gebhart/patrepeval huggingface dataset:
ROR2 is a novel prognostic biomarker and a potential therapeutic target in leiomyosarcoma and gastrointestinal stromal tumour (2012)

Soft-tissue sarcomas are a group of malignant tumours whose clinical management is complicated by morphological heterogeneity, inadequate molecular markers and limited therapeutic options. Receptor tyrosine kinases (RTKs) have been shown to play important roles in cancer, both as therapeutic targets and as prognostic biomarkers. An initial screen of gene expression data for 48 RTKs in 148 sarcomas showed that ROR2 was expressed in a subset of leiomyosarcoma (LMS), gastrointestinal stromal tumour (GIST) and desmoid-type fibromatosis (DTF). This was further confirmed by immunohistochemistry (IHC) on 573 tissue samples from 59 sarcoma tumour types. Here we provide evidence that ROR2 expression plays a role in the invasive abilities of LMS and GIST cells in vitro. We also show that knockdown of ROR2 significantly reduces tumour mass in vivo using a xenotransplantation model of LMS. Lastly, we show that ROR2 expression, as measured by IHC, predicts poor clinical outcome in patients with LMS and GIST, although it was not independent of other clinico-pathological features in a multivariate analysis, and that ROR2 expression is maintained between primary tumours and their metastases. Together, these results show that ROR2 is a useful prognostic indicator in the clinical management of these soft-tissue sarcomas and may represent a novel therapeutic target.
Energy bands in ferromagnetic iron (1977)

Energy bands in ferromagnetic iron have been calculated self-consistently using three different potentials. The first is the Kohn-Sham-Gaspar local-exchange approximation; second, a similar potential used in a previous calculation ($X\ensuremath{\alpha}$ with $\ensuremath{\alpha}=0.64$); third, the spin-polarized exchange-correlation potential of von Barth and Hedin. The linear-combination-of-atomic-orbitals method was employed using a basis set of independent Gaussian orbitals. Spin-orbit coupling and other relativistic effects were ignored. Results are presented for the Fermi surface, charge and spin form factors, contact charge and spin densities, and the Compton profile. Use of the exchange-correlation potential leads to improvement of calculated results in comparison with experiment, but some discrepancies still remain.
Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function (2007)

It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.
Capture and emission of electrons at 2.4-eV-deep trap level in SiO2films (1975)

Capture, photoionization, and impact-ionization cross sections for a 2.4-eV-deep electron trapping center in the silicon-dioxide layer of a metal-oxide-semiconductor structure have been determined using the photoinjection-photodepopulation technique. The electric field dependence of both capture and impact-ionization cross sections have been determined for accelerating fields in the range 0.1-1.0 MV/cm. Capture cross sections are of order ${10}^{\ensuremath{-}14}$ ${\mathrm{cm}}^{2}$ and uv photoionization cross sections greater than ${10}^{\ensuremath{-}18}$ ${\mathrm{cm}}^{2}$. High-field impact-ionization rates are 1-10 ${\mathrm{cm}}^{\ensuremath{-}1}$ for filled trap densities of order 5 \ifmmode\times\else\texttimes\fi{} ${10}^{13}$ ${\mathrm{cm}}^{\ensuremath{-}3}$.
High-Rate Space–Time Coded Large-MIMO Systems: Low-Complexity Detection and Channel Estimation (2009)

In this paper, we present a low-complexity algorithm for detection in high-rate, non-orthogonal space-time block coded (STBC) large-multiple-input multiple-output (MIMO) systems that achieve high spectral efficiencies of the order of tens of bps/Hz. We also present a training-based iterative detection/channel estimation scheme for such large STBC MIMO systems. Our simulation results show that excellent bit error rate and nearness-to-capacity performance are achieved by the proposed multistage <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">likelihood ascent search</i> ( <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">M</i> -LAS) detector in conjunction with the proposed iterative detection/channel estimation scheme at low complexities. The fact that we could show such good results for large STBCs like 16×16 and 32×32 STBCs from Cyclic Division Algebras (CDA) operating at spectral efficiencies in excess of 20 bps/Hz (even after accounting for the overheads meant for pilot based training for channel estimation and turbo coding) establishes the effectiveness of the proposed detector and channel estimator. We decode perfect codes of large dimensions using the proposed detector. With the feasibility of such a low-complexity detection/channel estimation scheme, large-MIMO systems with tens of antennas operating at several tens of bps/Hz spectral efficiencies can become practical, enabling interesting high data rate wireless applications.
Co-inhibition of NF-κB and JNK is synergistic in TNF-expressing human AML (2014)

Leukemic stem cells (LSCs) isolated from acute myeloid leukemia (AML) patients are more sensitive to nuclear factor κB (NF-κB) inhibition-induced cell death when compared with hematopoietic stem and progenitor cells (HSPCs) in in vitro culture. However, inadequate anti-leukemic activity of NF-κB inhibition in vivo suggests the presence of additional survival/proliferative signals that can compensate for NF-κB inhibition. AML subtypes M3, M4, and M5 cells produce endogenous tumor necrosis factor α (TNF). Although stimulating HSPC with TNF promotes necroptosis and apoptosis, similar treatment with AML cells (leukemic cells, LCs) results in an increase in survival and proliferation. We determined that TNF stimulation drives the JNK-AP1 pathway in a manner parallel to NF-κB, leading to the up-regulation of anti-apoptotic genes in LC. We found that we can significantly sensitize LC to NF-κB inhibitor treatment by blocking the TNF-JNK-AP1 signaling pathway. Our data suggest that co-inhibition of both TNF-JNK-AP1 and NF-κB signals may provide a more comprehensive treatment paradigm for AML patients with TNF-expressing LC.
Resolvins, docosatrienes, and neuroprotectins, novel omega‐3‐derived mediators, and their endogenous aspirin‐triggered epimers (2004)

The molecular basis for the beneficial impact of essential omega-3 (n-3) FA remains of interest. Recently, we identified novel mediators generated from eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) that displayed potent bioactions identified first in resolving inflammatory exudates and in tissues enriched with DHA. The trivial names resolvin (resolution phase interaction products) and docosatrienes were introduced for the bioactive compounds from these novel series since they possess potent anti-inflammatory and immunoregulatory actions. Compounds derived from EPA carrying potent biological actions (i.e., 1-10 nM range) are designated E series and denoted resolvins of the E series (resolvin E1 or RvE1), and those biosynthesized from the precursor DHA are denoted resolvins of the D series (resolvin D1 or RvD1). The number 1 designates the bioactive compounds in this family (#1-4). Bioactive members from DHA-containing conjugated triene structures or docosatrienes (DT) that possess immunoregulatory and neuroprotective actions were termed neuroprotectins. Aspirin treatment initiates a related epimeric series by triggering endogenous formation of the 17R-D series resolvins and docosatrienes. These epimers are denoted as aspirin-triggered (AT)-RvD and DT, and possess potent anti-inflammatory actions in vivo essentially equivalent to their 17S series pathway products. These include five distinct series: (i) 18R resolvins from EPA (i.e., RvE1); (ii) 17R series (AT) resolvins from DHA (RvD1 through RvD4); (iii) 17S series resolvins from DHA (RvD1 through RvD4), (iv) DT from DHA; and (v) their AT form 17R series DT. In this article, we provide an overview of the formation and actions of these newly uncovered pathways and products.
Identification of signal sequences that control transcription of borna disease virus, a nonsegmented, negative-strand RNA virus (1994)

Borna disease virus (BDV) is a nonsegmented, negative-strand RNA virus that causes neurologic disorders in a wide range of animal species. Although the virus is unclassified, sequence analysis of the 8.9-kb viral genome has shown that it is related to rhabdoviruses and paramyxoviruses. We have mapped subgenomic RNAs of BDV strain He80-1 to the viral genome by determining the precise sequences at their 5' and 3' termini. This analysis showed that the genome contains three transcription initiation sites and four termination sites. A 14- to 16-nucleotide semiconserved sequence was present at the gene start sites and partially copied into the subgenomic RNAs. The termination sites contained a U-rich motif reminiscent of termination signals in rhabdoviruses and paramyxoviruses. In contrast to the genomes of other nonsegmented, negative-strand RNA viruses, the BDV genome lacked the typical configuration of termination signal, intergenic region, and initiation signal at the gene boundaries. Instead, transcription units and transcription signals frequently overlapped. These differences have implications for our understanding of the control of viral transcription and may relate to the low-level replication and persistence of BDV.
Collectins and Pulmonary Host Defense (1998)

The surfactant-associated proteins SP-A and SP-D are members of a family of collagenous host defense lectins, designated collectins. There is increasing evidence that these pulmonary epithelial-derived proteins are important components of the innate immune response to microbial challenge, and that they participate in other aspects of immune and inflammatory regulation within the lung. The collectins bind to glycoconjugates and/or lipid moieties expressed by a wide variety of microorganisms and certain other organic particles in vitro. Although binding may facilitate microbial clearance through aggregation or other direct effects on the organism, SP-A and SP-D also have the capacity to modulate leukocyte function and, in some circumstances, to enhance their killing of microorganisms. The biologic activity of cell wall components, such as gram-negative bacterial polysaccharides, may be altered by interactions with collectins. Complementary or cooperative interactions between SP-A and SP-D could contribute to the efficiency of this defense system. Collectins may play particularly important roles in settings of inadequate or impaired specific immunity. Acquired or genetic alterations in the levels of active proteins within the airspaces and distal airways may increase susceptibility to infection.
Detection of subpicogram quantities of specific DNA sequences on blot hybridization with biotinytated probes (1985)

A sensitive method for detecting biotinylated DNA probes on dot and Southern blots is described which is based on the principle outlined by Leary et al (1). This system has two main components: detection of biotinylated DNA by a two-step procedure with streptavidin and poly(alkaline phosphatase); and blocking background with Tween 20. 32fg and 80fg of lambda phage DNA was detected on dot and Southern blot hybridizations respectively. 150fg of beta-globin was detected on Southern blots of genomic DNA. This method is fast, reproducible and can detect single copy genes in 0.25 micrograms genomic DNA on Southern blots.
Bone morphogenetic protein-2 stimulates chondrogenic expression in human nasal chondrocytes expandedin vitro (2008)

Articular cartilage contains an extracellular matrix with characteristic macromolecules such as type II collagen. Because this tissue is avascular and mature chondrocytes do not proliferate, cartilage lesions have a limited capacity for healing after trauma. Autologous chondrocyte implantation (ACI) is widely used for the treatment of patients with focal damage to articular cartilage. However, this method faces a major issue: dedifferentiation of chondrocytes occurs during the long-term culture necessary for mass cell production. The aim of this study was to determine if the step of cell amplification required for ACI could benefit from the use of bone morphogenetic protein (BMP)-2, a potent regulator of chondrogenic expression. Chondrocytes were isolated from human nasal cartilage, a hyaline cartilage like articular cartilage and were serially cultured in monolayers. After one, two or three passages, BMP-2 was used to evaluate the chondrogenic potential of the dedifferentiated chondrocytes, at the gene and protein level. We found that BMP-2 can reactivate the program of chondrogenic expression in dedifferentiated chondrocytes. To gain insight into the molecular mechanisms involved in the responsiveness of chondrocytes to BMP-2, we examined the phosphorylation of Smad proteins and the interaction of the Sry-type high-mobility-group box (Sox) transcription factors with the cartilage-specific enhancer of the type II procollagen gene. Our results show that BMP-2 acts by stimulating Smad phosphorylation and by enhancing DNA-binding of the Sox transcription factors to the specific enhancer of the type II procollagen gene. Thus, this study reveals the potential use of BMP-2 as a stimulatory agent in conventional ACI strategies.
Functional assembly in vitro of phycobilisomes with isolated photosystem II particles of eukaryotic chloroplasts. (1986)

Phycobiliproteins obtained by dissociation of phycobilisomes were reassociated in vitro with intact thylakoids or isolated photosystems I and I1 preparations obtained from cyanophytes (prokaryotes) or green algae (eukaryotes) to form bound phycobilisome complexes.Energy transfer from Fremyella diplosiphon phycobiliproteins to chlorophyll a of reaction centers I and 1 1 was measured in: (i) complexes containing intact thylakoids of the cyanophytes F. diplosiphon or A m -
Effects of melittin on expressions of mitochondria membrane protein 7A6, cell apoptosis-related gene products Fas and Fas Ligand in hepatocarcinoma cells (2007)

The effects of melittin in inducing hepatocarcinoma cell apoptosis may be related with up-regulating the expressions of mitochondria membrane protein 7A6 and Fas protein.
Equivalent Circuit Models and Optimization of a Split-Ring Resonator Lattice. (2016)

Abstract not provided.
Identification of the glmU gene encoding N-acetylglucosamine-1-phosphate uridyltransferase in Escherichia coli (1993)

The physiological properties of the EcoURF-1 open reading frame, which precedes the glmS gene at 84 min on the Escherichia coli chromosome (J. E. Walker, N. J. Gay, M. Saraste, and A. N. Eberle, Biochem. J. 224:799-815, 1984), were investigated. A thermosensitive conditional mutant in which the synthesis of the gene product was impaired at 43 degrees C was constructed. The inactivation of the gene in exponentially growing cells rapidly inhibited peptidoglycan synthesis. As a result, various alterations of cell shape were observed, and cell lysis finally occurred when the peptidoglycan content was 37% lower than that of normally growing cells. Analysis of the pools of peptidoglycan precursors revealed a large accumulation of N-acetylglucosamine-1-phosphate and the concomitant depletion of the pools of the seven peptidoglycan nucleotide precursors located downstream in the pathway, a result indicating that the mutational block was in the step leading from N-acetylglucosamine-1-phosphate and UTP to the formation of UDP-N-acetylglucosamine. In vitro assays showed that the overexpression of this gene in E. coli cells, directed by appropriate plasmids, led to a high overproduction (from 25- to 410-fold) of N-acetylglucosamine-1-phosphate uridyltransferase activity. This allowed us to purify this enzyme to homogeneity in only two chromatographic steps. The gene for this enzyme, which is essential for peptidoglycan and lipopolysaccharide biosyntheses, was designated glmU.
Alkali‐modified soy proteins: Effect of salts and disulfide bond cleavage on adhesion and viscosity (1996)

Abstract Soy protein isolates were treated with NaCl, Na 2 SO 4 , or Na 2 SO 3 (disulfide bond‐cleaving agent) at a pH of 10.0 and 50°C, and the effects of these salts on viscosity, adhesive strength on woods, and water resistance of the treated isolates were investigated. Viscosity and adhesive strength decreased with increasing concentrations of these salts. At a concentration of 0.1 M, these three salts reduced the viscosity of soy proteins with no significant adverse effects on adhesive strength and water resistance. Addition of 0.1 M NaCl, Na 2 SO 4 , or Na 2 SO 3 reduced adhesive strength insignificantly from 1230 N to 1120, 1060, or 1013 N, respectively. The viscosity of protein isolate modified at pH 10.0 and 50°C in the absence of salts was &gt;30,000 cP. Treatment with NaCl or Na 2 SO 4 resulted in viscosity reductions to 6000 or 1050 cP, respectively. The Na 2 SO 3 treatment yielded an isolate with the lowest viscosity of 110 cP and which retained adhesive and water‐resistive properties. The water resistance of modified soy proteins with and without 0.1 M Na 2 SO 3 treatment was not significantly different with 3.3 and 6.6% cumulative delaminations occurring after four water soaking cycles. Treatment with 0.1 M Na 2 SO 3 resulted in an isolate with a 28% decrease in disulfide linkages.
Leukocyte Ig-like Receptor B4 (LILRB4) Is a Potent Inhibitor of FcγRI-mediated Monocyte Activation via Dephosphorylation of Multiple Kinases (2009)

The leukocyte immunoglobulin-like receptor (LILR) B4 belongs to a family of cell surface receptors that possesses cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIMs). LILRB4 is believed to down-regulate activation signals mediated by non-receptor tyrosine kinase cascades through the recruitment of SHP-1. However, the exact mechanisms of LILRB4-mediated inhibition are not fully elucidated. In this study, we demonstrate high level surface expression of LILRB4 on THP-1 cells and primary peripheral blood monocytes, which profoundly inhibited production of a key pro-inflammatory cytokine (TNFalpha) induced by FcgammaRI (CD64). We also report that LILRB4 aggregated to sites of activation upon co-ligation with CD64 and that this may enhance its inhibitory effects. Cross-linking of CD64 on THP-1 cells markedly increased phosphorylation of multiple proteins including tyrosine kinases and signaling molecules (Lck, Syk, LAT, and Erk), an adaptor protein that targets protein-tyrosine kinases for degradation (c-Cbl) and a protein involved in the formation of actin cytoskeletal rearrangement (alpha-actinin-4). Co-ligation of LILRB4 considerably reduced CD64-mediated phosphorylation of Lck, Syk, LAT, Erk, and c-Cbl but not alpha-actinin-4, suggesting selective inhibition of signaling molecules. Treatment of cells with a broad-spectrum phosphatase inhibitor, sodium pervanadate (SP), significantly reversed LILRB4-mediated inhibition of TNFalpha production and protein tyrosine phosphorylation. In comparison, treatment with an SHP-1 specific inhibitor, sodium stibogluconate (SS) has no effects indicating involvement of phosphatase(s) other than SHP-1 in LILRB4 signaling. Collectively, our data show LILRB4 is a potent inhibitor of monocytes activation. This may provide a new potential therapeutic strategy for inflammatory conditions characterized by excessive TNFalpha production.
27.5L: Late‐News Paper: Multiphoton Organic EL device having Charge Generation Layer (2003)

Abstract Novel structure of Multiphoton Emission (MPE) organic EL (OEL) device capable of exceeding 100% quantum efficiency was fabricated. The principle of the device is that a plurality of conventional OEL structure (emissive unit) are stacked and divided by Charge Generation Layer (CGL) that works as an injector of electron‐hole pair upon voltage application. Tripled stacked MPE successfully achieved 48 cd/A for the emission from fluorescent green dye coumarin C545T.
Sensory Neuropathy Attributable to Loss of Bcl-w (2011)

Small fiber sensory neuropathy is a common disorder in which progressive degeneration of small-diameter nociceptors causes decreased sensitivity to thermal stimuli and painful sensations in the extremities. In the majority of patients, the cause of small fiber sensory neuropathy is unknown, and treatment options are limited. Here, we show that Bcl-w (Bcl-2l2) is required for the viability of small fiber nociceptive sensory neurons. Bcl-w(-/-) mice demonstrate an adult-onset progressive decline in thermosensation and a decrease in nociceptor innervation of the epidermis. This denervation occurs without cell body loss, indicating that lack of Bcl-w results in a primary axonopathy. Consistent with this phenotype, we show that Bcl-w, in contrast to the closely related Bcl-2 and Bcl-xL, is enriched in axons of sensory neurons and that Bcl-w prevents the dying back of axons. Bcl-w(-/-) sensory neurons exhibit mitochondrial abnormalities, including alterations in axonal mitochondrial size, axonal mitochondrial membrane potential, and cellular ATP levels. Collectively, these data establish bcl-w(-/-) mice as an animal model of small fiber sensory neuropathy and provide new insight regarding the role of Bcl-w and of mitochondria in preventing axonal degeneration.
The Development of Methane Production in Childhood and Adolescence (1985)

Methane concentration in the expired air was analyzed in 393 infants, children, and adolescents. There was no methane production below the age of 3 years. In the age group 3-4 years, 6.4% of the children produced methane. The percentages were 14.3-18.2% in children aged 7-14. A rise in methane production to 39.4-45.9% was recorded from age 14 to 18, as compared with 49.4% in adults in Israel. The reasons for these changes in methane production with age are not known. Alterations in the colonic flora or the production of a specific substrate(s) are the main possibilities. In our opinion, the latter possibility deserves further investigation.