Proper Motion of the Faint Star near KIC 8462852 (Boyajian's Star) - Not a Binary System

A faint star located 2 arcsec from KIC 8462852 was discovered in Keck 10 m adaptive optics imaging in the $JHK$ near-infrared (NIR) in 2014 by Boyajian et al. (2016). The closeness of the star to KIC 8462852 suggested the two could constitute a binary, which might have implications for the cause of the brightness dips seen by {\it Kepler} (Boyajian et al. (2016) and in ground-based optical studies Boyajian et al. (2018). Here, NIR imaging in 2017 using the Mimir instrument resolved the pair and enabled measuring their separation. The faint star had moved $67 \pm 7$ milliarcsec (mas) relative to KIC 8462852 since 2014. The relative proper motion of the faint star is $23.9 \pm 2.6$ mas yr$^{-1}$, for a tangential velocity of $45 \pm 5$ km s$^{-1}$ if it is at the same 390 pc distance as KIC 8462852. Circular velocity at the 750 AU current projected separation is $1.5$ km s$^{-1}$, hence the star pair cannot be bound.Comment: 10 pages, 2 figure

Development of an Intelligent System for IoT using Web Services and Cyber Physical Approaches

The Internet of Things (IoT) is changing the way we perceive information. It has inspired solutions for a variety of everyday problems. With the advent of IoT, the internet will house several ldquointelligent ldquoobjects capable of making their own decisions and communicate with each other in an efficient manner. Cyber-Physical Systems (CPSs) represent a new paradigm of future intelligent systems. They consist of loosely coupled subsystems which interact with mechanisms of Service oriented Architecture (SoA). One of the most important goals for many organizations is to satisfy their clientsrsquo service level agreements with respect to the response time and throughput. Web services are one of the popular technologies to achieve SOA solutions.Web service is a very important candidate technology to achieve SOA requirements that allows the service providers to publish their services to many service consumers. nbs

Early and Late Chronotype Have Similar Glucose Effectiveness in adults with Metabolic Syndrome

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Can a flavoured spray (Pill Glide) help children swallow their medicines? A pilot study

Pediatric pharmacists are constantly faced with the challenges of supporting children and caregivers for whom the difficulties of swallowing medicines can be a daily struggle. Most medicines are only available as tablets and capsules, and where liquid alternatives exist, these products often have issues with palatability and high costs. The objective of this study was to evaluate whether the swallowing spray, Pill Glide, could help children in taking their solid and liquid medicines. This open label pilot study compared the spray with a behavioral approach alone, the current standard of care at the pediatric hospital. Patients were children on long-term drug therapies, either transitioning from liquid preparations to tablets and capsules, or known to be experiencing swallowing difficulties. Using age-adapted diaries, patients self-reported the difficulty of taking medicines on a 6-point hedonic scale for 2 weeks before the intervention, and then for 1 week while using Pill Glide. Data were analyzed from 10 children aged 6 to 16 years, with an average burden of 3.5 tablets per day. Pill Glide (strawberry was the most popular flavor) was shown to significantly decrease the overall medicine taking difficulty score by 0.93 (range, 0.33–1.53), almost 1 hedonic face point on the scale used (P = .002). There was insufficient data for liquid medicines. Pill Glide could help children with pill swallowing, thus improving patient acceptability of medicines and potentially adherence. It could also be implemented as a useful cost-saving intervention because solid dosage forms are cheaper

Intercellular trafficking of a KNOTTED1 green fluorescent protein fusion in the leaf and shoot meristem of Arabidopsis

Dominant mutations in the maize homeobox gene knotted1 (kn1) act nonautonomously during maize leaf development, indicating that Kn1 is involved in the generation or transmission of a developmental signal that passes from the inner layers of the leaf to epidermal cells. We previously found that this nonautonomous activity is correlated with the presence of KN1 protein in leaf epidermal cells, where KN1 mRNA could not be detected. Furthermore, KN1 protein expressed in Escherichia coli and labeled with a fluorescent dye can traffic between leaf mesophyll cells in microinjection assays. Here we show that green fluorescent protein (GFP)-tagged KN1 is able to traffic between epidermal cells of Arabidopsis and onion. When expressed in vivo, the GFP approximately KN1 fusion trafficked from internal tissues of the leaf to the epidermis, providing the first direct evidence, to our knowledge, that KN1 can traffic across different tissue layers in the leaf. Control GFP fusions did not show this intercellular trafficking ability. GFP approximately KN1 also trafficked in the shoot apical meristem, suggesting that cell-to-cell trafficking of KN1 may be involved in its normal function in meristem initiation and maintenance

ARID1B is a specific vulnerability in ARID1A-mutant cancers

Summary Recent studies have revealed that ARID1A is frequently mutated across a wide variety of human cancers and also has bona fide tumor suppressor properties. Consequently, identification of vulnerabilities conferred by ARID1A mutation would have major relevance for human cancer. Here, using a broad screening approach, we identify ARID1B, a related but mutually exclusive homolog of ARID1A in the SWI/SNF chromatin remodeling complex, as the number one gene preferentially required for the survival of ARID1A-mutant cancer cell lines. We show that loss of ARID1B in ARID1A-deficient backgrounds destabilizes SWI/SNF and impairs proliferation. Intriguingly, we also find that ARID1A and ARID1B are frequently co-mutated in cancer, but that ARID1A-deficient cancers retain at least one ARID1B allele. These results suggest that loss of ARID1A and ARID1B alleles cooperatively promotes cancer formation but also results in a unique functional dependence. The results further identify ARID1B as a potential therapeutic target for ARID1A-mutant cancers

Targeting Tumour-Initiating Cells with TRAIL Based Combination Therapy Ensures Complete and Lasting Eradication of Multiple Myeloma Tumours In Vivo

Multiple myeloma (MM) remains an incurable disease despite improvements to available treatments and efforts to identify new drug targets. Consequently new approaches are urgently required. We have investigated the potential of native tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), in combination with doxorubicin, to induce apoptotic cell death in phenotypically distinct populations of myeloma cells in vitro and in vivo. The cytotoxic potential of TRAIL alone, and in combination with DOX, was assessed in vitro in purified CD138+ and CD138− cells from the MM cell lines and samples from patients with MM. Mouse xenografts obtained by implanting CD138− MM cells were used to assess the efficacy of TRAIL, alone and in combination with DOX, in vivo. CD138− cells were shown to be more resistant to the cytotoxic activity of TRAIL than CD138+ cells and have reduced expression of TRAIL death receptors. This resistance results in preferential killing of CD 138+ cells during exposure of MM culture to TRAIL. Furthermore, prolonged exposure results in the appearance of TRAIL-resistant CD138− cells. However, when TRAIL is combined with doxorubicin, this results in complete eradication of MM cells in vivo. Most importantly, this treatment successfully eliminates CD138− cells implicated in tumour initiation and growth maintenance. These findings may explain the failure of current therapies and offer a promising new approach in the quest to cure MM and disseminated cancers

A Simple Mathematical Model Based on the Cancer Stem Cell Hypothesis Suggests Kinetic Commonalities in Solid Tumor Growth

Background: The Cancer Stem Cell (CSC) hypothesis has gained credibility within the cancer research community. According to this hypothesis, a small subpopulation of cells within cancerous tissues exhibits stem-cell-like characteristics and is responsible for the maintenance and proliferation of cancer. Methodologies/Principal Findings: We present a simple compartmental pseudo-chemical mathematical model for tumor growth, based on the CSC hypothesis, and derived using a ‘‘chemical reaction’ ’ approach. We defined three cell subpopulations: CSCs, transit progenitor cells, and differentiated cells. Each event related to cell division, differentiation, or death is then modeled as a chemical reaction. The resulting set of ordinary differential equations was numerically integrated to describe the time evolution of each cell subpopulation and the overall tumor growth. The parameter space was explored to identify combinations of parameter values that produce biologically feasible and consistent scenarios. Conclusions/Significance: Certain kinetic relationships apparently must be satisfied to sustain solid tumor growth and to maintain an approximate constant fraction of CSCs in the tumor lower than 0.01 (as experimentally observed): (a) the rate of symmetrical and asymmetrical CSC renewal must be in the same order of magnitude; (b) the intrinsic rate of renewal and differentiation of progenitor cells must be half an order of magnitude higher than the corresponding intrinsic rates for cancer stem cells; (c) the rates of apoptosis of the CSC, transit amplifying progenitor (P) cells, and terminally differentiate

Targeting the IGF-1R signaling and mechanisms for epigenetic gene silencing in human multiple myeloma

Multiple myeloma (MM) is a B cell malignancy characterized by the expansion of clonal plasmablast/plasma cells within the bone-marrow. It is well established that the bone-marrow microenvironment has a pivotal role in providing critical cytokines and cell–cell interactions to support the growth and survival of the MM tumor clone. The pathogenesis of MM is, however, only fragmentarily understood. Detailed genomic analysis reveals a heterogeneous and complex pattern of structural and numerical chromosomal aberrations. In this review we will discuss some of the recent results on the functional role and potential clinical use of the IGF-1R, one of the major mediators of growth and survival for MM. We will also describe some of our results on epigenetic gene silencing in MM, as it may indeed constitute a novel basis for the understanding of tumor initiation and maintenance in MM and thus may change the current view on treatment strategies for MM