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1 amina propria) and targeting the epithelium (urothelium).
2 fections without causing lasting harm to the urothelium.
3 advanced transitional-cell carcinoma of the urothelium.
4 nd normally to mannosylated receptors in the urothelium.
5 thways including primary afferent nerves and urothelium.
6 wards developing specific endodermal derived urothelium.
7 erficial, 72 invasive lesions, and 52 normal urothelium.
8 eatment of patients with advanced TCC of the urothelium.
9 line expressing a cyclin D1 oncogene in the urothelium.
10 een UPEC and terminally differentiated human urothelium.
11 ponents originate from the same cells in the urothelium.
12 ill develop recurrent lesions throughout the urothelium.
13 id not cause histologic abnormalities of the urothelium.
14 el of expression compared to adjacent normal urothelium.
15 cell lineages in the prostate epithelium and urothelium.
16 24 was elevated compared with normal bladder urothelium.
17 ceptor (B1R) is expressed in control bladder urothelium.
18 study as compared to their respective normal urothelium.
19 l pilus for UPEC persistence in the inflamed urothelium.
20 here through the interstitium to beneath the urothelium.
21 major differentiation products of mammalian urothelium.
22 ced transitional-cell carcinoma (TCC) of the urothelium.
23 iously shown that p63 is expressed in normal urothelium.
24 m; strong expression was also seen in normal urothelium.
25 matic BK virus latency is established in the urothelium.
26 g growth, differentiation, and repair of the urothelium.
27 e specific differentiation of a transitional urothelium.
28 hanically evoked purinergic signaling by the urothelium.
29 vivo involved a direct effect on neoplastic urothelium.
30 itional cell carcinomas compared with normal urothelium.
31 and one major type in the sub-urothelium and urothelium.
32 te in promoting COM crystal retention by the urothelium.
33 th the level of potential carcinogens in the urothelium.
34 in the treatment of advanced cancers of the urothelium.
35 for patients with advanced carcinoma of the urothelium.
36 duction pathway in TCC cell lines and normal urothelium.
37 major differentiation products of mammalian urothelium.
38 ngle-agent activity against carcinoma of the urothelium.
39 ssary for the proliferative action of KGF on urothelium.
40 in mechanically-induced ATP release from the urothelium.
41 alized pannexin 1 to all three layers of the urothelium.
42 naling, Ret expression, and apoptosis of the urothelium.
43 by the urethra and external adherence to the urothelium.
44 y and raised P2X3 receptor expression in the urothelium.
45 uld contribute to spread of cells within the urothelium.
46 ctivated beta-catenin signaling in the adult urothelium.
47 d invade the epithelial cells of the bladder urothelium.
48 ld higher than in wild type mice with intact urothelium.
49 ormation and terminal differentiation of the urothelium.
50 in the developing and mature murine bladder urothelium.
51 d ATP release which presumably occurs in the urothelium.
52 P and type 1 pili for attachment to the host urothelium.
53 commonly predicted were biliary tract (18%), urothelium (11%), colorectal (10%), and non-small-cell l
54 rcinomatous urothelium but not in the normal urothelium; (2) uptake was detected at a very early stag
55 , synthesis of the HB-EGF precursor by human urothelium also suggests the possibility of using the DT
56 ed to increased proliferation of the bladder urothelium although this was not associated with hyperpl
59 amined the expression of PPARgamma in normal urothelium and bladder cancer in an attempt to assess it
60 distinct layer of smooth muscle between the urothelium and bladder detrusor, termed the muscularis m
61 in nine bladder cancer cells, paired normal urothelium and bladder tumor samples (n = 25), and tissu
64 family member expressed in both normal human urothelium and cultured normal human urothelial (NHU) ce
66 ic hedgehog secreted by the nascent ureteric urothelium and ending with ureteric smooth muscle cell d
67 fection, we showed that MRSA attached to the urothelium and implant in patterns that colocalized with
68 erents, but new findings have pointed to the urothelium and interstitial cells as key participants in
73 he PTCH, SMOH and GLI3 transcripts in normal urothelium and TCC cell lines and rare PTCH mutations in
75 m of transitional cells of the human bladder urothelium and that the soluble form of the growth facto
76 y be attributed to the interplay between the urothelium and the release of urothelially derived media
77 y signal feedback between basal cells of the urothelium and the stromal cells that underlie them.
78 erally, a prominent role has emerged for the urothelium and the underlying suburothelium in mechanose
79 ophosphamide (CYP)-induced cystitis) bladder urothelium and their contribution to lower urinary tract
80 s not expressed by normal or malignant human urothelium and therefore is unlikely to play a role in a
82 s that block bacterial interactions with the urothelium and vaccines focused on preventing both acute
83 le of regenerating all cell types within the urothelium, and are marked by expression of the secreted
85 increases with age, is not present in normal urothelium, and occurs early in tumorigenesis, it can be
87 onal crystals covering the apical surface of urothelium, and provide unique opportunities for studyin
88 to the permeability barrier function of the urothelium, and UPIII deficiency can lead to global anom
89 nvasive tumors with matched normal-appearing urothelium, and urothelium from 12 age-matched UC-free p
90 VNUT was abundantly expressed in the bladder urothelium, and when the urothelium was weakly stimulate
91 m the apical and basolateral surfaces of the urothelium appears to be mediated by separate mechanisms
92 een low-grade, noninvasive tumors and normal urothelium are needed to identify genes involved in earl
93 It is proposed that ATP is released from the urothelium as a sensory mediator for the degree of diste
94 ER1 interaction, and identification of human urothelium as a site of HB-EGF precursor (proHB-EGF) syn
95 e examined the distribution of nAChRs in the urothelium, as well as their ability to influence the re
96 Deletion of Klf5 from the developing bladder urothelium blocked epithelial cell differentiation, impa
97 served in the hyperplastic and carcinomatous urothelium but not in the normal urothelium; (2) uptake
98 rategy: 67LR was not expressed in the normal urothelium but was present in the tumor, whereas TATI ex
99 was confined to umbrella cells in the normal urothelium, but extended to all cell layers in the tumor
101 ns innervated the detrusor, vasculature, and urothelium, but only part of this innervation was sensor
102 esent in most normal human tissues including urothelium, but was reduced or absent in the majority of
103 reduce contact time between carcinogens and urothelium by diluting urinary metabolites and increasin
104 GFR3 may confer a selective advantage in the urothelium by overcoming normal contact inhibition of pr
105 ctivation of tumor suppressor p53 and pRb in urothelium by SV40 T antigen resulted in urothelial carc
106 ne, our data establish that normal mammalian urothelium can function not only as a permeability barri
107 ith our recent finding that transgenic mouse urothelium can secrete ectopically expressed human growt
108 ur data strongly support the hypothesis that urothelium can undergo at least three pathways of differ
109 ct4 is expressed in normal and in neoplastic urothelium carrying implications for a bladder cancer st
110 e developing prostate epithelium and bladder urothelium, cell lineages in these endoderm-derived epit
111 toxicity to telomerase-negative human normal urothelium cells but was highly cytotoxic to telomerase-
112 null mice develop a bladder with an abnormal urothelium, constituted by a single layer of cells that
113 cultures from the rat demonstrated that the urothelium contains both alpha3* and alpha7 receptors.
114 inogen activators of ruminants are therefore urothelium derived rather then kidney derived as in some
115 der tumour-derived cell lines and one normal urothelium-derived cell line for genome-wide copy number
116 s to examine p63 isoforms in mouse and human urothelium during embryogenesis and tumor progression, r
117 thogenic Escherichia coli (UPEC) in the host urothelium during urinary tract infection (UTI) via the
118 interplay between invading bacteria and the urothelium elicits a mucosal response aimed at clearing
122 However, our findings also indicate that urothelium expresses a variety of other Oct4 splice-vari
124 epithelial lining of the urinary bladder, or urothelium, expresses two subtypes of nicotinic acetylch
125 expressing FGFR3b-S243C in transgenic mouse urothelium expressing SV40T converted carcinoma-in-situ
126 al inactivation of both RB1 alleles in mouse urothelium failed to accelerate urothelial proliferation
129 luding the bladder, is lined by a stratified urothelium forming a highly differentiated, superficial
132 ethylation patterns between normal-appearing urothelium from bladders with cancer and urothelium from
133 ci were hypermethylated in apparently normal urothelium from bladders with cancer, indicating an epig
135 the various stages in the differentiation of urothelium from ES cells, including the commitment to an
136 n and, in ketamine-induced cystitis, loss of urothelium from large areas of the bladder wall is a rep
137 with the prostate findings, analysis of the urothelium from rescued p63-/- chimeras shows that umbre
140 ced transitional-cell carcinoma (TCC) of the urothelium has promising activity and acceptable toxicit
141 ve diseases of the human bladder epithelium (urothelium), however a cognate HER1 ligand that can act
142 atic carcinoma, but not in the nonneoplastic urothelium, implicates BKV as an etiologic agent in the
145 he release of several neurotransmitters from urothelium in response to distension and its action on r
147 K3CA may confer a selective advantage in the urothelium in vivo by overcoming normal contact-mediated
148 evels were greatly reduced (to <5% of normal urothelium) in cultured urothelial cells, which synthesi
149 from the bladder epithelium, also termed the urothelium, in response to mechanical or chemical stimul
150 n of a constitutively active Ha-ras in mouse urothelium induces simple urothelial hyperplasia that is
152 rom being a passive container for urine, the urothelium is a crucial area within the bladder wall and
156 enes or inactivation of tumor suppressors in urothelium is considered critical for development of uro
159 The apical surface of mammalian bladder urothelium is covered by large (500-1000 nm) two-dimensi
163 tivation of all Rb family genes in the mouse urothelium is sufficient to initiate bladder cancer deve
166 ncer arises in the superficial lining of the urothelium, it is a likely candidate for site-directed a
170 g in the ureteral mesenchyme, but not in the urothelium itself, led to urothelial disorganization, hi
172 e direct effects of ketamine on normal human urothelium maintained in organ culture or as finite cell
175 e-driven system ablating Foxa1 expression in urothelium of adult mice resulted in sex-specific histol
179 we eliminated beta1-integrin selectively in urothelium of mice using Cre-LoxP targeted gene deletion
180 increase in cytokeratin 14 expression in the urothelium of the female Foxa1 knockout mouse and an inc
182 akin II gene promoter, we have targeted into urothelium of transgenic mice a dominant-negative mutant
183 of an activated form of beta-catenin to the urothelium of transgenic mice using Cre-Lox technology (
184 provide compelling evidence, indicating that urothelium, one of the slowest cycling epithelia, is rem
185 rase (ChAT) were performed in wholemounts of urothelium or detrusor or cryostat sections of the bladd
186 d in quiescent (G(0)) cells, indicating that urothelium overexpressing the cyclin D1 (an 8-fold incre
191 d that disrupting the uroplakin layer of the urothelium resulted in water and urea permeabilities (P)
192 onclude that loss of integrin signaling from urothelium results in incontinence and overactive bladde
193 both patients relative to a panel of normal urothelium samples obtained from individuals free of bla
196 ty of the UPII promoter in the generation of urothelium-specific adenoviral vectors and provide a pot
202 (Uro) A subtype shares features with normal urothelium such as keratin 5 (KRT5), P-cadherin (P-Cad),
203 diminish the proliferative effect of KGF on urothelium, suggesting that the contribution of urinary
204 Hierarchical clustering classified normal urothelium, superficial, and invasive tumors with 82.2%
205 ltilayered water-tight epithelium called the urothelium, surrounded by smooth muscle layers that, by
209 , and intrinsic signalling mechanisms of the urothelium that may contribute to the altered sensory pr
210 lving ATP and NO release presumably from the urothelium, that in turn could act on bladder C-fiber af
211 Cs are progenitors in the adult regenerating urothelium, that P cells, a transient population, are pr
214 lls, followed by rapid reconstitution of the urothelium through differentiation of underlying basal a
215 GF-beta1) may stimulate ATP release from the urothelium through vesicular exocytosis mechanisms with
217 evidence that p53 deficiency predisposes the urothelium to hyperproliferation, but is insufficient fo
220 either low- or high-grade carcinomas in the urothelium transitional epithelium supporting a key role
221 least three pathways of differentiation: (a) urothelium-type pathway; (b) epidermis-type pathway; and
223 -dsP21-322-2'F into mouse bladder results in urothelium uptake and extends survival of mice with esta
224 imian vacuolating virus 40 T (SV40T), in the urothelium (Uro-SV40T-AR(-/y)) had a similar incidence o
225 ering to mannosylated receptors on the human urothelium via the carbohydrate-binding domain of the Fi
226 tability by stimulating ATP release from the urothelium via vesicular exocytosis mechanisms with mini
230 ing of the urethral diameter and with normal urothelium was noted in all dogs surviving at least 28 d
231 ssed in the bladder urothelium, and when the urothelium was weakly stimulated (i.e. in the early fill
233 arker of exposure, and are found also in the urothelium, where they give rise to a unique mutational
235 dinary high level (0.1% of total protein) in urothelium, whereas Rab27b levels were greatly reduced (
236 in PNCA in Uro-AR(-/y) than that found in WT urothelium, which suggests that Uro-AR may modulate blad
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