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Melanoma is a deadly skin cancer with high mortality, and its incidence is increasing every year. Although numerous anticancer drugs have been developed, these treatments have various side effects, such as skin rash, fatigue, diarrhea, cough, and muscle pain. Therefore, there is a need for research on novel anticancer drugs with low cytotoxicity and few side effects. In this study, we investigated whether afrormosin (7-hydroxy-4′,6-dimethoxyisoflavone), a member of the isoflavonoid family, could have the potential as a novel anticancer drug. Afrormosin decreased the viability of B16F10 melanoma cells in a time- and dose-dependent manner. We also found that the afrormosin-induced decrease in cell viability was caused by the reduction of cell proliferation through Go/G1 arrest and the induction of apoptosis in B16F10 melanoma cells. Furthermore, afrormosin decreased the metastatic activity (cell invasion and migration) of B16F10 melanoma cells. At the molecular level, afrormosin reduced the levels of Bcl-2, an anti-apoptotic protein, and augmented the levels of Bax, a pro-apoptotic protein, and p53, a tumor suppressor. Additionally, procaspase-3 levels were reduced by afrormosin treatment. When we examined the signaling pathways affected by afrormosin, we found that the AKT/ERK pathways were inhibited and the p38/JNK pathway was activated by afrormosin. Collectively, these results suggest the potential anticancer effect of afrormosin, making it a prospective candidate for development as an anticancer drug.

OBJECTIVES: The first confirmed case of coronavirus disease 2019 (COVID-19) in South Korea was reported in January 2020, with 28 confirmed cases reported as of February 14th, 2020. The epidemiological and clinical characteristics of all 28 cases were analyzed in response to this disease. METHODS: The epidemiological characteristics and early clinical features of the 28 patients from Korea with confirmed COVID-19 were analyzed using COVID-19 reporting and surveillance data and the epidemiological investigation reports prepared by the rapid response team. RESULTS: There were 16 patients that entered Korea from foreign countries: Wuhan, China (11 patients), Zhuhai, China, (1 patient), Singapore (2 patients), Japan (1 patient), and Thailand (1 patient). The early symptoms were fever, sore throat, cough or sputum production, chills, and muscle ache. Three patients were asymptomatic, however, 18 developed pneumonia. Of the 28 cases, 16 were index cases imported from abroad, with 10 cases of secondary infection originating in Korea, and the route of transmission still under investigation for 2 patients. The 10 patients with secondary infection were infected from contact with family members or acquaintances of primary patients, and the suspected sites of transmission were mostly at home. CONCLUSION: COVID-19 in Korea was spread by 16 infected individuals traveling from other countries, leading to second-generation cases. The initial symptoms were mostly minor, but the disease was infectious at this stage, resulting from close contact, particularly at home. Establishing an early detection strategy for COVID-19 is crucial for managing the transmission of the disease.

Melanoma is one of the most aggressive and lethal skin cancers. Lucidadiol is a triterpenoid isolated from Ganoderma lucidum and is known to have various biological functions, including antibacterial effects. However, the anti-cancer effects and mechanism of action of lucidadiol in malignant melanoma are unknown. In this study, lucidadiol significantly reduced B16 melanoma cell viability in a dose- and time-dependent manner. In addition, lucidadiol induced apoptosis and suppressed cell mobility in B16 melanoma cells. Moreover, our findings revealed that lucidadiol remarkably downregulated phospho-Akt/ERK/JNK, but not p38. Taken together, our results suggest that lucidadiol could exerts its anti-cancer effects by inducing apoptosis via modulation of the Akt/MAPK pathway. Therefore, lucidadiol may be a potential cancer therapeutic agent for malignant melanoma.

Signaling lymphocytic activating molecule family member 1 (SLAMF1 or CD150) is a cell surface glycoprotein expressed on various immune populations, regulating cell-cell interactions, activation, differentiation, and inflammatory responses and has been suggested as a potential target for inflammatory diseases. Signaling is believed to be mediated by high-affinity homophilic interactions; the recombinant soluble form of SLAMF1 has optimal activity in the range of 20 μg/mL. This contradicts with a rather weak homo-dimerization binding constant (KD) value reported previously; however, the analytical approach and data analysis suffered from various technical limitations at the time and therefore warrants re-examination. To address this apparent discrepancy, we determined the KD of soluble SLAMF1 using sedimentation velocity analytical ultracentrifuge (SV-AUC). A globally fitted monomer-dimer model properly explains the data from a wide concentration range obtained with both UV and fluorescence detection systems. The analysis suggests the dimerization KD value for human SLAMF1 is 0.48 μM. Additionally, our data show that SLAMF1 self-association is not driven by non-specific binding to glycans supporting the view of specific protein-protein interaction. We anticipate antibody biotherapeutics capable of modulating the biological consequences of SLAMF1 interactions will be readily identified.

The clearance of apoptotic cells is known to be a critical step in maintaining tissue and organism homeostasis. This process is rapidly/promptly mediated by recruited or resident phagocytes. Phagocytes that engulf apoptotic cells have been closely linked to the release of anti-inflammatory cytokines to eliminate inflammatory responses. Defective clearance of apoptotic cells can cause severe inflammation and autoimmune responses due to secondary necrosis of apoptotic cells. Recently accumulated evidence indicates that apoptotic cells and their clearance have important physiological roles in addition to immune-related functions. Herein, we review the current understanding of the mechanisms and fundamental roles of apoptotic cell clearance and the beneficial roles of apoptotic cells in physiological processes such as differentiation and development.

This dissertation identifies Korean international students as immigrants, as conduits of knowledge transfer, and as agents of change. Part of the American Cold War policy was to establish Korea's higher educational institutions with a core group of US-educated people. Figuring prominently in this story is the US government's use of foreign assistance as a diplomatic tool to build its influence abroad. The Korean government readily accepted the aid but imprinted its designs on the American blueprint to reflect its own goal of building a modern nation-state. American universities under contract with the US government assisted the redesign of key departments at Seoul National University (SNU) and the establishment of Korea Advanced Institute of Science (KAIS). Planned as model universities or paradigms for other Korean institutes of higher education, both national institutes became the standard bearers of "modern" knowledge. Both projects favored US-educated Koreans. To this end, the majority of the faculty members in the departments selected for restructuring at SNU was sent to the US to be trained and the overwhelming majority of KAIS' inaugural faculty members held doctoral degrees from the United States. The benefits and prestige associated with an American education in the Korean society contributed to a positive cultural representation of the US as a whole. This caused a growing number of Koreans to immigrate to the US to pursue their studies. These international students were central to Korean American immigration. They were information brokers, the first links to chain migration, and contributors to the changing racial and ethnic make-up of the American population in the twentieth century.

The simulation programs with the kalman filter for the naval Electro Optical Tracking System(EOTS) is presented. We achieve that the dependency tracking aiming systems performance of EOTS can be enhanced by minimizing the target information error which including transfer delay and measurement. According to our experiment results, kalman filter can be used for various electro optical systems to eliminate error value.

The Diamond Like Carbon(DLC) films for the Electro Optical Tracking System(EOTS) by using Plasma Enhanced Chemical Vapor Deposition(PECVD) method is presented. We achieve that the DLC films can reduce the surface delamination of thermal observation sensor front window due to the high hardness, low friction and chemical inertness which is comparable to a Si film. According to our experiment results, DLC films can be used for various electro optical systems to eliminate surface delamination.

Naive T cell populations are maintained in the periphery at relatively constant levels via mechanisms that control expansion and contraction and are associated with competition for homeostatic cytokines. It has been shown that in a lymphopenic environment naive T cells undergo expansion due, at least in part, to additional availability of IL-7. We have previously found that T cell–intrinsic deletion of TNFR-associated factor (TRAF) 6 (TRAF6ΔT) in mice results in diminished peripheral CD8 T cell numbers. In this study, we report that whereas naive TRAF6ΔT CD8 T cells exhibit normal survival when transferred into a normal T cell pool, proliferation of naive TRAF6ΔT CD8 T cells under lymphopenic conditions is defective. We identified IL-18 as a TRAF6–activating factor capable of enhancing lymphopenia-induced proliferation (LIP) in vivo, and that IL-18 synergizes with high-dose IL-7 in a TRAF6-dependent manner to induce slow, LIP/homeostatic-like proliferation of naive CD8 T cells in vitro. IL-7 and IL-18 act synergistically to upregulate expression of IL-18R genes, thereby enhancing IL-18 activity. In this context, IL-18R signaling increases PI3K activation and was found to sensitize naive CD8 T cells to a model noncognate self-peptide ligand in a way that conventional costimulation via CD28 could not. We propose that synergistic sensitization by IL-7 and IL-18 to self-peptide ligand may represent a novel costimulatory pathway for LIP.

Fatty acids (FAs) are essential constituents of cell membranes, signaling molecules, and bioenergetic substrates. Because CD8+ T cells undergo both functional and metabolic changes during activation and differentiation, dynamic changes in FA metabolism also occur. However, the contributions of de novo lipogenesis to acquisition and maintenance of CD8+ T cell function are unclear. In this article, we demonstrate the role of FA synthesis in CD8+ T cell immunity. T cell–specific deletion of acetyl coenzyme A carboxylase 1 (ACC1), an enzyme that catalyzes conversion of acetyl coenzyme A to malonyl coenzyme A, a carbon donor for long-chain FA synthesis, resulted in impaired peripheral persistence and homeostatic proliferation of CD8+ T cells in naive mice. Loss of ACC1 did not compromise effector CD8+ T cell differentiation upon listeria infection but did result in a severe defect in Ag-specific CD8+ T cell accumulation because of increased death of proliferating cells. Furthermore, in vitro mitogenic stimulation demonstrated that defective blasting and survival of ACC1-deficient CD8+ T cells could be rescued by provision of exogenous FA. These results suggest an essential role for ACC1-mediated de novo lipogenesis as a regulator of CD8+ T cell expansion, and may provide insights for therapeutic targets for interventions in autoimmune diseases, cancer, and chronic infections.

In this paper, underwater acoustic image classification of a cylindrical object using the Hough transformation is proposed. Hough transformation is often used to classify a cylindrical object in the optical systems. However, it is difficult to apply to the underwater acoustic image system because of lower resolution and noisier underwater environments. Thus, the cylindrical object was modeled and its geometric depth(GD) pixels were restored in order to make them suitable for the Hough transformation by using moving average filter and a polynomial interpolation method. As a result, restored GD pixels are similar to original ones and test results show high performance in classification.

We investigated the anti-inflammatory effects of minocycline in EAE, an animal model of MS. Minocycline, administered for two weeks after the clinical onset, significantly decreased the cumulative and mean clinical scores of EAE. This was associated with the reduction of both CD4(+) and CD8(+) T cell numbers in the spinal cord and the downregulation of LFA-1 on T cells without affecting the cytokine production profile. The predominant cytokine produced by T cells in the spleen was IFN-gamma whereas in the CNS it was IL-17. Our results indicate that minocycline regulates T cell infiltration into the CNS without modifying the dominant cytokine production.

Dendritic cells (DCs) appear in higher numbers within the CNS as a consequence of inflammation associated with autoimmune disorders, such as multiple sclerosis, but the contribution of these cells to the outcome of disease is not yet clear. Here, we show that stimulatory or tolerogenic functional states of intracerebral DCs regulate the systemic activation of neuroantigen-specific T cells, the recruitment of these cells into the CNS and the onset and progression of experimental autoimmune encephalomyelitis (EAE). Intracerebral microinjection of stimulatory DCs exacerbated the onset and clinical course of EAE, accompanied with an early T-cell infiltration and a decreased proportion of regulatory FoxP3-expressing cells in the brain. In contrast, the intracerebral microinjection of DCs modified by tumor necrosis factor α induced their tolerogenic functional state and delayed or prevented EAE onset. This triggered the generation of interleukin 10 (IL-10)-producing neuroantigen-specific lymphocytes in the periphery and restricted IL-17 production in the CNS. Our findings suggest that DCs are a rate-limiting factor for neuroinflammation.

Multiple sclerosis and an animal model resembling multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), are inflammatory demyelinating diseases of the CNS that are suppressed by systemic mycobacterial infection in mice and BCG vaccination in humans. Host defense responses against Mycobacterium in mice are influenced by T lymphocytes and their cytokine products, particularly IFN-γ, which plays a protective regulatory role in EAE. To analyze the counter-regulatory role of mycobacterial infection-induced IFN-γ in the CNS on the function of the pathological Th17 cells and the clinical outcome of EAE, we induced EAE in mice that were intracerebrally infected with Mycobacterium bovis bacille Calmette-Guerin (BCG). In this study, we demonstrate that intracerebral (i.c.) BCG infection prevented inflammatory cell recruitment to the spinal cord and suppressed the development of EAE. Concomitantly, there was a significant decrease in the frequency of myelin oligodendrocyte glycoprotein-specific IFN-γ-producing CD4+ T cells in the CNS. IL-17+CD4+ T cell responses were significantly suppressed in i.c. BCG-infected mice following EAE induction regardless of T cell specificity. The frequency of Foxp3+CD4+ T cells in these mice was equivalent to that of control mice. Intracerebral BCG infection-induced protection of EAE and suppression of myelin oligodendrocyte glycoprotein-specific IL-17+CD4+ T cell responses were similar in both wild-type and IFN-γ-deficient mice. These data show that live BCG infection in the brain suppresses CNS autoimmunity. These findings also reveal that the regulation of Th17-mediated autoimmunity in the CNS can be independent of IFN-γ-mediated mechanisms.

Wireless Mesh Networks (WMNs) are one of the few commonly implemented types of mobile ad-hoc networks (MANETs); several companies offer WMNs for broadband Internet access and for extending the coverage of wireless local area networks. Several particularities differentiate WMNs from MANETs. First, in WMNs, most of the traffic originates or terminates at the gateways (nodes connected to the wired infrastructure/Internet). Second, in most applications, WMN nodes tend to be neatly differentiated as either stationary nodes (providing connectivity and coverage) or mobile nodes (utilizing the coverage afforded by the stationary nodes). While general MANET routing protocols can be used in WMNs, it is expected that a protocol that takes the particularities of WMNs into account will outperform the general protocol. In this paper, we propose such a routing protocol and evaluate its performance via simulations. Results show that, for WMNs, the proposed routing protocol outperforms general purpose MANET protocols in terms of routing overhead, packet delivery ratio, network throughput, end-to-end delay, and average hop-count.

Wireless mesh networks are an alternative technology for last-mile broadband Internet access. In WMNs, similar to ad hoc networks, each user node operates not only as a host but also as a router; user packets are forwarded to and from an Internet-connected gateway in multihop fashion. The meshed topology provides good reliability, market coverage, and scalability, as well as low upfront investments. Despite the recent startup surge in WMNs, much research remains to be done before WMNs realize their full potential. This article tackles the problem of determining the exact capacity of a WMN. The key concept we introduce to enable this calculation is the bottleneck collision domain, defined as the geographical area of the network that bounds from above the amount of data that can be transmitted in the network. We show that for WMNs the throughput of each node decreases as O(1/n), where n is the total number of nodes in the network. In contrast with most existing work on ad hoc network capacity, we do not limit our study to the asymptotic case. In particular, for a given topology and the set of active nodes, we provide exact upper bounds on the throughput of any node. The calculation can be used to provision the network, to ensure quality of service and fairness. The theoretical results are validated by detailed simulations.

We treated the surface of indium-tin oxide (ITO) substrates in two ways, (i) coating of thin insulating ITO layer or (ii) irradiation of the surface with accelerated ions, and investigated the change in sheet resistance (R s h ) and the water-contact angle (WCA). R s h increased with the thickness of the insulating ITO layer or with the ion dose. WCA dropped as a result of the surface treatment to

Fatty acids (FAs) are essential constituents of cell membranes, signaling molecules, and bioenergetic substrates. Because CD8(+) T cells undergo both functional and metabolic changes during activation and differentiation, dynamic changes in FA metabolism also occur. However, the contributions of de novo lipogenesis to acquisition and maintenance of CD8(+) T cell function are unclear. In this article, we demonstrate the role of FA synthesis in CD8(+) T cell immunity. T cell-specific deletion of acetyl coenzyme A carboxylase 1 (ACC1), an enzyme that catalyzes conversion of acetyl coenzyme A to malonyl coenzyme A, a carbon donor for long-chain FA synthesis, resulted in impaired peripheral persistence and homeostatic proliferation of CD8(+) T cells in naive mice. Loss of ACC1 did not compromise effector CD8(+) T cell differentiation upon listeria infection but did result in a severe defect in Ag-specific CD8(+) T cell accumulation because of increased death of proliferating cells. Furthermore, in vitro mitogenic stimulation demonstrated that defective blasting and survival of ACC1-deficient CD8(+) T cells could be rescued by provision of exogenous FA. These results suggest an essential role for ACC1-mediated de novo lipogenesis as a regulator of CD8(+) T cell expansion, and may provide insights for therapeutic targets for interventions in autoimmune diseases, cancer, and chronic infections.

Dendritic cells (DCs) are a heterogeneous group of professional antigen presenting cells that lie in a nexus between innate and adaptive immunity because they recognize and respond to danger signals and subsequently initiate and regulate effector T-cell responses. Initially thought to be absent from the CNS, both plasmacytoid and conventional DCs as well as DC precursors have recently been detected in several CNS compartments where they are seemingly poised for responding to injury and pathogens. Additionally, monocyte-derived DCs rapidly accumulate in the inflamed CNS where they, along with other DC subsets, may function to locally regulate effector T-cells and/or carry antigens to CNS-draining cervical lymph nodes. In this review we highlight recent research showing that (a) distinct inflammatory stimuli differentially recruit DC subsets to the CNS; (b) DC recruitment across the blood-brain barrier (BBB) is regulated by adhesion molecules, growth factors, and chemokines; and (c) DCs positively or negatively regulate immune responses in the CNS.