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排序方式: 共有1416条查询结果,搜索用时 15 毫秒
131.
Yokoyama K Ogawa T Fujita A Asaoka K Sakai J 《Journal of biomedical materials research. Part A》2007,82(3):558-567
The fracture of Ni-Ti superelastic alloy has been investigated by a sustained tensile-loading test in physiological saline solution containing hydrogen peroxide (0.15M NaCl + 0.3M H(2)O(2)). The fracture always occurs when the applied stress exceeds the critical stress for martensite transformation. In contrast, under a low applied stress, the fracture does not always occur within 1000 h. The fracture is probably mainly caused by localized corrosion associated with the preferential dissolution of nickel ions. In 0.3M H(2)O(2) solution without NaCl, the fracture does not occur even under a high applied stress. The results of the present study imply that one reason for the fracture of the Ni-Ti superelastic alloy in vivo is localized corrosion due to the synergistic effects of hydrogen peroxide and sodium chloride under applied stress. 相似文献
132.
133.
Kosuke Kanazawa Kazuhiro Kishimoto Miyuki Nomura Koreyuki Kurosawa Hiroyuki Kato Yui Inoue Koh Miura Katsuya Fukui Yoji Yamashita Ikuro Sato Hiroyuki Tsuji Toshio Watanabe Takuji Tanaka Jun Yasuda Nobuhiro Tanuma Hiroshi Shima 《Cancer science》2021,112(6):2233-2244
According to TCGA database, mutations in PPP6C (encoding phosphatase PP6) are found in c. 10% of tumors from melanoma patients, in which they coexist with BRAF and NRAS mutations. To assess PP6 function in melanoma carcinogenesis, we generated mice in which we could specifically induce BRAF(V600E) expression and delete Ppp6c in melanocytes. In these mice, melanoma susceptibility following UVB irradiation exhibited the following pattern: Ppp6c semi-deficient (heterozygous) > Ppp6c wild-type > Ppp6c-deficient (homozygous) tumor types. Next-generation sequencing of Ppp6c heterozygous and wild-type melanoma tumors revealed that all harbored Trp53 mutations. However, Ppp6c heterozygous tumors showed a higher Signature 1 (mitotic/mitotic clock) mutation index compared with Ppp6c wild-type tumors, suggesting increased cell division. Analysis of cell lines derived from either Ppp6c heterozygous or wild-type melanoma tissues showed that both formed tumors in nude mice, but Ppp6c heterozygous tumors grew faster compared with those from the wild-type line. Ppp6c knockdown via siRNA in the Ppp6c heterozygous line promoted the accumulation of genomic damage and enhanced apoptosis relative to siRNA controls. We conclude that in the presence of BRAF(V600E) expression and UV-induced Trp53 mutation, Ppp6c haploinsufficiency promotes tumorigenesis. 相似文献
134.
Takahiro Suyama Terue Yui Atsuo Horiuchi Rie Irie Yoshiyuki Osamura Naoki Miyao 《Journal of Clinical and Experimental Hematopathology》2021,61(1):48
Tumor flare reaction (TFR) is a unique immune-mediated tumor recognition phenomenon presenting as rapid enlargement of the tumor, which mimics disease progression, developing in the early stage of treatment using immunomodulatory drugs or immune checkpoint inhibitors. A 59-year-old man with follicular lymphoma had residual tumor burden in the left hilar lymph nodes after R-CHOP therapy, and received lenalidomide and rituximab (R2) therapy. He developed respiratory distress on day 11 of R2 therapy. Chest X-ray and CT demonstrated left lung atelectasis due to left hilar lymph node swelling. We performed transbronchial lung biopsy on day 20 of R2 therapy. The biopsied left bronchus tissue exhibited extensive necrosis, which had a B-cell phenotype consistent with that of follicular lymphoma. Neither NK cells nor cytotoxic T cells were detected. It was unclear whether the immune effector cells disappeared at the time of transbronchial lung biopsy. Atelectasis in our patient improved by continuing R2 therapy beyond TFR. 相似文献
135.
Baba Yuto Kikuchi Eiji Shigeta Keisuke Ogihara Koichiro Matsushima Masashi Nishimoto Yui Murata Yasuaki Asakura Hirotaka Oyama Masafumi Mizuno Ryuichi Oya Mototsugu 《International journal of clinical oncology / Japan Society of Clinical Oncology》2021,26(11):2094-2103
International Journal of Clinical Oncology - The effects of the type of anesthesia (spinal (SA) vs. general (GA)) used for transurethral resection of bladder tumor (TURBT) on non-muscle invasive... 相似文献
136.
Underrecognized entity of the transient rise in the atrial capture threshold early after dual‐chamber pacemaker implantation 下载免费PDF全文
137.
Miwa H Asaoka D Hojo M Iijima K Sato N 《Nihon rinsho. Japanese journal of clinical medicine》2004,62(8):1441-1446
Recent advancement in the research of GERD has revealed that endoscopy negative GERD may not be a milder form of erosive GERD and may have different pathogenesis. We have previously proven that hypersensitivity to the acid of the esophageal mucosa plays an important role in its pathogenesis. Regarding the mechanisms for the esophageal hypersensitivity, we hypothesized that the tight junction proteins of the esophageal mucosa are fully or partially impaired in GERD patients. Accordingly, we immunohistologically studied the expression of various tight junction proteins using the rat reflux esophagitis model. The results demonstrated that the several kinds of tight junction proteins are expressed differently in the various parts of esophagus and their expression altered according to the development of reflux esophagitis. 相似文献
138.
Guleng B Tateishi K Kanai F Jazag A Ohta M Asaoka Y Ijichi H Tanaka Y Imamura J Ikenoue T Fukushima Y Morikane K Miyagishi M Taira K Kawabe T Omata M 《World journal of gastroenterology : WJG》2005,11(35):5455-5459
AIM: Vascular endothelial growth factor (VEGF) is a potent mediator of peritoneal fluid accumulation following tumor progression. This study investigated the role of VEGF secreted by cancerous cells in the formation of malignant ascites. METHODS: VEGF expression was eliminated by knockdown in the pancreas cancer cell-line PancO2 using vector-based short-hairpin type RNA interference (RNAi). Malignant ascites formation in the mouse was analyzed by intraperitoneal injection of PancO2 cells expressing VEGF or with expression knockdown. RESULTS: The VEGF knockdown PancO2 cell was successfully established. Knockdown of VEGF did not affect cancer cell proliferation in vitro or in vivo. The volume of ascites following peritoneal expansion of the tumor in VEGF knockdown cells and control cells did not differ statistically in this in vivo study. Moreover, the VEGF concentration in the ascites did not differ statistically. CONCLUSION: Malignant ascites formation might be mediated by VEGF production in noncancerous tissues, such as stromal compartments. An anti-VEGF strategy against malignant ascites could be applied to various tumors regardless of whether they secrete VEGF. 相似文献
139.
Garcia-Calvo M Lisnock J Bull HG Hawes BE Burnett DA Braun MP Crona JH Davis HR Dean DC Detmers PA Graziano MP Hughes M Macintyre DE Ogawa A O'neill KA Iyer SP Shevell DE Smith MM Tang YS Makarewicz AM Ujjainwalla F Altmann SW Chapman KT Thornberry NA 《Proceedings of the National Academy of Sciences of the United States of America》2005,102(23):8132-8137
Ezetimibe is a potent inhibitor of cholesterol absorption that has been approved for the treatment of hypercholesterolemia, but its molecular target has been elusive. Using a genetic approach, we recently identified Niemann-Pick C1-Like 1 (NPC1L1) as a critical mediator of cholesterol absorption and an essential component of the ezetimibe-sensitive pathway. To determine whether NPC1L1 is the direct molecular target of ezetimibe, we have developed a binding assay and shown that labeled ezetimibe glucuronide binds specifically to a single site in brush border membranes and to human embryonic kidney 293 cells expressing NPC1L1. Moreover, the binding affinities of ezetimibe and several key analogs to recombinant NPC1L1 are virtually identical to those observed for native enterocyte membranes. KD values of ezetimibe glucuronide for mouse, rat, rhesus monkey, and human NPC1L1 are 12,000, 540, 40, and 220 nM, respectively. Last, ezetimibe no longer binds to membranes from NPC1L1 knockout mice. These results unequivocally establish NPC1L1 as the direct target of ezetimibe and should facilitate efforts to identify the molecular mechanism of cholesterol transport. 相似文献
140.
Relationship between flow dynamics in the left atrium and hemostatic abnormalities in patients with nonvalvular atrial fibrillation 总被引:10,自引:0,他引:10
Shinohara H Fukuda N Soeki T Takeichi N Yui Y Tamura Y Oki T 《Japanese heart journal》1998,39(6):721-730
To investigate the relationship between left atrial (LA) flow dynamics and hemostatic markers in nonvalvular atrial fibrillation (AF), 45 patients with nonvalvular AF who had not received anticoagulants were evaluated by transesophageal echocardiography. We determined the LA appendage flow and the presence of LA spontaneous echo contrast (SEC) or thrombus. We measured plasma levels of thrombin-antithrombin III complex (TAT), fibrinopeptide A, D-dimer, beta-thromboglobulin, and platelet factor 4 in peripheral blood as hemostatic markers. The patients were divided into a low-velocity group (n = 19; sum of peak emptying and filling LA appendage flow velocities < 40 cm/s) and a high-velocity group (n = 26; > or = 40 cm/s). The maximum LA diameter was significantly greater and the LA expansion fraction was significantly smaller in the low-velocity group than in the high-velocity group. LA SEC or thrombus was observed in 11 patients (58%) in the low-velocity group, but not in any patients in the high-velocity group (p < 0.001). The plasma levels of TAT, fibrinopeptide A, D-dimer, beta-thromboglobulin, and platelet factor 4 were significantly higher in the low-velocity group than in the high-velocity group. The plasma levels of TAT, fibrinopeptide A, beta-thromboglobulin, and platelet factor 4 were significantly higher in 8 patients without LA SEC or thrombus in the low-velocity group than in 26 patients in the high-velocity group. Patients with nonvalvular AF accompanied by an enlarged and dysfunctioning LA and a decreased LA appendage flow velocity had increased intravascular coagulation-fibrinolysis activity and platelet activation. These abnormalities may be closely related to the thrombogenetic state in patients with nonvalvular AF. 相似文献