Fiber shape theory

筑波大学University of Tsukuba博士（理学）Doctor of Philosophy in Science1981【要旨】thesi

Surgical management of a patient with anomalous origin of the left circumflex coronary artery undergoing aortic and mitral valve surgery

Background The anomalous origin of the left circumflex coronary artery is rare and, when isolated, typically has minimal pathological significance. However, it can cause damage or compression of the coronary artery during aortic and mitral valve surgery. Case presentation The patient was a 34-year-old male diagnosed with severe aortic regurgitation due to a bicuspid aortic valve following infective endocarditis at the mitral valve. He was referred to our hospital owing to worsening heart failure. Preoperative evaluation revealed a mitral valve aneurysm and an anomalous left circumflex coronary artery originating from the right coronary artery and running posteriorly along the aortic valve annulus. During surgery, dissection of the anomalous left circumflex coronary artery was challenging. Mitral valve aneurysm repair and aortic valve replacement were performed. For the aortic valve replacement, a 23-mm St. Jude Medical Regent valve, one size smaller than optimal, was secured in the supra-annular position. Additionally, a coronary artery bypass graft was performed on the distal circumflex artery using a saphenous vein graft. The patient experienced no ischemic myocardial damage and was discharged in stable condition on postoperative day 14. Conclusions The anomalous origin of the left circumflex coronary artery should be recognized, and appropriate measures must be taken during valve surgery. Preemptive coronary artery bypass grafting is a reasonable option for patients undergoing aortic and mitral valve surgeries

Mitral valve repair in severe mitral regurgitation due to Barlow’s disease with concomitant mitral annular disjunction: a case report

Background Mitral annular disjunction (MAD) is characterized by the detachment of the mitral valve-left atrial junction from the left ventricular myocardium. The association of MAD with Barlow’s disease and its relevance to treatment are increasingly recognized. Case presentation A 75-year-old male with a history of mitral regurgitation (MR) and ablation for paroxysmal atrial fibrillation was diagnosed with severe MR due to Barlow’s disease, as confirmed by echocardiography. Imaging revealed disjunction at the mitral valve’s posterior annulus. During surgery, the posterior leaflet was resected along the annulus with precise height adjustments. A 6-mm separation between the mitral valve–left atrial junction and the left ventricular myocardium was sutured using a four-stitch mattress technique. The procedure included leaflet repair, insertion of artificial chordae, and mitral annuloplasty. Postoperatively, the MAD was corrected successfully, eliminating the severe MR. Conclusions Confirming the presence of MAD before surgery is essential for patients with MR. Surgical correction of MAD is imperative when present to address the disjunction effectively

Measurement of the Lifetime Difference in D0 Meson Decays

journal articl

Visual Computing: Constructing a Digital Bridge to the World of Dreams

video/mp4期間: 2014年8月4日講義場所: 情報科学研究科大講義室(L1)講演者所属: University of StuttgartSymposium: Making Augmented Reality Real Presentation-1vide

研究速報 : Anisotropic Deformation and Strength Properties of Wet-Tamped Sand in Plane Strain Compression at Low Pressures (Part 3) : Shear Deformation Characteristics

departmental bulletin pape

無作為抽出(ランダムサンプリング)による社会調査実施の手続き －京都市の女性調査から

departmental bulletin pape

Kinetics of Env(wt)- and Env(NYP)-induced fusion with HeLa-CD4 cells expressing CCR5(wt) (A) or CCR5(Δ18) (B)

<p><b>Copyright information:</b></p><p>Taken from "The role of the N-terminal segment of CCR5 in HIV-1 Env-mediated membrane fusion and the mechanism of virus adaptation to CCR5 lacking this segment"</p><p>http://www.retrovirology.com/content/4/1/55</p><p>Retrovirology 2007;4():55-55.</p><p>Published online 8 Aug 2007</p><p>PMCID:PMC1995219.</p><p></p> (A) Fusion with CCR5(wt)-expressing cells induced by Env(wt) and Env(NYP) is shown by filled circles and filled squares, respectively. Fusion after establishing the 18°-TAS (pre-incubation for 2 hr at 18°C) is shown by open circles (Env(wt)) and open squares (Env(NYP)). (B) Fusion with CCR5(Δ18)-expressing cells induced by Env(wt) and by Env(NYP) is shown by semifilled circles and filled triangles, respectively. The kinetics of fusion between Env(NYP)- and CCR5(Δ18)-expressing cells after establishing the 27°-TAS (pre-incubation for 2 hr at 27°C) is shown by open triangles. The experimental points are means ± SE

Inhibition of fusion with HeLa-CD4/CCR5(wt)-expressing cells by the CCR5 binding inhibitor, Sch-C

<p><b>Copyright information:</b></p><p>Taken from "The role of the N-terminal segment of CCR5 in HIV-1 Env-mediated membrane fusion and the mechanism of virus adaptation to CCR5 lacking this segment"</p><p>http://www.retrovirology.com/content/4/1/55</p><p>Retrovirology 2007;4():55-55.</p><p>Published online 8 Aug 2007</p><p>PMCID:PMC1995219.</p><p></p> (A) The inhibitory activity of Sch-C was measured upon direct co-culture of effector and target cells at 37°C for 2 hr (filled symbols) and after creating TAS (open symbols). TAS was created by pre-incubating cells at 18°C for 2 hr, and fusion was triggered by additional incubation at 37°C for 1.5 hr. Fusion mediated by Env(wt) and Env(NYP) is shown by squares and circles, respectively. (B) Effector cells expressing Env(wt) (squares) or Env(NYP) (circles) were pre-incubated with HeLa-CD4/CCR5(wt) cells at 18°C for varied times, exposed to 1.35 μM Sch-C for 5 min, and warmed to 37°C for 1.5 hr. (C) Following the creation of TAS (18°C, 2 hr), the cells were incubated for additional 5 or 50 min at 18°C with or without 300 nM Sch-C before raising the temperature to 37°C. The resulting fusogenic activity was normalized to the extent of fusion without the inhibitor. The Env(wt)- and Env(NYP)-induced fusion is shown by squares and circles, respectively

Env(NYP) is more readily inactivated by treatment with sCD4 than Env(wt)

<p><b>Copyright information:</b></p><p>Taken from "The role of the N-terminal segment of CCR5 in HIV-1 Env-mediated membrane fusion and the mechanism of virus adaptation to CCR5 lacking this segment"</p><p>http://www.retrovirology.com/content/4/1/55</p><p>Retrovirology 2007;4():55-55.</p><p>Published online 8 Aug 2007</p><p>PMCID:PMC1995219.</p><p></p> Cells expressing either Env(wt) or Env(NYP) were collected from the culture dish using a non-enzymatic cell dissociation solution and treated with 25 μg/ml sCD4 for 30 min at 37°C. Cells were washed twice to remove free sCD4 and co-incubated with HeLa-CD4/CCR5(wt) cells for 2 hr at 37°C. The results are plotted as percentage of fusion observed for untreated effector cells