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Masamitsu Ubukata Isao Ohsawa Hiroki Suzuki Rin Asao Yuya Nakamura Hirofumi Nishida Masayuki Nakamura Kosaku Nitta Yoshikazu Goto Hiromichi Gotoh 《Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy》2020,24(4):393-399
Ceftriaxone‐associated biliary pseudolithiasis is common among children; however, there are only a few reports of pseudolithiasis in adult patients on HD. This retrospective cohort study included 278 adult patients on ceftriaxone therapy from 1 February 2016 to 1 September 2018. Pseudolithiasis was defined as a new development of sludge or stones in the gallbladder within 60 days of ceftriaxone therapy. After excluding patients with preexisting gallstones and a history of cholecystectomy, 113 patients on maintenance HD, and another 98 patients were enrolled as the HD and control group, respectively. Thirteen patients developed pseudolithiasis. Its incidence was significantly higher in the HD group than that in the control group. Multivariate logistic regression analyses showed that development of pseudolithiasis was significantly associated with HD and ceftriaxone dose. Therefore, HD in patients receiving ceftriaxone therapy appears to be associated with a risk of pseudolithiasis. These findings highlight the need for careful follow‐up. 相似文献
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Rin Asao Katsuhiko Asanuma Fumiko Kodama Miyuki Akiba-Takagi Yoshiko Nagai-Hosoe Takuto Seki Yukihiko Takeda Isao Ohsawa Satoshi Mano Kiyoshi Matsuoka Hiroyuki Kurosawa Shinya Ogasawara Yoshiaki Hirayama Sakari Sekine Satoshi Horikoshi Masanori Hara Yasuhiko Tomino 《Clinical journal of the American Society of Nephrology》2012,7(9):1385-1393
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Shin Y Kim JB Choi JS Lee KM Shin SR Park SH Kim JW Lee MS 《Taehan Sohwagi Hakhoe chi》2012,59(3):257-259
A colonic muco-submucosal elongated polyp (CMSEP) was identified at colonoscopy in a 53-year-old male patient with lower gastrointestinal bleeding. Non-polypoid depressed type of early cancer was noted at the tip of the colonic polyp. The CMSEP is very rare and incidentally found in most cases. Moreover, its association with colonic neoplasia is extremely rare. To our knowledge, this is the second case report of CMSEP associated with a cancerous transformation. 相似文献
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Cilostazol suppresses β‐amyloid production by activating a disintegrin and metalloproteinase 10 via the upregulation of SIRT1‐coupled retinoic acid receptor‐β 下载免费PDF全文
Hye Rin Lee Hwa Kyoung Shin So Youn Park Hye Young Kim Won Suk Lee Byung Yong Rhim Ki Whan Hong Chi Dae Kim 《Journal of neuroscience research》2014,92(11):1581-1590
The accumulation of plaques of β‐amyloid (Aβ) peptides, a hallmark of Alzheimer's disease, results from the sequential cleavage of amyloid precursor protein (APP) by activation of β‐ and γ‐secretases. However, the production of Aβ can be avoided by alternate cleavage of APP by α‐and γ‐secretases. We hypothesized that cilostazol attenuates Aβ production by increasing a disintegrin and metalloproteinase 10 (ADAM10)/α‐secretase activity via SIRT1‐coupled retinoic acid receptor‐β (RARβ) activation in N2a cells expressing human APP Swedish mutation (N2aSwe). To evoke endogenous Aβ overproduction, the culture medium was switched from medium containing 10% fetal bovine serum (FBS) to medium containing 1% FBS, and cells were cultured for 3~24 hr. After depletion of FBS in media, N2aSwe cells showed increased accumulations of full‐length APP (FL‐APP) and Aβ in a time‐dependent manner (3–24 hr) in association with decreased ADAM10 protein expression. When pretreated with cilostazol (10–30 μM), FL‐APP and Aβ levels were significantly reduced, and ADAM10 and α‐secretase activities were restored. Furthermore, the effect of cilostazol on ADAM10 expression was antagonized by pretreating Rp‐cAMPS and sirtinol and by SIRT1‐gene silencing. In the N2aSwe cells overexpressing the SIRT1 gene, ADAM10, and sAPPα levels were significantly elevated. In addition, like all‐trans retinoic acid, cilostazol enhanced the protein expressions of RARβ and ADAM10, and the cilostazol‐stimulated ADAM10 elevation was significantly attenuated by LE135 (a RARβ inhibitor), sirtinol, and RARβ‐gene silencing. In conclusion, cilostazol suppresses the accumulations of FL‐APP and Aβ by activating ADAM10 via the upregulation of SIRT1‐coupled RARβ. © 2014 Wiley Periodicals, Inc. 相似文献