This study analyzed the relationship between efficient pitchers and teams advancing to the postseason in Korean professional baseball through DEA. A total of 1,133 pitchers who threw more than one inning from the 2014 season to the 2018 season were selected for this study. For DEA analysis, input variables were selected as annual salary and inning output variables as Wins, Saves, and Holds and the number of efficient pitchers for each season was classified using the input-oriented BCC model. After that, it was divided into two groups based on joining the postseason or not, and the number of efficient pitchers was compared through a prop test. As a result of the analysis, the groups that advanced to the postseason in the rest of the season except for the 2014 and 2017 seasons had more efficient pitchers. Considering that the 2014 season recorded the highest WAR (Wins Above Replacement) at 183.56 compared to other seasons, most pitchers threw well, and in the 2017 season, they made more mistakes in pitching than in other seasons, but they performed well in batters. The results of this study have expanded the research field using efficiency analysis in professional baseball and can be used as useful data for practical research.

Some mutations in FOXL2 are responsible for premature ovarian failure accompanied with blepharophimosis-ptosis-epicanthusinversus syndrome (BPES) typeI disease, and FOXL2-null mice exhibit developmental defects of granulosa cells. Recently, a new somatic mutation in FOXL2,c.402C>G, leading top. C134W change, has been identified in a vast majority of adult-type ovarian garnulosa cell tumors (GCTs). In the current study, we investigated possible mechanisms by which the C134W mutation could contribute to GCT development. The wild-type (WT) FOXL2 and its mutant form displayed differential apoptotic activities, in which WT induced a significant granulosa cell death while the mutant exhibited a minimal cell death effect. The FOXL2-induced apoptotic response was greatly dependent on caspase8, BID, or BAK since the depletion of either of them prevented FOXL2 to elicitits full apoptotic responses. Stimulated activation of caspase8, consequently resulting increased production of truncated BID (tBID), up-regulation and oligomerization of BAK, and release of cytochromec were all associated with the apoptosis followed by WT FOXL2 expression. In contrast, the mutant FOXL2 was deficient to elicit the full apoptotic signaling responses. In addition, we found the differential up-regulations of expression of death receptors including Fas and TNF-R1 between the WT and the mutant. Moreover, granulosa cells expressing either the WT FOXL2 or its variant form (C134W) exhibited distinct cell death sensitivities by the activation of death receptors. Thus, these differential activities of FOXL2 and it mutant may partly account for the pathophysiology of GCT development occurred by the somatic mutation (C134W) of FOXL2.

본 논문은 인공적인 단백질인 MCL-1ES BH3M에 관한 것으로 MCL-1ES BH3M를 과발현시 세포사멸을 유도한다. MCL-1L을 주형으로 재조합 PCR을 통해서 MCL-1ES BH3M를 클로닝하였다. 새롭게 클로닝한 단백질인 MCL-1ES BH3M 단백질은 안정성을 유지하기 위해서 PEST 도메인이 제거되어 있으며, 다른 BCL-2 패밀리 단백질과의 결합을 조절하기 위해서 BH3도메인의 Leu-Arg-Arg-Val-Gly-Asp-Gly 서열을 7개의 Ala 잔기로 인위적으로 돌연변이를 유도하였다. MCL-1ES BH3M를 293T 세포에서 과발현할 경우 세포사멸을 유도하였고, 항-세포사멸 단백질인 MCL-1L을 같이 과발현하더라도 세포사멸을 유도하였다. 또한, 과발현시 Caspase 9과 3를 활성화하였으며 면역염색법을 통해서 MCL-1ES BH3M 과발현시 미토콘드리아에 MCL-1ES BH3M 단백질이 부분적으로 위치하는 것을 확인하였다. 이상의 결과로 MCL- 1ES BH3M는 Caspase 9과 3의 활성을 통해서 세포사멸을 유도한다. 결론적으로 본 연구는 세포사멸을 유도하는 새로운 molecule을 클로닝하였고, 이 molecule에 의한 세포사멸 기능을 확인하였다.