무선 디지털카메라의 소유자 특정 방안에 대한 연구

송선범,이상진,박정흠 한국디지털포렌식학회 2022 디지털 포렌식 연구 Vol.16 No.3

Recently, smaller wearable cameras are being released. The wearable camera is connected to the smartphone using Wi-Fi communication and provides a function to view the recorded video in real time. In spite of this increased convenience, crimes related to illegal filming have increased dramatically. In recent criminal cases, small wearable cameras such as an action-cam which does not have media storage are being utilized. Criminals install the smaller wearable camera at a toilet or a fitting room, and then connect it to their smartphone using Wi-Fi communication. In this process, camera image is streaming to the smartphone and make it to video or graphic files on a real-time basis. Without media storage, it is difficult to specify who had installed the small wearable camera which was found in the crime scene. In this paper, we propose a method to identify Wi-Fi MAC address of a paired smartphone using a small wearable camera without media storage. Using a Wi-Fi MAC address information of smartphone, we can check manufacturer of the smartphone. Also, the IMEI value of the smartphone can be obtained through the manufacturer. And then, if we send the obtained information to the telecommunications company, we can check the smartphone subscriber who involved in illegal filming crime. 사용자의 몸에 직접 부착하는 소형 웨어러블 카메라가 출시되고 있다. 현재 웨어러블 카메라는 Wi-Fi 통신을 이용하여 스마트폰과 연결한 뒤 촬영된 영상을 실시간으로 볼 수 있는 기능을 제공하고 있고, 편리성이 더욱 커질 전망이지만 이러한 편리성을 활용하여 불법 촬영 범죄로 악용되는 사례가 대폭 증가했다. 최근에는 카메라에 영상을 저장하는 메모리를 삽입하지 않고, 화장실 또는 탈의실에 설치하고 Wi-Fi 통신을 이용하여 용의자의 스마트폰에 연결한 뒤 설치 장소에서 이동하여 근거리에서 촬영된 영상을 실시간으로 영상을 녹화 및 캡처하는 방식으로 범죄 수법이 고도화되고 있다. 이때 사건 현장에서 발견된 카메라에는 인쇄회로기판에 부착된 메모리만 존재하여 용의자를 확인하는 것은 어려운 실정이다. 본 논문에서는 무선 디지털카메라 내부에 인쇄회로기판에 부착된 메모리만 존재하는 경우에 포렌식 조사하는 기법을 제안한다. 제안한 분석기법을 활용하여 스마트폰과 연결된 Wi-Fi MAC 주소를 확보하고, 확보된 Wi-Fi MAC 주소로 스마트폰 제조사를 확인 및 IMEI 정보를 확인한 다음, 확인된 IMEI 정보를 통신사에 의뢰한다면 스마트폰 가입자를 확인할 수 있어 불법 촬영 범죄의 혐의자를 확인할 수 있다.

Modulation of Mitochondrial Membrane Potential and ROS Generation by Nicotinamide in a Manner Independent of SIRT1 and Mitophagy

송선범,장소영,강현태,Bie Wei,전운우,윤계순,황은성 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.7

Nicotinamide (NAM) plays essential roles in physiology through facilitating NAD+ redox homeostasis. Importantly, at high doses, it protects cells under oxidative stresses, and has shown therapeutic effectiveness in a variety of disease conditions. In our previous studies, NAM lowered reactive oxygen species (ROS) levels and extended cellular life span in primary human cells. In the treated cells, levels of NAD+/NADH and SIRT1 activity increased, while mitochondrial content decreased through autophagy activation. The remaining mitochondria were marked with low superoxide levels and high membrane potentials (Δψm); we posited that the treatment of NAM induced an activation of mitophagy that is selective for depolarized mitochondria, which produce high levels of ROS. However, evidence for the selective mitophagy that is mediated by SIRT1 has never been provided. This study sought to explain the mechanisms by which NAM lowers ROS levels and increases Δψm. Our results showed that NAM and SIRT1 activation exert quite different effects on mitochondrial physiology. Furthermore, the changes in ROS and Δψm were not found to be mediated through autophagy or SIRT activation. Rather, NAM suppressed superoxide generation via a direct reduction of electron transport, and increased Δψm via suppression of mitochondrial permeability transition pore formation. Our results dissected the effects of cellular NAD+ redox modulation, and emphasized the importance of the NAD+/NADH ratio in the mitochondria as well as the cytosol in maintaining mitochondrial quality.

식물추출물 항산화효능 기전의 일부로서의 활성산소 발생 억제 효과

송선범(Seon Beom Song),정구준(Gu June Chung),정희진(Hee Jin Jung),장정윤(Jung Yoon Jang),정해영(Hae Young Chung),김남득(Nam Deuk Kim),이지현(Ji-Hyeon Lee),민경진(Kyungjin Min),박순영(Sun Yeong Park),곽충실(Chung Shil Kwak),황은성(Eun 한국식품과학회 2021 한국식품과학회지 Vol.53 No.6

세포 내에서의 활성산소(ROS) 생성을 억제하는 일은 항산화제의 작동방식으로 기존에 알려진 ROS의 화학적 소거보다 조직의 산화적 손상을 줄이는 방법으로서 효과가 뛰어날 것으로 기대되지만, 이러한 전략은 지금까지의 연구들에서 거의 검토되지 않고 있다. 본 연구에서는 항산화 효능이 알려진 식물시료들이 실제로 세포에서 ROS 생성을 제어하여 항산화 효과를 발휘하는지를 쇠뜨기, 가죽나무잎, 달맞이순, 그리고 토마토의 에탄올 추출물을 가지고 조사하였다. 이 네 가지 식물 시료들은 모두 비슷하게 세포내 ROS의 수준을 감소시켰다. 그러나, 가죽나무잎, 달맞이순, 그리고 토마토 시료들만이 미토콘드리아 질을 개선하여 미토콘드리아로부터의 ROS 생성을 감소시켰는데, 이들은 또한 세포와 조직내 lipofuscin과 malondialdehyde의 축적을 줄여서 뚜렷한 산화적 손상을 억제하는 효과를 보였다. 이들은 나아가서 초파리의 수명을 연장시키는 효과도 보였다. 미토콘드리아 질 향상 효과가 거의 없었던 쇠뜨기 시료는 산화적 손상물과 초파리 수명에 거의 영향을 미치지 못하였다. 이러한 결과는 식물 시료들의 항산화 효과가 ROS의 화학적 소거와 미토콘드리아 질의 향상을 통해 발현될 수 있는데, 후자의 효과가 실제로 체내에서 산화적 손상을 억제하는데 중요하게 작용할 가능성을 시사해 준다. 향후, 식물시료들의 항산화 효능에 대해서 이러한 ROS 발생억제 기전을 대상으로 조사하는 일은 그 유용성을 판단하는데 있어서 큰 도움이 될 것으로 기대된다. Chemical scavenging of reactive oxygen species (ROS) is considered a major mechanism of antioxidant effects, but preventing ROS generation can be more efficient in attenuating oxidative damage. In this study, the extracts of plants, Solanum lycopersicum, Ailanthus altissima, Equisetum arvense, and Oenothera biennis, were tested to determine whether their antioxidative effects are driven by the prevention of superoxide generation from mitochondria, a major ROS generator. While all the extracts efficiently attenuated the elevation of ROS levels in human fibroblasts and inflammation-induced mice, those of S. lycopersicum, A. altissima, and O. laciniata only suppressed mitochondrial ROS generation and reduced levels of lipofuscin and lipid peroxidation. Furthermore, the extracts of A. altissima and O. laciniata extended the lifespan of fruit flies. Our results suggest that plant extracts with anti-oxidative effects differ in their ability to prevent ROS generation, which may be associated with the attenuation of oxidative damage in cells and animal tissues.

Lipofuscin Granule Accumulation Requires Autophagy Activation

황은성,송선범,Woosung Shim 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.8

Lipofuscins are oxidized lipid and protein complexes that accumulate during cellular senescence and tissue aging, regarded as markers for cellular oxidative damage, tissue aging, and certain aging-associated diseases. Therefore, understanding their cellular biological properties is crucial for effective treatment development. Through traditional microscopy, lipofuscins are readily observed as fluorescent granules thought to accumulate in lysosomes. However, lipofuscin granule formation and accumulation in senescent cells are poorly understood. Thus, this study examined lipofuscin accumulation in human fibroblasts exposed to various stressors. Our results substantiate that in glucose-starved or replicative senescence cells, where elevated oxidative stress levels activate autophagy, lipofuscins predominately appear as granules that co-localize with autolysosomes due to lysosomal acidity or impairment. Meanwhile, autophagosome formation is attenuated in cells experiencing oxidative stress induced by a doxorubicin pulse and chase, and lipofuscin fluorescence granules seldom manifest in the cytoplasm. As Torin-1 treatment activates autophagy, granular lipofuscins intensify and dominate, indicating that autophagy activation triggers their accumulation. Our results suggest that high oxidative stress activates autophagy but fails in lipofuscin removal, leaving an abundance of lipofuscin-filled impaired autolysosomes, referred to as residual bodies. Therefore, future endeavors in treating lipofuscin pathology-associated diseases and dysfunctions through autophagy activation demand meticulous consideration.

Impaired Autophagic Flux in Glucose-Deprived Cells: An Outcome of Lysosomal Acidification Failure Exacerbated by Mitophagy Dysfunction

황은성,송선범 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.11

Autophagy dysfunction is associated with human diseases and conditions including neurodegenerative diseases, metabolic issues, and chronic infections. Additionally, the decline in autophagic activity contributes to tissue and organ dysfunction and aging-related diseases. Several factors, such as down-regulation of autophagy components and activators, oxidative damage, microinflammation, and impaired autophagy flux, are linked to autophagy decline. An autophagy flux impairment (AFI) has been implicated in neurological disorders and in certain other pathological conditions. Here, to enhance our understanding of AFI, we conducted a comprehensive literature review of findings derived from two well-studied cellular stress models: glucose deprivation and replicative senescence. Glucose deprivation is a condition in which cells heavily rely on oxidative phosphorylation for ATP generation. Autophagy is activated, but its flux is hindered at the autolysis step, primarily due to an impairment of lysosomal acidity. Cells undergoing replicative senescence also experience AFI, which is also known to be caused by lysosomal acidity failure. Both glucose deprivation and replicative senescence elevate levels of reactive oxygen species (ROS), affecting lysosomal acidification. Mitochondrial alterations play a crucial role in elevating ROS generation and reducing lysosomal acidity, highlighting their association with autophagy dysfunction and disease conditions. This paper delves into the underlying molecular and cellular pathways of AFI in glucose-deprived cells, providing insights into potential strategies for managing AFI that is driven by lysosomal acidity failure. Furthermore, the investigation on the roles of mitochondrial dysfunction sheds light on the potential effectiveness of modulating mitochondrial function to overcome AFI, offering new possibilities for therapeutic interventions.