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( Sin Gi Park ),( Jong Bhak ),( Jong Soo Kim ),( Tae Hyung Kim ),( Jee Hyun An ),( Sang Youl Rhee ),( Hee Kyung Kim ),( Min Joo Kim ),( Hyun Jeong Jeon ),( Taekeun Oh ),( Hyung Jin Choi ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Agranulocytosis is a rare but life-threatening side effect of antithyroid drugs. Several reports, including familial cases, suggested that there could be substantial genetic susceptibility determinants which could predict the risk of antithyroid drug induced agranulocytosis. However, no tests are currently available to predict the risk of antithyroid drug induced agranulocytosis. Methods: In this study, we performed whole-exome sequencing to comprehensively identify the genetic variations responsible for antithyroid drug induced agranulocytosis. For discovery stage 1, whole-exome sequencing was performed for seven antithyroid drug induced agranulocytosis cases. Variant based approach and gene based approach were performed to discover candidate variants or genes for antithyroid drug induced agranulocytosis. For HLA loci, HLA-sequence-based typing was performed. For validation stage 2, Sanger sequencing and HLA-sequence-based typing were performed for eight additional independent antithyroid drug induced agranulocytosis cases. Antithyroid drug users without agranulocytosis side effect, Korean local healthy controls and public HLA database were used as control group. Results: Discovery stage genome-wide association study results revealed strong signals in chromosome 6 (P=2.7×10-8) and chromosome 19 (P=1.7×10-14). HLA typing of seven discovery cases and eight validation cases revealed several HLA types, which showed strong association with antithyroid drug induced agranulocytosis (odds ratio=4.6-6.3, P=3×10-3-5×10-5). Gene based approach indicated several candidate genes for antithyroid drug induced agranulocytosis. In these genes, several loss of function variants were found, which were common among antithyroid drug induced agranulocytosis cases, but these variants were very rare among controls (P=2.0×10-3-1.8×10-4). Conclusions: In conclusion, several strong genetic predictors of antithyroid drug induced agranulocytosis were discovered. To avoid the risk of life-threatening agranulocytosis side effect, these pharmacogenomics markers could be tested in clinic before initiation of antithyroid drugs.
Lee, Hyung-Geol,Kim, Sungchul,Jung, Da-Jung,Choi, Yoo-Min,Sin, Min-Seop,Choi, Seok-Woo,Song, Beom-Yong,Kim, Jong-Uk,Hong, Seung-Won,Yook, Tae-Han KOREAN PHARMACOPUNCTURE INSTITUTE 2014 Journal of pharmacopuncture Vol.17 No.1
Objectives: This experiment was conducted to examine the toxicity of Water soluble Carthmi-Flos herbal acupuncture (WCF) by administering a single intramuscular dose of WCF in 6-week-old, male and female Sprague-Dawley rats and to find the lethality dose for WCF. Methods: The experiment was conducted at Biotoxtech according to Good Laboratory Practices under a request by the Korean Pharmacopuncture Institute. This experiment was performed based on the testing standards of "Toxicity Test Standards for Drugs" by the Ministry of Food and Drug Safety. Subjects were divided into 4 groups: 1 control group in which normal saline was administered and 3 test groups in which 0.1, 0.5 or 1.0 mL of WCF was administered; a single intramuscular dose was injected into 5 males and 5 females in each group. General symptoms and body weights were observed/measured for 14 days after injection. At the end of the observation period, hematological and clinical chemistry tests were performed, followed by necropsy and histopathological examinations of the injected sections. Results: No mortalities were observed in any group. Also, symptoms, body weight, hematology, clinical chemistry and necropsy were not affected. However, histopathological examination of the injected part in one female in the 1.0-mL group showed infiltration of mononuclear cells and a multi-nucleated giant cell around eosinophilic material. Conclusion: Administration of single intramuscular doses of WCF in 3 groups of rats showed that the approximate lethal dose of WCF for all rats was in excess of 1.0 mL, as no mortalities were observed for injections up to and including 1.0 mL.
Lee, Sin‐,Ae,Ryu, Hyung Won,Kim, Young Mee,Choi, Suyong,Lee, Mi Ji,Kwak, Tae Kyoung,Kim, Hyeon Jung,Cho, Moonjae,Park, Ki Hun,Lee, Jung Weon Wiley Subscription Services, Inc., A Wiley Company 2009 Hepatology Vol.49 No.4
<P><B>Abstract</B></P><P>We previously reported that the four‐transmembrane L6 family member 5 (TM4SF5) was highly expressed in hepatocarcinoma, induced morphological elongation and epithelial‐mesenchymal transition, and caused abnormal cell growth in multilayers <I>in vitro</I> and tumor formation <I>in vivo</I>. In this study, we identified a synthetic compound, 4′‐(<I>p</I>‐toluenesulfonylamido)‐4‐hydroxychalcone (TSAHC) that antagonized both the TM4SF5‐mediated multilayer growth and TM4SF5‐enhanced migration/invasion. TSAHC treatment induced multilayer‐growing cells to grow in monolayers, recovering contact inhibition without accompanying apoptosis, and inhibited chemotactic migration and invasion. Tumor formation in nude mice injected with TM4SF5‐expressing cells and the growth of cells expressing endogenous TM4SF5, but not of TM4SF5‐null cells, was suppressed by treatment with TSAHC, but not by treatment with its analogs. The structure‐activity relationship indicated the significance of 4′‐<I>p</I>‐toluenesulfonylamido and 4‐hydroxy groups for the anti‐TM4SF5 effects of TSAHC. Point mutations of the putative <I>N</I>‐glycosylation sites abolished the TM4SF5‐specific TSAHC responsiveness. <I>Conclusion:</I> These observations suggest that TM4SF5‐enhanced tumorigenic proliferation and metastatic potential can be blocked by TSAHC, likely through targeting the extracellular region of TM4SF5, which is important for protein‐protein interactions. (H<SMALL>EPATOLOGY</SMALL> 2009.)</P>
( Jae Hyung Park ),( Joong Goo Kwon ),( Sun Joo Kim ),( Dae Kyu Song ),( Seok Guen Lee ),( Eun Soo Kim ),( Kwang Bum Cho ),( Byung Ik Jang ),( Dae Hwan Kim ),( Jeong Im Sin ),( Tae Wan Kim ),( In Hwan 대한소화기기능성질환·운동학회 2015 Journal of Neurogastroenterology and Motility (JNM Vol.21 No.1
Background/Aims Inflammatory bowel disease is commonly accompanied by colonic dysmotility and causes changes in intestinal smooth muscle contractility. In this study, colonic smooth muscle contractility in a chronic inflammatory condition was investigated using smooth muscle tissues prepared from interleukin-10 knockout (IL-10./.) mice. Methods Prepared smooth muscle sections were placed in an organ bath system. Cholinergic and nitrergic neuronal responses were observed using carbachol and electrical field stimulation with L-NG-nitroarginine methyl ester (L-NAME). The expression of interstitial cells of Cajal (ICC) networks, muscarinic receptors, neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) was observed via immunofluorescent staining. Results The spontaneous contractility and expression of ICC networks in the proximal and distal colon was significantly decreased in IL-10./. mice compared to IL-10+/+ mice. The contractility in response to carbachol was significantly decreased in the proximal colon of IL-10./. mice compared to IL-10+/+ mice, but no significant difference was found in the distal colon. In addition, the expression of muscarinic receptor type 2 was reduced in the proximal colon of IL-10./. mice. The nictric oxide-mediated relaxation after electrical field stimulation was significantly decreased in the proximal and distal colon of IL-10./. mice. In inflamed colon, the expression of nNOS decreased, whereas the expression of iNOS increased.Conclusions These results suggest that damage to the ICC network and NOS system in the proximal and distal colon, as well as damage to the smooth muscle cholinergic receptor in the proximal colon may play an important role in the dysmotility of the inflamed colon.