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김성렬,조영일,이해운,이정연,안해련,송종오,명승운 건국대학교 의과학연구소 2002 건국의과학학술지 Vol.12 No.-
Gitelman's syndrome is a rare disorder with a characteristic set of metabolic abnormalities. These include hypokalemia, metabolic alkalosis, hypocalciuria and hypomagnesemia. The clinical manifestations of Gitelman's syndrome are very similar with those of Bartter's syndrome and diuretic abuse. Gitelman' syndrome and Bartter's syndrome can be distinguished by renal clearance study after administration of furosemide and thiazide, since the primary defect in each of these disorders is an impairment in sodium reabsorption in the distal tubule and loop of Henle, respectively. Pseudo-Bartter's syndrome due to diuretic abuse can be distinguished by history of diuretic use and a positive urine assay for diuretics. We have experienced a case of pseudo-Gitelman's syndrome in 56-year old woman with unexplained hypokalemic metabolic alkalosis, hypocalciuria, and hypomagnesemia. The patient denied ingestion of diuretic medication. The results of renal clearance study using furosemide and thiazide in this case suggested the presence of the primary defect of sodium reabsorption in the distal tubule rather than in the loop of Henle. These clinical and laboratory findings were consistent with those of Gitelman's syndrome. But, this case was confirmed as pseudo-Gitelman's syndrome since diuretics were detected by a urine assay for diuretics. Furosemide and hydrochlorothiazide were contained in the pill that she had been taking due to constipation. Herein, we report the case of pseudo-Gitelman's syndrome by abuse of cathartics containig diuretics presented as Gitelman's syndrome in renal clearance study.
Kim, Kyu-pyo,Park, Seong Joon,Kim, Jeong-Eun,Hong, Yong Sang,Lee, Jae-Lyun,Bae, Kyun-Seop,Cha, Hyunju,Kwon, Sool-Ki,Ro, Seonggu,Cho, JoongMyung,Kim, Tae Won Springer-Verlag 2015 Investigational new drugs Vol.33 No.5
<P>Purpose The aim of the present study was to assess the safety, maximum tolerated dose (MTD), pharmacokinetics, pharmacodynamics, and efficacy of single and multiple doses of intravenous CG200745, a novel histone deacetylase (HDAC) inhibitor, in patients with advanced solid malignancies. Experimental Design Two to six patients received intravenous CG200745 according to the 2?+?4 dose-escalating method. This first-in-human trial was comprised of two parts: Part 1 was a single ascending dose, and Part 2 was multiple ascending doses weekly for 3?weeks, and then 1?week off. For the first cycle, pharmacokinetic sampling for CG200745 and pharmacodynamic sampling for acetylated histone H4 in peripheral blood mononuclear cells (PBMCs) were performed on day 1 for Part 1 and on days 1 and 15 for Part 2. Examination of acetylated histone H4 in pre- and post-biopsy samples was performed in accessible patients. Results In all, 28 patients were treated at 13 dose levels (1.8-250?mg/m(2)) and received a total of 71 cycles of CG200745. Hematologic toxicities included grade 3/4 neutropenia (22.2?%) that did not last a week and non-hematologic toxicities included fatigue (22.2?%) and anorexia (16.7?%) that did not exceed grade 2. No dose-limiting toxic effects were noted. Dose proportionality was observed for both the maximum concentration and area under the curve. The elimination half-life was 5.67??2.69?h (mean??standard deviation). An increase in PBMC acetylated histone H4 was observed at dose levels up to 51?mg/m(2), which plateaued at higher dose levels. At 24?h, 75?% of patients (6/8) showed higher relative acetylation in tumor tissue compared to PBMCs. Although there was no partial or complete response, 57.1?% of patients (16/28) had stable disease that lasted at least 6?weeks. Conclusions CG200745 can be safely administered at effective dose levels that inhibit HDAC in PBMCs and tumor tissue. Although MTD was not reached, further escalation was not performed because acetylated histone H4 plateaued at dose levels higher than 51?mg/m(2). Additional phase II trials are recommended at 250?mg/m(2).</P>
A Traffic and Interference Adaptive DCA Algorithm with Rearrangement in Microcellular Systems
Kim, Seong-Lyun,Han, Youngnam 한국경영과학회 1995 한국경영과학회 학술대회논문집 Vol.- No.1(2)
A new dynamic channel assigument (DCA) algorithm with rearrangement for cellular mobile communication systems is suggested. Our DCA algorithm is both traffic and interference adaptive, which is based on the mathematical formulation of the maximum packing under a realistic propagation mode. In developing the algorithm, we adopt the Lagrangean relaxation technique that bas been successfully used in the area of mathematical programming. Computational experiments of the algorithm reveal quite encouraging results. Although our algorithm primarily focuses on microcellular systems, it can be effectively applied to conventional cellular systems under highly nonuniform traffic distributions and interference conditions.
Delay Performance of Two-Stage Access in Cellular Internet-of-Things Networks
Kim, Jeemin,Lee, Hyun-Kwan,Kim, Dong Min,Kim, Seong-Lyun IEEE 2018 IEEE Transactions on Vehicular Technology VT Vol.67 No.4
<P>In this paper, two-stage random-access-based massive Internet-of-things uplink transmission is investigated. In this scheme, aggregator nodes are additionally deployed to relay packets to deal with a massive number of arrivals. A user node determines whether to utilize aggregator nodes according to the received signal strength from base stations and aggregator nodes. If the user node selects and transmits a packet to an aggregator node, the aggregator node stores and forwards the received packet to the base station. The use of aggregator nodes can reduce the per-hop delay as well as the user energy consumption by reducing the transmission distance from user nodes. However, in the two-stage random access protocol, an increase in the number of aggregator nodes incurs collisions in the wireless medium, and hence, increases the queueing delay at the aggregator node. Thus, improved radio resource allocation and network design are required to reduce additional delay in the two-hop uplink system. We, therefore, focus on optimizing the transmission probabilities of transmitting nodes and the aggregator node density to minimize the delay in two-stage random access networks.</P>
Park, Seong Joon,Hong, Yong Sang,Lee, Jae-Lyun,Ryu, Min-Hee,Chang, Heung Moon,Kim, Kyu-pyo,Ahn, Yong Chel,Na, Young-Soon,Jin, Dong-Hoon,Yu, Chang Sik,Kim, Jin Cheon,Kang, Yoon-Koo,Kim, Tae Won S. Karger AG 2012 Oncology Vol.82 No.2
<P>Abstract</P><P><I>Objective:</I> The anti-epidermal growth factor receptor monoclonal antibody cetuximab has been shown to be effective in patients with wild-type<I> KRAS</I> metastatic colorectal cancer (mCRC). Fragment C γ receptor <I>(Fc</I>γ<I>R)</I> polymorphisms may predict the effectiveness of cetuximab, but this has not been established. This study investigated the clinical relevance of <I>Fc</I>γ<I>R</I> gene polymorphisms and <I>KRAS</I> status in iri-notecan-refractory mCRC patients treated with cetuximab. <I>Methods:</I> The total number of irinotecan-refractory mCRC patients studied was 118. Among them, 117 and 107 patients were screened for <I>KRAS</I> mutations and genetic polymorphisms of <I>Fc</I>γ<I>RIIa-131H/R</I> and <I>Fc</I>γ<I>RIIIa-158V/F</I>, respectively. The association of <I>Fc</I>γ<I>R </I>polymorphisms and<I> KRAS </I>mutations with clinical outcome was analyzed. <I>Results:</I><I>KRAS</I> mutations were found in 33 patients (27.1%). Wild-type <I>KRAS</I> was associated with a better response rate (p < 0.001), longer progression-free survival (p < 0.001) and longer overall survival (p < 0.001). <I>Fc</I>γ<I>RIIa H/H, H/R </I>and<I> R/R </I>polymorphisms were observed in 54, 49 and 4 patients, respectively, and <I>Fc</I>γ<I>RIIIa V/V, V/F </I>and <I>F/F </I>polymorphisms were observed in 6, 65, and 36 patients, respectively. Clinical outcomes were not significantly associated with either <I>Fc</I>γ<I>RIIa</I> or <I>Fc</I>γ<I>RIIIa</I> polymorphisms or with combinations of <I>KRAS </I>status and <I>Fc</I>γ<I>R </I>polymorphisms. <I>Conclusion:</I> The <I>Fc</I>γ<I>RIIa</I> and <I>Fc</I>γ<I>RIIIa</I> polymorphisms may not be useful molecular biomarkers for the activity of cetuximab in patients with mCRC.</P><P>Copyright © 2012 S. Karger AG, Basel</P>