12,898 research outputs found
Rapamycin increases the incidence of neuropsychiatric illness in kidney transplant patients through the suppression of neural stem cells
No full text© 2020, The Author(s).Rapamycin inhibits protein translation in cells, including neural stem cells (NSCs), by suppressing the mechanistic target of rapamycin (mTOR). This drug has been widely used together with calcineurin inhibitors in transplantation patients to prevent graft rejection. Previous studies have reported an association between mTOR and depression, but few investigations of this have occurred in transplant recipients. We have here tested the psychiatric effects of rapamycin in mice. The animals treated with rapamycin showed decreased locomotion and sugar consumption. In these rapamycin-treated mice also, the granule cells in the dentate gyrus (DG), which actively differentiate and proliferate from NSC, showed decreases in both excitatory and inhibitory synaptic transmission. Furthermore, the SOX2/NeuN ratio in the DG was decreased in mice treated with rapamycin. We further show that kidney transplantation patients who are receiving rapamycin have more psychiatric disorder such as adjustment disorder. Clinical attention is thus needed when administering rapamycin to transplant recipients due to its behavioral effects and its impact on NSC11Nsciescopu
Hyperactive ACC-MDT Pathway Suppresses Prepulse Inhibition in Mice
No full textAltered prepulse inhibition (PPI) is an endophenotype associated with multiple brain disorders, including schizophrenia. Circuit mechanisms that regulate PPI have been suggested, but none has been demonstrated through direct manipulations. IRSp53 is an abundant excitatory postsynaptic scaffold implicated in schizophrenia, autism spectrum disorders, and attention-deficit/hyperactivity disorder. We found that mice lacking IRSp53 in cortical excitatory neurons display decreased PPI. IRSp53-mutant layer 6 cortical neurons in the anterior cingulate cortex (ACC) displayed decreased excitatory synaptic input but markedly increased neuronal excitability, which was associated with excessive excitatory synaptic input in downstream mediodorsal thalamic (MDT) neurons. Importantly, chemogenetic inhibition of mutant neurons projecting to MDT normalized the decreased PPI and increased excitatory synaptic input onto MDT neurons. In addition, chemogenetic activation of MDT-projecting layer 6 neurons in the ACC decreased PPI in wild-type mice. These results suggest that the hyperactive ACC-MDT pathway suppresses PPI in wild-type and IRSp53-mutant mice.11Nsciessciscopu
Author Correction: Evaluation of skin cancer resection guide using hyper‑realistic in‑vitro phantom fabricated by 3D printing
No full textThe original version of this Article contained an error in the spelling of the author Taehun Kim which was incorrectly given as Teahun Kim. The original Article has been corrected
IRSp53 Deletion in Glutamatergic and GABAergic Neurons and in Male and Female Mice Leads to Distinct Electrophysiological and Behavioral Phenotypes
No full textIRSp53 (also known as BAIAP2) is an abundant excitatory postsynaptic scaffolding protein implicated in autism spectrum disorders (ASD), schizophrenia, and attention-deficit/hyperactivity disorder (ADHD). IRSp53 is expressed in different cell types across different brain regions, although it remains unclear how IRSp53 deletion in different cell types affects brain functions and behaviors in mice. Here, we deleted IRSp53 in excitatory and inhibitory neurons in mice and compared resulting phenotypes in males and females. IRSp53 deletion in excitatory neurons driven by Emx1 leads to strong social deficits and hyperactivity without affecting anxiety-like behavior, whereas IRSp53 deletion in inhibitory neurons driven by Viaat has minimal impacts on these behaviors in male mice. In female mice, excitatory neuronal IRSp53 deletion induces hyperactivity but moderate social deficits. Excitatory neuronal IRSp53 deletion in male mice induces an increased ratio of evoked excitatory and inhibitory synaptic transmission (E/I ratio) in layer V pyramidal neurons in the prelimbic region of the medial prefrontal cortex (mPFC), whereas the same mutation does not alter the E/I ratio in female neurons. These results suggest that IRSp53 deletion in excitatory and inhibitory neurons and in male and female mice has distinct impacts on behaviors and synaptic transmission. Copyright © 2020 Kim, Noh, Kim, Yang, Kim and Kim. This is an open-access article
distributed under the terms of the Creative Commons Attribution License (CC BY).11Nsciescopu
세포 특이적 IRSp53 결손 생쥐의 특성 연구
No full text학위논문(박사) - 한국과학기술원 : 의과학대학원, 2019.2,[iii, 107 p. :]IRSp53 as an actin modulator is critical for growth and maintenance of dendritic spine, and its knockout in mice showed social deficit. Social deficit makes great burden to psychiatric patients such as schizophrenia and autism. But still, it is needed to be investigated its beneath mechanism and effective therapy for social deficit. Here I show telencephalic excitatory neuron specific Emx1-CreIRSp53 flox/flox (f/f) conditional knockout (cKO) mice have social deficit. Chemogenetic modulation of LH restores social deficit in Emx1-CreIRSp53 f/f cKO mice, butaggravates social deficit in f/f mice. In addition, I measure inhibitory/excitatory (I/E) ratio from optogenetically evoked synaptic transmission on neurons of the ventral tegmental area (VTA). It is presented with increasing I/E ratio with Emx1-CreIRSp53 f/f cKO mice and decreasing I/E ratio with f/f mice during chemogenetic modulation, respectively. Furthermore, inhibitory neuron specific chemogenetic modulation in LH makes social behavior increase in both Emx1-CreIRSp53 f/f cKO and control mice. This is the first study to utilise the circuit between LH and VTA for rescue of social behavior in disease-model mouse. In addition, this finding has clinical implication to treat social deficit in psychiatric patients.한국과학기술원 :의과학대학원
DBLP-derived labeled data for author name disambiguation
No full textThis is a DBLP-derived labeled data originally created by Dr. C. Lee Giles at Penn State University and filtered for duplicate removal and error correction by Dr. Jinseok Kim at University of Michigan. For more details, see references below.1. Kim, Jinseok (2018). Evaluating author name disambiguation for digital libraries: a case of DBLP. Scientometrics. doi:10.1007/s11192-018-2824-5 2. Kim, Jinseok & Kim, Jenna (2018). The impact of imbalanced training data on machine learning for author name disambiguation. Scientometrics. doi: 10.1007/s11192-018-2865-9Each row refers to an author name instance with following feature information separated by tab.author name: full name string extracted from DBLPunique author id: labels assigned manually by Dr. C. Lee Giles's teampaper id: assigned by Dr. Jinseok Kimauthor list: names of authors in the byline of the paperyear: publication yearvenue: conference or journal namestitle: stopwords removed and stemmed by the Porter's stemmerIf you want to use this dataset, please consider to cite papers below.For the original dataset: Han, H., Giles, L., Zha, H., Li, C., & Tsioutsiouliklis, K. (2004). Two Supervised Learning Approaches for Name Disambiguation in Author Citations. JCDL 2004: Proceedings of the Fourth ACM/IEEE Joint Conference on Digital Libraries, 296-305. doi:10.1145/996350.996419For the filtered dataset: 1. Kim, Jinseok (2018). Evaluating author name disambiguation for digital libraries: a case of DBLP. Scientometrics. doi:10.1007/s11192-018-2824-5 or2. Kim, Jinseok & Kim, Jenna (2018). The impact of imbalanced training data on machine learning for author name disambiguation. Scientometrics. doi: 10.1007/s11192-018-2865-9</div
Abstract 4657: LOX and ZFPM2 as novel diagnostic biomarkers for malignant pleural mesothelioma
No full textAbstract
Malignant pleural mesothelioma (MPM) is a rare, aggressive cancer being developed on outlayer of lung tissues and caused by mostly occupational exposure to asbestos. Poor prognosis needs to develop therapeutic drug as well as early diagnostic biomarker. Currently, mesothelin (MSLN), osteopontin (OPN), and fibulin 3 (FBLN3) have been reported as potential diagnostic biomarkers for MPM. In this study, we first performed bioinformatics analysis for public database to find diagnostic biomarkers for MPM. From the analysis using Cancer Cell Line Encyclopedia (CCLE) and Gene Expression Omnibus (GEO) databases, included were 7 genes involving LOX, LOXL1, LOXL2, ZFPM2, THBS2, SULF1, CDH11 identified as potential diagnostic biomarkers. These genes showed a similar diagnostic ability to FBLN3 or MSLN as MPM biomarker candidates. Further molecular approach using quantitative real-time polymerase chain reaction (QPCR) confirmed the higher mRNA expression of these candidates in MPM cell lines and patient samples. Moreover, two particular genes, LOX and ZFPM, showed MPM specific patterns of mRNA expression that were further confirmed in protein level by western blot assay. Together with biological approach, biostatistical analysis of receiver operating characteristic (ROC) analysis using the GEO database revealed significantly higher diagnostic potential of LOX and ZFPM2 genes compared to the FBLN3, one of the best diagnostic biomarkers currently reported. From this study, we believe these genes together with FBLN3 and MSLN would become novel potential biomarker candidates for MPM diagnosis.
Citation Format: Minkyu Kim, Hyun-Won Kim, Soon-Hee Jung, Sung Soo Oh, Yangsik Jeong, Jong-Whan Choi. LOX and ZFPM2 as novel diagnostic biomarkers for malignant pleural mesothelioma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4657. doi:10.1158/1538-7445.AM2017-4657</jats:p
Khoo Kay Kim, professor of Malaysian history : a biobibliometric study
No full textPresents an analysis of the publication productivity, authorship pattern, channels of communication, journal preference and language preference of Professor Dato' Khoo Kay Kim, Professor of Malaysian History in the University of Malaya, Kuala Lumpur. The results of this biobibliometric study indicate that he can be a role model for future Malaysian historians to emulate his various achievements especially in the field of history education
Anxious, Dismal, Giddy, Aggressive: Seth Kim-Cohen interviewed by Mark Peter Wright for Ear Room.
No full textA conversation with author Seth Kim-Cohen
Kim Gordon - no icon
No full textAs cofounder of legendary rock band Sonic Youth, best-selling author, and celebrated artist, Kim Gordon is one of the most singular and influential figures of the modern era. This personally curated scrapbook is an edgy and evocative portrait of Gordon s life, art, and style. Spanning from her childhood on Californian surf beaches in the 60s and 70s to New York s downtown art and music scene in the 80s and 90s where Sonic Youth was born. Through unpublished personal photographs, magazine and newspaper clippings, fashion editorials, and advertising campaigns, interspersed with Gordon s song lyrics, writings, artworks, private objects, and ephemera, this book demonstrates how Kim Gordon has been a role model for generations of women and me
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