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The Interface between Syntax and Morphology: Taiwanese Verbal Complexes
( Huei Ling Lin ) 한국언어정보학회 2002 국제 워크샵 Vol.2002 No.-
Taiwanese abounds with verbal complexes. Among them, phasal complexes, resultative complexes, and directional complexes are alike in that their second component denotes some sort of result. Moreover, they behave similarly in that they can occur in V-ho-V, V-e/be-V, and V-bo-V forms. Despite the similarities, they still differ from one another in several aspects, such as whether objects are allowed inside or after the verbal complex, whether infixing changes their basic meaning, etc. This paper examines their individual properties carefully and proposes that these three types of complexes are all different from one another in their formation and thus the difference in their syntactic behavior. Directional complexes are syntactic phrases, resultative complexes are compounds derived in syntax, and while some phasal complexes are also syntactically derived compounds, others are compounds formed in the lexicon. This paper aims to argue that words (or compounds in this case) can be formed in syntax as well as in the lexicon.
Angel Chao,Yi-Hao Lin,Lan-Yan Yang,Ren-Chin Wu,Wei-Yang Chang,Pi-Yueh Chang,Shih-Cheng Chang,Chiao-Yun Lin,Huei-Jean Huang,Cheng-Tao Lin,Hung-Hsueh Chou,Kuan-Gen Huang,Wen-Ling Kuo,Ting-Chang Chang,Ch 대한부인종양학회 2020 Journal of Gynecologic Oncology Vol.31 No.3
Objective: The characteristics of patients with metachronous breast and ovarian malignancies and the pathogenic role of BRCA1/2 mutations remain poorly understood. We investigated these issues through a review of hospital records and nationwide Taiwanese registry data, followed by BRCA1/2 mutation analysis in hospital-based cases. Methods: We retrospectively retrieved consecutive clinical records of Taiwanese patients who presented with these malignancies to our hospital between 2001 and 2017. We also collected information from the Data Science Center of the Taiwan Cancer Registry (TCR) between 2007 and 2015. Next-generation sequencing and multiplex ligation-dependent probe amplification were used to identify BRCA1/2 mutations and large genomic rearrangements, respectively. When BRCA1/2 mutations were identified in index cases, pedigrees were reconstructed and genetic testing was offered to family members. Results: A total of 12,769 patients with breast cancer and 1,537 with ovarian cancer were retrieved from our hospital records. Of them, 28 had metachronous breast and ovarian malignancies. We also identified 113 cases from the TCR dataset. Eighteen hospital-based cases underwent BRCA1/2 sequencing and germline pathogenic mutations were detected in 7 patients (38.9%, 5 in BRCA1 and 2 in BRCA2). All BRCA1/2 mutation carriers had ovarian high-grade serous carcinomas. Of the 12 patients who were alive at the time of analysis, 5 were BRCA1/2 mutation carriers. All of them had family members with BRCA1/2-associated malignancies. Conclusions: Our results provide pilot evidence that BRCA1/2 mutations are common in Taiwanese patients with metachronous breast and ovarian malignancies, supporting the clinical utility of genetic counseling.
Hung-Jen Liu,Ping-Yuan Lin,Ling-Rung Wang,Hsue-Yin Hsu,Ming-Huei Liao,Wen-Ling Shih 한국분자세포생물학회 2008 Molecules and cells Vol.26 No.4
The first ORF of the ARV S1133 S1 segment encodes the nonstructural protein p10, which is responsible for the induction of cell syncytium formation. However, p10-dependent signaling during syncytium formation is fully unknown. Here, we show that dominant negative RhoA, Rho inhibitor C3 exoenzyme, ROCK/Rho-kinase inhibitor Y-27632 and Rac1 inhibitor NSC23766 inhibit p10-mediated cell fusion. p10 over-expression is concomitant with activation and membrane translocation of RhoA and Rac1, but not cdc42. RhoA and Rac1 downstream events, including JNK phosphorylation and transcription factor AP-1 and NF-B activation, as well as MLC expression and phosphorylation are simultaneously activated by p10. p10 point mutant T13M possessed 20% fusion-inducing ability and four p10 fusion-deficient mutants V15M, V19M, C21S and L32A reduced or lost their ability to activate RhoA and Rac1 signaling. We conclude that p10-mediated syncytium formation proceeds by utilizing RhoA and Rac1-dependent signaling.