Comparison of ensemble simple feed forward neural network and deep learning neural network on Phishing Detection

Phishing attack is one of wide spread cybercrimes due to the advancement of the Internet. There are many forms of phishing attack and the most common one is through email. The attacker tries to pretend by sending email from an official organization or body to deceive the user in giving in their credential user name and password. The username and password are then used for malicious purpose. Many methods have been used to detect these phishing attacks; however, the attack evolved too quickly to be solved by manual approach. Therefore, automated phishing detection through artificial intelligence approach would be more feasible. In this paper, a comparison study for phishing detection between two neural networks which are the feedforward neural network and the deep learning neural network is carried out. The result is empirically evaluated to determine which method performs better in phishing detection

Рифма в рамках средневекового крымскотатарского силлабического стиха

В предложенной статье представлен теоретический материал, который раскрывает сущность и особенности рифмы, подкреплённый необходимым материалом из крымскотатарской литературы.У запропонованій статті представлений теоретичний матеріал, що розкриває сутність і особливості рими, підкріплений необхідним матеріалом із кримськотатарської літератури.In offered article the theoretical material which opens essence and features of the rhyme, supported by a necessary material from crimean tatars literatures is submitted

Modelling of photonic wire Bragg Gratings

Some important properties of photonic wire Bragg grating structures have been investigate. The design, obtained as a generalisation of the full-width gap grating, has been modelled using 3D finite-difference time-domain simulations. Different types of stop-band have been observed. The impact of the grating geometry on the lowest order (longest wavelength) stop-band has been investigated - and has identified deeply indented configurations where reduction of the stop-bandwidth and of the reflectivity occurred. Our computational results have been substantially validated by an experimental demonstration of the fundamental stop-band of photonic wire Bragg gratings fabricated on silicon-on-insulator material. The accuracy of two distinct 2D computational models based on the effective index method has also been studied - because of their inherently much greater rapidity and consequent utility for approximate initial designs. A 2D plan-view model has been found to reproduce a large part of the essential features of the spectral response of full 3D models

The Influences of Diesel Particulate Filter Installation on Air Pollutant Emissions for Used Vehicles

Three kinds of diesel particulate filters (DPFs) were installed on used diesel-powered vehicles to investigate their influences on air pollutant emissions. The air pollutant emissions were measured before, after and running for specific distances to assess the deterioration effect. The emission measurement was performed on a chassis dynamometer. The results show that emissions of smoke, CO and HC are all reduced after DPF installation. After 20000 km driving, the emission concentrations of the above 3 criteria air pollutants do not increase in comparison with that right after installation. When DPFs are installed, the emissions of PAHs (polycyclic aromatic hydrocarbons) are reduced by 85.6-89.4% and 69.0-89.2% for heavy-duty diesel vehicles (HDVs) and light-duty diesel vehicles (LDVs), respectively. After driving 20000 km for HDVs and 2500 km for LDVs, PAH emissions do not increase in comparison with that right after installation, indicating that the DPFs do not deteriorate after driving for the test mileages. The lower molecular weight PAHs predominates in the exhaust both before and after DPF installation. The results also show the reduction rate is higher for higher molecular weight PAHs due to their tendency to adsorb on particulate

The synthesized 2-(2-fluorophenyl)-6,7-methylenedioxyquinolin-4-one (CHM-1) promoted G2/M arrest through inhibition of CDK1 and induced apoptosis through the mitochondrial-dependent pathway in CT-26 murine colorectal adenocarcinoma cells

In this study, we investigated the effects of 2-(2-fluorophenyl)-6,7-methylenedioxyquinolin-4-one (CHM-1) on cell viability, cell cycle arrest and apoptosis in CT-26 murine colorectal adenocarcinoma cells. For determining cell viability, the MTT assay was used. CHM-1 promoted G2/M arrest by PI staining and flow cytometric analysis. Apoptotic cells were evaluated by DAPI staining. We used CDK1 kinase assay, Western blot analysis and caspase activity assays for examining the CDK1 activity and proteins correlated with apoptosis and cell cycle arrest. The in vivo anti-tumor effects of CHM-1-P were evaluated in BALB/c mice inoculated with CT-26 cells orthotopic model. CHM-1 induced CT-26 cell viability inhibition and morphologic changes in a dose-dependent and time-dependent manner and the approximate IC(50) was 742.36 nM. CHM-1 induced significant G2/M arrest and apoptosis in CT-26 cells. CHM-1 inhibited the CDK1 activity and decreased CDK1, Cyclin A, Cyclin B protein levels. CHM-1 induced apoptosis in CT-26 cells and promoted increasing of cytosolic cytochrome c, AIF, Bax, BAD, cleavage of pro-caspase-9, and -3. The significant reduction of caspase-9 and -3 activity and increasing the viable CT-26 cells after pretreated with caspase-9 and -3 inhibitor indicated that CHM-1-induced apoptosis was mainly mediated a mitochondria-dependent pathway. CHM-1-P improved mice survival rate, and enlargement of the spleen and liver metastasis were significantly reduced in groups treated with either 10 mg/kg and 30 mg/kg of CHM-1-P and 5-FU in comparison to these of CT-26/BALB/c mice. Taken together, CHM-1 acted against colorectal adenocarcinoma cells in vitro via G2/M arrest and apoptosis, and CHM-1-P inhibited tumor growth in vivo

Low-Luminosity Accretion in Black Hole X-ray Binaries and Active Galactic Nuclei

At luminosities below a few percent of Eddington, accreting black holes switch to a hard spectral state which is very different from the soft blackbody-like spectral state that is found at higher luminosities. The hard state is well-described by a two-temperature, optically thin, geometrically thick, advection-dominated accretion flow (ADAF) in which the ions are extremely hot (up to $10^{12}$ K near the black hole), the electrons are also hot ($\sim10^{9-10.5}$ K), and thermal Comptonization dominates the X-ray emission. The radiative efficiency of an ADAF decreases rapidly with decreasing mass accretion rate, becoming extremely low when a source reaches quiescence. ADAFs are expected to have strong outflows, which may explain why relativistic jets are often inferred from the radio emission of these sources. It has been suggested that most of the X-ray emission also comes from a jet, but this is less well established.Comment: To appear in "From X-ray Binaries to Quasars: Black Hole Accretion on All Mass Scales" edited by T. Maccarone, R. Fender, L. Ho, to be published as a special edition of "Astrophysics and Space Science" by Kluwe

Photoproduction of mesons off nuclei

Recent results for the photoproduction of mesons off nuclei are reviewed. These experiments have been performed for two major lines of research related to the properties of the strong interaction. The investigation of nucleon resonances requires light nuclei as targets for the extraction of the isospin composition of the electromagnetic excitations. This is done with quasi-free meson photoproduction off the bound neutron and supplemented with the measurement of coherent photoproduction reactions, serving as spin and/or isospin filters. Furthermore, photoproduction from light and heavy nuclei is a very efficient tool for the study of the interactions of mesons with nuclear matter and the in-medium properties of hadrons. Experiments are currently rapidly developing due to the combination of high quality tagged (and polarized) photon beams with state-of-the-art 4pi detectors and polarized targets

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society