Miracle-dz/UniFAR-FTUs huggingface dataset:
The effects of taxanes, vorinostat and doxorubicin on growth and proliferation of Echinococcus multilocularis metacestodes assessed with magnetic resonance imaging and simultaneous positron emission tomography

Cytostatic drugs used in cancer therapy were evaluated for their capacity to inhibit Echinococcus multilocularis metacestode growth and proliferation. Metacestode tissues were exposed in vitro to docetaxel, doxorubicin, navelbine, paclitaxel, and vorinostat for 1 week, then incubated in drug-free culture, and thereafter metacestodes were injected into the peritoneum of Meriones unguiculatus. Magnetic resonance imaging (MRI) and simultaneous positron emission tomography (PET) were applied to monitor in vivo growth of drug-exposed E. multilocularis in Meriones. At 3 month p.i. , docetaxel (at 10 μM, 5 μM and 2 μM) inhibited in vivo growth and proliferation of E. multilocularis, and at 5 months p.i. , only in the 2 μM docetaxel exposure group 0.3 cm3 of parasite tissue was found. With paclitaxel and navelbine the in vivo growth of metacestodes was suppressed until 3 months p.i. , thereafter, parasite tissues enlarged up to 3 cm3 in both groups. E. multilocularis tissues of more than 10 g developed in Meriones injected with metacestodes which were previously exposed in vitro to doxorubicin, navelbine, paclitaxel or vorinostat. In Meriones infected with metacestodes previously exposed to docetaxel, the in vivo grown parasite tissues weighted 0.2 g. In vitro cultured E. multilocularis metacestodes exposed to docetaxel did not produce vesicles until 7 weeks post drug exposure, while metacestodes exposed to doxorubicin, navelbine and vorinostat proliferated continuously. In summary, docetaxel, and less efficaciously paclitaxel, inhibited in vivo and in vitro parasite growth and proliferation, and these observations suggest further experimental studies with selected drug combinations which may translate into new treatment options against alveolar echinococcosis.
Methods for Coding Tobacco-Related Twitter Data: A Systematic Review

Background As Twitter has grown in popularity to 313 million monthly active users, researchers have increasingly been using it as a data source for tobacco-related research. Objective The objective of this systematic review was to assess the methodological approaches of categorically coded tobacco Twitter data and make recommendations for future studies. Methods Data sources included PsycINFO, Web of Science, PubMed, ABI/INFORM, Communication Source, and Tobacco Regulatory Science. Searches were limited to peer-reviewed journals and conference proceedings in English from January 2006 to July 2016. The initial search identified 274 articles using a Twitter keyword and a tobacco keyword. One coder reviewed all abstracts and identified 27 articles that met the following inclusion criteria: (1) original research, (2) focused on tobacco or a tobacco product, (3) analyzed Twitter data, and (4) coded Twitter data categorically. One coder extracted data collection and coding methods. Results E-cigarettes were the most common type of Twitter data analyzed, followed by specific tobacco campaigns. The most prevalent data sources were Gnip and Twitter’s Streaming application programming interface (API). The primary methods of coding were hand-coding and machine learning. The studies predominantly coded for relevance, sentiment, theme, user or account, and location of user. Conclusions Standards for data collection and coding should be developed to be able to more easily compare and replicate tobacco-related Twitter results. Additional recommendations include the following: sample Twitter’s databases multiple times, make a distinction between message attitude and emotional tone for sentiment, code images and URLs, and analyze user profiles. Being relatively novel and widely used among adolescents and black and Hispanic individuals, Twitter could provide a rich source of tobacco surveillance data among vulnerable populations.
Two siblings with Bardet?Biedl syndrome caused by mutations in BBS10 : the first case identified in Korea

features or 3 primary and 2 secondary features [1,4]. In addition to the pleiotropic symptoms and signs observed clinically in multiple organ systems, the genetic background of BBS is quite heterogeneous with significant interand intrafamilial variations. The inheritance pattern of BBS is traditionally considered to be autosomal recessive [1]. To date, mutations in 16 genes have been identified as causative of BBS. All of these genes account for approximately 80% of clinically diagnosed cases of BBS. Among them, BBS1 and BBS10 are the 2 main genes involved in BBS, and each of these gene mutations presents in more than 20% of the cases [1]. To date, 7 clinically diagnosed cases of BBS have been reported Two siblings with Bardet–Biedl syndrome caused by mutations in BBS10: the first case identified in Korea
Oxidative burden in familial hypercholesterolemia

Familial hypercholesterolemia (FH) is a genetic disorder characterized by high serum levels of low‐density lipoprotein cholesterol (LDL‐c). FH is characterized by accelerated development of atherosclerosis and represents the most frequent hereditary cause of premature coronary heart disease. Mutations of the LDL receptor gene are the genetic signature of FH, resulting in abnormal levels of circulating LDLs. Moreover, FH promotes the generation of reactive oxygen species (ROS) which is another key mechanism involved in atherosclerosis development and progression. The aim of this narrative review is to update the current knowledge on the pathophysiological mechanisms linking FH to ROS generation and their detrimental impact on atherosclerotic pathophysiology. With this purpose, we reviewed experimental and clinical data on the association between FH and OS and the functional role of OS as a promoter of inflammation and atherosclerosis. In this regard, oxidant species such as oxidized LDL, malondialdehyde, ROS, and isoprostanes emerged as leading mediators of the oxidative injury in FH. In conclusion, targeting oxidative stress may be a promising therapeutic strategy to reduce atherogenesis in patients with FH.
Factors Influencing the Cardiovascular Response to Subanesthetic Ketamine: A Randomized, Placebo-Controlled Trial

Abstract Background The increasing use of ketamine as a potential rapid-onset antidepressant necessitates a better understanding of its effects on blood pressure and heart rate, well-known side effects at higher doses. For the subanesthetic dose used for depression, potential predictors of these cardiovascular effects are important factors influencing clinical decisions. Since ketamine influences the sympathetic nervous system, we investigated the impact of autonomic nervous system-related factors on the cardiovascular response: a genetic polymorphism in the norepinephrine transporter and gender effects. Methods Blood pressure and heart rate were monitored during and following administration of a subanesthetic dose of ketamine or placebo in 68 healthy participants (mean age 26.04 ±5.562 years) in a double-blind, randomized, controlled, parallel-design trial. The influences of baseline blood pressure/heart rate, gender, and of a polymorphism in the norepinephrine transporter gene (NET SLC6A2, rs28386840 [A-3081T]) on blood pressure and heart rate changes were investigated. To quantify changes in blood pressure and heart rate, we calculated the maximum change from baseline (ΔMAX) and the time until maximum change (TΔMAX). Results Systolic and diastolic blood pressure as well as heart rate increased significantly upon ketamine administration, but without reaching hypertensive levels. During administration, the systolic blood pressure at baseline (TP0Sys) correlated negatively with the time to achieve maximal systolic blood pressure (TΔMAXSys, P<.001). Furthermore, women showed higher maximal diastolic blood pressure change (ΔMAXDia, P<.001) and reached this peak earlier than men (TΔMAXDia, P=.017) at administration. NET rs28386840 [T] carriers reached their maximal systolic blood pressure during ketamine administration significantly earlier than [A] homozygous (TΔMAXSys, P=.030). In a combined regression model, both genetic polymorphism and TP0Sys were significant predictors of TΔMAXSys (P<.0005). Conclusions Subanesthetic ketamine increased both blood pressure and heart rate without causing hypertensive events. Furthermore, we identified gender and NET rs28386840 genotype as factors that predict increased cardiovascular sequelae of ketamine administration in our young, healthy study population providing a potential basis for establishing monitoring guidelines.
On Achieving Group-Strategyproof Multicast

In computer networks, multicast models a class of data dissemination applications, where a common data item is routed to multiple receivers simultaneously. The routing of multicast flows across the network may incur a cost, and such a cost is to be recovered from payments by receivers who enjoy the multicast service. In reality, a group of potential multicast receivers exist at different network locations. Each receiver has a valuation for receiving the multicast service, but such valuation is private information known to itself. A multicast scheme asks each potential receiver to report her valuation, then decides which subset of potential receivers to serve, how to route the multicast flow to them, and how much to charge each of them. A multicast scheme is stragegyproof if no receiver has incentive to lie about her true valuation. It is further group strategyproof if no group of colluding receivers has incentive to lie. We study multicast schemes that target group strategyproofness, in both directed and undirected networks. Our main results reveal that under group strategyproofness, a compromise is necessary in either routing optimality or budget balance. We also design multicast schemes that pursue maximum budget balance while guaranteeing group stragetyproofness and routing optimality.
Regulation of RNA polymerase II processivity by Spt5 is restricted to a narrow window during elongation

Spt5 is a highly conserved RNA polymerase II (Pol II)‐associated pausing and elongation factor. However, its impact on global elongation and Pol II processivity in mammalian cells has not been clarified. Here, we show that depleting Spt5 in mouse embryonic fibroblasts (MEFs) does not cause global elongation defects or decreased elongation rates. Instead, in Spt5‐depleted cells, a fraction of Pol II molecules are dislodged during elongation, thus decreasing the number of Pol II complexes that complete the transcription cycle. Most strikingly, this decrease is restricted to a narrow window between 15 and 20 kb from the promoter, a distance which coincides with the stage where accelerating Pol II attains maximum elongation speed. Consequently, long genes show a greater dependency on Spt5 for optimal elongation efficiency and overall gene expression than short genes. We propose that an important role of Spt5 in mammalian elongation is to promote the processivity of those Pol II complexes that are transitioning toward maximum elongation speed 15–20 kb from the promoter.
CAVER 3.0: A Tool for the Analysis of Transport Pathways in Dynamic Protein Structures

Tunnels and channels facilitate the transport of small molecules, ions and water solvent in a large variety of proteins. Characteristics of individual transport pathways, including their geometry, physico-chemical properties and dynamics are instrumental for understanding of structure-function relationships of these proteins, for the design of new inhibitors and construction of improved biocatalysts. CAVER is a software tool widely used for the identification and characterization of transport pathways in static macromolecular structures. Herein we present a new version of CAVER enabling automatic analysis of tunnels and channels in large ensembles of protein conformations. CAVER 3.0 implements new algorithms for the calculation and clustering of pathways. A trajectory from a molecular dynamics simulation serves as the typical input, while detailed characteristics and summary statistics of the time evolution of individual pathways are provided in the outputs. To illustrate the capabilities of CAVER 3.0, the tool was applied for the analysis of molecular dynamics simulation of the microbial enzyme haloalkane dehalogenase DhaA. CAVER 3.0 safely identified and reliably estimated the importance of all previously published DhaA tunnels, including the tunnels closed in DhaA crystal structures. Obtained results clearly demonstrate that analysis of molecular dynamics simulation is essential for the estimation of pathway characteristics and elucidation of the structural basis of the tunnel gating. CAVER 3.0 paves the way for the study of important biochemical phenomena in the area of molecular transport, molecular recognition and enzymatic catalysis. The software is freely available as a multiplatform command-line application at http://www.caver. cz.
Growth and Characterization of M-Plane GaN Thin Films Grown on γ-LiAlO2 (100) Substrates

M-plane GaN thin films were grown on LiAlO2 substrates under different N/Ga flux ratios by plasma-assisted molecular beam epitaxy. An anisotropic growth of M-plane GaN was demonstrated against the N/Ga flux ratio. As the N/Ga flux ratio decreased by increasing Ga flux, the GaN surface trended to a flat morphology with stripes along [112-0]. According to high-resolution X-ray diffraction analysis, Li5GaO4 was observed on the interface between GaN and LiAlO2 substrate. The formation of Li5GaO4 would influence the surface morphology and crystal quality.
Potential role of type I interferon in the pathogenic process leading to type 1 diabetes

Purpose of review Understanding the relationship between viral infections and the development of type 1 diabetes (T1D) is essential for T1D prevention. Virus-induced innate immune responses, specifically type I interferon (IFN-I) and the IFN gene signature, orchestrate early events of &bgr;-cell dysfunction preceding islet autoimmunity. We summarize recent advances in how IFN-I and the IFN gene signature can drive T1D development. Recent findings IFN-I, particularly IFN-&agr;, and the IFN gene signature have been detected in islets and peripheral blood of T1D patients. T1D risk genes in the IFN-I signaling pathway regulate antiviral responses in &bgr; cells driven by IFN-I and proinflammatory cytokines. Polymorphisms in these genes may cause chronic dysregulated IFN signaling in islets, characterized by hyperexpression of IFN-I, the IFN gene signature, and major histocompatibility complex class I during viral infection. Islet-cell inflammation mediated by aberrant IFN signaling drives &bgr;-cell apoptosis by initiating autoreactivity against &bgr;-cell antigens. The profound elevation in IFN-I and the IFN gene signature observed in some forms of T1D are also seen in a novel group of human autoimmune and autoinflammatory diseases called interferonopathies. Summary Despite significant advances, further studies are required to functionally dissect the mechanisms by which excessive IFN-I contributes to the evolution of autoimmunity that destroys &bgr; cells.
A FinFET SRAM cell design with BTI robustness at high supply voltages and high yield at low supply voltages

In this paper, a SRAM cell structure which uses pMOS access transistors and predischarged bitlines is presented. By using the strained pMOS transistor technology, the degradation of the read static noise margin (SNM) at high supply voltages due to the aging, especially in the presence of symmetric stress, is suppressed. In contrast to conventional cell, the write margin of the proposed cell does not degrade considerably at low supply voltages. To assess the efficacy, the proposed cell is compared with conventional cell for two cases of unstrained and strained pMOS. A comparative study is performed using mixed mode device/circuit simulations for a gate length of 22 nm. The results show that the read SNM degradation due to the symmetric aging at the supply voltage of 1 V is about 6% after three years for the proposed strained structure, while degradations are 14%, 12%, and 11% for the unstrained proposed structure, unstrained, and strained conventional structures, respectively. In addition, the proposed cell has both read and write cell sigma yields higher than six for supply voltages ranging from 1 V down to 0.5 V while the other structures have read or write yields less than six at the minimum supply voltage. Through some work function tuning, the cell sigma yields of the other structures reach above six for both read and write while being still lower than those of the proposed structure. Copyright © 2015 John Wiley & Sons, Ltd.
Algorithmic identification of discrepancies between published ratios and their reported confidence intervals and P‐values

Motivation: Studies, mostly from the operations/management literature, have shown that the rate of human error increases with task complexity. What is not known is how many errors make it into the published literature, given that they must slip by peer‐review. By identifying paired, dependent values within text for reported calculations of varying complexity, we can identify discrepancies, quantify error rates and identify mitigating factors. Results: We extracted statistical ratios from MEDLINE abstracts (hazard ratio, odds ratio, relative risk), their 95% CIs, and their P‐values. We re‐calculated the ratios and P‐values using the reported CIs. For comparison, we also extracted percent‐ratio pairs, one of the simplest calculation tasks. Over 486 000 published values were found and analyzed for discrepancies, allowing for rounding and significant figures. Per reported item, discrepancies were less frequent in percent‐ratio calculations (2.7%) than in ratio‐CI and P‐value calculations (5.6‐7.5%), and smaller discrepancies were more frequent than large ones. Systematic discrepancies (multiple incorrect calculations of the same type) were higher for more complex tasks (14.3%) than simple ones (6.7%). Discrepancy rates decreased with increasing journal impact factor (JIF) and increasing number of authors, but with diminishing returns and JIF accounting for most of the effect. Approximately 87% of the 81 937 extracted P‐values were ≤ 0.05. Conclusion: Using a simple, yet accurate, approach to identifying paired values within text, we offer the first quantitative evaluation of published error frequencies within these types of calculations. Contact: jonathan‐wren@omrf.org or jdwren@gmail.com Supplementary information: Supplementary data are available at Bioinformatics online.
Self-Organized Dynamic Caching Space Sharing in Virtualized Wireless Networks

Both virtualization and content caching are promising techniques for the future 5G wireless networks. Meanwhile, self-organized based resource management is one fundamental capability enabling the wireless networking more flexible and efficient. In this work, we focus on the virtualized wireless networks deployed by a common wireless network operator (WNO), where the caching spaces of heterogenous BSs (macrocell BSs and small cell BSs) are dynamically shared by multiple self-organized service operators (SPs) to perform content pre-caching and provide users better services. Particularly, by well considering the strategic interactions among the WNO and SPs, we formulate this problem as a double auction game, where the WNO and SPs are the seller and bidders, respectively. In contrast to the traditional double auction based formulation, each bidder is permitted to bid multiple goods here. To address this, the concept of virtual SP is incorporated and a multi-round based auction algorithm has been developed. Then, the key economic properties, i.e., individual rationality, budget balance and truthfulness, of our proposed algorithm are also established. Finally, simulation results verify the effectiveness of our proposed algorithm in terms of both the SP's revenue and user's satisfaction.
Multiuser rate-diverse network-coded multiple access

This paper presents the first Network-Coded Multiple Access (NCMA) system with multiple users adopting different signal modulations, referred to as rate-diverse NCMA. A distinguishing feature of NCMA is the joint use of physical-layer network coding (PNC) and multiuser decoding (MUD) to boost throughput of multipacket reception systems. In previous NCMA systems, users adopt the same modulation regardless of their individual channel conditions. This leads to suboptimal throughput for many practical scenarios, especially when different users have widely varying channel conditions. A rate-diverse NCMA system allows different users to use modulations that are commensurate with their channel conditions. A key challenge is the design of PNC mapping and decoding mechanisms in NCMA when different users adopt different modulations. While there have been past work on non-channel-coded rate-diverse PNC, this paper is the first attempt to design channel-coded rate-diverse PNC to ensure the reliability of the overall NCMA system. Specifically, we put forth a symbol-splitting channel coding and modulation design so that PNC/NCMA can work over different modulations. We implemented our rate-diverse NCMA system on software-defined radios. Experimental results show that the throughput of rate-diverse NCMA can outperform the state-of-the-art rate-homogeneous NCMA by 80%. Overall, the introduction of rate diversity significantly boosts the NCMA system throughput in practical scenarios.
Phase Only RF Precoding for Massive MIMO Systems With Limited RF Chains

Massive MIMO systems promise high spectrum efficiency by deploying M ≫ 1 antennas at the base station (BS). However, to achieve the full gain provided by massive MIMO, the BS requires M radio frequency (RF) chains, which are expensive. This motivates us to consider RF-chain limited massive MIMO systems with M antennas but only S ≪ M RF chains. We propose a two-stage precoding scheme to efficiently exploit the large spatial degree of freedom (DoF) gain in massive MIMO systems with limited RF chains and reduced channel state information (CSI) signaling overhead. In this scheme, the MIMO precoder is partitioned into a high-dimensional phase only RF precoder followed by a low-dimensional baseband precoder. The RF precoder is adaptive to the spatial correlation matrices for inter-cluster interference mitigation. The baseband precoder is adaptive to the reduced dimensional “effective” CSI for intra-cluster spatial multiplexing. We formulate the two stage precoding problem such that the minimum (weighted) average data rate of users is maximized under the phase only constraint on the RF precoder and the limited RF chain constraint. This is a combinatorial optimization problem which is in general NP-hard. We propose a low complexity solution based on a novel bi-convex approximation approach. Simulations show that the proposed design has significant gain over various baselines.