Under pressure: Response urgency modulates striatal and insula activity during decision-making under risk

When deciding whether to bet in situations that involve potential monetary loss or gain (mixed gambles), a subjective sense of pressure can influence the evaluation of the expected utility associated with each choice option. Here, we explored how gambling decisions, their psychophysiological and neural counterparts are modulated by an induced sense of urgency to respond. Urgency influenced decision times and evoked heart rate responses, interacting with the expected value of each gamble. Using functional MRI, we observed that this interaction was associated with changes in the activity of the striatum, a critical region for both reward and choice selection, and within the insula, a region implicated as the substrate of affective feelings arising from interoceptive signals which influence motivational behavior. Our findings bridge current psychophysiological and neurobiological models of value representation and action-programming, identifying the striatum and insular cortex as the key substrates of decision-making under risk and urgency

Common genetic variation in cellular transport genes and epithelial ovarian cancer (EOC) risk

Background Defective cellular transport processes can lead to aberrant accumulation of trace elements, iron, small molecules and hormones in the cell, which in turn may promote the formation of reactive oxygen species, promoting DNA damage and aberrant expression of key regulatory cancer genes. As DNA damage and uncontrolled proliferation are hallmarks of cancer, including epithelial ovarian cancer (EOC), we hypothesized that inherited variation in the cellular transport genes contributes to EOC risk. Methods In total, DNA samples were obtained from 14,525 case subjects with invasive EOC and from 23,447 controls from 43 sites in the Ovarian Cancer Association Consortium (OCAC). Two hundred seventy nine SNPs, representing 131 genes, were genotyped using an Illumina Infinium iSelect BeadChip as part of the Collaborative Oncological Gene-environment Study (COGS). SNP analyses were conducted using unconditional logistic regression under a log-additive model, and the FDR q<0.2 was applied to adjust for multiple comparisons. Results The most significant evidence of an association for all invasive cancers combined and for the serous subtype was observed for SNP rs17216603 in the iron transporter gene HEPH (invasive: OR = 0.85, P = 0.00026; serous: OR = 0.81, P = 0.00020); this SNP was also associated with the borderline/low malignant potential (LMP) tumors (P = 0.021). Other genes significantly associated with EOC histological subtypes (p<0.05) included the UGT1A (endometrioid), SLC25A45 (mucinous), SLC39A11 (low malignant potential), and SERPINA7 (clear cell carcinoma). In addition, 1785 SNPs in six genes (HEPH, MGST1, SERPINA, SLC25A45, SLC39A11 and UGT1A) were imputed from the 1000 Genomes Project and examined for association with INV EOC in white-European subjects. The most significant imputed SNP was rs117729793 in SLC39A11 (per allele, OR = 2.55, 95% CI = 1.5-4.35, p = 5.66x10-4). Conclusion These results, generated on a large cohort of women, revealed associations between inherited cellular transport gene variants and risk of EOC histologic subtypes

Containere i Windows server 2016

Denne bacheloroppgaven ble utformet for å besvare Ikomms spørsmål angående implementasjon av Windows Container i Windows Server 2016. Gruppen har i denne oppgaven utforsket funksjonaliteten til containere i Windows Server 2016 - technical preview 4 og arkitekturen bak, og deretter målt ressursutnyttelse opp mot eksisterende virtualiseringsteknologier. Gruppen sitter i etterkant igjen med et inntrykk av at Windows Container ikke er en moden teknologi. Mangelen på et grafisk grensesnitt og RDP-støtte innsnevrer bruksområdene til containere betraktelig. Microsoft har gitt utrykk for at dette heller ikke vil bli støttet i endelig utgave av Windows Server 2016. Windows er i stor grad et grafisk operativsystem, og de fleste programmer har grafiske komponenter som de er avhengig av, noe som forsterker denne problematikken. Under vår testing kommer Windows Container ytelsesmessig ut både svakere og mer ustabil satt opp mot virtuelle maskiner kjørt i Hyper-V, men stort sett med små marginer. Ettersom målet med containere er å få en bedre utnyttelse av eksisterende hardware, tyder dette på at Windows Container ikke er godt nok optimalisert. Med denne begrunnelsen sammen med et manglende behov for horisontal skalering fra Ikomms side, anbefales de ikke å implementere Windows Container i sin serverpark.This bachelor thesis was designed to answer a series of questions from Ikomm regarding the implementation of Windows Container in Windows Server 2016. This thesis explores the functionality of containers in Windows Server 2016 - technical preview 4, the architecture behind, and compared resource utilization benchmarks to existing virtualization technologies. After finishing the thesis the group is left with the impression that Windows Container is not yet a mature technology. The lack of a graphical interface and RDP support narrows the usecases for containers considerably. Microsoft has expressed that this will not be a functionality in the final release of Windows Server 2016 either. Windows is largely a graphical operating system, and most programs have graphical components that they depend on, which reinforces this issue. During our testing, the performance of Windows Container has been shown to be both weaker and more unstable when compared to virtual machines running in Hyper-V, albeit not by much. However, since the objective of containers is to achieve a better utilization of existing hardware, it suggests that Windows Container is not sufficiently optimized. With this rationale along with Ikomm not being limited by horizontal scaling, we advice them not to implement Windows Container in their server park

Heart rate variability: Measurement and emerging use in critical care medicine

Variation in the time interval between consecutive R wave peaks of the QRS complex has long been recognised. Measurement of this RR interval is used to derive heart rate variability. Heart rate variability is thought to reflect modulation of automaticity of the sinus node by the sympathetic and parasympathetic components of the autonomic nervous system. The clinical application of heart rate variability in determining prognosis post myocardial infarction and the risk of sudden cardiac death is well recognised. More recently, analysis of heart rate variability has found utility in predicting foetal deterioration, deterioration due to sepsis and impending multiorgan dysfunction syndrome in critically unwell adults. Moreover, reductions in heart rate variability have been associated with increased mortality in patients admitted to the intensive care unit. It is hypothesised that heart rate variability reflects and quantifies the neural regulation of organ systems such as the cardiovascular and respiratory systems. In disease states, it is thought that there is an ‘uncoupling’ of organ systems, leading to alterations in ‘inter-organ communication’ and a clinically detectable reduction in heart rate variability. Despite the increasing evidence of the utility of measuring heart rate variability, there remains debate as to the methodology that best represents clinically relevant outcomes. With continuing advances in technology, our understanding of the physiology responsible for heart rate variability evolves. In this article, we review the current understanding of the physiological basis of heart rate variability and the methods available for its measurement. Finally, we review the emerging use of heart rate variability analysis in intensive care medicine and conditions in which heart rate variability has shown promise as a potential physiomarker of disease

Systematically Debugging IoT Control System Correctness for Building Automation

ABSTRACT Advances and standards in Internet of Things (IoT) have simplified the realization of building automation. However, non-expert IoT users still lack tools that can help them to ensure the underlying control system correctness: userprogrammable logics match the user intention. In fact, nonexpert IoT users lack the necessary know-how of domain experts. This paper presents our experience in running a building automation service based on the Salus framework. Complementing efforts that simply verify the IoT control system correctness, Salus takes novel steps to tackle practical challenges in automated debugging of identified policy violations, for non-expert IoT users. First, Salus leverages formal methods to localize faulty user-programmable logics. Second, to debug these identified faults, Salus selectively transforms the control system logics into a set of parameterized equations, which can then be solved by popular model checking tools or SMT (Satisfiability Modulo Theories) solvers. Through office deployments, user studies, and public datasets, we demonstrate the usefulness of Salus in systematically debugging the correctness of IoT control systems for building automation

Potentiation of Anticancer Drugs: Effects of Pentoxifylline on Neoplastic Cells

The drug efflux activity of P-glycoprotein (P-gp, a product of the mdr1 gene, ABCB1 member of ABC transporter family) represents a mechanism by which tumor cells escape death induced by chemotherapeutics. In this study, we investigated the mechanisms involved in the effects of pentoxifylline (PTX) on P-gp-mediated multidrug resistance (MDR) in mouse leukemia L1210/VCR cells. Parental sensitive mouse leukemia cells L1210, and multidrug-resistant cells, L1210/VCR, which are characterized by the overexpression of P-gp, were used as experimental models. The cells were exposed to 100 μmol/L PTX in the presence or absence of 1.2 μmol/L vincristine (VCR). Western blot analysis indicated a downregulation of P-gp protein expression when multidrug-resistant L1210/VCR cells were exposed to PTX. The effects of PTX on the sensitization of L1210/VCR cells to VCR correlate with the stimulation of apoptosis detected by Annexin V/propidium iodide apoptosis necrosis kit and proteolytic activation of both caspase-3 and caspase-9 monitored by Western blot analysis. Higher release of matrix metalloproteinases (MMPs), especially MMP-2, which could be attenuated by PTX, was found in L1210/VCR than in L1210 cells by gelatin zymography in electrophoretic gel. Exposure of resistant cells to PTX increased the content of phosphorylated Akt kinase. In contrast, the presence of VCR eliminated the effects of PTX on Akt kinase phosphorylation. Taken together, we conclude that PTX induces the sensitization of multidrug-resistant cells to VCR via downregulation of P-gp, stimulation of apoptosis and reduction of MMPs released from drug-resistant L1210/VCR cells. These facts bring new insights into the mechanisms of PTX action on cancer cells