Miracle-dz/UniFAR-FTUs huggingface dataset:
Frame-patch matching based robust video watermarking using KAZE feature

A frame-patch matching based robust video watermarking using KAZE feature is proposed in this paper. We employed the KAZE feature for matching the feature points of frame-patch with those of all frames in video. In our method, the watermark information is embedded in Discrete Cosine Transform (DCT) domain of randomly generated blocks in the matched region. In the extraction process, we synchronized the embedded region from the distorted video by using KAZE feature matching. RST (rotation, scaling, translation) parameters are estimated and the watermark information can be extracted. Experimental results showed that our proposed method is very robust against geometrical attacks, video processing attacks, temporal attacks, and so on.
An mRNA Capping Enzyme Targets FACT to the Active Gene To Enhance the Engagement of RNA Polymerase II into Transcriptional Elongation

ABSTRACT We have recently demonstrated that an mRNA capping enzyme, Cet1, impairs promoter-proximal accumulation/pausing of RNA polymerase II (Pol II) independently of its capping activity in Saccharomyces cerevisiae to control transcription. However, it is still unknown how Pol II pausing is regulated by Cet1. Here, we show that Cet1's N-terminal domain (NTD) promotes the recruitment of FACT (facilitates chromatin transcription that enhances the engagement of Pol II into transcriptional elongation) to the coding sequence of an active gene, ADH1, independently of mRNA-capping activity. Absence of Cet1's NTD decreases FACT targeting to ADH1 and consequently reduces the engagement of Pol II in transcriptional elongation, leading to promoter-proximal accumulation of Pol II. Similar results were also observed at other genes. Consistently, Cet1 interacts with FACT. Collectively, our results support the notion that Cet1's NTD promotes FACT targeting to the active gene independently of mRNA-capping activity in facilitating Pol II's engagement in transcriptional elongation, thus deciphering a novel regulatory pathway of gene expression.
Adaptive Dynamic Scheduling on Multifunctional Mixed-Criticality Automotive Cyber-Physical Systems

A function model for the description of distributed end-to-end computations is called a task graph. Multiple functions with different criticality levels are supported by one electronic control unit (ECU), and one function is distributed over multiple ECUs in integrated automotive architecture. Considering the inherent heterogeneity, interaction, and diverse nature of such an architecture, automotive embedded systems have evolved to automotive cyber-physical systems (ACPS), which consist of multiple distributed automotive functions with different criticality levels. Efficient scheduling strategies can fully utilize ECUs in ACPS for high performance. However, ACPS should deal with joint challenges of heterogeneity, dynamics, parallelism, safety, and criticality, and these challenges are the key issues that will be solved in the next generation automotive open system architecture adaptive platform. This study first proposes a fairness-based dynamic scheduling algorithm FDS_MIMF to minimize the individual makespans (i.e., schedule lengths) of functions from a high performance perspective. FDS_MIMF can respond autonomously to the joint challenges of heterogeneity, dynamics, and parallelism of ACPS. To further respond autonomously to the joint challenges of heterogeneity, dynamics, parallelism, safety, and criticality of ACPS, we present an adaptive dynamic scheduling algorithm ADS_MIMF to achieve low deadline miss ratios (DMRs) of safety-critical functions from a timing constraint perspective while maintaining the acceptable overall makespan of ACPS from a high performance perspective. ADS_MIMF is implemented by changing up and down the criticality level of ACPS to adjust the execution of different functions on different criticality levels without increasing the time complexity. Experimental results indicate that FDS_MIMF can obtain short overall makespan, whereas ADS_MIMF can reduce the DMR values of high-criticality functions while still keeping satisfactory performance of ACPS.
Objectively-measured sedentary time and its association with markers of cardiometabolic health and fitness among cardiac rehabilitation graduates

Background Sedentary time is an independent risk factor for cardiometabolic disease and mortality. It is unknown how much time individuals with coronary artery disease spend being sedentary or how their sedentary time relates to markers of health. The objectives of this study were to: (a) quantify sedentary time in a post-cardiac rehabilitation (CR) population, and (b) assess association with cardiometabolic risk, independent of moderate-to-vigorous physical activity. Design Cross-sectional. Methods As part of a larger trial, 263 recent CR graduates (∼10 days post-CR, mean age 63.6 ± 9.3 years, 75% male) wore an ActiGraph GT3X accelerometer during waking hours (≥4 days, ≥10 hours/day) to quantify sedentary time (≤150 counts per minute). Spearman correlations were computed to assess relationships between sedentary time (adjusted for wear time) with markers of cardiometabolic health and fitness. Significant markers were examined using multiple linear regressions. Results Participants spent an average of 8 hours/day sedentary (∼14 bouts/day). Sedentary time was negatively correlated with high-density lipoprotein and V · O2peak and positively correlated with triglycerides, body mass index and waist circumference. After adjusting for age, sex, medications and moderate-to-vigorous physical activity, hours/day of sedentary time remained significantly associated with log V · O2peak (β = −0.02, p = 0.001) and body mass index (β = 0.49, p = 0.02). Conclusions Findings suggest that even among a group of post-CR individuals who are already probably more active than patients who have not undergone CR, sedentary time remains high and is associated with poorer cardiorespiratory fitness, suggesting a possible new area of focus among CR programs.
Endurance training and maximal oxygen consumption with ageing: Role of maximal cardiac output and oxygen extraction

Background The increase in maximal oxygen consumption (VO2max) with endurance training is associated with that of maximal cardiac output (Qmax), but not oxygen extraction, in young individuals. Whether such a relationship is altered with ageing remains unclear. Therefore, we sought systematically to review and determine the effect of endurance training on and the associations among VO2max, Qmax and arteriovenous oxygen difference at maximal exercise (Ca-vO2max) in healthy aged individuals. Design and methods We conducted a systematic search of MEDLINE, Scopus and Web of Science, from their inceptions until May 2015 for articles assessing the effect of endurance training lasting 3 weeks or longer on VO2max and Qmax and/or Ca-vO2max in healthy middle-aged and/or older individuals (mean age ≥40 years). Meta-analyses were performed to determine the standardised mean difference (SMD) in VO2max, Qmax and Ca-vO2max between post and pre-training measurements. Subgroup and meta-regression analyses were used to evaluate the associations among SMDs and potential moderating factors. Results Sixteen studies were included after systematic review, comprising a total of 153 primarily untrained healthy middle-aged and older subjects (mean age 42–71 years). Endurance training programmes ranged from 8 to 52 weeks of duration. After data pooling, VO2max (SMD 0.89; P < 0.0001) and Qmax (SMD 0.61; P < 0.0001) were increased after endurance training; no heterogeneity among studies was detected. Ca-vO2max was only increased with endurance training interventions lasting more than 12 weeks (SMD 0.62; P = 0.001). In meta-regression, the SMD in Qmax was positively associated with the SMD in VO2max (B = 0.79, P = 0.04). The SMD in Ca-vO2max was not associated with the SMD in VO2max (B = 0.09, P = 0.84). Conclusions The improvement in VO2max following endurance training is a linear function of Qmax, but not Ca-vO2max, through healthy ageing.
NOS1AP Functionally Associates with YAP To Regulate Hippo Signaling

ABSTRACT Deregulation of cellular polarity proteins and their associated complexes leads to changes in cell migration and proliferation. The nitric oxide synthase 1 adaptor protein (NOS1AP) associates with the tumor suppressor protein Scribble to control cell migration and oncogenic transformation. However, how NOS1AP is linked to the cell signaling events that curb oncogenic progression has remained elusive. Here we identify several novel NOS1AP isoforms, NOS1APd, NOS1APe, and NOS1APf, with distinct cellular localizations. We show that isoforms with a membrane-interacting phosphotyrosine binding (PTB) domain can associate with Scribble and recognize acidic phospholipids. In a screen to identify novel binding proteins, we have discovered a complex consisting of NOS1AP and the transcriptional coactivator YAP linking NOS1AP to the Hippo signaling pathway. Silencing of NOS1AP reduces the phosphorylation of YAP and of the upstream kinase Lats1. Conversely, expression of NOS1AP promotes YAP and Lats1 phosphorylation, which correlates with reduced TEAD activity and restricted cell proliferation. Together, these data implicate a role for NOS1AP in the regulation of core Hippo signaling and are consistent with the idea that NOS1AP functions as a tumor suppressor.
Anti‐Aβ: The good, the bad, and the unforeseen

Alzheimer's disease (AD) is characterized in part by the deposition of amyloid β protein (Aβ) in compact fibrillar plaques. These structures can induce an innate immune response in the brain, which triggers progressive inflammation, neuronal loss, and further acceleration of Aβ plaque formation. Compared with the case in normal individuals, the T and B lymphocytes in AD patients and murine models are hyporesponsive to Aβ. However, depending on the route of delivery, tolerance can be overcome by vaccination, with the induction of an anti‐Aβ‐mediated immune response. Through mechanisms that are incompletely understood, immunized APP transgenic animals show markedly reduced Aβ deposition, preservation of normal neuronal architecture, and improved performance in memory and spatial learning tasks. In human trials, Aβ vaccination stabilized cognition and slowed the progression of dementia. Neuropathologic examination of a vaccinated subject showed reduced cortical Aβ without changes in other AD‐associated pathology. However, in some patients, vaccination induced severe meningoencephalitis, causing the trial to be terminated. Thus, vaccination appears to activate both beneficial and deleterious anti‐Aβ immunity, suggesting that the vaccine can have potent clinical utility if an appropriate immunologic response can be generated. © 2003 Wiley‐Liss, Inc.
Low aerobic capacity in middle-aged men associated with increased mortality rates during 45 years of follow-up

Background Low aerobic capacity has been associated with increased mortality in short-term studies. The aim of this study was to evaluate the predictive power of aerobic capacity for mortality in middle-aged men during 45-years of follow-up. Design The study design was a population-based prospective cohort study. Methods A representative sample from Gothenburg of men born in 1913 was followed from 50–99 years of age, with periodic medical examinations and data from the National Hospital Discharge and Cause of Death registers. At 54 years of age, 792 men performed an ergometer exercise test, with 656 (83%) performing the maximum exercise test. Results In Cox regression analysis, low predicted peak oxygen uptake ( VO 2 max ), smoking, high serum cholesterol and high mean arterial blood pressure at rest were significantly associated with mortality. In multivariable analysis, an association was found between predicted VO 2 max tertiles and mortality, independent of established risk factors. Hazard ratios were 0.79 (95% confidence interval (CI) 0.71–0.89; p < 0.0001) for predicted VO 2 max , 1.01 (1.002–1.02; p < 0.01) for mean arterial blood pressure, 1.13 (1.04–1.22; p < 0.005) for cholesterol, and 1.58 (1.34–1.85; p < 0.0001) for smoking. The variable impact (Wald’s χ2) of predicted VO 2 max tertiles (15.3) on mortality was secondary only to smoking (31.4). The risk associated with low predicted VO 2 max was evident throughout four decades of follow-up. Conclusion In this representative population sample of middle-aged men, low aerobic capacity was associated with increased mortality rates, independent of traditional risk factors, including smoking, blood pressure and serum cholesterol, during more than 40 years of follow-up.
An In Vitro TORC1 Kinase Assay That Recapitulates the Gtr-Independent Glutamine-Responsive TORC1 Activation Mechanism on Yeast Vacuoles

ABSTRACT Evolutionarily conserved target of rapamycin (TOR) complex 1 (TORC1) responds to nutrients, especially amino acids, to promote cell growth. In the yeast Saccharomyces cerevisiae, various nitrogen sources activate TORC1 with different efficiencies, although the mechanism remains elusive. Leucine, and perhaps other amino acids, was reported to activate TORC1 via the heterodimeric small GTPases Gtr1-Gtr2, the orthologues of the mammalian Rag GTPases. More recently, an alternative Gtr-independent TORC1 activation mechanism that may respond to glutamine was reported, although its molecular mechanism is not clear. In studying the nutrient-responsive TORC1 activation mechanism, the lack of an in vitro assay hinders associating particular nutrient compounds with the TORC1 activation status, whereas no in vitro assay that shows nutrient responsiveness has been reported. In this study, we have developed a new in vitro TORC1 kinase assay that reproduces, for the first time, the nutrient-responsive TORC1 activation. This in vitro TORC1 assay recapitulates the previously predicted Gtr-independent glutamine-responsive TORC1 activation mechanism. Using this system, we found that this mechanism specifically responds to l-glutamine, resides on the vacuolar membranes, and involves a previously uncharacterized Vps34-Vps15 phosphatidylinositol (PI) 3-kinase complex and the PI-3-phosphate [PI(3)P]-binding FYVE domain-containing vacuolar protein Pib2. Thus, this system was proved to be useful for dissecting the glutamine-responsive TORC1 activation mechanism.
Longer-term effects of home-based exercise interventions on exercise capacity and physical activity in coronary artery disease patients: A systematic review and meta-analysis

Background Exercise-based cardiovascular rehabilitation (CR) improves exercise capacity (EC), lowers cardiovascular risk profile and increases physical functioning in the short term. However, uptake of and adherence to a physically active lifestyle in the long run remain problematic. Home-based (HB) exercise programmes have been introduced in an attempt to enhance long-term adherence to recommended levels of physical activity (PA). The current systematic review and meta-analysis aimed to compare the longer-term effects of HB exercise programmes with usual care (UC) or centre-based (CB) CR in patients referred for CR. Design Systematic review and meta-analysis. Methods Non-randomised controlled trials (RCTs) or randomised trials comparing the effects of HB exercise programmes with UC or CB rehabilitation on EC and/or PA, with a follow-up period of ≥12 months and performed in coronary artery disease patients, were searched in four databases (PubMed, EMBASE, the Cumulative Index to Nursing and Allied Health Literature (CINAHL) and the Cochrane Central Register of Controlled trials (CENTRAL)) from their inception until September 7, 2016. Standardised mean differences (SMDs) were calculated and pooled by means of random effects models. Risk of bias, publication bias and heterogeneity among trials were also assessed. Results Seven studies could be included in the meta-analysis on EC, but only two studies could be included in the meta-analysis on PA (total number of 1440 patients). The results showed no significant differences in EC between HB rehabilitation and UC (SMD 0.10, 95% confidence interval (CI) –0.13 to 0.33). There was a small but significant difference in EC in favour of HB compared to CB rehabilitation (SMD 0.25, 95% CI 0.02–0.48). No differences were found for PA (SMD 0.37, 95% CI –0.18 to 0.92). Conclusions HB exercise is slightly more effective than CB rehabilitation in terms of maintaining EC. The small number of studies warrants the need for more RCTs evaluating the long-term effects of different CR interventions on EC and PA behaviour, as this is the ultimate goal of CR.
Osteotomia em Chevron modificada: análise preliminar do comportamento baropodométrico

OBJECTIVE: To evaluate the clinical and baropodometric characteristics of the gaits of individuals with a hallux valgus deformity after modified Chevron osteotomy, in isolation or in association with the Weil osteotomy. METHODS: Foot evaluation happened before and three months after surgery analyzing 27 mildly and moderately deformed feet. The clinical evaluation included the AOFAS score and radiographic measurements. The baropodometric evaluation was done with the Emed-at platform. Peak of Pressure, Pressure-Time Integral and Relative Load were calculated in 10 different regions of the feet: calcaneous, midfoot, first to fifth metatarsal regions, hallux, second and third to fifth toes. RESULTS: After the surgical procedure, an increase in AOFAS scores and a decrease of radiographic parameters were seen. The baropodometric evaluation, after isolated Chevron osteotomy, showed a reduction in pressure and strength under the first metatarsal and hallux, as well as an increase in the same variables on central and lateral metatarsals. After Chevron/Weil osteotomy significant alterations had only occurred in the region of the hallux and toes. CONCLUSION: In the short-term, the modified Chevron technique promoted improvements in clinical conditions and radiographic parameters. The baropodometric evaluation evidenced a load transference from medial to lateral regions of the forefoot, possibly due to the short postoperative period.
Distinct Roles of Mus81, Yen1, Slx1-Slx4, and Rad1 Nucleases in the Repair of Replication-Born Double-Strand Breaks by Sister Chromatid Exchange

ABSTRACT Most spontaneous DNA double-strand breaks (DSBs) arise during replication and are repaired by homologous recombination (HR) with the sister chromatid. Many proteins participate in HR, but it is often difficult to determine their in vivo functions due to the existence of alternative pathways. Here we take advantage of an in vivo assay to assess repair of a specific replication-born DSB by sister chromatid recombination (SCR). We analyzed the functional relevance of four structure-selective endonucleases (SSEs), Yen1, Mus81-Mms4, Slx1-Slx4, and Rad1, on SCR in Saccharomyces cerevisiae. Physical and genetic analyses showed that ablation of any of these SSEs leads to a specific SCR decrease that is not observed in general HR. Our work suggests that Yen1, Mus81-Mms4, Slx4, and Rad1, but not Slx1, function independently in the cleavage of intercrossed DNA structures to reconstitute broken replication forks via HR with the sister chromatid. These unique effects, which have not been detected in other studies unless double mutant combinations were used, indicate the formation of distinct alternatives for the repair of replication-born DSBs that require specific SSEs.
The Small Molecule GMX1778 Is a Potent Inhibitor of NAD+ Biosynthesis: Strategy for Enhanced Therapy in Nicotinic Acid Phosphoribosyltransferase 1-Deficient Tumors

ABSTRACT GMX1777 is a prodrug of the small molecule GMX1778, currently in phase I clinical trials for the treatment of cancer. We describe findings indicating that GMX1778 is a potent and specific inhibitor of the NAD+ biosynthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT). Cancer cells have a very high rate of NAD+ turnover, which makes NAD+ modulation an attractive target for anticancer therapy. Selective inhibition by GMX1778 of NAMPT blocks the production of NAD+ and results in tumor cell death. Furthermore, GMX1778 is phosphoribosylated by NAMPT, which increases its cellular retention. The cytotoxicity of GMX1778 can be bypassed with exogenous nicotinic acid (NA), which permits NAD+ repletion via NA phosphoribosyltransferase 1 (NAPRT1). The cytotoxicity of GMX1778 in cells with NAPRT1 deficiency, however, cannot be rescued by NA. Analyses of NAPRT1 mRNA and protein levels in cell lines and primary tumor tissue indicate that high frequencies of glioblastomas, neuroblastomas, and sarcomas are deficient in NAPRT1 and not susceptible to rescue with NA. As a result, the therapeutic index of GMX1777 can be widended in the treatment animals bearing NAPRT1-deficient tumors by coadministration with NA. This provides the rationale for a novel therapeutic approach for the use of GMX1777 in the treatment of human cancers.
Performance analysis of an FFH/BFSK receiver with product-combining in a fading channel under multitone interference

The bit-error probability (BEP) is evaluated for a fast frequency-hopping binary frequency-shift-keying (FFH/BFSK) spread-spectrum communication system over Rician fading channels in the presence of worst-case multitone jamming (MTJ) and additive white Gaussian noise (AWGN). A diversity reception scheme of product-combining is applied at the receiver. Two types of MTJ models, namely n=1-band MTJ and independent MTJ, are considered in this letter. To obtain the final decision statistics, the closed-form or a single finite integral expressions of cumulative distribution functions (CDFs) of the ratio of two square-law detectors' outputs per hop are derived. According to the numerical results, it is shown, unlike the known knowledge for the AWGN channel, that independent MTJ is more harmful than n=1-band MTJ for the product-combining receivers (L/spl ges/2) in fading channels.
Coronary artery disease: Risk stratification and patient selection for more aggressive secondary prevention

In patients with stable coronary artery disease, clinical outcomes are predominantly characterized by the consequences of atherosclerosis on the myocardium, but also by complications of atherosclerosis, notably recurrent acute coronary syndrome or stroke. Secondary prevention therapy is therefore key in this patient population. Intensification of secondary prevention therapy is possible, at the price of a therapeutic risk or a high cost, therefore justifying careful selection of patients with a high residual risk and low therapeutic risk. Two lines of therapy can be intensified, independently of each other, namely anti-thrombotics and lipid-lowering agents. Intensification of anti-thrombotic therapy is efficacious in terms of ischaemic events and cardiovascular mortality, but incurs an excess haemorrhagic risk. Patients aged over 65 years of age and those with a history of intra-cranial haemorrhage are not eligible for intensification of anti-thrombotic therapy. Conversely, patients with prior or recurrent myocardial infarction may benefit from this strategy, especially if they are current smokers or have diabetes mellitus. Intensification of lipid-lowering therapy can be achieved through an association of high-intensity statins with ezetimibe or PCSK9 inhibitors. This strategy engenders little risk, but the cost of PCSK9 inhibition is high, and should be considered based on the level of low-density lipoprotein cholesterol achieved with statin treatment at the maximal tolerated dose. In addition to this patient selection based on low-density lipoprotein cholesterol levels, the presence of diabetes or documented progression of atherosclerosis should be considered.