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Seasonal performance of a non-hydrostatic global atmospheric model on a cubed-sphere grid
Jung-Eun Esther Kim,Myung-Seo Koo,Changhyun Yoo,Song-You Hong 한국기상학회 2021 한국기상학회 학술대회 논문집 Vol.2021 No.4
A new operational weather forecast model, Korean Integrated Model (KIM), is evaluated on a seasonal simulation framework to extend its operations into prediction longer than the weather time scale. The simulated results are compare with those produced by the conventional spectral transform model using an identical physics package, in order to isolate the errors introduced by imperfect physics parameterizations. The simulated mean states of the KIM are very close to the reanalysis for the selected cases. Moreover, most large-scale fields from the KIM are comparable to those from the spectral transform model, which implies that the general features of large-scale variables and precipitation are highly governed by physical parameterizations, and that the physics – dynamics coupling in the KIM is stable in a long-term simulation. To understand the systematic biases of the KIM, the eddy transports on mean states, tropical large-scale circulations, and precipitation would be analyzed in detail.
Modified CGA for Frequently Moving Mobile Nodes in Secure Neighbor Discovery
( Esther Kim ),( Nam-uk Kim ),( Soo-duek Kim ),( Tae-myoung Chung ) 한국정보처리학회 2009 한국정보처리학회 학술대회논문집 Vol.16 No.2
IPv6 is newly introduced to solve limitations and problems of IPv4 and in IPv6 network, nodes use Neighbor Discovery protocol to discover the subnet prefix and configure its own address. However, Neighbor Discovery is vulnerable to various attacks as it does not have secure mechanism to protect itself. Thus, the Secure Neighbor Discovery has introduced and the main mechanism used in Secure Neighbor Discovery is Cryptographically Generated Address. In this paper, we provide a brief of Cryptographically Generated Address and its limitation in a case where a mobile node moves from one network to another frequently. The proposed scheme resolves this limitation by using the fixed interface identifier.
Severe Human Rhinovirus Lower Respiratory Tract Infections in Young Children
( Doo Ri Kim ),( Kyung-ran Kim ),( Hwanhee Park ),( Esther Park ),( Joongbum Cho ),( Jihyun Kim ),( Hee Jae Huh ),( Kangmo Ahn ),( Nam Yong Lee ),( Yae-jean Kim ) 대한소아감염학회 2023 Pediatric Infection and Vaccine Vol.30 No.3
목적: 리노바이러스의 감염은 하기도 감염을 일으키기도 한다. 본 연구에서는 리노바이러스에 의한 중증 하기도 감염을 보이는 소아환자의 특성을 알아보고자 하였다. 방법: 2016년부터 2020년까지 삼성서울병원 소아청소년과에 리노바이러스 하기도감염으로 입원한 환자의 의무기록을 후향적으로 분석하였다. 입원 시 연령이 생후90일 이상, 5세 미만인 소아 환자를 대상으로 하였다. 다른 호흡기 병원체와의 동시 감염이 확인된 환자는 제외하였다. 리노바이러스에 의한 중증 하기도감염은 고유량 산소요법 치료가 필요한 경우, 기계 호흡이 필요한 경우 또는 중환자실 입원하는 경우로 정의하였다. 결과: 해당 기간 동안 총 115건의 리노바이러스 하기도 감염 입원이 확인되었다. 연령 중앙값은 17개월 (범위, 3-56개월) 이었으며, 입원 일수 중앙값은 4일 (범위, 2-31일) 이었다. 115 건 중 18건의 입원 (15.7%)은 중증 리노바이러스 하기도 감염 그룹으로 분류되었다. 중증 경과 그룹 환자의 연령 중앙값은 그렇지 않은 그룹에 비해 연령 중앙값이 낮았다 (9.5개월 vs. 19.0 개월, P=0.001). 18명의 중증 리노바이러스 하기도 감염 그룹 환자 중 11명 (61.1%)는 기저질환을 가지고 있었으며, 만성 폐질환이 가장 많은 비율을 차지하였다 (63.6%). 여섯 명의 환자는 (33.3%) 기계 호흡을 필요로 하였다. 일곱 명의 기저질환이 없는 환자도 중증 리노바이러스 하기도 감염 그룹에 포함되어 있었다. 이들 일곱 명의 환자 중 네 명은 추후에 천식으로 진단되었다. 115건의 입원을 기저질환이 없는 환자군 (n=60)과 기저질환이 있는 환자군 (n=55)으로 나누어 분석하였을 때, 리노바이러스에 의한 중증 하기도 감염을 보이는 비율은 각각 11.7% 와 20.0%였다 (P=0.219). 결론: 리노바이러스 감염은 중증 하기도감염의 원인이 될 수 있으며, 기저질환자 뿐 아니라 건강한 소아에서도 중증 하기도감염을 일으킬 수 있다 Purpose: Human rhinovirus (HRV) infections can result in lower respiratory tract infections (LRTIs). We aimed to investigate the characteristics of severe HRV LRTI in young children. Methods: Medical records were reviewed retrospectively in patients who were hospitalized for HRV LRTIs from 2016 to 2020 at the Samsung Medical Center in Seoul, Korea. Patients aged 90 days or older and younger than 5 years were included. Patients with co-infections with other respiratory pathogens were excluded. Severe HRV LRTI was defined as the following: the need for high-flow oxygenation, mechanical ventilation, or intensive care unit admission. Results: A total of 115 cases were identified. The median age was 17 months (range, 3-56 months) and the median hospital days were 4 days (range, 2-31 days). Of the 115 cases, 18 patients (15.7%) developed severe HRV LRTI. The median age was younger in the severe group compared to the non-severe group (9.5 months vs. 19.0 months, P=0.001). Of 18 patients with severe HRV LRTI, 11 (61.1%) had underlying diseases - chronic lung diseases accounted for the largest proportion (63.6%). Six patients (33.3%) required mechanical ventilation. Of note, 7 previously healthy children were diagnosed with severe HRV LRTI. Of those 7 children, 4 of them were diagnosed with asthma later. When the 115 cases were divided into previously healthy (n=60) and underlying disease (n=55) groups, severe courses of HRV LRTI were observed in 11.7% and 20.0% of children, respectively (P=0.219). Conclusions: HRV can cause severe LRTI even in previously healthy children as well as in children with comorbidities
Li, Yan,Kim, Ryunhee,Cho, Yi Sul,Song, Woo Seok,Kim, Doyoun,Kim, Kyungdeok,Roh, Junyeop Daniel,Chung, Changuk,Park, Hanwool,Yang, Esther,Kim, Soo-Jeong,Ko, Jaewon,Kim, Hyun,Kim, Myoung-Hwan,Bae, Yong- Society for Neuroscience 2018 The Journal of neuroscience Vol.38 No.26
<P>SALM1 (SALM (synaptic adhesion-like molecule), also known as LRFN2 (leucine rich repeat and fibronectin type III domain containing), is a postsynaptic density (PSD)-95-interacting synaptic adhesion molecule implicated in the regulation of NMDA receptor (NMDAR) clustering largely based on in vitro data, although its in vivo functions remain unclear. Here, we found that mice lacking SALM1/LRFN2 (Lrfn2(-/-) mice) show a normal density of excitatory synapses but altered excitatory synaptic function, including enhanced NMDAR-dependent synaptic transmission but suppressed NMDAR-dependent synaptic plasticity in the hippocampal CA1 region. Unexpectedly, SALM1expression was detected in both glutamatergic and GABAergic neurons and Lrfn2(-/-) CA1 pyramidal neurons showed decreases in the density of inhibitory synapses and the frequency of spontaneous inhibitory synaptic transmission. Behaviorally, ultrasonic vocalization was suppressed in Lrfn2(-/-) pups separated from their mothers and acoustic startle was enhanced, but locomotion, anxiety-like behavior, social interaction, repetitive behaviors, and learning and memory were largely normal in adult male Lrfn2(-/-) mice. These results suggest that SALM1/LRFN2 regulates excitatory synapse function, inhibitory synapse development, and social communication and startle behaviors in mice.</P>
DRG2 Deficient Mice Exhibit Impaired Motor Behaviors with Reduced Striatal Dopamine Release
Lim, Hye Ryeong,Vo, Mai-Tram,Kim, Dong Jun,Lee, Unn Hwa,Yoon, Jong Hyuk,Kim, Hyung-Jun,Kim, Jeongah,Kim, Sang Ryong,Lee, Jun Yeon,Yang, Chae Ha,Kim, Hee Young,Choi, June-Seek,Kim, Kijeong,Yang, Esther MDPI AG 2020 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.21 No.1
<P>Developmentally regulated GTP-binding protein 2 (DRG2) was first identified in the central nervous system of mice. However, the physiological function of DRG2 in the brain remains largely unknown. Here, we demonstrated that knocking out DRG2 impairs the function of dopamine neurons in mice. DRG2 was strongly expressed in the neurons of the dopaminergic system such as those in the striatum (Str), ventral tegmental area (VTA), and substantia nigra (SN), and on neuronal cell bodies in high-density regions such as the hippocampus (HIP), cerebellum, and cerebral cortex in the mouse brain. DRG2 knockout (KO) mice displayed defects in motor function in motor coordination and rotarod tests and increased anxiety. However, unexpectedly, DRG2 depletion did not affect the dopamine (DA) neuron population in the SN, Str, or VTA region or dopamine synthesis in the Str region. We further demonstrated that dopamine release was significantly diminished in the Str region of DRG2 KO mice and that treatment of DRG2 KO mice with l-3,4-dihydroxyphenylalanine (L-DOPA), a dopamine precursor, rescued the behavioral motor deficiency in DRG2 KO mice as observed with the rotarod test. This is the first report to identify DRG2 as a key regulator of dopamine release from dopamine neurons in the mouse brain.</P>