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Short-term Trading and Stock Mispricing
JinGi Ha 한국자료분석학회 2023 Journal of the Korean Data Analysis Society Vol.25 No.6
This paper examines the influence of short-term trading on stock mispricing. Using a mispricing index proposed by Stambaugh, Yu, Yuan (2012, 2015) as a proxy for stock mispricing, This paper investigates how sensitive quarterly short-term institutional trading is to changes in the level of stock mispricing. This paper’s main finding is that trading by short-term institutions is negatively associated with the change-of-stock mispricing index, especially when stock liquidity is high. This paper supports the theoretical view of Cespa, Vives (2015), in which short-term trading can improve price informativeness when liquidity trading is persistent. Also, this research contributes to a better understanding of the interplay between short-term trading and stock mispricing, offering insights into its role in enhancing price efficiency and market dynamics.
JinGi Ha 한국재무학회 2023 한국재무학회 학술대회 Vol.2023 No.11
This study examines how board independence affects fund performance related to the investment experience of independent directors. Using the 2001 SEC amendment as an exogenous shock, I find that board independence does not affect fund performance on average. However, when a board has independent directors with investment experience, it boosts fund performance. This study also finds that a fund manager is less constrained and contractual management fee is more aligned with fund performance under such a board. The findings suggest that board independence is not always beneficial to fund shareholders. Instead, its effectiveness varies depending on independent directors’ investment experience.
Effects of Pruning and Fertilization on the Growth of Highbush Blueberry ‘Jersey’
Yeong-Ha Kwon,In-Kyu Kang,Jingi Yoo,Hyong Woo Choi,Sang-Wook Koh,Su Jin Kim,Kyo-Sun Park,Cheol Choi 한국원예학회 2018 원예과학기술지 Vol.36 No.4
This study examined the effect of different pruning and fertilization methods on the growth and development of highbush blueberry ‘Jersey’. A higher degree of thinning resulted in the formation of more suckers on the crown of the plants compared to other thinning methods. Combinational use of recommended fertilization and heavy thinning (HT) induced the highest average number of sucker formation. The average lengths of the shoots were 21.4-25.2, 17.4-20.1, and 12.0-15.3 cm for HT-, LT- (light thinning), and HP- (heading-back pruning) treated plants, respectively. HT also induced the highest number of mother shoots that were longer than 20 cm (36.6-41.1%), while LT (27.5-33.8%) and HP (15.8-23.8%) treatments produced fewer mother shoots. Analysis of fruit characteristics revealed that a higher degree of thinning increased fruit weight in 2013 as well as total soluble solid content in 2014. The pruning method had a greater impact on fruit yield than fertilization, as increased thinning led to a higher growth rate (HT 467.4-1036.2%, LT 234.9-314.3%, and HP 171.7-203.9%).
Kim Dong-Kyu,Jeong Hyobin,Bae Jingi,Cha Moon-Yong,Kang Moonkyung,Shin Dongjin,Ha Shinwon,Hyeon Seung Jae,Kim Hokeun,Suh Kyujin,Choi Mi-Sun,Ryu Hoon,Yu Seong-Woon,Kim Jong-Il,Kim Yeon-Sook,Lee Sang-Won 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Mitochondria in neural progenitors play a crucial role in adult hippocampal neurogenesis by being involved in fate decisions for differentiation. However, the molecular mechanisms by which mitochondria are related to the genetic regulation of neuronal differentiation in neural progenitors are poorly understood. Here, we show that mitochondrial dysfunction induced by amyloid-beta (Aβ) in neural progenitors inhibits neuronal differentiation but has no effect on the neural progenitor stage. In line with the phenotypes shown in Alzheimer’s disease (AD) model mice, Aβ-induced mitochondrial damage in neural progenitors results in deficits in adult hippocampal neurogenesis and cognitive function. Based on hippocampal proteome changes after mitochondrial damage in neural progenitors identified through proteomic analysis, we found that lysine demethylase 5A (KDM5A) in neural progenitors epigenetically suppresses differentiation in response to mitochondrial damage. Mitochondrial damage characteristically causes KDM5A degradation in neural progenitors. Since KDM5A also binds to and activates neuronal genes involved in the early stage of differentiation, functional inhibition of KDM5A consequently inhibits adult hippocampal neurogenesis. We suggest that mitochondria in neural progenitors serve as the checkpoint for neuronal differentiation via KDM5A. Our findings not only reveal a cell-type-specific role of mitochondria but also suggest a new role of KDM5A in neural progenitors as a mediator of retrograde signaling from mitochondria to the nucleus, reflecting the mitochondrial status.