関: pepsinogen II

WordNet

the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system
precursor of pepsin; stored in the stomach walls and converted to pepsin by hydrochloric acid in the stomach

PrepTutorEJDIC

carbonの化学記号
cesiumの化学記号
cadmiumの化学記号

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1. 胃酸分泌の生理学 physiology of gastric acid secretion
2. 胃炎および胃障害の分類と診断 classification and diagnosis of gastritis and gastropathy
3. 栄養の吸収および吸収不良の機序 mechanisms of nutrient absorption and malabsorption
4. Gastric cancer screening
5. 胃癌の臨床的特徴、診断、および病期分類 clinical features diagnosis and staging of gastric cancer

English Journal

Cancer development based on chronic active gastritis and resulting gastric atrophy as assessed by serum levels of pepsinogen and Helicobacter pylori antibody titer.

Yoshida T1, Kato J, Inoue I, Yoshimura N, Deguchi H, Mukoubayashi C, Oka M, Watanabe M, Enomoto S, Niwa T, Maekita T, Iguchi M, Tamai H, Utsunomiya H, Yamamichi N, Fujishiro M, Iwane M, Takeshita T, Ushijima T, Ichinose M.Author information 1Second Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama City, Wakayama, Japan.AbstractOur study investigated the relationship between gastric cancer development and activity of Helicobacter pylori-associated chronic gastritis or the resulting chronic atrophic gastritis (CAG). A cohort of 4,655 healthy asymptomatic subjects, in whom serum pepsinogen (PG) and H. pylori antibody titer had been measured to assess the activity and stage of H. pylori-associated chronic gastritis, was followed for up to 16 years, and cancer development was investigated. In subjects with a serologically diagnosed healthy stomach (H. pylori-negative/CAG-negative), cancer incidence rate was low, at 16/100,000 person-years. With the establishment of H. pylori infection and progression of chronic gastritis, significant stepwise cancer risk elevations were seen from CAG-free subjects (H. pylori-positive/CAG-negative) [hazard ratio (HR) = 8.9, 95% confidence interval (CI) = 2.7-54.7] to subjects with CAG (H. pylori-positive/CAG-positive) (HR = 17.7, 95% CI = 5.4-108.6) and finally to subjects with metaplastic gastritis (H. pylori-negative/CAG-positive) (HR = 69.7, 95% CI = 13.6-502.9). In H. pylori-infected CAG-free subjects, significantly elevated cancer risk was observed in the subgroup with active inflammation-based high PG II level or potent immune response-based high H. pylori antibody titer; the former was associated with a particularly high risk of diffuse-type cancer, and both subgroups showed high cancer incidence rates of around 250/100,000 person-years, comparable to that in subjects with CAG. No such risk elevation was observed in H. pylori-infected subjects with CAG. These results clearly indicate that gastric cancer develops mainly from the gastritis-atrophy-metaplasia-cancer sequence and partly from active inflammation-based direct carcinogenesis, and that serum levels of PG and H. pylori antibody titer provide indices of cancer development in H. pylori-infected subjects.
International journal of cancer. Journal international du cancer.Int J Cancer.2014 Mar 15;134(6):1445-57. doi: 10.1002/ijc.28470. Epub 2013 Oct 3.
Our study investigated the relationship between gastric cancer development and activity of Helicobacter pylori-associated chronic gastritis or the resulting chronic atrophic gastritis (CAG). A cohort of 4,655 healthy asymptomatic subjects, in whom serum pepsinogen (PG) and H. pylori antibody titer h
PMID 24009139

Amplification of steroid-mediated SP-B expression by physiological levels of caffeine.

Fehrholz M1, Hütten M, Kramer BW, Speer CP, Kunzmann S.Author information 1Univ. Children's Hospital, Univ. of Wuerzburg, Josef-Schneider-Str. 2, D-97080 Wuerzburg, Germany. markus.fehrholz@uni-wuerzburg.de.AbstractFactors positively influencing surfactant homeostasis in general and surfactant protein B (SP-B) expression in particular are considered of clinical importance regarding an improvement of lung function in preterm infants. The objective of this study was to identify effects of physiological levels of caffeine on glucocorticoid-mediated SP-B expression in vitro and in vivo. Levels of SP-B and pepsinogen C were quantified by quantitative real-time RT-PCR or immunoblotting in NCI-H441 cells daily exposed to caffeine and/or dexamethasone (DEX). In vivo, SP-B expression was analyzed in bronchoalveolar lavage (BAL) of preterm sheep exposed to antenatal DEX and/or postnatal caffeine. If DEX and caffeine were continuously present, SP-B mRNA and protein levels were increased for up to 6 days after induction (P < 0.05). Additionally, caffeine enhanced SP-B mRNA expression in DEX-pretreated cells (P < 0.05). Moreover, caffeine amplified DEX-induced pepsinogen C mRNA expression (P < 0.05). After short-term treatment with caffeine in vivo, only slightly higher SP-B levels could be detected in BAL of preterm sheep following antenatal DEX, combined with an increase of arterial oxygen partial pressure (P < 0.01). Our data demonstrated that the continuous presence of caffeine in vitro is able to amplify DEX-mediated SP-B expression. In contrast, short-term improvement of lung function in vivo is likely to be independent of altered SP-B transcription and translation. An impact of caffeine on release of surfactant reservoirs from lamellar bodies could, however, quickly affect SP-B content in BAL, which has to be further investigated. Our findings indicate that caffeine is able to amplify main effects of glucocorticoids that result from changes in surfactant production, maturation, and release.
American journal of physiology. Lung cellular and molecular physiology.Am J Physiol Lung Cell Mol Physiol.2014 Jan 1;306(1):L101-9. doi: 10.1152/ajplung.00257.2013. Epub 2013 Oct 25.
Factors positively influencing surfactant homeostasis in general and surfactant protein B (SP-B) expression in particular are considered of clinical importance regarding an improvement of lung function in preterm infants. The objective of this study was to identify effects of physiological levels of
PMID 24163141

The Interaction Effects of pri-let-7a-1 rs10739971 with PGC and ERCC6 Gene Polymorphisms in Gastric Cancer and Atrophic Gastritis.

Xu Q, Liu JW, He CY, Sun LP, Gong YH, Jing JJ, Xing CZ, Yuan Y.Author information Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China ; Key Laboratory of Cancer Etiology and Prevention, China Medical University, Liaoning Provincial Education Department, Shenyang, Liaoning, People's Republic of China.AbstractBACKGROUND: The aim of this study was to investigate the interaction effects of pri-let-7a-1 rs10739971 with pepsinogen C (PGC) and excision repair cross complementing group 6 (ERCC6) gene polymorphisms and its association with the risks of gastric cancer and atrophic gastritis. We hoped to identify miRNA polymorphism or a combination of several polymorphisms that could serve as biomarkers for predicting the risk of gastric cancer and its precancerous diseases.
PloS one.PLoS One.2014 Feb 25;9(2):e89203. doi: 10.1371/journal.pone.0089203. eCollection 2014.
BACKGROUND: The aim of this study was to investigate the interaction effects of pri-let-7a-1 rs10739971 with pepsinogen C (PGC) and excision repair cross complementing group 6 (ERCC6) gene polymorphisms and its association with the risks of gastric cancer and atrophic gastritis. We hoped to identify
PMID 24586594

Japanese Journal

血清ペプシノーゲン値による低用量アスピリン胃粘膜傷害のリスク評価 (特集高齢化社会におけるNSAIDs消化管障害)

飯島克則,小池智幸,下瀬川徹
消化器内科 59(2), 111-113, 2014-08
NAID 40020195602

ABCC11/MRP8 Expression in the Gastrointestinal Tract and a Novel Role for Pepsinogen Secretion

Matsumoto Hirofumi,Tsuchiya Tomoshi,Yoshiura Koh-ichiro,Hayashi Tomayoshi,Hidaka Shigekazu,Nanashima Atsushi,Nagayasu Takeshi
ACTA HISTOCHEMICA ET CYTOCHEMICA 47(3), 85-94, 2014-06-28
… Additional immuno-fluorescence assays revealed co-localization of ABCC11/MRP8 and pepsinogen I in normal gastric chief cells. … Furthermore, the ABCC11 mRNA-suppressed NCI-N87 gastric cancer cell line failed to secret pepsinogen I extracellularly. … Our results indicated a novel function of ABCC11/MRP8 in the regulation of pepsinogen I secretion in the normal gastric chief cells. …
NAID 120005477059