gebhart/patrepeval huggingface dataset:
Mutations in the Endodomain of Sindbis Virus Glycoprotein E2 Define Sequences Critical for Virus Assembly (2006)

ABSTRACT Envelopment of Sindbis virus at the plasma membrane is a multistep process in which an initial step is the association of the E2 protein via a cytoplasmic endodomain with the preassembled nucleocapsid. Sindbis virus is vectored in nature by blood-sucking insects and grows efficiently in a number of avian and mammalian vertebrate hosts. The assembly of Sindbis virus, therefore, must occur in two very different host cell environments. Mammalian cells contain cholesterol which insect membranes lack. This difference in membrane composition may be critical in determining what requirements are placed on the E2 tail for virus assembly. To examine the interaction between the E2 tail and the nucleocapsid in Sindbis virus, we have produced substitutions and deletions in a region of the E2 tail (E2 amino acids 408 to 415) that is initially integrated into the endoplasmic reticulum. This sequence was identified as being critical for nucleocapsid binding in an in vitro peptide protection assay. The effects of these mutations on virus assembly and function were determined in both vertebrate and invertebrate cells. Amino acid substitutions (at positions E2: 408, 410, 411, and 413) reduced infectious virus production in a position-dependent fashion but were not efficient in disrupting assembly in mammalian cells. Deletions in the E2 endodomain (Δ406-407, Δ409-411, and Δ414-417) resulted in the failure to assemble virions in mammalian cells. Electron microscopy of BHK cells transfected with these mutants revealed assembly of nucleocapsids that failed to attach to membranes. However, introduction of these deletion mutants into insect cells resulted in the assembly of virus-like particles but no assayable infectivity. These data help define protein interactions critical for virus assembly and suggest a fundamental difference between Sindbis virus assembly in mammalian and insect cells.
Cell-type specific potent Wnt signaling blockade by bispecific antibody (2018)

Cell signaling pathways are often shared between normal and diseased cells. How to achieve cell type-specific, potent inhibition of signaling pathways is a major challenge with implications for therapeutic development. Using the Wnt/β-catenin signaling pathway as a model system, we report here a novel and generally applicable method to achieve cell type-selective signaling blockade. We constructed a bispecific antibody targeting the Wnt co-receptor LRP6 (the effector antigen) and a cell type-associated antigen (the guide antigen) that provides the targeting specificity. We found that the bispecific antibody inhibits Wnt-induced reporter activities with over one hundred-fold enhancement in potency, and in a cell type-selective manner. Potency enhancement is dependent on the expression level of the guide antigen on the target cell surface and the apparent affinity of the anti-guide antibody. Both internalizing and non-internalizing guide antigens can be used, with internalizing bispecific antibody being able to block signaling by all ligands binding to the target receptor due to its removal from the cell surface. It is thus feasible to develop bispecific-based therapeutic strategies that potently and selectively inhibit signaling pathways in a cell type-selective manner, creating opportunity for therapeutic targeting.
Potent mitochondria-targeted peptides reduce myocardial infarction in rats (2007)

This study shows that pretreatment with both SS-31 and SS-20 significantly reduced myocardial lipid peroxidation and infarct size in ischemia-reperfusion injury, and suggests that the cardioprotective properties of 2',6'-dimethyl-tyrosine-D-Arg-Phe-Lys-NH2 was primarily mediated by its antioxidant properties. As SS-20 does not scavenge reactive oxygen species, it most likely reduces reactive oxygen species production during ischemia-reperfusion.
Glow: Generative Flow with Invertible 1x1 Convolutions (2018)

Flow-based generative models (Dinh et al., 2014) are conceptually attractive due to tractability of the exact log-likelihood, tractability of exact latent-variable inference, and parallelizability of both training and synthesis. In this paper we propose Glow, a simple type of generative flow using an invertible 1x1 convolution. Using our method we demonstrate a significant improvement in log-likelihood on standard benchmarks. Perhaps most strikingly, we demonstrate that a generative model optimized towards the plain log-likelihood objective is capable of efficient realistic-looking synthesis and manipulation of large images. The code for our model is available at https://github.com/openai/glow
The glioblastoma‐derived t cell suppressor factor/ transforming growth factor‐β2 inhibits t cell growth without affecting the interaction of interleukin 2 with its receptor (1988)

Human glioblastoma cells secrete a peptide termed glioblastoma-derived T cell suppressor factor (G-TsF) which inhibits T cell activation. Recently, purification and cloning of G-TsF revealed that G-TsF is identical to transforming growth factor-beta 2. As shown here, G-TsF suppresses the growth of an ovalbumin-specific mouse T helper cell clone (OVA-7T) independently of the stimulus used being either (a) antigen in the presence of antigen-presenting cells, or (b) interleukin 2 (IL2) or (c) phorbol ester and calcium ionophore. Furthermore, in the presence of antibodies against IL2 receptors, G-TsF was able to suppress the residual proliferation still observed when OVA-7T were stimulated with phorbol ester/ionophore. G-TsF failed to inhibit the release of IL3 from OVA-7T activated with IL2. Taken together, the data provide evidence that G-TsF does not directly interfere with interactions of IL2 with its receptor but rather inhibits T cell activation by interfering with an as yet unidentified pathway used by both IL2 and phorbol ester/ionophore. When analyzing different monokines and lymphokines for its effect on G-TsF-induced suppression of T cell growth the only factor found to partially neutralize the effect of G-TsF was tumor necrosis factor-alpha.
Injection of a dopamine antagonist into Holstein steers to relieve symptoms of fescue toxicosis. (1997)

Two experiments were conducted to determine whether administering a dopamine antagonist to steers fed endophyte-infected (E+) tall fescue would increase serum prolactin (PRL) and reduce rectal temperature. Steers in both experiments were housed in environmentally controlled chambers (32 degrees C; 50% relative humidity). In Exp. 1, 10 steers were allotted randomly to receive s.c. injections of either 0, .006, .03, or .06 mg of Ro 24-0409 (dopamine antagonist)/kg BW. The experiment was designed in four phases: endophyte-free seed (E-) without antagonist (d -11 to 0); E- with antagonist (d 0 to 7); E+ with antagonist (d 7 to 28); E+ without antagonist (d 28 to 38). In Exp. 2, 22 Holstein steers were allotted randomly to the same treatments and design, except three steers were maintained on E- without antagonist. Steers were fed individually with intakes measured daily. In Exp. 1, feed intake and rectal temperature were not improved (P > .05) by antagonist injection. In Exp. 2, antagonist injections increased (P < .05) PRL. Ingestion of E+ decreased (P < .05) feed intake and serum PRL. Antagonist injection decreased (P < .05) rectal temperature and increased (P < .05) serum PRL.
A high performance cabac decoding architecture (2005)

In this paper, we propose a high performance hardware architecture of CABAC decoder CABAC is the context adaptive binary arithmetic coding used in H.264/AVC video standard, which achieves significant compression enhancement while bringing greater complexity and costs in implementation. The necessity of hardware implementation for real-time CABAC decoders is introduced, and then a fast and cost effective architecture is proposed. The new architecture can achieve decoding speed of averagely 500 cycles/macroblock, for typical 4M bit stream of DI resolution, 30 frame/s. An ASIC implementation of the new architecture is carried out in a 0.18 /spl mu/m silicon technology. The estimated area is 0.3 mm/sub 2/ and the critical path is limited within 6.7 ns.
A Low Power Phase-Change Random Access Memory using a Data-Comparison Write Scheme (2007)

A low power PRAM using a data-comparison write (DCW) scheme is proposed. The PRAM consumes large write power because large write currents are required during long time. At first, the DCW scheme reads a stored data during write operation. And then, it writes an input data only when the input and stored data are different. Therefore, it can reduce the write power consumption to a half. The 1K-bit PRAM test chip with 128×8bits is implemented with a 0.8μm CMOS technology with a 0.5μm GST cell.
Near-capacity dirty-paper code designs based on TCQ and IRA codes (2005)

This paper addresses near-capacity dirty-paper code designs based on TCQ and IRA codes, where the former is employed as the most efficient means of vector quantization and the latter for their capacity-approaching performance. By bringing together TCQ - the best quantizer from the source coding community and EXIT chart based IRA code designs - the best from the channel coding community, we are able to approach the theoretical limit of dirty-paper coding. For example, at 0.25 b/s, one of our code designs (with 1024-state TCQ) performs 0.83 dB away from the capacity
Anti‐PrP antibodies block PrPSc replication in prion‐infected cell cultures by accelerating PrPC degradation (2004)

The use of anti-PrP antibodies represents one of the most promising strategies for the treatment of prion diseases. In the present study, we screened various anti-PrP antibodies with the aim of identifying those that would block PrP(Sc) replication in prion-infected cell culture. Two antibodies, SAF34 recognizing the flexible octarepeats region on HuPrP protein, and SAF61 directed against PrP amino acid residues (144-152), not only inhibited PrP(Sc) formation in prion-infected neuroblastoma cells but also decreased the PrP(C) levels in non-infected N2a cells. In addition, treatment with both SAF34 and SAF61 antibodies decreased PrP(C) and PrP(Sc) levels in the cells synergistically. In the presence of both antibodies, our results showed that the mode of action which leads to the disappearance of PrP(Sc) in cells is directly coupled to PrP(C) degradation by reducing the half-life of the PrP(C) protein.
Site-specific N-terminal labelling of proteinsin vitro and in vivo using N-myristoyl transferase and bioorthogonal ligation chemistry (2007)

N-Myristoyl transferase-mediated modification with azide-bearing substrates is introduced as a highly selective and practical method for in vitro and in vivo N-terminal labelling of a recombinant protein using bioorthogonal ligation chemistry.
Epstein–Barr Virus Infection (2000)

The Epstein–Barr virus (EBV) was discovered 36 years ago by electron microscopy of cells cultured from Burkitt's lymphoma tissue by Epstein, Achong, and Barr.1 Four years later, in 1968, EBV was shown to be the etiologic agent of heterophile-positive infectious mononucleosis.2 EBV DNA was detected in tissues from patients with nasopharyngeal carcinoma in 1970.3 In the 1980s, EBV was found to be associated with non-Hodgkin's lymphoma and oral hairy leukoplakia in patients with the acquired immunodeficiency syndrome (AIDS).4,5 Since then, EBV DNA has been found in tissues from other cancers, including T-cell lymphomas and Hodgkin's disease.6,7 EBV is . . .
Pax-2, kidney development, and oncogenesis (1996)

The development of a complex tissue from a few simple precursor cells requires the precise activation and repression of tissue-specific genes that determine cell lineages, tissue patterning, and cellular proliferation. In the kidney, a number of recently identified genes are critical for normal development. Among these, the Pax-2 gene encodes a transcription factor that is expressed in the ureter bud, in the induced kidney mesenchyme, and in the progenitor cells of the glomerular and tubular epithelium. Although the differentiation of the renal epithelium requires Pax-2 function, failure to suppress the gene in mature epithelium is detrimental to normal renal function. Recent, data suggest that the Wilms' tumor-suppressor gene WT1 can down-regulate Pax-2 expression, consistent with high levels of Pax-2 in Wilms' tumors. Additional studies suggest that reactivation of this developmental regulator can contribute to a variety of other renal diseases.
A wide variety of DNA sequences can functionally replace a yeast TATA element for transcriptional activation. (1990)

We created a library of DNA molecules in which the required TATA element of a yeast gal-his3 promoter is replaced by random-sequence oligomers averaging 16 bp in length. Surprisingly, 1% of such random sequences functionally replace the native yeast TATA element. In many cases, sequences completely unrelated to the consensus TATA element (TATAAA) stimulate transcription with equal or increased efficiency. Transcription mediated by these synthetic elements requires GAL4 and is initiated from normal his3 initiation sites, suggesting that it occurs by a mechanism indistinguishable from that involving wild-type TATA elements. Many, but not all, of these elements act as substrates for yeast TFIID in reconstituted transcription reactions in vitro. These observations indicate that yeast TFIID can stimulate transcription from TATA elements whose sequences differ from the consensus, and they suggest the possibility of alternative factors that may provide a related function for transcriptional activation.
The clinical utility of HTLV-1 viral load measurement (2011)

High levels of HTLV-1 proviral load in peripheral blood mononuclear cells (PBMCs) have been observed in patients with Adult T-cell Leukaemia Lymphoma (ATLL) and HTLV-1 Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). The proviral load has been reported to fluctuate in both asymptomatic carriers and in symptomatic patients. We aimed to quantify intra-patient variability, to identify “outliers”, and to characterise the range of viral loads in asymptomatic carriers and in patients with HTLV-1-associated diseases.
The extracellular domain of p185/neu is released from the surface of human breast carcinoma cells, SK-BR-3 (1991)

The human breast carcinoma cell line SK-BR-3, expresses the neu oncogene product, p185, which is a receptor tyrosine kinase. Using a double monoclonal antibody capture enzyme-linked immunosorbent assay for p185, activity was detected in conditioned media from cultures of SK-BR-3 cells. Two monoclonal antibodies specific for the extracellular domain of p185/neu immunoprecipitated a protein with a molecular mass of approximately 105 kDa. p105 was further shown to compete with p185 for binding to monoclonal antibodies and pulse-chase experiments indicate that it was generated by post-translational processing. Peptide maps showed that p105 and p185 are related polypeptides. Since p105 is close to the predicted size for the extracellular domain of p185/neu, we propose that SK-BR-3 cells specifically process and release this portion of the receptor into the medium. The release of the extracellular domain may have implications in oncogenesis and its detection could prove useful as a cancer diagnostic.
A wide dynamic range switched-LNA in SiGe BiCMOS (2002)

A wide dynamic range, high current efficient switched-LNA has been developed by using SiGe BiCMOS technology. The low loss RF MOSFET reduced silicon substrate effect at high frequency is used as a bypass switch of LNA. The 800-900 MHz LNA is demonstrated in this work in high gain/low distortion mode for transmitting and receiving simultaneously, the amplifier achieves 15.3 dB gain, 1.4 dB noise figure and +1.6 dBm IIP3 with 5.9 mA DC current. In high gain/low current mode for receiving only, 13.3 dB gain, 1.6 dB noise figure and -0.6 dBm IIP3 are achieved with 3.0 mA. In low gain mode, 1.5 dB insertion loss and +16.1 dBm IIP3 with <10 uA are realized by the bypass switch. The switched-LNA is housed in a very small and low cost SON12 plastic package with a Down-Mixer.
A MAGE-6-encoded peptide is recognized by expanded lymphocytes infiltrating a spontaneously regressing human primary melanoma lesion (1999)

In recent years, experiments based on the in vitro stimulation of either autologous peripheral blood lymphocytes or tumor-infiltrating lymphocytes with melanoma cells have shown that distinct members of the large MAGE gene family encode tumor-associated antigenic peptides. However, little is still known about natural anti-MAGE responses in vivo. We have studied a case of spontaneously regressing human melanoma, hypothesizing that in this unique situation, the host immune system had developed an efficient cytotoxic T lymphocyte (CTL) response against the cancer cells. Amongst the dense tumor infiltrate, certain clonal populations of T cells were shown to be amplified, thereby suggesting that an antigen-driven selection had occurred at the tumor site. One of the expanded tumor-infiltrating lymphocytes was shown to be a Vβ13+ CD8+ CTL displaying a strong and selective cytotoxic activity against the autologous melanoma cells. Here we show that this cytotoxic T cell clone recognizes a MAGE-6-encoded peptide. MAGE-6 is therefore the fourth gene of the MAGE family shown to encode antigenic peptide recognized by T cells. Together, these data provide further evidence that T cell responses against MAGE antigens may naturally develop in vivo.
Blood Markers for the Prognosis of Ischemic Stroke (2009)

Blood biomarkers might provide useful information to improve the prediction of outcome after acute ischemic stroke. However, this review showed that many studies were subject to bias. Although some markers had some predictive ability, none of the studies was able to demonstrate that the biomarker added predictive power to a validated clinical model. The clinical usefulness of blood biomarkers for predicting prognosis in the setting of ischemic stroke has yet to be established.
Analysis of Topoisomerase-DNA Interactions by Electrophoretic Mobility Shift Assay (2003)

DNA topoisomerases break and rejoin DNA strands through a covalent pro-tein-DNA intermediate. The reaction chemistry involves nucleophilic attack by a tyrosine moiety of the enzyme on the phosphodiester backbone of DNA to form a phosphotyrosyl linkage to one (in the case of type I enzymes) or both (type II enzymes) of the DNA strands. Although the distribution of topoisomerase cleavage sites in DNA is nonrandom, the principles governing cleavage site choice are not fully understood. The question of how topoisomerases recognize their DNA cleavage sites is of definite interest, insofar as site specificity may have implications for topoisomerase action in vivo, and because the topoisomerase-DNA complex is the pharmacological target of many antimicrobial and anticancer drugs. An extensive battery of footprinting techniques has been applied to analyzing the topoisomerase-DNA interface in selected model systems, including deoxyribonuclease protection, base-specific modification protection, base-specific modification interference, phosphate modification interference, and site-specific photocrosslinking. This chapter focuses on the use of the electrophoretic mobility shift assay (EMSA) to study topoisomerase binding to DNA.
Modeling and Characterizing Power Variability in Multicore Architectures (2007)

Parameter variation due to manufacturing error is an unavoidable consequence of technology scaling in future generations. The impact of random variation in physical factors such as gate length and interconnect spacing have a profound impact on not only performance of chips, but also their power behavior. While circuit-level techniques such as adaptive body-biasing can help to mitigate mal-fabricated chips, they cannot completely alleviate severe within die variations forecasted for near future designs. Despite the large impact that power variability have on future designs, there is a lack of published work that examines architectural implications of this phenomenon. In this work, we develop architecture level models that model power variability due to manufacturing error and examine its influence on multicore designs. We introduce VariPower, a tool for modeling power variability based on an microarchitectural description and floorplan of a chip. In particular, our models are based on layout level SPICE simulations and project power variability for different microarchitectural blocks using statistical analysis. Using VariPower: (1) we characterize power variability for multicore processors, (2) explore application sensitivity to power variability, and (3) examine clustering techniques that can appropriately classify groups of processors and chips that have similar variability characteristics
Two monoclonal anticarbohydrate antibodies directed to glycosphingolipids with a lacto-N-glycosyl type II chain. (1981)

Two monoclonal antibodies directed to the Type II carbohydrate chain of glycosphingolipids have been prepared by the murine hybridoma technique. Their reactivity was determined by liposome lysis, plate-binding assay, complement fixation, and hemagglutination inhibition. One antibody was specific for glycolipids having the nonreducing terminal N-acetyllactosamine (Gal beta 1 leads to 4GlcNAc beta 1 leads to R) structure and did not react with glycolipids having either a Type I chain (Gal beta 1 leads to 3GlcNAc beta 1 leads to R), a ganglio-series structure (Gal beta 1 leads to 3GalNAc beta 1 leads to R), or a sialosyl or fucosyl substitution at the N-acetyllactosamine residue. This antibody readily agglutinated adult human erythrocytes of all ABO types but did not agglutinate umbilical cord cells. The other antibody reacted with the Type II chain H structure (Fuc alpha 1 leads to 2Gal beta 1 leads to 4GlcNAc beta 1 leads to R) but reacted only weakly with the Type I chain H (Fuc alpha 1 leads to 2Gal beta 1 leads to 3GlcNAc beta 1 leads to R) and ganglio-series H (Fuc alpha 1 leads to 2Gal beta 1 leads to 3GalNAc beta 1 leads to R) structures. At 37 degrees C this antibody agglutinated human erythrocytes of types O and A2 but was unable to cause detectable agglutination of types B and A1. Because of their narrow, well defined specificity, these monoclonal anticarbohydrate reagents will be useful in the study of the distribution, quantity, and function of specific carbohydrates on the cell surface.
Thermal sensitivity of tellurite and germanate optical fibers (2007)

The temperature coefficients of optical phase have been measured at 1536 nm wavelength for short fiber Fabry-Perot cavities of tellurite and germanate glass fibers spliced to silica fiber. The results are consistent with the thermal expansion and thermo-optic coefficients of the bulk glasses.
Aggressive Combination Treatment for Invasive Fungal Sinusitis in Immunocompromised Patients (2000)

Invasive sinonasal fungal disease is a potentially fatal complication of chemotherapy-induced immunosuppression and neutropenia. We reviewed the outcomes of seven cancer patients who had been diagnosed with invasive fungal sinusitis; six patients had hematologic malignancies and one had breast cancer. At the time of their sinus diagnosis, all patients had been hospitalized and were receiving combination chemotherapy for their underlying malignancy. Impairment of their immune function was characterized by an absolute neutrophil count of less than 1,000/mm3. Aggressive management of their sinonasal fungal disease consisted of surgical debridement and systemic amphotericin B for all patients, and treatment with granulocyte colony-stimulating factor for two patients. Invasive Aspergillus infection was identified in six patients and invasive Candida albicans infection in one. Although the prognosis for these patients was poor and two patients died of the fungal infection, the aggressive treatment strategy resulted in long-term survival for the remaining five patients.