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1 nce, reduced social participation, bowel and bladder dysfunction).
2 d differential mechanisms driving neurogenic bladder dysfunction.
3 spasticity and weakness, as well as frequent bladder dysfunction.
4 ts might be effective drugs for treatment of bladder dysfunction.
5 or vesicoureteral reflux grade and bowel and bladder dysfunction.
6 inary bladder and exhibit varying degrees of bladder dysfunction.
7  multiple sclerosis, spinal cord injury, and bladder dysfunction.
8 procedure for pediatric patients with severe bladder dysfunction.
9 n urinary bladder neurotrophic factors after bladder dysfunction.
10 in patients with multiple system atrophy and bladder dysfunction.
11  disrupting normal function and resulting in bladder dysfunction.
12 ontribute to developing better therapies for bladder dysfunction.
13 h ketamine + COX-2 inhibitor prevented these bladder dysfunctions.
14 V4 may be a promising therapeutic target for bladder dysfunctions.
15 .2 agonists as potential novel therapies for bladder dysfunctions.
16 ked immunosorbent assay and displayed marked bladder dysfunction 12 weeks after STZ injection.
17  participation (56.5%; 95% CI, 52.1%-60.8%), bladder dysfunction (45.9%; 95% CI, 38.0%-53.8%), and fa
18 slatable method for therapeutic targeting of bladder dysfunction acutely after SCI.
19                                   Neurogenic bladder dysfunction affects up to 80% of individuals wit
20  However, the underlying mechanisms inducing bladder dysfunction after prostatic inflammation are not
21      These changes may contribute to urinary bladder dysfunction after SCI.
22 nderstand the mechanisms whereby TMS reduced bladder dysfunction after SCI.
23 nent in the pathogenesis of diabetes-induced bladder dysfunction, although the molecular mechanisms h
24 instay of surgical treatment for neuropathic bladder dysfunction and detrusor instability.
25  stress urinary incontinence, renal disease, bladder dysfunction and erectile dysfunction.
26 spinal cord level, BDNF is a key mediator of bladder dysfunction and pain during cystitis, it is pres
27 mmatory mediator provides novel insight into bladder dysfunction and supports new avenues for therape
28  constipation, reduced social participation, bladder dysfunction, and fatigue were most prevalent.
29 e study on placebo or antibiotics, bowel and bladder dysfunction, and renal scarring.
30 cations, plane of surgery, 30-day mortality, bladder dysfunction, and sexual dysfunction, none showed
31 the precise mechanisms of TGF-beta mediating bladder dysfunction are not yet known.
32      Thus, recurrence of UTIs and associated bladder dysfunction are the outcome of the preferential
33 icles that have been published on neurogenic bladder dysfunction as well as on posterior urethral val
34 nsights into how brain degeneration leads to bladder dysfunction, as well as novel strategies to trea
35  disease characterized by congenital urinary bladder dysfunction, associated with a significant risk
36  Subjects had to have urodynamic evidence of bladder dysfunction, be ambulatory, and not have dementi
37                                      Urinary bladder dysfunction can be caused by environmental, gene
38 to Lewy body disorders, whereas younger age, bladder dysfunction, catheter use, and dream enactment b
39                                   Neurogenic bladder dysfunction causes urological complications and
40                                              Bladder dysfunction characterized by abnormal bladder sm
41                                     Diabetic bladder dysfunction, characterized by detrusor overactiv
42 ly impaired locomotor function and prolonged bladder dysfunction compared with wild-type (WT) litterm
43 te deficits, consisting of paresis and bowel/bladder dysfunction, completely recovered neurologic fun
44                                     Diabetic bladder dysfunction (DBD) is a common urological complic
45                                     Diabetic bladder dysfunction (DBD) is common and affects 80% of d
46                                     Diabetic bladder dysfunction (DBD) is the most common complicatio
47  studies have investigated NLRP3 in diabetic bladder dysfunction (DBD), despite a high clinical preva
48 al therapy for obstruction-induced myopathic bladder dysfunction (from benign prostatic hyperplasia o
49  as a target for new therapy for BPH-induced bladder dysfunction in aging men.
50                           This review covers bladder dysfunction in children.
51 activated K2P channels may underlie myogenic bladder dysfunction in humans.
52 egeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced en
53  loop for inflammatory responses involved in bladder dysfunction in MS.
54  of candidates for intervention, but ongoing bladder dysfunction in patients after valve ablation rem
55 ond to nicotine despite the absence of major bladder dysfunction in vivo.
56 on which characterizes many types of urinary bladder dysfunctions including urinary incontinence.
57 n Continence Society discussed the issues of bladder dysfunction, including enuresis, and this review
58 tic brain injury (TBI) often leads to severe bladder dysfunction, including incontinence and lower ur
59 y characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a
60                                              Bladder dysfunction is a common clinical problem attribu
61                                              Bladder dysfunction is associated with the overexpressio
62                                              Bladder dysfunction is common in Multiple Sclerosis (MS)
63 estation of spinal cord injury (SCI)-induced bladder dysfunction is detrusor overactivity (DO).
64  pathogenic GFAP variants had higher odds of bladder dysfunction (OR 3.17, p<0.0001), upper airway dy
65 paraplegic patient with neurogenic bowel and bladder dysfunction poses radiation safety challenges, a
66        Here, we demonstrate that a prevalent bladder dysfunction, produced by partial obstruction in
67             Cognitive decline and neurogenic bladder dysfunction progressed over time in most patient
68                         Neuropathic pain and bladder dysfunction represent significant quality-of-lif
69          In this model of brain degeneration bladder dysfunction results from rostral, and not hindbr
70 ced cardiovascular fitness, ataxia, fatigue, bladder dysfunction, spasticity, pain, cognitive deficit
71 turition center may contribute to the severe bladder dysfunction that characterizes multiple system a
72                                   Because of bladder dysfunction, there were 8 infectious events of t
73 irst time that mutations in CHRNA3 can cause bladder dysfunction, urinary tract malformations, and dy
74  candidate of possible surgical solution for bladder dysfunction, we propose a novel orthotropic mous
75 n among the patients with renal scarring and bladder dysfunction were acceptable.
76            In conclusion, renal scarring and bladder dysfunction were predictors of vesicoureteral re
77 tivariable analysis, only renal scarring and bladder dysfunction were significantly associated with p
78                                        These bladder dysfunctions were accompanied by increases in th
79  recognized prodromal markers (constipation, bladder dysfunction) were more common at baseline.
80 ere disorders with endpoints of irreversible bladder dysfunction with vesicoureteral reflux, urinary
81 gulation of Rho A signaling and reversed the bladder dysfunction, without affecting hyperglycemia.