http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Imaging Spectrum after Pancreas Transplantation with Enteric Drainage
Jian-Ling Chen,Rheun-Chuan Lee,Yi-Ming Shyr,Sing-E Wang,Hsiuo-Shan Tseng,Hsin-Kai Wang,Shan-Su Huang,Cheng-Yen Chang 대한영상의학회 2014 Korean Journal of Radiology Vol.15 No.1
Since the introduction of pancreas transplantation more than 40 years ago, surgical techniques and immunosuppressive regiments have improved and both have contributed to increase the number and success rate of this procedure. However, graft survival corresponds to early diagnosis of organ-related complications. Thus, knowledge of the transplantation procedure and postoperative image anatomy are basic requirements for radiologists. In this article, we demonstrate the imaging spectrum of pancreas transplantation with enteric exocrine drainage.
Wei-Teh Li,Jau-Ming Chen,Ruo-Shan Tseng,Tzu-Ling Lai 한국기상학회 2022 Asia-Pacific Journal of Atmospheric Sciences Vol.58 No.1
September 2016 harbored record-breaking three tropical cyclones (TCs) affecting Taiwan within a month. Multiple modulating processes governing these three TC events and associated rainfall and intensification features are examined. September 2016 fell in a La Niña phase. For interannual variability, major warm sea surface temperature (SST) anomalies in September 2016 shifted eastward toward the tropical western North Pacific (WNP) compared to the Maritime Continent during other La Niña events. These SST anomalies induced strong convergence and convection anomalies facilitating TC formation. The TCs formed in the joint region between a northern anticyclonic anomaly over the northern WNP and a southern cyclonic anomaly extending from the tropical WNP toward Taiwan. They were steered by anomalous easterly/southeasterly flows northwestward toward an anomalous cyclonic center overlying Taiwan, leading to intensive TC activity affecting Taiwan. For intraseasonal variability, the three TCs of September 2016 were steered by anomalous easterly/southeasterly flows in the southern section of a 30–60-day anomalous anticyclone over the subtropical WNP northwestward toward a 30–60-day anomalous cyclone that lay over Taiwan. During these events, local rainfall in Taiwan was mainly affected by moisture convergence due to 3–10-day transient anomalies, rather than intraseasonal anomalies. For TC intensification processes, faster intensification was assisted by decreases in vertical wind shear and increases in upward motion, moisture convergence, upper-level divergence, and SST. Intensification processes were mainly affected by transient anomalies. Overall, interannual and intraseasonal anomalies modulated TC genesis and movement, while transient anomalies influenced local rainfall and intensification processes.
Chun-Yu Liu,Tzu-Ting Huang,Pei-Yi Chu,Chun-Teng Huang,Chia-Han Lee,Wan-Lun Wang,Ka-Yi Lau,Wen-Chun Tsai,Tzu-I Chao,Jung-Chen Su,Ming-Huang Chen,Chung-Wai Shiau,Ling-Ming Tseng,Kuen-Feng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Triple-negative breast cancer (TNBC) remains difficult to treat and urgently needs new therapeutic options. Nintedanib, a multikinase inhibitor, has exhibited efficacy in early clinical trials for HER2-negative breast cancer. In this study, we examined a new molecular mechanism of nintedanib in TNBC. The results demonstrated that nintedanib enhanced TNBC cell apoptosis, which was accompanied by a reduction of p-STAT3 and its downstream proteins. STAT3 overexpression suppressed nintedanib-mediated apoptosis and further increased the activity of purified SHP-1 protein. Moreover, treatment with either a specific inhibitor of SHP-1 or SHP-1-targeted siRNA reduced the apoptotic effects of nintedanib, which validates the role of SHP-1 in nintedanib-mediated apoptosis. Furthermore, nintedanib-induced apoptosis was attenuated in TNBC cells expressing SHP-1 mutants with constantly open conformations, suggesting that the autoinhibitory mechanism of SHP-1 attenuated the effects of nintedanib. Importantly, nintedanib significantly inhibited tumor growth via the SHP-1/p-STAT3 pathway. Clinically, SHP-1 levels were downregulated, whereas p-STAT3 was upregulated in tumor tissues, and SHP-1 transcripts were associated with improved disease-free survival in TNBC patients. Our findings revealed that nintedanib induces TNBC apoptosis by acting as a SHP-1 agonist, suggesting that targeting STAT3 by enhancing SHP-1 expression could be a viable therapeutic strategy against TNBC.