Balanced Encoding of Near-Zero Correlation for an AES Implementation

Power analysis poses a significant threat to the security of cryptographic algorithms, as it can be leveraged to recover secret keys. While various software-based countermeasures exist to mitigate this non-invasive attack, they often involve a trade-off between time and space constraints. Techniques such as masking and shuffling, while effective, can noticeably impact execution speed and rely heavily on run-time random number generators. On the contrary, internally encoded implementations of block ciphers offer an alternative approach that does not rely on run-time random sources, but it comes with the drawback of requiring substantial memory space to accommodate lookup tables. Internal encoding, commonly employed in white-box cryptography, suffers from a security limitation as it does not effectively protect the secret key against statistical analysis. To overcome this weakness, this paper introduces a secure internal encoding method for an AES implementation. By addressing the root cause of vulnerabilities found in previous encoding methods, we propose a balanced encoding technique that aims to minimize the problematic correlation with key-dependent intermediate values. We analyze the potential weaknesses associated with the balanced encoding and present a method that utilizes complementary sets of lookup tables. In this approach, the size of the lookup tables is approximately 512KB, and the number of table lookups is 1,024. This is comparable to the table size of non-protected white-box AES-128 implementations, while requiring only half the number of lookups. By adopting this method, our aim is to introduce a non-masking technique that mitigates the vulnerability to statistical analysis present in current internally-encoded AES implementations.Comment: 36 pages, 17 figures, submitte

Design of Web-based Security Management for Intrusion Detection

Electronic business is rapidly popularized and extended through Internet. Internet has many security weaknesses, so we need the security solution such Intrusion Detection System that minimizes the damage of hacking and responds the intrusion dynamically. It is difficult for legacy management system to process the security environments and electronic business, because legacy system lacks of security policies and integrated security methods. In order to resolve these problems, we need security management system that has standard security policy, consulting, diagnosis, maintenance, and repair function. In this paper, we design and implement Web-based security management for intrusion detection. Our security system consists of network nodes, general hosts and a management node. A management node manages a network node, that is a secure router, and general hosts by security policies. We design the channel between the management node and the network node using IPsec (IP Security). We have applied java and Web to implementing user interface of security system. As the proposed system makes use of Web, security management system is easily accessed through the Web

Regulation of Microglia and Macrophage Polarization via Apoptosis Signal-Regulating Kinase 1 Silencing after Ischemic/Hypoxic Injury

Inflammation is implicated in ischemic stroke and is involved in abnormal homeostasis. Activation of the immune system leads to breakdown of the blood–brain barrier and, thereby, infiltration of immune cells into the brain. Upon cerebral ischemia, infiltrated macrophages and microglia (resident CNS immune cell) are activated, change their phenotype to M1 or M2 based on the microenvironment, migrate toward damaged tissue, and are involved in repair or damage. Those of M1 phenotype release pro-inflammatory mediators, which are associated with tissue damage, while those of M2 phenotype release anti-inflammatory mediators, which are related to tissue recovery. Moreover, late inflammation continually stimulates immune cell infiltration and leads to brain infarction. Therefore, regulation of M1/M2 phenotypes under persistent inflammatory conditions after cerebral ischemia is important for brain repair. Herein, we focus on apoptosis signal-regulating kinase 1 (ASK1), which is involved in apoptotic cell death, brain infarction, and production of inflammatory mediators after cerebral ischemia. We hypothesized that ASK1 is involved in the polarization of M1/M2 phenotype and the function of microglia and macrophage during the late stage of ischemia/hypoxia. We investigated the effects of ASK1 in mice subjected to middle cerebral artery occlusion and on BV2 microglia and RAW264.7 macrophage cell lines subjected to oxygen-glucose deprivation. Our results showed that ASK1 silencing effectively reduced Iba-1 or CD11b-positive cells in ischemic areas, suppressed pro-inflammatory cytokines, and increased anti-inflammatory mediator levels at 7 days after cerebral ischemia. In cultured microglia and macrophages, ASK1 inhibition, induced by NQDI-1 drug, decreased the expression and release of M1-associated factors and increased those of M2-associated factors after hypoxia/reperfusion (H/R). At the gene level, ASK1 inhibition suppressed M1-associated genes and augmented M2-associated genes. In gap closure assay, ASK1 inhibition reduced the migration rate of microglia and macrophages after H/R. Taken together, our results provide new information that suggests ASK1 controls the polarization of M1/M2 and the function of microglia and macrophage under sustained-inflammatory conditions. Regulation of persistent inflammation via M1/M2 polarization by ASK1 is a novel strategy for repair after ischemic stroke

Three-way Translocation of MLL/MLLT3, t(1;9;11)(p34.2;p22;q23), in a Pediatric Case of Acute Myeloid Leukemia

The chromosome band 11q23 is a common target region of chromosomal translocation in different types of leukemia, including infantile leukemia and therapy-related leukemia. The target gene at 11q23, MLL, is disrupted by the translocation and becomes fused to various translocation partners. We report a case of AML with a rare 3-way translocation involving chromosomes 1, 9, and 11: t(1;9;11)(p34.2;p22;q23). A 3-yr-old Korean girl presented with a 5-day history of fever. A diagnosis of AML was made on the basis of the morphological evaluation and immunophenotyping of bone marrow specimens. Flow cytometric immunophenotyping showed blasts positive for myeloid lineage markers and aberrant CD19 expression. Karyotypic analysis showed 46,XX,t(1;9;11)(p34.2;p22;q23) in 19 of the 20 cells analyzed. This abnormality was involved in MLL/MLLT3 rearrangement, which was confirmed by qualitative multiplex reverse transcription-PCR and interphase FISH. She achieved morphological and cytogenetic remission after 1 month of chemotherapy and remained event-free for 6 months. Four cases of t(1;9;11)(v;p22;q23) have been reported previously in a series that included cases with other 11q23 abnormalities, making it difficult to determine the distinctive clinical features associated with this abnormality. To our knowledge, this is the first description of t(1;9;11) with clinical and laboratory data, including the data for the involved genes, MLL/MLLT3