190 research outputs found

    Efficient Wu-Manber Pattern Matching Hardware for Intrusion and Malware Detection.

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    Network intrusion detection systems and antivirus software are essential in detecting malicious network traffic and attacks such as denial-of-service and malwares. Each attack, worm or virus has its own distinctive signature. Signature-based intrusion detection and antivirus systems depend on pattern matching to look for possible attack signatures. Pattern matching is a very complex task, which requires a lot of time, memory and computing resources. Software-based intrusion detection is not fast enough to match high network speeds and the increasing number of attacks. In this paper, we propose special purpose hardware for Wu-Manber pattern matching algorithm. FPGAs form an excellent choice because of their massively parallel structure, reprogrammable logic and memory resources. The hardware is designed in Verilog and implemented using Xilinx ISE. For evaluation, we dope network traffic traces collected using Wireshark with 2500 signatures from the ClamAV virus definitions database. Experimental results show high speed that reaches up to 216 Mbps. In addition, we evaluate time, device usage, and power consumption

    The Level Of Possession Of The Students At The Hashemite University Of Professional And Family Counseling Skills In Light Of Achievement And Gender Variables

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    The present study aimed to identify the level of owning a field training students majoring in psychological counseling at the Hashemite University of professional and family counseling skills in light of achievement and gender variables. The subjects of the study comprised of (100) subjects of field training students in the second semester of the academic year 2014-2015. A questionnaire was used in this study to identify the professional counseling skills and another questionnaire for family counseling skills. Results of the study have shown that field training students majoring in psychological counseling at the Hashemite University own professional and family counseling skills moderately. The results also indicated that the level of students' possession of the professional and family counseling skills rises as GPA rises and that females are more equipped to those skills, compared with males

    Moral Disengagement and its Relationship to Moral Identity among Adolescents

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    ملخص: هدفت الدراسة الحالية إلى دراسة العلاقة بين التحرّر الأخلاقي والهويّة الأخلاقيّة، كما هدفت إلى معرفة مستوى التحرّر الأخلاقي والهويّة الأخلاقيّة، ومعرفة ما إذا كانت هنالك فروق في مستوى التحرّر الأخلاقي والهويّة الأخلاقيّة تُعزى لمُتغيّريّ الجنس، والصف الدّراسي. ولتحقيق أهداف الدّراسة، اُستُخدم مقياس التحرّر الأخلاقي، ومقياس الهويّة الأخلاقيّة. تكونت عينة الدّراسة من (1032) من المراهقين تم اختيارهم بالطريقة القصدية. أسفرت نتائج الدراسة عن مستويات منخفضة من التحرّر الأخلاقي ومرتفعة من الهويّة الأخلاقيّة لدى عينة الدراسة. وأظهرت النتائج وجود فروق دالّة إحصائيًّا في مستوى التحرّر الأخلاقي وأبعاده (التبرير الأخلاقي، والمسميات الملطفة، والمقارنة المفيدة، وإزاحة المسؤولية، ونشر المسؤولية، وتجاهل العواقب، وعزو اللوم، والتجريد من الخصائص الإنسانية) تُعزى لمُتغيّر الجنس، حيث إنّ مستوى التحرّر الأخلاقي وأبعاده لدى الذّكور أعلى منه لدى الإناث، ووجود فروق دالّة إحصائيًّا في مستوى التحرّر الأخلاقي وأبعاده (التبرير الأخلاقي، والمسميات الملطفة، ونشر المسؤولية، وعزو اللوم، والتجريد من الخصائص الإنسانية) تُعزى لمُتغيّر الصف الدّراسي، حيث إنّ مستوى التحرّر الأخلاقي وأبعاده لدى طلبة الصف السابع أعلى منه لدى طلبة الصف الثامن والصف التاسع. وكذلك أظهرت النتائج وجود فروق دالّة إحصائيا في مستوى الهويّة الأخلاقيّة وبعديها (الترميز، والاستيعاب) تُعزى لمُتغيّر الجنس، ولصالح الإناث، ووجود فروق دالّة إحصائيًّا في مستوى الهويّة الأخلاقيّة وبُعديها (الترميز، والاستيعاب) تُعزى لمُتغيّر الصف الدّراسي، ولصالح طلبة الصف الثامن. وأخيرًا أظهرت النتائج وجود علاقة ارتباطية سالبة ودالّة إحصائيًّا بين التحرّر الأخلاقي والهويّة الأخلاقيّة. واستنادًا الى النتائج، توصي الدراسة بالاستفادة من المستوى المرتفع للهوية الأخلاقيّة عند المراهقين في تنمية، وتطوير جوانب الشخصيّة الأخرى، كالمسؤولية الاجتماعيّة.Abstract: This study aimed to examine the relationship between moral disengagement and moral identity; moreover, it aimed at identifying the level of moral disengagement as well as the moral identity. Furthermore, this paper also aimed to see whether there are statistically significant differences in the level of moral disengagement and moral identity can attributed to so gender and class levels. To achieve the objective of the study, both moral disengagement scale, and moral identity scale were used. The sample of the study consisted of (1032) adolescents chosen purposive method. The results of the study revealed low levels of moral disengagement and high levels of moral identity. Male adolescents were significantly higher than their female counterpart regarding the moral disengagement and its dimensions (moral justification, euphemistic language, advantageous comparison, displacement of responsibility, diffusion of responsibility, distorting consequence, attribution of blame, and dehumanization), and seventh-grade were significantly higher than their eighth and ninth grade counterpart regarding the moral disengagement and its dimensions (moral justification, euphemistic language, diffusion of responsibility,  attribution of blame, and dehumanization). It was found that the levels of moral identity and its dimensions (symbolization and internalization) were significantly higher in females than males. It was also found that the levels of moral identity and its dimensions (symbolization and internalization) were significantly higher eighth-grade than seventh and ninth grade. Finally, the results showed a negative relationship between moral disengagement and moral identity. Based on the results, the study recommends taking advantage of the high level of moral identity among adolescents in the development of other aspects of personality, such as social responsibility

    Temozolomide induces senescence but not apoptosis in human melanoma cells

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    Temozolomide (TMZ), a DNA alkylating agent used in the treatment of melanoma, is believed to mediate its effect by addition of a methyl group to the O6 position of guanine in DNA. Resistance to the agent may be in part due to the activity of O6-methylguanine-DNA methyl transferase (MGMT). In the present study, we show that sensitivity of melanoma cells to TMZ was dependent on their p53 status and levels of MGMT. Analysis of the mechanisms underlying reduced viability showed no evidence for induction of apoptosis even though marked levels of apoptosis was seen in TK6 lymphoma cells. Sensitivity of melanoma cells was associated with p53-dependent G2/M cell cycle arrest and induction of senescence. To verify the role of p53, the assays were repeated in presence of pifithrin-α, an inhibitor of p53. This resulted in increased viability of melanoma cells with wild-type p53 and reversed G2/M cell cycle arrest. Paradoxically, apoptosis was increased in melanoma but decreased as expected in TK6 lymphoma cells. These results are consistent with the view that TMZ is relatively ineffective against melanoma due to defective apoptotic signalling resulting from activation of p53. The nature of the defects in apoptotic signalling remains to be explored

    WWOX sensitises ovarian cancer cells to paclitaxel via modulation of the ER stress response

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    There are clear gaps in our understanding of genes and pathways through which cancer cells facilitate survival strategies as they become chemoresistant. Paclitaxel is used in the treatment of many cancers, but development of drug resistance is common. Along with being an antimitotic agent paclitaxel also activates endoplasmic reticulum (ER) stress. Here, we examine the role of WWOX (WW domain containing oxidoreductase), a gene frequently lost in several cancers, in mediating paclitaxel response. We examine the ER stress-mediated apoptotic response to paclitaxel in WWOX-transfected epithelial ovarian cancer (EOC) cells and following siRNA knockdown of WWOX. We show that WWOX-induced apoptosis following exposure of EOC cells to paclitaxel is related to ER stress and independent of the antimitotic action of taxanes. The apoptotic response to ER stress induced by WWOX re-expression could be reversed by WWOX siRNA in EOC cells. We report that paclitaxel treatment activates both the IRE-1 and PERK kinases and that the increase in paclitaxel-mediated cell death through WWOX is dependent on active ER stress pathway. Log-rank analysis of overall survival (OS) and progression-free survival (PFS) in two prominent EOC microarray data sets (Tothill and The Cancer Genome Atlas), encompassing ~800 patients in total, confirmed clinical relevance to our findings. High WWOX mRNA expression predicted longer OS and PFS in patients treated with paclitaxel, but not in patients who were treated with only cisplatin. The association of WWOX and survival was dependent on the expression level of glucose-related protein 78 (GRP78), a key ER stress marker in paclitaxel-treated patients. We conclude that WWOX sensitises EOC to paclitaxel via ER stress-induced apoptosis, and predicts clinical outcome in patients. Thus, ER stress response mechanisms could be targeted to overcome chemoresistance in cancer

    MGMT gene promoter methylation correlates with tolerance of temozolomide treatment in melanoma but not with clinical outcome

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    BACKGROUND: Despite limited clinical efficacy, treatment with dacarbazine or temozolomide (TMZ) remains the standard therapy for metastatic melanoma. In glioblastoma, promoter methylation of the counteracting DNA repair enzyme O(6)-methylguanine-DNA-methyltransferase (MGMT) correlates with survival of patients exposed to TMZ in combination with radiotherapy. For melanoma, data are limited and controversial. METHODS: Biopsy samples from 122 patients with metastatic melanoma being treated with TMZ in two multicenter studies of the Dermatologic Cooperative Oncology Group were investigated for MGMT promoter methylation. We used the COBRA (combined bisulphite restriction analysis) technique to determine aberrant methylation of CpG islands in small amounts of genomic DNA isolated from paraffin-embedded tissue sections. To detect aberrant methylation, bisulphite-treated DNA was amplified by PCR, enzyme restricted, and visualised by gel electrophoresis. RESULTS: Correlation with clinical data from 117 evaluable patients in a best-response evaluation indicated no statistically significant association between MGMT promoter methylation status and response. A methylated MGMT promoter was observed in 34.8% of responders and 23.4% of non-responders (P=0.29). In addition, no survival advantage for patients with a methylated MGMT promoter was detectable (P=0.79). Interestingly, we found a significant correlation between MGMT methylation and tolerance of therapy. Patients with a methylated MGMT promoter had more severe adverse events, requiring more TMZ dose reductions or discontinuations (P=0.007; OR 2.7 (95% CI: 1.32-5.7)). Analysis of MGMT promoter methylation comparing primaries and different metastases over the clinical course revealed no statistical difference (P=0.49). CONCLUSIONS: In advanced melanoma MGMT promoter, methylation correlates with tolerance of therapy, but not with clinical outcome

    The Combination of BH3-Mimetic ABT-737 with the Alkylating Agent Temozolomide Induces Strong Synergistic Killing of Melanoma Cells Independent of p53

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    Metastatic melanoma has poor prognosis and is refractory to most conventional chemotherapies. The alkylating agent temozolomide (TMZ) is commonly used in treating melanoma but has a disappointing response rate. Agents that can act cooperatively with TMZ and improve its efficacy are thus highly sought after. The BH3 mimetic ABT-737, which can induce apoptosis by targeting pro-survival Bcl-2 family members, has been found to enhance the efficacy of many conventional chemotherapeutic agents in multiple cancers. We found that combining TMZ and ABT-737 induced strong synergistic apoptosis in multiple human melanoma cell lines. When the drugs were used in combination in a mouse xenograft model, they drastically reduced tumor growth at concentrations where each individual drug had no significant effect. We found that TMZ treatment elevated p53 levels, and that the pro-apoptotic protein Noxa was elevated in TMZ/ABT-737 treated cells. Experiments with shRNA demonstrated that the synergistic effect of TMZ and ABT-737 was largely dependent on Noxa. Experiments with nutlin-3, a p53 inducer, demonstrated that p53 induction was sufficient for synergistic cell death with ABT-737 in a Noxa-dependent fashion. However, p53 was not necessary for TMZ/ABT-737 synergy as demonstrated by a p53-null line, indicating that TMZ and ABT-737 together induce Noxa in a p53-independent fashion. These results demonstrate that targeting anti-apoptotic Bcl-2 members is a promising method for treating metastatic melanoma, and that clinical trials with TMZ and Bcl-2 inhibitors are warranted

    GRP78 Knockdown Enhances Apoptosis via the Down-Regulation of Oxidative Stress and Akt Pathway after Epirubicin Treatment in Colon Cancer DLD-1 Cells

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    INTRODUCTION: The 78-kDa glucose-regulated protein (GRP78) is induced in the cancer microenvironment and can be considered as a novel predictor of responsiveness to chemotherapy in many cancers. In this study, we found that intracellular reactive oxygen species (ROS) and nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation were higher in GRP78 knockdown DLD-1 colon cancer cells compared with scrambled control cells. METHODOLOGY/PRINCIPAL FINDINGS: Treatment with epirubicin in GRP78 knockdown DLD-1 cells enhanced apoptosis and was associated with decreased production of intracellular ROS. In addition, apoptosis was increased by the antioxidants propyl gallate (PG) and dithiothreitol (DTT) in epirubicin-treated scrambled control cells. Epirubicin-treated GRP78 knockdown cells resulted in more inactivated Akt pathway members, such as phosphorylated Akt and GSK-3β, as well as downstream targets of β-catenin expression. Knockdown of Nrf2 with small interfering RNA (siRNA) increased apoptosis in epirubicin-treated GRP78 knockdown cells, which suggested that Nrf2 may be a primary defense mechanism in GRP78 knockdown cells. We also demonstrated that epirubicin-treated GRP78 knockdown cells could decrease survival pathway signaling through the redox activation of protein phosphatase 2A (PP2A), which is a serine/threonine phosphatase that negatively regulates the Akt pathway. CONCLUSIONS: Our results indicate that epirubicin decreased the intracellular ROS in GRP78 knockdown cells, which decreased survival signaling through both the Akt pathway and the activation of PP2A. Together, these mechanisms contributed to the enhanced level of epirubicin-induced apoptosis that was observed in the GRP78 knockdown cells
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