gebhart/patrepeval huggingface dataset:
Improved Texture Networks: Maximizing Quality and Diversity in Feed-Forward Stylization and Texture Synthesis (2017)

The recent work of Gatys et al., who characterized the style of an image by the statistics of convolutional neural network filters, ignited a renewed interest in the texture generation and image stylization problems. While their image generation technique uses a slow optimization process, recently several authors have proposed to learn generator neural networks that can produce similar outputs in one quick forward pass. While generator networks are promising, they are still inferior in visual quality and diversity compared to generation-by-optimization. In this work, we advance them in two significant ways. First, we introduce an instance normalization module to replace batch normalization with significant improvements to the quality of image stylization. Second, we improve diversity by introducing a new learning formulation that encourages generators to sample unbiasedly from the Julesz texture ensemble, which is the equivalence class of all images characterized by certain filter responses. Together, these two improvements take feed forward texture synthesis and image stylization much closer to the quality of generation-via-optimization, while retaining the speed advantage.
Furo[2,3‐d]pyrimidines and Oxazolo[5,4‐d]pyrimidines as Inhibitors of Receptor Tyrosine Kinases (RTK) (2004)

Abstract Receptor tyrosine kinases such as VEGFR2 (vascular endothelial growth factor receptor 2, KDR) or EGFR (epidermal growth factor receptor) play crucial roles in a variety of diseases, such as cancer. Recently, some pyrrolopyrimidines were shown to be potent EGFR inhibitors. Therefore, new types of oxazolo[5,4‐ d ]pyrimidines and furo[2,3‐ d ]pyrimidines were synthesized ( Schemes 1 and 2 ). Appropriately substituted derivatives of these classes of compounds inhibited VEGFR2 and EGFR with IC 50 values in the low nanomolar range (see Table ). Generally, the furopyrimidines were somewhat more active than the oxazolopyrimidines. The best inhibitors, 20m, 20p , and 20r , had an IC 50 of 3 n M towards EGFR and showed a good selectivity, being distinctly less active towards VEGFR2.
In vitro–differentiated TH17 cells mediate lethal acute graft-versus-host disease with severe cutaneous and pulmonary pathologic manifestations (2008)

The morbidity and mortality associated with graft-host-disease (GVHD) is a significant obstacle to the greater use of allogeneic stem cell transplantation. Donor T cells that predominantly differentiate into TH1/Tc1 T cells and generate pro-inflammatory cytokines such as interferon-gamma (IFN-gamma) mediate GVHD. Although numerous studies have described a pathogenic role for IFN-gamma, multiple reports have demonstrated that the lack of IFN-gamma paradoxically exacerbated GVHD lethality. This has led to speculation that another subset of T cells may significantly contribute to GVHD mortality. Several groups have demonstrated a new lineage of CD4+ T helper cell development distinct from TH1 or TH2 differentiation. This lineage is characterized by production of interleukin (IL)-17A, IL-17F, IL-22, and IL-21 and has been termed TH17 cells. Here, we demonstrate that a highly purified population of TH17 cells is capable of inducing lethal GVHD, hallmarked by extensive pathologic cutaneous and pulmonary lesions. Upon transfer, these cells migrate to and expand in GVHD target organs and secondary lymphoid tissues. Finally, we demonstrate differential roles for tumor necrosis factor-alpha (TNF-alpha) and IL-17A in the clinical manifestations of GVHD induced by TH17 cells. Our studies demonstrate that cells other than TH1/Tc1 can mediate acute GVHD.
Malignant cells fuel tumor growth by educating infiltrating leukocytes to produce the mitogen Gas6 (2009)

The transforming and tumor growth-promoting properties of Axl, a member of the Tyro3, Axl, and Mer (TAM) family of receptor tyrosine kinases (TAMRs), are well recognized. In contrast, little is known about the role of the TAMR ligand growth arrest-specific gene 6 (Gas6) in tumor biology. By using Gas6-deficient (Gas6(-/-)) mice, we show that bone marrow-derived Gas6 promotes growth and metastasis in different experimental cancer models, including one resistant to vascular endothelial growth factor inhibitors. Mechanistic studies reveal that circulating leukocytes produce minimal Gas6. However, once infiltrated in the tumor, leukocytes up-regulate Gas6, which is mitogenic for tumor cells. Consistent herewith, impaired tumor growth in Gas6(-/-) mice is rescued by transplantation of wild-type bone marrow and, conversely, mimicked by transplantation of Gas6(-/-) bone marrow into wild-type hosts. These findings highlight a novel role for Gas6 in a positive amplification loop, whereby tumors promote their growth by educating infiltrating leukocytes to up-regulate the production of the mitogen Gas6. Hence, inhibition of Gas6 might offer novel opportunities for the treatment of cancer.
Strategy for enhanced transgenic strain development for embryonic conditional lethality in Anastrepha suspensa (2012)

Here the first reproductive sterility system for the tephritid fruit fly pest, Anastrepha suspensa, is presented, based on lethality primarily limited to embryos heterozygous for a conditional lethal transgene combination. This tetracycline (Tet)-suppressible system uses a driver construct having the promoter from the newly isolated embryo-specific A. suspensa serendipity α gene linked to the Tet-transactivator. This was used to drive expression of a phosphomutated variant of the pro-apoptotic cell death gene, hid, from A. ludens, that was isolated, based on its identity to A. suspensa hid. The Alhid(Ala2) variant was shown to have the highest cell death activity in an in vitro A. suspensa cell death assay compared to the orthologous genes Ashid, Dmhid, and the variant Dmhid(Ala5). These cell death assays also allowed a determination of the most-efficient driver-effector cassette combinations for use in A. suspensa transformants, resulting in two hybrid strains exhibiting 100% lethality. One strain was 96% lethal in embryos in the absence of tetracycline, with none surviving past the first larval instar, which is critical for pests that are most damaging in late-larval stages. We demonstrate that the isolation and in vitro validation of species-specific promoters and lethal effector genes can greatly improve the efficiency of creating high-performance conditional lethality strains that may be extended to other insect pest species.
A functional polymorphism in the reduced folate carrier gene and DNA hypomethylation in mothers of children with autism (2010)

The biologic basis of autism is complex and is thought to involve multiple and variable gene-environment interactions. While the logical focus has been on the affected child, the impact of maternal genetics on intrauterine microenvironment during pivotal developmental windows could be substantial. Folate-dependent one carbon metabolism is a highly polymorphic pathway that regulates the distribution of one-carbon derivatives between DNA synthesis (proliferation) and DNA methylation (cell-specific gene expression and differentiation). These pathways are essential to support the programmed shifts between proliferation and differentiation during embryogenesis and organogenesis. Maternal genetic variants that compromise intrauterine availability of folate derivatives could alter fetal cell trajectories and disrupt normal neurodevelopment. In this investigation, the frequency of common functional polymorphisms in the folate pathway was investigated in a large population-based sample of autism case-parent triads. In case-control analysis, a significant increase in the reduced folate carrier (RFC1) G allele frequency was found among case mothers, but not among fathers or affected children. Subsequent log linear analysis of the RFC1 A80G genotype within family trios revealed that the maternal G allele was associated with a significant increase in risk of autism whereas the inherited genotype of the child was not. Further, maternal DNA from the autism mothers was found to be significantly hypomethylated relative to reference control DNA. Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.
Non-contrast T1-mapping detects acute myocardial edema with high diagnostic accuracy: a comparison to T2-weighted cardiovascular magnetic resonance (2012)

Non-contrast T1-mapping using ShMOLLI is a novel method for objectively detecting myocardial edema with a high diagnostic performance. T1-mapping may serve as a complementary technique to T2-weighted imaging for assessing myocardial edema in ischemic and non-ischemic heart disease, such as quantifying area-at-risk and diagnosing myocarditis.
One-step ultrasensitive detection of microRNAs with loop-mediated isothermal amplification (LAMP) (2010)

An ultrasensitive microRNA assay was developed with one-step loop-mediated isothermal amplification (LAMP) initiated by the target microRNA.
2-Amino-6-furan-2-yl-4-substituted Nicotinonitriles as A2A Adenosine Receptor Antagonists (2008)

A 2A adenosine receptor antagonists usually have bi- or tricyclic N aromatic systems with varying substitution patterns to achieve desired receptor affinity and selectivity. Using a pharmacophore model designed by overlap of nonxanthine type of previously known A 2A antagonists, we synthesized a new class of compounds having a 2-amino nicotinonitrile core moiety. From our data, we conclude that the presence of at least one furan group rather than phenyl is beneficial for high affinity on the A 2A adenosine receptor. Compounds 39 (LUF6050) and 44 (LUF6080) of the series had K i values of 1.4 and 1.0 nM, respectively, with reasonable selectivity toward the other adenosine receptor subtypes, A 1, A 2B, and A 3. The high affinity of 44 was corroborated in a cAMP second messenger assay, yielding subnanomolar potency for this compound.
Interaction of the human insulin receptor tyrosine kinase from the baculovirus expression system with protein kinase C in a cell-free system. (1993)

The cytoplasmic domain of the human insulin receptor (HIR) from the baculovirus expression system (BIRK) is a soluble, constitutively activated protein-tyrosine kinase. In a cell-free system, BIRK is phosphorylated on serine and threonine residues by protein kinase C (PKC) purified from rat brain. Two-dimensional tryptic phosphopeptide mapping of PKC-phosphorylated BIRK identified one phosphothreonine and three phosphoserine peptides, which were also in tryptic digests of insulin receptors from insulin- or PMA-treated Chinese hamster ovary (CHO) cells transfected with the HIR. After Lys-C proteolysis of PKC-phosphorylated BIRK, radioactive phosphopeptides were purified on a C8 reverse-phase high pressure liquid chromatography column. Amino acid sequence analysis identified a phosphothreonine peptide corresponding to amino acids 1331-1340 of the HIR. This peptide contains only one threonine, amino acid 1336, which is identified as a site for PKC phosphorylation in BIRK. CHO cells transfected with the wild type (CHO/HIR) or a mutant human insulin receptor (CHO/HIRT1336N), in which threonine 1336 was substituted with asparagine, were 32P labeled and then stimulated with insulin or phorbol 12-myristate 13-acetate (PMA). Two-dimensional phosphopeptide analysis of the HIR revealed that phosphorylation of phosphothreonine peptide T, shown to be in PKC-phosphorylated BIRK, was increased by insulin or PMA. However, the corresponding peptide was not in the mutant receptor. Therefore, the present study directly identifies threonine 1336 in the HIR as a phosphorylation site for insulin and PMA. These data also show that BIRK can be used as a model for the study of the regulation of the insulin receptor kinase.
Systemic and regional hemodynamic effects of angiotensin-(1–7) in rats (2003)

The systemic and regional hemodynamics effects of ANG-(1–7) were examined in urethane-anesthetized rats. The blood flow distribution (kidneys, skin, mesentery, lungs, spleen, brain, muscle, and adrenals), cardiac output, and total peripheral resistance were investigated by using fluorescent microspheres. Blood pressure and heart rate were recorded from the brachial artery. ANG-(1–7) infusion (110 fmol · min −1 · 10 min −1 iv) significantly increased blood flow to the kidney (5.10 ± 1.07 to 8.30 ± 0.97 ml · min −1 · g −1 ), mesentery (0.73 ± 0.16 to 1.17 ± 0.49 ml · min −1 · g −1 ), brain (1.32 ± 0.44 to 2.18 ± 0.85 ml · min −1 · g −1 ), and skin (0.07 ± 0.02 to 0.18 ± 0.07 ml · min −1 · g −1 ) and the vascular conductance in these organs. ANG-(1–7) also produced a significant increase in cardiac index (30%) and a decrease in total peripheral resistance (2.90 ± 0.55 to 2.15 ± 0.28 mmHg · ml −1 · min · 100 g). Blood flow to the spleen, muscle, lungs, and adrenals, as well as the blood pressure and heart rate, were not altered by the ANG-(1–7) infusion. The selective ANG-(1–7) antagonist A-779 reduced the blood flow in renal, cerebral, mesenteric, and cutaneous beds and blocked the ANG-(1–7)-induced vasodilatation in the kidney, mesentery, and skin, suggesting a significant role of endogenous ANG-(1–7) in these territories. The effects of ANG-(1–7) on the cerebral blood flow, cardiac index, systolic volume, and total peripheral resistance were partially attenuated by A-779. A high dose of ANG-(1–7) (11 pmol · min −1 · 10 min −1 ) caused an opposite effect of that produced by the low dose. Our results show for the first time that ANG-(1–7) has a previously unsuspected potent effect in the blood flow distribution and systemic hemodynamics.
A novel, human Atg13 binding protein, Atg101, interacts with ULK1 and is essential for macroautophagy (2009)

Macroautophagy is an intracellular, vesicle-mediated mechanism for the sequestration and ultimate lysosomal degradation of cytoplasmic proteins, organelles and macromolecules. The macroautophagy process and many of the autophagy-specific (Atg) proteins are remarkably well conserved in higher eukaryotes. In yeast, the Atg1 kinase complex includes Atg1, Atg13, Atg17, and at least four other interacting proteins, some of which are phosphorylated in a TOR-dependent manner, placing the Atg1 signaling complex downstream of a major nutrient-sensing pathway. Atg1 orthologs, including mammalian unc-51-like kinase 1 (ULK1), have been identified in higher eukaryotes and have been functionally linked to autophagy. This suggests that other components of the Atg1 complex exist in higher eukaryotes. Recently, a putative human Atg13 ortholog, FLJ20698, was identified by gapped-BLAST analysis. We show here that FLJ20698 (Atg13) is a ULK1-interacting phosphoprotein that is essential for macroautophagy. Furthermore, we identify a novel, human Atg13-interacting protein, FLJ11773, which we have termed Atg101. Atg101 is essential for autophagy and interacts with ULK1 in an Atg13-dependent manner. Additionally, we present evidence that intracellular localization of the ULK1 complex is regulated by nutrient conditions. Finally, we demonstrate that Atg101 stabilizes the expression of Atg13 in the cell, suggesting that Atg101 contributes to Atg13 function by protecting Atg13 from proteasomal degradation. Therefore, the identification of the novel protein, Atg101, and the validation of Atg13 and Atg101 as ULK1-interacting proteins, suggests an Atg1 complex is involved in the induction of macroautophagy in mammalian cells.
Atorvastatin Inhibits ABCA1 Expression and Cholesterol Efflux in THP-1 Macrophages by an LXR-dependent Pathway (2008)

The effect of atorvastatin on adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and cholesterol efflux remains controversial. In an effort to clarify this issue, ABCA1 expression and apolipoprotein AI (apoAI)-mediated cholesterol efflux after atorvastatin treatment were investigated in THP-1 macrophages. Atorvastatin from 2 microM to 40 microM dose-dependently inhibited ABCA1 expression in human monocyte-derived macrophages and phorbol 12-myristate 13-acetate (PMA)-stimulated THP-1 monocytes. ApoAI-mediated cholesterol efflux was reduced in PMA-stimulated THP-1 cells treated with atorvastatin, this effect was abolished with acetylated low-density lipoprotein (LDL) pretreatment. Atorvastatin treatment also dose-dependently reduced liver X receptor alpha (LXRalpha) expression and Rho activation. Rho activation by farnysylpyophosphate (FPP) and lysophosphatidic acid (LPA) did not salvage, but further depressed, the cholesterol efflux and ABCA1 expression in the presence of atorvastatin. Without atorvastatin, Rho activation by mevalonate, FPP, and LPA diminished apoAI-mediated cholesterol efflux, and Rho activation by GTPgammaS also decreased ABCA1 messenger ribonucleic acid (mRNA) by 16%. Furthermore, Rho inhibition by C3 exoenzyme increased ABCA1 mRNA by 48% despite a 17% decrease in apoAI-mediated cholesterol efflux. LXRalpha agonists (T01901317 and 22(R)-hydroxycholesterol) prevented any reductions in cholesterol efflux or ABCA1 expression associated with atorvastatin treatment. Furthermore, Western blot analysis demonstrated the reciprocal inhibition of Rho and LXRalpha. In conclusion, atorvastatin decreases ABCA1 expression in noncholesterol-loaded macrophages in an LXRalpha- but not Rho-dependent pathway; this effect can be compromised after acetylated LDL cholesterol loading.
Long duration strapdown stellar-inertial navigation using satellite tracking (2003)

A strapdown stellar-inertial navigation system (INS) is currently being developed which can be used to correct for the gyro drift in an INS throughout a long-duration mission. The star sensor provides updates of the inertial angle error derived from stellar observations. However, since the star sensor updates are unable to correct for INS drifts due to accelerometer errors, the stellar inertial navigation solution accuracy degrades with time. A study has been performed on the number of visible satellites that can be tracked by the stellar-inertial system. The authors discuss the results of this study and include simulation results showing the performance improvement possible using both star and satellite observations to bound the system error growth. The results have shown that the combination of measurements can maintain the system error growth to within 700 ft over a long-duration mission.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
RNAi in Budding Yeast (2009)

RNA interference (RNAi), a gene-silencing pathway triggered by double-stranded RNA, is conserved in diverse eukaryotic species but has been lost in the model budding yeast Saccharomyces cerevisiae. Here, we show that RNAi is present in other budding yeast species, including Saccharomyces castellii and Candida albicans. These species use noncanonical Dicer proteins to generate small interfering RNAs, which mostly correspond to transposable elements and Y' subtelomeric repeats. In S. castellii, RNAi mutants are viable but have excess Y' messenger RNA levels. In S. cerevisiae, introducing Dicer and Argonaute of S. castellii restores RNAi, and the reconstituted pathway silences endogenous retrotransposons. These results identify a previously unknown class of Dicer proteins, bring the tool of RNAi to the study of budding yeasts, and bring the tools of budding yeast to the study of RNAi.
Thermal reversibility in electrical characteristics of ultraviolet/ozone-treated graphene (2013)

Changes in electrical properties of a bilayer graphene-based field-effect transistor (G-FET) after being oxidized through ultraviolet (UV)/ozone (O3) treatment are presented. A decrease in conductivity and carrier mobility was observed after oxidation. However, electrical properties recovered after annealing oxidized G-FET with H2/Ar, indicating that oxidation with UV/O3 treatment was thermally reversible. Raman spectroscopy was conducted to verify that no defects were introduced after oxidation. The existence of chemical bonds between oxygen and graphene was confirmed from the X-ray photoelectron spectroscopy. Moreover, we found that graphene's sheet resistance increased after oxidation. Nevertheless, contact resistivity at graphene-Au/TiN electrode interface remained unchanged.
Whole set of constitutive promoters for RpoN sigma factor and the regulatory role of its enhancer protein NtrC in Escherichia coli K-12 (2021)

The promoter selectivity of <i>Escherichia coli</i> RNA polymerase (RNAP) is determined by its promoter-recognition sigma subunit. The model prokaryote <i>E. coli</i> K-12 contains seven species of the sigma subunit, each recognizing a specific set of promoters. Using genomic SELEX (gSELEX) screening <i>in vitro</i>, we identified the whole set of 'constitutive' promoters recognized by the reconstituted RNAP holoenzyme alone, containing RpoD (σ<sup>70</sup>), RpoS (σ<sup>38</sup>), RpoH (σ<sup>32</sup>), RpoF (σ<sup>28</sup>) or RpoE (σ<sup>24</sup>), in the absence of other supporting regulatory factors. In contrast, RpoN sigma (σ<sup>54</sup>), involved in expression of nitrogen-related genes and also other cellular functions, requires an enhancer (or activator) protein, such as NtrC, for transcription initiation. In this study, a series of gSELEX screenings were performed to search for promoters recognized by the RpoN RNAP holoenzyme in the presence and absence of the major nitrogen response enhancer NtrC, the best-characterized enhancer. Based on the RpoN holoenzyme-binding sites, a total of 44 to 61 putative promoters were identified, which were recognized by the RpoN holoenzyme alone. In the presence of the enhancer NtrC, the recognition target increased to 61-81 promoters. Consensus sequences of promoters recognized by RpoN holoenzyme in the absence and presence of NtrC were determined. The promoter activity of a set of NtrC-dependent and -independent RpoN promoters was verified <i>in vivo</i> under nitrogen starvation, in the presence and absence of RpoN and/or NtrC. The promoter activity of some RpoN-recognized promoters increased in the absence of RpoN or NtrC, supporting the concept that the promoter-bound NtrC-enhanced RpoN holoenzyme functions as a repressor against RpoD holoenzyme. Based on our findings, we propose a model in which the RpoN holoenzyme fulfils the dual role of repressor and transcriptase for the same set of genes. We also propose that the promoter recognized by RpoN holoenzyme in the absence of enhancers is the 'repressive' promoter. The presence of high-level RpoN sigma in growing <i>E. coli</i> K-12 in rich medium may be related to the repression role of a set of genes needed for the utilization of ammonia as a nitrogen source in poor media. The list of newly identified regulatory targets of RpoN provides insight into <i>E. coli</i> survival under nitrogen-depleted conditions in nature.
Synthesis of highly active and stable Au–PtCu core–shell nanoparticles for oxygen reduction reaction (2012)

Au-PtCu core-shell nanoparticles were successfully synthesized via galvanic replacement of Cu by Pt on hollow Au nano-spheres. Characterizations of the nanoparticles were conducted by X-ray diffraction (XRD), transmission electron microscopy (TEM), and electrochemical measurements. Results indicate 2-2.5 times higher specific activity and mass activity of the Au-PtCu catalysts than commercial Pt black and Pt/C in oxygen reduction reaction (ORR), measured in a rotating disk electrode system. Besides, thinner PtCu coating (25 nm thick, deposition time of 20 min) on the hollow Au nano-spheres demonstrated a pronounced CO oxidation peak shift (by 0.13 V) and long-term durability probably due to the unique core-shell structure and strong electronic coupling between the Au core and the PtCu shell.