Гомосексуальный субъект в пространстве публичного: нарративное измерение камин-аута

<div><p>Background</p><p>Although <i>Helicobacter pylori</i> (<i>H</i>. <i>pylori</i>) infection is closely associated with the development of peptic ulcer, its involvement in pathophysiology in the lower intestinal tract and gastrointestinal (GI) motility remains unclear. Glucagon-like peptide-1 (GLP-1) is a gut hormone produced in the lower intestinal tract and involved in GI motility. Here, we investigated the effect of <i>H</i>. <i>pylori</i> infection on the link between GLP-1 expression and motility of the GI tract.</p><p>Methods</p><p>C57BL/6 mice were inoculated with a <i>H</i>. <i>pylori</i> strain. Twelve weeks later, the <i>H</i>. <i>pylori</i>-infected mice underwent <i>H</i>. <i>pylori</i> eradication treatment. GI tissues were obtained from the mice at various time intervals, and evaluated for the severity of gastric inflammatory cell infiltration and immunohistochemical expression of GLP-1 and PAX6 in the colonic mucosa. Gastrointestinal transit time (GITT) was measured by administration of carmine-red solution.</p><p>Results</p><p>GLP-1 was expressed in the endocrine cells of the colonic mucosa, and PAX6 immunoreactivity was co-localized in such cells. The numbers of GLP-1- and PAX6-positive cells in the colon were significantly increased at 12 weeks after <i>H</i>. <i>pylori</i> infection and showed a positive correlation with each other. The GITT was significantly longer in <i>H</i>. <i>pylori</i>-infected mice than in non-infected controls and showed a positive correlation with GLP-1 expression. When <i>H</i>. <i>pylori</i>-infected mice underwent <i>H</i>. <i>pylori</i> eradication, GITT and PAX6/GLP-1 expression did not differ significantly from those in untreated <i>H</i>. <i>pylori</i>-infected mice.</p><p>Conclusions</p><p><i>H</i>. <i>pylori</i> infection may impair GI motility by enhancing the colonic GLP-1/PAX6 expression.</p></div

Pathological Approach for Surveillance of Ulcerative Colitis-associated cancer:Usefulness of Immunohistochemistry for p53

The patients with long-standing ulcerative colitis( UC) have a high-risk of neoplastic lesions in the colonicmucosa. The UC-associated neoplastic lesion is difficult to detect by endoscopic examination or diagnosehistologically. In the present study, we aimed to clarify whether immunohistochemistry for p53 is useful todiscriminate the UC-associated neoplasia from inflammed regenerating epithelium. Tissue samples were obtainedfrom colorectomy specimens from 20 patients with long-standing UC (range 6-29 years). The surfaceof microstructure of the tissues was observed by stereomicroscopy, and the sections were examined usingimmunohistochemistry for p53. All of T2-4 carcinomas were detectable by endoscopic examination beforesurgery, whereas considerable number of dysplasias (52.5%), Tis carcinomas (33.3%), and T1 carcinomas(60.0%) were undetectable. Fifty-three of 67 UC-associated neoplastic lesions (79.1%) were of flat-typemacroscopically. The detection rate of flat-type neoplasias( 45.3%) was significantly lower than that of protrudingones (100%). The positivity of p53 overexpression was 0 % in UC-II, 52.5 % in UC-III, and 70.4 %in UC-IV, respectively. UC-II lesions had lower positivity of p53 overexpression than UC-III( P=0.027) or-IV lesions( P=0.003). Immunohistochemical analysis of p53 protein is useful to discriminate the UC-associatedneoplasia from inflammed regenerating epithelium

Association of Human Leukocyte Antigen with Interstitial Lung Disease in Rheumatoid Arthritis: A Protective Role for Shared Epitope

INTRODUCTION: Interstitial Lung Disease (ILD) is frequently associated with Rheumatoid Arthritis (RA) as one of extra-articular manifestations. Many studies for Human Leukocyte Antigen (HLA) allelic association with RA have been reported, but few have been validated in an RA subpopulation with ILD. In this study, we investigated the association of HLA class II alleles with ILD in RA. METHODS: An association study was conducted on HLA-DRB1, DQB1, and DPB1 in 450 Japanese RA patients that were or were not diagnosed with ILD, based on the findings of computed tomography images of the chest. RESULTS: Unexpectedly, HLA-DRB1*04 (corrected P [Pc] = 0.0054, odds ratio [OR] 0.57), shared epitope (SE) (P = 0.0055, OR 0.66) and DQB1*04 (Pc = 0.0036, OR 0.57) were associated with significantly decreased risk of ILD. In contrast, DRB1*16 (Pc = 0.0372, OR 15.21), DR2 serological group (DRB1*15 and *16 alleles) (P = 0.0020, OR 1.75) and DQB1*06 (Pc = 0.0333, OR 1.57, respectively) were significantly associated with risk of ILD. CONCLUSION: HLA-DRB1 SE was associated with reduced, while DR2 serological group (DRB1*15 and *16) with increased, risk for ILD in Japanese patients with RA

Immunohistochemical Localization of REG Ia Protein in Salivary Gland Tumors

The regenerating gene( Reg) Ia protein has a trophic effect on gastric epithelial cells, and its overexpressionis reported in gastrointestinal cancers. The salivary gland is a component of the digestive system, andtherefore, REG Ia protein may play some role in the pathophysiology of salivary gland tumors. In the presentstudy, we determined the immunohistochemical localization of REG Ia protein in salivary gland tumorsand moreover investigated its relationship to clinicopathological features. Twenty-eight patients with salivarygland tumor were enrolled. The specimens resected by surgery from those patients were examinedusing immunohistochemistry for REG Ia protein and Ki67. Five of the 16 pleomorphic adenomas (31.3%)were positive for REG Ia protein. Regarding salivary gland carcinomas, four of five mucoepidermoid carcinomas(80%), three of five adenoid cystic carcinomas (60%), one of two polymorphous low-grade adenocarcinomas(50%) were also positive for REG Ia protein. However, no relationships were found betweenREG Ia protein expression and clinicopathological features. Regarding the Ki67 expression, strong signalwas observed in the tumor cells of patients with salivary gland adenoma as well as carcinoma. REG Ia proteinis expressed not only in adenocarcinoma but also precancerous adenoma cells proliferating actively,suggesting that REG Ia protein may play a role at least in part in the development of salivary gland tumors

The Japanese Clinical Practice Guideline for acute kidney injury 2016

Acute kidney injury (AKI) is a syndrome which has a broad range of etiologic factors depending on different clinical settings. Because AKI has significant impacts on prognosis in any clinical settings, early detection and intervention are necessary to improve the outcomes of AKI patients. This clinical guideline for AKI was developed by a multidisciplinary approach with nephrology, intensive care medicine, blood purification, and pediatrics. Of note, clinical practice for AKI management which was widely performed in Japan was also evaluated with comprehensive literature search

Selection of Postoperative Systemic Chemotherapy for Advanced Gastric Cancer Patients with Hepatic Metastasis Using the Histoculture Drug Response Assay

The usefulness of histoculture drug response assay (HDRA) before the start of antitumor chemotherapy was explored to predict the antitumor response of chemotherapy for progressive gastric cancer patients with hepatic metastasis. Cancer tissue was collected from 6 advanced gastric cancer patients with hepatic metastasis, to assess whether the tumor is sensitive to chemotherapeutic agents of 5-fluorouracil (5-FU), mitomycin C (MMC), docetaxel hydrate (TXT), and cisplatin (CDDP) by the HDRA method. The size of hepatic tumor was measured by CT scan 3 and 6 months after the start of the chemotherapy and examined the relationship between the selected chemotherapy and antitumor response. Of 6 patients investigated in the present study, 3 patients received monotherapy with TS-1[○!R], which was found to be effective in 2 patients (66.7%). In the patient who received MMC monotherapy, the HDRA showed the cancer tissue to be less sensitive to any of antitumor agents tested, resultantly indicating no antitumor response. In the remaining 2 patients with combination therapy with TS-1[○!R] and MMC, the selected chemotherapeutic agents showed anti-tumor effect. The HDRA is useful to predict the antitumor response of postoperative adjunctive chemotherapy for advanced gastric cancer patients with hepatic metastasis, and plays an important role in selection of antitumor agents

JASMINE: Near-infrared astrometry and time-series photometry science

The Japan Astrometry Satellite Mission for INfrared Exploration (JASMINE) is a planned M-class science space mission by the Institute of Space and Astronautical Science, the Japan Aerospace Exploration Agency. JASMINE has two main science goals. One is Galactic archaeology with a Galactic Center survey, which aims to reveal the Milky Way’s central core structure and formation history from Gaia-level (∼25 ${\mu}$as) astrometry in the near-infrared (NIR) Hw band (1.0–1.6 ${\mu}$m). The other is an exoplanet survey, which aims to discover transiting Earth-like exoplanets in the habitable zone from NIR time-series photometry of M dwarfs when the Galactic Center is not accessible. We introduce the mission, review many science objectives, and present the instrument concept. JASMINE will be the first dedicated NIR astrometry space mission and provide precise astrometric information on the stars in the Galactic Center, taking advantage of the significantly lower extinction in the NIR. The precise astrometry is obtained by taking many short-exposure images. Hence, the JASMINE Galactic Center survey data will be valuable for studies of exoplanet transits, asteroseismology, variable stars, and microlensing studies, including discovery of (intermediate-mass) black holes. We highlight a swath of such potential science, and also describe synergies with other missions

Mitochondrial Involvement in the Accumulation of Misfolded Proteins in Neurodegenerative Diseases

Mitochondrial respiratory chain deficiency and increased oxidative stress have been closely associated with major age-associated neurodegenerative diseases. I hypothesized that mitochondrial oxidative phosphorylation defects or elevated oxidative stress, which could arise in a stochastic manner during our normal aging process, might modulate the formation of protein aggregates or production of misfolded proteins, contributing to the initiation of these diseases. To test this hypothesis, we (i) have developed and characterized mouse and cellular models of Alzheimer\u27s and Huntington\u27s diseases expressing aggregate-prone pathogenic proteins, beta-amyloid and mutant huntingtin (Chapters 1 and 2), (ii) have developed mouse models that exhibit neuron-specific defects in mitochondrial oxidative phosphorylation (Chapters 2 and 3), and (iii) have evaluated the alterations in the amount of aggregate loads upon genetic and pharmacological manipulations of mitochondrial oxidative phosphorylation activities (Chapters 1 and 2). The evaluation of the impacts of mitochondrial defects on the amount of huntingtin aggregates has revealed that a defect in complex III promotes the accumulation of huntingtin aggregates via the impairment of proteasome activity (Chapter 1). On the other hand, ablation of complex IV activity in a subset of postmitotic neurons revealed that complex IV deficiency does not promote either oxidative stress or the deposition of amyloid plaques in a mouse model of Alzheimer\u27s disease, questioning the mitochondrial origin of Alzheimer\u27s disease (Chapter 2). However, as shown previously, the tight correlation between oxidative stress and accumulation of amyloid plaques was found. Chapter 3 involved the generation of an improved mouse model, in which mitochondrial defects can be induced in a subset of forebrain neurons (cortex, hippocampus, and striatum) in a doxycycline-dependent manner. This system relies on the regulated expression of a mitochondria-targeted restriction enzyme, PstI, which digests mitochondrial DNA and thereby impairs the activity of oxidative phosphorylation. In conclusion, our studies highlighted the disease-specific complex pathways that may modulate the accumulation of misfolded proteins during aging. Future studies employing the newly-developed mouse model may reveal a contribution of age-associated global defects of oxidative phosphorylation to oxidative stress and neurodegenerative diseases

Regenerating gene蛋白の、高ガストリン血症ラットにおける胃粘膜増殖作用に関する研究

京都大学0048新制・課程博士博士(医学)甲第7763号医博第2116号新制||医||713(附属図書館)UT51-99-G357京都大学大学院医学研究科内科系専攻(主査)教授 中尾 一和, 教授 今村 正之, 教授 千葉 勉学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDA