An Intrusion Detection Using Machine Learning Algorithm Multi-Layer Perceptron (MlP): A Classification Enhancement in Wireless Sensor Network (WSN)

During several decades, there has been a meteoric rise in the development and use of cutting-edge technology. The Wireless Sensor Network (WSN) is a groundbreaking innovation that relies on a vast network of individual sensor nodes. The sensor nodes in the network are responsible for collecting data and uploading it to the cloud. When networks with little resources are deployed harshly and without regulation, security risks occur. Since the rate at which new information is being generated is increasing at an exponential rate, WSN communication has become the most challenging and complex aspect of the field. Therefore, WSNs are insecure because of this. With so much riding on WSN applications, accuracy in replies is paramount. Technology that can swiftly and continually analyse internet data streams is essential for spotting breaches and assaults. Without categorization, it is hard to simultaneously reduce processing time while maintaining a high level of detection accuracy. This paper proposed using a Multi-Layer Perceptron (MLP) to enhance the classification accuracy of a system. The proposed method utilises a feed-forward ANN model to generate a mapping for the training and testing datasets using backpropagation. Experiments are performed to determine how well the proposed MLP works. Then, the results are compared to those obtained by using the Hoeffding adaptive tree method and the Restricted Boltzmann Machine-based Clustered-Introduction Detection System. The proposed MLP achieves 98% accuracy, which is higher than the 96.33% achieved by the RBMC-IDS and the 97% accuracy achieved by the Hoeffding adaptive tree

Molecular analysis of LITAF-mediated inflammatory pathways

PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact [email protected] (D.Sc.)--Boston University, Henry M. Goldman School of Dental Medicine, 2008 (Dept. of Oral Biology and Periodontology).Includes bibliographical references: leaves 93-104.TNF-a is a critical cytokine secreted predominantly by macrophages in response to bacterial toxins, inflammatory products and other noxious stimuli. This cytokine plays a significant role in various chronic inflammatory diseases, autoimmune diseases and in endotoxic/septic shock. LITAF is a transcription factor that forms a complex in the cytoplasm with STAT-6B and translocates into the nucleus to bind to the promoter of TNF-a, to participate in the TNF-a gene expression independently of the NF-KB pathway of regulation. It has become essential to elucidate and establish the role of LITAF in inflammatory processes in order to better understand the molecular mechanisms involved in inflammatory processes in hope of designing therapeutic strategies for TNF-a-mediated inflammatory diseases. Based on previous data generated in our laboratory, we hypothesized that (1) LITAF plays a role in the activation of several inflammatory mediators in response to endotoxemia and (2) the absence of LITAF protects animals from the deleterious effects of endotoxemia. Mice genetically deficient of LITAF in monocytes/macrophages (macLITAF-/-) were established in order to aid in the characterization of the functional role of LITAF in vivo. Peritoneal macrophages were collected from each mouse and the animals were screened for LITAF deficiency by PCR and confirmed by Western Blot analysis to determine the expression of LITAF protein and by ELISA to determine the TNF-a level. Characterization of the functional role of LITAF in vivo was elucidated using two inflammatory models: lethal and sub-lethal endotoxemia. LITAF deficient animals better tolerated the lethal endotoxic shock compared to the wild-type animals, when administered with LPS along with D-Galactosamine. Analysis of the profile of inflammatory mediators revealed that the macLITAF-/- mice showed a decreased production of most of the proinflammatory cytokines including TNF-a, as well as all the anti-inflammatory cytokines. Based on the literature, this phenomena can be interpreted that LITAF deficiency causes an immediate reduction in the systemic inflammatory response syndrome (SIRS) which effects the immediate reduction in the compensatory anti-inflammatory response syndrome (CARS), thus protecting the animal from death. In order to determine the systemic effect of LITAF deficiency, the profile of mediators when a sub-lethal dose of LPS was administered, revealed that, there was a delayed peak in the proinflammatory response leading to a similar delay in the anti-inflammatory response. Thus, when inflammation is re-established such as in sub-lethal bacteremia, the anti-inflammatory response follows suit to limit the detrimental effects of a prolonged release of the proinflammatory mediators. To begin to dissect the molecular pathways associated with LITAF-mediated inflammatory response, we tested the role of major serine/threonine kinases in this process. LPS-induced macLITAF-/- exhibited an upregulation of pro-survival kinases Akt, Erkl/2 and RSK compared to wild-type macrophages suggesting that these kinases may be involved in the survival of LITAF deficient animals when exposed to a bacterial challenge. Further studies are in progress to comprehensibly test this hypothesis. Altogether the present data provide new understanding of LITAF mediated inflammatory process and pave the way for further molecular analyses of the kinases involved in this process

Beneficial Dysregulation of the Time Course of Inflammatory Mediators in Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Factor-Deficient Mice▿

To begin to understand the surprising survival of macrophage-specific lipopolysaccharide-induced tumor necrosis factor alpha factor-deficient (macLITAF−/−) animals after a lethal dose of lipopolysaccharide (LPS), as reported earlier, the present follow-up study focuses on the role of LITAF in the regulation of inflammatory cytokines secreted in response to lethal or sublethal doses of LPS administered to wild-type (WT) and macLITAF−/− mice. A time course study of kinase expression in peritoneal macrophages revealed increased phosphorylation of prosurvival kinases Akt, Erk1/2, and ribosomal S6 kinase (RSK) in macLITAF−/− mice compared to that in WT mice (n = 8), confirming their role in LPS-mediated diseases. macLITAF−/− mice (n = 8) survived a lethal dose of LPS plus d-galactosamine (d-GalN), expressing lower serum levels of pro- and anti-inflammatory cytokines than the WT levels. To extend our knowledge on LPS-induced inflammatory events, an effective sublethal dose of LPS was administered to the animals (n = 14). WT animals exhibited an acute inflammatory response that decreased after 4 h. Interestingly, macLITAF−/− mice exhibited an initial delay in the secretion of proinflammatory cytokines that peaked after 8 h and reached WT levels after 18 h. Anti-inflammatory cytokine secretions were initially delayed but increased after 4 h and remained elevated compared to WT levels, even after 18 h. Our results demonstrate that LITAF deficiency in vivo affects cytokines other than TNF-α and influences the balance between the pro- and anti-inflammatory cytokines, which protects the animals from the deleterious effects of an LPS-induced inflammatory response, resulting in a beneficial host regulation of inflammatory cytokines and in enhanced survival. Therapeutic intervention aimed at reducing LITAF via kinase modulators may prove useful in preventing LPS-induced mortality

Evaluation of crown-root angulation of lateral incisors adjacent to palatally impacted canines

The objective of this study is to explore differences in crown-to-root angulation between lateral incisors adjacent to palatally impacted canines (PICs) and lateral incisors adjacent to normally erupted canines (NECs).; Orthodontic records of 100 subjects (51 with PICs and 49 with NECs) were reviewed. Crown-to-root angulations of all lateral incisors were measured manually on the final panoramic radiographs. Also, three experienced orthodontists were asked to visually inspect the morphology of the lateral incisors on the panoramic radiographs. A mixed model was used to test the difference in crown-to-root angulation of the lateral incisor between the experimental and the control groups. The association between the examiners' observations and the presence of a canine impaction was assessed by means of a chi-square test. All analyses were performed at the 0.05 level of statistical significance.; A significant (p = 0.009) difference of 2.3° in crown-to-root angulation was found between groups. Also, 66.7% of the lateral incisors that were identified as "abnormal" by the panel of orthodontists were adjacent to a PIC. A percentage of 65.2 of lateral incisors that were identified as "normal" were located adjacent to NECs.; The root of lateral incisors adjacent to PICs is angulated more mesially compared to lateral incisors adjacent to NECs. In addition, clinicians are somewhat able to predict if a canine is palatally impacted by visually observing the crown-to-root angulation of the adjacent lateral incisor. Evaluating the crown-to-root angulation of a lateral incisor on a panoramic image might facilitate an early diagnosis of palatally impacted canines

Time-Dependent Density Functional Theoretical Investigation of Photoinduced Excited-State Intramolecular Dual Proton Transfer in Diformyl Dipyrromethanes

In recent research [Chem. Commun. 2014, 50, 8667], it was found that photoinduced enolization occurred in 1,9-diformyl-5,5-diaryldipyrromethane (DA_KK) by excited-state dual proton transfer resulting in a red-shifted absorption, a phenomena not observed in 1,9-diformyl-5,5-dimethyldipyrromethane (DM_KK) and 1,9-diformyl-5-aryldipyrromethane (MA_KK). The observation was supported by preliminary density functional theoretical (DFT) calculations. In the work reported here, a detailed and systematic study was undertaken considering four molecules, 1,9-diformyldipyrromethane (DH_KK), DM_KK, MA_KK, and DA_KK and their rotational isomers using DFT methods. Different processes, namely, cis–trans isomerization and single and double proton transfer processes, and their mechanistic details were investigated in the ground and excited states. From the simulation studies, it was seen that the presence of different substituents at the meso carbon does not affect the λ_abs values during cis → trans isomerization. However, enolization by proton transfer processes were found to be influenced by the substituents, as seen in the experiments. Enolization was observed to follow a stepwise mechanism, that is, diketo → monoenol → dienol. While monoenols showed negligible substituent effects on the λ_abs values, a large red shift in λ_abs was seen only in DA_KK, in agreement with the experimental findings. This observation can be attributed to the lowering of the keto → enol activation barrier, stabilization of DA_EE in the S₁ state, and the charge transfer nature of the transitions involved in DA_EE

<i>ansa</i>-Ferrocene-Incorporated Calixpyrroles and Calixphyrins: Syntheses and Spectral/Structural Characterization

The syntheses and spectral/structural characterization of <i>ansa</i>-ferrocene-incorporated <i>normal</i> calixphyrins and <i>core-modified</i> calixpyrroles and calixphyrins are reported. Acid-promoted dehydrative condensation of 1,1′-bis­(dimethylpyrrolylmethyl)­ferrocene and 2,5-bis­(dimethylhydroxymethyl)­thiophene/furan yielded <i>ansa</i>-ferrocene-based <i>core-modified</i> calixpyrroles, while acid-catalyzed dehydrative condensation of 1,1′-bis­(diphenylpyrrolylmethyl)­ferrocene with the aryl aldehydes and 2,5-bis­(phenylhydroxymethyl)­thiophene followed by DDQ oxidation resulted in the formation of <i>ansa</i>-ferrocene-appended <i>normal</i> and <i>core-modified</i> calixphyrins, respectively. The newly synthesized macrocycles were characterized by FAB-MS, NMR, and UV–vis spectral analyses and finally confirmed by single-crystal X-ray structural analysis. All these studies clearly revealed the introduction of ferrocene in the main framework of the corresponding macrocycles in an <i>ansa</i>-type way. The <i>core-modified</i> calixpyrroles adopt a 1,3-alternate conformation, while the corresponding calixphyrins maintained partial planarity along the tripyrrin plane due to the presence of <i>meso</i> sp² carbon and generated curved staircase conformation. In addition to the intramolecular hydrogen-bonding interactions, calixphyrins generate self-assembled dimers, one- and two-dimensional supramolecular assemblies through intermolecular hydrogen bonding in the solid state

Amelioration of emphysema in mice through lentiviral transduction of long-lived pulmonary alveolar macrophages

Directed gene transfer into specific cell lineages in vivo is an attractive approach for both modulating gene expression and correcting inherited mutations such as emphysema caused by human α1 antitrypsin (hAAT) deficiency. However, somatic tissues are mainly comprised of heterogeneous, differentiated cell lineages that can be short lived and difficult to specifically transfect. Here, we describe an intratracheally instilled lentiviral system able to deliver genes selectively to as many as 70% of alveolar macrophages (AMs) in the mouse lung. Following a single in vivo lentiviral transduction, genetically tagged AMs persisted in lung alveoli and expressed transferred genes for the lifetime of the adult mouse. A prolonged macrophage lifespan, rather than precursor cell proliferation, accounted for the surprisingly sustained presence of transduced AMs. We utilized this long-lived population to achieve localized secretion of therapeutic levels of hAAT protein in lung epithelial lining fluid. In an established mouse model of emphysema, lentivirally delivered hAAT ameliorated the progression of emphysema, as evidenced by attenuation of increased lung compliance and alveolar size. After 24 weeks of sustained gene expression, no humoral or cellular immune responses to hAAT protein were detected. Our results challenge the dogma that AMs are short lived and suggest that these differentiated cells may be a possible target cell population for in vivo gene therapy applications, including the sustained correction of hAAT deficiency