gebhart/patrepeval huggingface dataset:
Oleoresinosis in Grand Fir (Abies grandis) Saplings and Mature Trees (Modulation of this Wound Response by Light and Water Stresses) (1993)

The stem content of diterpene resin acids (rosin) increases dramatically following wounding of grand fir (Abies grandis) saplings, but the level of monoterpene olefins (turpentine) in the stem decreases following injury, in spite of a significant increase in monoterpene cyclase (synthase) activity. However, this observation was explained when rapid evaporative losses of the volatile monoterpenes from the wound site was demonstrated by trapping experiments, a finding consistent with a role of turpentine as a solvent for the mobilization and deposition of rosin to seal the injury. Mature forest trees responded to stem wounding by the enhancement of monoterpene cyclization capacity in a manner similar to 2-year-old grand fir saplings raised in the greenhouse. Light and water stresses greatly reduced the constitutive level of monoterpene cyclase activity and abolished the wound-induced response. The diminution in monoterpene biosynthetic capacity was correlated with a dramatic decrease in cyclase protein as demonstrated by immunoblotting. Relief of stress conditions resulted in the restoration of cyclase activity (both constitutive and wound induced) to control levels. The results of these experiments indicate that grand fir saplings are a suitable model for studies of the regulation of defensive oleoresinosis in conifers.
Double-Stranded RNA Binding by Human Cytomegalovirus pTRS1 (2005)

The human cytomegalovirus (HCMV) TRS1 and IRS1 genes rescue replication of vaccinia virus (VV) that has a deletion of the double-stranded RNA binding protein gene E3L (VVDeltaE3L). Like E3L, these HCMV genes block the activation of key interferon-induced, double-stranded RNA (dsRNA)-activated antiviral pathways. We investigated the hypothesis that the products of these HCMV genes act by binding to dsRNA. pTRS1 expressed by cell-free translation or by infection of mammalian cells with HCMV or recombinant VV bound to dsRNA. Competition experiments revealed that pTRS1 preferentially bound to dsRNA compared to double-stranded DNA or single-stranded RNA. 5'- and 3'-end deletion analyses mapped the TRS1 dsRNA-binding domain to amino acids 74 through 248, a region of identity to pIRS1 that contains no homology to known dsRNA-binding proteins. Deletion of the majority of this region (Delta86-246) completely abrogated dsRNA binding. To determine the role of the dsRNA-binding domain in the rescue of VVDeltaE3L replication, wild-type or deletion mutants of TRS1 were transfected into HeLa cells, which were then infected with VVDeltaE3L. While full-length TRS1 rescued VVDeltaE3L replication, deletion mutants affecting a carboxy-terminal region of TRS1 that is not required for dsRNA binding failed to rescue VVDeltaE3L. Analyses of stable cell lines revealed that the carboxy-terminal domain is necessary to prevent the shutoff of protein synthesis and the phosphorylation of eIF2alpha after VVDeltaE3L infection. Thus, pTRS1 contains an unconventional dsRNA-binding domain at its amino terminus, but a second function involving the carboxy terminus is also required for countering host cell antiviral responses.
Hepatitis B Virus X Protein Modulates Apoptosis in Primary Rat Hepatocytes by Regulating both NF-κB and the Mitochondrial Permeability Transition Pore (2009)

The hepatitis B virus (HBV) X protein (HBx) is a multifunctional protein that regulates numerous cellular signal transduction pathways, including those that modulate apoptosis. However, different HBx-dependent effects on apoptosis have been reported; these differences are likely the consequence of the exact conditions and cell types used in a study. Many of the previously reported studies that analyzed HBx regulation of apoptosis were conducted in immortalized or transformed cells, and the alterations that have transformed or immortalized these cells likely impact apoptotic pathways. We examined the effects of HBx on apoptotic pathways in cultured primary rat hepatocytes, a biologically relevant system that mimics normal hepatocytes in the liver. We analyzed the effects of HBx on apoptosis both when HBx was expressed in the absence of other HBV proteins and in the context of HBV replication. HBx stimulation of NF-kappaB inhibited the activation of apoptotic pathways in cultured primary rat hepatocytes. However, when HBx-induced activation of NF-kappaB was blocked, HBx stimulated apoptosis; blocking the activity of the mitochondrial permeability transition pore inhibited HBx activation of apoptosis. These results suggest that HBx can be either proapoptotic or antiapoptotic in hepatocytes, depending on the status of NF-kappaB, and confirm previous studies that link some HBx activities to modulation of the mitochondrial permeability transition pore. Overall, our studies define apoptotic pathways that are regulated by HBx in cultured primary hepatocytes and provide potential mechanisms for the development of HBV-associated liver cancer.
Broken bar detection in induction motors using current and flux spectral analysis (2004)

Spectrum analysis of the stator current is commonly used for detecting broken rotor bar faults in induction motors. In this paper we examine the practicality of estimating the number of broken bars using stator current and axial leakage flux measurements. The work is based on experimental current and flux measurements taken from induction motors as the number of broken rotor bars is progressively increased. The test results are compared with theoretical predictions and empirical results from other researchers. The effect of partial load operation is also examined.
The synthesis of head-to-tail cyclic sulfono-γ-AApeptides (2014)

We report an efficient method for the preparation of unprecedented head-to-tail cyclic sulfono-γ-AApeptides. Following this method, a number of cyclic sequences bearing two to five subunits were efficiently synthesized. In addition, the X-ray crystal structure study of a three-membered cyclic sulfono-γ-AApeptide revealed a type II β-turn-like character.
Hydrophobicity indices for amino acid residues as determined by high-performance liquid chromatography. (1992)

The retention times of compounds on reversed-phase high-performance liquid chromatography columns are determined by their overall hydrophobicity. This paper exploits this relationship to derive hydrophobicity indices for amino acid residues. Retention times of 20 Z-amino acids and their methyl, ethyl and benzyl esters were determined under standard conditions on reversed-phase high-performance liquid chromatography at pH 3.0 and pH 7.5. Retention times of derivatives of six of the amino acids were used to calculate amino acid residue hydrophobicity values relative to glycine and leucine by a computer-based iterative procedure that used splines to optimize the smoothness of fit. Using these derived curves, values for each derivative of the remaining 14 Z-amino acids were determined and averages calculated. The curves, generated independently for pH 3.0 and pH 7.5 were effectively identical and the determined hydrophobicity values (other than for charged residues) were also similar at the two pHs. The values obtained vary significantly from other published values. Comparisons with some of the more commonly used hydrophobicity/hydropathy tables are presented. The highest correlation was found with constants determined for water/octanol partitioning of N- and C-terminal protected amino acids.
Transcriptional Repression by Blimp-1 (PRDI-BF1) Involves Recruitment of Histone Deacetylase (2000)

B-lymphocyte-induced maturation protein (Blimp-1) is a transcriptional repressor that is considered to be a master regulator of terminal B-cell development because it is sufficient to trigger differentiation in the BCL(1)-cell model. Transcription of the c-myc gene is repressed by Blimp-1 during B-cell differentiation. In this study, we have explored the mechanism by which Blimp-1 represses transcription by using Gal4-fusion protein assays and assays in which Blimp-1 represses the natural c-myc promoter. The results show that Blimp-1 represses the c-myc promoter by an active mechanism that is independent of the adjacently bound activator YY1. Blimp-1 contains two regions that independently associate with histone deacetylase (HDAC) and endogenous Blimp-1 in nuclear extracts binds in vitro to the c-myc Blimp-1 site in a complex containing HDAC. The functional importance of recruiting HDAC for Blimp-1-dependent repression of c-myc transcription is supported by two experiments. First, the HDAC inhibitor tricostatin A inhibits Blimp-1-dependent repression in cotransfection assays. Second, a chromatin immunoprecipitation assay shows that expression of Blimp-1 causes deacetylation of histone H3 associated with the c-myc promoter, and this deacetylation depends on the Blimp-1 binding site in the c-myc promoter.
USE OF THE METHYLXANTHINE DERIVATIVE A802715 IN TRANSPLANTATION IMMUNOLOGY (1997)

These in vitro data indicate that the A802715 (1) is a stronger immunosuppressant for T cells than PTX, (2) suppresses T cell activation pathways that are resistant to PTX or CsA, and (3) acts synergistically with CsA.
The chimeric TAC receptor co-opts the T cell receptor yielding robust anti-tumor activity without toxicity (2018)

Engineering T cells with chimeric antigen receptors (CARs) is an effective method for directing T cells to attack tumors, but may cause adverse side effects such as the potentially lethal cytokine release syndrome. Here the authors show that the T cell antigen coupler (TAC), a chimeric receptor that co-opts the endogenous TCR, induces more efficient anti-tumor responses and reduced toxicity when compared with past-generation CARs. TAC-engineered T cells induce robust and antigen-specific cytokine production and cytotoxicity in vitro, and strong anti-tumor activity in a variety of xenograft models including solid and liquid tumors. In a solid tumor model, TAC-T cells outperform CD28-based CAR-T cells with increased anti-tumor efficacy, reduced toxicity, and faster tumor infiltration. Intratumoral TAC-T cells are enriched for Ki-67<sup>+</sup> CD8<sup>+</sup> T cells, demonstrating local expansion. These results indicate that TAC-T cells may have a superior therapeutic index relative to CAR-T cells.
Improved Murine Model of Malaria UsingPlasmodium falciparumCompetent Strains and Non-Myelodepleted NOD-scid IL2RγnullMice Engrafted with Human Erythrocytes (2009)

Murine models of Plasmodium falciparum malaria may become crucial tools in drug discovery. Here we show that non-myelodepleted NOD-scid IL2Rgamma(null) mice engrafted with human erythrocytes support an infectious burden up to tenfold higher than that supported by engrafted NOD-scid beta2microglobulin(null) mice. The new model was validated for drug discovery and was used to assess the therapeutic efficacy of 4-pyridones, selective inhibitors of P. falciparum cytochrome bc1.
An update to the list of mouse mutants with neural tube closure defects and advances toward a complete genetic perspective of neural tube closure (2010)

The number of mouse mutants and strains with neural tube defects (NTDs) now exceeds 240, including 205 representing specific genes, 30 for unidentified genes, and 9 multifactorial strains. These mutants identify genes needed for embryonic neural tube closure. Reports of 50 new NTD mutants since our 2007 review (Harris and Juriloff, 2007) were considered in relation to the previously reviewed mutants to obtain new insights into mechanisms of NTD etiology. In addition to null mutations, some are hypomorphs or conditional mutants. Some mutations do not cause NTDs on their own, but do so in digenic, trigenic, and oligogenic combinations, an etiology that likely parallels the nature of genetic etiology of human NTDs. Mutants that have only exencephaly are fourfold more frequent than those that have spina bifida aperta with or without exencephaly. Many diverse cellular functions and biochemical pathways are involved; the NTD mutants draw new attention to chromatin modification (epigenetics), the protease-activated receptor cascade, and the ciliopathies. Few mutants directly involve folate metabolism. Prevention of NTDs by maternal folate supplementation has been tested in 13 mutants and reduces NTD frequency in six diverse mutants. Inositol reduces spina bifida aperta frequency in the curly tail mutant, and three new mutants involve inositol metabolism. The many NTD mutants are the foundation for a future complete genetic understanding of the processes of neural fold elevation and fusion along mechanistically distinct cranial-caudal segments of the neural tube, and they point to several candidate processes for study in human NTD etiology.
3H-Benzophosphepine Complexes:  Versatile Phosphinidene Precursors (2005)

The synthesis of a variety of benzophosphepine complexes [R = Ph, t-Bu, Me; ML(n )()= W(CO)(5), Mo(CO)(5), Cr(CO)(5), Mn(CO)(2)Cp] by two successive hydrophosphinations of 1,2-diethynylbenzene is discussed in detail. The first hydrophosphination step proceeds at ambient temperature without additional promoters, and subsequent addition of base allows full conversion to benzophosphepines. Novel benzeno-1,4-diphosphinanes were isolated as side products. The benzophosphepine complexes themselves serve as convenient phosphinidene precursors at elevated, substituent-dependent temperatures (>55 degrees C). Kinetic and computational analyses support the proposal that the phosphepine-phosphanorcaradiene isomerization is the rate-determining step. In the absence of substrate, addition of the transient phosphinidene to another benzophosphepine molecule is observed, and addition to 1,2-diethynylbenzene furnishes a delicate bidentate diphosphirene complex.
A sensorless, stable v/f control method for permanent-magnet synchronous motor drives (2003)

When permanent-magnet synchronous motors (PMSMs) are used for pump and fan applications, V/f control methods can be used to control them. The problem with open-loop V/f control of PMSMs without having damper windings in the rotor is the inherent instability after exceeding a certain applied frequency. In this paper, a new V/f control method is proposed for motor drives for stable operation in a wide frequency range. The magnitude of the voltage is controlled in order to maintain a constant stator flux linkage in the PMSM. The applied frequency is modulated proportional to the input power perturbations to stabilize the drive for a wide frequency range. No position sensor is required to implement this stabilizing technique. The small-signal analysis and the experimental results confirm the effectiveness of this stabilizing technique. The experimental results also indicate the satisfactory performance of the drive for pump and fan applications.
Inhibition of vascular smooth muscle cell proliferation by a novel fibroblast growth factor receptor antagonist (2002)

We have identified an FGF antagonist, which may serve in clinical practice as a preventive measure of restenosis.
Phosphorylation of tyrosine 474 of the enteropathogenic Escherichia coli (EPEC) Tir receptor molecule is essential for actin nucleating activity and is preceded by additional host modifications (1999)

The enteropathogenic Escherichia coli (EPEC) Tir protein becomes tyrosine phosphorylated in host cells and displays an increase in apparent molecular mass. The interaction of Tir with the EPEC outer membrane protein, intimin, triggers actin nucleation beneath the adherent bacteria. The enterohaemorrhagic E. coli O157:H7 (EHEC) Tir molecule is not tyrosine phosphorylated. In this paper, Tir tyrosine phosphorylation is shown to be essential for actin nucleation activity, but not for the increase in apparent molecular mass observed in target cells. Tyrosine phosphorylation had no role in Tir molecular mass shift, indicating additional host modifications. Analysis of Tir intermediates indicates that tyrosine-independent modification functions to direct Tir's correct insertion from the cytoplasm into the host membrane. Deletion analysis identified Tir domains participating in translocation, association with the host membrane, modification and antibody recognition. Intimin was found to bind a 55-amino-acid region (TIBA) within Tir that topological and sequence analysis suggests is located in an extracellular loop. Homologous TIBA sequences exist in integrins, which also bind intimin. Collectively, this study provides definitive evidence for the importance of tyrosine phosphorylation for EPEC Tir function and reveals differences in the pathogenicity of EPEC and EHEC. The data also suggest a mechanism for Tir insertion into the host membrane, as well as providing clues to the mode of intimin-integrin interaction.
HIV-1 drug resistance surveillance using dried whole blood spots (2007)

The results suggest that genotypes obtained from DBS are equivalent to those from plasma. DBS are a promising public health tool for HIVDR surveillance of treatment-naive subjects, especially in regions where specimens might be exposed to severe environmental conditions and where logistical difficulties could prevent timely specimen processing. More studies are needed to validate DBS for patient monitoring.
Gene therapy for Duchenne muscular dystrophy (2012)

Significant steps have been made in the development of gene therapy approaches for Duchenne muscular dystrophy. These approaches aim to slow down disease progression, requiring robust outcome measures to assess efficacy.
Molecular evolution of rodent insulins. (1987)

Several trees of amino acid sequences of rodent insulins were derived with the maximum-parsimony procedure. Possible orthologous and paralogous relationships were investigated. Except for a recent gene duplication in the ancestor of rat and mouse, there are no strong arguments for other paralogous relationships. Therefore, a tree in agreement with other biological data is the most reasonable one. According to this tree, the capacity to form zinc-binding hexamers was lost once in the ancestor of the hystricomorph rodents, followed by moderately increased evolutionary rates in the lineages to African porcupine and chinchilla but highly increased rates in at least three independent lines to other taxa of this suborder: guinea pig, cuis, and Octodontoidea (coypu and casiragua).
Modeling stream processing applications for dependability evaluation (2011)

This paper describes a modeling framework for evaluating the impact of faults on the output of streaming applications. Our model is based on three abstractions: stream operators, stream connections, and tuples. By composing these abstractions within a Stochastic Activity Network, we allow the modeling of complete applications. We consider faults that lead to data loss and to silent data corruption (SDC). Our framework captures how faults originating in one operator propagate to other operators down the stream processing graph. We demonstrate the extensibility of our framework by evaluating three different fault tolerance techniques: checkpointing, partial graph replication, and full graph replication. We show that under crashes that lead to data loss, partial graph replication has a great advantage in maintaining the accuracy of the application output when compared to checkpointing. We also show that SDC can break the no data duplication guarantees of a full graph replication-based fault tolerance technique.
Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. (1995)

In this study, human monocyte-derived macrophages were shown to induce collagen breakdown in fibrous caps of human atherosclerotic plaques associated with cellular expression and zymographic evidence of MMP activity; no evidence of collagen breakdown was found in the presence of an MMP inhibitor. These findings support the hypothesis that increased macrophage density and/or activation in the atherosclerotic plaque may induce collagen breakdown in the fibrous cap by secreting MMPs and possibly other proteases, thus contributing to vulnerability to plaque rupture.
The Molecular Interaction of Fas and FAP-1 (1997)

Fas (APO-1/CD95), which is a member of the tumor necrosis factor receptor superfamily, is a cell surface receptor that induces apoptosis. A protein tyrosine phosphatase, Fas-associated phosphatase-1 (FAP-1), that was previously identified as a Fas binding protein interacts with the C-terminal 15 amino acids of the regulatory domain of the Fas receptor. To identify the minimal region of the Fas C-terminal necessary for binding to FAP-1, we employed an in vitro inhibition assay of Fas/FAP-1 binding using a series of synthetic peptides as well as a screen of random peptide libraries by the yeast two-hybrid system. The results showed that the C-terminal three amino acids (SLV) of human Fas were necessary and sufficient for its interaction with the third PDZ (GLGF) domain of FAP-1. Furthermore, the direct cytoplasmic microinjection of this tripeptide (Ac-SLV) resulted in the induction of Fas-mediated apoptosis in a colon cancer cell line that expresses both Fas and FAP-1. Since t(S/T)X(V/L/I) motifs in the C termini of several other receptors have been shown to interact with PDZ domain in signal transducing molecules, this may represent a general motif for protein-protein interactions with important biological functions.
Activation of the Erk Pathway Is Required for TGF-β1-Induced EMT In Vitro (2004)

Transforming growth factor-beta1 (TGF-beta1) can be tumor-suppressive through the activation of the Smad-mediated signaling pathway. TGF-beta1 can also enhance tumor progression by stimulating epithelial-to-mesenchymal transition (EMT) through additional pathways. EMT is characterized by the acquisition of a fibroblast-like cell morphology, dissolution of tight junctions, disruption of adherence junctions, and formation of actin stress fibers. There is evidence linking the activation of mitogen-activated protein kinase pathways to the induction of TGF-beta1-mediated EMT. However, the role of Erk in the induction of TGF-beta1-mediated EMT remains unclear. TGF-beta1 treatment of normal murine mammary gland (NMuMG) epithelial cells resulted in increased gene expression of Ras, Raf, MEK1/2, and Erk1/2, as shown by microarray analysis and real-time polymerase chain reaction. Upon 24 and 48 hours of treatment with TGF-beta1, NMuMG and mouse cortical tubule (MCT) epithelial cells underwent EMT as shown by changes in cell morphology, delocalization of zonula occludens-1 and E-cadherin from cell-cell junctions, and formation of actin stress fibers. TGF-beta1 treatment also resulted in increased levels of phosphorylated Erk and Erk kinase activity. Treatment with an MEK inhibitor, U0126, inhibited increased Erk phosphorylation and kinase activity, and blocked TGF-beta1-induced EMT in both cell lines. These data show that TGF-beta1 induces the activation of the Erk signaling pathway, which is required for TGF-beta1-mediated EMT in vitro.
Hydrophilic Zeolite Coatings for Improved Heat Transfer (2005)

The evaporation time and wetting limit temperature for a water droplet on the surface of a bare, Zeolite-A-coated, or ZSM-5-coated stainless steel substrate have been experimentally studied. Three stainless steel substrates are prepared with different finishes. The surface finishing of a substrate is shown to cause observable changes in the wettability of a bare or ZSM-5-coated surface. Contact angle measurements reveal that Zeolite-A coatings are the most hydrophilic and that bare stainless steel is the least hydrophilic. The evaporation time and wetting limit temperature of a water droplet placed on the surface of the bare and coated substrates are examined as surface temperature increases. The zeolite coatings decrease the evaporation time and increase the wetting limit temperature on the bare stainless steel substrate, with Zeolite-A coatings offering the best improvement. For the bare substrate and the substrates coated with the same zeolite, as hydrophilicity increases, the evaporation time decreases and wetting limit temperature increases.