Miracle-dz/UniFAR-FTUs huggingface dataset:
Join cost for unit selection speech synthesis

In unit-selection speech synthesis systems, synthetic speech is produced by concatenating speech units selected from a large database, or inventory, which contains many instances of each speech unit with varied prosodic and spectral characteristics. Hence, by selecting an appropriate sequence of units, it is possible to synthesize highly natural-sounding speech. The selection of the best unit sequence from the database is typically treated as a search problem in which the best sequence of candidates from the inventory is the one that has the lowest overall cost [1]. This cost is often decomposed into two costs: a target cost (how closely candidate units in the inventory match the specification of the target phone sequence) and join cost (how well neighboring units can be joined) [1]. If, as is usually the case, the cost functions used to compute these costs take into account only properties of the fixed target sequence and local properties of the candidates, the optimal unit sequence can be found efficiently by a Viterbi search for the lowest cost path through the lattice of the target and join costs. In this chapter we focus on the calculation of the join cost (also known as concatenation cost). The ideal join cost is one that, although based solely on measurable properties of the candidate units—such as spectral parameters, amplitude, and F0—correlates highly with human listeners’ perceptions of discontinuity at concatenation points. In other words, the join cost should predict the degree of perceived discontinuity. We use this terminology: a join cost is computed using a join cost function, which generally uses a distance measure on some parameterization of the speech signal.
Second-hit mosaic mutation in mTORC1 repressor DEPDC5 causes focal cortical dysplasia–associated epilepsy

DEP domain–containing 5 protein (DEPDC5) is a repressor of the recently recognized amino acid–sensing branch of the mTORC1 pathway. So far, its function in the brain remains largely unknown. Germline loss-of-function mutations in DEPDC5 have emerged as a major cause of familial refractory focal epilepsies, with case reports of sudden unexpected death in epilepsy (SUDEP). Remarkably, a fraction of patients also develop focal cortical dysplasia (FCD), a neurodevelopmental cortical malformation. We therefore hypothesized that a somatic second-hit mutation arising during brain development may support the focal nature of the dysplasia. Here, using postoperative human tissue, we provide the proof of concept that a biallelic 2-hit — brain somatic and germline — mutational mechanism in DEPDC5 causes focal epilepsy with FCD. We discovered a mutation gradient with a higher rate of mosaicism in the seizure-onset zone than in the surrounding epileptogenic zone. Furthermore, we demonstrate the causality of a Depdc5 brain mosaic inactivation using CRISPR-Cas9 editing and in utero electroporation in a mouse model recapitulating focal epilepsy with FCD and SUDEP-like events. We further unveil a key role of Depdc5 in shaping dendrite and spine morphology of excitatory neurons. This study reveals promising therapeutic avenues for treating drug-resistant focal epilepsies with mTORC1-targeting molecules.
Glacsweb: a sensor network for hostile environments

A sensor network is described which obtains data from nodes on and inside glaciers. Power management through scheduling and selective control is used to allow a lifetime of at least one year on batteries. Radio links in the glacier and across 2.5 km distances are used for data and commands. The prototype system was installed in Norway in 2003 and this paper describes details of the full design for 2004 through discussion of the lessons learnt.
Factors Affecting Attitudes Towards Broadband Adoption in the Kingdom of Saudi Arabia

Utilizing a survey approach, this research set out to explore the reasons for the slow progress in broadband adoption and investigates the factors that may be affecting the adoption of broadband by KSA consumers. Particular emphasis was placed on individual-level factors such as social and cultural influences. The key findings were that the factors with the main influence on attitude towards adoption of broadband were: (1) usefulness, (2) service quality, (3) age, (4) usage, (5) type of connection, and (6) type of accommodation. Contrary to prediction, although socio-cultural factors such as regulation through filtration of broadband were found to have no significant influence on the adoption of broadband, consumers were aware and largely did not like the regulation. The chapter also provides a discussion on research implications, limitations, and future directions.
Consolidating a Link Centered Neural Connectivity Framework with Directed Transfer Function Asymptotics

We present a unified mathematical derivation of the asymptotic behaviour of three of the main forms of \textit{directed transfer function} (DTF) complementing recent partial directed coherence (PDC) results \cite{Baccala2013}. Based on these results and numerical examples we argue for a new directed `link' centered neural connectivity framework to replace the widespread correlation based effective/functional network concepts so that directed network influences between structures become classified as to whether links are \textit{active} in a \textit{direct} or in an \textit{indirect} way thereby leading to the new notions of \textit{Granger connectivity} and \textit{Granger influenciability} which are more descriptive than speaking of Granger causality alone.
Multiuser precoding in MIMO two-way relay transmission

This paper is concerned with the problem of multiuser precoding design for multiple-output multiple-input (MIMO) two-way relay transmission. In the literature, most of existing studies on multiuser transmission over two-way relay channels have assumed that user terminals (i.e., source nodes) are equipped with a single antenna. To increase the capacity of the multiuser two-way relay network, this paper introduces precoding designs at source and relay nodes for space division multiple access (SDMA) transmissions between source nodes. Numerical simulation results show that the proposed precoding designs at multi-antenna source nodes (i.e., user terminals) can improve the capacity of the network.
Empirical mode decomposition as a filter bank

Empirical mode decomposition (EMD) has recently been pioneered by Huang et al. for adaptively representing nonstationary signals as sums of zero-mean amplitude modulation frequency modulation components. In order to better understand the way EMD behaves in stochastic situations involving broadband noise, we report here on numerical experiments based on fractional Gaussian noise. In such a case, it turns out that EMD acts essentially as a dyadic filter bank resembling those involved in wavelet decompositions. It is also pointed out that the hierarchy of the extracted modes may be similarly exploited for getting access to the Hurst exponent.
Genomic Adaptation of the Lactobacillus casei Group

Lactobacillus casei, L. paracasei, and L. rhamnosus form a closely related taxonomic group (Lactobacillus casei group) within the facultatively heterofermentative lactobacilli. Here, we report the complete genome sequences of L. paracasei JCM 8130 and L. casei ATCC 393, and the draft genome sequence of L. paracasei COM0101, all of which were isolated from daily products. Furthermore, we re-annotated the genome of L. rhamnosus ATCC 53103 (also known as L. rhamnosus GG), which we have previously reported. We confirmed that ATCC 393 is distinct from other strains previously described as L. paracasei. The core genome of 10 completely sequenced strains of the L. casei group comprised 1,682 protein-coding genes. Although extensive genome-wide synteny was found among the L. casei group, the genomes of ATCC 53103, JCM 8130, and ATCC 393 contained genomic islands compared with L. paracasei ATCC 334. Several genomic islands, including carbohydrate utilization gene clusters, were found at the same loci in the chromosomes of the L. casei group. The spaCBA pilus gene cluster, which was first identified in GG, was also found in other strains of the L. casei group, but several L. paracasei strains including COM0101 contained truncated spaC gene. ATCC 53103 encoded a higher number of proteins involved in carbohydrate utilization compared with intestinal lactobacilli, and extracellular adhesion proteins, several of which are absent in other strains of the L. casei group. In addition to previously fully sequenced L. rhamnosus and L. paracasei strains, the complete genome sequences of L. casei will provide valuable insights into the evolution of the L. casei group.
JITProf: pinpointing JIT-unfriendly JavaScript code

Most modern JavaScript engines use just-in-time (JIT) compilation to translate parts of JavaScript code into efficient machine code at runtime. Despite the overall success of JIT compilers, programmers may still write code that uses the dynamic features of JavaScript in a way that prohibits profitable optimizations. Unfortunately, there currently is no way to measure how prevalent such JIT-unfriendly code is and to help developers detect such code locations. This paper presents JITProf, a profiling framework to dynamically identify code locations that prohibit profitable JIT optimizations. The key idea is to associate meta-information with JavaScript objects and code locations, to update this information whenever particular runtime events occur, and to use the meta-information to identify JIT-unfriendly operations. We use JITProf to analyze widely used JavaScript web applications and show that JIT-unfriendly code is prevalent in practice. Furthermore, we show how to use the approach as a profiling technique that finds optimization opportunities in a program. Applying the profiler to popular benchmark programs shows that refactoring these programs to avoid performance problems identified by JITProf leads to statistically significant performance improvements of up to 26.3% in 15 benchmarks.
The radio luminosity function of the NEP distant cluster radio galaxies

A complete sample of 18 X-ray selected clusters of galaxies belonging to the ROSAT North Ecliptic Pole (NEP) survey has been observed with the Very Large Array at 1.4 GHz in B configuration. These are the most distant clusters in the X-ray survey with redshift in the range $0.3 -1 , except for three sources, belonging to the same cluster, which have a higher peak brightness limit of 0.26 mJy beam -1 . The NEP field source counts are in good agreement with the source counts of a comparison survey, the VLA-VIRMOS deep field survey, indicating that the NEP sample is statistically complete. Thirty-two out of the 79 sources are within 0.2 Abell radii, twenty-two of them are considered cluster members based on spectroscopic redshifts or their optical magnitude and morphological classification. The cluster radio galaxies are used to construct the Radio Luminosity Function (RLF) of distant X-ray selected clusters. A comparison with two nearby cluster RLFs shows that the NEP RLF lies above the local ones, has a steeper slope at low radio powers ( ≤ 10 24 W Hz -1 ) and shows no evidence for a break at ${\approx}6 \times 10^{24}$ W Hz -1 which is observed in the nearby cluster RLFs. We discuss briefly the origin and possible explanations of the differences observed in the radio properties of nearby and distant clusters of galaxies. The main result of this study is that the RLF of the distant X-ray clusters is very different from that of the local rich Abell clusters.
TAP binds to the constitutive transport element (CTE) through a novel RNA‐binding motif that is sufficient to promote CTE‐dependent RNA export from the nucleus

The constitutive transport element (CTE) of the simian type D retroviruses overcomes nuclear retention and allows nuclear export of unspliced viral RNAs by recruiting TAP, a host factor which is thought to be required for export of cellular mRNAs. In this report, we show that the first 372 amino acid residues of TAP, comprising a stretch of leucine‐rich repeats, are both necessary and sufficient for binding to the CTE RNA and promoting its export to the cytoplasm. Moreover, like the full‐length protein, this domain migrates to the cytoplasm upon nuclear co‐injection with the CTE RNA. Together, these results indicate that the CTE‐binding domain includes the signals for nuclear export. We also describe a derivative of TAP that bears a triple amino acid substitution within the CTE‐binding domain and substantially reduces the export of mRNAs from the nucleus. This provides further evidence for a role for TAP in this process. Thus, the CTE‐binding domain of TAP defines a novel RNA‐binding motif which has dual functions, both recognizing the CTE RNA and interacting with other components of the nuclear transport machinery.
A New Representation for Device Color

Introduction An important part of color reproduction is the rendering of colors onto display devices [1], where the colors may be spot colors (e.g., tints) or the colors of a digitized photograph. Display devices, such as monitors and printers, are capable of showing only a subset of all perceivable colors; this subset is called the device color gamut. Colors subjected to a reproduction system may not fall within the gamut of the target display device. In these cases, the colors cannot be exactly reproduced. If no corrective action is taken, the reproduction of graphics having out of gamut colors results in undesirable distortions of the tonal and color range of the graphic. When this occurs, some action is required, either notifying the user to modify the colors to fit within the gamut, or employing an algorithm to automatically compress the colors according to some predetermined strategy to fit within the gamut. In either case, a reliable technique is needed to determine whether or not a color lies inside a device gamut. When considering applications involving high resolution digitized images containing millions of colors, this gamut test must be very fast.
GM‐CSF and IL‐4 are not involved in IVIG‐mediated amelioration of ITP in mice: a role for IL‐11 cannot be ruled out

Previously, we have reported that interleukin (IL)‐4, granulocyte–macrophage colony‐stimulating factor (GM‐CSF), and IL‐11, but not IL‐33, are up‐regulated in two strains of mice with immune thrombocytopenia (ITP) that are responsive to intravenous immunoglobulin (IVIg) treatment. Previously, IL‐4 was ruled out in the mechanism of IVIg; however, other publications have suggested this cytokine as a major player in the mechanism of IVIg action. Thus, we sought to further investigate a role for IL‐4 and, in addition, GM‐CSF and IL‐11 in the mechanism of action of IVIg using a murine model of ITP. A passive platelet antibody model was used to generate ITP in IL‐4 receptor knock‐out (IL‐4R–/–), IL‐11 receptor knock‐out (IL‐11Rα–/–) and GM‐CSF knock‐out (Csf2–/–) mice. We also used a neutralizing antibody to IL‐11 and recombinant human IL‐11 (rhIL‐11) in addition to depleting basophils in vivo to study the effect of IVIg to ameliorate ITP. Our results showed that basophils, IL‐4 and GM‐CSF were unimportant in both ITP induction and its amelioration by IVIg. The role of IL‐11 in these processes was less clear. Even though IL‐11Rα–/– mice with ITP responded to IVIg similarly to wild‐type (WT) mice, treatment of ITP WT mice with rhIL‐11 instead of IVIg showed an increase in platelet numbers and WT mice administered anti‐IL‐11 showed a significant reduction in the ability of IVIg to ameliorate the ITP. Our findings indicate that neither IL‐4, basophils or GM‐CSF have roles in IVIg amelioration of ITP; however, a role for IL‐11 requires further study.
Osthole induces lung cancer cell apoptosis through inhibition of inhibitor of apoptosis family proteins

In the present study, we investigated the effects and mechanisms of Osthole on the apoptosis of non-small cell lung cancer (NSCLC) cells and its synergistic effect with Embelin. Our results revealed that treatment with both Osthole and Embelin inhibited cell proliferation. Notably, combination treatment of Osthole and Embelin inhibited cell proliferation more significantly compared with monotherapy. In addition, morphological analysis and Annexin V/propidium iodide analysis revealed that the combination of Osthole and Embelin enhanced their effect on cell apoptosis. We further examined the effect of Osthole on the expression of inhibitor of apoptosis protein (IAP) family proteins. That treatment of A549 lung cancer cells with various concentrations of Osthole was observed to decrease the protein expression of X-chromosome-encoded IAP, c-IAP1, c-IAP2 and Survivin, and increase Smac expression in a dose-dependent manner. Furthermore, it was noted that Osthole or Embelin alone increased the expression of BAX, caspase-3, caspase-9, cleaved caspase-3 and cleaved caspase-9, and decreased Bcl-2 levels following treatment. Osthole and Embelin combination treatment had a synergistic effect on the regulation of these proteins. In conclusion, our study demonstrated that Osthole inhibited proliferation and induced the apoptosis of lung cancer cells via IAP family proteins in a dose-dependent manner. Osthole enhances the antitumor effect of Embelin, indicating that combination of Osthole and Embelin has potential clinical significance in the treatment of NSCLC.
Prospective Development of Small Molecule Targets to Oncogenic Ras Proteins

Abnormal expression or mutations in Ras proteins has been found in up to 30% of cancer cell types, making them excellent protein models to probe structure-function relationships of cell-signaling processes that mediate cell transformtion. Yet, there has been very little development of therapies to help tackle Ras-related diseased states. The development of small molecules to target Ras proteins to potentially inhibit abnormal Ras-stimulated cell signaling has been conceptualized and some progress has been made over the last 16 or so years. Here, we briefly review studies characterizing Ras protein-small molecule interactions to show the importance and potential that these small molecules may have for Ras-related drug discovery. We summarize recent results, highlighting small molecules that can be directly targeted to Ras using Structure-Based Drug Design (SBDD) and Fragment-Based Lead Discovery (FBLD) methods. The inactivation of Ras oncogenic signaling in vitro by small molecules is currently an attractive hurdle to try to and leap over in order to attack the oncogenic state. In this regard, important features of previously characterized properties of small molecule Ras targets, as well as a current understanding of conformational and dynamics changes seen for Ras-related mutants, relative to wild type, must be taken into account as newer small molecule design strategies towards Ras are developed.
A candidate gene approach to genetic prognostic factors of IgA nephropathy--a result of Polymorphism REsearch to DIstinguish genetic factors Contributing To progression of IgA Nephropathy (PREDICT-IgAN).

BACKGROUND Renal prognosis of IgA nephropathy (IgAN) is affected by environmental and genetic factors. Other studies demonstrated that some atherosclerotic disease-related genes were significantly associated with renal prognosis. METHODS The Polymorphism REsearch to DIstinguish genetic factors Contributing To progression of IgAN (PREDICT-IgAN) was a multicentre retrospective observational study to investigate associations between progression of IgAN (a 50% increase of serum creatinine level and slope of eGFR) and a hundred atherosclerotic disease-related gene polymorphisms, mainly single nucleotide polymorphisms (SNPs) in 320 IgAN patients who had more than a normal range of urinary protein (> or =0.25 g/day) at diagnosis. RESULTS During 8.3 +/- 4.2 years of a follow-up period, 83 patients (25.9%) developed progression. In log-rank tests, glycoprotein Ia GPIa C807T and G873A and intercellular adhesion molecule-1 ICAM-1 A1548G (K469E) were found to be significantly associated with progression even after adjustment for multiple comparisons by the method of Bonferroni (adjusted P = 0.0174, 0.0176 and 0.0430, respectively). In a multivariate Cox proportional-hazards model, GPIa 807TT (873CC) [versus 807TT, adjusted hazard ratio 2.05 (95% confidence interval 1.13-3.71)] and ICAM-1 1548GG [versus 1548AA, 2.55 (1.40-4.65)] were identified as independent genetic predictors of progression, along with conventional clinical prognostic factors such as eGFR, urinary protein and use of antihypertensives at diagnosis. CONCLUSIONS PREDICT-IgAN distinguished GPIa C807T/ G873A and ICAM-1 A1548G from multiple athero- sclerotic disease-related gene polymorphisms by their predictive indicator for progression of IgAN.
Stem Cell Quiescence

Adult stem cells are maintained in a quiescent state but are able to exit quiescence and rapidly expand and differentiate in response to stress. The quiescent state appears to be necessary for preserving the self-renewal of stem cells and is a critical factor in the resistance of cancer stem cells (CSCs) to chemotherapy and targeted therapies. Limited knowledge about quiescence mechanisms has prevented significant advances in targeting of drug-resistant quiescent CSCs populations in the clinic. Thus, an improved understanding of the molecular mechanisms of quiescence in adult stem cells is critical for the development of molecularly targeted therapies against quiescent CSCs in different cancers. Recent studies have provided a better understanding of the intrinsic and extrinsic regulatory mechanisms that control stem cell quiescence. It is now appreciated that the p53 gene plays a critical role in regulating stem cell quiescence. Other intrinsic regulatory mechanisms include the FoxO, HIF-1α, and NFATc1 transcription factors and signaling through ATM and mTOR. Extrinsic microenvironmental regulatory mechanisms include angiopoietin-1, TGF-β, bone morphogenic protein, thrombopoietin, N-cadherin, and integrin adhesion receptors; Wnt/β-catenin signaling; and osteopontin. In this article, we review current advances in understanding normal stem cell quiescence, their significance for CSC quiescence and drug resistance, and the potential clinical applications of these findings. Clin Cancer Res; 17(15); 4936–41. ©2011 AACR.