Stability and Effective Process Control for Secure Email Filtering

A fantastic tool for both commercial and personal communication is electronic mail. It has increasingly become a necessary component of our working life since it is straightforward, available, and simple to use. Spam emails have started to tarnish internet experiences and threaten the integrity of email. Due to the exponential growth of spam, both people and organisations are under a great deal of financial and other strain. In order to prevent the future of email itself from being in jeopardy, a solution to the spam problem must be discovered. There is an urgent need to solve the Email spam issue since spam volume has been rising over the last several decades. As part of this effort, many effects of spam emails on businesses and people were noted and thoroughly examined. In order to properly assess current technologies, solutions, and methods, a comprehensive literature review was conducted throughout the procedures. The goals of this work is to develop new methodologies for the implementation of new strategies for the efficient management of email spam and to construct a proof-of-concept software system for the Process controlled assessment of such strategies

Modulation of Macrophage Function by Lactobacillus-Conditioned Medium

open access articleProbiotics are used as microbial food supplements for health and well-being. They are thought to have immunomodulatory effects although their exact physiological mechanism of action is not clear. This study investigated the influence of probiotic Lactobacillus rhamnosus GG conditioned media (LGG-CM) on macrophage phagocytosis of non-pathogenic Escherichia coli HfrC. The gentamicin protection assay was used to study the bacterial killing phases of phagocytosis. Macrophages co-incubated with E. coli for an hour allowed them to ingest bacteria and then the rate of E. coli killing was monitored for up to 300 min to determine the killing or digestion of the bacteria by recovering them from the macrophage lysate. We found that the LGG-CM significantly increased the bacterial killing by approximately 6-fold when compared with that of controls. By contrast, this killing process was found to be associated with enhanced free radical production via the activation of NADPH oxidase, stimulated by the LGG conditioned medium. We also found that the conditioned medium had small effect on nitric oxide (NO) generation, albeit to a lesser extent. This work suggests that LGG-CM may play an important role in suppressing the total microbial load within the macrophages and hence, the extent to which pro-inflammatory molecules such as free radicals and NO are generated. The modulation of inflammation-promoting signals by LGG-CM may be beneficial as it modulates bacterial killing, and thereby prevents any collateral damage to host

A Novel Role for IκBζ in the Regulation of IFNγ Production

IκBζ is a novel member of the IκB family of NFκB regulators, which modulates NFκB activity in the nucleus, rather than controlling its nuclear translocation. IκBζ is specifically induced by IL-1β and several TLR ligands and positively regulates NFκB-mediated transcription of genes such as IL-6 and NGAL as an NFκB binding co-factor. We recently reported that the IL-1 family cytokines, IL-1β and IL-18, strongly synergize with TNFα for IFNγ production in KG-1 cells, whereas the same cytokines alone have minimal effects on IFNγ production. Given the striking similarities between the IL-1R and IL-18R signaling pathways we hypothesized that a common signaling event or gene product downstream of these receptors is responsible for the observed synergy. We investigated IκBζ protein expression in KG-1 cells upon stimulation with IL-1β, IL-18 and TNFα. Our results demonstrated that IL-18, as well as IL-1β, induced moderate IκBζ expression in KG-1 cells. However, TNFα synergized with IL-1β and IL-18, whereas by itself it had a minimal effect on IκBζ expression. NFκB inhibition resulted in decreased IL-1β/IL-18/TNFα-stimulated IFNγ release. Moreover, silencing of IκBζ expression led to a specific decrease in IFNγ production. Overall, our data suggests that IκBζ positively regulates NFκB-mediated IFNγ production in KG-1 cells

IFNγ and IL-12 restrict Th2 responses during Helminth/Plasmodium co-infection and promote IFNγ from Th2 cells

Parasitic helminths establish chronic infections in mammalian hosts. Helminth/Plasmodium co-infections occur frequently in endemic areas. However, it is unclear whether Plasmodium infections compromise anti-helminth immunity, contributing to the chronicity of infection. Immunity to Plasmodium or helminths requires divergent CD4+ T cell-driven responses, dominated by IFNγ or IL-4, respectively. Recent literature has indicated that Th cells, including Th2 cells, have phenotypic plasticity with the ability to produce non-lineage associated cytokines. Whether such plasticity occurs during co-infection is unclear. In this study, we observed reduced anti-helminth Th2 cell responses and compromised anti-helminth immunity during Heligmosomoides polygyrus and Plasmodium chabaudi co-infection. Using newly established triple cytokine reporter mice (Il4gfpIfngyfpIl17aFP635), we demonstrated that Il4gfp+ Th2 cells purified from in vitro cultures or isolated ex vivo from helminth-infected mice up-regulated IFNγ following adoptive transfer into Rag1-/- mice infected with P. chabaudi. Functionally, Th2 cells that up-regulated IFNγ were transcriptionally re-wired and protected recipient mice from high parasitemia. Mechanistically, TCR stimulation and responsiveness to IL-12 and IFNγ, but not type I IFN, was required for optimal IFNγ production by Th2 cells. Finally, blockade of IL-12 and IFNγ during co-infection partially preserved anti-helminth Th2 responses. In summary, this study demonstrates that Th2 cells retain substantial plasticity with the ability to produce IFNγ during Plasmodium infection. Consequently, co-infection with Plasmodium spp. may contribute to the chronicity of helminth infection by reducing anti-helminth Th2 cells and converting them into IFNγ-secreting cells

Cytological evaluation of thyroid lesions by nuclear morphology and nuclear morphometry

Introduction: Fine needle aspiration (FNA) of the thyroid gland is an effective diagnostic method. The Bethesda system for reporting thyroid cytopathology classifies them into six categories and gives implied risk for malignancy and management protocol in each category. Though the system gives specific criteria, diagnostic dilemma still exists. Using nuclear morphometry, we can quantify the number of parameters, such as those related to nuclear size and shape. The evaluation of nuclear morphometry is not well established in thyroid cytology. Objective: To classify thyroid lesions on fine needle aspiration cytology (FNAC) using Bethesda system and to evaluate the significance of nuclear parameters in improving the prediction of thyroid malignancy. Materials and Methods: In the present study, 120 FNAC cases of thyroid lesions with histological diagnosis were included. Computerized nuclear morphometry was done on 81 cases which had confirmed cytohistological correlation, using Aperio computer software. One hundred nuclei from each case were outlined and eight nuclear parameters were analyzed. Results: In the present study, thyroid lesions were common in female with M: F ratio of 1:5 and most commonly in 40–60 yrs. Under Bethesda system, 73 (60.83%) were category II; 14 (11.6%) were category III, 3 (2.5%) were category IV, 8 (6.6%) were category V, and 22 (18.3%) were category VI, which were malignant on histopathological correlation. Sensitivity, specificity, and diagnostic accuracy of Bethesda reporting system are 62.5, 84.38, and 74.16%, respectively. Minimal nuclear diameter, maximal nuclear diameter, nuclear perimeter, and nuclear area were higher in malignant group compared to nonneoplastic and benign group. Conclusion: The Bethesda system is a useful standardized system of reporting thyroid cytopathology. It gives implied risk of malignancy. Nuclear morphometry by computerized image analysis can be utilized as an additional diagnostic tool

Security Infrastructure for Hybrid Clouds and Cloud Federation

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Biologic Width - Knowledge Key for Restorative Dentistry: A Review

Aim: To elaborate the importance of the concept of biologic width in terms of restorative dentistry. Background: Biological width is the natural distance (combine heights) between the base of the healthy gingival sulcus or epithelial attachment to the tooth and the height of the alveolar bone or connective tissue. For better description of relationship between the periodontal tissues and conservative procedures is to restore form, function, esthetics, and comfort for the dentition. Most of the dentists are aware of biological width, its maintenance and its importance during application of crown lengthening. However, this review will elaborate on its importance in restorative dentistry. This article reviews the anatomy, categories, evaluation, violation, methods to correct the violation of biologic width and its relationship to periodontal health and restorative dentistry. Review Results: Respecting the biologic width and designing restorations accordingly is crucial. Biologic Width is the dimension of space that the healthy gingival tissues occupy above the alveolar bone. Incorrectly placed margins of restorations are a common cause of biologic width violation. This can lead to gingival inflammation and bone loss, thereby damaging the periodontal health as well as reducing the life of the restoration