Academic literature on the topic 'Urinary detrusor'
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Journal articles on the topic "Urinary detrusor"
Musci, R., V. Franchini, T. Meroni, O. De Cobelli, B. Frea, G. Bovo, A. M. Milella, E. Rossi, F. Franzetti, and U. Pea. "Neurogenic urinary dysfunction in AIDS patients." Urologia Journal 61, no. 2 (April 1994): 137–41. http://dx.doi.org/10.1177/039156039406100209.
Full textSakakibara, Ryuji, Ayami Shimizu, Osamu Takahashi, Fuyuki Tateno, Masahiko Kishi, Yosuke Aiba, Hiroyoshi Suzuki, Tatsuya Yamamoto, Chiharu Shibata, and Tomonori Yamanishi. "Lower Urinary Tract Function in Familial Spastic Paraplegia." European Neurology 80, no. 3-4 (2018): 121–25. http://dx.doi.org/10.1159/000494030.
Full textAndersson, Karl-Erik, and Anders Arner. "Urinary Bladder Contraction and Relaxation: Physiology and Pathophysiology." Physiological Reviews 84, no. 3 (July 2004): 935–86. http://dx.doi.org/10.1152/physrev.00038.2003.
Full textGorbunov, Aleksandr I., Aleksandr N. Murav’ev, Evgenij G. Sokolovich, and Petr K. Yablonsky. "Neurogenic urinary disorders in patients with tuberculous spondylitis before and after surgical treatment." Urology reports (St. - Petersburg) 11, no. 1 (May 27, 2021): 27–32. http://dx.doi.org/10.17816/uroved52482.
Full textGriffiths, D. J., C. E. Constantinou, and R. van Mastrigt. "Urinary bladder function and its control in healthy females." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 2 (August 1, 1986): R225—R230. http://dx.doi.org/10.1152/ajpregu.1986.251.2.r225.
Full textOKAMOTO-KOIZUMI, Takako, Masayuki TAKEDA, Takeshi KOMEYAMA, Akihiko HATANO, Makoto TAMAKI, Takaki MIZUSAWA, Toshiki TSUTSUI, et al. "Pharmacological and molecular biological evidence for ETA endothelin receptor subtype mediating mechanical responses in the detrusor smooth muscle of the human urinary bladder." Clinical Science 96, no. 4 (April 1, 1999): 397–402. http://dx.doi.org/10.1042/cs0960397.
Full textHeppner, Thomas J., Jeffrey J. Layne, Jessica M. Pearson, Hagop Sarkissian, and Mark T. Nelson. "Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 2 (August 2011): R351—R362. http://dx.doi.org/10.1152/ajpregu.00656.2010.
Full textAl-Shukri, S. Kh, T. G. Giorgobiani, R. E. Amdiy, and A. S. Al-Shukri. "Urinary dysfunction in patients with unsatisfactory results of surgical treatment of benign prostatic hyperplasia." Grekov's Bulletin of Surgery 176, no. 6 (December 28, 2017): 66–70. http://dx.doi.org/10.24884/0042-4625-2017-176-6-66-70.
Full textNoronha, R., H. Akbarali, A. Malykhina, R. D. Foreman, and Beverley Greenwood-Van Meerveld. "Changes in urinary bladder smooth muscle function in response to colonic inflammation." American Journal of Physiology-Renal Physiology 293, no. 5 (November 2007): F1461—F1467. http://dx.doi.org/10.1152/ajprenal.00311.2007.
Full textRusina, Yelena Ivanovna. "The role of complex preoperative urodynamic testing of continent women when planning surgery for pelvic organ prolapse." Journal of obstetrics and women's diseases 63, no. 1 (December 15, 2014): 17–25. http://dx.doi.org/10.17816/jowd63117-25.
Full textDissertations / Theses on the topic "Urinary detrusor"
Sethia, Krishna Kumar. "The pathophysiology of detrusor instability." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235958.
Full textCutner, Alfred. "The lower urinary tract in pregnancy." Thesis, Imperial College London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338240.
Full textMoon, Annick. "Effect of nitric oxide on detrusor contractility." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313235.
Full textHasan, Tahseen. "Transcutaneous electrical nerve stimulation (TENS) and temporary S3 nerve root stimulation in idiopathic detrusor instability and characterization of the human detrusor smooth muscle contraction." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310132.
Full textMasters, Jonathan Grenville. "Sources of calcium involved in detrusor smooth muscle contraction." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312030.
Full textMills, Ian W. "The pathophysiology of Detrusor instability and the role of bladder ischaemia in its aetiology." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325284.
Full textGreyling, Linda Magdalena. "Histologiese veranderinge wat volg op distensie van die detrusor in die rot : Spraque-Dawley (Afrikaans)." Diss., University of Pretoria, 2001. http://hdl.handle.net/2263/30254.
Full textBau, Fernando Ricardo. "Avaliação do efeito relaxante do BAY 41-2272 em detrusor isolado de coelhos." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308919.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-14T06:23:28Z (GMT). No. of bitstreams: 1 Bau_FernandoRicardo_M.pdf: 739046 bytes, checksum: e73f0e5383c7082e68c3cbf81bdfce5f (MD5) Previous issue date: 2009
Resumo: A síndrome da bexiga hiperativa atinge grande parte da população mundial, e gera sintomas que prejudicam a qualidade de vida dos portadores. Está associada com a hiperatividade do detrusor que se dá por um aumento das contrações espontâneas. Alguns estudos têm mostrado que a deficiência de NO é um dos fatores responsáveis por gerar estas contrações espontâneas. É sabido que o mecanismo de sinalização do NO envolve a ativação da guanilil ciclase solúvel e produção de GMPc. Atualmente, algumas drogas têm sido sintetizadas para mimetizar o efeito exercido pelo NO, tal como o BAY 41-2272, um potente estimulador da guanilil ciclase solúvel independente de NO. Vários trabalhos mostraram que o BAY 41-2272 causa relaxamento de vários tipos de musculatura lisa, podendo ser um composto com grande potencial terapêutico em doenças onde a via do NO/GMPc está prejudicada. O objetivo deste trabalho é investigar a capacidade do BAY 41-2272 de relaxar detrusor isolado de camundongo, coelho e rato in vitro e os mecanismos farmacológicos envolvidos na resposta relaxante. Camundongos C57b6 machos (30-40 g), coelhos New Zealand machos (2-3 kg) e ratos Wistar machos (250-300 g) foram anestesiados e mortos. As bexigas foram removidas e fragmentos de detrusor foram montados em banho para órgãos isolados contendo 10 ml de solução de Krebs. Curvas concentração-resposta ao BAY 41-2272 (10-9 - 10-4 M) foram construídas em tecidos précontraídos com carbacol (10 µM) ou KCl (80 mM), na ausência ou na presença de LNAME (inibidor da óxido nítrico sintase; 100 µM), ODQ (inibidor da guanilato ciclase solúvel; 100 µM), Sildenafil (inibidor da fosfodiesterase tipo-5; 10 µM), ou inibidores de canais de potássio (0,1 µM charibdotoxina + 1 µM apamina; 1µM tetraetilamônio; ou 10 µM glibenclamida). Curvas concentração-resposta ao nitroprussiato de sódio (SNP; 10-8 - 10-4 M), gliceril trinitrato (GTN; 10-8 - 10-4 M) e 8Br-GMPc (10-8 - 10-4 M) foram também construídas. Contrações induzidas por CaCl2 extracelular foram avaliadas na presença do BAY 41-2272, bem como o efeito no influxo de cálcio em plaquetas isoladas de coelho. Níveis de GMPc e AMPc foram avaliados após a estimulação do detrusor com BAY 41- 2272 (10 e 100 µM) e SNP (100 µM) na ausência ou na presença de ODQ (100 µM), através de imunoensaio enzimático (ELISA). O BAY 41-2272 produziu relaxamento de detrusor isolado de camundongos, ratos e coelhos de maneira concentração-dependente, com valores de resposta máxima de 61,3 ± 6,6%, 91,7 ± 5,9% e 95,1 ± 9,9%, respectivamente. Detrusor de coelhos foram selecionados para os experimentos subseqüentes. Os doadores de NO, SNP e GTN, bem com o 8Br-GMPc produziram um discreto relaxamento comparado ao BAY 41-2272. O tratamento dos tecidos com L-NAME (100 µM) ou sildenafil (10 µM) não afetou de maneira significativa o relaxamento induzido pelo BAY 41-2272. Entretanto, o ODQ (100 µM), reduziu significativamente a resposta ao BAY 41-2272. Os bloqueadores de canais de K+ (apamin + charibdotoxina, glibenclamida ou tetraetilamônio) também não afetaram a resposta relaxante do BAY 41-2272. O BAY 41-2272 (10 e 100 µM) elevou os níveis de GMPc em cerca de 14 e 20 vezes respectivamente, sem afetar os níveis de AMPc. Na menor concentração do BAY 41-2272 (10 µM), o ODQ aboliu a elevação dos níveis de GMPc, ao passo que na maior concentração do BAY 41-2272 (100 µM), o ODQ inibiu parcialmente a elevação dos níveis de GMPc. A adição de CaCl2 (0,01-30 mM) extracelular em detrusor isolado de coelhos causou contração de maneira concentração-dependente que foi significativamente reduzida pelo tratamento prévio com BAY 41-2272 (1 e 10 µM), sendo que este efeito não foi prevenido pelo ODQ. O BAY 41-2272 reduziu significativamente o aumento dos níveis intracelulares de cálcio em plaquetas de coelho induzido por trombina. Em resumo, o BAY 41-2272 produz relaxamento em detrusor isolado de camundongos, coelhos e ratos através da produção de GMPc e da inibição do influxo de cálcio que independe de GMPc
Abstract: Overactive bladder (OAB) is a highly prevalent condition that affects millions of people worldwide with a profound effect on quality of life. The bladder overactivity is related to spontaneous contractions of the detrusor smooth muscle causing an increase in the intravesical pressure and consequently stimulation of the micturirion reflex. Evidences suggest that impairment of nitric oxide (NO) signaling pathway may account for OAB. It is well established that NO signaling pathways involves soluble guanylate cyclase (sGC) stimulation and cyclic GMP production. Recently, pharmacological agents capable of directly stimulating soluble guanylate cyclase independenly of NO, such as BAY 41-2272 has been reported to produce relaxation of different types of smooth muscle, showing great therapeutic potential in disturbs which NO pathway is impaired. The present study aimed to evaluate the capacity of BAY 41-2272 to relax isolated mouse, rat and rabbit DSM and the mechanism underlying these response. C57b6 male mice, Wistar male rats and New Zealand male rabbits were anesthetized, and urinary bladder removed. DSM was transferred to 10-mL organ baths containing oxygenated and warmed Krebs-Henseleit solution. Tissues were connected to force-displacement transducers and changes in isometric force were recorded. Concentration-response curves to BAY 41-2272 (10-9 - 10-4M) were constructed, in previously contracted tissues with carbachol (10 µM) or KCl (80 mM), in the absence and in the presence of L-NAME (Nitric Oxide Synthase inhibitor; 100 µM), ODQ (sGC inhibitor; 100 µM), Sildenafil (phosphodiesterase type-5 inhibitor; 10 µM), or potassium channel blockers (0.1 µM charybdotoxin + 1 µM apamin; 1 µM tetraethylammonium; or 10 µM glybenclamide). Concentration-response curves to sodium nitroprusside (SNP; 10-8 - 10-4 M), glyceryl trinitrate (GTN; 10-8 - 10-4 M) and 8Br-cGMP (10-8 - 10-4 M) were also constructed. CaCl2-induced contractions in DSM and calcium influx in rabbit isolated platelets were evaluated in the presence of BAY 41-2272. Levels of cAMP and cGMP in DSM strips were determined after treatment with BAY 41-2272 (10 and 100 µM), SNP (100 µM) in the absence or in the presence of ODQ (100 µM) using specific EIA kit. BAY 41-2272 (0.001-100 µM) produced concentration-dependent DSM relaxations in mouse, rat and rabbit with maximal responses of 61.3 ± 6.6%, 95.1 ± 9.9% and 91.7 ± 5.9%, respectively. The NO-donors sodium nitroprusside and glyceryl trinitrate, as well as 8-bromo-cGMP also produced concentration-dependent rabbit DSM relaxations, but to a lesser extent than BAY 41-2272. Pretreatment with L-NAME (NO synthesis inhibitor) or sildenafil (phosphodiesterase-5 inhibitor) had no effect in BAY 41-2272- induced responses. However, the soluble guanylyl cyclase inhibitor ODQ significantly reduced BAY 41-2272-induced relaxantions. BAY 41-2272 (10 and 100 µM) increased the bladder cGMP levels by about of 14- and 20-fold, respectively, without affecting the cAMP levels. The cGMP increases in response to BAY 41-2272 and SNP were markedly reduced by ODQ. CaCl2 caused a concentration-dependent contraction in DSM strips and BAY 41- 2272 significantly reduced the contractile responses to extracellular Ca2+ in an ODQinsensitive manner. BAY 41-2272 also significantly reduced the increase of intracellular calcium levels induced by thrombin. This inhibitory effect was completely reverted after the treatment with ODQ. BAY 41-2272 relaxes DSM of the three animal species studied. BAY 41-2272-induced DSM relaxation involves mainly cGMP production, but an additional mechanism involving Ca2+ influx blockade independently of cGMP production appears to be involved
Mestrado
Farmacologia
Mestre em Farmacologia
Rahmanou, Philip. "Assessment of lower urinary tract function in women with urodynamic stress incontinence with and without detrusor overactivity." Thesis, Imperial College London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589995.
Full textRamos, Filho Antonio Celso S. "Avaliação morfofuncional e molecular do detrusor isolado de ratos hipertensos renovasculares." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308915.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A hipertensão renovascular é uma forma secundária da hipertensão arterial, que corresponde de 1-5% dos casos de hipertensão. A associação entre hipertensão arterial e disfunções miccionais foi observada no modelo experimental de ratos espontaneamente hipertensos (SHR). Até o momento nenhum estudo avaliou as disfunções miccionais em animais hipertensos renovasculares. Dessa forma, neste estudo, caracterizamos a disfunção miccional em ratos hipertensos renovasculares através do modelo de dois rins, um clip (2K-1C). Em ratos Wistar (200-220 g) colocou-se um clip em torno da artéria renal. Depois de oito semanas, os ratos foram utilizados. Realizou-se estudo cistométrico em ratos anestesiados, assim como curvas concentração-resposta para agentes contráteis e relaxantes em detrusor isolado (DSM). Foram também realizados estudos histomorfométricos e da expressão de RNAm dos receptores muscarínicos M3 e M2 em DSM isolado. Os resultados histomorfométricos mostraram aumentos significantes na espessura da parede da bexiga, no volume intravesical, na densidade de musculatura lisa e na densidade de fibras neurais no grupo 2K-1C em comparação ao SHAM. O agonista muscarínico, carbacol, produziu contrações concentração-dependentes do DSM, as quais foram significantemente maiores no grupo 2K-1C. O inibidor da Rho-quinase, Y27-632 (10 µM), reduziu significantemente a contração induzida pelo carbacol nos ratos SHAM e 2K-1C; porém, no grupo 2K-1C, o DSM continuou hiperativo na presença do Y27-632. A estimulação elétrica (1 - 32 Hz) produziu contração freqüência-dependente do DSM as quais foram maiores no grupo 2K-1C. O agonista purinérgico P2X, ?,?-metileno-ATP (1 - 100 µM), o KCl (1 - 300 µM) e o Ca2+ extracelular (0,01-100 µM) produziram contrações concentração-dependente; porém, não observamos diferenças entre o grupo SHAM e 2K-1C. O agonista não seletivo ?-adrenérgico, isoproterenol, o agonista seletivo ?2-adrenérgico, metaproterenol, e o agonista seletivo ?3-adrenérgico, BRL37-344, produziram relaxamentos menores do DSM nos ratos 2K-1C, e também redução nos níveis intracelulares de AMPc nos detrusores. O efeito relaxante ao nitroprussiato de sódio e BAY41-2272 mantiveram-se iguais nos animais SHAM e 2K-1C. A expressão do RNAm do receptor muscarínico M3 (mas não do M2) no DSM foi significantemente maior nos ratos 2K-1C em comparação ao grupo controle. Os tratamentos crônicos com losartan e captopril normalizaram a pressão arterial sistólica dos animais 2K-1C, normalizaram a função miccional, e reduziram a hipercontratilidade do detrusor induzida pela estimulação elétrica e pelo carbacol, assim como restabeleceram o relaxamento induzido pelo isoproterenol ao nível do grupo SHAM. Concluimos que os ratos hipertensos renovasculares apresentam hiperatividade do detrusor, a qual envolve remodelamento tecidual e aumento da contração via receptor muscarínico M3 associado à redução no relaxamento ?-adrenérgico com redução da sinalização intracelular e produção de AMPc. Os tratamentos com losartan e captopril restauram a função miccional dos animais 2K-1C
Abstract: Renovascular hypertension is a secondary form of arterial hypertension, accounting for 1-5% of cases in unselected population. Association between arterial hypertension and urinary bladder dysfunction has been reported in spontaneously hypertensive rats, but no study evaluated the bladder dysfunction in renovascular hypertensive animals. Therefore, in this study, we explored the bladder dysfunction in renovascular hypertensive rats, using the two-kidney one-clip (2K-1C) model. A silver clip was placed around the renal artery of male Wistar Kyoto rats (200-220 g). After eight weeks, rats were used. Cystometric study in anesthetized rats, along with concentration-response curves to both contractile and relaxant agents in isolated detrusor smooth muscle (DSM) were performed. Histomorphometry and mRNA expression of muscarinic M3 and M2 receptors in DSM were also determined. The histomorphometric data showed significant increases in bladder wall thickness, intravesical volume and density of smooth muscle, as well as density of neural fibers in the 2K-1C group compared with SHAM. The muscarinic agonist carbachol produced concentration-dependent DSM contractions, which were markedly greater in 2K-1C rats. The Rho-kinase inhibitor Y27-632 (10 µM) significantly reduced the carbachol-induced contractions in sham and 2K-1C rats, but DSM in 2K-1C rats remained overactive in the presence of Y27632. Electrical-field stimulation (EFS; 1-32 Hz) produced frequency-dependent DSM contractions that were also greater in 2K-1C group. The P2X receptor agonist ?,?-methylene ATP (1-100 µM), KCl (1-300 mM) and extracellular Ca2+ (0.01-100 M) produced concentration-dependent DSM contractions, but no changes among sham and 2K-1C rats were seen. In 2K-1C rats, the non-selective ?-adrenoceptor agonist isoproterenol, the ?2-adrenoceptor agonist metaproterenol and the ?3-adrenoceptor agonist BRL 37-344 produced lower DSM relaxations, as well as decreased cAMP levels. The relaxant responses to sodium nitroprusside and BAY 41-2272 remained unchanged in 2K-1C rats. Expression of mRNA of muscarinic M3 (but not of M2) receptors in DSM was significantly increased in 2K-1C rats. The chronic treatment with losartan and captopril normalized the blood systolic pressure of 2K-1C animals, improved their urinary function by reducing DSM hypercontractility to EFS and carbacol stimulation, and restored the relaxation induced by the ?-adrenergic agonist isoproterenol to the level of SHAM group. In conclusion, renovascular hypertensive rats exhibit overactive DSM that involves tissue remodeling and enhanced muscarinic M3-mediated contractions associated with reduced ?-adrenoceptor-mediated signal transduction. The treatments with losartan and captopril improved urinary function of 2K-1C animals
Mestrado
Mestre em Farmacologia
Books on the topic "Urinary detrusor"
Jackson, Simon, and Natalia Price. Urinary incontinence. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0059.
Full textBeckman, Thomas J., and Haitham S. Abu-Lebdeh. Men’s Health. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0465.
Full textDaly, Donna, and Christopher Chapple. Anatomy, neurophysiology, and pharmacological control mechanisms of the bladder. Edited by Christopher R. Chapple. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0034.
Full textBryant, Richard J., and James W. F. Catto. General overview of bladder cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0074.
Full textBook chapters on the topic "Urinary detrusor"
Miftahof, Roustem N., and Hong Gil Nam. "Pharmacology of Detrusor Activity." In Biomechanics of the Human Urinary Bladder, 133–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36146-3_9.
Full textMiftahof, Roustem N., and Hong Gil Nam. "Continual Model of the Detrusor." In Biomechanics of the Human Urinary Bladder, 73–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36146-3_5.
Full textMiftahof, Roustem N., and Hong Gil Nam. "A Model of the Detrusor Fasciculus." In Biomechanics of the Human Urinary Bladder, 87–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36146-3_6.
Full textUvelius, Bengt, and Anders Arner. "Metabolism of Detrusor Smooth Muscle in Normal and Obstructed Urinary Bladder." In Advances in Experimental Medicine and Biology, 29–39. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1585-6_5.
Full textSahai, Arun, Jai Seth, Muhammed Shamim Khan, and Prokar Dasgupta. "Intravesical Therapy for Refractory Overactive Bladder and Detrusor Overactivity in Adults: Botulinum Toxin-A." In Minimally Invasive Therapy for Urinary Incontinence and Pelvic Organ Prolapse, 135–54. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0008-4_12.
Full text"Stents In Detrusor–Sphincter Dyssynergia." In Stenting the Urinary System, Second Edition, 501. CRC Press, 2004. http://dx.doi.org/10.3109/9780203427910-77.
Full textBeckman, Thomas J. "Men’s Health." In Mayo Clinic Internal Medicine Board Review, 337–44. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190464868.003.0030.
Full textCollins, Nerissa M. "Otolaryngology and Ophthalmology." In Mayo Clinic Internal Medicine Board Review, 345–48. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190464868.003.0031.
Full textMerwe, André. "The urethral stent and detrusor–sphincter dyssynergia." In Handbook of Urinary Stents: Basic Science and Clinical Applications, 299. Jaypee Brothers Medical Publishers (P) Ltd., 2016. http://dx.doi.org/10.5005/jp/books/12884_41.
Full textChancellor, M., and D. Rivas. "Complications related to Urolume sphincter stent used for the management of detrusor–sphincter dyssynergia." In Stenting the Urinary System, Second Edition, 507–13. CRC Press, 2004. http://dx.doi.org/10.3109/9780203427910-79.
Full textConference papers on the topic "Urinary detrusor"
Celik, Ismail B., Asaf Varol, Coskun Bayrak, and Jagannath R. Nanduri. "A One Dimensional Mathematical Model for Urodynamics." In ASME/JSME 2007 5th Joint Fluids Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/fedsm2007-37647.
Full textde Souza, Júlia Raquel Nunes, Ana Luiza Verissimo Jacob, Marco Antônio Rodrigues de Morais, and Carlos Augusto Faria. "Noctúria: etiologia e impacto sobre a qualidade de vida em mulheres atendidas em unidade terciária do sistema de saúde." In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130230.
Full textReports on the topic "Urinary detrusor"
Zhu, Zhihong, Yue Zhuo, Haitao Jin, Boyu Wu, and Zhijie Li. Chinese Medicine Therapies for Neurogenic Bladder after Spinal Cord Injury: A protocol for systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0084.
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