美國博士從事研究不端行為被抓，將面臨3篇文章被撤稿

　　Viravuth Yin 博士是Mount Desert Island Biological Laboratory (MDIBL) 的副教授。科研誠信辦公室 (ORI) 發現 Viravuth Yin 博士在美國公共衛生服務 (PHS) 等基金支持的研究中從事研究不端行為。

　　Viravuth Yin有意、故意和/或偽造和/或捏造以下三 (3) 篇已發表論文和兩 (2) 篇已提交手稿中的數據，從事研究不端行為。Viravuth Yin重復使用、重新標記和報告磷酸鹽緩沖鹽水 (PBS) 作為亂序反義鎖定核酸 (LNA)的對照；Viravuth Yin通過不做或者是少做實驗，得到相關的實驗結果。Viravuth Yin同意接受2年的監督及撤回已經發表在Development，iScience 等3篇文章的要求。

　　ORI對于科研誠信的調查案例及結果報告，這也能為中國的相關科研誠信部門等調查相關的案例，提供了借鑒。

　　Viravuth Yin 博士：基于Mount Desert Island Biological Laboratory (MDIBL) 進行的調查報告和科研誠信辦公室 (ORI) 在其監督審查中進行的額外分析，ORI發現 Viravuth Yin 博士（被調查人），前 MDIBL 副教授，在美國公共衛生服務 (PHS) 等基金支持的研究中從事研究不端行為。

　　Viravuth Yin既不承認也不否認 ORI 的研究不當行為調查結果。雙方簽訂本協議以完成此事項，無需進一步花費時間、財務或其他資源。

　　ORI 發現，Viravuth Yin有意、故意和/或偽造和/或捏造以下三 (3) 篇已發表論文和兩 (2) 篇已提交手稿中的數據，從事研究不端行為：

　　Smith AM, Dykeman CA, King BL, Yin VP. Modulation of TNFα Activity by the microRNA Let-7 Coordinates Heart Regeneration. iScience 2019；15:1-15； doi: 10.1016/j.isci.2019.04.009（以下簡稱“iScience 2019”）

　　Smith AM, Dykeman CA, King BL, Yin VP. Modulation of TNFα Activity by the microRNA Let-7 Coordinates Heart Regeneration. iScience 2019；17:225-29； doi: 10.1016/j.isci.2019.06.017（以下簡稱“iScience Correction”）

　　Beauchemin M, Smith A, Yin VP. Dynamic microRNA-101a and Fosab expression controls zebrafish heart regeneration. Development 2015；142:4026-37； doi: 10.1242/dev.126649（以下簡稱“Development 2015”）

　　Smith AM, Dykeman CA, Yin VP. Modulation of epicardial TNFα Activity by the microRNA Let-7 Coordinates the Zebrafish Heart Regeneration. Manuscript submitted to iScience in 2018（以下簡稱“iScience 2018稿件”）

　　Smith AM, Dykeman CA, Yin VP. Modulation of epicardial TNFα Activity by the microRNA let-7 coordinates the zebrafish heart regeneration. Manuscript submitted to PNAS in 2018（以下簡稱“PNAS 2018稿件”）

　　具體而言，Viravuth Yin通過以下方式有意、故意和/或不計后果地偽造和/或捏造數據：

　　在以下實驗結果中重復使用、重新標記和報告磷酸鹽緩沖鹽水 (PBS) 對照作為亂序反義鎖定核酸 (LNA)：

　　RT-qPCR data representing the knockdown of let7 expression in Figure 2B of PNAS 2018 draft, iScience 2018 draft, and iScience 2019

　　images of tcf21:Dsred expression in LNA-let-7 treated hearts at 3, 14, and 21 days post -amputation (dpa) showing defects in wound closure in Figure 2C of PNAS 2018 draft, iScience 2018 draft, and iScience 2019

　　quantification of tcf21:Dsred expression within the resection wound in LNA-let-7 treated hearts in Figure 2D of iScience 2019

　　images exhibiting proliferating cardiac muscle (CM) in Figure 3A of PNAS 2018 draft, iScience 2018 draft, and iScience 2019

　　suppression of CM proliferation indices in LNA-let-7 hearts at 3 and 7 dpa in Figure 3B of PNAS 2018 draft, iScience 2018 draft, and iScience 2019

　　severity of the injured heart phenotype in Figure 3C of PNAS 2018 draft, iScience 2018 draft, and iScience 2019

　　quantification of the severity of the injury heart phenotype in Figure 3D of iScience 2019

　　electron microscopy images of remote and injury zones of resected 7-dpa hearts in Figure 4A of PNAS 2018 draft, iScience 2018 draft, iScience 2019, and iScience Correction

　　images of Tg(gata4:GFP) expression in the primordial heart muscle layer in Figure 4B of PNAS 2018 draft, iScience 2018 draft, iScience 2019, and iScience Correction

　　quantification of gata4:GFP expression in control and LNA-let-7 treated hearts in Figure 4C of iScience 2019 and iScience Correction

　　RNA transcripts identifying differentially upregulated TNFα transcripts in Figure 5A of PNAS 2018 draft, iScience 2018 draft, iScience 2019, and their resultant qPCR results, which identified increased TNFα expression in Figure 5C of PNAS 2018 draft, Figure 5B of iScience 2018 draft, iScience 2019, and Table S1 of iScience 2019

　　CM proliferation analyses results in Figures S4B and S4C of PNAS 2018 draft and iScience 2018 draft, and Figures S5B and S5C of iScience 2019

　　images representing the function of let-7 in Figure 2C of iScience Correction and reusing and relabeling images from an unrelated experiment, such that let-7 function is not represented in the image

　　images reporting the function of let-7 in Figure 3A of iScience Correction

　　images representing differences in the effects of miR-101a depletion on Met2 and PNA expression and the quantification of cardiomyocyte proliferation in uninjured control and Tg(hs:miR-101a-sp) heat exposed hearts (CM proliferation analysis) in Figures 2A, 2B, 2C, and 2D, and results in Figure 2E of Development 2015

　　muscle, fibrin, and collagen staining images representing increased scar tissue presence in Tg(hs:miR-101a-sp) heat-treated hearts, as compared to wild type hearts in Figures 3A, 3B, 3C, 3D, 3E, and 3F of Development 2015

　　scarring indices and the size of the injured area in wild type versus Tg(hs:miR-101a-sp) heat-treated hearts in Figures 3G and 3H of Development 2015

　　differences in (1) the amount of scarring, as represented by AFOG staining in control and Tg (hs:miR-101-a-sp) ventricles from resected and heat-treated hearts in Figures 4B and 4C； (2) the amount of scar tissue in the presence of suppressed miR-101a expression in Tg(hs:miR-101a-sp) hearts, compared to control hearts in Figures 4H and 4I； and (3) the quantification of the scarring indices in control versus Tg(hs:miR-101a-sp) hearts in Figure 4J of Development 2015

　　differences in (1) the amount of scarring, as represented by comparing AFOG staining in control and Tg(hs:miR-101a-sp) and Tg(hs:miR-133a1-pre) hearts exposed to long term heat therapy in Figures 5A, 5B and 5C, or Tropomyosin staining in Figures 5D, 5E, and 5F； and (2) the quantification of the scarring indices, tropomyosin expression, and injury area in Figures 5G, 5H, and 5I of Development 2015

　　increased Fosab expression in Tg(hs:miR-101a-sp) ventricles relative to controls in Figures 6A and 6B, RNA in situ hybridization studies in control and regenerating hearts detecting miR-101a expression in Figures 6C, 6D, 6E, and 6E’, and Fosab expression in Figures 6F, 6G, 6H, and 6H’ of Development 2015

　　images reporting significant differences in Dsred expression, cardiomyocyte proliferation, collagen and fibrin staining, and scar tissue removal in ventricles from zebrafish treated with lna-Let-7, as compared to scrambled control, to support the importance of miR-101a in scar tissue removal/ventricular regeneration in Figures 6H, 6I, 6J, 7C, 7D, and 7E of Development 2015

　　報告未執行的研究方法和統計數據（以下實驗結果）

　　PCR data in the graph represented in Figure 2B of PNAS 2018 draft, iScience 2018 draft, and iScience 2019, by representing the data from two (2) remote PCR experiments as being from the same experiment

　　PCR data in the graph represented in Figure 2B of iScience Correction by reusing and relabeling a graph containing data that were the result of different experimental conditions (exposure to heat shock), to include scrambled control data

　　control data and statistical differences between control and experimental data represented in PNAS 2018 draft, iScience 2018 draft, iScience 2019, and iScience Correction, by falsely reporting the use of both antisense scrambled and LNA oligonucleotides that were designed and administered to adult animals via intraperitoneal injection at 10ug/g body weight

　　representing the “n” of one biological replicate or one experiment as being multiple independent samples or experiments in iScience 2019 and iScience Correction

　　control data and statistical differences between control and experimental data and the reported methods in Development 2015, concluding that miR-101a controls both CM proliferation and scar tissue removal, by falsely reporting the use of LNA oligonucleotides to modulate miR-101 activity in vivo to elucidate its contributions during adult heart regeneration

　　Viravuth Yin簽訂了自愿和解協議（協議）并自愿同意以下內容：

　　Viravuth Yin同意自 2021 年 8 月 2 日起對其研究進行為期兩 (2) 年的監督。

　　Viravuth Yin同意自愿退出 PHS 的任何咨詢職位。

　　作為本協議的一個條件，Viravuth Yin應該撤回Development 2015 Dec 1；142(23):4026-37；iScience 2019 May 31；15:1-15及iScience 2019 Jul 26；17:225-29等3篇文章。

　　參考消息：

　　https://ori.hhs.gov/content/case-summary-yin-viravuth-p-