start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=183
end-page=187
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=因島総合病院
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=杉本誠起
kn-aut-sei=杉本
kn-aut-mei=誠起
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=日立造船健康保険組合　因島総合病院
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=179
end-page=181
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=G タンパク共役型受要体 (GPCR) と Recepteor Transactivation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=吉井壮哲
kn-aut-sei=吉井
kn-aut-mei=壮哲
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院　医歯学総合研究所　腫瘍制御学講座　機能制御講座薬理学
en-keyword=GPCR
kn-keyword=GPCR
en-keyword=transactivation
kn-keyword=transactivation
en-keyword=EGF
kn-keyword=EGF
en-keyword=ErbB
kn-keyword=ErbB
en-keyword=EGF-R
kn-keyword=EGF-R
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=173
end-page=177
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=前立腺癌遺伝子治療の現状と展望
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=那須保友
kn-aut-sei=那須
kn-aut-mei=保友
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=公文裕巳
kn-aut-sei=公文
kn-aut-mei=裕巳
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯学総合研究所泌尿科病態学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯学総合研究所泌尿科病態学
en-keyword=前立腺癌
kn-keyword=前立腺癌
en-keyword=遺伝子治療
kn-keyword=遺伝子治療
en-keyword=アデノウイスルベクター
kn-keyword=アデノウイスルベクター
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=167
end-page=171
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Helicobacter pylori decreases mucin synthesis in human gastric mucosa via inhibution of UDP-galactosyltansferase
kn-title=Helicobacter Pylori 感染胃粘膜における胃ムチン生合成の変化 ―UDP-ガラクトース転移酵素活性測定による検討―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/aims : Alterations of gastric mucin have been postulated as important pathogenic properties of Helicobacter pylori. In this study, we investigated gastric mucin synthesis in H. pylori-infected gastric mucosa by measuring UDP-galactosyltransferase (UDP-Gal-T) activity, a key enzyme for the synthesis of mucin, and the amount of intracellular mucin in the gastric mucosa.
 Methods : Gastric biopsy specimens were obtained from thirty-seven patients(20 H. pylori-positive and 17 H. pylori-negative). UDP-Gal-T activity of the biopsy specimens was measured by an assay aystem we had developed, using a peanut agglutinin lectin. The amount of intracellular mucin in the gastric epithrlial cells was analyzed by measuring the cells' periodic acid-Schiff-alcian blue staining-positive subtances.
 Results : UDP-Gal-T activites in the antral mucosa of H. Pylori-positive patients were significantly lower than that of H. pylori-negative patients (p<0.05). The amount of intracelluar mucin in the antral epithelial cells of H. pylori-positive patients was significantly lower than that of H. pyolori-negative patients (p<0.01).
 Conclusions : H. pylori infection decreases gastric mucin synthesis by the inhibition of UDP-Gal-T activity. This effect may impair the gastric mucosal barrier and contribute to the mucosal injury induced by H. pylori infection.
en-copyright=
kn-copyright=

en-aut-name=TanakaShoichi
en-aut-sei=Tanaka
en-aut-mei=Shoichi
kn-aut-name=田中彰一
kn-aut-sei=田中
kn-aut-mei=彰一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Scinece,Okayama University Graduate School of Medicine and Dentistry
en-keyword=Helicobacter pylori
kn-keyword=Helicobacter pylori
en-keyword=胃粘膜
kn-keyword=胃粘膜
en-keyword=ムチン生合成
kn-keyword=ムチン生合成
en-keyword=ガラクトース転移酵素
kn-keyword=ガラクトース転移酵素
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=153
end-page=158
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Flowcytometric analysis of HBcAg-specific lymphocyte reaction in acute hepatitis B
kn-title=B型急性肝炎における HBc 抗原特異的リンパ球反応の解析
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Antigen specific T-cell responeses are important for the eradication of Hepatitis B virus (HBV) in acute infection. Flow cytometric analysis of intracellular cytokines is a simple method for studying the T-cell response at the single-cell level in a short period pf time. In the present syudy, we invesfisated the hepatitis B virus (HBV)-specific T-cell response using flow cytometry. Eight patients with acute hepatitis B and 2 patients with fulminant hepatitis B were studied. Heparinized peripheral blood was incubated with recombinant HB core antigen (HBcAg), and intracytoplasmic cytokines were analyzed by flow cytometry. HBcAg-specific interferon-gamma positive CD4 T-cella were positive in 4 of 10 patients while HBcAg-specific interferon-gamma positive CD8 T-cells and interleukin-4 positive T-cells were negatiive in all patients. No intracytoplasmic cytokines were demonstrated in healthy subjects or with recombinant hepatitis C virus (HCV) antigens. HBcAg-specific CD4 T-cells could be detected by a sensitive flow cytometric analysis of the peripherad blood and the cytokine profile of these cells was Th1. These results suggest that HBcAg-specific Th1-type CD4 T-cells may play an important role in controlling viral clearance during acute HBV infection.
en-copyright=
kn-copyright=

en-aut-name=SuzukiTakahiro
en-aut-sei=Suzuki
en-aut-mei=Takahiro
kn-aut-name=鈴木貴博
kn-aut-sei=鈴木
kn-aut-mei=貴博
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
en-keyword=B型急性肝炎
kn-keyword=B型急性肝炎
en-keyword=B型劇症肝炎
kn-keyword=B型劇症肝炎
en-keyword=細胞内サイトカイン
kn-keyword=細胞内サイトカイン
en-keyword=フローサイトメトリー
kn-keyword=フローサイトメトリー
en-keyword=HBcAg
kn-keyword=HBcAg
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=159
end-page=165
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Clinical significance of anti-asialoglycoprotein receptor autoantibodies, detected by a capture-immunoassay, in autoimmune liver diseases
kn-title=抗原捕捉免疫測定法による抗アシアロ糖タンパク質受容体抗体の検出 ―自己免疫性肝疾患における臨床的意義―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the development of autoimmune chronic acive hepatitis (AIH), the pathogenic relevance of antimmune responses against asialoglycoprotein recepter (ASGPR) has been implicated. We have previously developed a capture enzyme-linked immunsorbent assay (ELISA) for detection of anti-ASGPR antibodies and found a high prevalence of anti-ASGPR antibodies in AIH and primary biliary cirrhosis (PBC). IN this study, to clarify the clinical singnifi-cance of the measurement of anti-ASGPR antibodies in autimmune live diseases we studied correlations between thee isotype of the anti-ASGPR antibody.In AIH, the anti-ASGPR antibody titer was positively correlated with serum γ-globulin and IgM values, but not with serum transaminase. The anti-ASGPR antibody titer in histogically-active disease with piecmeal necrosis was signififcantly higher then that in quiescent disease. The most common Isotype of anti-ASGPR antibodies detected in active AIH was IgM. We encountered a case of AIH where the tirer of IgM anti-ASGPR antibody decreased by induction of remission with steroid therapy. These results suggest that the measurement of IgM isotope anti-ASGPR antiody might be useful for the evaluation of disease activity and effects of therapy in AIH patients.
en-copyright=
kn-copyright=

en-aut-name=MorisueYoshiko
en-aut-sei=Morisue
en-aut-mei=Yoshiko
kn-aut-name=森末佳子
kn-aut-sei=森末
kn-aut-mei=佳子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science,Okayama University Graduate School of Medicine and Dentistry
en-keyword=自己免疫性肝炎
kn-keyword=自己免疫性肝炎
en-keyword=原発性胆汁性肝硬変
kn-keyword=原発性胆汁性肝硬変
en-keyword=抗アシアロ糖タンパク質受容体抗体
kn-keyword=抗アシアロ糖タンパク質受容体抗体
en-keyword=自己抗体
kn-keyword=自己抗体
en-keyword=アイソタイプ
kn-keyword=アイソタイプ
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=145
end-page=152
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Abnormal polyunsaturated fatty acid pattern in plasma physholipiods and its clinical significance in patients with hepatocellular carcinoma snd live cirrhosis
kn-title=肝細胞癌症例および非坦癌肝硬変症例にみられる血漿リン脂質多価不飽和脂肪酸形成の異常と臨床の意義
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of present syudy is to analyze fatty acid composition in plasma phospolipids in patients with hepatocellular carcinoma (HCC) and live cirrhosis (LC) and to elucidate the significance of polunsaturated fatty acid on hepatocarcinogenesis. Arachidonic acid/Linoleic acid (AA/LA) molar ratios in plasma phosphatidylinositol in LC (1.42±0.29,p<0.01) and in HCC (1.24±0.12,p<0.001) were significantly lower than that in control subjects (2.78±0.16). The AA/LA molar ratio in plasma phoshatidylethanolamine in HCC(1.07±0.13) was significantly lower than that in control subjecls (1.94±0.21,p<0.01). The plasma lysophospatidyclholine (LysoPC) concentration in HCC (71.6±8.4nmol/ml, p<0.001) and in LC(80.9±12.0 nmol/ml, p<0.001) were siginificantly lower than that in control subjects (146.7±5.7nmol/ml). Plasma arachidonoy-LysoPC was siginificantly in HCC(3.2±0.5mol%) compared with that in LC (1.5±0.3mol%,p<0.01) and in control subjecys (1.9±0.1mol%,p<0.01). Plasma arachidonoy-LysoPC may play an importhant role in the pathophysiology of HCC patients.
en-copyright=
kn-copyright=

en-aut-name=YokoyamaJunko
en-aut-sei=Yokoyama
en-aut-mei=Junko
kn-aut-name=横山純子
kn-aut-sei=横山
kn-aut-mei=純子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
en-keyword=plasma phospholipids
kn-keyword=plasma phospholipids
en-keyword=arachidonic acird
kn-keyword=arachidonic acird
en-keyword=lysophosphatidylcholine
kn-keyword=lysophosphatidylcholine
en-keyword=hepatocellular carcinoma
kn-keyword=hepatocellular carcinoma
en-keyword=liver chrrhosis
kn-keyword=liver chrrhosis
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=139
end-page=144
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=In vivo and in vitro analysis of the effect of various acid-secretion blockers on UDP-galactosyltransferase activities in rat gastric mucosa
kn-title=各種酸分泌抑制剤の胃粘液糖蛋白質合成に対する影響 ―in vivo および in vitro における検討―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gastric mucus glycoprotein is important for the protection of gastric mucosa from acid. UDP-galactosyltransfer-ase (UDP-Gal-T) is a key enzyme for the synthesis of gastric mucus glycoprotein. In this study, we investigted the effects of five acid-secretion blockers, cimetidine, ranitidine, famotidine, roxatidine and omprazole on the UDP-Gal-T activity in rat gastric mucosa to clarify the interaction of the acid-secretion blocker and the gastric mucosal barrier. Intraperitoneal administration of these drugs to rat increased pH of the gastric mucosal suface and significantly decreased the gastric UDP-Gal-T activies. When we administered citrate phoshate buffer (pH 2) to the rat stomach to inhibit the change of gastric pH induced by the acid-secretion blockers, the effecer of famotidine, roxatidine and omeprazole on UDP-Gal T activties were abolished, but cimetidine and ranitidine significantly decreased the enzyme activiyty When we incubated the acid-secretion blockers with the homogenates of ral gastric mucosa, cimetidine and ranitidine significantly dereased UDP-Gal-T activites, whreas the other drugs showed no apparent influence on the enzyme sctivity. These findins suggest that the acid-secretion blockers decrease gastric mucin synthesis via the increase of the intragastric pH.In addition, among the acid-secretion blockers stydied here, cimetidine and rantidine also have direct inhibitory effects on the gastric UDP-Gal-T activity.
en-copyright=
kn-copyright=

en-aut-name=KiharaYasuhiro
en-aut-sei=Kihara
en-aut-mei=Yasuhiro
kn-aut-name=木原康裕
kn-aut-sei=木原
kn-aut-mei=康裕
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science,Okayama University Graduate School of Medicine and Dentistry
en-keyword=mucin
kn-keyword=mucin
en-keyword=galactosyltransferase
kn-keyword=galactosyltransferase
en-keyword=H2-receptor antagonist
kn-keyword=H2-receptor antagonist
en-keyword=proton pump inhibitor
kn-keyword=proton pump inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=133
end-page=138
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A study on thr effect of Heliobacter pylori to the gastric mucosal defensive mechanism
kn-title=Helicobacter pylori の胃粘膜防御機構に与える影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=UDP-galactosyltransferase (UDP-Gal-T) is a key enzyme in the synthesis of mucus glycoproteins, which play an important role in gastric mucosal defensive mechanisms. Helicobacter pylori (HP) induces gastritis and peptic ulceers but mechanisms of HP-induced mucosal injury sre not fully understood. To elucidate the mechanism whereby (HP) infection induces gastric mucosal injury, we investigated the effects HP on the gastric mucosal defensive mechanism by measuring UDP-Gal T activies in HGC-27, a mucin-producing gastric caneer cell line, treated with　various HP-relatd materials (sonicated HP, HP culture supernatants, live HP). HP-related materials induced no significant chages in UDP-Gal T activity, but the enzyme increased when we generated a low concentration of ammonia by adding sonicated HP. and urea simultaneousy. In contrast, UDP-Gal-T activity did not increase when we added live HP instead of sonicated HP. Next, we investigated the effects of HP on ethanol-induced injury in the HGC-27 cells. Pretreatment with ammonia of a low concetration significantly protected cells from ethanol-induced injury. In contrast, pretreatment with live HP and urea generated ammonia of the similar concentration but did not protect cells from the injoy. Our findings that HP has an inhibitory effect against adaptive cytoprotection induced by ammonia by inhibiting the induction of UDP-Gal T.
en-copyright=
kn-copyright=

en-aut-name=YoshinagaFumiya
en-aut-sei=Yoshinaga
en-aut-mei=Fumiya
kn-aut-name=吉永文哉
kn-aut-sei=吉永
kn-aut-mei=文哉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
en-keyword=Helicobacter pylori
kn-keyword=Helicobacter pylori
en-keyword=UDP-galactosyltansferase
kn-keyword=UDP-galactosyltansferase
en-keyword=ammonia
kn-keyword=ammonia
en-keyword=ethanol
kn-keyword=ethanol
en-keyword=adaptive cytoprotection
kn-keyword=adaptive cytoprotection
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=131
end-page=132
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=職業性ストレスの健康影響とその対策
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=川上憲人
kn-aut-sei=川上
kn-aut-mei=憲人
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯学総合研究所　衛生学・予防医学分野
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=125
end-page=130
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ＳＥＲＥＸ法によるマウス移植腫瘍の抗原解析
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=小野俊朗
kn-aut-sei=小野
kn-aut-mei=俊朗
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯学総合研究所　免疫学
en-keyword=SEREX
kn-keyword=SEREX
en-keyword=Meth A
kn-keyword=Meth A
en-keyword=Mouse
kn-keyword=Mouse
en-keyword=Antibody
kn-keyword=Antibody
en-keyword=Cancer/testis (CT) anigen
kn-keyword=Cancer/testis (CT) anigen
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=2
article-no=
start-page=117
end-page=123
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ikaros family とリンパ系腫瘍
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=中瀬浩一
kn-aut-sei=中瀬
kn-aut-mei=浩一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=愛媛県立中央病院
END