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1 inary bladder and exhibit varying degrees of bladder dysfunction.
2 multiple sclerosis, spinal cord injury, and bladder dysfunction.
3 procedure for pediatric patients with severe bladder dysfunction.
4 n urinary bladder neurotrophic factors after bladder dysfunction.
5 in patients with multiple system atrophy and bladder dysfunction.
6 or vesicoureteral reflux grade and bowel and bladder dysfunction.
7 h ketamine + COX-2 inhibitor prevented these bladder dysfunctions.
10 nent in the pathogenesis of diabetes-induced bladder dysfunction, although the molecular mechanisms h
12 spinal cord level, BDNF is a key mediator of bladder dysfunction and pain during cystitis, it is pres
13 mmatory mediator provides novel insight into bladder dysfunction and supports new avenues for therape
15 cations, plane of surgery, 30-day mortality, bladder dysfunction, and sexual dysfunction, none showed
17 icles that have been published on neurogenic bladder dysfunction as well as on posterior urethral val
18 disease characterized by congenital urinary bladder dysfunction, associated with a significant risk
19 Subjects had to have urodynamic evidence of bladder dysfunction, be ambulatory, and not have dementi
21 ly impaired locomotor function and prolonged bladder dysfunction compared with wild-type (WT) litterm
22 te deficits, consisting of paresis and bowel/bladder dysfunction, completely recovered neurologic fun
29 of candidates for intervention, but ongoing bladder dysfunction in patients after valve ablation rem
31 on which characterizes many types of urinary bladder dysfunctions including urinary incontinence.
32 n Continence Society discussed the issues of bladder dysfunction, including enuresis, and this review
36 ced cardiovascular fitness, ataxia, fatigue, bladder dysfunction, spasticity, pain, cognitive deficit
37 turition center may contribute to the severe bladder dysfunction that characterizes multiple system a
40 ere disorders with endpoints of irreversible bladder dysfunction with vesicoureteral reflux, urinary
41 gulation of Rho A signaling and reversed the bladder dysfunction, without affecting hyperglycemia.
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