Tunnel Structure Analysis by the Operational Method First Report

Article信州大学工学部紀要 25: 13-20 (1968)departmental bulletin pape

Finite Element Arch Analysis by the Operational Method

Article信州大学工学部紀要 25: 1-12 (1968)departmental bulletin pape

Operational Finite Element Analysis of Circular Rings Surrounded with Elastic Foundation

Article信州大学工学部紀要 27: 37-46 (1969)departmental bulletin pape

Direct Analysis of Continuous Beam-Columns

Article信州大学工学部紀要 23: 1-14 (1967)departmental bulletin pape

Operational Method for Various Continuous Beams

Article信州大学工学部紀要 24: 1-22 (1968)departmental bulletin pape

Z-360, a novel therapeutic agent for pancreatic cancer, prevents up-regulation of ephrin B1 gene expression and phosphorylation of NR2B via suppression of interleukin-1 β production in a cancer-induced pain model in mice

<p>Abstract</p> <p>Background</p> <p>Z-360 is an orally active cholecystokinin-2 (CCK2)/gastrin receptor antagonist currently under development as a therapeutic drug for pancreatic cancer. It was previously reported that Z-360 treatment in combination with gemcitabine prolonged the survival period in a lethal pancreatic cancer xenograft model in mice. In a phase Ib/IIa clinical study, Z-360 treatment displayed a trend of reduced pain in patients with advanced pancreatic cancer in combination with gemcitabine including analgesics such as opioids. Here, we investigated the mechanism of analgesic action of Z-360 in a severe cancer-induced pain model in mice, which is considered to be opioid-resistant, by examining ephrin B1 gene expression, <it>N</it>-methyl-D-aspartate receptor NR2B subunit phosphorylation, and interleukin-1β (IL-1β) production.</p> <p>Results</p> <p>In a mouse model of cancer-induced pain, ephrin B1 gene expression in dorsal root ganglia (DRGs) and the phosphorylation of NR2B in the spinal cord were induced. Z-360 treatment inhibited both ephrin B1 gene expression and the phosphorylation of NR2B. In addition, IL-1β production increased in the cancer-inoculated hind paw of mice, but could be suppressed by treatment with Z-360. Moreover, we observed that the CCK1 receptor antagonist devazepide similarly suppressed up-regulation of ephrin B1 gene expression and IL-1β production, and that the intraperitoneal injection of sulfated CCK-8 induced the production of IL-1β in the cancer-inoculated region.</p> <p>Conclusions</p> <p>We have identified a novel pain cascade, in which IL-1β production in cancer-inoculated regions induces ephrin B1 gene expression in DRGs and then ephrin B1 enhances the tyrosine phosphorylation of NR2B via Eph B receptor in the spinal cord. Notably, Z-360 relieves cancer-induced pain by preventing this pain cascade through the suppression of IL-1β production, likely via the blockade of CCK1 receptor. The pre-clinical results presented here support the analgesic action of Z-360 in pancreatic cancer patients with severe, opioid-resistant pain. Pre-clinical and clinical results have demonstrated that Z-360 combined with gemcitabine represents a promising pancreatic cancer therapy approach with characteristic analgesic effects in addition to the prolongation of survival.</p

Preliminary in vivo evaluation of a needle insertion manipulator for central venous catheterization

Central venous catheterization is associated with potential complications secondary to accidental puncture, including venous bleeding and pneumothorax. We developed a system that avoids these complications and simplifies the procedure using a robot to provide puncture assistance. We herein report a puncture experiment conducted in vivo in a porcine to evaluate the manipulator. The right and left jugular veins of a pig were punctured five times each through both opened and unopened skin at a puncture angle and speed. A venous placement rate of 80% was obtained with opened skin. A much lower rate of 40% was obtained with unopened skin. One of five attempts in opened skin was unsuccessful, likely because of the stick-slip phenomenon. This system was effective for jugular venous puncture of opened skin. Future studies should focus on puncture conditions that facilitate needle placement, inhibit the stick-slip phenomenon, and minimize needle bending due to the presence of skin. © 2014 Kobayashi et al.; licensee Springer.1

IL-17Aは赤痢アメーバの腸管感染においてIFN-γ/IL-4比の減少と持続感染に寄与する

Amebiasis is an infectious disease caused by Entamoeba histolytica, an anaerobic protozoan parasite, and is a major public health problem worldwide, particularly in areas with inadequate sanitation and poor hygiene. Th1 responses, represented by interferon gamma (IFN-γ), play a protective role by clearing the amebae from the gut, whereas Th2 responses are responsible for chronic infection. Th17 responses preconditioned by vaccination or by modulating the intestinal microbiome protect mice from the settlement of E. histolytica. However, the role of interleukin-17A (IL-17A), which is upregulated during the natural course of intestinal amebiasis, has not been clarified. The aim of this study was to investigate the role of IL-17A during intestinal amebiasis in a mouse model. IL-17A knockout and wild-type CBA/J mice were challenged intracecally with 2 × 106 E. histolytica trophozoites, and their infection, pathology, and immune responses were monitored. Neither the initial settlement of E. histolytica nor the inflammation of the cecum was affected by the absence of IL-17A for week 1, but the infection rate and parasite burden declined in a late stage of infection, accompanied by an increased IFN-γ/IL-4 ratio. Therefore, IL-17A contributes to the persistence of E. histolytica and modulates the immune response, including the IFN-γ/IL-4 ratio, which may be responsible for the reduction of the parasite burden in the IL-17A knockout mice during the chronic phase of intestinal amebiasis.長崎大学学位論文 学位記番号:博(医歯薬)甲第1005号 学位授与年月日:平成29年12月6日Author: Sharmina Deloer, Risa Nakamura, Mihoko Kikuchi, Taeko Moriyasu, Yombo Dan Justin Kalenda, Eman Sayed Mohammed, Masachika Senba, Yoichiro Iwakura, Hiroki Yoshida, Shinjiro HamanoCitation: Parasitology International, 66(6), pp.817-823; 2017Nagasaki University (長崎大学)課程博