM,
activates ses (e.g.,
m for viral should be
DK56338,
Special co
Faith IhekwClaire Bocc
1Section ofTexas ChilHospital, H4Departmeof PediatricChildren’s BACKGROrecurrent (must be taunderlying evaluate tincorporatiMETHODSfrom screeprotocol, fdisease (1significant day prior aThe fecal mRESULTS2 months fmonths aftHe was coconvergenhowever, radults. BasymptomaOut of the difficile direThe UC psubsequenOne patien2nd enemaCONCLUScomplicatinthe coursedonor baccarriage mwhen cons
Tex 6th Fron
onsideration
weazu1, Emichini5, Ruth
f Pediatric Gdren’s Hosp
Houston, TX,ent of Patholoc Infectious Hospital, Ho
OUND: Fecantibiotic re
aken with peclinical con
the microbiaon of these
S: Nine rCDened, self-defollowed by 1 ulcerative neurologic
and 8 weeksmicrobiomes: All 4 patienfollowing a ster FMT durionsidered ance of the rremained asacteroidetesatic carriage5 patients wected antibiopatient requnt clinical cont was diagna FMT. SIONS: FMTng clinical coe of rCDI incterial speci
may predisposidering FMT
xas MedicaAnnual Frntiers of In
ns for fecal
ly Hollister2,4
Ann Luna2,4
Gastroenteropital, Housto, USA; 3USDogy& ImmunDisease, Deouston, TX,
cal microbiofractory) Cloediatric rCDnditions wheal mechanispediatric coI patients (1esignated orenema FMcolitis [UC
impairment s after the firs were studients without usingle FMT.ng an uppern asymptomrecipient mis distant fros specificae of C. difficilwith complicaotic therapieuired FMT 3ourse. The Cnosed with
T is highly onditions. Cldicates a faes and rec
ose to CDI. T for rCDI in
al Center Drontiers in
nflammator
microbiotadiffic
4, Dorottya N4, James Ver
logy, Departn, TX, USA;
DA/ARS Chilnology, Baylepartment ofUSA
ota transplaostridium difI, given a h
en comparedsm of actionsiderations.5-16 year or universal d
MT, if clinica], 1 Crohn as underlyinrst FMT. Seed by 454 pyunderlying d One of ther respiratory
matic carrier.crobiomes
om the donolly increasle did not sigating clinical es prior to F3 times to
CD patient’s poorly mana
effective forlinical improavorable outconstitution A special appediatric pa
Digestive n Digestivery Bowel D
25
a transplantcile infectio
Nagy-Szakarsalovic2,4, a
tment of Ped 2Departmenldren's Nutritor College of Pediatrics,
ntation (FMfficile infectiohigher asympd to adults. on of FMT s. old) receiveddonors throu
ally indicateddisease [C
ng conditionlect patientsyrosequenciisease had r
ese patients infection, b. Metagenomto the donoor microbiomed in abugnificantly mconditions,
MT. These clear CDI, diarrhea didaged consti
r the treatmvement duritcome followof recipientpproach inco
atients with u
Diseases Ce Diseases
Diseases in 2
tation in pen
l1,3, Abria Haand Richard
diatrics, Baynt of Patholotion Researc
of Medicine, Baylor Colle
MT) is the on (rCDI). Sptomatic caWe performin a cohor
d filtered, frough colonosd. Two pati
CD]), 1 had ns. All patiens gave additng of the baresolution ofwas found
ut was withomic analyseor’s microbime as indeundance fo
modify microbonly 2 had opatients resbut still re
d not responpation and
ment of pediing C. difficilwing FMT. Ft microbiomorporating t
underlying di
Center s Symposi2015
diatric recu
aynes2,4, MilKellermayer
ylor College ogy, Texas Cch Center, HHouston, TX
ege of Medic
most effecSpecial consrriage rate a
med metagert of rCDI
ozen-thawedscopy underients had in
heart transnts providedtional samplacterial 16S f their symptto be positi
out gastrointes indicated iome. Recip
ependent heollowing FMbiome compobvious clinsponded weeceived colend to either C. difficile c
iatric rCDI ile directed aFMT results
mes. Asympthese findingisorders.
um:
urrent Clost
ena Pitashnr1,3
of Medicine,Children’s Houston, TXX, USA; 5Secine, Texas
ctive treatmesiderations foand more fr
enomic analypatients, w
d fecal prepr an IRB apnflammatorysplant, and d a stool saes to be anrRNA gene. toms for move for C. diftestinal comthat FMT in
pient microbealthy childreMT. Intere
position. ical benefit f
ell to a singleectomy duriantibiotics o
carriage dur
in patients wantibiotic thes in engraftmtomatic C. gs should be
tridium
ny2,4,
,
, USA; ection
ent for or FMT requent yses to
with the
paration pproved y bowel
2 had ample 1 alyzed. re than fficile 4 plaints. nduced biomes, en and
estingly,
from C. e FMT. ing his
or FMT. ing her
without erapy in ment of difficile
e taken
Li Jiao1,3, NMatthew WKanwal1,3, 1Departme3Section of Backgrouintestine, ain healthy i Methods: colonoscopand July 20cecum, ascsamples wfrom sampplatform. T(OTU) clas Results: WcomparablProteobactincrease asamples shsubject hadEscherichiathe compolevel. Varialevel. The a more equdiversity anindividual rrectum from Conclusioamong eacimplicationenvironme
Tex 6th Fron
Character
Nadim J. AjaWong2, Bhup
Maria Velez
ent of Medicif Gastroente
nd: Our undas well as onindividuals is
We enrolledpy suite at th014. We obtcending, tran
were also colples and the The sequencssification an
We obtained e amounts oteria accounbundance ofhowed an ind unique mica_Shigella, Asition of the
ations in comShannon divual distributinalysis (weigrather than bm other segm
ons: The intrch individual of mucosal ntal determi
xas MedicaAnnual Frntiers of In
ristics of m
ami2, David Ginderjit Anan
z1,3, Donna L
ne and 2Molerology, Mich
derstanding on the diversits limited.
d eight men (he Michael Etained a totansverse, deslected from 16S V4 regi
cing data wend calculatio
~3,450 seqof OTUs idennted for > 95f Proteobactcrease in Ficrobiota signAkkermansimucosal mi
mpositions wversity indexon in the abghted UniFraby sample sement.
ra-individual l. Mucosal mand fecal mnants of lon
al Center Drontiers in
nflammator
ucosal and
Graham1,3, Ynd1,3, RhondL. White1,3, H
ecular Virolohael E. DeBa
on longitudinty at lower ta
(age: 51-69 E. DeBakey al of 38 snapscending, sigthree men bon was ampre analyzed n of diversity
uences for entified for ea% of both mteria comparrmicutes andnature. Variaa, and Faeccrobiota alo
were seen fox scores werundances ofac PCoA) suegment. For
microbiota dmicrobiota wamicrobiota in
gitudinal var
Digestive n Digestivery Bowel D
26
fecal micro
Yasser Shaibda Cole1,3, CHashem El-S
ogy and Micakey VA Me
nal spatial daxonomic lev
years old, foVA Medical
p frozen normgmoid, and
before bowelplified and se
using QIIMEy indices.
each sampleach subject.
mucosal and red to colonid Bacteroideations in comcalilbacteriumng the larger Akkermansre higher for f the OTUs f
uggested thar the same in
diversity wasas under-precolon tumorriation of mic
Diseases Ce Diseases
Diseases in 2
obiota in he
b1,3, Jocelyn lark Hair1,3,
Serag1,3, Jos
robiology, Bedical Cente
iversity of mvel between
our non-HispCenter in H
mal colonic mrectum segml cleaning. Mequenced usE v1.8 for op
e. Feces andBacteroidetefecal sampleic mucosa, Ietes comparmposition wem at the Gene intestine resia and Lachcolonic muc
found in mucat the microbndividual, the
s greater thaesented in thrigenesis macrobial comm
Center s Symposi2015
ealthy indiv
Uriostegui1,
Jason Hou1,
eph F. Petro
Baylor Collegr
mucosal micr mucosal an
panic white) ouston betwmucosa surfment of the iMicrobial DNsing the Illumperational ta
d colonic mues, Firmicutees. NonetheIn contrast, cred to fecal sere seen for nus level. Foemained stabhnospiraceacosa than focosal samplbiome was ce separation
an the inter-he fecal samay be differemunity shou
um:
iduals
,3, Liang Che,3, Fasiha osino2
ge of Medicin
robiota in thend fecal micr
from the ween July 20face biopsiesintestine. ThA was extramina MiSeq axonomy uni
ucosa had es, and
eless, feces colonic mucosamples. EaLachnospira
or each subjeble at the ph
ae at the genor feces sugge. The beta-
clustered by n was seen f
segment divmples. The ent. Host andld be investi
en1,3,
ne
e large robiota
013 s from
he fecal acted
t
had osal
ach aceae, ect,
hylum nera gesting -each
for
versity
d igated.
Effects o Coreen Joand James 1Departme2Departme
Probiotics as inflammmicroorgancomponendecarboxyinflammatothe primaryproject soustudies shoinflammatogroups witshowed deby modulat
Tex 6th Fron
of L. reuteri
hnson1,2, Bhs Versalovic1
ent of Patholoent of Patholo
may affect tmatory bownism, Lactot, L-histidinelase. The p
ory cytokine y contact of ught to identowed that L.ory cytokine thout histamecreased expting pro-infla
xas MedicaAnnual Frntiers of In
derived his
hanu Priya G1,2
ogy and Immogy, Texas C
the disease wel diseasebacillus reu
e, to the bioproduced hisTNF in humthe L. reuteify how hista. reuteri deriIL-8 by HT
mine. In addpression of ammatory cy
al Center Drontiers in
nflammator
stamine on
Ganesh1,2, M
munology, BChildren’s H
course of pe via moduteri ATCC logically actstamine from
man myeloid eri derived hiamine affectived histami
T-29 cells stition, HT-29IL-8. Overaytokines
Digestive n Digestivery Bowel D
27
IL-8 expres
onica Lugo1
aylor CollegHospital, Hou
atients with ulation of PTA 6475,
tive immunom L. reutercells thereb
istamine is ts the expresne significantimulated wi9 cells treateall, L.reuteri d
Diseases Ce Diseases
Diseases in 2
ssion using
,2, Vanessa
ge of Medicinuston, Texas
chronic immthe host
, has been oregulatory sri has been by modulatinthe intestinassion of cytontly suppresith IL-1β, coed with comderived hista
Center s Symposi2015
in vitro cel
Jackson1,2
ne, s, USA
mune-mediaimmune sy shown to
signal histamshown to
ng host immal epithelial cokines from esses the expompared to mmercially aamine show
um:
l culture mo
ated disorderystem. One
convert a mine via a hsuppress thunity. Howe
cell (IEC) layepithelial cepression of tthat of the
available hisws beneficial
odels
rs such e such dietary istidine
he pro-ever, as yer, our lls. Our he pro-control
stamine effects
Systemic
Sunkuk Kw 1 Center foThe Univer 2 The UniveThe Univer Backgrouconditions important rmanifestatlymphatic farchitectur Methods: nitric oxidedisease acmethyl esteFL-C16. Lusing dynaindocyanin Results: Dthe skin of the mesenlymphatic vmice expossignificantlDSS treatmreduced asDSS-colitislymphatic pperipheral profile and Conclusioinvasively inflammatio
Tex 6th Fron
cally-altered
won,1 Germa
r Molecular rsity of Texa
ersity of Texrsity of Texa
nd: Altered including inf
role in the paions. Howevfunction. Thre are system
In the acutee synthase (ictivity. Mice er (L-NAME
Lymphatic coamic near-infne green (ICG
Dynamic NIRmice exposteric lymphavessels in thsed to DSS y higher freq
ment, the cos compared s mice treatepump activitylymph node dendritic ce
ons: Our stumonitor lympon and prov
xas MedicaAnnual Frntiers of In
d lymphatic
aine Agollah
Imaging, Thas Health Sc
xas Graduateas MD Ander
lymphatic fuflammation. athogenesis ver, it is unk
he aim of ourmically altere
DSS colitis NOS-/-) werwere also tr). Mesenter
ontractile funfrared fluoreG) to the hin
RF imaging ded to DSS.
atic vessels, he skin of mifor 4 days squency thanntractile freqto their resp
ed with L-NAy. Additionas of mice wi
ell migration.
dy demonstrphatic functiide informat
al Center Drontiers in
nflammator
c function in
,2 Grace Wu
e Brown Focience Cente
e School of rson Cancer
unction and s Recent datof inflamma
known if, andr study was ed in dextran
model, Balbre fed with Dreated with bric lymphaticnction and veescence (NIRnd paw in mi
data demonsMice with abut not in dece with DSShowed simil wild-type m
quency in bopective baseAME showedlly, histologyth DSS-indu.
rates showson and vession about re
Digestive n Digestivery Bowel D
28
n mice with
colitis
u,1 and Eva M
undation Inser, Houston,
Biomedical Sr Center, Ho
structure areta suggests tatory bowel dd how local ito investigatn sulfate sod
b/c and C57BDSS in the drboth DSS anc vessels weessel remodRF) imaging ce prior to a
strated systecute colitis sermal lymph
S-induced coar lymphatic
mice with the oth iNOS-/- alines and did
d partial but y and fluoresuced colitis r
s the feasibilisel remodelinesponse to th
Diseases Ce Diseases
Diseases in 2
dextran-su
M. Sevick-M
stitute of MoTX 77030,
Sciences at ouston, Texa
e implicated that the lymdisease (IBDnflammationte whether lydium (DSS)-
BL/6 mice arinking wate
nd a NOS inhere visualizedeling were lofollowing in
and 4 and 7
emically impshowed impahatics. Howeolitis. The lyc contraction same treatm
and wild-typed not statistinot completscence activreveal altere
ity of functiong in systemherapy.
Center s Symposi2015
ulfate sodium
Muraca1
lecular Med
Houston, as 77030,
in a numberphatic systeD) and extran in the gut aymphatic fun-induced acu
and mice lacker and monitohibitor, NG-nd after oral gongitudinallytradermal (i.days after D
aired lymphaaired lymphaever, we obs
ymphatic vesn frequency ment. Howeve mice was cally differ fre improvem
vated cell soed architectu
onal NIRF immic lymphatic
um:
m-induced
icine
r of pathologem may playintestinal affects systenction and ute colitis.
king inducibored to asse
nitro-l-arginingavage of Boy characteriz.d.) injection
DSS treatme
atic contractatic drainageserved dilatessels in iNOSas baseline,ver, at 7 daysignificantly rom each otent of systerting analysire, leukocyte
maging to noc response t
acute
gical an
emic
le ess ne odipy-zed n of nt.
tility in e in ed S-/- , but ys of
ther. mic is of e
n-to
C
Eric E. LloyRobert Bry 1Dept. of A3Texas ChiHouston, T Individualsrepeatedlycerebrovascerebral smbrain. CSVgrey mattealterations spontaneochronicallyassigned tapneas, cinstrumentcontinued through sethe Firmicsignificantlrespectivelincreased of microglmorphomepretreatingdrinking wrats, OSA damage tomicroglia (hypertensiostudy furthconsequen
Tex 6th Fron
erebral Sm
yd, PhD1, Dayan Jr, PhD1
Anesthesiologildren’s MicrTX, USA.
s suffering f collapses scular diseamall vessel VD produceser. In the pre
to the guusly hypert
y instrumenteto an OSA correspondined with a traeach day fo
equencing ofcutes:Bacteriy increased ly. Blood bra(n=6, p<0.05ia, the resi
etric analysig the SHRSPwater), which
induced no o the blood (n=4-9, p=0on, blood-bher suggesnces of OSA
xas MedicaAnnual Frntiers of In
all Vessel D
avid J. Durga.
gy, 2Dept. ofobiome Cen
from obstrucduring sle
ses or accedisease (CSs cognitive sent study w
ut microbiomtensive stroed with a tragroup, whe
ng to severacheal balloor 8 hr durinf the bacteriiodetes ratio(n=7-10, p<
ain barrier p5) in small vident immuns) in the OP OSA grouh dramatical
significant cbrain barri
0.001). Ourrain barrier
sts that bacA.
al Center Drontiers in
nflammator
Disease, Ob
an, PhD1, Em
f Pathology anter, Departm
ctive sleep eep to prolerating the
SVD), involvimpairment,
we tested theme (i.e., dyoke prone racheal ballooere the ballore OSA in
oon but wereng the sleepal 16s rRNAo (from 0.7
<0.05) in SHpermeability,vessels of thne cells in OSA group p with antibly decreasechange in ther (n=4-9, r studies linintegrity, an
cteriotherap
Digestive n Digestivery Bowel D
29
bstructive S
mily B. Hollis
and Immunoment of Path
apnea (OSoduce apneprogressiones patholog, resulting fre hypothesisysbiosis) resrats (SHRSon that couldoon was inf
humans, oe not subjecp cycle for 2A gene in fec76 to 0.48, RSP with O, as assesse
he OSA groubrain was compared
biotics (ampied Firmicutehe systolic bp=0.015), ank gut dysbnd activatioy could po
Diseases Ce Diseases
Diseases in 2
Sleep Apnea
ster, PhD2,3,
ology, Baylorhology, Texas
SA), a condea, are atn. One of theical alteratiorom damags that CSVDsulting from
SP), an anid be remotelflated 60 timor to a shcted to apne2 weeks. Ancal samplesp=0.046).
SA by 20 ± ed by IgG eups compare
significantlyto sham ccillin [1 gm/
es:Bacteriodeblood pressu
and attenuatbiosis, occun of residenossibly blun
Center s Symposi2015
a, and Gut D
Julia L. Cop
r College of s Children’s
ition where t risk for ese cerebroons to the sme to cerebr
D is acceleram OSA. 15imal model y inflated. R
mes/hr for 1am control as. In the Onalysis of ths, revealed aSystolic blo4 mm Hg ab
extravasationed to sham cy greater (
controls (n=/L] and neometes ratio inure (n=4-9, ted or aboli
urring as a nt immunitynt some of
um:
Dysbiosis
pe, PhD2,3, a
Medicine, Hospital,
the upper either deve
ovascular dismall vesselsal white andted by patho to 20 we
for CSVDRats were ra10 sec to p
group thaOSA group, ahe gut microa significant ood pressurbove the shan, was signicontrols. Acas determin6, p<0.05). mycin [0.5 gn another stp=0.478), reished activaresult of O
y in the braf the patho
and
airway eloping seases, s of the d deep ological eek old , were ndomly
produce t were apneas
obiome, shift in
re was am rats ficantly tivation ned by
When gm/L] in train of educed ation of OSA, to
in. Our ological
SPDEF in
Lo, Yuan-H 1. IntegrativMedicine 2
Center 3. D Backgrouthat resultconditions,and differefrequently β-catenin tmolecular between Ntargets andis regulateSPDEF plintestine. Wnegatively SPDEF me Material atranscriptiooverexpresimmunoprestaining. Win vivo by u Results: Wcatenin tarexpressioncatenin-driinteracts wphysiologicInterestingbind to β-cSPDEF binchromatin through probserved freveal metogether, thpathways, tumorigene
Tex 6th Fron
nhibits colo
Hung1,3; Noa
ve Molecular. Division of
Department o
nd: Colorects in the o, Wingless/Ientiation of dysregulatetranscriptiontargeted th
Notch and Wd strategies.ed by ATOHays an impWe have aregulates β
ediated repre
and Methodonal activityssed in humecipitation
We directly ausing inducib
We found thargets, such n, which is ven intestina
with β-catencal conditionly, our resul
catenin or to nds to β-cainteraction.
rotein-proteinfor β-cateninchanistic inhese resultscoordinatel
esis, but also
xas MedicaAnnual Frntiers of In
rectal cancthr
ah, Taeko2; S
r and BiomeGastroenter
of Medicine a
ctal carcinogoncogenic trnt (Wnt) anintestinal e
d. Although al activity is
herapies havWnt/β-catenin
We have shH1, a key gaportant role also previouβ-catenin traession of β-c
s: To invest, tagged w
man CRC ce(co-IP), chnalyzed the ble mouse m
at cellular pras Cyclin Dconsistent wal tumorigen
nin in both ns. The bindlts indicatedinhibit β-cattenin target We propos
n interactionn in this studsights into
s suggest thay maintainino intestinal s
al Center Drontiers in
nflammator
er cell growrough prote
Shroyer, Noa
edical Sciencrology, Hepaand Dan L. D
genesis is dransformationd Notch sigepithelium. H
constitutive believed to
ve limited en pathways hown that Satekeeper fo
in cell cycusly reportedanscriptionalcatenin trans
tigate the mwildtype SPDell lines follo
hromatin imeffects of S
model (Lgr5C
roliferation, D1 and c-Mywith our prenesis and shhuman CRding region that the DNtenin transcrsites on ch
se that SPDn, independy. Ongoing eSPDEF fun
at SPDEF mng intestinastem cell bio
Digestive n Digestivery Bowel D
30
wth by reguein-protein I
ah1,3
ce (IMBS) Gatology, and Duncan Can
riven by a son of normagnaling pathHowever, inactivation odrive most
efficacy. Thin CRCs mAM Pointed
or Notch-drivcle exit andd that SPDl activity. Hescriptional a
mechanism oDEF or trunowed by β-
mmunoprecipPDEF expre
CreERT2; β-cate
β-catenin trayc, is inhibiteevious studihrinks estab
RC cells in for SPDEF
NA-binding driptional actihromatin, reDEF could ent of its Dexperiments
nction in CRmay be a pivo
l homeostasology.
Diseases Ce Diseases
Diseases in 2
lating β-catInteraction
raduate ProNutrition, C
ncer Center,
series of geal colonic hways coordn intestinal of canonical human colo
herefore, idemay allow de
Domain Etsven differen regulates
DEF is a coere we test
activity in hum
of SPDEF-mncated SPD-catenin tranpitation (Chession in β-ceninexon3; Ro
anscriptionaed in humanes in vivo.
blished tumovitro and m
F and β-catedomain of Sivity. Finally,
esulting in thmediate oth
DNA bindings using ChIPRC and norotal link betwsis and imp
Center s Symposi2015
tenin transc
ogram, Bayloincinnati Ch Baylor Colle
enetic and emucosa. Udinately regcancers, thWnt signalinrectal cance
entifying traevelopment os transcriptiotiation of intterminal difolonic tumot the molecuman colon c
mediated inhDEF mutantsnscriptional hIP) and icatenin-driveosa26rtta-ires-E
al activity, ann CRC cell Moreover,
ors in vivo. Imouse intesenin interac
SPDEF is un, our ChIP dhe disruptionher transcripg capacity, sP-seq and Rrmal intestinween Notch pacting not
um:
criptional ac
or College ofhildren’s Hosege of Medi
epigenetic chnder physio
gulate homeese pathwang resulting ers (CRCs), nscriptional of new theraon Factor (Stestinal epitfferentiation or suppressular mechancancer cells.
ibition of β-cs were tranactivity assimmunofluoren intestinal EGFP; TRE-Sp
nd expressiolines after SSPDEF inhn addition, S
stinal cryptsction was mnnecessary fdata suggestn of β-catenption prograsimilar to wNA-seq assanal biology. and Wnt/β-conly on co
ctivity
f spital cine
hanges ological
eostasis ays are
in high current nodes
apeutic SPDEF) helium. in the
or that nism of
catenin nsiently ay, co-rescent tumors
pdef).
on of β-SPDEF ibits β-SPDEF under
mapped. for it to ted that nin and amming
what we ays will Taken
catenin lorectal
Pankajini M 1University2Baylor Co
Fatty liver National H(3 to 23 peto steatohedemonstramorbidity airinotecan based neotreatment associatedirinotecan t In hepatic including involved wliver toxicitof several involves (i)is further glucuronostwo inactivExcess acirinotecan homeostasbias causecomplex di To develop& 50 mg/k10, liver waSignificant Interestingtranscriptiotranscriptiomost likelydirect accudirecting pfatty acid possible pathe powerfDMEs in pa
Tex 6th Fron
An
Mallick1, Mic
y of Houstonollege of Med
disease (Fealth and Nu
er cent). FLDepatitis whe
ated that cheand mortaliwhich is wi
oadjuvant chof CLM by
d FLD and mtherapy is st
steatosis, increasing ith drugs thaty has been drug metab
) Bioactivatiodetoxified
syltransferesve metabolitccumulation
causes FLDsis. Therefored by pre-exisease.
p an irinotecg of irinotecas excised a
steatosis (ly, we found
on factor inon factor invy increased fumulation ofpossible acchomeostasiathogenic mful early stagathogenic m
xas MedicaAnnual Frntiers of In
nimal Mode
hael M Ittma
, Departmendicine, Patho
LD) is one utritional Exa
D manifests aen accompaemotherapyty in these dely used fohemotherap
hepatic resmorbidity/motill not known
fat accumuhepatic FFAat induce FLrelated to e
bolizing enzon by carbo to inacti
ses (UGTs);tes i.e. NPCof the SN-3
D by alteringre, our aim xisting inflam
can-induced can via intra and fixed in (Average std that irinotenvolved in volved in fafatty acid upf triglycerideumulation os. Thus, ou
mechanisms ges of disea
mechanisms
al Center Drontiers in
nflammator
el of Irinotec
ann2, and Ro
nt of Pharmaology and Im
of the leadiamination Sas simple st
anied with intreatment patients. O
or the treatmy effectivelysection. Howortality after n and need t
ulation occuA uptake, s
LD seems to nhanced geymes (DME
oxylesterasesive SN-38 (ii) Oxidatio
C and APC.38 causes fag the gene eis to develo
mmation to d
FLD animalperitoneal (10% formaleatosis sco
ecan significafatty acid tty acid me
ptake and/or es. Importanof toxic SN38ur novel in involved in i
ase models tof complex d
Digestive n Digestivery Bowel D
31
can-induced
omi Ghose1
aceutical Scimmunology,
ing causes urvey reportteatosis (fat nflammation is associate
Of particularment of coloy down-sizewever majohepatic surto be explor
rs by modisynthase abe diverse a
eneration of Es). Irinotecas (CEs) to f
glucuronidon by cytoc NPC is co
atal diarrheaexpression oop irinotecadetermine th
l model, we (i.p) route foin for fat acc
ore: 2+) wasantly down-rsynthesis, wtabolism. Thdecreased
ntly, the exp8 in the livevivo model irinotecan inthat may prodiseases.
Diseases Ce Diseases
Diseases in 2
d Fatty Live
iences, HouHouston, TX
of chronic lts, in USA oaccumulatio or fibrosis.
ed with FLDr importancorectal liver
es liver metor problem wrgery. The mred.
ifying free fnd reducingand unique. toxic metaban is a prodform more ade (SN-38Gchrome P45onverted to a in cancer of enzymesn-induced Fhe pathogen
treated aduor 9 consecucumulation as observed regulated gewhereas upherefore, it’sfatty acid ou
pression of er that migh
provides vanduced fatty ovide import
Center s Symposi2015
er Disease
ston, TX – 7X-77030
liver diseaseover 30 millioon in liver), w. Recent cli
D, which ince is the ch
r metastasisastases andwith irinotec
mechanism o
fatty acid (g oxidationIn certain caolites due todrug and itsactive metabG) by uri0 (CYP) 3ASN-38 by tpatients. W
s involved inFLD animal nesis and ro
ult male C57utive days, oassessment
at both doene expressp-regulated s reasonablutput mechaCyp3a11 wat contribute aluable infoliver. Our sttant new ins
um:
77030
e in the USon adults havwhich can prnical studie
creases the hemotherapys (CLM). Irind thereby ecan treatmeof FLD indu
FFA) home. The mecases, highero increased s biotransforbolite, SN-38dine dipho
A enzymes tthe CEs ene hypothesi
n regulation model witho
ole of DMEs
7BL6J mice wonce daily. Oby H & E st
oses of irinoion of enzymthe enzym
le to considanisms leadsas down-regto the chan
ormation abotudy is indicasights in the
S. Third ve FLD rogress s have risk of
y drug, notecan enables nt was
uced by
eostasis hanism r risk of activity rmation 8 which osphate to form zymes. ze that of lipid out the
s in this
with 25 On day taining. otecan. me and
me and der that s to the gulated nges in out the ative of role of
Dysregu
Maynard, JDolores6; F
1DepartmeLiver CenteCenter, BaBasic Scie6DepartmeBaylor Col Backgroustudies suhepatocytetissues. HoHypothesihepatocellu Methods: uninvoled Hep3B, SNwere validaof purinergand BrdU terminal Ki Results: Mcompared expressionreceptor exsufficient tincorporatiattenuatedP2X3 promdownregulaHCC patiereceptor isgenes of h Conclusiorole for dyphenotype
Tex 6th Fron
ulation of p
Janielle P1,2,
Finegold, Mil
ent of Pediater, 2 Program
aylor Collegence Researc
enf of Pathololege of Med
nd: Hepatouggest that e proliferatioowever, the is: Dysreguular carcinog
P2 purinergareas, n=4
NU387, PLCated by micrgic signaling
incorporationase inhibito
Multiple P2 to uninvolv
n was assoxpression wto induce con and incr nucleotide-moted prolifation of cycl
ents. Mst1/2soforms as ippo signalin
ons: Our anysregulation and identifie
xas MedicaAnnual Frntiers of In
urinergic spatie
3; Johnson, lton J2,3,6; Go
rics, Divisionm in Translae of Medicinech, 5Departmogy and Immicine, Houst
cellular carcextracellula
on in vitro apathophysio
ulation of pugenesis.
gic receptor 2), Mst1/2-/-
C/PRF/5) weroarray (mRon HCC ce
on of HCC or) or AF-35
purinergic ved areas iciated with
was observedcell cycle preased cycli-induced cycferation in lin D1 expre-/- mouse tucompared t
ng, implicate
alysis of HC of P2 pures P2X3 pur
al Center Drontiers in
nflammator
ignaling is ents with he
Randy L4; Loss, John A2
n of Gastroeational Biologe, 4Departmement of Systmunology, Bon, TX, Unit
cinoma (HCar ATP-mednd P2 purin
ologic relevaurinergic sign
expression - livers (hipere analyzed
RNA) analysiell cycle progcells expose
53 (P2X3 ant
receptor ison up to 60poor recur
d in HCC ceprogression in D3, E, aclin protein HCC cells.
ession in Huumors exhibto WT whileed in HCC pa
CC patients, rinergic signrinergic rece
Digestive n Digestivery Bowel D
32
associated epatocellula
ee, Ju-Seog2,7; Thevana
enterology, Hgy and Moleent of Biochtems Biologyaylor Collegted States.
C) is the 2ndiated activanergic recepance of purinnaling facilit
profiles (15 po-deficient d by qRT-PCs of a large
gression wased to ATPStagonist).
oforms were0% of patierrence-free ell lines. Ext
in Huh7 cnd A mRNAexpression. Interestingh7 cells, wh
bit dysregulae nucleotideathogenesis
Mst1/2-/- livenaling in theeptors as pot
Diseases Ce Diseases
Diseases in 2
with poor rar carcinom
g5; Sohn, Bonther, Sund
Hepatology &cular Medicemistry andy, UT MD Ange of Medicin
nd most letation of P2
ptors are ovenergic signatates aberra
isoforms) omice HCC
CR and immr cohort of Hs analyzed bS, ATP or A
e elevated ≥ents. High P
survival. Dytracellular ncells, as evA and prote Extracellula
gly, ATPS hich was assated expresse treatment s.
ers and HCCe induction tential new t
Center s Symposi2015
recurrence-ma
o Hwa5; Lopeararajah1,2,3
& Nutrition, Tine, 3Dan L. Molecular Bnderson Canne, 7Departm
hal cancer 2 purinergic erexpressedling in HCC
ant cell proli
of HCC patieC) and HCCmunohistochHCC patientby Western ADP +/- SP
≥2-fold in pP2X3 or lowysregulationucleotide trevidenced byein expressiar ATP-medtreatment i
sociated withsion of multof Huh7 ce
C cells in vitrof a hyper
targets for th
um:
-free surviv
ez-Terrada,
Texas ChildrDuncan Ca
Biology, Divincer Center,ment of Surg
worldwide. receptors
d in certain remains un
iferation und
ent livers (tuC cell lines hemistry. Fts (n=188). blotting, qR
P600125 (c-
atient liver w P2Y13 ren of P2 pureatment alony increasedion. JNK indiated activainduced a h poor progntiple P2 purells induced
ro identifies ar-proliferativeherapy.
val in
ren’s ancer sion of
gery,
Recent induce cancer known.
derlying
umor vs (Huh7, indings Impact
RT-PCR -Jun N-
tumors eceptor rinergic ne was d BrdU hibition ation of distinct
nosis in rinergic
d target
a novel e HCC
An outb
Adrienne LAttumi, Dia
Baylor ColMichael E.
The hypoththe etiologyperipheral to 50% of PCR detecmore convdisease-sporganism fwould supantibiotics.reveal a mtechniquespatients trein a villagafflicted widetection, a more covery high fand early r
Tex 6th Fron
break of IBD
L. McNees1, ane Markesic
lege of Med DeBakey V
hesis that a y of Crohn’sblood macrothese patien
ction methodvincing argupecific consifor studies o
pport unders We hypoth
more consiss viable orgeated at the e in Bahraiith Johne’s disolation and
onsistent assfrequency oresults of cul
xas MedicaAnnual Frntiers of In
D provides npa
Najah Zayyach3 , and Dav
icine1, BahraVA Medical C
mycobacters Disease (Cophages of nts has beends have imprument for Mistency of aof microbial
standing disehesized thatstent rate oanisms couHouston Den, which bedisease. Thd culture of sociation be
of detection lture.
al Center Drontiers in
nflammator
new evidenathogenesis
ani2, Fazal Tvid Y. Graha
ain SpecialtyCenter4
rium, specifCD) has been
patients withn widely reproved, labor
MAP as a cassociation, genomics, ease pathogt multiple saof detection uld be isolateBakey VA Megan recente causative MAP from
etween MAPof MAP in p
Digestive n Digestivery Bowel D
33
ce for a roles of Crohn's
Tabassam1, am1, 4
y Hospital, M
ically M. avin strengthenh CD. A posorted, but th
ratory culturecausative ag
compared molecular e
genesis andampling of p
among patted. These Medical Cently possibly agent of Jopatients wit
P and CD. Wperipheral b
Diseases Ce Diseases
Diseases in 2
e of M. avius disease
Jason Hou1
Manama, Ba
ium paratubned by the resitive MAP Phe detectione of these ogent for CDwith contro
epidemiologd an approaperipheral btients, and experiments
nter and in aafter the im
ohne’s diseah recently d
We will preslood of thes
Center s Symposi2015
um paratube
, 4, Antone R
ahrain2. Pulm
berculosis (Mecent detectPCR in bloo
n rate has berganisms ha
D would be ols. Further,gy, and antibach to treatblood from C
that with as are beingan “outbreakmportation oase is MAP.diagnosed Csent here ouse two CD p
um:
erculosis in
R. Opekun1,
motect, Inc. 3
MAP), has a tion of MAP od specimeneen variableas not advan
to demons cultivation biotic suscetment or cuCD patientsappropriate conducted
k” populationof a herd of We propoD will demour observatipatient popu
n the
Tariq
, and
role in DNA in
ns of up e. While nced. A strate a
of the eptibility re with
s would culture in CD
n of CD f cattle
ose that onstrate ons on
ulations
Christina MBaylor Col
In Lactobaproductionmetabolismrevealed nhistidine oror viabilitymedia whedeterminedproductionproviding bimproves hits sole soenteroids epithelium.
Tex 6th Fron
Morra and Jalege of Med
acillus reute of the pro-
m pathways o significantr 13C6
15N3 L-. While, theere all histidd that the . Together, benefit to thhistamine prource of L-hto determin. I will
xas MedicaAnnual Frntiers of In
L-Histidin
ames Versalicine, Houst
eri the deca-inflammatoin L. reuteri t changes inhistidine. Th
ere were no dine was re
addition ofthese data
he host, is roduction; anhistidine. Fute the effec
al Center Drontiers in
nflammator
ne metaboli
ovic M.D., Pon, TX
arboxylationry moleculeusing 13C6
15
n growth or vherefore, his
significant eplaced withf carnosine have demonot required
nd 3) L. reutture work w
cts of L. reu
Digestive n Digestivery Bowel D
34
ism by Lact
Ph.D.
of L-histide, TNF. We 5N3 L-histidinviability whetamine prodchanges to carnosine
e to the monstrated thd for L. reuteri strains c
will involve cuteri and hi
Diseases Ce Diseases
Diseases in 2
tobacillus r
dine to histahave begu
ne. Analysis en cultured induction is no growth or (β-alanyl-L-
medium signhat 1) histiduteri growth;can import, pco-culturing istamine me
Center s Symposi2015
reuteri
amine by Hun to elucida
of wild typen different c
ot essential foviability in L
-histidine), mnificantly incdine decarbo; 2) the addprocess, andof L. reuter
etabolism o
um:
HdcA reducate novel h and hdcA moncentrationor L. reuteriL. reuteri grmass spectrcreases hisoxylation, aldition of card use carnosri with human the huma
ces the istidine
mutants ns of L-growth
rown in roscopy stamine lthough rnosine sine as an ileal an ileal
Dorottya NSchady2,4, Kellermaye1Section ofTexas ChilHospital, H4Departme5Departme
BACKGROoption for treating UCin pediatricMETHODSwere stud(colonoscoimmunotheclinical anmicrobiomebacterial 1RESULTStolerated tremission. moderate tlength of cthe initiatioupon seriaCONCLUSconsideringmucosal renumber: N
Study ID
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opy and reteerapy. Filterend endoscoes were ana6S rRNA ge: Patients the treatme
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M W NH M W NH F W H M W NH F W NH F W H M W NH M W NH M W NH
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cal microbiocolitis (UC). red the clinics with mild tatients (9 tr
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37
30
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Hollister2,4,Fica E. Lopez
logy, Departn, TX, USA;DA/ARS Chinology, Baylollege of Me
ta transplanRecent tria
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Digestive n Digestivery Bowel D
35
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Faith D. Ihekz5, Ruth Ann
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o an FMT ) administerdonor stool
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28 (2) 25 22 32 (1) 10 17 (1) 9 2 24 (5)
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Center s Symposi2015
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Center s Symposi2015
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Digestive n Digestivery Bowel D
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Center s Symposi2015
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PhD2, Paman Lee, MD, ne, Texas Ccs and Microlecular and
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s1,2, Alex P1,2, Mathew
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Digestive n Digestivery Bowel D
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Center s Symposi2015
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Center s Symposi2015
on in IL-10-/
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nzler KW, VProc Natl Acais RN. Eico9
Mann M, DuBent. Oncogeen C, Hohenucleocapsid -8. PMID:11lski RJ. Cyt
of adeno-assol. 2012; 86:pekun AR. PMID:24815
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including biliary atresia
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Center s Symposi2015
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unique, coms of the mammal and cann this fractio
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nced as a fs maintains ssion and pus in malignession. The ch opportunima, Barrett
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ses in inflam0643 MxA protein
. Proc Natl A
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are needednd includes gnditions,2,3 srinucleus ha
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erinuclear microtubule
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cancer e, when d. The genetic
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Jennifer K.Runge1,2, E
1Texas ChBates AveMedicine, Oof MedicinAdministra
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Results Mabundancedeveloped antibiotics vancomyciwhich are mutant strReuterin (pdu-cbi-heglycerol is FurthermoC. difficile and patieunappreciae.g. surfacL. reuteri targeting m
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Tex 6th Fron
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. Spinler1,2, , Emily B. Hol
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Digestive n Digestivery Bowel D
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signaling me
ny Haag1,2, Avic1,2,3, Kevin
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or purified ration for usin
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s. We ident. difficile thaL. reuteri anaim to ch
his novel f
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Aaron Brown Garey4, Ro
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4Departmey, Houston,
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from CDI pecreased inacillus spp. CDI. ParticumL), and metowth in vitroeuterin, do reuteri requd that the ce in a humareuterin alonng L. reuterionstrate thaoteins that aifficile killing ment of a p
from CDI pt disease, wtified L. reutean vancomynd glycerol aharacterize tfinding to d
Center s Symposi2015
n gut-micro
wn1,2, Ruth Anobert A. Britt
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in the U.S.$3.5 billion, wn between here is still ae have idents as the phy
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is an increti1 has numess, while inhGLP-1 analognately, the ce gut microypercholeste
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Digestive n Digestivery Bowel D
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Center s Symposi2015
y human m
dt3, Robert A
of Medicinetate Universsity of Mich
ndocrine L cng promotingetion, β-cell sed as thera
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cells which lg insulin sec
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Digestive n Digestivery Bowel D
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Center s Symposi2015
ent, the perise to injury.
Department oO; 3Departmhe Children’sology, Hepat
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Purpose: several mainduced cowhich COXCOX-2, waTNBS.
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Tex 6th Fron
Perfusion wt
Song Gao, M
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The cyclooalignancies iolitis in rat cX-2 is substas assessed
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he concentran rate couldwith blank HBups perfuse03 and 0.0n was 156±427±36, 70±110μM celec
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n with celecof COX-2 ins colon perf
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Digestive n Digestivery Bowel D
46
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ctively. In thups perfusedectively. Coased the ha
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Center s Symposi2015
production rat colon
ge of Pharma
ssed in inflaobenzenesulmatory boweelective and with inflamm
the colon oments of prtion (HBSS)). The perfuted by solidrate were dendicator of
ng the perfuequation. In mined to beetermined togroup the and 10μM h the controE2 attenuatio
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Yuying LiuDepartmen 2Allergy/ImScience Ce Backgrouinflammatolevels of effector/mecells modudriven autodysregulatlymphoproWhen we MechanismAims: To mucosa, spMethods: C57BL/6J the offsprinscurfy phewas recognisolated froanti-CD4/Cby flow cycultured anpresence oPMA/Inom(Th17) andResults: Sin intestinathe expansSystemic acontain a hreduced thproinflammLR17938 tdirectly inhConclusiodemonstraTh1/Th17 human aut
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fed LR17ms by which determine ifpleen and peScurfy mic
normal maleng will be he
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d analyzed bSf mice showal mucosa csion and actanti-inflammhighly expanhe number
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sed activateOral feeding and inflamma938 were alsvated CD4+Trtantly, in ccreased in Lof CD4+T an and Th17 cflammatory
activation ofe of Foxp3+Tes.
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Center s Symposi2015
systemic ane
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s been shoNEC), assoc
while differeintestinal mu
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ty of Texas
own to havciated with reentially moducosa. Foxpses lethal, Csyndrome (Imerally die f life (DOL) ficantly incr
vestigated. 4+T cell in ination. ygous femaromosome, nerally deveOnce sf phedays. Immund were labelmmatory Temice were
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Hashem El-SDirector Baylor Colleghasheme@bc Mary K. EsteDirector EmeBaylor Collegmestes@bcm Lenard M. LicAssociate DirDirector, InteUniversity of Lenard.M.Lic Lopa Mishra, Associate DirMD Andersolmishra@mda Douglas BurrAssociate DirBaylor Collegdburrin@bcm Milton FinegoDirector, CellMorphology CBaylor Collegfinegold@bcm
ilesh Advani, Maduate ResearcHealth Scienc
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Michael MancinCo-Director, CMorphology CoBaylor College mancini@bcm Cecilia LjungbeAssociate DirecMolecular MorBaylor College [email protected] James VersalovDirector, FunctProteomics CoBaylor College [email protected] Lisa White, Ph.Co-Director, FGenomics & PBaylor College [email protected] Joseph PetrosinAssociate DirecGenomics & PBaylor College jpetrosino@bc
LIST OF Phabet ica l o
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Digestive n Digestivery Bowel D
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C LEADER
ni, Ph.D. Cellular & Molecore of Medicine .edu
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Sundararajah ThAssociate DirectBiology Core Baylor College [email protected]
Karen Uray, Ph.Associate DirectBiology Core University of TeKaren.L.David@
David Y. GrahamCo-Director, DDDirector, Study D& Clinical ReseaBaylor College odgraham@bcm.
Fasiha Kanwal, MCo-Director, StuClinical ResearchBaylor College [email protected]
Center ContactSara M. TristanTMC DDC AdTel: 713-798-2Fax: 713-798-0escamill@bcm
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Jennifer BaileyAssistant ProfUT Health SciJennifer.M.Bai
Robert Bryan,Professor and Baylor [email protected]
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