Chao-Wei Liu

Mr. Chao-Wei Liu

orcid

Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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29 August 2021 in Journal of Clinical Medicine
Verified
Journal Article
Open access
PDF file
TCTso-Hsiao Chen
Tso-Hsiao Chen
CLChao-Wei Liu
Chao-Wei Liu
YHYi-Hsien Ho
Yi-Hsien Ho
CHChun-Kai Huang
Chun-Kai Huang
Ching-Sheng HungChing-Sheng Hung
Ching-Sheng Hung
JLJung-Chun Lin
Jung-Chun Lin
A growing body of study have documented the association of gut dysbiosis or fecal metabolites with chronic kidney disease (CKD). However, it is not clear whether the phenomenon simply reflects the microenvironment changes correlated with the CKD severity or contributes to the progression of CKD. In this study, we identified the gut microbiota and metabolite in feces samples correlated with CKD severity using the Nanopore long-read sequencing platform and UPLC-coupled MS/MS approach. A cross-sectional cohort study was performed from 1 June 2020 to 31 December 2020. One hundred and fifty-six clinical participants, including 60 healthy enrollees and 96 Stage 1–5 CKD patients, were enrolled in this study. The ROC curve generated with the relative abundance of Klebsiella pneumonia or S-Adenosylhomocysteine showed a gradual increase with the CKD severity. Our results further revealed the positive correlation of increased K. pneumonia and S-Adenosylhomocysteine in gut environment, which may be of etiological importance to the deterioration of a CKD patient. In that sense, the microbiota or metabolite changes constitute potential candidates for evaluating the progression of CKD.

1 December 2020 in Neoplasia
Verified
Journal Article
Open access
YCYi-Su Chen
Yi-Su Chen
CLChao-Wei Liu
Chao-Wei Liu
YLYing-Chin Lin
Ying-Chin Lin
CTChia-Ying Tsai
Chia-Ying Tsai
CYChing-Hui Yang
Ching-Hui Yang
JLJung-Chun Lin
Jung-Chun Lin
• Differential splicing profiles of MBNL1 and Acin1 gene is noted in CRC tissues or cells. • Autoregulated exclusion of MBNL1 exons is altered with upregulated SRSF3 • MBNL1 isoform differentially modulates CRC-related AS events. • SRSF3 and MBNL1 exerts opposite impact on expression of the Acin1 isoform. • Acin1 isoform exhibits distinct influence on DNA fragmentation in CRC cells. • SRSF3-MBNL11-Acin1 constitutes an emerging circuit involved in apoptosis of CRC cells.