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1 es is present constitutively and modified by bladder inflammation.
2 phamide was used to induce acute and chronic bladder inflammation.
3 c and estrogen signaling could down-regulate bladder inflammation.
4 the bladder, synergistically reduced chronic bladder inflammation.
5 tor functions before developing histological bladder inflammation.
6 ic T cells induced OVA-mediated histological bladder inflammation.
7 le hypotheses regarding the roles of PARs in bladder inflammation.
8 1) spinal cord following CYP-induced urinary bladder inflammation.
9  was unchanged following CYP-induced urinary bladder inflammation.
10 o a localized immune response in the CNS and bladder inflammation.
11 on's nucleus/locus coeruleus area, prevented bladder inflammation.
12 F-alpha and TGF-B signaling pathways, due to bladder inflammation.
13 a experiments as well as in a mouse model of bladder inflammation.
14  (Trks) in micturition reflexes with urinary bladder inflammation.
15 er afferent pathways after visceral (urinary bladder) inflammation.
16 otype into these mice and found this blocked bladder inflammation and cystometric markers of DBD.
17 ing agents reversed cyclophosphamide-induced bladder inflammation and detrusor expansion.
18                      The opposing effects of bladder inflammation and HYPX on the potency of WIN in t
19                                         Both bladder inflammation and HYPX significantly increased th
20 cumulation of DNA damage in a mouse model of bladder inflammation and in cultured bladder muscle cell
21 ng to sustained cyclooxygenase-2 expression, bladder inflammation and mucosal wounding-responses asso
22 y, we confirmed that CNF1 expression induces bladder inflammation and, in particular, as shown in thi
23  circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting
24 nic signaling independently attenuated acute bladder inflammation by decreasing neutrophil recruitmen
25 he bladder, suggesting that GBS may suppress bladder inflammation during cystitis.
26 a of adult rats were evaluated after chronic bladder inflammation induced by 2 week treatment with cy
27 nd NGF, p75(NTR), after various durations of bladder inflammation induced by cyclophosphamide (CYP).
28 diated viscero-visceral interaction in which bladder inflammation influences uterine CB1 sensitivity,
29                                              Bladder inflammation or HYPX significantly decreased thi
30 erent nerve hyperexcitability during urinary bladder inflammation or irritation.
31 TP during pathological conditions of urinary bladder inflammation or irritation.
32 t PAR-4 mRNA is up-regulated in experimental bladder inflammation regardless of the initiating stimul
33                         Catheter use elicits bladder inflammation, releasing host serum proteins, inc
34 spite the functional presence of TGF-beta in bladder inflammation, the precise mechanisms of TGF-beta
35                                 During acute bladder inflammation, there was a predominant infiltrate
36  beta-estradiol and anabasine reduce chronic bladder inflammation through reduction of nuclear transl
37 tudy utilized cyclophosphamide (CYP)-induced bladder inflammation to identify and characterize bladde
38  tumor necrosis factor-alpha (TNFa)-mediated bladder inflammation upon subsequent bacterial challenge
39                                   Changes in bladder inflammation were measured histologically and by
40 kg) in three groups: (1) controls; (2) after bladder inflammation with intravesicular turpentine; and