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101.
Kentaro Wakamatsu Nobuhiko Nagata Hiroyuki Kumazoe Keishi Oda Hiroshi Ishimoto Michihiro Yoshimi Shohei Takata Minako Hamada Yoshifusa Koreeda Kouji Takakura Miwa Ishizu Makiko Hara Shinji Ise Miiru Izumi Takashi Akasaki Sanae Maki Masaharu Kawabata Hiroshi Mukae Masayuki Kawasaki 《Respiratory investigation》2017,55(1):16-23
Background
The prognostic significance of serial measurements of serum KL-6 levels in patients with idiopathic pulmonary fibrosis (IPF) is unclear; hence, it was assessed in this study.Methods
Medical records of 66 patients with IPF, who were not treated with pirfenidone prior to enrollment, were retrospectively reviewed for information on clinical progress, forced vital capacity (FVC), survival, and serum KL-6 levels. We assessed initial serum levels of KL-6, serial changes in serum KL-6 levels, yearly decline in FVC (ΔFVC), and the rate of decline (%ΔFVC).Results
Patients with increased serum KL-6 levels during follow-up had a significantly steeper decline in ΔFVC than those with no KL-6 increase (?201 vs. ?50.7 ml/year; p=0.0001). Patients with both initial serum KL-6 ≥1000 U/ml and serial increases in serum KL-6 had the steepest decline, while those with both initial serum KL-6 <1000 ml and no serial increases in KL-6 had the least decline in ΔFVC and %ΔFVC. Relative to the non-increased KL-6 group, survival in the increased KL-6 group tended to be poorer (p=0.0530). Patients with both initial serum KL-6 values <1000 U/ml and no serial increase in KL-6 had more favorable prognoses than those with serial increases in KL-6 or initial serum KL-6 values ≥1000 U/ml (p<0.0044). Prognosis was significantly poorer in patients with serial KL-6 changes >51.8 U/ml/year than in those with serial KL-6 changes <51.8 U/ml/year (p=0.0009).Conclusion
Thus, serial serum KL-6 measurements can be useful for assessing prognosis in patients with IPF. 相似文献102.
Tsuneyuki Sato Motokazu Naruse Kentaro Toyosu Makiko Seno 《Macromolecular chemistry and physics.》1996,197(11):3541-3554
The aged system of lanthanum versatate ( 1 ) and p-chlorobenzenediazonium tetrafluoroborate ( 2 ) was found to initiate effectively the radical polymerization of acrylic monomers including alkyl methacrylates, butyl acrylate and acrylonitrile, although its initiating activity is lower than that of the non-aged system. The polymerization of methyl methacrylate ( 3 ) with the aged 1/2 system was studied kinetically in acetone. The initial polymerization rate (Rp) is expressed by Rp = Kċ[aged 1/2 ]0.80 ċ [ 3 ]1.1 at 50°C. The overall activation energy of the polymerization is 59.0 kJ ċ mol−1. The molecular weight of the resulting poly( 3 ) formed in the early stage increases with increasing conversion. The polymerization system involves a persistent radical showing a four-line EPR spectrum with a g-value of 2.004. A three-line spectrum due to the nitroxyl radical was also observed at lower monomer concentrations. The total concentration of persistent radicals was found to correspond well to the instantaneous polymerization rate. The copolymerization of styrene (M1) and 3 (M2) with the aged initiator system was examined at 50°C in acetone. r1 and r2 are 0.19 and 0.47, respectively. The former is considerably smaller than that (0.52) reported for the conventional radical polymerization. 相似文献
103.
Zuo Shogo Sho Masayuki Sawai Toshio Kanehiro Hiromichi Maeda Kosaku Yoshida Makiko Tsukada Ryo Nomura Motonari Okuyama Hiroomi 《Pediatric surgery international》2020,36(2):137-143
Pediatric Surgery International - The programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) pathway has garnered much attention for its roles in clinical oncology. The aim of this study was... 相似文献
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Makiko Kawaguchi Koji Yamamoto Hiroaki Kataoka Aya Izumi Fumiki Yamashita Takumi Kiwaki Takahiro Nishida Eric Camerer Tsuyoshi Fukushima 《Cancer science》2020,111(4):1193-1202
Hepatocyte growth factor activator inhibitor‐1 (HAI‐1), encoded by the SPINT1 gene, is a membrane‐bound protease inhibitor expressed on the surface of epithelial cells. Hepatocyte growth factor activator inhibitor‐1 regulates type II transmembrane serine proteases that activate protease‐activated receptor‐2 (PAR‐2). We previously reported that deletion of Spint1 in ApcMin/+ mice resulted in accelerated formation of intestinal tumors, possibly through enhanced nuclear factor‐κB signaling. In this study, we examined the role of PAR‐2 in accelerating tumor formation in the ApcMin/+ model in the presence or absence of Spint1. We observed that knockout of the F2rl1 gene, encoding PAR‐2, not only eliminated the enhanced formation of intestinal tumors caused by Spint1 deletion, but also reduced tumor formation in the presence of Spint1. Exacerbation of anemia and weight loss associated with HAI‐1 deficiency was also normalized by compound deficiency of PAR‐2. Mechanistically, signaling triggered by deregulated protease activities increased nuclear translocation of RelA/p65, vascular endothelial growth factor expression, and vascular density in ApcMin/+‐induced intestinal tumors. These results suggest that serine proteases promote intestinal carcinogenesis through activation of PAR‐2, and that HAI‐1 plays a critical tumor suppressor role as an inhibitor of matriptase, kallikreins, and other PAR‐2 activating proteases. 相似文献
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Neutrophilic panniculitis with vasculitis in a melanoma patient treated with vemurafenib: a case report and its management
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110.