ライフサイエンスコーパス: voiding dysfunction

1 and smooth muscle contractility, leading to voiding dysfunction.

2 ed comfort for patients with incontinence or voiding dysfunction.

3 basis of lower renal tract malformations and voiding dysfunction.

4 th overactivity syndromes and nonobstructive voiding dysfunction.

5 offers promise for managing both storage and voiding dysfunction.

6 ck therapy for the treatment of recalcitrant voiding dysfunction.

7 reatment of benign prostatic hyperplasia and voiding dysfunction.

8 rned voiding patterns that contribute to the voiding dysfunction.

9 ative complications, and presence of de novo voiding dysfunction.

10 Voiding dysfunction after anti-incontinence procedures i

11 le of preoperative urodynamics in predicting voiding dysfunction after anti-incontinence surgery is r

12 of the urothelial barrier, a major cause of voiding dysfunction and bladder pain syndrome.

13 so assessed postoperative urge incontinence, voiding dysfunction, and adverse events.

14 lications (urinary tract infection, urgency, voiding dysfunction, and mesh erosion) were more common

15 eye movement behaviour disorder and urinary voiding dysfunction appear to precede the development of

16 urinary-tract infection, hydronephrosis, and voiding dysfunctions as a result of neurogenic bladders.

17 ase ALPL, which might mitigate the degree of voiding dysfunction by compensating for Nt5e deletion.

18 d contraction force, suggesting that bladder voiding dysfunction can be attributed to impaired BSM co

19 5-HT3A mutant mice had marked voiding dysfunction characterized by a loss of micturiti

20 of clinical presentations such as hematuria, voiding dysfunction, flank pain, abdominal pain, nephrol

21 of women who appear to be at higher risk of voiding dysfunction following incontinence surgery, and

22 ive complications, and de novo postoperative voiding dysfunction in a multicenter cohort.

23 Urinary voiding dysfunction in childhood, manifesting as inconti

24 Voiding dysfunction in children encompasses a wide spect

25 Over the last several decades voiding dysfunction in children has primarily been assoc

26 This overview of voiding dysfunction in children outlines the established

27 ill focus on the diagnosis and management of voiding dysfunction in neurologically and anatomically n

28 tive urodynamics in predicting postoperative voiding dysfunction in patients undergoing anti-incontin

29 th reduced tissue rigidity may contribute to voiding dysfunction in people with long-term DM.

30 Several aspects of voiding dysfunction in women remain under investigation,

31 hough not useful in the primary treatment of voiding dysfunction is equivalent in potency to biofeedb

32 Voiding dysfunction may play an etiological role in cong

33 Voiding dysfunction may spontaneously improve or require

34 se medications in the treatment of pediatric voiding dysfunction, neurogenic bladder, chronic lower u

35 also more likely to experience postoperative voiding dysfunction (OR, 3.5; 95% CI, 1.6-7.6; P = .001)

36 rates of positive provocative stress tests, voiding dysfunction, or adverse events.

37 eading to diminished BSM contractility and a voiding dysfunction phenotype that recapitulates human D

38 prognostic information regarding the risk of voiding dysfunction postoperatively and the possibility

39 The rates of voiding dysfunction requiring surgery were 2.7% in those

40 afferent neurons may therefore contribute to voiding dysfunction seen in diabetes mellitus.

41 Voiding dysfunction typically presents after toilet trai

42 complications include but are not limited to voiding dysfunction, urinary retention, vaginal extrusio

43 igher rate of lower urinary tract injury and voiding dysfunction when compared with transobturator ta

44 e CRH as a novel target for the treatment of voiding dysfunctions, which are highly prevalent disease