Sivertsendenton3955

Mobile technologies are capable of offering individual level health care services to users. Mobile Healthcare (m-Healthcare) frameworks, which feature smartphone (SP) utilizations of ubiquitous computing made possible by applying wireless Body Sensor Networks (BSNs), have been introduced recently to provide SP clients with health condition monitoring and access to medical attention when necessary. However, in see more -Healthcare framework, clients' personal info and sensitive data can easily be poached by intruders or any malicious party, causing serious security problems and confidentiality issues. In 2013, Lu et al. proposed a mobile-Healthcare emergency framework based on privacy-preserving opportunistic computing (SPOC), claiming that their splendid SPOC construction can opportunistically gather SP resources such as computing power and energy to handle computing-intensive Personal Health Information (PHI) with minimal privacy disclosure during an emergency. To balance between the risk of personal health information exposure and the essential PHI processing and transmission, Lu et al. presented a patient-centric privacy ingress control framework based on an attribute-based ingress control mechanism and a Privacy-Preserving Scalar Product Computation (PPSPC) technique. In spite of the ingenious design, however, Lu et al.'s framework still has some security flaws in such aspects as client anonymity and mutual authentication. In this article, we shall offer an improved version of Lu et al.'s framework with the security weaknesses mended and the computation efficiency further boosted. In addition, we shall also present an enhanced mobile-Healthcare emergency framework using Partial Discrete Logarithm (PDL) which does not only achieve flawless mutual authentication as well as client anonymity but also reduce the computation cost.In the search for new antiviral therapies against human immunodeficiency virus type 1 (HIV-1), several cellular targets are being investigated. Ataxia telangiectasia and Rad3-related protein (ATR) has been implicated in HIV-1 replication, namely during retroviral DNA integration. We studied the effect of the ATR inhibitor ETP-46464 on HIV-1 replication in peripheral blood mononuclear cells (PBMCs) and in the persistently HIV-1-infected cell line H61-D. After treatment with ETP-46464, a significant decrease in virus production was observed in both cell systems. Quantification of viral DNA forms in the acutely infected PBMCs suggests that inhibition could take place in the early phase of the viral life cycle before viral DNA integration. Moreover, after treatment of H61-D cells with 3'-azido-3'-deoxythymidine (AZT), which blocks new reverse transcription events, ETP-46464 decreased viral production, suggesting that inhibition of viral replication occurred in the late phase of the life cycle after viral DNA integration. A decrease in virus production after transfection of 293T cells with an HIV-1 infectious molecular clone also suggested that the effect of ETP-46464 is exerted at a post-integration step. We propose that ETP-46464 produces its inhibitory effect on HIV-1 replication by acting in both the early and late phases of the retroviral replication cycle. Thus, ATR could represent a new target for inhibition of HIV-1 replication.A novel virus of the genus Narnavirus, designated "Saccharomyces narnavirus I329" (ScNV-I329), was discovered in Saccharomyces cerevisiae strain I-329, which is used for industrial production of sherry-like wines. The genome of ScNV-I329 is 2509 nt in length with short terminal inverted repeats and a single open reading frame capable of encoding an RNA-dependent RNA polymerase most closely related to that of Saccharomyces 20S RNA narnavirus. This is the third known member of the genus Narnavirus from yeasts.PURPOSE OF REVIEW The bidirectional relationship between sleep disorders and inflammatory bowel disease (IBD) has gained considerable attention in recent years. It has been suggested that poor sleep and fatigue are extra-intestinal manifestations of IBD. This review reports recent studies exploring subjective and objective assessments of sleep in the adult IBD population. RECENT FINDINGS In ulcerative colitis patients, poor sleep has been independently linked to depression and poorer IBD-related quality of life. Using home polysomnography, IBD patients were shown to have less rapid eye movement sleep and Crohn's patient had increased lighter sleep. A study utilizing surveys assessing circadian rhythms described circadian misalignment in IBD patients and reported that circadian misalignment in Crohn's disease was associated with a more aggressive disease phenotype. The use of biologics may improve sleep disturbances in patients with IBD. Translational and clinical studies have reported that disturbances in sleep quality are linked to intestinal inflammation and a heighted systemic immune response. IBD patients appear to have disturbed sleep. Poor sleep is also suggested as a marker for subclinical disease activity. #link# Recent studies have suggested circadian misalignment in IBD patients, and future studies are needed to assess these clinical implications.The piriform cortex (paleocortex) is the olfactory cortex or the primary cortex for the sense of smell. It receives the olfactory input from the mitral and tufted cells of the olfactory bulb and is involved in the processing of information pertaining to odors. The piriform cortex and the adjoining neocortex have different cytoarchitectures; while the former has a three-layered structure, the latter has a six-layered structure. The regulatory mechanisms underlying the building of the six-layered neocortex are well established; in contrast, less is known about of the regulatory mechanisms responsible for structure formation of the piriform cortex. The differences as well as similarities in the regulatory mechanisms between the neocortex and the piriform cortex remain unclear. Here, the expression of neocortical layer-specific genes in the piriform cortex was examined. Two sublayers were found to be distinguished in layer II of the piriform cortex using Ctip2/Bcl11b and Brn1/Pou3f3. The sequential expression pattern of Ctip2 and Brn1 in the piriform cortex was similar to that detected in the neocortex, although the laminar arrangement in the piriform cortex exhibited an outside-in arrangement, unlike that observed in the neocortex.