Miracle-dz/UniFAR-FTUs huggingface dataset:
Immune Cell Toll-Like Receptor 4 Is Required for Cardiac Myocyte Impairment During Endotoxemia

The aim of this study was to investigate the importance of Toll-like receptor 4 (TLR4) signaling on cardiac myocytes versus immune cells in lipopolysaccharide (LPS)-induced cardiac dysfunction. Cardiac myocytes isolated from LPS-treated C57Bl/6 mice showed reduced shortening and calcium transients as compared with myocytes from untreated mice. In addition, LPS-treated C57Bl/6 mice showed impaired cardiac mitochondrial function, including reduced respiration and reduced time of induction of permeability transition. All of the aforementioned cardiac dysfunction was dependent on TLR4, because LPS-treated TLR4-deficient mice did not have reduced myocyte shortening or mitochondrial dysfunction. To evaluate the role of cardiac myocyte versus leukocyte TLR4, LPS was injected into chimeric mice with TLR4-positive leukocytes and TLR4-deficient myocytes. These mice showed reduced myocyte shortening in response to LPS. Myocytes from chimeric mice with TLR4-deficient leukocytes and TLR4-positive myocytes had no response to LPS. In addition, isolated myocytes from C57Bl/6 mice subsequently treated with LPS and serum for various times did not have reduced shortening, despite the presence of TLR4 mRNA and protein, as determined by reverse-transcription polymerase chain reaction and fluorescent-activated cell sorting. In fact, cardiac myocytes had equivalent amounts of TLR4 as endothelium; however, only the latter is responsive to LPS. Furthermore, signaling pathways downstream of TLR4 were not activated during direct LPS treatment of myocytes. In conclusion, TLR4 on leukocytes, and not on cardiac myocytes, is important for cardiac myocyte impairment during endotoxemia.
First-Order Indefinability of Answer Set Programs on Finite Structures

An answer set program with variables is first-order definable on finite structures if the set of its finite answer sets can be captured by a first-order sentence, otherwise this program is first-order indefinable on finite structures. In this paper, we study the problem of first-order indefinability of answer set programs. We provide an Ehrenfeucht-Fraisse game-theoretic characterization for the first-order indefinability of answer set programs on finite structures. As an application of this approach, we show that the well-known finding Hamiltonian cycles program is not first-order definable on finite structures. We then define two notions named the 0-1 property and unbounded cycles or paths under the answer set semantics, from which we develop two sufficient conditions that may be effectively used in proving a program's first-order indefinability on finite structures under certain circumstances.
Ieee Transactions on Pattern Analysis and Machine Intelligence 1 Identifying Behaviors in Crowd Scenes Using Stability Analysis for Dynamical Systems

—A method is proposed for identifying five crowd behaviors (bottlenecks, fountainheads, lanes, arches, and blocking) in visual scenes. In the algorithm, a scene is overlaid by a grid of particles initializing a dynamical system defined by the optical flow. Time integration of the dynamical system provides particle trajectories that represent the motion in the scene; these trajectories are used to locate regions of interest in the scene. Linear approximation of the dynamical system provides behavior classification through the Jacobian matrix; the eigenvalues determine the dynamic stability of points in the flow and each type of stability corresponds to one of the five crowd behaviors. The eigenvalues are only considered in the regions of interest, consistent with the linear approximation and the implicated behaviors. The algorithm is repeated over sequential clips of a video in order to record changes in eigenvalues, which may imply changes in behavior. The method was tested on over 60 crowd and traffic videos.
Soft-Boosted Self-Constructing Neural Fuzzy Inference Network

This correspondence paper proposes an improved version of the self-constructing neural fuzzy inference network (SONFIN), called soft-boosted SONFIN (SB-SONFIN). The design softly boosts the learning process of the SONFIN in order to decrease the error rate and enhance the learning speed. The SB-SONFIN boosts the learning power of the SONFIN by taking into account the numbers of fuzzy rules and initial weights which are two important parameters of the SONFIN, SB-SONFIN advances the learning process by: 1) initializing the weights with the width of the fuzzy sets rather than just with random values and 2) improving the parameter learning rates with the number of learned fuzzy rules. The effectiveness of the proposed soft boosting scheme is validated on several real world and benchmark datasets. The experimental results show that the SB-SONFIN possesses the capability to outperform other known methods on various datasets.
The $\chi$-Divergence for Approximate Inference

Variational inference enables Bayesian analysis for complex probabilistic models with massive data sets. It posits a family of approximating distributions and finds the member closest to the posterior. While successful, variational inference methods can run into pathologies; for example, they typically underestimate posterior uncertainty. In this paper we propose CHIVI, a complementary algorithm to traditional variational inference. CHIVI is a black box algorithm that minimizes the $\chi$-divergence from the posterior to the family of approximating distributions and provides an upper bound of the model evidence. We studied CHIVI in several scenarios. On Bayesian probit regression and Gaussian process classification it yielded better classification error rates than expectation propagation (EP) and classical variational inference (VI). When modeling basketball data with a Cox process, it gave better estimates of posterior uncertainty. Finally, we show how to use the CHIVI upper bound and classical VI lower bound to sandwich estimate the model evidence.
Circadian Gating of the Cell Cycle Revealed in Single Cyanobacterial Cells

Cycle Entrainment Cells manage many cyclic processes that must coordinate with each other for best cellular performance. Yang et al. (p. 1522) present a general theoretical framework that quantitatively describes coupled cyclic processes and then apply this to the interaction between the circadian and cell-division cycles in single cyanobacteria. Simultaneously tracking individual cell divisions and circadian phases and fitting the data with the model suggest that cell-cycle progression slows down dramatically during a specific circadian interval, whereas cell-cycle progression is independent of the cell-cycle phase. Modeling and observation of cyanobacteria show entrainment of the cell cycle by their biological clock. Although major progress has been made in uncovering the machinery that underlies individual biological clocks, much less is known about how multiple clocks coordinate their oscillations. We simultaneously tracked cell division events and circadian phases of individual cells of the cyanobacterium Synechococcus elongatus and fit the data to a model to determine when cell cycle progression slows as a function of circadian and cell cycle phases. We infer that cell cycle progression in cyanobacteria slows during a specific circadian interval but is uniform across cell cycle phases. Our model is applicable to the quantification of the coupling between biological oscillators in other organisms.
The Protein Synthesis Inhibitor Anisomycin Induces Macrophage Apoptosis in Rabbit Atherosclerotic Plaques through p38 Mitogen-Activated Protein Kinase

Because macrophages play a major role in atherosclerotic plaque destabilization, selective removal of macrophages represents a promising approach to stabilize plaques. We showed recently that the protein synthesis inhibitor cycloheximide, in contrast to puromycin, selectively depleted macrophages in rabbit atherosclerotic plaques without affecting smooth muscle cells (SMCs). The mechanism of action of these two translation inhibitors is dissimilar and could account for the differential effects on SMC viability. It is not known whether selective depletion of macrophages is confined to cycloheximide or whether it can also be achieved with translation inhibitors that have a similar mechanism of action. Therefore, in the present study, we investigated the effect of anisomycin, a translation inhibitor with a mechanism of action similar to cycloheximide, on macrophage and SMC viability. In vitro, anisomycin induced apoptosis of macrophages in a concentration-dependent manner, whereas SMCs were only affected at higher concentrations. In vivo, anisomycin selectively decreased the macrophage content of rabbit atherosclerotic plaques through apoptosis. The p38 mitogen-activated protein kinase (MAPK) inhibitor SB202190 [4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)-1H-imidazole] prevented anisomycin-induced macrophage death, without affecting SMC viability. SB202190 decreased anisomycin-induced p38 MAPK phosphorylation, did not alter c-Jun NH2-terminal kinase (JNK) phosphorylation, and increased extracellular signal-regulated kinase (ERK) 1/2 phosphorylation. The latter effect was abolished by the mitogen-activated protein kinase kinase 1/2 inhibitor U0126 [1,4-diamino-2,3-dicyano-1,4-bis(2-aminophynyltio)butadiene ethanolate], although the prevention of anisomycin-induced macrophage death by SB202190 remained unchanged. The JNK phosphorylation inhibitor SP600125 did not affect anisomycin-induced macrophage or SMC death. In conclusion, anisomycin selectively decreased the macrophage content in rabbit atherosclerotic plaques, indicating that this effect is not confined to cycloheximide. p38 MAPK, but not ERK1/2 or JNK, plays a major role in anisomycin-induced macrophage death.
Computational Analysis of Host–Pathogen Protein Interactions between Humans and Different Strains of Enterohemorrhagic Escherichia coli

Serotype O157:H7, an enterohemorrhagic Escherichia coli (EHEC), is known to cause gastrointestinal and systemic illnesses ranging from diarrhea and hemorrhagic colitis to potentially fatal hemolytic uremic syndrome. Specific genetic factors like ompA, nsrR, and LEE genes are known to play roles in EHEC pathogenesis. However, these factors are not specific to EHEC and their presence in several non-pathogenic strains indicates that additional factors are involved in pathogenicity. We propose a comprehensive effort to screen for such potential genetic elements, through investigation of biomolecular interactions between E. coli and their host. In this work, an in silico investigation of the protein–protein interactions (PPIs) between human cells and four EHEC strains (viz., EDL933, Sakai, EC4115, and TW14359) was performed in order to understand the virulence and host-colonization strategies of these strains. Potential host–pathogen interactions (HPIs) between human cells and the “non-pathogenic” E. coli strain MG1655 were also probed to evaluate whether and how the variations in the genomes could translate into altered virulence and host-colonization capabilities of the studied bacterial strains. Results indicate that a small subset of HPIs are unique to the studied pathogens and can be implicated in virulence. This subset of interactions involved E. coli proteins like YhdW, ChuT, EivG, and HlyA. These proteins have previously been reported to be involved in bacterial virulence. In addition, clear differences in lineage and clade-specific HPI profiles could be identified. Furthermore, available gene expression profiles of the HPI-proteins were utilized to estimate the proportion of proteins which may be involved in interactions. We hypothesized that a cumulative score of the ratios of bound:unbound proteins (involved in HPIs) would indicate the extent of colonization. Thus, we designed the Host Colonization Index (HCI) measure to determine the host colonization potential of the E. coli strains. Pathogenic strains of E. coli were observed to have higher HCIs as compared to a non-pathogenic laboratory strain. However, no significant differences among the HCIs of the two pathogenic groups were observed. Overall, our findings are expected to provide additional insights into EHEC pathogenesis and are likely to aid in designing alternate preventive and therapeutic strategies.
New time-frequency derived cepstral coefficients for automatic speech recognition

The goal is to improve recognition rate by optimisation of Mel Frequency Cepstral Coefficients (MFCCs): modifications concern the time-frequency representation used to estimate these coefficients. There are many ways to obtain a spectrum out of a signal which differ in the method itself (Fourier, Wavelets,…), and in the normalisation. We show here that we can obtain noise resistant cepstral coefficients, for speaker independent connected word recognition. The recognition system is based on a continuous whole word hidden Markov model. An error reduction rate of approximately 50% is achieved. Moreover evaluation tests demonstrate that these results can be obtained with smaller databases: halving the training database have small effects on recognition rates (which is not the case with traditional MFCCs).
Survival predictors of preterm neonates: Hospital based study in Iran (2010-2011)

Background: Preterm birth (PTB) is responsible for 70% of neonatal mortalities. Various factors influence the risk of neonatal mortality in different populations. Objective: Our objective was to evaluate neonatal survival rate of preterm infants, and to define its predictors in Iranian population. Materials and Methods: This retrospective cohort study included all preterm (26-37 weeks) infants (n=1612) born alive in Shahid Akbar-abadi university hospital, during one year period (April 2010-2011). These infants were evaluated for fetal-neonatal, maternal, and pregnancy data. Survival analysis was performed and viability threshold and risk factors of neonatal mortality were evaluated. Results: Total overall mortality rate was 9.1%. Survival rate were 11.11% for extremely low birth weights (LBW) and 45.12% for very early PTBs. The smallest surviving infant was a 750 gr female with gestational age (GA) of 30 weeks and the youngest infants was a 970 gram female with GA of 25weeks plus 2 days. History of previous dead neonate, need to cardio-pulmonary resuscitation (CPR), need to neonatal intensive care unit (NICU) admission, postnatal administration of surfactant, presence of anomalies, Apgar score <7, multiple pregnancy, non-cephalic presentation, early PTB, very early PTB, LBW, very low birth weight (VLBW) and extremely low birth weight (ELBW), were risk factors for mortality in preterm neonates. Conclusion: Our study revealed that neonatal survival rate is dramatically influenced by birth weight especially under 1000grams, GA especially below 30 weeks, neonatal anomalies, history of previous dead fetus, multiple pregnancy, non- cephalic presentation, and need for NICU admission, resuscitation and respiratory support with surfactant
A Natural Human Retrovirus Efficiently Complements Vectors Based on Murine Leukemia Virus

Background Murine Leukemia Virus (MLV) is a rodent gammaretrovirus that serves as the backbone for common gene delivery tools designed for experimental and therapeutic applications. Recently, an infectious gammaretrovirus designated XMRV has been identified in prostate cancer patients. The similarity between the MLV and XMRV genomes suggests a possibility that the two viruses may interact when present in the same cell. Methodology/Principal Findings We tested the ability of XMRV to complement replication-deficient MLV vectors upon co-infection of cultured human cells. We observed that XMRV can facilitate the spread of these vectors from infected to uninfected cells. This functional complementation occurred without any gross rearrangements in the vector structure, and the co-infected cells produced as many as 104 infectious vector particles per milliliter of culture medium. Conclusions/Significance The possibility of encountering a helper virus when delivering MLV-based vectors to human cells in vitro and in vivo needs to be considered to ensure the safety of such procedures.
A 15.8 pJ/bit/iter quasi-cyclic LDPC decoder for IEEE 802.11n in 90 nm CMOS

We present a low-power quasi-cyclic (QC) low density parity check (LDPC) decoder that meets the throughput requirements of the highest-rate (600 Mbps) modes of the IEEE 802.11n WLAN standard. The design is based on the layered offset-min-sum algorithm and is runtime-programmable to process different code matrices (including all rates and block lengths specified by IEEE 802.11η). The register-transfer-level implementation has been optimized for best energy efficiency. The corresponding 90 nm CMOS ASIC has a core area of 1.77 mm2 and achieves a maximum throughput of 680 Mbps at 346 MHz clock frequency and 10 decoding iterations. The measured energy efficiency is 15.8pJ/bit/iteration at a nominal operating voltage of 1.0 V.
One Trillion Edges: Graph Processing at Facebook-Scale

Analyzing large graphs provides valuable insights for social networking and web companies in content ranking and recommendations. While numerous graph processing systems have been developed and evaluated on available benchmark graphs of up to 6.6B edges, they often face significant difficulties in scaling to much larger graphs. Industry graphs can be two orders of magnitude larger - hundreds of billions or up to one trillion edges. In addition to scalability challenges, real world applications often require much more complex graph processing workflows than previously evaluated. In this paper, we describe the usability, performance, and scalability improvements we made to Apache Giraph, an open-source graph processing system, in order to use it on Facebook-scale graphs of up to one trillion edges. We also describe several key extensions to the original Pregel model that make it possible to develop a broader range of production graph applications and workflows as well as improve code reuse. Finally, we report on real-world operations as well as performance characteristics of several large-scale production applications.
Information-Theoretic Operating Regimes of Large Wireless Networks

In analyzing the point-to-point wireless channel, insights about two qualitatively different operating regimes-bandwidth and power-limited-have proven indispensable in the design of good communication schemes. In this paper, we propose a new scaling law formulation for wireless networks that allows us to develop a theory that is analogous to the point-to-point case. We identify fundamental operating regimes of wireless networks and derive architectural guidelines for the design of optimal schemes. Our analysis shows that in a given wireless network with arbitrary size, area, power, bandwidth, etc., there are three parameters of importance: the short-distance signal-to-noise ratio (SNR), the long-distance SNR, and the power path loss exponent of the environment. Depending on these parameters, we identify four qualitatively different regimes. One of these regimes is especially interesting since it is fundamentally a consequence of the heterogeneous nature of links in a network and does not occur in the point-to-point case; the network capacity is both power and bandwidth limited. This regime has thus far remained hidden due to the limitations of the existing formulation. Existing schemes, either multihop transmission or hierarchical cooperation, fail to achieve capacity in this regime; we propose a new hybrid scheme that achieves capacity.
STAR FORMATION AROUND SUPERGIANT SHELLS IN THE LARGE MAGELLANIC CLOUD

We examine the recent star formation associated with four supergiant shells in the Large Magellanic Cloud (LMC): LMC 1, 4, 5, and 6, which have been shown to have simple expanding-shell structures. H ii regions and OB associations are used to infer star formation in the last few Myr, while massive young stellar objects reveal the current ongoing star formation. Distributions of ionized H i and molecular components of the interstellar gas are compared with the sites of recent and current star formation to determine whether triggering has taken place. We find that a great majority of the current star formation has occurred in gravitationally unstable regions, and that evidence of triggered star formation is prevalent at both large and local scales.
Aerosolized iloprost for pulmonary vasoreactivity testing in children with long‐standing pulmonary hypertension related to congenital heart disease

Background: In congenital heart disease with increased pulmonary blood flow and pressure, progressive changes in the vascular structure can lead to irreversible pulmonary hypertension (PH). Pulmonary hemodynamic parameters are used to determine whether surgical correction is no longer indicated. In this study, aerosolized iloprost was used to assess pulmonary vasoreactivity in children with long‐standing PH related to congenital heart disease. Methods: Children with long‐standing and severe PH secondary to congenital heart disease were included in this study. Various hemodynamic parameters were measured before and after iloprost inhalation (0.5 μg/kg), and vascular resistance was determined. Responders to the iloprost test were defined as those with a decrease in both pulmonary vascular resistance (PVR) and pulmonary‐to‐systemic vascular resistance ratio (Rp/Rs) of >10%. Results: Eighteen children aged between 7 months and 13 years with long‐standing and severe PH secondary to congenital heart disease were studied. Thirteen children had a positive response, resulting in a mean (± SD) decrease of PVR from 9.3 ± 4.6 to 4.6 ± 2.7 Wood U · m2 (P < 0.001), and a mean decrease of Rp/Rs from 0.54 ± 0.37 to 0.24 ± 0.14 (P = 0.005). Conclusions: Iloprost‐induced pulmonary vasodilator responses vary among children with PH related to congenital heart disease. The use of inhale iloprost in the cardiac catheterization laboratory results in pulmonary vasoreactivity for some of these children particularly a reduction in PVR and the pulmonary‐to‐systemic vascular resistance ratio. © 2008 Wiley‐Liss, Inc.
Phorbol myristate acetate stimulates pinocytosis and membrane spreading in mouse peritoneal macrophages

Phorbol myristate acetate (PMA) at a concentration of 0.01 microgram/ml causes an approximately threefold increase in surface area of resident, proteose-peptone-elicited, and thioglycolate-broth-elicited mouse peritoneal macrophages. Resident and proteose-peptone-elicited macrophages, cultured for 24 h in the presence of PMA, increase their pinocytic rate twofold in response to addition of PMA (0.01 microgram/ml) to the medium. Thioglycolate-broth-elicited macrophages, cultured for 24 h in the absence of PMA, immediately increase their pinocytic rate 2- to 3.5-fold in response to a single challenge with PMA (0.01 microgram/ml). Cytochalasin B, colchicine, and podophyllotoxin have only modest inhibitory effects on the basal rate of pinocytosis and on PMA-induced cellular spreading, but completely block the stimulatory effects of PMA on pinocytosis in thioglycolate- broth-elicited macrophages. Cytochalasin D markedly inhibits both basal and PMA-stimulated pinocytosis in these cells. Thus, PMA is a useful tool for studying mechanisms of macrophage spreading and for enhancing the overall rate of pinosome formation.
Near optimal LQR step tracking for a finite set of LTI plants

In this paper we consider the use of periodic controllers for simultaneous stabilization and step tracking, including the case when there is an occasional, though persistent, plant change. We consider the case of a finite set of admissible models; we provide a design procedure which yields a controller which stabilizes each such model and provides near optimal LQR step tracking, and then demonstrate, via simulation, that it has the facility to tolerate occasional (but persistent) switches between these models without an undue effect on the performance. The controller is periodic with a slight nonlinearity.