gebhart/patrepeval huggingface dataset:
<title>A resilient and quick data compression method of prediction errors for space missions</title> (2009)

It has passed more than a decade since the Consultative Committee for Space Data Systems (CCSDS) made its recommendation for lossless data compression. The CCSDS standard is commonly used for scientific missions because it is a general-purpose lossless compression technique with a low computational cost which results in acceptable compression ratios. At the core of this compression algorithm it is the Rice coding method. Its performance rapidly degrades in the presence of noise and outliers, as the Rice coder is conceived for noiseless data following geometric distributions. To overcome this problem we present here a new coder, the so-called Prediction Error Coder (PEC), as well as its fully adaptive version (FAPEC) which we show is a reliable alternative to the CCSDS standard. We show that PEC and FAPEC achieve large compression ratios even when high levels of noise are present in the data. This is done testing our compressors with synthetic and real data, and comparing the compression ratios and processor requirements with those obtained using the CCSDS standard.
Direct observation of half-metallic energy gap in Co2MnSi by tunneling conductance spectroscopy (2006)

Magnetic tunnel junctions with a Co2MnSi∕Al–O∕CoFe structure are prepared by magnetron sputtering and investigated with respect to the energy gap near the Fermi energy level. The plasma oxidation time for the Al–O barrier is found to affect the condition of the Co2MnSi∕Al–O interface. The optimized sample (50s oxidation time) exhibits a magnetoresistance ratio of 159% and tunneling spin polarization of 0.89 at 2K. The bias voltage dependence of tunneling conductance (dI∕dV−V) reveals a clear half-metallic energy gap at 350–400meV for Co2MnSi, with an energy separation of just 10meV between the Fermi energy and the bottom edge of conduction band.
PE-202 : Expression Analysis of Immune Markers in Non-Alcoholic Steatohepatitis Identifies Activated Macrophages as Key Mediators of Inflammation and Fibrosis Progression (2020)

Aims: The pathophysiology of non-alcoholic steatohepatitis (NASH) is multifactorial and not yet completely understood; however, innate immunity is a major contributing factor in which liver-resident macrophages (Kupffer cells) and recruited macrophages play a central part in disease progression. In this study, we aimed to demonstrate that activated macrophages are as key mediators of inflammation and fibrosis progression in NASH livers.
Methods: Ninety-four, snap-frozen benign liver tissues with various chronic liver diseases in the different fibrosis stages (0: n=17, 1: n=12, 2: n=12, 3: n=25, 4: n=28) were subjected to the expression analyses. Gene expression analysis was performed using the nCounter PanCancer Pathway Panel (NanoString Technologies, Seattle, WA, USA). Liver biopsy was performed for NASH livers with various fibrosis stages. Immunohistochemistry and multicolor flow cytometry were performed with the biopsy specimen. Mouse model of NASH-induced liver cirrhosis was established using high-fat, high-cholesterol (HFHC) diet with intraperitoneal streptozocin injection. All statistical analyses in this study were performed using the open source statistical programming environment R language (version 3.4.3).
Results: Gene expression analysis with 94 patient liver samples using the nCounter PanCancer Pathway Panel identified that expression level of IL12B, SOCS1, and STAT1, which are robustly expressed in activated macrophages, was higher in the livers with advanced fibrosis (stage 3 and 4) than those with low-grade fibrosis (stage 1 and 2) or no fibrosis (P<0.001). Immunohistochemical staining demonstrated that the number of CD68+ macrophages increases as the fibrosis progresses in NASH livers (P<0.05). Flow cytometry using liver biopsy specimen demonstrated that macrophages in the livers with advanced fibrosis show higher expression of HLA-DR and PDL1, suggesting that these macrophages contribute not only to the inflammation and fibrosis, but also to dismantling anti-tumor immune surveillance in fibrotic NASH livers. Mice fed with HFHC diet with intraperitoneal streptozocin injection developed NASH, liver cirrhosis, and hepatocellular carcinoma, and the number of activated macrophages increased as the disease progressed.
Conclusions: Our data using expression analysis of immune markers showed that activated macrophages are key mediators of inflammation and fibrosis progression in NASH livers. This study was supported by The Research Supporting Program of The Korean Association for the Study of the Liver and The Korean Liver Foundation. This study was also supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (2020R1A2C3011569).
Uncoupling gene activity from chromatin structure: promoter mutations can inactivate transcription of the yeast HSP82 gene without eliminating nucleosome-free regions. (1992)

DNase I-hypersensitive sites represent "nucleosome-free" regions in chromatin where the underlying DNA sequence is highly accessible to trans-acting proteins. Here we demonstrate that it is possible to uncouple gene activity from hypersensitive site formation. Point or substitution mutations were introduced into the promoter of the yeast chromosomal HSP82 gene, encoding the 83-kDa heat shock protein (HSP), via site-directed integration. Mutating either the TATA box or heat shock element 1 (HSE1) significantly reduced basal and heat-induced transcription while mutating both essentially inactivated expression. Dormant transcription units exhibited arrays of sequence-positioned nucleosomes; nevertheless, the inactivated genes still retained a hypersensitive site within their mutated promoters. In addition, all yeast strains maintained a heat-inducible hypersensitive site at -600 base pairs (bp), while several mutant strains converted a constitutive hypersensitive site at -300 bp into a heat-inducible one. Thus, mutations in cis-acting elements within a promoter can inactivate transcription without eliminating nucleosome-free regions.
Solar cells with thin Cu(In1-xGax)Se<inf>2</inf> absorbers: Optical analysis and quantum efficiency simulations (2014)

We present in-depth quantum efficiency analyses of of Cu(In,Ga)Se <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sub> (CIGS) solar cells. Ex-situ spectroscopic ellipsometry (SE) analysis is applied to partially and fully completed solar cells with standard thickness and thin CIGS absorbers. Optical properties and multilayer structural data are deduced and used to predict the maximum obtainable quantum efficiency spectra and short-circuit current densities (J <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">sc</sub> ). We validate optical model development and the resulting quantum efficiency (QE) simulations with experimental results for CIGS solar cells incorporating standard 2.2 μm thick absorbers. We find that both the bulk CIGS layer and the CdS-CIGS interface layer serve as active layer components and together contribute 100% of the photo-generated current. Thus, essentially all photo-generated carriers are collected from these layers. Solar cells with thin absorbers were also fabricated and efficiencies of 13.2% at 0.73 μm CIGS thickness, 10.1% at 0.50 μm and 8.0% at 0.36 μm were obtained. Although J <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">sc</sub> is expected to decrease with decreasing absorber thickness due to reduced optical collection, modeling results suggest that electronic losses are also occurring upon thinning the absorber, ranging from ~ 1.3 to 1.9 mA/cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> for cells with CIGS thicknesses from 0.73 to 0.36 μm, respectively.
Data from EGFR Blockade Reverts Resistance to KRAS<sup>G12C</sup> Inhibition in Colorectal Cancer (2023)

&lt;div&gt;Abstract&lt;p&gt;Most patients with &lt;i&gt;KRAS&lt;/i&gt;&lt;sup&gt;G12C&lt;/sup&gt;–mutant non–small cell lung cancer (NSCLC) experience clinical benefit from selective KRAS&lt;sup&gt;G12C&lt;/sup&gt; inhibition, whereas patients with colorectal cancer bearing the same mutation rarely respond. To investigate the cause of the limited efficacy of KRAS&lt;sup&gt;G12C&lt;/sup&gt; inhibitors in colorectal cancer, we examined the effects of AMG510 in &lt;i&gt;KRAS&lt;/i&gt;&lt;sup&gt;G12C&lt;/sup&gt; colorectal cancer cell lines. Unlike NSCLC cell lines, &lt;i&gt;KRAS&lt;/i&gt;&lt;sup&gt;G12C&lt;/sup&gt; colorectal cancer models have high basal receptor tyrosine kinase (RTK) activation and are responsive to growth factor stimulation. In colorectal cancer lines, KRAS&lt;sup&gt;G12C&lt;/sup&gt; inhibition induces higher phospho-ERK rebound than in NSCLC cells. Although upstream activation of several RTKs interferes with KRAS&lt;sup&gt;G12C&lt;/sup&gt; blockade, we identify EGFR signaling as the dominant mechanism of colorectal cancer resistance to KRAS&lt;sup&gt;G12C&lt;/sup&gt; inhibitors. The combinatorial targeting of EGFR and KRAS&lt;sup&gt;G12C&lt;/sup&gt; is highly effective in colorectal cancer cells and patient-derived organoids and xenografts, suggesting a novel therapeutic strategy to treat patients with &lt;i&gt;KRAS&lt;/i&gt;&lt;sup&gt;G12C&lt;/sup&gt; colorectal cancer.&lt;/p&gt;Significance:&lt;p&gt;The efficacy of KRAS&lt;sup&gt;G12C&lt;/sup&gt; inhibitors in NSCLC and colorectal cancer is lineage-specific. RTK dependency and signaling rebound kinetics are responsible for sensitivity or resistance to KRAS&lt;sup&gt;G12C&lt;/sup&gt; inhibition in colorectal cancer. EGFR and KRAS&lt;sup&gt;G12C&lt;/sup&gt; should be concomitantly inhibited to overcome resistance to KRAS&lt;sup&gt;G12C&lt;/sup&gt; blockade in colorectal tumors.&lt;/p&gt;&lt;p&gt;&lt;i&gt;See related commentary by Koleilat and Kwong, p. 1094&lt;/i&gt;.&lt;/p&gt;&lt;p&gt;&lt;i&gt;This article is highlighted in the In This Issue feature, p. 1079&lt;/i&gt;&lt;/p&gt;&lt;/div&gt;
Enhanced X-Ray Detectors Using Polar Dopants for KCD Digital Radiography (1996)

The goal of this study is to develop high resolution imaging detectors with applications in digital radiography and computed tomography. A physical treatment aimed at a better understanding of the line-spread function response of kinestatic charge detector (KCD) gas media, using dopants with permanent electric dipoles, is presented. Experimental results were obtained by operating a KCD krypton-filled detector at pressures up to 60 atm and constant electric field-to-gas density ratio doped with small amounts of polar or nonpolar polyatomic molecules with low or high ionization potential. The results clearly indicate that the addition of dopants having both low ionization potential and high dipole moment significantly enhance the imaging signal quality. An analysis of the experimental results aimed at providing a plausible interpretation of the reported observations is offered.
The Rho ADP-ribosylating C3 exoenzyme binds cells via an Arg–Gly–Asp motif (2017)

The Rho ADP-ribosylating C3 exoenzyme (C3bot) is a bacterial protein toxin devoid of a cell-binding or -translocation domain. Nevertheless, C3 can efficiently enter intact cells, including neurons, but the mechanism of C3 binding and uptake is not yet understood. Previously, we identified the intermediate filament vimentin as an extracellular membranous interaction partner of C3. However, uptake of C3 into cells still occurs (although reduced) in the absence of vimentin, indicating involvement of an additional host cell receptor. C3 harbors an Arg-Gly-Asp (RGD) motif, which is the major integrin-binding site, present in a variety of integrin ligands. To check whether the RGD motif of C3 is involved in binding to cells, we performed a competition assay with C3 and RGD peptide or with a monoclonal antibody binding to β1-integrin subunit and binding assays in different cell lines, primary neurons, and synaptosomes with C3-RGD mutants. Here, we report that preincubation of cells with the GRGDNP peptide strongly reduced C3 binding to cells. Moreover, mutation of the RGD motif reduced C3 binding to intact cells and also to recombinant vimentin. Anti-integrin antibodies also lowered the C3 binding to cells. Our results indicate that the RGD motif of C3 is at least one essential C3 motif for binding to host cells and that integrin is an additional receptor for C3 besides vimentin.
Neural Networks and Artificial Intelligence for Biomedical Engineering (1999)

From the Publisher:
Using examples drawn from biomedicine and biomedical engineering, this reference text provides comprehensive coverage of all the major techniques currently available to build computer-assisted decision support systems. You will find practical solutions for biomedicine based on current theory and applications of neural networks, artificial intelligence and other methods for the development of decision-making aids, including hybrid systems.
The EGFR T790M Mutation in Acquired Resistance to an Irreversible Second-Generation EGFR Inhibitor (2012)

Molecular target therapies using first-generation, reversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI), such as gefitinib or erlotinib, have been shown to be effective for patients with non-small cell lung cancer (NSCLC) who harbor activating mutations in EGFR. However, these patients eventually develop resistance to the reversible TKIs, and this has led to the development of second-generation, irreversible EGFR inhibitors. Currently, the mechanism of acquired resistance to irreversible EGFR inhibitors is not clear. Using an in vitro cell culture system, we modeled the acquired resistance to first-line treatment with second-generation EGFR-TKIs using an EGFR-mutant NSCLC cell line. Here, we report a mechanism of resistance involving T790M secondary mutation as well as a corresponding clinical case. The results of these findings suggest that inhibition of EGFR by currently available second-generation EGFR-TKIs may not be sufficient to physiologically prevent the emergence of cells that are still dependent on EGFR signaling. This finding bears important implications on the limitations of currently available second-generation EGFR-TKIs.
Elevated Plasma YKL-40, Lipids and Lipoproteins, and Ischemic Vascular Disease in the General Population (2015)

Elevated YKL-40 was associated with a 34% increase in triglyceride levels and with a 2-fold increased risk of ischemic stroke, whereas genetically elevated YKL-40 were not.
Trends in advanced process technology—Submicrometer CMOS device design and process requirements (1986)

Some of the trends in integrated circuit process development are described. The motivations or technical reasons for this activity are discussed. This effort will continue to develop the downsizing that increases functional density and performance. Limiting factors are examined and new technical developments that could enable CMOS density to be comparable with NMOS density are explored. Various isolation techniques are described and the influence on performance of well profiles and doping concentrations are examined. These trends have a beating on the choice of gate electrode materials. Reliability factors governing the gate dielectric thickness are discussed briefly. MOSFET diode capacitance is shown to be the predominant limiting factor at the device level. Methodologies that could be used to reduce device parasitics are considered in detail. Device scaling below 1-µm calls for changes in contact metallization techniques. Trends in metallization technology and the various methods of fabricating multilevel interconnections when the via sizes become very small are described. The processing methods being investigated to overcome device limitations are examined and compared. In some cases, the present technical difficulties of these methods are discussed. The general conclusion of this work is that "downsizing" will continue, but advances will be more dependent upon innovative processes and device research, whereas in the past, scaling rules were adequate and progress was evolutionary.
Activation of hedgehog signaling associates with early disease progression in chronic lymphocytic leukemia (2019)

Targeted sequencing of 103 leukemia-associated genes in leukemia cells from 841 treatment-naive patients with chronic lymphocytic leukemia (CLL) identified 89 (11%) patients as having CLL cells with mutations in genes encoding proteins that putatively are involved in hedgehog (Hh) signaling. Consistent with this finding, there was a significant association between the presence of these mutations and the expression of GLI1 (χ<sup>2</sup> test, <i>P</i> < .0001), reflecting activation of the Hh pathway. However, we discovered that 38% of cases without identified mutations also were GLI1<sup>+</sup> Patients with GLI1<sup>+</sup> CLL cells had a shorter median treatment-free survival than patients with CLL cells lacking expression of GLI1 independent of IGHV mutation status. We found that GANT61, a small molecule that can inhibit GLI1, was highly cytotoxic for GLI1<sup>+</sup> CLL cells relative to that of CLL cells without GLI1. Collectively, this study shows that a large proportion of patients have CLL cells with activated Hh signaling, which is associated with early disease progression and enhanced sensitivity to inhibition of GLI1.
Allopurinol might improve response to azathioprine and 6‐mercaptopurine by correcting an unfavorable metabolite ratio (2010)

In those with a high 6-MMPN:6-TGN ratio (>20), response to thiopurine treatment might be improved by the addition of allopurinol, together with a reduced thiopurine dose and close hematological monitoring.
Antiproliferative property of hexadecyloxypropyl 9-[2-(phosphonomethoxy) ethyl] guanine (HDP-PMEG) for unwanted ocular proliferation. (2011)

HDP-PMEG possesses a significant inhibitory effect on the proliferation of RPE, retinal glial cells, scleral fibroblasts, and ocular melanoma cells. HDP-PMEG is also genotoxic and may be used as a single short application for the modulation of unwanted ocular proliferation.
Humoral control of cell proliferation: the role of fibroblast growth factor in regeneration, angiogenesis, wound healing, and neoplastic growth. (1976)

The Fibroblast Growth Factor (FGF) is a mitogenic agent in the brain and pituitary of mammals. Recent investigations of the effect of FGF on diverse cell types has shown that FGF stimulates the division of cells from a wide variety of tissues of mesodermal origin including fibroblasts, chondrocytes, myoblasts, smooth muscle cells, glial cells, normal adrenal cells, and the Y1 adrenal cell line. Cell types of endodermal or ectodermal origin do not appear to be sensitive to FGF. Since FGF can be found in neural tissues and since it induces the proliferation of two cell types involved in the formation of regeneration blastemas (chondrocytes and myoblasts), we have investigated the possibility that FGF could be similar or identical to the neurotrophic factors present in nerve and responsible for the regeneration of limbs in lower vertebrates. Our results have shown that FGF could indeed substitute for the neurotropic factor and replace the nerves in inducing blastema formation and sustaining proliferation of mesenchymal cells which can differentiate into chrondrocytes and myoblasts. Since the blastema has been described as a benign tumor, the role of FGF in the formation of blastemas and benign tumors is currently under investigation. In addition to stimulating fibroblasts, FGF also has a striking growth-promoting effect on primary cultures of vascular endothelial cells. This suggests that FGF could be an angiogenesis factor. Thus, FGF, one of the most potent mitogenic agents found in tissue extracts has two properties expected of an agent which could induce tumors: it can induce blastema formation (direct mitogenic effect) and, through its mitogenic effect on endothelial cells, it could induce formation of capillaries (amplification step), permitting unlimited growth. Repair processes under FGF control will, under normal circumstances, lead to wound healing. In contrast, if cells become transplanted to the wrong environment (hormonal imbalance), growth factors such as FGF could make them proliferate in an anarchic way since negative feedback from surrounding cells will be lacking.
Immortalization of plasma cells by plasmid DNA and its hybridoma (1995)

Human plasma cell lines producing IgG were cloned by the limiting dilution method from polyclonally immortalized B-cell lines with the plasmid DNA (pSVTLbsr) containing simian virus 40 (SV40)-gene from primary peripheral blood mononuclear cells of healthy and nonimmune volunteers. The plasma cell lines fused well with conventional partner cells and became evenly IgG-producing hybridomas at high efficiency, especially with the partner cell from human origin. One of the difficulties in obtaining stable IgG-producing hybridoma using Epstein-Barr virus (EBV) transformation followed by back fusion with partner cells, might mainly be attributed to the inability to immortalize plasma cells on account of the very low density of CD21 (EBV receptor) on the cell surface. The present CD21-independent immortalization by plasmid DNA and by the infection with SV40 protein-coated plasmid DNA will be a potentially effective method to obtain IgG-producing human monoclonal antibodies.
Kinematics of the Subaxial Cervical Spine in Rotation In Vivo Three-Dimensional Analysis (2004)

In Brief Study Design. Three-dimensional intervertebral motions of the subaxial cervical spine during head rotation were investigated in healthy volunteers using three-dimensional magnetic resonance imaging (MRI). Objectives. To document intervertebral coupled motions of the subaxial cervical spine during rotation. Summary of Background Data. In vivo three-dimensional kinematics of the subaxial cervical spine in rotation have not previously been well described, since they are too complicated to follow using conventional radiography or computed tomography techniques. Methods. Ten healthy volunteers underwent three-dimensional MRI of the cervical spine in 11 positions with 15° increments during head rotation using a 1.0-T imager. Relative motions of the subaxial cervical spine were calculated by automatically superimposing a segmented three-dimensional MRI of the vertebra in the neutral position over images of each position using volume registration. Three-dimensional motions of adjacent vertebrae were represented with 6 df (6 degrees of freedoms) by Euler angles and translations on the coordinate system defined by Panjabi, then visualized in animations using surface bone models. Results. Mean axial rotation of the subaxial cervical spine in maximum head rotation (69.5°) was 2.2° at C2–C3, 4.5° at C3–C4, 4.6° at C4–C5, 4.0° at C5–C6, 1.6° at C6–C7, and 1.5° at C7–T1. Coupled lateral bending with axial rotation was observed in the same direction as axial rotation at all levels (C2–C3, 3.6°; C3–C4, 5.4°; C4–C5, 5.0°; C5–C6, 5.3°; C6–C7, 4.9°; C7–T1, 1.2°). Coupled extension with axial rotation occurred in the middle cervical region (C2–C3, 1.4°; C3–C4, 2.3°; C4–C5, 1.5°), while in the lower cervical region, flexion was coupled with axial rotation (C5–C6, 0.9°; C6–C7, 2.4°; C7–T1, 3.0°). Conclusions. We investigated intervertebral motions of the subaxial cervical spine during head rotation using a three-dimensional imaging system, and obtained the first accurate depictions of in vivo coupled motion. These findings will be helpful as the basis for understanding abnormal conditions. This study investigated three-dimensional intervertebral motions of the subaxial cervical spine during head rotation using three-dimensional MRI and provides the first accurate elucidation of in vivo coupled motion.