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Cho Sung-Ae,Huh Inho,Lee Seok-Jin,Sung Tae-Yun,구관우,조춘규,지영석 대한마취통증의학회 2022 Korean Journal of Anesthesiology Vol.75 No.1
Background: Catheter-related bladder discomfort (CRBD) is common in patients with a urinary catheter and is a risk factor for emergence agitation (EA). The mainstay of CRBD management is anticholinergics. Dexamethasone inhibits acetylcholine release. This study aimed to evaluate the effects of dexamethasone on postoperative CRBD and EA.Methods: In this prospective study, 90 patients undergoing urological surgery requiring urinary catheterization were allocated randomly to one of two groups (each n = 45). Before induction of anesthesia, the dexamethasone group received 10 mg (2 ml) of dexamethasone intravenously, while the control group received 2 ml of saline in the same manner. The incidence and severity of CRBD were assessed 0, 1, 2, and 6 h after the patient arrived in the post-anesthesia care unit (PACU) as the primary outcomes. The incidence and severity of EA were also compared during emergence and recovery from anesthesia as secondary outcomes.Results: The incidences of CRBD in the control group and dexamethasone group at 0, 1, 2, and 6 h postoperatively were 28.9% and 15.6%, 55.6% and 55.6%, 57.8% and 46.7%, and 53.3% and 51.1%, respectively. The incidence and severity of CRBD assessed at 0, 1, 2, and 6 h postoperatively did not show intergroup differences. The incidence and severity of EA in the operating room and PACU also showed no difference between the groups.Conclusions: Dexamethasone (10 mg) administered before induction of anesthesia did not further reduce the incidence or severity of CRBD or EA in patients undergoing urological surgery.
Transthyretin: A Transporter Protein Essential for Proliferation of Myoblast in the Myogenic Program
Lee, Eun Ju,Pokharel, Smritee,Jan, Arif Tasleem,Huh, Soyeon,Galope, Richelle,Lim, Jeong Ho,Lee, Dong-Mok,Choi, Sung Wook,Nahm, Sang-Soep,Kim, Yong-Woon,Park, So-Young,Choi, Inho MDPI 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.1
<P>Irregularities in the cellular uptake of thyroid hormones significantly affect muscle development and regeneration. Herein, we report indispensable role of transthyretin (TTR) in maintaining cellular thyroxine level. TTR was found to enhance recruitment of muscle satellite cells to the site of injury, thereby regulating muscle regeneration. Fluorescence-activated cell sorting (FACS) and immunofluorescence analysis of TTR<SUB>wt</SUB> (TTR wild type) and TTR<SUB>kd</SUB> (TTR knock-down) cells revealed that TTR controlled cell cycle progression by affecting the expression of Cyclin A2. Deiodinase 2 (D2) mediated increases in triiodothyronine levels were found to regulate the expression of myogenic marker, myogenin (MYOG). Moreover, use of a coumarin derivative (CD) revealed a significant reduction in cellular thyroxine, thereby indicating that TTR play a role in the transport of thyroxine. Taken together, these findings suggest that TTR mediated transport of thyroxine represents a survival mechanism necessary for the myogenic program. The results of this study will be highly useful to the strategic development of novel therapeutics to combat muscular dystrophies.</P>
Urokinase의 적출심장의 심근허혈에 대한 보호작용과 invitro 및 exvivo항혈전작용 실험
권광일,신홍섭,윤정옥,김보신,민지하,이병호,허인회 충남대학교 약학대학 의약품개발연구소 1992 藥學論文集 Vol.8 No.-
Protective effect of urokinase on reperfusion were studied followed by global ischemia in the isolated perfused rat heart. Separately, anti-platelet aggregation effect of urokinase also investigated. Urokinase exhibited positive effect for the protection of rat heart function by increasing the LV dp/dt, coronary flow (CF) and the rate pressure product (RPP), and by decreasing the LVEDP on reperfusion. Urokinase also decreased arrhythmia by 74.7%(P<0.05) induced by global ischemia in the rat heart. In the platelet aggregation study, urokinase did not show the inhibitory effect of ADP or collagen induced platelet aggregation invitro and exvivo.
Park, Jae-Sun,Kim, Hyung-Seok,Kim, Jun-Dae,Seo, Jungwon,Chung, Kyung-Sook,Lee, Ho-Sa,Huh, Tae-Lin,Jo, Inho,Kim, Yong-Ou Wiley-Liss, Inc. 2009 Developmental dynamics Vol.238 No.6
<P>We investigated chamber-specific gene expression by isolating a 2.2-kb polymerase chain reaction product containing the 5′-flanking region of the zebrafish ventricular myosin heavy-chain gene (vmhc). Promoter analysis revealed that the fragment, consisting of nucleotides from −301 to +26, is sufficient for vmhc promoter activity. Among several putative cis-acting elements in the region, a GATA-binding site was identified to be crucial for the activity of the promoter, as evidenced by the complete abolishment of promoter activity by a single nucleotide substitution of GATA-binding site (−287, C→T). Knockdown of GATA-binding proteins 4 and 6 (GATA4 and -6) by their antisense morpholino oligonucleotides resulted in reduced green fluorescent protein (GFP) reporter gene and endogenous vmhc expression. These findings suggest that GATA4 and -6 play a key role in the regulation of vmhc expression in the ventricle. In addition, the vmhc promoter and the transgenic zebrafish (vmhc:gfp) are useful tools to study the formation and function of the ventricle. Developmental Dynamics 238:1574–1581, 2009. © 2009 Wiley-Liss, Inc.</P>