1.

論文

論文
正源寺, 美穂 ; 泉, キヨ子 ; 平松, 知子
出版情報: 金沢大学つるま保健学会誌.  32  pp.39-41,  2008-12-25.  金沢大学つるま保健学会
URL: http://hdl.handle.net/2297/12696
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論文

論文
Kadono, Yoshifumi ; Ueno, Satoru ; Kadomoto, Suguru ; Iwamoto, Hiroaki ; Takezawa, Yuta ; Nakashima, Kazufumi ; Nohara, Takahiro ; Izumi, Kouji ; Mizokami, Atsushi ; Gabata, Toshifumi ; Namiki, Mikio
出版情報: Neurourology and Urodynamics.  35  pp.1034-1039,  2016-11-01.  John Wiley and Sons Inc.
URL: http://hdl.handle.net/2297/46502
概要: Aims: To examine which preoperative factors, including urodynamic evaluations, and operative procedures could predict continence status after robot-assisted radical prostatectomy (RARP) in this study. Materials and Methods: Univariate and multivariate logistic regression analyses of preoperative factors such as age, body mass index, prostate-specific antigen level before biopsy, prostate size before surgery, membranous urethral length measured using magnetic resonance imaging (MRI), bladder compliance and maximum urethral closure pressure (MUCP) measured by urodynamic study (UDS), and nerve-sparing (NS) status predicting 24-hr pad test >2 g/day at 1 year after RARP were examined in 111 patients enrolled in this study. Results: The number of patients with incontinence at 1 year after RARP was 39 (35.1%). The only predictive factor for urinary continence was NS grades. To investigate the contribution of NS to urinary continence, 84 patients underwent UDS three times; before, immediately after, and 1 year after RARP. Chronological UDS revealed that recovery patterns of storage and voiding functions were the same among non-NS, unilateral-NS, and bilateral-NS groups, and that higher degrees of NS contributed to lesser decreases in MUCP and longer functional urethral length (FUL) after RARP. Conclusion: Preoperative factors, including the results of UDS, could not predict continence 1 year after RARP. The NS procedure contributed to continence status. NS favorably affected MUCP and FUL; however, it did not affect bladder function after RARP. Neurourol. Urodynam. 35:1034–1039, 2016. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.<br />Embarogo Period 12 months 続きを見る
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論文

論文
横山, 修 ; Yokoyama, Osamu
出版情報: 平成11(1999)年度 科学研究費補助金 基盤研究(B) 研究成果報告書 = 1999 Fiscal Year Final Research Report Summary.  1998-1999  pp.46p.-,  2000-03.  金沢大学医学部附属病院
URL: http://hdl.handle.net/2297/00049362
概要: Ibotenic acidを用いた前脳基底核破壊により、アルツハイマー型痴呆の類似した病態モデルを作成し、排尿反射の亢進が生じることを確認した。このモデルを用いてアルツハイマー型痴呆による過活動型神経因性膀胱の発生機序について薬理学的検討を 行った。1)Ibotenic acid注入による前脳基底核破壊により、大脳皮質CAT活性は、約30%の低下がみられた。2)前脳基底核破壊ラット(basal forebrain lesion rats;BF群)は偽手術ラット(sham operated rats;SO群)に比べ有意な膀胱容量の減少が認められた。3)M1、M2受容体アゴニストであるoxotremorineMの右側脳室内累積投与によりSO群では膀胱容量の有意な減少がみられた。BF群では低用量で有意な膀胱容量の増大がみられ、高用量で膀胱容量は逆に減少し二相性の作用が認められた。5)M1受容体アンタゴニストであるpirenzepineの右側脳室内単回投与によりSO群、BF群とも膀胱容量の有意な増大がみられた。BF群はSO群に比べ10分の1の低用量より増大反応が認められた。6)膀胱容量を変化させない低用量のpirenzepineを前投与したラットにoxotremorineMを投与すると、BF群では、膀胱容量の増大が認められなかった。7)橋排尿中枢へのoxotremorineM局所投与により膀胱容量は減少した。pirenzepine投与により膀胱容量に変化は認められなかった。前脳基底核より大脳皮質に投射するACh系は排尿反射中枢に対し抑制性に投射していると考えられる。この投射系はpirenzepineにより遮断されることよりM1受容体を介するものであると思われる。脳幹部の橋排尿中枢におけるACh系は、おもにM2受容体を介すると考えられ、これは排尿反射に対し促進性に作用していると推測された。<br />OBJECTS : To investigate the mechanisms of neurogenic bladder overactivity in Alzheimer type senile dementia in a conscious rat model.METHODS : Male Wistar rats were placed in a stereotaxic apparatus, and subjected to bilateral lesion of the basal forebrain by means of ibotenic acid (IA) injection (7.5 μg/rat on each side)(BF rats). Phosphate buffered saline (PBS) was injected to control rats (sham operated rats ; SO rats). Cystometrograms (CMG) were obtained 7 to 10 days after IA/PBS injection. After CMG recording, choline-acetyltransferase (CAT) activities in the frontal cortices were assayed to assess the damage to cholinergic neuronal projections from basal forebrain to frontal cortices. The influences of intracerebroventricular administration of Oxotremorine M, muscarinic receptor agonist, or pirenzepine, M1 muscarinic receptor antagonist were investigated in conscious BF or SO rats. Antagonized effects of pirenzepine were also examined in BF rats. The effects of oxotremorine M or pirensepine directly injected into the PMC (pontine micturition center) were examined under urethane anesthesia.RESULTS : Bladder capacity become significantly smaller than before IA injection. Seven to 10 days after IA injection, bladder capacity was approximately 43% of SO rats. CAT activity in the frontal cortices was reduced in BF rats. Oxotremorine M increased bladder capacity in BF rats, while decreased in SO rats. Pirensepine significantly increased bladder capacity both in BF and SO rats, and antagonised the effect of oxotremorine M. Direct injection of oxotremorine M into the PMC decreased bladder capacity in BF and SO rats, while injection of pirensepine had no effects on CMG.CONCLUSIONS : These results indicate that M1 muscarinic system in the cerebral cortex has inhibitory influence to micturition reflex pathway. Down-regulation of this inhibitory mechanism plays an important role on overactive bladder in Alzheimer type dementia. M2 muscarinic system in the brainstem is likely to have excitatory influence on micturition reflex pathway.<br />研究課題/領域番号:10470334, 研究期間(年度):1998-1999 続きを見る
4.

論文

論文
横山, 修 ; Yokoyama, Osamu
出版情報: 平成13(2001)年度 科学研究費補助金 基盤研究(B) 研究成果報告書 = 2001 Fiscal Year Final Research Report Summary.  2000-2001  pp.10p.-,  2002-03.  金沢大学医学部附属病院
URL: http://hdl.handle.net/2297/00049361
概要: これまでの研究により、脳血管障害に伴い生ずる頻尿・尿失禁は記憶/学習に関与すると推測されている海馬の長期増強(long-term potentiation, LTP)に類似していることが解明された。すなわち脳梗塞時橋排尿中枢では、興奮性神経 伝達物質であるglutamateのN-methyl-D-aspartate(NMDA)受容体開口に始まる一連のシグナル伝達と最終的には新たなmRNAと蛋白質の合成が必要と推測された。本研究ではprotein kinase A inhibitorによるシグナル伝達や核内遺伝子の転写が、どのように排尿反射亢進に関与し、c-fosやzif268などの神経可塑性関連遺伝子の発現がNMDA受容体とどのようにリンクしているのかを検討した.また転写因子としてのc-fosやzif268で制御される下流遺伝子、COX-2/nNOSが尿失禁遺伝子である可能性についても検討した。1)protein kinase Aは転写因子の1つであるcAMP responsive element-binding protein(CREB)をリン酸化し、核内遺伝子の転写を促進する。この酵素の阻害剤(H-89)を橋背外側被蓋にmicroinjectionすると排尿反射を抑制することが可能であった.さらにこの抑制は脳梗塞後2時間の時点で1番効果的であった。従ってprotein kinase A依存性の反応が橋背外側被蓋において脳梗塞2時間以後に排尿反射の亢進をもたらし、脳梗塞4時間以後には作用していないことが明らかになった。2)actinomycin Dを背外側被蓋野にmicroinjetionしてDNAからRNAへの転写を阻害すると排尿反射の亢進は抑制されるという結果、さらに神経可塑性関連遺伝子の発現が抑制されるという結果は、排尿反射亢進に本質的な脳部位は吻側部橋の背外側被蓋野で、ここに頻尿/尿失禁遺伝子ともいうべき遺伝子が存在することを意味している。3)その候補の1つとしてCOX-2が挙げられると思われるが、COX-2 inhibitorが脳梗塞作成後でも排尿反射の抑制に有効か、あるいはCOX-2の下流に存在する遣伝子は何か、など今後検討すべき課題は多いと考えられる。<br />Object: To investigate the signal transduction and molecular mechanisms in the pontine tegmental area (PTA) associated with bladder overactivity after cerebral infarction. Methods: Cerebral infarction was induced by left middle cerebral artery occlusion (MCAO) in SD rats. Bladder activity was monitored with continuous infusion cystometrography in awake rats. The influences of H-89 (protein kinase A inhibitor), actinomycin D (ACD; RNA synthesis inhibitor), or NS-398 (COX-2 inhibitor) on bladder activity and gene expression (c-fos and zif268) were examined. Expressions of c-fos and zif268 mRNA in the DPT were monitored with real-time PCR. Results: In cerebral infarcted (CI) rats pretreated with vehicle, bladder capacity (BC) was significantly reduced after MCAO and remained consistently below half of pre-occlusion capacity. H-89, when administered 2 hours after MCAO, inhibited the reduction in BC. ACD also blocked reduction in BC in CI rats. In ACD-treated CI rats, BC gradually recovered and returned to the control level prior to MCAO within 10 hours. Treatment with NS-398 before MCAO prevented the development of bladder overactivity dose-dependently, and did not influence infarction volume. One hour after MCAO, c-fos and COX-2 mRNA expression, three hours after MCAO, zif268 mRNA expression had significantly increased as compared to those in sham operated rats. Pretreatment with MK-801, glutamatergic NMDA receptor antagonist, inhibited the development bladder overactivity and significantly reduced these gene expressions in the PTA. ACD suppressed an increase in c-fos mRNA expression 1hour after MCA occlusion as well as in zif268 3hours after MCAO. Conclusion: These results indicate that the development of bladder overactivity following MCAO is mediated by the activation of an NMDA receptor and by an RNA synthesis. Transcription in the DPT was found to be necessary for maintenance of long-lasting bladder overactivity caused by cerebral infarction. Furthermore, COX-2 molecular mechanism in the brain seems to be related to bladder overactivity. Further research on the molecular mechanisms in the brain related to bladder overactivity may lead to pharmacological therapy which targets the micturition center.<br />研究課題/領域番号:12470331, 研究期間(年度):2000-2001 続きを見る