Miracle-dz/UniFAR-FTUs huggingface dataset:
Inside Debt and the Design of Corporate Debt Contracts

Theory posits that managerial holdings of debt “inside debt” align managers' incentives with those of outside debtholders. Executive pensions, consisting of rank-and-file RAF plans and supplemental executive retirement plans SERPs, and other deferred compensation ODC have debt-like payoffs, and could therefore function as inside debt. However, whereas SERPs are often unfunded and unsecured, RAF plans are funded and secured to some extent, and ODC may be invested in equity and withdrawn flexibly before retirement. Special arrangements in executive debt-like compensation could hence weaken or even nullify any incentive-alignment effect. We find that higher CEO debt-like compensation leads to lower promised yield and fewer covenants in a sample of loans originated in 2006--2008. This effect is driven entirely by benefits accrued under SERPs, consistent with SERPs more closely resembling risky corporate debt; balances accrued under RAF and ODC plans do not provide similar effects. Furthermore, promised yields are lower when debt-like compensation claims can be withdrawn only after outside debt claims are expected to settle. Our findings persist after accounting for endogeneity using state personal income tax rates as an instrument for CEOs' willingness to defer compensation. Overall, the evidence suggests that executive debt-like compensation is only effective at resolving stockholder--debtholder conflicts when its payoffs are truly debt-like and that lenders' perceptions are affected not only by the magnitude of debt-like compensation but also by its seniority. Data, as supplemental material, are available at http://dx.doi. org/10.1287/mnsc.2013. 1813 . This paper was accepted by Wei Jiang, finance.
Expression of HOXB2, a Retinoic Acid Signaling Target in Pancreatic Cancer and Pancreatic Intraepithelial Neoplasia

Purpose: Despite significant progress in understanding the molecular pathology of pancreatic cancer and its precursor lesion: pancreatic intraepithelial neoplasia (PanIN), there remain no molecules with proven clinical utility as prognostic or therapeutic markers. Here, we used oligonucleotide microarrays to interrogate mRNA expression of pancreatic cancer tissue and normal pancreas to identify novel molecular pathways dysregulated in the development and progression of pancreatic cancer. Experimental Design: RNA was hybridized to Affymetrix Genechip HG-U133 oligonucleotide microarrays. A relational database integrating data from publicly available resources was created to identify candidate genes potentially relevant to pancreatic cancer. The protein expression of one candidate, homeobox B2 (HOXB2), in PanIN and pancreatic cancer was assessed using immunohistochemistry. Results: We identified aberrant expression of several components of the retinoic acid (RA) signaling pathway (RARα, MUC4, Id-1, MMP9, uPAR, HB-EGF, HOXB6, and HOXB2), many of which are known to be aberrantly expressed in pancreatic cancer and PanIN. HOXB2, a downstream target of RA, was up-regulated 6.7-fold in pancreatic cancer compared with normal pancreas. Immunohistochemistry revealed ectopic expression of HOXB2 in 15% of early PanIN lesions and 48 of 128 (38%) pancreatic cancer specimens. Expression of HOXB2 was associated with nonresectable tumors and was an independent predictor of poor survival in resected tumors. Conclusions: We identified aberrant expression of RA signaling components in pancreatic cancer, including HOXB2, which was expressed in a proportion of PanIN lesions. Ectopic expression of HOXB2 was associated with a poor prognosis for all patients with pancreatic cancer and was an independent predictor of survival in patients who underwent resection.
Decreased Neuronal Synchronization during Experimental Seizures

Synchronization between CA1 pyramidal neurons was studied using dual-cell patch-clamp techniques simultaneous with an extracellular measurement of network activity. We explored various linear and nonlinear methods to detect weak synchronization in this network, using cross-correlation, mutual information in one and two dimensions, and phase correlation in both broad and narrow band. The linear and nonlinear methods demonstrated different patterns of sensitivity to detect synchrony in this network, depending on the dynamical state of the network. Bursts in 4-amino-pyridine (4AP) were highly synchronous events. Unexpectedly, seizure-like events in 4AP were desynchronous events, both in comparison with interictal periods preceding the seizure without bursts (cut Schaffer collateral tract) and in comparison with bursts preceding the seizures (intact Schaffer collateral tract). The finding that seizure-like events are associated with desynchronization in such networks is consistent with recent theoretical work, suggesting that asynchrony is necessary to maintain a high level of activity in neuronal networks for sustained periods of time and that synchrony may disrupt such activity.
The Newtonian and Relativistic Theory of Orbits and the Emission of Gravitational Waves

This review paper is devoted to the theory of orbits. We start with the discussion of the Newtonian problem of motion then we consider the relativistic problem of motion, in particular the PN approximation and the further gravitomagnetic corrections. Finally by a classification of orbits in accordance with the conditions of motion, we calculate the gravitational waves luminosity for different types of stellar encounters and orbits.
A Framework for Deflated and Augmented Krylov Subspace Methods

We consider deflation and augmentation techniques for accelerating the convergence of Krylov subspace methods for the solution of nonsingular linear algebraic systems. Despite some formal similarity, the two techniques are conceptually different from preconditioning. Deflation (in the sense the term is used here) “removes” certain parts from the operator making it singular, while augmentation adds a subspace to the Krylov subspace (often the one that is generated by the singular operator); in contrast, preconditioning changes the spectrum of the operator without making it singular. Deflation and augmentation have been used in a variety of methods and settings. Typically, deflation is combined with augmentation to compensate for the singularity of the operator, but both techniques can be applied separately. We introduce a framework of Krylov subspace methods that satisfy a Galerkin condition. It includes the families of orthogonal residual and minimal residual methods. We show that in this framework augmen.
Improvements to Secure Computation with Penalties

Motivated by the impossibility of achieving fairness in secure computation [Cleve, STOC 1986], recent works study a model of fairness in which an adversarial party that aborts on receiving output is forced to pay a mutually predefined monetary penalty to every other party that did not receive the output. These works show how to design protocols for secure computation with penalties that tolerate an arbitrary number of corruptions. In this work, we improve the efficiency of protocols for secure computation with penalties in a hybrid model where parties have access to the "claim-or-refund" transaction functionality. Our first improvement is for the ladder protocol of Bentov and Kumaresan (Crypto 2014) where we improve the dependence of the script complexity of the protocol (which corresponds to miner verification load and also space on the blockchain) on the number of parties from quadratic to linear (and in particular, is completely independent of the underlying function). Our second improvement is for the see-saw protocol of Kumaresan et al. (CCS 2015) where we reduce the total number of claim-or-refund transactions and also the script complexity from quadratic to linear in the number of parties. We also present a 'dual-mode' protocol that offers different guarantees depending on the number of corrupt parties: (1) when s n/2 parties are corrupt, this protocol guarantees fairness with penalties (i.e., if the adversary gets the output, then either the honest parties get output as well or they get compensation via penalizing the adversary). The above protocol works as long as t+s < n, matching the bound obtained for secure computation protocols in the standard model (i.e., replacing "fairness with penalties" with "security-with-abort" (full security except fairness)) by Ishai et al. (SICOMP 2011).
Adapted Domain Specific Class Means

We address the problem of domain adaptation (DA) from one or multiple source domains to a target domain. Most of the existing DA methods assume that source data is largely available. Such an assumption rarely holds in real applications, for both technical and legal reasons. More realistic are situations where source domain observations become quickly unavailable, but only some domain representatives can be retained, either as source instances or as their aggregation. In this paper therefore we focus on the Domain Specific Class Means (DSCM) classifier [5] that can handle such scenario and we combine it with the sMDA framework [4]. We show, on a variety of datasets and tasks, that the method can be applied successfully even when no labeled target is available and also that it can provide performance comparable to the case where dense knowledge (all source data) is available.
A Dominant-Negative FGF1 Mutant (the R50E Mutant) Suppresses Tumorigenesis and Angiogenesis

Fibroblast growth factor-1 (FGF1) and FGF2 play a critical role in angiogenesis, a formation of new blood vessels from existing blood vessels. Integrins are critically involved in FGF signaling through crosstalk. We previously reported that FGF1 directly binds to integrin αvβ3 and induces FGF receptor-1 (FGFR1)-FGF1-integrin αvβ3 ternary complex. We previously generated an integrin binding defective FGF1 mutant (Arg-50 to Glu, R50E). R50E is defective in inducing ternary complex formation, cell proliferation, and cell migration, and suppresses FGF signaling induced by WT FGF1 (a dominant-negative effect) in vitro. These findings suggest that FGFR and αvβ3 crosstalk through direct integrin binding to FGF, and that R50E acts as an antagonist to FGFR. We studied if R50E suppresses tumorigenesis and angiogenesis. Here we describe that R50E suppressed tumor growth in vivo while WT FGF1 enhanced it using cancer cells that stably express WT FGF1 or R50E. Since R50E did not affect proliferation of cancer cells in vitro, we hypothesized that R50E suppressed tumorigenesis indirectly through suppressing angiogenesis. We thus studied the effect of R50E on angiogenesis in several angiogenesis models. We found that excess R50E suppressed FGF1-induced migration and tube formation of endothelial cells, FGF1-induced angiogenesis in matrigel plug assays, and the outgrowth of cells in aorta ring assays. Excess R50E suppressed FGF1-induced angiogenesis in chick embryo chorioallantoic membrane (CAM) assays. Interestingly, excess R50E suppressed FGF2-induced angiogenesis in CAM assays as well, suggesting that R50E may uniquely suppress signaling from other members of the FGF family. Taken together, our results suggest that R50E suppresses angiogenesis induced by FGF1 or FGF2, and thereby indirectly suppresses tumorigenesis, in addition to its possible direct effect on tumor cell proliferation in vivo. We propose that R50E has potential as an anti-cancer and anti-angiogenesis therapeutic agent (“FGF1 decoy”).
Anti-autophagic and anti-apoptotic effects of memantine in a SH-SY5Y cell model of Alzheimer's disease via mammalian target of rapamycin-dependent and -independent pathways

Memantine non-competitively blocks the N-methyl-d-aspartate receptor in order to inhibit beta-amyloid (Aβ) secretion, and has been used to treat moderate-to-severe Alzheimer's disease (AD). However, the mechanisms underlying the role of memantine in the autophagy and apoptosis of neuronal cells in AD, as well as the association between neuronal autophagy and apoptosis have yet to be elucidated. The present study aimed to establish an AD cell model overexpressing the 695-amino-acid Swedish mutant of Aβ precursor protein (APP695swe) in order to observe the effects of memantine on the cell viability, autophagy and apoptosis of SH-SY5Y cells in the AD model, and to investigate the associated underlying mechanisms. A pcDNA3.1-APP695 plasmid was transfected into the SH-SY5Y cells. Reverse transcription-quantitative polymerase chain reaction and western blot analyses demonstrated that the AD cell model was successfully established. MTT assays demonstrated that memantine was able to upregulate neuronal cell survival, and acridine orange staining and flow cytometry demonstrated that memantine (5 µM) was able to inhibit neuronal autophagy and apoptosis. Following neuronal autophagy induction by rapamycin, cell apoptosis rates increased significantly. Further experiments revealed that memantine was able to upregulate the expression of signaling molecules phosphorylated (p)-phosphoinositide 3-kinase, p-Akt and p-mammalian target of rapamycin (mTOR), and also inhibited the phosphorylation of the B-cell lymphoma 2/Beclin-1 complex via mitogen-activated protein kinase 8. In conclusion, the results of the present study demonstrated that in the AD cell model, autophagy was able to promote apoptosis. Memantine exerted anti-autophagic and anti-apoptotic functions, and mTOR-dependent as well as-independent autophagic signaling pathways were involved in this process. Therefore, these results of the present study strongly supported the use of memantine as a potential therapeutic strategy for AD treatment.
Propagation of Seizurelike Activity in a Model of Neocortex Running title: Seizurelike Activity in a Model of Neocortex

Seizures in pediatric epilepsy are often associated with spreading, repetitive bursting activity in neocortex. We examined onset and propagation of seizurelike activity using a computational model of cortical circuitry. The model includes two pyramidal cell types and four types of inhibitory interneurons; each neuron is represented by a multicompartmental model with biophysically realistic ion channels. We determined the role of bursting neurons and found that their capability of driving network oscillations is most prominent in networks with either weak or relatively strong excitatory synaptic coupling. Synaptic coupling strength was varied in a separate set of simulations to examine its role in network bursting. Oscillations both between cortical layers (vertical oscillations) and between cortical areas (horizontal oscillations) emerge at moderate excitatory coupling strengths. For horizontal propagation, existence of a fast conducting fiber system and its properties are critical. We conclude that seizurelike oscillatory activity may originate from single neurons or small networks and that activity may propagate in two principal fashions: one that can be represented by a unidirectional (pacemaker)-type process and the other as multior bidirectional propagating waves. The frequency of the bursting patterns relates to underlying propagating activity that can either sustain or disrupt the ongoing oscillation.
A Novel Iterative Multilateral Localization Algorithm for Wireless Sensor Networks

In many applications of wireless sensor networks, location is very important information. It can be used to identify the location at which sensor readings originate, in routing and data storage protocols based on geographical areas and so on. Location information can come from manual setting or GPS device. However, manual setting requires huge cost of human time, and GPS setting requires expensive device cost. Both approaches are not applicable to localization task of large scale wireless sensor networks. In this paper, we propose an accurate and efficient localization algorithm, called iterative multilateral localization algorithm based on time rounds. This Algorithm uses time round mechanism and anchor nodes triangle placement scheme to reduce error accumulation caused by iteratively localization. And it also reduces location errors and prevents abnormal phenomena caused by trilateral localization through limiting the minimum number of neighboring beacon nodes used in different localizing time rounds. Experimental results reveal that this algorithm has high localization accuracy, even if in large range errors, it can achieve good result.
Altered levels and distribution of microtubule‐associated proteins before disease onset in a mouse model of amyotrophic lateral sclerosis

Alterations of the axonal transport and microtubule network are potential causes of motor neurodegeneration in mice expressing a mutant form of the superoxide dismutase 1 (SOD1G37R) linked to amyotrophic lateral sclerosis (ALS). In the present study, we investigated the biology of microtubule‐associated proteins (MAPs), responsible for the formation and stabilization of microtubules, in SOD1G37R mice. Our results show that the protein levels of MAP2, MAP1A, tau 100 kDa and tau 68 kDa species decrease significantly as early as 5 months before onset of symptoms in the spinal cord of SOD1G37R mice, whereas decrease in levels of tau 52–55 kDa species is most often noted with the manifestation of the clinical symptoms. Interestingly, there was no change in the protein levels of MAPs in the brain of SOD1G37R mice, a CNS organ spared by the mutant SOD1 toxicity. Remarkably, as early as 5 months before disease onset, the binding affinities of MAP1A, MAP2 and tau isoforms to the cytoskeleton decreased in spinal cord of SOD1G37R mice. This change correlated with a hyperphosphorylation of the soluble tau 52–55 kDa species at epitopes recognized by the antibodies AT8 and PHF‐1. Finally, a shift in the distribution of MAP2 from the cytosol to the membrane is detected in SOD1G37R mice at the same stage. Thus, alterations in the integrity of microtubules are early events of the neurodegenerative processes in SOD1G37R mice.
Biotin-4-Fluorescein Based Fluorescence Quenching Assay for Determination of Biotin Binding Capacity of Streptavidin Conjugated Quantum Dots

The valency of quantum dot nanoparticles conjugated with biomolecules is closely related to their performance in cell tagging, tracking, and imaging experiments. Commercially available streptavidin conjugates (SAv QDs) are the most commonly used tool for preparing QD−biomolecule conjugates. The fluorescence quenching of biotin-4-fluorscein (B4F) provides a straightforward assay to quantify the number of biotin binding sites per SAv QD. The utility of this method was demonstrated by quantitatively characterizing the biotin binding capacity of commercially available amphiphilic poly(acrylic acid) Qdot ITK SAv conjugates and poly(ethylene glycol) modified Qdot PEG SAv conjugates with emission wavelengths of 525, 545, 565, 585, 605, 625, 655, 705, and 800 nm. Results showed that 5- to 30-fold more biotin binding sites are available on ITK SAv QDs compared to PEG SAv QDs of the same color with no systematic variation of biotin binding capacity with size.
Uncertainty and Disagreement in Economic Prediction: The Bank of England Survey of External Forecasters

This article introduces a new source of survey data, namely the Bank of England Survey of External Forecasters. The survey collects point and density forecasts of inflation and GDP growth, and hence offers the opportunity of constructing direct measures of uncertainty. We present a simple statistical framework in which to define and interrelate measures of uncertainty and disagreement. The resulting measures are compared with other direct measures of uncertainty, nationally and internationally. A significant, sustained reduction in inflation uncertainty followed the 1997 granting of operational independence to the Bank of England to pursue a monetary policy of inflation targeting.
Caenorhabditis elegans lin-35/Rb, efl-1/E2F and Other Synthetic Multivulva Genes Negatively Regulate the Anaphase-Promoting Complex Gene mat-3/APC8

Retinoblastoma (Rb)/E2F complexes repress expression of many genes important for G1-to-S transition, but also appear to regulate gene expression at other stages of the cell cycle. In C. elegans, lin-35/Rb and other synthetic Multivulva (SynMuv) group B genes function redundantly with other sets of genes to regulate G1/S progression, vulval and pharyngeal differentiation, and other unknown processes required for viabilty. Here we show that lin-35/Rb, efl-1/E2F, and other SynMuv B genes negatively regulate a component of the anaphase-promoting complex or cyclosome (APC/C). The APC/C is a multisubunit complex that promotes metaphase-to-anaphase progression and G1 arrest by targeting different substrates for ubiquitination and proteasome-mediated destruction. The C. elegans APC/C gene mat-3/APC8 has been defined by temperature-sensitive embryonic lethal alleles that strongly affect germline meiosis and mitosis but only weakly affect somatic development. We describe severe nonconditional mat-3 alleles and a hypomorphic viable allele (ku233), all of which affect postembryonic cell divisions including those of the vulval lineage. The ku233 lesion is located outside of the mat-3 coding region and reduces mat-3 mRNA expression. Loss-of-function alleles of lin-35/Rb and other SynMuv B genes suppress mat-3(ku233) defects by restoring mat-3 mRNA to wild-type levels. Therefore, Rb/E2F complexes appear to repress mat-3 expression.
Induction of ROS Overload by Alantolactone Prompts Oxidative DNA Damage and Apoptosis in Colorectal Cancer Cells

Cancer cells typically display higher than normal levels of reactive oxygen species (ROS), which may promote cancer development and progression but may also render the cancer cells more vulnerable to further ROS insult. Indeed, many of the current anticancer therapeutics kill cancer cells via induction of oxidative stress, though they target both cancer and normal cells. Recently, alantolactone (ATL), a natural sesquiterpene lactone, has been shown to induce apoptosis by increasing ROS levels specifically in cancer cells; however, the molecular mechanisms linking ROS overproduction to apoptosis remain unclear. Here we show that the ATL-induced ROS overload in human SW480 and SW1116 colorectal cancer cells was followed by a prominent accumulation of cellular oxidized guanine (8-oxoG) and immediate increase in the number of DNA strand breaks, indicating that increased ROS resulted in extensive oxidative DNA damage. Consequently, the G1/S-CDK suppresser CDKN1B (p21) and pro-apoptotic proteins Bax and activated caspase-3 were upregulated, while anti-apoptotic Bcl-2 was downregulated, which were followed by cell cycle arrest at G1 and marked apoptosis in ATL-treated cancer but not non-cancer cells. These results suggest that the ATL-induced ROS overload triggers cell death through induction of massive oxidative DNA damage and subsequent activation of the intrinsic apoptosis pathway.