Specific sensitivity of the skin to ultraviolet B (UVB) rays is one of the mechanisms responsible for widespread skin damage. This study tested whether 1,3,5-trihydroxybenzene (THB), a compound abundant in marine products, might inhibit UVB radiationinduced NADPH oxidase 4 (NOX4) in both human HaCaT keratinocytes and mouse dorsal skin and explore its cytoprotective mechanism. The mechanism of action was determined using western blotting, immunocytochemistry, NADP+/NADPH assay, reactive oxygen species (ROS) detection, and cell viability assay. THB attenuated UVB-induced NOX4 expression both in vitro and in vivo, and suppressed UVB-induced ROS generation via NADP+ production, resulting in increased cell viability with decreased apoptosis. THB also reduced the expression of UVB-induced phosphorylated AMP-activated protein kinase (AMPK) and phosphorylated c-Jun N-terminal kinase (JNK). THB suppressed UVB-induced NOX4 expression and ROS generation by inhibiting AMPK and JNK signaling pathways, thereby inhibiting cellular damage. These results showed that THB could be developed as a UV protectant.
Journal of the Korea Institute of Information Security & Cryptology
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v.34
no.4
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pp.651-666
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2024
Android devices employ lock screens with various authentication methods to protect user data. However, even with the lock screen active, the device can be accessed via the Android Debug Bridge(ADB), a powerful development tool that controls devices connected through USB. In this paper, we explore methods to bypass the lock screen security mechanism by leveraging the characteristics of ADB. To achieve this, we analyze ADB commands to categorize those that can severely impact the Android system and propose LockPickFuzzer, a fuzzing test tool that automatically explores ways to combine these commands to disable lock screen security. To demonstrate LockPickFuzzer's ability to detect security vulnerabilities using ADB, we conducted experiments on the Galaxy S23 and Pixel 8, both running Android 14. The results revealed two ADB command combinations that could either steal authentication information or bypass the lock screen. We submitted a report on these discovered vulnerabilities to the Samsung security team and received official acknowledgment (SVE-2023-1344) from Samsung Electronics for one ADB command combination that can be reproduced on user devices. LockPickFuzzer is a practical tool that operates automatically without user intervention and is expected to contribute to the effective detection of security vulnerabilities caused by ADB command combinations on Android devices.
In recent years, the needs for WLANs(Wireless Local Area Networks) technology which can access to Internet anywhere have been dramatically increased particularly in SOHO(Small Office Home Office) and Hot Spot. However, unlike wired networks, there are some unique characteristics of wireless networks. These characteristics include the burst packet losses due to unreliable wireless channel. Note that burst packet losses, which occur when the distance between the wireless station and the AP(Access Point) increase or when obstacles move temporarily between the station and AP, are very frequent in 802.11 networks. Conversely, due to burst packet losses, the performance of 802.11 networks are not always as sufficient as the current application require, particularly when they use TCP at the transport layer. The high packet loss rate over wireless links can trigger unnecessary execution of TCP congestion control algorithm, resulting in performance degradation. In order to overcome the limitations of WLANs environment, MAC-layer LDA(Loss Differentiation Algorithm)has been proposed. MAC-layer LDA prevents TCP's timeout by increasing CRD(Consecutive Retry Duration) higher than burst packet loss duration. However, in the wireless channel with high packet loss rate, MAC-layer LDA does not work well because of two reason: (a) If the CRD is lower than burst packet loss duration due to the limited increase of retry limit, end-to-end performance is degraded. (b) energy of mobile device and bandwidth utilization in the wireless link are wasted unnecessarily by Reducing the drainage speed of the network buffer due to the increase of CRD. In this paper, we propose a new retransmission module based on Cross-layer approach, called BLD(Burst Loss Detection) module, to solve the limitation of previous link layer retransmission schemes. BLD module's algorithm is retransmission mechanism at IEEE 802.11 networks and performs retransmission based on the interaction between retransmission mechanisms of the MAC layer and TCP. From the simulation by using ns-2(Network Simulator), we could see more improved TCP throughput and energy efficiency with the proposed scheme than previous mechanisms.
In this Paper, we propose the new face detection and tracking method based on template matching for real-time applications such as, teleconference, telecommunication, front stage of surveillance system using face recognition, and video-phone applications. Since the main purpose of paper is to track a face regardless of various environments, we use template-based face tracking method. To generate robust face templates, we apply wavelet transform to the average face image and extract three types of wavelet template from transformed low-resolution average face. However template matching is generally sensitive to the change of illumination conditions, we apply Min-max normalization with histogram equalization according to the variation of intensity. Tracking method is also applied to reduce the computation time and predict precise face candidate region. Finally, facial components are also detected and from the relative distance of two eyes, we estimate the size of facial ellipse.
The p16 protein is a cyclin dependent kinase inhibitor that inhibits cell cycle progression from $G_1$ phase to S phase in cell cycle. Many p16 gene mutations have been noted in many cancer-cell lines and in some primary cancers, and alterations of p16 gene function by DNA methylation have been noticed in various kinds of cancer tissues and cell-lines. There have been a large body of literature has accumulated indicating that abnormal patterns of DNA methylation (both hypomethylation and hypermethylation) occur in a wide variety of human neoplasma and that these aberrations of DNA methylation may play an important epigenetic role in the development and progression of neoplasia. DNA methylation is a part of the inheritable epigenetic system that influences expression or silencing of genes necessary for normal differentiation and proliferation. Gene activity may be silenced by methylation of up steream regulatory regions. Reactivation is associated with demethylation. Although evidence or a high incidence of p16 alterations in a variety of cell lines and primary tumors has been reported, that has been contested by other investigators. The precise mechanisms by which abnormal methylation might contribute to carcinogenesis are still not fully elucidated, but conceivably could involve the modulation of oncogene and other important regulatory gene expression, in addition to creating areas of genetic instability, thus predisposing to mutational events causing neoplasia. There have been many variable results of studies of head and neck squamous cell carcinoma(HNSCC). This investigation was studied on 13 primary HNSCC for p16 gene status by protein expression in immunohistochemistry, and DNA genetic/epigenetic analyzed to determine the incidence, the mechanisms, and the potential biological significance of its Inactivation. As methylation detection method of p16 gene, the methylation specific PCR(MSP) is sensitive and specific for methylation of any block of CpG sites in a CpG islands using bisulfite-modified DNA. The genomic DNA is modified by treatment with sodium bisulfate, which converts all unmethylated cytosines to uracil(thymidine). The primers designed for MSP were chosen for regions containing frequent cytosines (to distinguish unmodified from modified DNA), and CpG pairs near the 5' end of the primers (to provide maximal discrimination in the PCR between methylated and unmethylated DNA). The two strands of DNA are no longer complementary after bisulfite treatment, primers can be designed for either modified strand. In this study, 13 paraffin embedded block tissues were used, so the fragment of DNA to be amplified was intentionally small, to allow the assessment of methylation pattern in a limited region and to facilitate the application of this technique to samlples. In this 13 primary HNSCC tissues, there was no methylation of p16 promoter gene (detected by MSP and automatic sequencing). The p16 protein-specific immunohistochemical staining was performed on 13 paraffin embedded primary HNSCC tissue samples. Twelve cases among the 13 showed altered expression of p16 proteins (negative expression). In this study, The author suggested that low expression of p16 protein may play an important role in human HNSCC, and this study suggested that many kinds of genetic mechanisms including DNA methylation may play the role in carcinogenesis.
The objective of the present studies was to develop and validate a system for isolation, purification and extended culture of pigment-producing cells in alpaca skin (melanocytes) responsible for coat color and to determine the effect of alpha melanocyte stimulating hormone treatment on mRNA expression for the melanocortin 1 receptor, a key gene involved in coat color regulation in other species. Skin punch biopsies were harvested from the dorsal region of 1-3 yr old alpacas and three different enzyme digestion methods were evaluated for effects on yield of viable cells and attachment in vitro. Greatest cell yields and attachment were obtained following dispersion with dispase II relative to trypsin and trypsin-EDTA treatment. Culture of cells in medium supplemented with basic fibroblast growth factor, bovine pituitary extract, hydrocortisone, insulin, 12-O-tetradecanolphorbol-13-acetate and cholera toxin yielded highly pure populations of melanocytes by passage 3 as confirmed by detection of tyrosinase activity and immunocytochemical localization of melanocyte markers including tyrosinase, S-100 and micropthalmia-associated transcription factor. Abundance of mRNA for tyrosinase, a key enzyme in melanocyte pigment production, was maintained through 10 passages showing preservation of melanocyte phenotypic characteristics with extended culture. To determine hormonal responsiveness of cultured melanocytes and investigate regulation of melanocortin 1 receptor expression, cultured melanocytes were treated with increasing concentrations of ${\alpha}$-melanocyte stimulating hormone. Treatment with ${\alpha}$-melanocyte stimulating hormone increased melanocortin receptor 1 mRNA in a dose dependent fashion. The results demonstrated culture of pure populations of alpaca melanocytes to 10 passages and illustrate the potential utility of such cells for studies of intrinsic and extrinsic regulation of genes controlling pigmentation and coat color in fiber-producing species.
Sensor networks consist of many tiny sensor nodes that collaborate among themselves to collect, process, analyze, and disseminate data. In sensor networks, sensor nodes are typically powered by batteries, and have limited computing resources. Moreover, the redeployment of nodes by energy exhaustion or their movement makes network topology change dynamically. These features incur problems that do not appear in traditional, wired networks. Security in sensor networks is challenging problem due to the nature of wireless communication and the lack of resources. Several efforts are underway to provide security services in sensor networks, but most of them are preventive approaches based on cryptography. However, sensor nodes are extremely vulnerable to capture or key compromise. To ensure the security of the network, it is critical to develop suity mechanisms that can survive malicious attacks from "insiders" who have access to the keying materials or the full control of some nodes. In order to protect against insider attacks, it is necessary to understand how an insider can attack a sensor network. Several attacks have been discussed in the literature. However, insider attacks in general have not been thoroughly studied and verified. In this paper, we study the insider attacks against routing protocols in sensor networks using the Ad-hoc On-Demand Distance Vector (AODV) protocol. We identify the goals of attack, and then study how to achieve these goals by modifying of the routing messages. Finally, with the simulation we study how an attacker affects the sensor networks. After we understand the features of inside attacker, we propose a detect mechanism using hop count information.
UWB signal with high resolution capability can be used to estimate ranging and positioning in wireless personal area network. The node works on its local clock and the frequency differences of nodes have serious affects on ranging algorithms estimating locations of mobile nodes. The low rate UWB, IEEE802.15.4a, describes asynchronous two way ranging methods such as TWR and SDS-TWR working without any additional network synchronization, but the algorithms can not eliminate the effect of clock frequency differences. Therefore, the mechanisms to characterize the crystal difference is essential in typical UWB PHY implementations. In high rate UWB, characterizing of crystal offset with tracking loop is not required. But, detection of the clock frequency offset between the local clock and remote clock can be performed if there is little noise induced jitter. In this paper, we complete related ranging equations of high rate UWB based on TWR with relative frequency offset, and analyze a residual error in the ideal equations. We also evaluate the performance of the relative frequency offset algorithm by simulation and analyze the ranging errors according to the number of TWR to compensate coarse clock resolution. The results show that the relative frequency offset compensation and many times of TWR enhance the performance to converge to a limited ranging errors even with coarse clock resolutions.
The purpose of this study was to provide a detailed explanation of the mechanism of bisanthracycline, WP 631 in comparison to doxorubicin (DOX), a first generation anthracycline, currently the most widely used pharmaceutical in clinical oncology. Experiments were performed in SKOV-3 ovarian cancer cells which are otherwise resistant to standard drugs such as cis-platinum and adriamycin. As attention was focused on the ability of WP 631 to induce apoptosis, this was examined using a double staining method with Annexin V and propidium iodide probes, with measurement of the level of intracellular calcium ions and cytosolic cytochrome c. The western blotting technique was performed to confirm PARP cleavage. We also investigated the involvement of caspase activation and DNA degradation (comet assay and immunocytochemical detection of phosphorylated H2AX histones) in the development of apoptotic events. WP 631 demonstrated significantly higher effectiveness as a pro-apoptotic drug than DOX. This was evident in the higher levels of markers of apoptosis, such as the externalization of phosphatidylserine and the elevated level of cytochrome c. An extension of incubation time led to an increase in intracellular calcium levels after treatment with DOX. Lower changes in the calcium content were associated with the influence of WP 631. DOX led to the activation of all tested caspases, 8, 9 and 3, whereas WP 631 only induced an increase in caspase 8 activity after 24h of treatment and consequently led to the cleavage of PARP. The lack of active caspase 3 had no outcome on the single and double-stranded DNA breaks. The obtained results show that WP 631 was considerably more genotoxic towards the investigated cell line than DOX. This effect was especially visible after longer times of incubation. The above detailed studies indicate that WP 631 generates early apoptosis and cell death independent of caspase-3, detected at relatively late time points. The observed differences in the mechanisms of the action of WP631 and DOX suggest that this bisanthracycline can be an effective alternative in ovarian cancer treatment.
Kim, Dong-Hyun;Heo, Tae-Hwe;Kim, June-Bum;Kim, Sung-Jo
Journal of Life Science
/
v.20
no.8
/
pp.1281-1286
/
2010
Gaucher disease (GD) is caused by glucocerebrosidase functional deficiency and the most prevalent lysosomal storage disorder (LSD), with an incidence of about 1 in 20,000 new births. Resveratrol, one kind of phytoalexin, is a produced naturally by several plants and has anti-tumor, anti-aging, anti-inflammatory and neuro-protective effects. In this paper we provide the cellular protective effect of resveratrol in both type I and type II Gaucher disease cells. Resveratrol treatment did not show any significant change in the p21 and p53 mRNA expression level, however expression level of the p21 protein, a cell cycle arrest factor, shows significant increment in both types of Gaucher disease cells. These cell cycle arrest patterns were confirmed by both MTT assay measurement and microscopy detection. In comparison, expression level of poly ADP ribose polymerase (PARP), an apoptosis indicator protein, was significantly decreased in both type I and II Gaucher disease cells after treatment with resveratrol. This result indicates that resveratrol relievescellular apoptotic stress fromtype I and II Gaucher disease cells. Therefore, we demonstrate that resveratrol inhibits cell proliferation via p21 activity and activates cellular repair systems for Gaucher disease cells. Our results provide at least one of the molecular mechanisms of Gaucher disease and may allow the verification of potential drug targets for therapeutic trials.
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