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연산자 조작 공격과 피연산자 조작 공격에 대한 기존 CRT-RSA Scheme의 안전성 분석
허순행(Soonhaeng Hur),이형섭(Hyungsub Lee),이현승(Hyunseung Rhee),최동현(Donghyun Choi),원동호(Dongho Won),김승주(Seungjoo Kim) 한국정보보호학회 2009 정보보호학회논문지 Vol.19 No.6
CRT-RSA의 사용이 대중화됨에 따라, CRT-RSA에 대한 보안 또한 중요 이슈가 되었다. 1996년, Bellcore 연구원들에 의해 CRT-RSA가 오류 주입 공격에 취약하다고 밝혀진 이래로, 많은 대응책들이 제안되었다. 첫 번째 대응책은 1999년 Shamir에 의해 제안되었으며, Shamir의 대응책은 오류 검사 기법에 기반을 두고 있다. Shamir의 대응책이 소개된 이후, 오류 검사 기법을 사용하는 많은 대응책들이 제안되었다. 그러나 Shamir의 대응책은 2001년 Joey 등에 의하여 피연산자 조작 공격에 취약함이 밝혀졌으며, 오류 검사 기법 또한 2003년 Yen 등에 의하여 연산자 조작 공격에 취약하다고 알려졌다. 이에 Yen 등은 오류 검사 기법을 사용하지 않고 오류 확산 기법을 사용하여 새로운 대응책을 제안하였으나, Yen 등이 제안한 대응책 또한 2007년에 Yen과 Kim에 의하여 안전하지 않음이 밝혀졌다. 최근에는 Kim 등이 Yen 등의 대응책을 보완한 새로운 대응책을 제안하였으며, Ha 등 또한 오류 확산 기법을 사용한 대응책을 제안하였다. 그러나 Kim 등과 Ha 등이 제안한 대응책들을 포함한 기존 대응책들은 연산자 조작 공격에 대해서는 안전성이 증명되지 않았기 때문에 본 논문에서는 피연산자 조작 공격은 물론, 연산자 조작 공격도 고려하여 지금까지 제안된 대응책들의 안전성을 분석할 것이다. As the use of RSA based on chinese remainder theorem(CRT-RSA) is being generalized, the security of CRT-RSA has been important. Since Bellcore researchers introduced the fault attacks on CRT-RSA, various countermeasures have been proposed. In 1999, Shamir firstly proposed a countermeasure using checking procedure. After Shamir's countermeasure was introduced, various countermeasures based on checking procedure have been proposed. However, Shamir's countermeasure was known to be vulnerable to the modified operand attack by Joey et al. in 2001, and the checking procedure was known to be vulnerable to the modified opcode attack by Yen et al. in 2003. Yen et al. proposed a new countermeasure without checking procedure, but their countermeasure was known to be also vulnerable to the modified operand attack by Yen and Kim in 2007. In this paper, we point out that pre, but countermeasures were vulnerable to the modified operand attack or the modified opcode attack.
Jae Hyun Kim,Hee-Won Jeong,Yoon-Hee Choo,Moinay Kim,Eun Jin Ha,Jiwoong Oh,Youngbo Shim,Seung Bin Kim,Han-Gil Jung,So Hee Park,Jungook Kim,Junhyung Kim,Hye Seon Kim,Seungjoo Lee 대한신경손상학회 2023 Korean Journal of Neurotrauma Vol.19 No.2
Mannitol, derived from mannose sugar, is crucial in treating patients with elevated intracranial pressure (ICP). Its dehydrating properties at the cellular and tissue levels increase plasma osmotic pressure, which is studied for its potential to reduce ICP through osmotic diuresis. While clinical guidelines support mannitol use in these cases, the best approach for its application continues to be debated. Important aspects needing further investigation include: 1) bolus administration versus continuous infusion, 2) ICP-based dosing versus scheduled bolus, 3) identifying the optimal infusion rate, 4) determining the appropriate dosage, 5) establishing fluid replacement plans for urinary loss, and 6) selecting monitoring techniques and thresholds to assess effectiveness and ensure safety. Due to the lack of adequate high-quality prospective research data, a comprehensive review of recent studies and clinical trials is crucial. This assessment aims to bridge the knowledge gap, improve understanding of effective mannitol use in elevated ICP patients, and provide insights for future research. In conclusion, this review aspires to contribute to the ongoing discourse on mannitol application. By integrating the latest findings, this review will offer valuable insights into the function of mannitol in decreasing ICP, thereby informing better therapeutic approaches and enhancing patient outcomes.
Auxiliary Role of Oct-1 for the Soluble Expression of Recombinant Protein in Escherichia coli
SeungJoo KIM,Jihwan CHUN,Wonbeom PARK,NaYeon KIM,MinJu KIM,Yong Hwan LEE,Dae-Hyuk KWEON 한국생물공학회 2021 한국생물공학회 학술대회 Vol.2021 No.10
E. coli has been favored for the expression of various heterologous proteins due to its biological properties including fast growth, high cultivation density, and ease of genetic manipulation. However, hydrophobic nature of some proteins makes it extremely difficult to express and acquire the desired products in a soluble and active form. For example, the presence of transmembrane domain and the lack of glycosidic moieties greatly hampered the expression and purification of influenza hemagglutinin (HA), the main target of influenza vaccine, in E. coli. In this study, we employed Oct-1 DNA binding domain as a fusion partner to express and acquire full-length HA in E. coli system. It has been reported that Oct-1 can form plasmid-protein complexes in E. coli cytoplasm, thereby facilitating the soluble expression of recombinant proteins. In the current study, we confirmed that the expression level of Oct-1-HA was significantly increased compared to that of native HA, and the purified Oct-1-HA retained its activity as a consequence of improved solubility. Regarding the data, we suggest that Oct-1 can effectively contribute to the soluble production of heterologous proteins.
Deficiency of Endothelium-Specific Transcription Factor <i>Sox17</i> Induces Intracranial Aneurysm
Lee, Seungjoo,Kim, Il-Kug,Ahn, Jae Sung,Woo, Dong-Cheol,Kim, Sang-Tae,Song, Sukhyun,Koh, Gou Young,Kim, Hyung-Seok,Jeon, Byeong Hwa,Kim, Injune American Heart Association 2015 Circulation Vol.131 No.11
<P><B>Background—</B></P><P>Intracranial aneurysm (IA) is a common vascular disorder that frequently leads to fatal vascular rupture. Although various acquired risk factors associated with IA have been identified, the hereditary basis of IA remains poorly understood. As a result, genetically modified animals accurately modeling IA and related pathogenesis have been lacking, and subsequent drug development has been delayed.</P><P><B>Methods and Results—</B></P><P>The transcription factor Sox17 is robustly expressed in endothelial cells of normal intracerebral arteries. The combination of <I>Sox17</I> deficiency and angiotensin II infusion in mice induces vascular abnormalities closely resembling the cardinal features of IA such as luminal dilation, wall thinning, tortuosity, and subarachnoid hemorrhages. This combination impairs junctional assembly, cell-matrix adhesion, regeneration capacity, and paracrine secretion in endothelial cells of intracerebral arteries, highlighting key endothelial dysfunctions that lead to IA pathogenesis. Moreover, human IA samples showed reduced Sox17 expression and impaired endothelial integrity, further strengthening the applicability of this animal model to clinical settings.</P><P><B>Conclusions—</B></P><P>Our findings demonstrate that <I>Sox17</I> deficiency in mouse can induce IA under hypertensive conditions, suggesting <I>Sox17</I> deficiency as a potential genetic factor for IA formation. The <I>Sox17</I>-deficient mouse model provides a novel platform to develop therapeutics for incurable IA.</P>