ライフサイエンスコーパス: bladder inflammation

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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 a experiments as well as in a mouse model of bladder inflammation.

10 was unchanged following CYP-induced urinary bladder inflammation.

11 o a localized immune response in the CNS and bladder inflammation.

12 on's nucleus/locus coeruleus area, prevented bladder inflammation.

13 (Trks) in micturition reflexes with urinary bladder inflammation.

14 er afferent pathways after visceral (urinary bladder) inflammation.

15 ing agents reversed cyclophosphamide-induced bladder inflammation and detrusor expansion.

16 The opposing effects of bladder inflammation and HYPX on the potency of WIN in t

17 Both bladder inflammation and HYPX significantly increased th

18 cumulation of DNA damage in a mouse model of bladder inflammation and in cultured bladder muscle cell

19 y, we confirmed that CNF1 expression induces bladder inflammation and, in particular, as shown in thi

20 circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting

21 nic signaling independently attenuated acute bladder inflammation by decreasing neutrophil recruitmen

22 he bladder, suggesting that GBS may suppress bladder inflammation during cystitis.

23 a of adult rats were evaluated after chronic bladder inflammation induced by 2 week treatment with cy

24 nd NGF, p75(NTR), after various durations of bladder inflammation induced by cyclophosphamide (CYP).

25 diated viscero-visceral interaction in which bladder inflammation influences uterine CB1 sensitivity,

26 Bladder inflammation or HYPX significantly decreased thi

27 erent nerve hyperexcitability during urinary bladder inflammation or irritation.

28 TP during pathological conditions of urinary bladder inflammation or irritation.

29 t PAR-4 mRNA is up-regulated in experimental bladder inflammation regardless of the initiating stimul

30 spite the functional presence of TGF-beta in bladder inflammation, the precise mechanisms of TGF-beta

31 During acute bladder inflammation, there was a predominant infiltrate

32 beta-estradiol and anabasine reduce chronic bladder inflammation through reduction of nuclear transl

33 Changes in bladder inflammation were measured histologically and by

34 kg) in three groups: (1) controls; (2) after bladder inflammation with intravesicular turpentine; and

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