gebhart/patrepeval huggingface dataset:
Potentiation of pathogen-specific defense mechanisms in Arabidopsis by β-aminobutyric acid (2000)

The nonprotein amino acids gamma-aminobutyric acid (GABA) and beta-aminobutyric acid (BABA) have known biological effects in animals and plants. Their mode of action has been the object of thorough research in animals but remains unclear in plants. Our objective was to study the mode of action of BABA in the protection of Arabidopis plants against virulent pathogens. BABA protected Arabidopsis against the oomycete pathogen Peronospora parasitica through activation of natural defense mechanisms of the plant such as callose deposition, the hypersensitive response, and the formation of trailing necroses. BABA was still fully protective against P. parasitica in transgenic plants or mutants impaired in the salicylic acid, jasmonic acid, and ethylene signaling pathways. Treatment with BABA did not induce the accumulation of mRNA of the systemic acquired resistance (SAR)-associated PR-1 and the ethylene- and jasmonic acid-dependent PDF1.2 genes. However, BABA potentiated the accumulation of PR-1 mRNA after attack by virulent pathogenic bacteria. As a result, BABA-treated Arabidopsis plants were less diseased compared with the untreated control. In the case of bacteria, BABA protected mutants insensitive to jasmonic acid and ethylene but was not active in plants impaired in the SAR transduction pathway. Thus, BABA protects Arabidopsis against different virulent pathogens by potentiating pathogen-specific plant resistance mechanisms. In addition, we provide evidence that BABA-mediated papilla formation after P. parasitica infection is independent of the SAR signaling pathway.
Effects of scatter in dual-energy imaging: an alternative analysis (1989)

Dual-energy imaging provides images in which the conspicuity of the signal of interest is heightened by selectively cancelling intervening structures. Area detectors for dual-energy imaging offer some advantages over line-scanning systems because they make efficient use of the source. Area detectors, however, collect scattered radiation. To determine the seriousness of the scatter problem and how effective scatter correction is at reducing scatter's deleterious effects, dual-energy imaging in the presence of scatter is simulated. The coefficients are modified so that the intervening material and the scatter are cancelled in some particular region of the image. Results for simulations of two clinically important material-subtraction-the bone-subtraction image and the soft-tissue-subtraction image-are presented. The effects of scatter on contrast, noise variance, and SNR for the two subtractions are examined.
Mucin synthesis. II. Substrate specificity and product identification studies on canine submaxillary gland UDP-GlcNAc:Gal beta 1-3GalNAc(GlcNAc leads to GalNAc) beta 6-N-acetylglucosaminyltransferase. (1980)

The preceding paper (Williams, D., and Schachter, H. (1980) J. Biol. Chem. 255, 0000-0000) described a novel N-acetylglucosaminyltransferase in canine submaxillary gland microsomes which catalyzed the incorporation of GlcNAc into mucin acceptors. We show in the present report that the enzyme catalyzes th following reaction: UDP-GlcNAc + Gal beta 1-3GalNAc-X leads to Gal beta 1-3(GlcNAc beta 1-6) GalNAc-X + UDP, where X can be porcine submaxillary mucin polypeptide (Km = 5.2 mM), antifreeze glycoprotein polypeptide (Km = 23 mM), alpha-O-p-nitrophenyl (Km = 0.52 mM), beta-O-p-nitrophenyl (Km = 0.92 mM), alpha-O-o-nitrophenyl (Km = 0.86 mM), alpha-O-benzyl (Km = 0.77 mM), alpha-O-methyl (Km = 4.2 mM), or -H (Km = 1.2 mM). Ineffective acceptors (< 5% of the activity with Gal beta 1-3GalNAc-alpha-p-nitrophenyl) are asialo-ovine submaxillary mucin, asialo-alpha 1 acid glycoprotein, Gal beta 1-3GlcNAc-beta-p-nitrophenyl, Gal beta 1-3GlcNAc-alpha-methyl, Gal beta1-3GlcNAc, Gal beta 1-3-N-acetylgalactosaminitol, and D-fucose beta 1-3GalNAc-alpha-benzyl, indicating that both the Gal and GalNAc residues are essential for acceptor activity. The beta 1 leads to 6-linkage of GlcNAc to GalNAc in the acceptor Gal beta 1-3GalNAc-alpha-O-benzyl was established by methylation analysis and high resolution 1H nuclear magnetic resonance spectroscopy of a large scale preparation of product. Preliminary evidence has been obtained indicating that sialic acid linked alpha 2-6 to GalNAc or L-fucose linked alpha 1-2 to Gal inhibit the action of the beta 6-N-acetylglucosaminyltransferase on Gal beta 1-3GalNAc-porcine submaxillary mucin polypeptide.
Bone marrow-derived dendritic cells can process bacteria for MHC-I and MHC-II presentation to T cells (1997)

Dendritic cells can engulf particulate Ags and induce T cell proliferative responses after pulsing with particulate Ag. However, their capacity to process viable Gram-negative bacteria for presentation by MHC-I and MHC-II has not been shown. We therefore characterized the ability of murine bone marrow-derived dendritic cells to process Escherichia coli and Salmonella typhimurium, expressing defined epitopes for presentation by MHC-I and MHC-II molecules. The I-Ak-restricted 46-61 epitope from hen egg white lysozyme (HEL(46-61)) or the Kb-restricted 257-264 epitope from chicken egg OVA (OVA(257-264)) was expressed as fusion proteins in the bacterial cytoplasm as the Crl-HEL and Crl-OVA fusion proteins, respectively. Bacteria expressing Crl-HEL or Crl-OVA, or beads coated with HEL or OVA, were coincubated with murine bone marrow-derived dendritic cells, and Ag processing and presentation were quantitated using T cell hybridomas. The data show that granulocyte-macrophage CSF-stimulated dendritic cells can process live intact Gram-negative bacteria for peptide presentation by MHC-I and MHC-II. Cytochalasin D inhibition studies revealed that processing for both MHC-I and MHC-II presentation required cytoskeletal rearrangements. Processing for MHC-I and MHC-II presentation was inhibited by ammonium chloride, suggesting that acidic compartments were required. Thus, granulocyte-macrophage CSF-stimulated murine bone marrow dendritic cells are capable of processing exogenous particulate Ags, including bacteria with no known mechanism for phagosomal escape, for peptide presentation by both MHC-I and MHC-II. These data suggest that dendritic cells may be important in priming both CD4+ and CD8+ T cells to bacterial Ags.
Engineering of TEV protease variants by yeast ER sequestration screening (YESS) of combinatorial libraries (2013)

Myriad new applications of proteases would be enabled by an ability to fine-tune substrate specificity and activity. Herein we present a general strategy for engineering protease selectivity and activity by capitalizing on sequestration of the protease to be engineered within the yeast endoplasmic reticulum (ER). A substrate fusion protein composed of yeast adhesion receptor subunit Aga2, selection and counterselection substrate sequences, multiple intervening epitope tag sequences, and a C-terminal ER retention sequence is coexpressed with a protease library. Cleavage of the substrate fusion protein by the protease eliminates the ER retention sequence, facilitating transport to the yeast surface. Yeast cells that display Aga2 fusions in which only the selection substrate is cleaved are isolated by multicolor FACS with fluorescently labeled antiepitope tag antibodies. Using this system, the Tobacco Etch Virus protease (TEV-P), which strongly prefers Gln at P1 of its canonical ENLYFQ↓S substrate, was engineered to recognize selectively Glu or His at P1. Kinetic analysis indicated an overall 5,000-fold and 1,100-fold change in selectivity, respectively, for the Glu- and His-specific TEV variants, both of which retained high catalytic turnover. Human granzyme K and the hepatitis C virus protease were also shown to be amenable to this unique approach. Further, by adjusting the signaling strategy to identify phosphorylated as opposed to cleaved sequences, this unique system was shown to be compatible with the human Abelson tyrosine kinase.
Amino acid sequence similarities of the mitochondrial short chain delta 3, delta 2-enoyl-CoA isomerase and peroxisomal multifunctional delta 3, delta 2-enoyl-CoA isomerase, 2-enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase enzyme in rat liver. The proposed occurrence of isomerization and hydration in the same catalytic domain of the multifunctional enzyme (1991)

We report the isolation and characterization of a cDNA encoding the mitochondrial short chain delta 3, delta 2-enoyl-CoA isomerase from rat liver. Tryptic fragments of the purified protein were generated, purified, and sequenced. A rat liver cDNA library, constructed in the plasmid vector pUEX1 was screened with oligonucleotides synthesized on the basis of peptide sequences. The obtained clone contained 783 bases predicting to code the entire mature protein of 261 amino acids. The molecular weight of 29,300 predicted from cDNA-derived sequences was consistent with the subunit size determined earlier. A high degree of similarity was noted between the amino acid sequence of isomerase and that of the amino-terminal half of peroxisomal multifunctional isomerase-hydratase-dehydrogenase enzyme and mitochondrial 2-enoyl-CoA hydratase in rat liver. These similarities also appeared at the level of predicted secondary structural elements, suggesting that hte rat multifunctional enzyme has both the isomerization and hydration activities in the amino-terminal domain. This idea is further supported by the proposed existence of only one CoA-binding site in the amino-terminal half of the multifunctional enzyme and by previous studies suggesting that the transfer of the substrate from the isomerization site to the hydration site occurs without aqueous bulk phase (Palosaari P.M., and Hiltunen, J. K. (1990) J. Biol. Chem. 265, 2446-2449).
Compressing the X graphics protocol (1994)

This dissertation is about compressing networked graphics for transmission across low bandwidth networks like phone lines and wireless networks. It concentrates on the X Window System Version 11 (X) because X is the most widely available networked window system today. The dissertation is divided into three main sections: The first section describes a system for tracing the X protocol, the traces gathered, and an analysis of the results. The traces were analyzed by breaking the protocol down into discrete instructions or messages, and analyzing the frequency and network resource requirements of these messages. This analysis has resulted in preliminary results in 4 areas: the relative importance of X messages, how X usage changes during different application stages, differing application idioms for accomplishing similar tasks, and the size distributions of X messages and groups of X messages. Some of these results have architectural implications for network protocols and implementations....
Glutaraldehyde-Cross-linked Meniscal Allografts: Clinical, Gross, and Histological Results (1988)

Osteoarthritic changes in the knee are often a late result of total meniscectomy. In cases of total resection, availability of a prosthetic meniscus might limit development of these changes. The objective of this research was to evaluate a glutaraldehyde-cross-linked medial meniscus as a morphologically and biologically compatible prosthesis in a canine model. Medial and lateral menisci were harvested from donor dogs, frozen in saline, and cross-linked with glutaraldehyde. Five host animals were selected and matched with donors. Glutaraldehyde-cross-linked medial menisci were implanted bilaterally in the stifle joints and one glutaraldehyde cross-linked lateral meniscus was implanted subcutaneously. Clinical results showed asymptomatic limb and joint usage during the 12 postoperative weeks. Gross and histological evaluations indicated acceptable biocompatibility. The subcutaneous implants were encapsulated with a thin fibrous tissue capsule that was only mildly inflamed. Within the joints, the anterior attachment and periphery were maintained in position by their sutures; however, there was dehiscence of the posterior suture in all cases. The articulating surfaces of the implants were intact. There was an initial loss in the quantity of proteoglycans following glutaraldehyde treatment, with significant recovery after implantation into the joints. There were significant degenerative changes (loss of proteoglycans and fibrillation) in the articular cartilage on the femoral condyle and tibial plateau most likely a result of the posterior attachment failure. It was concluded that glutaraldehyde-cross-linked meniscal allografts showed an acceptable degree of histocompatibility. However, failure of the posterior attachment interfered with testing the efficacy of the prosthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
Genetic risk for severe periodontal disease. (1997)

The discovery of a genetic marker that is highly associated with increased risk for severe periodontitis is a major breakthrough in the clinical management of all dental patients. The marker is not diagnostic; rather, it is a prognostic test, and it is used to identify patients who are much more susceptible to plaque. Individuals who have the marker have a 6 to 19 times higher chance of getting severe periodontitis than those who do not have the marker. It is estimated that 30% of the US population will test positive. This new information supplements existing microbiology and immunology research. A limitation with the established view of the etiology of periodontal disease makes it difficult to explain to patients why they are more or less at risk based solely on their level of oral hygiene. It has also been difficult to predict the clinical outcomes of various treatments for individual patients because each person responds differently to their own plaque. The genetic discovery helps to explain why some people with a little plaque have a lot of disease, and why other people with a lot of plaque have only minor problems. By incorporating the constant factor, genetics, into your philosophy of practice, the patient's periodontal needs and desires can be better understood and managed.
Design of peptides for sequence-specific recognition of the minor groove of DNA. (1994)

Insulin is both a hormone regulating energy metabolism and a growth factor. We and others have shown that physiological doses of insulin initiate complex signals in primary human and mouse β-cells, but the functional significance of insulin's effects on this cell type remains unclear. In the present study, the role of insulin in β-cell apoptosis was examined. Exogenous insulin completely prevented apoptosis induced by serum withdrawal when given at picomolar or low nanomolar concentrations but not at higher concentrations, indicating that physiological concentrations of insulin are antiapoptotic and that insulin signaling is self-limiting in islets. Insulin treatment was associated with the nuclear localization of Pdx1 and the prosurvival effects of insulin were largely absent in islets 50% deficient in Pdx1, providing direct evidence that Pdx1 is a signaling target of insulin. Physiological levels of insulin did not increase Akt phosphorylation, and the protective effects of insulin were only partially altered in islets lacking 80% of normal Akt activity, suggesting the presence of additional insulin-regulated antiapoptotic pathways. Proteomic analysis of insulin-treated human islets revealed significant changes in multiple proteins. Bridge-1, a Pdx1-binding partner and regulator of β-cell survival, was increased significantly at low insulin doses. Together, these data suggest that insulin can act as a master regulator of islet survival by regulating Pdx1.
United States v. Pedro Lara, Nos. 93-1750, 93-1780, 93-1794, 93-1795, 93-1837 (2nd Cir. February 2, 1995) (1995 U.S. App. LEXIS 2188) (1994)

Research Article| November 01 1994 United States v. Pedro Lara, Nos. 93-1750, 93-1780, 93-1794, 93-1795, 93-1837 (2nd Cir. February 2, 1995) (1995 U.S. App. LEXIS 2188) Newman Newman Search for other works by this author on: This Site PubMed Google Scholar Federal Sentencing Reporter (1994) 7 (3): 159–163. https://doi.org/10.2307/20639777 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Newman; United States v. Pedro Lara, Nos. 93-1750, 93-1780, 93-1794, 93-1795, 93-1837 (2nd Cir. February 2, 1995) (1995 U.S. App. LEXIS 2188). Federal Sentencing Reporter 1 November 1994; 7 (3): 159–163. doi: https://doi.org/10.2307/20639777 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentFederal Sentencing Reporter Search This content is only available via PDF. Copyright 1994 Vera Institute of Justice, Inc. Article PDF first page preview Close Modal You do not currently have access to this content.
Family Home Visitors: Increasing Minority Women’s Access to Health Services (2009)

The article describes how service access barriers (language, trust) were addressed at different levels (organization, service provider, community) by involving Family Home Visitors to support Nurse Practitioners in providing pre- and postnatal services to linguis­tic minority women in Ontario. The investigators undertook a secondary analysis of 18 semi-structured interviews with health unit informants, Nurse Practitioners, program us­ers, and community leaders, including Family Home Visitors. Health units facilitated col­laboration between two programs aimed at serving mothers with young children, result­ing in both programs using Family Home Visitors. They enhanced minority women’s trust in Nurse Practitioner services by providing interpretation, outreach and support. Family Home Visitors increased Nurse Practitioners’ community knowledge and insights of the family situation. The findings contribute to our understanding of strategies to overcome language and trust barriers and improve access to programs for isolated women from linguistic minority backgrounds. Family Home Visitors’ role has the potential for being expanded and deserves more system support.
A brief history of RNAi: the silence of the genes (2006)

The use of the RNA interference (RNAi) pathway to eliminate gene products has greatly facilitated the understanding of gene function. Behind this remarkable pathway is an intricate network of proteins that ensures the degradation of the target mRNA. In this review, we explore the history of RNAi as well as highlighting recent discoveries.
The maizedek1gene functions in embryonic pattern formation and cell fate specification (2002)

Mutants in the maize defective kernel1 (dek1) gene are blocked in embryogenesis and the endosperm is chalky and lacks an aleurone layer. Here we show that intermediate alleles result in embryos that lack a shoot axis while weak alleles result in endosperms with mosaic aleurone and deformed plants with epidermal cells that resemble bulliform cells, a specialized epidermal cell type. This indicates that dek1 functions in embryonic pattern formation, cell fate specification and pattern formation in the leaf epidermis, and cell fate specification in the endosperm. Thus, the dek1 gene product appears to control different cellular-developmental processes depending on cellular context. The phenotype of the weak dek1-Dooner allele resembles the crinkly4 (cr4) mutant phenotype. Double mutants between dek1 and cr4 showed elements of epistasis, additivity and synergy, suggesting that the gene products may function in overlapping developmental processes. cr4 transcript was detectable in dek1 mutant kernels indicating that DEK1 was not required for Cr4 transcript accumulation. To test whether DEK1 regulated the ligand for the CR4 receptor kinase, a genetic mosaic analysis was performed. The dek1 phenotype appeared to be generally cell-autonomous, leading to the conclusion that it was not likely to produce a diffusible signal molecule, and therefore was not likely to regulate the CR4 ligand.
Vaccinia as a vector for gene delivery (2004)

Gene therapy is a promising approach, yet so far it has shown limited effectiveness in many clinical trials, mainly due to insufficient gene transduction. Recombinant vaccinia virus (rVV) has been well developed as a gene delivery vector, initially for protein expression in mammalian cells. rVV has been further developed to express antigens in vivo in generating immunity for protection against specific infectious diseases and cancer. rVVs, as non-replicating viral vectors, have been demonstrated for their great potential as vaccines, for their diminished cytopathic effects, high levels of protein expression and strong immunogenicity, and they are relatively safe in animals and in human patients. A number of clinical trials using rVVs as vaccines have shown promising results for treating infectious diseases and cancer. In the last few years, due to its exceptional ability to replicate in tumour cells, the Western Reserve strain vaccinia has been explored as a replicating oncolytic virus for cancer virotherapy. As more is learned about the functions of viral gene products in controlling the mammalian cell cycle and in disabling cellular defence mechanisms, specific viral functions can be augmented or eliminated to enhance antitumour efficacy and improve tumour cell targeting. General mechanisms by which this oncolytic virus achieves the antitumour efficacy and specificity are reviewed. Specifically, the deletion of the viral genes for thymidine kinase and vaccinia growth factor resulted in a vaccinia mutant with enhanced tumour targeting activity and fully retaining its efficiency of replication in cancer cells. Other potential strategies for improving this vector for gene delivery will also be discussed in this review.
Proteomic Profiling of Endothelial Cells in Human Lung Cancer (2008)

Genomic and proteomic analysis of normal and diseased tissues have yielded an abundance of molecular information for diagnostic and potential therapeutic targets. Changing the target of analysis from poorly accessible cells within tissues to easily accessible vascular endothelium has theoretical advantages in tissue-specific targeting. In this study, we sought to map a large-scale proteome of microvascular endothelium in human non-small cell lung cancer (NSCLC) and normal lung tissues, and identify lung cancer-related endothelial cell (EC)-selective proteins. Endothelial cells were isolated within NSCLC tissues and adjacent-normal lung tissue of lung cancer patients by using CD31-immunomagnetic beads. The complex proteins from the ECs were separated by one-dimensional gel electrophoresis, and the proteins in each gel band were digested by trypsin. Peptides were separated by online reverse-phase liquid-chromatography and analyzed by electrospray ionization (ESI) ion trap tandem mass spectrometry. Approximately 600-1000 proteins were identified in each individual sample. Five patient cases of paired individual data, extracted from the protein identification data sets of both normal- and cancer-derived ECs, were analyzed by subtractive proteomics. An average of 300 proteins was specifically identified from each lung cancer-derived EC isolate, compared to normal lung-derived ECs. With the use of several comparative analyses, we identified among those 300 proteins, 16 common candidate proteins that were detected in at least 3 of 5 cases specific to lung cancer-derived ECs. Proteins selectively identified in cancer-derived ECs, including coatomer protein complex, subunit gamma (COPG), and peroxiredoxin 4 (PRDX4), were validated by Western blot analysis. In an additional experiment in which 16 cancer samples were analyzed by immunohistochemistry, PRDX4, thymopoietin (TMPO), and COPG were confirmed to be abundantly expressed in lung cancer-derived ECs and in cancerous lung cells. Further ongoing analysis of these 16 candidate proteins will determine their potential applicability to NSCLC-specific diagnosis and therapeutics.