An Awareness of Japanese Crew in the EMS Helicopter on Organizational Management

Abstract. Kushiro city general hospital and Kojinkai Memorial Hospital started EMS Project on 5 October 2009. It had worked 14 times on 26 November, and save a lot of lives. The EMS helicopter plays an important role of regional differences in medication. The EMS operates three institutions -an Aviation Organization, a Medical Organization and a Fire Organization. However, the cooperation of labor doesn't happen in their division of labors. It does not make divide the work. This is because the EMS does not divide work and responsibilities clearly one solution is to have a common field of responsibility across the 3 organization order to improve cooperation. Since this study analyzes the EMS organization from the knowledge creation point of view. This paper is based on a month-long research study at hospital waiting rooms

The lived experience of a woman in her 50 s with a lower limb prosthetic device

It is imperative that a concern of physical function is addressed such as ability to walk, and how the disease and the sophistication of artificial devices influence person’s quality of life（QOL）. A woman in her ５０s who has a lower limb prosthetic device after amputation. She lived with this prosthesis for more than ２０ years. Interviews were recorded, transcribed, and analyzed. The findings of the study revealed that hoping for a better QOL can be lost due to unbearable suffering from adverse reactions during chemotherapy. This lived experience made her decide to discontinue chemotherapy giving her greater than expected grief experience than her postamputation. Watchful ambulation became distinctive and purposive with each step so as not to fall. This walking style was to show her normal gait, rather than worrying about the gaze from people. Furthermore, it was found that feelings of incompleteness still existed even with the prosthetic device. This was often attributed to the physical pain and discomfort while wearing this device even while knowing that she is now a whole person. Still she felt incomplete in the moment. Visible artificial device becoming her essential part, provided a meaningful life that enabled her to grow with the family

Truncated KCNQ1 mutant, A178fs/105, forms hetero-multimer channel with wild-type causing a dominant-negative suppression due to trafficking defect

AbstractWe identified a novel mutation Ala178fs/105 missing S3–S6 and C-terminus portions of KCNQ1 channel. Ala178fs/105-KCNQ1 expressed in COS-7 cells demonstrated no current expression. Co-expression with wild-type (WT) revealed a dominant-negative effect, which suggests the formation of hetero-multimer by mutant and WT. Confocal laser microscopy displayed intracellular retention of Ala178fs/105-KCNQ1 protein. Co-expression of the mutant and WT also increased intracellular retention of channel protein compared to WT alone. Our findings suggest a novel mechanism for LQT1 that the truncated S1–S2 KCNQ1 mutant forms hetero-multimer and cause a dominant-negative effect due to trafficking defect

Tcap gene mutations in hypertrophic cardiomyopathy and dilated cardiomyopathy

ObjectivesWe sought to explore the relationship between a Tcap gene (TCAP)abnormality and cardiomyopathy.BackgroundHypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) cause severe heart failure and sudden death. Recent genetic investigations have revealed that mutations of genes encoding Z-disc components, including titin and muscle LIM protein (MLP), are the primary cause of both HCM and DCM. The Z-disc plays a role in establishing the mechanical coupling of sarcomeric contraction and stretching, with the titin/Tcap/MLP complex serving as a mechanical stretch sensor. Tcap interacts with the calsarcin, which tethers the calcineurin to the Z-disc.MethodsThe TCAPwas analyzed in 346 patients with HCM (236 familial and 110 sporadic cases) and 136 patients with DCM (34 familial and 102 sporadic cases). Two different in vitro qualitative assays—yeast two-hybrid and glutathion S-transferase pull-down competition—were performed in order to investigate functional changes in Tcap's interaction with MLP, titin, and calsarcin-1 caused by the identified mutations and a reported DCM-associated mutation, R87Q.ResultsTwo TCAPmutations, T137I and R153H, were found in patients with HCM, and another TCAPmutation, E132Q, was identified in a patient with DCM. It was demonstrated by the qualitative assays that the HCM-associated mutations augment the ability of Tcap to interact with titin and calsarcin-1, whereas the DCM-associated mutations impair the interaction of Tcap with MLP, titin, and calsarcin-1.ConclusionsThese observations suggest that the difference in clinical phenotype (HCM or DCM) may be correlated with the property of altered binding among the Z-disc components

Cleavage of Toll-Like Receptor 9 Ectodomain Is Required for In Vivo Responses to Single Strand DNA

Mouse toll-like receptor 9 (TLR9) is an endosomal sensor for single-stranded DNA. TLR9 is transported from the endoplasmic reticulum to endolysosomes by a multiple transmembrane protein Unc93 homolog B1, and proteolytically cleaved at its ectodomain. The structure of TLR9 and its biochemical analyses have shown that the proteolytic cleavage of TLR9 ectodomain enables TLR9-dimerization and TLR9 activation. However, the requirement of TLR9 cleavage in vivo has not been studied. We here show that the 13 amino acids deletion at the cleavage site made TLR9 resistant to proteolytic cleavage. The deletion mutation in the Tlr9 gene impaired TLR9-dependent cytokine production in conventional dendritic cells from the mutant mice. Not only in vitro, in vivo production of inflammatory cytokines (TNF-α and IL-12p40), chemokine (CCR5/RANTES), and type I interferon (IFN-α) induced by administration of TLR9 ligand was also impaired. These results demonstrate that the TLR9 cleavage is required for TLR9 responses in vivo

経頸静脈的肝内門脈大循環短絡術が著効した難治性腹水の1例

京都府立医科大学附属北部医療センター放射線科京都府立医科大学附属北部医療センター外科京都府立医科大学大学院医学研究科放射線診断治療学京都府立医科大学大学院医学研究科消化器外科学市立福知山市民病院腫瘍内科市立福知山市民病院放射線科Department of Radiology, North Medical Center, Kyoto Prefectural University of MedicineDepartment of Surgery, North Medical Center, Kyoto Prefectural University of MedicineDepartment of Radiology, Kyoto Prefectural University of MedicineDepartment of Digestive Surgery, Kyoto Prefectural University of MedicineDepartment of Medical Oncology, Fukuchiyama City HospitalDepartment of Medical Radiology, Fukuchiyama City Hospital切除不能肝内胆管癌の58 歳男性に難治性腹水を生じ、著明な腹部膨満感に対し頻回な穿刺排液を要した。腹水性状は漏出性で進行した肝病変による門脈圧亢進症に起因すると判断した。介入治療として経頸静脈的肝内門脈大循環短絡術を適用した。腹部膨満感のNRS は9 から1 に低下し、35 日後の原病死まで有害事象や症状再発なく経過した。難治性腹水に対する介入治療には、腹水の性状診断を含めて治療方針を決定することが重要である

Measurement of serum hepcidin-25 levels as a potential test for diagnosing hemochromatosis and related disorders

石川県立中央病院金沢大学医薬保健研究域医学系Iron overload syndromes include a wide spectrum of genetic and acquired conditions. Recent studies suggest suppressed hepcidin synthesis in the liver to be the molecular basis of hemochromatosis. However, a liver with acquired iron overload synthesizes an adequate amount of hepcidin. Thus, hepcidin could function as a biochemical marker for differential diagnosis of iron overload syndromes. Methods We measured serum iron parameters and hepcidin- 25 levels followed by sequencing HFE, HJV, HAMP, TFR2, and SLC40A1 genes in 13 Japanese patients with iron overload syndromes. In addition, we performed direct measurement of serum hepcidin-25 levels using liquid chromatography-tandem mass spectrometry in 3 Japanese patients with aceruloplasminemia and 4 Italians with HFE hemochromatosis. Results One patient with HJV hemochromatosis, 2 with TFR2 hemochromatosis, and 3 with ferroportin disease were found among the 13 Japanese patients. The remaining 7 Japanese patients showed no evidence for genetic basis of iron overload syndrome. As far as the serum hepcidin-25 was concerned, seven patients with hemochromatosis and 3 with aceruloplasminemia showed markedly decreased serum hepcidin-25 levels. In contrast, 3 patients with ferroportin disease and 7 with secondary iron overload syndromes showed serum hepcidin levels parallel to their hyperferritinemia. Patients with iron overload syndromes were divided into 2 phenotypes presenting as low and high hepcidinemia. These were then associated with their genotypes. Conclusion Determining serum hepcidin-25 levels may aid differential diagnosis of iron overload syndromes prior to genetic analysis. © Springer 2010

大学祭

写真あり大学祭の展示 : 本釜菜津子(英語英米文学科)ワークショップ しおり作り : 林陽子(音楽芸術学科