Miracle-dz/UniFAR-FTUs huggingface dataset:
Corporate dividend Policy Determinants: Intelligent versus a Traditional Approach

SUMMARY Dividend is the return that an investor receives when purchasing a company's shares. The decision to pay these dividends to shareholders concerns several other groups of people, such as financial managers, consulting firms, individual and institutional investors, government and monitoring authorities, and creditors, just to name a few. The prediction and modelling of this decision has received a significant amount of attention in the corporate finance literature. However, the methods used to study the aforementioned question are limited to the logistic regression method without any implementation of the advanced and expert methods of data mining. These methods have proven their superiority in other business-related fields, such as marketing, production, accounting and auditing. In finance, bankruptcy prediction has the vast majority among data-mining implementations, but to the best of the authors’ knowledge such an implementation does not exist in dividend payment prediction. This paper satisfies this gap in the literature and provides answers that help to understand the so-called ‘dividend puzzle’. Specifically, this paper provides evidence supporting the hypothesis that data-mining methods perform better in accuracy measures against the traditional methods used. The prediction of dividend policy determinants provides valuable benefits to all related parties, as they can manage, invest, consult and monitor the dividend policy in a more effective way. Copyright © 2013 John Wiley & Sons, Ltd.
Distinct Domains of the GATA-1 Cofactor FOG-1 Differentially Influence Erythroid versus Megakaryocytic Maturation

ABSTRACT FOG family zinc finger proteins play essential roles in development through physical interaction with GATA factors. FOG-1, like its interacting partner GATA-1, is required for normal differentiation of erythroid and megakaryocytic cells. Here, we have developed a functional assay for FOG-1 based on its ability to rescue erythroid and megakaryocytic maturation of a genetically engineered FOG-1−/− cell line. We demonstrate that interaction through only one of FOG-1's four GATA-binding zinc fingers is sufficient for rescue, providing evidence against a model in which FOG-1 acts to bridge multiple GATA-binding DNA elements. Importantly, we find that distinct regions of FOG-1 differentially influence erythroid versus megakaryocyte maturation. As such, we propose that FOG-1 may modulate the fate of a bipotential erythroid/megakaryocytic precursor cell.
A Literature Analysis on the Adoption of Mobile Commerce Services by Individuals

Mobile commerce has been a huge success in terms of adoption by individuals in some markets like Japan, while, surprisingly, not as flourishing in others. Many studies have been conducted using traditional adoption models and theories (such as TAM) that mainly focus on technology aspects. A more complete understanding of the issue requires the need to integrate three roles that mcommerce users play: as technology users, network members and consumers. In this study, we review existing literature on individuals’ voluntary adoption of mobile commerce services to highlight the adequacy/inadequacy of previous studies’ coverage of these three roles. We observe that there is a lack of a complete understanding of mobile commerce adoption in the current literature. Several implications for future research and practice are discussed.
The evolutionary dynamics of influenza A virus adaptation to mammalian hosts

Few questions on infectious disease are more important than understanding how and why avian influenza A viruses successfully emerge in mammalian populations, yet little is known about the rate and nature of the virus’ genetic adaptation in new hosts. Here, we measure, for the first time, the genomic rate of adaptive evolution of swine influenza viruses (SwIV) that originated in birds. By using a curated dataset of more than 24 000 human and swine influenza gene sequences, including 41 newly characterized genomes, we reconstructed the adaptive dynamics of three major SwIV lineages (Eurasian, EA; classical swine, CS; triple reassortant, TR). We found that, following the transfer of the EA lineage from birds to swine in the late 1970s, EA virus genes have undergone substantially faster adaptive evolution than those of the CS lineage, which had circulated among swine for decades. Further, the adaptation rates of the EA lineage antigenic haemagglutinin and neuraminidase genes were unexpectedly high and similar to those observed in human influenza A. We show that the successful establishment of avian influenza viruses in swine is associated with raised adaptive evolution across the entire genome for many years after zoonosis, reflecting the contribution of multiple mutations to the coordinated optimization of viral fitness in a new environment. This dynamics is replicated independently in the polymerase genes of the TR lineage, which established in swine following separate transmission from non-swine hosts.
Integrin-linked kinase is required for radial sorting of axons and Schwann cell remyelination in the peripheral nervous system

During development, Schwann cells (SCs) interpret different extracellular cues to regulate their migration, proliferation, and the remarkable morphological changes associated with the sorting, ensheathment, and myelination of axons. Although interactions between extracellular matrix proteins and integrins are critical to some of these processes, the downstream signaling pathways they control are still poorly understood. Integrin-linked kinase (ILK) is a focal adhesion protein that associates with multiple binding partners to link integrins to the actin cytoskeleton and is thought to participate in integrin and growth factor–mediated signaling. Using SC-specific gene ablation, we report essential functions for ILK in radial sorting of axon bundles and in remyelination in the peripheral nervous system. Our in vivo and in vitro experiments show that ILK negatively regulates Rho/Rho kinase signaling to promote SC process extension and to initiate radial sorting. ILK also facilitates axon remyelination, likely by promoting the activation of downstream molecules such as AKT/protein kinase B.
Elevated cardiac troponin I and functional recovery and disability in patients after aneurysmal subarachnoid hemorrhage.

BACKGROUND Patients with aneurysmal subarachnoid hemorrhage experience myocardial injury at the time of rupture, but its effect on functional recovery and disability is unclear. OBJECTIVE To describe the prevalence of myocardial injury, as indicated by high serum levels of cardiac troponin I (≥0.3 ng/mL), within the first 5 days after aneurysmal subarachnoid hemorrhage and the effect of the injury on 3-month functional recovery and disability. METHODS In a prospective longitudinal study, 239 patients with Hunt/Hess grade 3 or greater and/or Fisher grade 2 or greater at admission had serum level of troponin I measured on days 0 to 5. Patients were interviewed at 3 months to evaluate functional recovery (Glasgow Outcome Scale) and functional disability (Modified Rankin Scale). Statistics included χ² analysis, t tests, and binary logistic regression. RESULTS Troponin values were elevated in 33.5% of the patients, and few patients in either group had a history of coronary artery disease (7.4% with troponin levels ≥0.3 ng/mL vs 2.7% with levels <0.3 ng/mL, P = .12). Higher troponin levels were significantly related to age and Hunt/Hess and Fisher grades, but not race, and were significantly associated with poorer functional recovery (P < .001) and more functional disability (P < .001). Even after controls for age, race, and more severe Hunt/Hess grades, higher levels remained a significant predictor of poorer functional recovery (P = .04) and disability (P = .01). CONCLUSION Elevated levels of cardiac troponin I after aneurysmal subarachnoid hemorrhage are common in patients with no cardiac history, are associated with severity of the hemorrhage, and are independently predictive of poorer functional recovery and increased disability.
Vitamin D: Moving Forward to Address Emerging Science

The science surrounding vitamin D presents both challenges and opportunities. Although many uncertainties are associated with the understandings concerning vitamin D, including its physiological function, the effects of excessive intake, and its role in health, it is at the same time a major interest in the research and health communities. The approach to evaluating and interpreting the available evidence about vitamin D should be founded on the quality of the data and on the conclusions that take into account the totality of the evidence. In addition, these activities can be used to identify critical data gaps and to help structure future research. The Office of Dietary Supplements (ODS) at the National Institutes of Health has as part of its mission the goal of supporting research and dialogues for topics with uncertain data, including vitamin D. This review considers vitamin D in the context of systematically addressing the uncertainty and in identifying research needs through the filter of the work of ODS. The focus includes the role of systematic reviews, activities that encompass considerations of the totality of the evidence, and collaborative activities to clarify unknowns or to fix methodological problems, as well as a case study using the relationship between cancer and vitamin D.
Hyperfixation of HMPAO in subacute ischemic stroke leading to spuriously high estimates of cerebral blood flow by SPECT.

W e want to report an error in interpreting d,l-hexamethylpropylene amine oxime (HMPAO) tomograms as cerebral blood flow (CBF) in subacute ischemic stroke cases. By simultaneously studying CBF by `33Xe dynamic single-photon emission computed tomography (SPECT), an obvious discrepancy was noted in that the HMPAO tomograms grossly exaggerated the reflow hyperemia following spontaneous reperfusion. To interpret 'Tc-HMPAO images in terms of CBF distribution, it is essential that the same or almost the same fraction of locally supplied tracer is fixed in the various regions, healthy as well as diseased, at the time imaging is performed. This fixation is due to extraction across the blood-brain barrier (BBB) and to retention of the extracted tracer molecules, a retention caused by chemical conversion to a hydrophilic metabolite that is unable to cross cell membranes as well as the BBB. A constant degree of fractional fixation in all brain regions of 40-50% has been found in humans.1 A few series comparing 'Tc-HMPAO images with CBF tomography obtained by `33Xe as well as with C1502 positron emission tomography images have consistently shown a good agreement in normal humans and in various disease states including acute ischemic stroke,2-4 but the number of such comparisons is rather limited. Nevertheless, the impression gained from this factual basis is that 9Tc-HMPAO can be trusted to image CBF distribution after correction for a minor nonlinearity due to back-diffusion in the first few minutes.5 The fidelity of 9`Tc-HMPAO to map CBF has been taken for granted to such an extent that it has been used as a "gold standard" of CBF distribution in comparative studies with other SPECT tracers of CBF such as N-isopropyl-p-(1231)iodoamphetamine (123I-IMP)6 or 99mTc-N,N'-1,2-ethylenediylbis-L-cysteine diethyl ester (`9Tc-ECD). 7 We report here three cases of focal hyperfixation of 9`Tc-HMPAO in patients with subacute stroke (2-3 weeks) with evidence of infarct reperfusion. By hyperfixation we mean a higher counting rate over the infarct (relative to that of the opposite side) than can be explained by CBF as measured by 133Xe tomography at the same time. This can only occur if the fractional fixation exceeds the normal level of 40-50%. In case 1, on October 26, 1992, a 62-year-old man suddenly developed massive right-sided hemiparesis and aphasia. On day 3, SPECT with 'Tc-HMPAO showed massive reduction of tracer uptake in the anterior half of the left middle cerebral artery (MCA) distribution territory. When restudied on day 15, we first measured CBF by 133Xe tomography. As shown in Figure 1, the infarct
Pulse shrinkage based pre-bond through silicon vias test in 3D IC

Defects in TSV not only lead to variation in the propagation delay but also in the transition delay of the net connected to the TSV. A non-invasive approach for pre-bond TSV test based on pulse shrinkage is proposed to detect resistive open and leakage fault. TSVs are used as capacitive loads of their driving gates, then the pulse visiting the cyclic shrinkage cells will be shrunk until it vanishes completely. The shrinkage amount is digitized into a digital code to compare with an expected value of fault free. Experiments on fault detection are presented through HSPICE simulations using realistic models for a 45 nm CMOS technology. The results show the effectiveness in the detection of resistive open defects 0. 2kΩ above and equivalent leakage resistance less than 40MΩ. The estimated design for testability area cost of our method is negligible for realistic dies.
Microbial communities at the borehole observatory on the Costa Rica Rift flank (Ocean Drilling Program Hole 896A)

The microbiology of subsurface, hydrothermally influenced basaltic crust flanking mid-ocean ridges has remained understudied, due to the difficulty in accessing the subsurface environment. The instrumented boreholes resulting from scientific ocean drilling offer access to samples of the formation fluids circulating through oceanic crust. We analyzed the phylogenetic diversity of bacterial communities of fluid and microbial mat samples collected in situ from the observatory at Ocean Drilling Program Hole 896A, drilled into ~6.5 million-year-old basaltic crust on the flank of the Costa Rica Rift in the equatorial Pacific Ocean. Bacterial 16S rRNA gene sequences recovered from borehole fluid and from a microbial mat coating the outer surface of the fluid port revealed both unique and shared phylotypes. The dominant bacterial clones from both samples were related to the autotrophic, sulfur-oxidizing genus Thiomicrospira. Both samples yielded diverse gamma- and alphaproteobacterial phylotypes, as well as members of the Bacteroidetes, Planctomycetes, and Verrucomicrobia. Analysis of ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) genes (cbbL and cbbM) from the sampling port mat and from the borehole fluid demonstrated autotrophic carbon assimilation potential for in situ microbial communities; most cbbL genes were related to those of the sulfur-oxidizing genera Thioalkalivibrio and Thiomicrospira, and cbbM genes were affiliated with uncultured phylotypes from hydrothermal vent plumes and marine sediments. Several 16S rRNA gene phylotypes from the 896A observatory grouped with phylotypes recovered from seawater-exposed basalts and sulfide deposits at inactive hydrothermal vents, but there is little overlap with hydrothermally influenced basaltic boreholes 1026B and U1301A on the Juan de Fuca Ridge flank, suggesting that site-specific characteristics of Hole 896A (i.e., seawater mixing into borehole fluids) affect the microbial community composition.
Machine learning, statistical learning and the future of biological research in psychiatry

Psychiatric research has entered the age of ‘Big Data’. Datasets now routinely involve thousands of heterogeneous variables, including clinical, neuroimaging, genomic, proteomic, transcriptomic and other ‘omic’ measures. The analysis of these datasets is challenging, especially when the number of measurements exceeds the number of individuals, and may be further complicated by missing data for some subjects and variables that are highly correlated. Statistical learning-based models are a natural extension of classical statistical approaches but provide more effective methods to analyse very large datasets. In addition, the predictive capability of such models promises to be useful in developing decision support systems. That is, methods that can be introduced to clinical settings and guide, for example, diagnosis classification or personalized treatment. In this review, we aim to outline the potential benefits of statistical learning methods in clinical research. We first introduce the concept of Big Data in different environments. We then describe how modern statistical learning models can be used in practice on Big Datasets to extract relevant information. Finally, we discuss the strengths of using statistical learning in psychiatric studies, from both research and practical clinical points of view.
Compressive K-means

The Lloyd-Max algorithm is a classical approach to perform K-means clustering. Unfortunately, its cost becomes prohibitive as the training dataset grows large. We propose a compressive version of K-means (CKM), that estimates cluster centers from a sketch, i.e. from a drastically compressed representation of the training dataset. We demonstrate empirically that CKM performs similarly to Lloyd-Max, for a sketch size proportional to the number of centroids times the ambient dimension, and independent of the size of the original dataset. Given the sketch, the computational complexity of CKM is also independent of the size of the dataset. Unlike Lloyd-Max which requires several replicates, we further demonstrate that CKM is almost insensitive to initialization. For a large dataset of 107 data points, we show that CKM can run two orders of magnitude faster than five replicates of Lloyd-Max, with similar clustering performance on artificial data. Finally, CKM achieves lower classification errors on handwritten digits classification.
Abdominal Obesity is Associated with Peripheral Artery Disease in Hemodialysis Patients

Background Peripheral arterial disease (PAD) is a leading cause of morbidity in hemodialysis (HD) patients. Recent evidence suggests that abdominal obesity (AO) may play a role in PAD. However, the association between AO and PAD has not been thoroughly studied in HD patients. Methods The present cross-sectional study aimed to examine the relationship between AO and PAD in a cohort of 204 chronic HD patients. The ankle brachial index (ABI) was used as an estimate of the presence of PAD. Plasma adiponectin levels, interleukin-6 (IL-6) levels, high sensitivity C-reactive protein (hs-CRP) levels, asymmetric dimethylarginine (ADMA) levels, and lipid profiles were measured. Logistic regression was used to estimate the association between the presence of PAD and AO as well as other potential risk factors. Results The metabolic risk factors and all individual traits, including elevated ln-transformed hs-CRP, were found to be significant (P<0.05) more frequently in HD patients with AO than that in control subjects. Patients with AO had a higher prevalence of PAD than the control individuals, with a mean ABI of 0.96±0.23 and 1.08±0.16 (P<0.0001) and PAD prevalence of 26.9% and 10.8% (P = 0.003), respectively. By multivariate analysis, AO (odds ratio [OR], 4.532; 95% CI, 1.765–11.639; P = 0.002), elevated serum ln-transformed ADMA (OR, 5.535; 95% CI, 1.323–23.155; P = 0.019), and ln-transformed IL-6 (OR, 1.567; 95% CI, 1.033–2.378; P = 0.035) were independent predictors of the presence of PAD. Conclusions HD patients with AO exhibited a cluster of metabolic risk factors and lower ABI. AO, elevated serum ln-transformed ADMA, and ln-transformed IL-6 were independent predictors of the presence of PAD.
Negative Regulation of Mast Cell Signaling and Function by the Adaptor LAB/NTAL

Engagement of the Fcɛ receptor I (FcɛRI) on mast cells and basophils initiates signaling pathways leading to degranulation. Early activation events include tyrosine phosphorylation of two transmembrane adaptor proteins, linker for activation of T cells (LAT) and non–T cell activation linker (NTAL; also called LAB; a product of Wbscr5 gene). Previous studies showed that the secretory response was partially inhibited in bone marrow–derived mast cells (BMMCs) from LAT-deficient mice. To clarify the role of NTAL in mast cell degranulation, we compared FcɛRI-mediated signaling events in BMMCs from NTAL-deficient and wild-type mice. Although NTAL is structurally similar to LAT, antigen-mediated degranulation responses were unexpectedly increased in NTAL-deficient mast cells. The earliest event affected was enhanced tyrosine phosphorylation of LAT in antigen-activated cells. This was accompanied by enhanced tyrosine phosphorylation and enzymatic activity of phospholipase C γ1 and phospholipase C γ2, resulting in elevated levels of inositol 1,4,5-trisphosphate and free intracellular Ca2+. NTAL-deficient BMMCs also exhibited an enhanced activity of phosphatidylinositol 3-OH kinase and Src homology 2 domain–containing protein tyrosine phosphatase-2. Although both LAT and NTAL are considered to be localized in membrane rafts, immunogold electron microscopy on isolated membrane sheets demonstrated their independent clustering. The combined data show that NTAL is functionally and topographically different from LAT.
Disordered methionine/homocysteine metabolism in premature vascular disease. Its occurrence, cofactor therapy, and enzymology.

Mild homocysteinemia occurs surprisingly often in patients with premature vascular disease. We studied the possible enzymatic sources of this mild hyperhomocysteinemia and the control of homocysteine levels in plasma by treatment of patients with the cofactors and cosubstrates of homocysteine catabolism. We assessed homocysteine metabolism in 131 patients who had premature disease in their coronary, peripheral, or cerebrovascular circulation by using a standard oral methionine-load test. Impaired homocysteine metabolism occurred in 28 patients. We assayed levels of the primary enzymes of homocysteine catabolism in cultured skin fibroblast extracts from 15 of these 28 patients. The patients' cystathionine beta-synthase levels (3.68 +/- 2.52 nmol/h per milligram of cell protein, mean +/- SD) were markedly depressed compared with those from 31 healthy adult control subjects (7.61 +/- 4.49, P < .001). The patients' levels of 5-methyltetrahydrofolate: homocysteine methyltransferase were normal. While betaine: homocysteine methyltransferase was not expressed in skin fibroblasts, 24-hour urinary betaine and N,N-dimethylglycine measurements were consistent with normal or enhanced remethylation of homocysteine by betaine: homocysteine methyltransferase in the 13 patients tested. When treated daily with choline and betaine, pyridoxine, or folic acid, there was a normalization of the postmethionine plasma homocysteine level in 16 of 19 patients. Our results indicate that mild homocysteinemia in premature vascular disease may be caused by either a folate deficiency or deficiencies in cystathionine beta-synthase activity. It does not necessarily involve deficiencies of either 5-methyltetrahydrofolate:homocysteine methyltransferase or betaine:homocysteine methyltransferase. Effective treatment regimens are also defined.