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논문 기본 정보

자료유형
학술저널
저자정보
Satoshi Sugino (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Ken Inoue (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Reo Kobayashi (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Ryohei Hirose (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Toshifumi Doi (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Akihito Harusato (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Osamu Dohi (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Naohisa Yoshida (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Kazuhiko Uchiyama (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Takeshi Ishikawa (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Tomohisa Takagi (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Hiroaki Yasuda (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Hideyuki Konishi (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr) Yasuko Hirai (Department of Human Immunology and Nutrition Science Kyoto Prefectural University of Medicine Kyoto) Katsura Mizushima (Department of Human Immunology and Nutrition Science Kyoto Prefectural University of Medicine Kyoto) Yuji Naito (Department of Human Immunology and Nutrition Science Kyoto Prefectural University of Medicine Kyoto) Toshifumi Tsuji (Department of Gastroenterology and Hepatology Fukuchiyama City Hospital Kyoto Japan) Takashi Okuda (Department of Gastroenterology and Hepatology Fukuchiyama City Hospital Kyoto Japan) Keizo Kagawa (Department of Gastroenterology and Hepatology Fukuchiyama City Hospital Kyoto Japan) Makoto Tominaga (Division of Cell Signaling National Institute for Physiological Sciences National Institutes of Nat) Yoshito Itoh (Department of Molecular Gastroenterology and Hepatology Kyoto Prefectural University of Medicine Gr)
저널정보
대한소화관운동학회(현 대한소화기능성질환.운동학회) Journal of Neurogastroenterology and Motility (JNM) Journal of Neurogastroenterology and Motility (JNM) Vol.28 No.4
발행연도
2022.10
수록면
693 - 705 (13page)
DOI
10.5056/jnm21198

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"Background/Aims Several studies have assessed the effect of cool temperature on colonic peristalsis. Transient receptor potential melastatin 8 (TRPM8) is a temperature-sensitive ion channel activated by mild cooling expressed in the colon. We examined the antispasmodic effect of cool temperature on colonic peristalsis in a prospective, randomized, single-blind trial and based on the video imaging and intraluminal pressure of the proximal colon in rats and TRPM8-deficient mice. Methods In the clinical trial, we randomly assigned a total of 94 patients scheduled to undergo colonoscopy to 2 groups: the mildly cool water (n = 47) and control (n = 47) groups. We used 20 mL of 15°C water for the mildly cool water. The primary outcome was the proportion of subjects with improved peristalsis after treatment. In the rodent proximal colon, we evaluated the intraluminal pressure and performed video imaging of the rodent proximal colon with cool water administration into the colonic lumen. Clinical trial registry website (Trial No. UMIN-CTR; UMIN000030725). Results In the randomized controlled trial, after treatment, the proportion of subjects with no peristalsis with cool water was significantly higher than that in the placebo group (44.7% vs 23.4%; P < 0.05). In the rodent colon model, cool temperature water was associated with a significant decrease in colonic peristalsis through its suppression of the ratio of peak frequency (P < 0.05). Cool temperature-treated TRPM8-deficient mice did not show a reduction in colonic peristalsis compared with wild-type mice. Conclusion For the first time, this study demonstrates that cool temperature-dependent suppression of colonic peristalsis may be associated with TRPM8 activation."

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