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| 2. |
- Chakrabarty, Basu, et al.
(författare)
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Nitric oxide signaling pathways in the normal and pathological bladder: Do they provide new pharmacological pathways?—ICI-RS 2023
- 2023
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Ingår i: Neurourology and Urodynamics. - 0733-2467 .- 1520-6777.
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Forskningsöversikt (refereegranskat)abstract
- Aims: The nitric oxide (NO•)/soluble guanylate cyclase/cyclic-GMP (cGMP) signaling pathway is ubiquitous and regulates several functions in physiological systems as diverse as the vascular, nervous, and renal systems. However, its roles in determining normal and abnormal lower urinary tract functions are unclear. The aim was to identify potential therapeutic targets associated with this pathway to manage lower urinary tract functional disorders. Methods: This review summarizes a workshop held under the auspices of ICI-RS with a view to address these questions. Results: Four areas were addressed: NO• signaling to regulate neurotransmitter release to detrusor smooth muscle; its potential dual roles in alleviating and exacerbating inflammatory pathways; its ability to act as an antifibrotic mediator; and the control by nitrergic nerves of lower urinary tract vascular dynamics and the contractile performance of muscular regions of the bladder wall. Central to much of the discussion was the role of the NO• receptor, soluble guanylate cyclase (sGC) in regulating the generation of the enzyme product, the second messenger cGMP. The redox state of sGC is crucial in determining its enzymic activity and the role of a class of novel agents, sGC activators, to optimize activity and to potentially alleviate the consequences of lower urinary tract disorders was highlighted. In addition, the consequences of a functional relationship between nitrergic and sympathetic nerves to regulate vascular dynamics was discussed. Conclusions: Several potential NO•-dependent drug targets in the lower urinary tract were identified that provide the basis for future research and translation to clinical trials.
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| 3. |
- Hashim, Hashim, et al.
(författare)
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Desmopressin, as a "Designer-Drug," in the Treatment of Overactive Bladder Syndrome
- 2009
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Ingår i: Neurourology and Urodynamics. - : Wiley. - 0733-2467 .- 1520-6777. ; 28:1, s. 40-46
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Tidskriftsartikel (refereegranskat)abstract
- Aims: This study looked at whether oral desmopressin, by decreasing kidney urine production, would prolong bladder filling-time thereby increasing the time to reach maximum capacity, thus reducing overactive bladder (OAB) symptoms, and providing an alternative method of treatment to OAB sufferers. Methods: An investigator-initiated, 2-week, multi-national, multi-centre, "proof-of-concept," phase IIb, double-blind, placebo-controlled, prospective, randomized, cross-over study was conducted using 0.2 mg of oral desmopressin in adults suffering with OAB. Patients were included in the trial period if they had >= 4 voids in the first 8-hr of the day after rising, excluding the first morning void. The primary endpoint was evaluation of effectiveness of desmopressin in increasing the time to the first OAB symptom episodes during the first 8-hr following treatment. Results: Time to first void was 8-min later on the drug than on placebo (P = 0.27). However, the drug led to one less void (3.2 vs. 4.2) in the same period (P < 0.001). There was an increase in the time to first urgency episode with a decrease in the number of urgency episodes in the drug days compared to placebo (P < 0.003). There was a subjective improvement in frequency and urgency and overall quality-of-life as measured by the ICIQ-OAB. Twenty-seven people reported adverse events which were all mild, headache being the commonest and no hyponatremia was recorded. Conclusions: Antidiuresis, using oral desmopressin tablets, is a novel, feasible and safe (short-term basis) method of treatment for adults with OAB, and could be considered in the armamentarium of drugs available for the treatment of OAB. Neurourol. Urodynam. 28:40-46, 2009. (C) 2008 Wiley-Liss, Inc.
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| 5. |
- Sievert, Karl-Dietrich, et al.
(författare)
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Can we prevent incontinence? ICI-RS 2011.
- 2012
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Ingår i: Neurourology and urodynamics. - : Wiley. - 1520-6777 .- 0733-2467. ; 31:3, s. 390-9
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Tidskriftsartikel (refereegranskat)abstract
- A review of the current state of research with regard to prevention of incontinence.
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| 6. |
- Schafer, Werner, et al.
(författare)
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Good urodynamic practices: uroflowmetry, filling cystometry, and pressure-flow studies
- 2002
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Ingår i: Neurourology and Urodynamics. - : Wiley. - 0733-2467. ; 21:3, s. 261-274
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Tidskriftsartikel (refereegranskat)abstract
- This is the first report of the International Continence Society (ICS) on the development of comprehensive guidelines for Good Urodynamic Practice for the measurement, quality control, and documentation of urodynamic investigations in both clinical and research environments. This report focuses on the most common urodynamics examinations; uroflowmetry, pressure recording during filling cystometry, and combined pressure-flow studies. The basic aspects of good urodynamic practice are discussed and a strategy for urodynamic measurement, equipment set-up and configuration, signal testing, plausibility controls, pattern recognition, and artifact correction are proposed. The problems of data analysis are mentioned only when they are relevant in the judgment of data quality. In general, recommendations are made for one specific technique. This does not imply that this technique is the only one possible. Rather, it means that this technique is well-established, and gives good results when used with the suggested standards of good urodynamic practice.
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| 7. |
- Wyndaele, Michel, et al.
(författare)
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Beyond the urothelium: Interplay between autonomic nervous system and bladder inflammation in urinary tract infection, bladder pain syndrome with interstitial cystitis and neurogenic lower urinary tract dysfunction in spinal cord injury-ICI-RS 2023.
- 2023
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Ingår i: Neurourology and urodynamics. - 1520-6777.
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Forskningsöversikt (refereegranskat)abstract
- Inflammation and neuronal hypersensitivity are reactive protective mechanisms after urothelial injury. In lower urinary tract dysfunctions (LUTD), such as urinary tract infection (UTI), bladder pain syndrome with interstitial cystitis (BPS/IC) and neurogenic LUTD after spinal cord injury (SCI), chronic inflammation can develop. It is unclear how the protective reactionary inflammation escalates into chronic disease in some patients.During its 2023 meeting in Bristol, the International Consultation on Incontinence-Research Society (ICI-RS) reviewed the urothelial and inflammatory changes after UTI, BPS/IC and SCI. Potential factors contributing to the evolution into chronic disease were explored in a think-tank.Five topics were discussed. (1) Visceral fat metabolism participates in the systemic pro-inflammatory effect of noradrenalin in BPS/IC and SCI. Sympathetic nervous system-adipocyte-bladder crosstalk needs further investigation. (2) Sympathetic hyperactivity also potentiates immune depression in SCI and needs to be investigated in BPS/IC. Gabapentin and tumor necrosis factor-α are promising research targets. (3) The exact peripheral neurons involved in the integrative protective unit formed by nervous and immune systems need to be further identified. (4) Neurotransmitter changes in SCI and BPS/IC: Neurotransmitter crosstalk needs to be considered in identifying new therapeutic targets. (5) The change from eubiosis to dysbiosis in SCI can contribute to UTI susceptibility and needs to be unraveled.The think-tank discussed whether visceral fat metabolism, immune depression through sympathetic hyperactivity, peripheral nerves and neurotransmitter crosstalk, and the change in microbiome could provide explanations in the heterogenic development of chronic inflammation in LUTD. High-priority research questions were identified.
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