gebhart/patrepeval huggingface dataset:
Phosphorescent top-emitting organic light-emitting devices with improved light outcoupling (2003)

A dielectric capping layer has been used to increase the light output and to tune the spectral characteristics of top-emitting, phosphorescent organic light-emitting devices (OLEDs). By controlling the thickness of the dielectric layer deposited on top of a thin metal cathode, the transmittance of the top electrode can be adjusted. Maximum light output is not achieved at highest cathode transmittance, indicating that the interplay between different interference effects can be controlled by means of the capping-layer thickness. Furthermore, we demonstrate that the electrical device characteristic is not influenced by the capping layer. The strength of our concept in particular lies in the fact that the optical and the electrical device performance can be optimized separately. Using the capping-layer concept, we have achieved an OLED efficiency of 64 cd/A with pure green emission.
Nitric oxide synthase, cyclooxygenase 2, and vascular endothelial growth factor in the angiogenesis of non-small cell lung carcinoma. (2000)

We have investigated the hypothesis that nitric oxide synthase (NOS2), cyclooxygenase-2 (COX2), and vascular endothelial growth factor (VEGF) protein levels individually demonstrate a direct correlation with microvessel density (MVD) and clinical outcome in human non-small cell lung cancer (NSCLC). Furthermore, we hypothesized that MVD may explain the propensity of certain histological lung cancer subtypes for early metastasis via a hematological route. Immunohistochemically, we studied the protein expression levels of NOS2, COX2, and VEGF and MVD by counting CD31-reactive blood vessels (BVs) in 106 surgically resected NSCLC specimens. NOS2, COX2, and VEGF immunoreactivity were observed in 48, 48, and 58%, respectively, of the study subjects, and their levels correlated with MVD at the tumor-stromal interphase (P < or = 0.001). More adenocarcindmas and large cell carcinomas displayed overexpression of NOS2 when compared with squamous cell carcinoma (SCC; r = 0.44; P < 0.001). NOS2 and COX2 levels were found to correlate positively with VEGF status (r = 0.44; P < 0.001, 0.01, and 0.03, respectively). These results attest to the significant interaction of these factors in the angiogenesis of NSCLC. Although neither angiogenic factors nor MVD correlated with patient survival, the latter correlated with tumor clinical stage in both squamous (SCC; 73 BVs/mm2) and non-SCC (78 BVs/mm2) tumors. These results indicate that angiogenesis is a complex process that involves multiple factors including NOS2, COX2, and VEGF. Furthermore, the role of angiogenesis in the biology of various histological lung cancer types may be different. The complexity of angiogenesis may explain the modest results observed in antiangiogenesis therapy that target a single protein.
Technique for controlling effective Vth in multi-Gbit DRAM sense amplifier (2002)

We propose the use of a capacitor couple structure to control the effective threshold voltage (Vth) and its application to Vth fluctuation compensation in flip-flop sense amplifiers for multi-gigabit DRAMs. Our proposed sense amplifier functions correctly at up to a 500 mV fluctuation in Vth for the transistor pair in the latch. It does not require extra charging time in the sensing operation for compensation. In addition, the sense-amplifier speed is independent of the Vth value, so our S/A can also compensate the sensing speed fluctuation. This Vth control method and Vth-compensated sense amplifier opens up the possibility of utilizing transistors with gate lengths of less than 0.1 /spl mu/m, where the Vth variations could not be reduced.
Quorum Sensing in Staphylococcus aureus Biofilms (2004)

Several serious diseases are caused by biofilm-associated Staphylococcus aureus, infections in which the accessory gene regulator (agr) quorum-sensing system is thought to play an important role. We studied the contribution of agr to biofilm development, and we examined agr-dependent transcription in biofilms. Under some conditions, disruption of agr expression had no discernible influence on biofilm formation, while under others it either inhibited or enhanced biofilm formation. Under those conditions where agr expression enhanced biofilm formation, biofilms of an agr signaling mutant were particularly sensitive to rifampin but not to oxacillin. Time lapse confocal scanning laser microscopy showed that, similar to the expression of an agr-independent fluorescent reporter, biofilm expression of an agr-dependent reporter was in patches within cell clusters and oscillated with time. In some cases, loss of fluorescence appeared to coincide with detachment of cells from the biofilm. Our studies indicate that the role of agr expression in biofilm development and behavior depends on environmental conditions. We also suggest that detachment of cells expressing agr from biofilms may have important clinical implications.
RF1 attenuation enables efficient non-natural amino acid incorporation for production of homogeneous antibody drug conjugates (2017)

Amber codon suppression for the insertion of non-natural amino acids (nnAAs) is limited by competition with release factor 1 (RF1). Here we describe the genome engineering of a RF1 mutant strain that enhances suppression efficiency during cell-free protein synthesis, without significantly impacting cell growth during biomass production. Specifically, an out membrane protease (OmpT) cleavage site was engineered into the switch loop of RF1, which enables its conditional inactivation during cell lysis. This facilitates extract production without additional processing steps, resulting in a scaleable extract production process. The RF1 mutant extract allows nnAA incorporation at previously intractable sites of an IgG1 and at multiple sites in the same polypeptide chain. Conjugation of cytotoxic agents to these nnAAs, yields homogeneous antibody drug conjugates (ADCs) that can be optimized for conjugation site, drug to antibody ratio (DAR) and linker-warheads designed for efficient tumor killing. This platform provides the means to generate therapeutic ADCs inaccessible by other methods that are efficient in their cytotoxin delivery to tumor with reduced dose-limiting toxicities and thus have the potential for better clinical impact.
From chemoprevention to chemotherapy: common targets and common goals (2004)

Three decades of research have revealed that cancer is easier to prevent than to treat and that consumption of certain fruits and vegetables can reduce the risk of cancer. Whereas chemotherapy is designed to destroy cancer after it appears, chemoprevention involves the abrogation or delay in the onset of cancer. Regardless of whether a chemopreventive or chemotherapeutic approach is taken, cancer is a multifactorial disease that requires modulation of multiple pathways and multiple targets. Various molecular targets of chemoprevention are also relevant to the therapy of cancer. These targets include the activation of apoptosis; suppression of growth factor expression or signalling; downregulation of antiapoptotic proteins; suppression of phosphatidylinositol-3'-kinase/Akt, NF-kappaB, Janus kinase-signal transducer and activator of transcription and activator protein-1 signalling pathways; and downregulation of angiogenesis through inhibition of vascular endothelial growth factor expression, cyclooxygenase-2, matrix metalloproteinase-9, urokinase-type plasminogen activator, adhesion molecules and cyclin D1. Pharmacologically safe phytochemicals that have been identified from plants or their variant forms can modulate these molecular targets. These phytochemicals include genistein, resveratrol, dially sulfide, S-ally cysteine, allicin, lycopene, capsaicin, curcumin, 6-gingerol, ellagic acid, ursolic acid, betulinic acid, flavopiridol, silymarin, anethol, catechins and eugenol. Recent work has shown that these phytochemicals also can reverse chemoresistance and radioresistance. Because of their pharmacological safety, these agents can be used alone to prevent cancer and in combination with chemotherapy to treat cancer.
C3d of Complement as a Molecular Adjuvant: Bridging Innate and Acquired Immunity (1996)

An optimal immune response should differentiate between harmful and innocuous antigens. Primitive systems of innate immunity, such as the complement system, may play a role in this distinction. When activated, the C3 component of complement attaches to potential antigens on microorganisms. To determine whether this alters acquired immune recognition, mice were immunized with a recombinant model antigen, hen egg lysozyme (HEL), fused to murine C3d. HEL bearing two and three copies of C3d was 1000- and 10,000-fold more immunogenic, respectively, than HEL alone. Thus, C3d is a molecular adjuvant of innate immunity that profoundly influences an acquired immune response.
Effects of human chromosome 12 on interactions between Tat and TAR of human immunodeficiency virus type 1 (1994)

Rates of transcriptions of the human immunodeficiency virus are greatly increased by the viral trans activator Tat. In vitro, Tat binds to the 5' bulge of the trans-activation response (TAR) RNA stem-loop, which is present in all viral transcripts. In human cells, the central loop in TAR and its cellular RNA-binding proteins are also critical for the function of Tat. Previously, we demonstrated that in rodent cells (CHO cells), but not in those which contain the human chromosome 12 (CHO12 cells), Tat-TAR interactions are compromised. In this study, we examined the roles of the bulge and loop in TAR in Tat trans activation in these cells. Whereas low levels of trans activation depended solely on interactions between Tat and the bulge in CHO cells, high levels of trans activation depended also on interactions between Tat and the loop in CHO12 cells. Since the TAR loop binding proteins in these two cell lines were identical and different from their human counterpart, the human chromosome 12 does not encode TAR loop binding proteins. In vivo binding competition studies with TAR decoys confirmed that the binding of Tat to TAR is more efficient in CHO12 cells. Thus, the protein(s) encoded on human chromosome 12 helps to tether Tat to TAR via its loop, which results in high levels of trans activation.
Synthesis, Stereochemical, and Conformational Studies of Selected 3,7-Diheterabicyclo[3.3.1]nonan-9-ols: X-Ray Diffraction Analyses of 7-Benzyl-9-phenyl-3-oxa-7-azabicyclo[3.3.1]nonan-9-ol and 7-Benzyl-9-(4-N,N′-dimethylaminophenyl)-3-thia-7-azabicyclo[3.3.1]nonan-9-ol, a Rare Stable Chair–Boat Form With Trigonal Nitrogen (2006)

A systematic study of 1,2-additions to 3,7-diheterabicyclo[3.3.1]nonan-9-ones (3,7-DHBCN-9-ONES) by symmetrically substituted aryl Grignard reagents in anhydrous THF or ether has been conducted. 1,2-Additions of aryl Grignard reagents to the carbonyl group at C-9 in 7-benzyl-3-oxa-7-azabicyclo[3.3.1]nonan-9-one and 7-benzyl-3-thia-7-azabicyclo[3.3.1]nonan-9-one resulted in the formation of tertiary alcohols with the aryl group “syn” to the oxygen or sulfur atoms in the respective rings. The X-ray analyses demonstrated that the solid, bicyclic, oxygen-containing alcohol was in chair–chair form while the solid, bicyclic, sulfur-containing alcohol existed in chair–boat form. A tentative mechanism is that the Grignard reagent may coordinate with the oxygen atom and / or sulfur atom in a boat conformer of the bicyclic system prior to the attack from the “oxygen or sulfur sides.”
Test Cases for HMAC-MD5 and HMAC-SHA-1 (1997)

This document provides two sets of test cases for HMAC-MD5 and HMAC-SHA-1, respectively. HMAC-MD5 and HMAC-SHA-1 are two constructs of the HMAC [HMAC] message authentication function using the MD5 [MD5] hash function and the SHA-1 [SHA] hash function. Both constructs are used by IPSEC [OG,CG] and other protocols to authenticate messages. The test cases and results provided in this document are meant to be used as a conformance test for HMAC-MD5 and HMAC-SHA-1 implementations.
Escherichia coli YqhD Exhibits Aldehyde Reductase Activity and Protects from the Harmful Effect of Lipid Peroxidation-derived Aldehydes (2008)

Evidence that Escherichia coli YqhD is involved in bacterial response to compounds that generate membrane lipid peroxidation is presented. Overexpression of yqhD results in increased resistance to the reactive oxygen species-generating compounds hydrogen peroxide, paraquat, chromate, and potassium tellurite. Increased tolerance was also observed for the lipid peroxidation-derived aldehydes butanaldehyde, propanaldehyde, acrolein, and malondialdehyde and the membrane-peroxidizing compound tert-butylhydroperoxide. Expression of yqhD was also associated with changes in the concentration of intracellular peroxides and cytoplasmic protein carbonyl content and with a reduction in intracellular acrolein levels. When compared with the wild type strain, an yqhD mutant exhibited a sensitive phenotype to all these compounds and also augmented levels of thiobarbituric acid-reactive substances, which may indicate an increased level of lipid peroxidation. Purified YqhD catalyzes the in vitro reduction of acetaldehyde, malondialdehyde, propanaldehyde, butanaldehyde, and acrolein in a NADPH-dependent reaction. Finally, yqhD transcription was induced in cells that had been exposed to conditions favoring lipid peroxidation. Taken together these results indicate that this enzyme may have a physiological function by protecting the cell against the toxic effect of aldehydes derived from lipid oxidation. We speculate that in Escherichia coli YqhD is part of a glutathione-independent, NADPH-dependent response mechanism to lipid peroxidation.
Expression of CD44 Variants in Lung Cancer and Its Relationship to Hyaluronan Binding (2000)

We examined the expression of CD44 variant forms and their binding to hyaluronan (HA) in lung cancer cell lines. There was no relationship between the level of expression of CD44 variants and HA binding in different lung cancer cell lines. The expression of CD44v6 and CD44E in some cell lines was not always associated with HA binding. There was no relationship between the tissue pathological type and CD44 expression or HA binding. Deglycosylation by neuraminidase induced CD44-HA binding in human lung cancer cell lines. Our findings suggest that the HA binding ability of CD44, which is negatively regulated by glycosylation, might be a more important factor in tumorigenesis or metastasis than the expression of CD44 variant forms.
Histone deacetylase inhibitors: a new class of immunosuppressors targeting a novel signal pathway essential for CD154 expression (2003)

Here we report that histone deacetylase inhibitors (HDAC-i) comprise a new class of immunosuppressive agents. HDAC-i inhibited CD4 T-cell proliferation in a dose-dependent manner, which was not caused by apoptosis or decreased viability. Although early intracellular signals such as tyrosine kinase activity and elevation of intracellular calcium concentration were not affected, the characteristic aggregation of T cells following activation was completely abrogated. This correlated with diminished activation-induced expression of the adhesion molecules. HDAC-i furthermore inhibited activation-induced CD25 and CD154 expression on CD4 cells, without affecting induction of CD69. HDAC-i inhibited CD154 expression by a mechanism distinctly different from cyclosporine-mediated inhibition. HDAC-i thus inhibited interleukin 2 (IL-2)-induced CD154 expression on effector T cells and constitutively expressed CD154 on various tumor cells, events that were not affected by cyclosporine. Additional studies showed that HDAC-i treatment inhibited c-Myc expression, which was further shown to be important for CD154 gene activation. These results demonstrate pronounced T-cell inhibitory activity of HDAC-i, which may form the basis of novel therapeutic interventions against autoimmune diseases and allograft rejection.
Single-scan dual-tracer FLT+FDG PET tumor characterization (2013)

Rapid multi-tracer PET aims to image two or more tracers in a single scan, simultaneously characterizing multiple aspects of physiology and function without the need for repeat imaging visits. Using dynamic imaging with staggered injections, constraints on the kinetic behavior of each tracer are applied to recover individual-tracer measures from the multi-tracer PET signal. The ability to rapidly and reliably image both (18)F-fluorodeoxyglucose (FDG) and (18)F-fluorothymidine (FLT) would provide complementary measures of tumor metabolism and proliferative activity, with important applications in guiding oncologic treatment decisions and assessing response. However, this tracer combination presents one of the most challenging dual-tracer signal-separation problems--both tracers have the same radioactive half-life, and the injection delay is short relative to the half-life and tracer kinetics. This work investigates techniques for single-scan dual-tracer FLT+FDG PET tumor imaging, characterizing the performance of recovering static and dynamic imaging measures for each tracer from dual-tracer datasets. Simulation studies were performed to characterize dual-tracer signal-separation performance for imaging protocols with both injection orders and injection delays of 10-60 min. Better performance was observed when FLT was administered first, and longer delays before administration of FDG provided more robust signal-separation and recovery of the single-tracer imaging measures. An injection delay of 30 min led to good recovery (R > 0.96) of static image values (e.g. SUV), K(net), and K(1) as compared to values from separate, single-tracer time-activity curves. Recovery of higher order rate parameters (k(2), k(3)) was less robust, indicating that information regarding these parameters was harder to recover in the presence of statistical noise and dual-tracer effects. Performance of the dual-tracer FLT(0 min)+FDG(32 min) technique was further evaluated using PET/CT imaging studies in five patients with primary brain tumors where the data from separate scans of each tracer were combined to synthesize dual-tracer scans with known single-tracer components; results demonstrated similar dual-tracer signal recovery performance. We conclude that rapid dual-tracer FLT+FDG tumor imaging is feasible and can provide quantitative tumor imaging measures comparable to those from conventional separate-scan imaging.
Criteria for standardization of pH measurements in organic solvents and water + organic solvent mixtures of moderate to high permittivities (1985)

Abstract
Serum C‐reactive protein levels predict survival in hepatocellular carcinoma (2007)

The prognosis of H-CRP-positive patients was poorer compared with H-CRP-negative patients. This study confirmed that H-CRP, like CRP, is a marker of poor prognosis in HCC patients.
Medium‐chain fatty acids stimulate interleukin‐8 production in Caco‐2 cells with different mechanisms from long‐chain fatty acids1 (2001)

These findings suggest that not only OA but also CA stimulates IL-8 production in intestinal epithelial cells, and the mechanisms of action differ between OA and CA.
Compensation of spectral and RF errors in swept-source OCT for high extinction complex demodulation (2015)

We provide a framework for compensating errors within passive optical quadrature demodulation circuits used in swept-source optical coherence tomography (OCT). Quadrature demodulation allows for detection of both the real and imaginary components of an interference fringe, and this information separates signals from positive and negative depth spaces. To achieve a high extinction (∼60 dB) between these positive and negative signals, the demodulation error must be less than 0.1% in amplitude and phase. It is difficult to construct a system that achieves this low error across the wide spectral and RF bandwidths of high-speed swept-source systems. In a prior work, post-processing methods for removing residual spectral errors were described. Here, we identify the importance of a second class of errors originating in the RF domain, and present a comprehensive framework for compensating both spectral and RF errors. Using this framework, extinctions >60 dB are demonstrated. A stability analysis shows that calibration parameters associated with RF errors are accurate for many days, while those associated with spectral errors must be updated prior to each imaging session. Empirical procedures to derive both RF and spectral calibration parameters simultaneously and to update spectral calibration parameters are presented. These algorithms provide the basis for using passive optical quadrature demodulation circuits with high speed and wide-bandwidth swept-source OCT systems.
Ia expression by vascular endothelium is inducible by activated T cells and by human gamma interferon. (1983)

We have used monoclonal antibody binding, measured by radioimmunoassay, fluorescence flow cytometry, and ultrastructural immunocytochemistry, to measure expression of Ia antigens on cultured human umbilical vein endothelial (HUVE) cells. Under standard culture conditions, HUVE cells do not express Ia antigens. However, treatment of primary HUVE cultures with phytohemagglutinin induces the expression of Ia antigens. Every endothelial cell in the culture becomes Ia-positive and endothelial cells appear to synthesize Ia. HLA-A,B is concomitantly increased. The expression of Ia appears to be mediated by T cells because (a) pretreatment of primary HUVE cultures with OKT3 plus complement blocks the action of the lectins but not of medium conditioned by lectin-activated peripheral blood mononuclear cells; (b) co-culture of endothelial cells with allogeneic T cells, in the absence of lectin, also induces endothelial Ia; and (c) human immune (gamma) interferon, produced by Chinese hamster ovary cells transfected with the human gamma interferon gene, directly induces endothelial Ia. During co-culture with lymphocytes, about one-third of the endothelial cells are Ia-positive after 24 h and all of the endothelial cells are Ia-positive by 72 h. Proliferation of allogeneic T cells starts by 96 h and peaks at 144 h. Thus, endothelial Ia appears sufficiently early to be a determinant for the proliferation of allogeneic T cells. Inducible expression of Ia by endothelium may be important both for allograft rejection and for recruitment of circulating T cells into the site of an immune response.
Influence of Age, Diabetes, and Cataract on Calcium, Lipid-Calcium, and Protein-Calcium Relationships in Human Lenses (2003)

The data support the hypothesis that increased intracellular calcium concentrations and a diminished capacity of lens lipids to bind to calcium initiate a cascade of events that culminates in increased light-scattering from lipids and especially proteins. Calcium binding to lipid membranes cannot directly contribute to light-scattering in cataractous lenses. It has been suggested that most of the diffusible calcium in the lens is in the intercellular spaces and that lens lipids in the outer leaflet of the bilayer bind to that calcium. If so, this could account for the 150-fold difference between free and bound calcium levels in the lens.