gebhart/patrepeval huggingface dataset:
Graph-based motion estimation and compensation for dynamic 3D point cloud compression (2015)

This paper addresses the problem of motion estimation in 3D point cloud sequences that are characterized by moving 3D positions and color attributes. Motion estimation is key to effective compression of these sequences, but it remains a challenging problem as the temporally successive frames have varying sizes without explicit correspondence information. We represent the time-varying geometry of these sequences with a set of graphs, and consider 3D positions and color attributes of the points clouds as signals on the vertices of the graph. We then cast motion estimation as a feature matching problem between successive graphs. The motion is estimated on a sparse set of representative vertices using new spectral graph wavelet descriptors. A dense motion field is eventually interpolated by solving a graph-based regularization problem. The estimated motion is finally used for color compensation in the compression of 3D point cloud sequences. Experimental results demonstrate that our method is able to accurately estimate the motion and to bring significant improvement in terms of color compression performance.
ENHANCEMENT OF THYMIC RECOVERY AFTER CYCLOSPORINE BY RECOMBINANT HUMAN GROWTH HORMONE AND INSULIN-LIKE GROWTH FACTOR I (1991)

Correlation of thymic changes with the development of CsA-associated syngeneic graft-versus-host disease (sGVHD) suggested that the development of tolerance depends on the prompt regeneration of the thymus after stopping CsA. Accordingly, we have tested recombinant human growth hormone (rhGH) and recombinant human insulin-like growth factor I (rhIGF-1) to determine if they accelerate reconstitution of the rat thymus after CsA-induced involution. After 14 days of CsA, the thymus has marked medullary involution but normally recovers fully in 6 weeks. In this study, LEW rats were injected with vehicle, rhGH, or rhIGF-1 for 21 days after stopping CsA and were examined. The vehicle-treated rats showed partial recovery with respect to Hassall's corpuscles, class II antigen expression, medullary size, medullary dendritic cells (DC), and T cell maturation. The mature thymocytes were predominantly CD8+ T cells. Both rhGH and rhIGF-1 induced significant thymic enlargement compared with the vehicle-treated rats. They also both significantly enhanced regeneration with respect to Hassall's corpuscles. The mature thymocyte population had significantly greater CD4+ cells. In addition, rhIGF-1 induced a significant improvement in the medullary size and medullary DC. While the medullae of a normal thymus are in intimate contact with cortical class II antigen, after CsA the cortex adjacent to the medulla is primarily class II antigen negative. RhGH significantly increased the class II antigen in the deep cortex while rhIGF-1 demonstrated a trend toward greater expression in this region (P = 0.06). We conclude that rhGH and rhIGF-1 accelerate thymic regeneration post-CsA. Further studies are now indicated to establish the potential for these factors to enhance the development of antigen-specific tolerance.
Histidine-rich glycoprotein modulation of the anticoagulant activity of heparin. Evidence for a mechanism involving competition with both antithrombin and thrombin for heparin binding. (1987)

Heparin binding to rabbit histidine-rich glycoprotein (HRG) was studied in a purified system, allowing for determination of a heparin dissociation constant of approximately 5.5 X 10(-8) M for the interaction with HRG at pH 7.0. The strong interaction between heparin and HRG was demonstrated to be competitive with the binding of both antithrombin and thrombin to the heparin chain. HRG was further tested as a modulator of the anticoagulant activity of heparin by comparing rates of the heparin-catalyzed reaction between antithrombin and thrombin in the presence and absence of added HRG. The heparin-antithrombin-thrombin reaction was modeled using the formalism of a two-substrate enzyme-catalyzed reaction with heparin as the enzyme and HRG analyzed as an enzyme inhibitor. HRG was shown to compete with both antithrombin and thrombin for binding to heparin by this kinetic analysis. Thus, both the kinetic and heparin-binding data indicate that the mechanism by which HRG modulates heparin anticoagulant activity involves competition for heparin with both the inhibitor and the protease. Inhibition by HRG of the heparin-catalyzed reaction was found to be highly dependent on pH, with a sharp increase in inhibition from about 15% to greater than 90% observed as pH was lowered from 7.4 to 7.0. Since little change in the rate of the heparin-catalyzed inhibition of thrombin by antithrombin occurs in this pH region, the dramatic change in HRG inhibition seen upon pH titration may reflect increasing ionic interaction between heparin and HRG due to the protonation of histidine residues which occurs in this pH region.
Development of Chemical Substances Regulating Biofilm Formation (1997)

Abstract The chemical substances which regulate biofilm formation were examined, and a bioassay system which uses marine bacteria with adhering properties was developed. This bioassay system is suitable for screening crude extracts from marine organisms. Using this system, those substances which regulate biofilm formation were isolated from marine organisms. For example, bis(deacetyl)solenolide D was obtained from the marine sponge Psammaplysilla purpurea. Novel nitroalkanes were also isolated from the Okinawan sponge Callyspongia sp. Ethyl N-(2-phenylethyl)carbamate isolated from the marine bacteria SCRC3P79 (Cytophaga sp.) inhibited biofilm formation. Furthermore, the N,N-dichloro, isocyanide, isothiocyanate, and dithiocarbamate derivatives of 2-(4-nitrophenyl)ethylamine, significantly inhibited the growth of marine attaching bacteria. Interestingly, most of the marine sponges examined contained anti-biofilm compounds, such as benzoic acid, aeroplysinin-I, and bromoageliferin.
Metalloproteinases Shed TREM-1 Ectodomain from Lipopolysaccharide-Stimulated Human Monocytes (2007)

Triggering receptors expressed on myeloid cell (TREM) proteins are a family of cell surface receptors that participate in diverse cellular processes such as inflammation, coagulation, and bone homeostasis. TREM-1, in particular, is expressed on neutrophils and monocytes and is a potent amplifier of inflammatory responses. LPS and other microbial products induce up-regulation of cell surface-localized TREM-1 and the release of its soluble form, sTREM-1. Two hypotheses have been advanced to explain the origin of sTREM-1: alternative splicing of TREM-1 mRNA and proteolytic cleavage(s) of mature, membrane-anchored TREM-1. In this report, we present conclusive evidence in favor of the proteolytic mechanism of sTREM-1 generation. No alternative splicing forms of TREM-1 were detected in monocytes/macrophages. Besides, metalloproteinase inhibitors increased the stability of TREM-1 at the cell surface while significantly reducing sTREM-1 release in cultures of LPS-challenged human monocytes and neutrophils. We conclude that metalloproteinases are responsible for shedding of the TREM-1 ectodomain through proteolytic cleavage of its long juxtamembrane linker.
Handbook of Liver Disease (2011)

Well-organized and vibrantly illustrated throughout, Handbook of Liver Disease is a comprehensive yet concise handbook providing authoritative guidance on key clinical issues in liver disease. The quick-reference outline format ensures that you'll find answers when you need them, and cover-to-cover updates keep you abreast of the recent rapid changes in the field. Written by leading international experts in hepatology, this reference is ideal for gastroenterologists, hepatologists, internists, family practitioners, trainees, and others who diagnose and manage patients with liver disorders
Pooled Analysis of Long-Term Survival Data From Phase II and Phase III Trials of Ipilimumab in Unresectable or Metastatic Melanoma (2015)

To our knowledge, this is the largest analysis of OS to date for ipilimumab-treated patients with advanced melanoma. We observed a plateau in the survival curve, beginning at approximately 3 years, which was independent of prior therapy or ipilimumab dose. These data add to the evidence supporting the durability of long-term survival in ipilimumab-treated patients with advanced melanoma.
T-614, a Novel Antirheumatic Drug, Inhibits Both the Activity and Induction of Cyclooxygenase-2 (COX-2) in Cultured Fibroblasts (1995)

To elucidate the mechanism for the selective inhibition of prostaglandin E2 (PGE2) production in inflammatory tissue by T-614 (3-formylamino-7-methylsulfonylamino-6-phenoxy-4H-1-benzopyran-4-o ne), its effects on both the activity and the induction of cyclooxygenase (COX)-2 were investigated in vitro. T-614 inhibited the activity of purified COX-2 enzyme (IC50: 7.7 micrograms/ml), but was inactive against both COX-1 activities of microsomal and purified enzymes (IC50: > 300 micrograms/ml). On the other hand, when the inhibition of PGE2 production by T-614 was examined in the cultured fibroblasts stimulated with bradykinin, T-614 at 1 microgram/ml or less inhibited PGE2 release more effectively than that in the above cell-free system. Therefore, we examined which of the COX enzymes was expressed in bradykinin-stimulated fibroblasts by using both the reverse transcriptase-polymerase chain reaction (RT-PCR) and Northern blot analyses. As a result, COX-1 mRNA was constitutively expressed in the cells, whereas COX-2 mRNA was not detected without stimulation with bradykinin, but was expressed within 30 min when stimulated. Furthermore, it was found that the addition of T-614 reduced the COX-2 mRNA levels in 30 min after stimulation. These studies suggest that at least some of inhibitory effects of T-614 on prostanoids production are mediated by the synergy of the inhibition of COX-2 activity and the inhibition of induction, and such an action of T-614 may explain the pharmacological properties of this drug.
Highly Stereoselective Addition of Organometallic Reagents to N-tert-Butanesulfinyl Imines Derived from 3- and 4-Substituted Cyclohexanones (2004)

Addition of alkyl or aryl Grignard reagents to N-sulfinyl imines derived from 3- and 4-substituted cyclohexanones proceeds with good yields and with excellent diasteroselectivity. The selectivity of the reaction is controlled by the ring substituent rather than the sulfinyl group stereochemistry, and therefore racemic tert-butanesulfinamide can be employed.
The novel isoxazoline ectoparasiticide fluralaner: Selective inhibition of arthropod γ-aminobutyric acid- and l-glutamate-gated chloride channels and insecticidal/acaricidal activity (2013)

Isoxazolines are a novel class of parasiticides that are potent inhibitors of γ-aminobutyric acid (GABA)-gated chloride channels (GABACls) and L-glutamate-gated chloride channels (GluCls). In this study, the effects of the isoxazoline drug fluralaner on insect and acarid GABACl (RDL) and GluCl and its parasiticidal potency were investigated. We report the identification and cDNA cloning of Rhipicephalus (R.) microplus RDL and GluCl genes, and their functional expression in Xenopus laevis oocytes. The generation of six clonal HEK293 cell lines expressing Rhipicephalus microplus RDL and GluCl, Ctenocephalides felis RDL-A285 and RDL-S285, as well as Drosophila melanogaster RDLCl-A302 and RDL-S302, combined with the development of a membrane potential fluorescence dye assay allowed the comparison of ion channel inhibition by fluralaner with that of established insecticides addressing RDL and GluCl as targets. In these assays fluralaner was several orders of magnitude more potent than picrotoxinin and dieldrin, and performed 5-236 fold better than fipronil on the arthropod RDLs, while a rat GABACl remained unaffected. Comparative studies showed that R. microplus RDL is 52-fold more sensitive than R. microplus GluCl to fluralaner inhibition, confirming that the GABA-gated chloride channel is the primary target of this new parasiticide. In agreement with the superior RDL on-target activity, fluralaner outperformed dieldrin and fipronil in insecticidal screens on cat fleas (Ctenocephalides felis), yellow fever mosquito larvae (Aedes aegypti) and sheep blowfly larvae (Lucilia cuprina), as well as in acaricidal screens on cattle tick (R. microplus) adult females, brown dog tick (Rhipicephalus sanguineus) adult females and Ornithodoros moubata nymphs. These findings highlight the potential of fluralaner as a novel ectoparasiticide.
Development of an improved CAD scheme for automated detection of lung nodules in digital chest images (1997)

Lung cancer is the leading cause of cancer deaths in men and women in the United States, with a 5-year survival rate of only about 13%. However, this survival rate can be improved to 47% if the disease is diagnosed and treated at an early stage. In this study, we developed an improved computer-aided diagnosis (CAD) scheme for the automated detection of lung nodules in digital chest images to assist radiologists, who could miss up to 30% of the actually positive cases in their daily practice. Two hundred PA chest radiographs, 100 normals and 100 abnormals, were used as the database for our study. The presence of nodules in the 100 abnormal cases was confirmed by two experienced radiologists on the basis of CT scans or radiographic follow-up. In our CAD scheme, nodule candidates were selected initially by multiple gray-level thresholding of the difference image (which corresponds to the subtraction of a signal-enhanced image and a signal-suppressed image) and then classified into six groups. A large number of false positives were eliminated by adaptive rule-based tests and an artificial neural network (ANN). The CAD scheme achieved, on average, a sensitivity of 70% with 1.7 false positives per chest image, a performance which was substantially better as compared with other studies. The CPU time for the processing of one chest image was about 20 seconds on an IBM RISC/6000 Powerstation 590. We believe that the CAD scheme with the current performance is ready for initial clinical evaluation.
VASE‐encoded peptide modifies NCAM‐ and L1‐mediated neurite outgrowth (1997)

Interactions between the neural cell adhesion molecule (NCAM) with NCAM-expressing neurons (trans-interaction) stimulate outgrowth of neurites. The extent of NCAM-triggered neurite outgrowth depends on the presence of 10 amino acids derived from the variable alternatively spliced exon (VASE or π-exon) in the fourth immunoglobulin-like domain of NCAM (Ig4): NCAM with VASE reduces and without VASE enhances neurite outgrowth in cis- or trans-interaction. We have investigated the role of VASE in neurite outgrowth by characterizing the receptors at the cell surface of cultured cerebellar neurons. Results from experiments with L1 and NCAM antibodies and with cerebellar neurons derived from wild-type or NCAM-deficient mice show that substrate-coated Ig4 with VASE (Ig4+) or without VASE (Ig4−) stimulates neurite outgrowth by a trans-interaction with L1 and that Ig4− promotes neurite outgrowth more strongly than Ig4+ by a transinteraction with NCAM. J. Neurosci. Res. 50:62–68, 1997. © 1997 Wiley-Liss, Inc.
Clustering short text using Ncut-weighted non-negative matrix factorization (2012)

Non-negative matrix factorization (NMF) has been successfully applied in document clustering. However, experiments on short texts, such as microblogs, Q&A documents and news titles, suggest unsatisfactory performance of NMF. An major reason is that the traditional term weighting schemes, like binary weight and tfidf, cannot well capture the terms' discriminative power and importance in short texts, due to the sparsity of data. To tackle this problem, we proposed a novel term weighting scheme for NMF, derived from the Normalized Cut (Ncut) problem on the term affinity graph. Different from idf, which emphasizes discriminability on document level, the Ncut weighting measures terms' discriminability on term level. Experiments on two data sets show our weighting scheme significantly boosts NMF's performance on short text clustering.
Salmonella enterica Serovars Enteritidis Infection Alters the Indigenous Microbiota Diversity in Young Layer Chicks (2015)

Avian gastrointestinal (GI) tracts are highly populated with a diverse array of microorganisms that share a symbiotic relationship with their hosts and contribute to the overall health and disease state of the intestinal tract. The microbiome of the young chick is easily prone to alteration in its composition by both exogenous and endogenous factors, especially during the early posthatch period. The genetic background of the host and exposure to pathogens can impact the diversity of the microbial profile that consequently contributes to the disease progression in the host. The objective of this study was to profile the composition and structure of the gut microbiota in young chickens from two genetically distinct highly inbred lines. Furthermore, the effect of the Salmonella Enteritidis infection on altering the composition makeup of the chicken microbiome was evaluated through the 16S rRNA gene sequencing analysis. One-day-old layer chicks were challenged with S. Enteritidis and the host cecal microbiota profile as well as the degree of susceptibility to Salmonella infection was examined at 2 and 7 days post infection. Our result indicated that host genotype had a limited effect on resistance to S. Enteritidis infection. Alpha diversity, beta diversity, and overall microbiota composition were analyzed for four factors: host genotype, age, treatment, and postinfection time points. S. Enteritidis infection in young chicks was found to significantly reduce the overall diversity of the microbiota population with expansion of Enterobacteriaceae family. These changes indicated that Salmonella colonization in the GI tract of the chickens has a direct effect on altering the natural development of the GI microbiota. The impact of S. Enteritidis infection on microbial communities was also more substantial in the late stage of infection. Significant inverse correlation between Enterobacteriaceae and Lachnospiraceae family in both non-infected and infected groups, suggested possible antagonistic interaction between members of these two taxa, which could potentially influences the overall microbial population in the gut. Our results also revealed that genetic difference between two lines had minimal effect on the establishment of microbiota population. Overall, this study provided preliminary insights into the contributing role of S. Enteritidis in influencing the overall makeup of chicken's gut microbiota.
Superoxide Mediated Reduction of Organically Complexed Iron(III):  Comparison of Non-Dissociative and Dissociative Reduction Pathways (2007)

We have investigated the mechanism of reduction of organically complexed iron(III) in the presence of superoxide, the one-electron reduced form of dioxygen that is produced in natural waters by thermal, photochemical, and biological pathways. Experimental results show that reduction of organically complexed iron(III) by superoxide may occur by either (or, in some instances, both) reaction of superoxide with inorganic iron(III) after its dissociation from the complex (dissociative reduction) or by direct reaction of superoxide with the complex (non-dissociative reduction). In the presence of low concentrations of ligands such as citrate and sulfosalicylate that bind iron(III) relatively weakly and result in complexes with high dissociation rate constants (kd > 1 x 10(-4) s(-1)), a dissociative reduction pathway dominates. However, in the presence of strong ligands or high concentrations of weak ligands, only non-dissociative reduction of complexed iron(III) occurs. The relative contribution of each pathway has major implications for the lability and hence potential bioavailablity of iron in natural waters. The simple kinetic model developed here can be used to correctly predict the superoxide-mediated formation rates of iron(II) in natural systems.
Heterogeneously Integrated Optoelectronic Devices Enabled by Micro‐Transfer Printing (2015)

Transfer printing is a materials assembly technique that uses elastomeric stamps for heterogeneous integration of various classes of micro‐ and nanostructured materials into two‐ and three‐dimensionally organized layouts on virtually any type of substrate. Work over the past decade demonstrates that the capabilities of this approach create opportunities for a wide range of device platforms, including component‐ and system‐level embodiments in unusual optoelectronic technologies with characteristics that cannot be replicated easily using conventional manufacturing or growth techniques. This review presents recent progress in functional materials and advanced transfer printing methods, with a focus on active components that emit, absorb, and/or transport light, ranging from solar cells to light‐emitting diodes, lasers, photodetectors, and integrated collections of these in functional systems, where the key ideas provide unique solutions that address limitations in performance and/or functionality associated with traditional technologies. High‐concentration photovoltaic modules based on multijunction, micro‐ and millimeter‐scale solar cells and high‐resolution emissive displays based on microscale inorganic light‐emitting diodes provide examples of some of the most sophisticated systems, geared toward commercialization.
IL-13 is a therapeutic target in radiation lung injury (2016)

Pulmonary fibrosis is a potentially lethal late adverse event of thoracic irradiation. Prior research indicates that unrestrained TGF-β1 and/or type 2 cytokine-driven immune responses promote fibrosis following radiation injury, but the full spectrum of factors governing this pathology remains unclear. Interleukin 13 (IL-13) is a key factor in fibrotic disease associated with helminth infection, but it is unclear whether it plays a similar role in radiation-induced lung fibrosis. Using a mouse model, we tested the hypothesis that IL-13 drives the progression of radiation-induced pulmonary fibrosis. Irradiated lungs from wild-type c57BL/6NcR mice accumulated alternatively-activated macrophages, displayed elevated levels of IL-13, and extensive fibrosis, whereas IL-13 deficient mice were resistant to these changes. Furthermore, plasma from irradiated wild-type mice showed a transient increase in the IL-13 saturated fraction of the circulating decoy receptor IL-13Rα2. Finally, we determined that therapeutic neutralization of IL-13, during the period of IL-13Rα2 saturation was sufficient to protect mice from lung fibrosis. Taken together, our results demonstrate that IL-13 is a major regulator of radiation-induced lung injury and demonstrates that strategies focusing on IL-13 may be useful in screening for timely delivery of anti-IL-13 therapeutics.