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Hwang Soojin,Lee Yena,Yoon Ji-Hee,Kim Ja Hye,Kim Hyery,Koh Kyung-Nam,Im Ho Joon,Yoo Han-Wook,Choi Jin-Ho 대한소아내분비학회 2024 Annals of Pediatirc Endocrinology & Metabolism Vol.29 No.2
Purpose: As the survival rate from pediatric cancers has increased significantly with advances in treatment modalities, long-term endocrine complications have also risen. This study investigated the frequencies and risks of endocrine sequelae in childhood cancer survivors who received hematopoietic stem cell transplantation (HSCT).Methods: This study included 200 pediatric patients who underwent HSCT. Clinical and endocrinological findings were collected retrospectively. The median follow-up duration after HSCT was 14 years.Results: Endocrine complications occurred in 135 patients (67.5%). Children who underwent HSCT at pubertal age (n=100) were at higher risk of endocrine complications than those who received it at prepubertal age (79% vs. 56%, <i>P</i>=0.001). The most common complication was hypogonadism (40%), followed by dyslipidemia (22%). Short stature and diabetes mellitus were more prevalent in the prepubertal group, whereas hypogonadism and osteoporosis were more common in the pubertal group. Being female, pubertal age at HSCT, and glucocorticoid use were predictors of an increased risk for any complication. Radiation exposure increased the risk of short stature and hypothyroidism. Hypogonadism was significantly associated with being female, pubertal age at HSCT, and high-dose radiation. Pubertal age at HSCT also increased the risks of osteoporosis and dyslipidemia.Conclusion: This study demonstrates that long-term endocrine complications are common after HSCT in children and adolescents. Age at HSCT is a critical factor for endocrine complications after HSCT. These findings suggest that surveillance strategies for endocrine complications in childhood cancer survivors should be specified according to age at HSCT.
Hwang, Soojin,Song, Saera,Hong, Yoon Ki,Choi, Gahee,Suh, Yoon Seok,Han, Seung Yeop,Lee, Minjung,Park, Seung Hwan,Lee, Jang Ho,Lee, Soojin,Bang, Se Min,Jeong, Yuji,Chung, Won-Ju,Lee, Im-Soon,Jeong, Gil Public Library of Science 2013 PLoS genetics Vol.9 No.4
<▼1><P><I>DJ-1</I>, a Parkinson's disease (PD)–associated gene, has been shown to protect against oxidative stress in <I>Drosophila</I>. However, the molecular mechanism underlying oxidative stress-induced phenotypes, including apoptosis, locomotive defects, and lethality, in <I>DJ-1</I>-deficient flies is not fully understood. Here we showed that <I>Daxx-like protein</I> (<I>DLP</I>), a <I>Drosophila</I> homologue of the mammalian <I>Death domain-associated protein</I> (<I>Daxx</I>), was upregulated under oxidative stress conditions in the loss-of-function mutants of <I>Drosophila DJ-1β</I>, a <I>Drosophila</I> homologue of <I>DJ-1</I>. <I>DLP</I> overexpression induced apoptosis via the c-Jun N-terminal kinase (JNK)/<I>Drosophila</I> forkhead box subgroup O (dFOXO) pathway, whereas loss of <I>DLP</I> increased resistance to oxidative stress and UV irradiation. Moreover, the oxidative stress-induced phenotypes of <I>DJ-1β</I> mutants were dramatically rescued by <I>DLP</I> deficiency, suggesting that enhanced expression of <I>DLP</I> contributes to the <I>DJ-1β</I> mutant phenotypes. Interestingly, we found that dFOXO was required for the increase in <I>DLP</I> expression in <I>DJ-1β</I> mutants and that dFOXO activity was increased in the heads of <I>DJ-1β</I> mutants. In addition, subcellular localization of DLP appeared to be influenced by <I>DJ-1</I> expression so that cytosolic DLP was increased in <I>DJ-1β</I> mutants. Similarly, in mammalian cells, Daxx translocation from the nucleus to the cytosol was suppressed by overexpressed <I>DJ-1β</I> under oxidative stress conditions; and, furthermore, targeted expression of <I>DJ-1β</I> to mitochondria efficiently inhibited the Daxx translocation. Taken together, our findings demonstrate that DJ-1β protects flies against oxidative stress- and UV-induced apoptosis by regulating the subcellular localization and gene expression of DLP, thus implying that Daxx-induced apoptosis is involved in the pathogenesis of <I>DJ-1</I>-associated PD.</P></▼1><▼2><P><B>Author Summary</B></P><P>DJ-1 is an antioxidant protein that has been implicated in autosomal recessive Parkinson's disease (PD), although the mechanism by which <I>DJ-1</I> deficiency causes PD remains elusive. <I>Drosophila DJ-1</I> mutants are highly sensitive to oxidative stress and UV irradiation, and oxidative stress-induced cell death is significantly increased in dopaminergic neurons. In this study, we characterized a <I>Drosophila</I> homologue of death domain-associated protein (Daxx), <I>Daxx-like protein</I> (<I>DLP</I>), as a key player in the process of the oxidative stress-induced cell death in <I>DJ-1</I> mutants. Upon oxidative stress, <I>DLP</I> expression was increased in the <I>DJ-1</I> mutants, and locomotive defects and oxidative stress-induced phenotypes including apoptosis and lethality were dramatically rescued by <I>DLP</I> deficiency. More interestingly, we revealed that <I>Drosophila</I> forkhead box subgroup O was required for the increased <I>DLP</I> expression in <I>DJ-1</I> mutants. Additionally, <I>Drosophila</I> DJ-1 suppressed DLP and Daxx translocation from the nucleus to the cytosol in both fly brain and mammalian cells. Interestingly, targeted expression of <I>Drosophila DJ-1</I> to mitochondria efficiently inhibited Daxx translocation. Our results show that <I>Drosophila</I> DJ-1 protects dopaminergic neurons from oxidative stresses by regulating the subcellular localization and gene expression of <I>DLP</I>, providing a clue to understanding the molecular mechanism underlying oxidative stress-induced neuronal death in PD.</P></▼2>
Soojin Hwang,Darae Kim,Gahee Choi,Seon Woo An,Yoon Ki Hong,Yoon Seak Suh,Min Jung Lee,조경상 한국분자세포생물학회 2010 Molecules and cells Vol.29 No.6
Parkin is the most prevalent genetic factor in the onset of autosomal recessive juvenile parkinsonism (AR-JP), and mutations in parkin has been reported to cause motor defects, which result from dopamine deficiency caused by dopaminergic neuronal cell death. Activation of c-Jun N-terminal kinase (JNK) has also been implicated in neuronal cell death in Parkinson’s disease (PD). Moreover, Droso-phila models for AR-JP, loss of function mutants of Dro-sophila parkin, also show dopaminergic neural degenera-tion associated with hyperactivation of JNK, increased apoptosis, and mitochondrial defects. However, the mo-lecular mechanism by which Parkin protects cells from apoptosis remains unclear. In the present study, we tested whether Drosophila Parkin suppressed the JNK signaling pathway in developing tissues. Ectopically expressed parkin strongly suppressed the constitutively active form of Hemipterous (HepCA), a Drosophila JNK kinase that in-duces an eye degeneration phenotype and apoptosis in the eye imaginal disc. Moreover, parkin also suppressed extra vein formation induced by Basket (Bsk), a Drosophila JNK. Interestingly, the bsk mRNA level was markedly re-duced by parkin over-expression, suggesting that the ef-fect of parkin on the phenotype induced by activation of JNK signaling was achieved by transcriptional regulation. Furthermore, we found that the expression level of JNK target genes was reduced by parkin over-expression. Taken together, these results suggest that Drosophila Parkin suppresses JNK signaling by reducing bsk transcription.
Hwang, Gaeun,Park, Hyungmin,Bok, Taesoo,Choi, Sinho,Lee, Sungjun,Hwang, Inchan,Choi, Nam-Soon,Seo, Kwanyong,Park, Soojin The Royal Society of Chemistry 2015 Chemical communications Vol.51 No.21
<P>Nanostructured micrometer-sized Al-Si particles are synthesized via a facile selective etching process of Al-Si alloy powder. Subsequent thin Al2O3 layers are introduced on the Si foam surface via a selective thermal wet oxidation process of etched Al-Si particles. The resulting Si/Al2O3 foam anodes exhibit outstanding cycling stability (a capacity retention of 78% after 300 cycles at the C/5 rate) and excellent rate capability.</P>
황수진 ( Soojin Hwang ),김애련 ( Aeryun Kim ),문선혜 ( Sunhye Moon ),김지희 ( Jihee Kim ),김진휘 ( Jinhwi Kim ),하영혜 ( Younghea Ha ),양옥영 ( Okyoung Yang ) 한국보건행정학회 2016 보건행정학회지 Vol.26 No.4
Background: Rehabilitations in subacute phase are different from acute treatments regarding the characteristics and required resource consumption of the treatments. Lack of accuracy and validity of the Korean Diagnosis Related Group and Korean Out-Patient Group for the acute patients as the case-mix and payment tool for rehabilitation inpatients have been problematic issues. The objective of the study was to develop the Korean Rehabilitation Patient Group (KRPG) reflecting the characteristics of rehabilitation inpatients. Methods: As a retrospective medical record survey regarding rehabilitation inpatients, 4,207 episodes were collected through 42 hospitals. Considering the opinions of clinical experts and the decision-tree analysis, the variables for the KRPG system demonstrating the characteristics of rehabilitation inpatients were derived, and the splitting standards of the relevant variables were also set. Using the derived variables, we have drawn the rehabilitation inpatient classification model reflecting the clinical situation of Korea. The performance evaluation was conducted on the KRPG system. Results: The KRPG was targeted at the inpatients with brain or spinal cord injury. The etiologic disease, functional status (cognitive function, activity of daily living, muscle strength, spasticity, level and grade of spinal cord injury), and the patient`s age were the variables in the rehabilitation patients. The algorithm of KRPG system after applying the derived variables and total 204 rehabilitation patient groups were developed. The KRPG explained 11.8% of variance in charge for rehabilitation inpatients. It also explained 13.8% of variance in length of stay for them. Conclusion: The KRPG version 1.0 reflecting the clinical characteristics of rehabilitation inpatients was classified as 204 groups.