gebhart/patrepeval huggingface dataset:
SPATIAL VARIABILITY OF FIELD TOPOGRAPHY ANDWHEAT YIELD IN THE PALOUSE REGION OF THE PACIFIC NORTHWEST (1998)

Measurement and analysis of the spatial variability of fields are two important aspects of site-specific cropmanagement. In this study, data for wheat yield, ground slope and aspect were intensively collected from five fields in the Palouse region of Washington using a set of sensors and a Global Positioning System (GPS) receiver. A Geographic Information System (GIS) database was developed to manage the field-collected data and information from topographic maps and to group the data from each field into different regions for analysis. Relative elevation differences across the five fields ranged from 29 to 70 m. Slope steepness ranged from 0 to 30 with field means of 9 to 12. Geostatistical analyses showed that the spatial patterns of variability in wheat yields differed not only from one field to another but also from one region to another within a field. The ranges of influence in wheat yield for the five whole fields were from 55 to 86 m, while those for the within-field regions varied from 20 to over 100 m. Regression analyses indicated that topographic attributes including elevation, slope and aspect had significant effects on wheat yield. These topographic attributes could explain 13 to 35% of the variability in wheat yield for the whole fields, though 49 to 84% of the yield variability could be explained by topography in some regions within the five fields. These results provided useful quantitative information about the influence of topography on crop yield in the Palouse region.
Way2Home: Assertive Outreach Service for the Inner City of Sydney (2011)

The Way2Home is a new assertive outreach service in the inner city of Sydney that provides proactive and long-term support to rough sleepers who are chronically homeless. The role performed by the Outreach and Support Team is highlighted.
Specific down‐regulation of connective tissue growth factor attenuates progression of nephropathy in mouse models of type 1 and type 2 diabetes (2007)

ABSTRACT Diabetic nephropathy (DN) remains a major complication in both type 1 and type 2 diabetes. Systemic administration of antitransforming growth factor‐β (TGF‐β) antibody has shown some promise in mouse models of DN. However, chronic blockade of the multifunctional TGB‐β could be problematic. Several downstream effects of TGF‐β are mediated by connective tissue growth factor (CTGF), which is up‐regulated in several renal cells and secreted in the urine in the diabetic state. Using murine models of DN (type 1 and type 2) and a CTGF antisense oligonucleotide (ASO) of novel chimeric chemistry, we evaluated the specific role of this target in DN. In the type 1 model of DN, C57BL6 mice were made diabetic using streptozo‐tocin injections and hyperglycemic animals were treated with CTGF ASOs (20 mg/kg/2 qw) for 4 months. ASO, but not mismatch control oligonucleo‐tide, ‐treated animals showed significant reduction in target CTGF expression in the kidney with a concomitant decrease in proteinuria and albuminuria. Treatment with the CTGF ASO for 8 wk reduced serum creatinine and attenuated urinary albuminuria and pro‐teinuria in diabetic db/db mice, a model of type 2 DN. The ASO also reduced expression of genes involved in matrix expansion such as fibronectin and collagen (I and IV) and an inhibitor of matrix degradation, PAI‐1, in the renal cortex, contributing to significant reversal of mesangial expansion in both models of DN. Pathway analyses demonstrated that diabetes‐induced phosphory‐lation of p38 MAPK and its downstream target CREB was also inhibited by the ASO. Our results strongly suggest that blocking CTGF using a chimeric ASO holds substantial promise for the treatment of DN.—Guha, M., Xu, Z.‐G., Tung, D., Lanting, L., Natarajan, R. Specific down‐regulation of connective tissue growth factor attenuates progression of nephropathy in mouse models of type 1 and type 2 diabetes. FASEB J. 21, 3355–3368 (2007)
The epipolythiodioxopiperazine (ETP) class of fungal toxins: distribution, mode of action, functions and biosynthesis (2005)

Epipolythiodioxopiperazines (ETPs) are toxic secondary metabolites made only by fungi. The best-known ETP is gliotoxin, which appears to be a virulence factor associated with invasive aspergillosis of immunocompromised patients. The toxicity of ETPs is due to the presence of a disulphide bridge, which can inactivate proteins via reaction with thiol groups, and to the generation of reactive oxygen species by redox cycling. With the availability of complete fungal genome sequences and efficient gene-disruption techniques for fungi, approaches are now feasible to delineate biosynthetic pathways for ETPs and to gain insights into the evolution of such gene clusters.
Exosomes Derived from IL-10-Treated Dendritic Cells Can Suppress Inflammation and Collagen-Induced Arthritis (2005)

We have demonstrated previously that local, adenoviral-mediated gene transfer of viral IL-10 to a single joint of rabbits and mice with experimental arthritis can suppress disease in both the treated and untreated contralateral joints. This contralateral effect is mediated in part by APCs able to traffic from the treated joint to lymph nodes as well as to untreated joints. Moreover, injection of dendritic cells (DC) genetically modified to express IL-4 or Fas ligand was able to reverse established murine arthritis. To examine the ability of exosomes derived from immunosuppressive DCs to reduce inflammation and autoimmunity, murine models of delayed-type hypersensitivity and collagen-induced arthritis were used. In this study, we demonstrate that periarticular administration of exosomes purified from either bone marrow-derived DCs transduced ex vivo with an adenovirus expressing viral IL-10 or bone marrow-derived DCs treated with recombinant murine IL-10 were able to suppress delayed-type hypersensitivity responses within injected and untreated contralateral joints. In addition, the systemic injection of IL-10-treated DC-derived exosomes was able suppress the onset of murine collagen-induced arthritis as well as reduce severity of established arthritis. Taken together, these data suggest that immature DCs are able to secrete exosomes that are involved in the suppression of inflammatory and autoimmune responses. Thus DC-derived exosomes may represent a novel, cell-free therapy for the treatment of autoimmune diseases.
Ligand-dependent activation of ER lowers blood pressure and attenuates cardiac hypertrophy in ovariectomized spontaneously hypertensive rats (2007)

Ligand-dependent activation of ERbeta confers blood pressure lowering effects in SHR that are superior to those of 17beta-estradiol or the ERalpha agonist 16alpha-LE2 and attenuates cardiac hypertrophy primarily by a reduction of cardiac afterload without promoting uterine growth.
Genes acrA and acrB encode a stress‐induced efflux system of Escherichia coli (1995)

Defined mutations of acrA or acrB (formerly acrE) genes increased the susceptibility of Escherichia coli to a range of small inhibitor molecules. Deletion of acrAB increased susceptibility to cephalothin and cephaloridine, but the permeability of these beta-lactams across the outer membrane was not increased. This finding is inconsistent with the earlier hypothesis that acrAB mutations increase drug susceptibility by increasing the permeability of the outer membrane, and supports our model that acrAB codes for a multi-drug efflux pump. The natural environment of an enteric bacterium such as E. coli is enriched in bile salts and fatty acids. An acrAB deletion mutant was found to be hypersusceptible to bile salts and to decanoate. In addition, acrAB expression was elevated by growth in 5 mM decanoate. These results suggest that one major physiological function of AcrAB is to protect E. coli against these and other hydrophobic inhibitors. Transcription of acrAB is increased by other stress conditions including 4% ethanol, 0.5 M NaCl, and stationary phase in Luria-Bertani medium. Finally, acrAB expression was shown to be increased in mar (multiple-antibiotic-resistant) mutants.
Quantum error correction of dephasing in 3 qubits (1996)

We show how to perform error correction of single qubit dephasing by encoding a single qubit into a minimum of three. This may be performed in a manner closely analogous to classical error correction schemes. Further, the resulting quantum error correction schemes are trivially generalized to the minimal encoding of arbitrarily many qubits so as to allow for multiqubit dephasing correction under the sole condition that the environment acts independently on each qubit.
Presenilin 1 facilitates the constitutive turnover of beta-catenin: differential activity of Alzheimer's disease-linked PS1 mutants in the beta-catenin-signaling pathway. (1999)

Although an association between the product of the familial Alzheimer's disease (FAD) gene, presenilin 1 (PS1), and beta-catenin has been reported recently, the cellular consequences of this interaction are unknown. Here, we show that both the full length and the C-terminal fragment of wild-type or FAD mutant PS1 interact with beta-catenin from transfected cells and brains of transgenic mice, whereas E-cadherin and adenomatous polyposis coli (APC) are not detected in this complex. Inducible overexpression of PS1 led to increased association of beta-catenin with glycogen synthase kinase-3beta (GSK-3beta), a negative regulator of beta-catenin, and accelerated the turnover of endogenous beta-catenin. In support of this finding, the beta-catenin half-life was dramatically longer in fibroblasts deficient in PS1, and this phenotype was completely rescued by replacement of PS1, demonstrating that PS1 normally stimulates the degradation of beta-catenin. In contrast, overexpression of FAD-linked PS1 mutants (M146L and DeltaX9) failed to enhance the association between GSK-3beta and beta-catenin and interfered with the constitutive turnover of beta-catenin. In vivo confirmation was demonstrated in the brains of transgenic mice in which the expression of the M146L mutant PS1 was correlated with increased steady-state levels of endogenous beta-catenin. Thus, our results indicate that PS1 normally promotes the turnover of beta-catenin, whereas PS1 mutants partially interfere with this process, possibly by failing to recruit GSK-3beta into the PS1-beta-catenin complex. These findings raise the intriguing possibility that PS1-beta-catenin interactions and subsequent activities may be consequential for the pathogenesis of AD.
RNA catalytic properties of the minimum (-)sTRSV sequence (1989)

We have identified an RNA catalytic domain within the sequence of the 359 base long negative-strand satellite RNA of tobacco ringspot virus. The catalytic domain contains two minimal sequences of satellite RNA, a 50-base catalytic RNA sequence, and a 14-base substrate RNA sequence. The catalytic complex of catalytic RNA/substrate RNA represents a structure not previously found in any RNA catalytic reaction described to date. The reaction is truly catalytic since the catalytic RNA has multiple substrate cleavage events and is not consumed during the course of the reaction. A linear relationship is seen between reaction rate and catalytic RNA concentration. The reaction has a Km of 0.03 microM, a kcat of 2.1/min, a temperature optimum of near 37 degrees C, and an energy of activation of 19 kcal/mol.
MicroRNA Expression Profiling in Prostate Cancer (2007)

MicroRNAs (miRNA) are small, endogenously expressed noncoding RNAs that negatively regulate expression of protein-coding genes at the translational level. Accumulating evidence, such as aberrant expression of miRNAs, suggests that they are involved in the development of cancer. They have been identified in various tumor types, showing that different sets of miRNAs are usually deregulated in different cancers. To identify the miRNA signature specific for prostate cancer, miRNA expression profiling of 6 prostate cancer cell lines, 9 prostate cancer xenografts samples, 4 benign prostatic hyperplasia (BPH), and 9 prostate carcinoma samples was carried out by using an oligonucleotide array hybridization method. Differential expression of 51 individual miRNAs between benign tumors and carcinoma tumors was detected, 37 of them showing down-regulation and 14 up-regulation in carcinoma samples, thus identifying those miRNAs that could be significant in prostate cancer development and/or growth. There was a significant trend (P=0.029) between the expression of miRNAs and miRNA locus copy number determined by array comparative genomic hybridization, indicating that genetic aberrations may target miRNAs. Hierarchical clustering of the tumor samples by their miRNA expression accurately separated the carcinomas from the BPH samples and also further classified the carcinoma tumors according to their androgen dependence (hormone naive versus hormone refractory), indicating the potential of miRNAs as a novel diagnostic and prognostic tool for prostate cancer.
In situdetection of activated Bruton’s tyrosine kinase in the Ig signaling complex by phosphopeptide-specific monoclonal antibodies (1999)

Bruton's tyrosine kinase (Btk) is a critical transducer of signals originating from the B cell antigen receptor (BCR). Dosage, sequential phosphorylation, and protein interactions are interdependent mechanisms influencing Btk function. Phosphopeptide-specific mAbs recognizing two distinct phosphotyrosine modifications were used to quantify Btk activation by immunofluorescent techniques during B cell stimulation. In a population of cultured B cells stimulated by BCR crosslinking and analyzed by flow cytometry, transient phosphorylation of the regulatory Btk tyrosine residues (551Y and 223Y) was detected. The kinetics of phosphorylation of the residues were temporally distinct. Tyrosine 551, a transactivating substrate site for Src-family kinases, was maximally phosphorylated within approximately 30 seconds of stimulation as monitored by flow cytometry. Tyrosine 223, an autophosphorylation site within the SH3 domain, was maximally phosphorylated at approximately 5 minutes. Btk returned to a low tyrosine phosphorylation level within 30 minutes, despite persistent elevation of global tyrosine phosphorylation. Colocalization of activated Btk molecules with the crosslinked BCR signaling complex was observed to coincide with the period of maximal Btk tyrosine phosphorylation when stimulated B cells were analyzed with confocal microscopy. The results of these in situ temporal and spatial analyses imply that Btk signaling occurs in the region of the Ig receptor signaling complex, suggesting a similar location for downstream targets of its activity.
Glycolipids as Immunomodulators: Syntheses and Properties (1991)

Abstract Although the most successful vaccines still consist of attenuated or killed pathogens, it is evident that genetic engineering will eventually provide pure antigens in sufficient quantities. To achieve a protective effect, however, the immune response to these structures, which are only weakly immunogenic, must be activated by adjuvants. The discovery of chemically defined, well‐tolerated. synthetic adjuvants is therefore especially important in effective immunoprophylaxis. A very promising class of compounds in this respect are synthetic glycosylamides, with two long alkyl chains consisting of alkylamines and fatty acids. Unlike natural glycolipids, which exert an immunosuppressive effect, the new glycolipid analogues described here show marked immunostimulation. In vaccination experiments with various antigens they provide efficient protection. Their mode of action, which differs from that of known adjuvants, makes glycolipid analogues particularly interesting for immunization of patients with defective T lymphocyte function, for example AIDS patients.
Obesity-Related Derangements in Metabolic Regulation (2006)

An epidemic surge in the incidence of obesity has occurred worldwide over the past two decades. This alarming trend has been triggered by lifestyle habits that encourage overconsumption of energy-rich foods while also discouraging regular physical activity. These environmental influences create a chronic energy imbalance that leads to persistent weight gain in the form of body fat and a host of other abnormalities in metabolic homeostasis. As adiposity increases, so does the risk of developing comorbidities such as diabetes, hypertension, and cardiovascular disease. The intimate association between obesity and systemic metabolic dysregulation has inspired a new area of biochemistry research in which scientists are seeking to understand the molecular mechanisms that link chronic lipid oversupply to tissue dysfunction and disease development. The purpose of this chapter is to review recent findings in this area, placing emphasis on lipid-induced functional impairments in the major peripheral organs that control energy flux: adipose tissue, the liver, skeletal muscle, and the pancreas.
Alzheimer's disease. (1985)

Alzheimer's disease is an extremely prevalent illness that has been more clearly understood in recent years. Although its cause is unknown, it is in some cases genetically transmissable. Symptoms include forgetfulness, memory loss, and confusion early in the illness and culminate in loss of personality and total cognitive degeneration. Diagnosis can be made with certainty only at autopsy, but the clinician must carefully eliminate treatable and partially treatable illnesses that present as dementia. A deficit of choline acetyltransferase seems specific to the disease and has been correlated to the neuropathologic changes in brains of patients with AD as well as to clinical symptomatology. While pharmacologic treatment strategies have attempted to increase brain acetylcholine function, they have not been clinically successful to date. Antipsychotic agents remain the treatment of choice for many AD patients, although helping the family care for such patients may be the most valuable service the physician can provide.
Decreased Expression of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinase in the Kidneys of Hereditary Nephrotic (ICGN) Mice (2005)

Matrix metalloporoteinases (MMPs), which are dominantly regulated by tissue inhibitors of metalloproteinase (TIMPs), play important roles in extracellular matrix (ECM) degradation and are involved in the progression of kidney diseases. In glomeruli and tubulointerstitum of hereditary nephrotic (ICR-derived glomerulonephritis: ICGN) mouse kidneys, hyper-accumulation of ECM components occurred, and MMP activity decreased. In the present study, because lower levels of MMP activity may contribute to the progression of renal fibrosis in ICGN mice, Western blotting analysis and immunohistochemical staining for MMPs and TIMPs were performed to verify the expression levels of these proteins. Levels of MMP-2, MMP-9, MT1-MMP, TIMP-1 and TIMP-2 in the kidneys were decreased in ICGN mice in comparison with normal ICR mice. These results indicate that small amounts and low levels of activity of MMPs cause the progression of renal fibrosis in ICGN mice.
Inhibitory effects of anti-miRNA oligonucleotides (AMOs) on A549 cell growth (2008)

MicroRNAs (miRNAs) are a new class of non-protein-coding, endogenous small RNA molecules of 18-24 nt in size. miRNAs can specifically down-regulate gene expression involved in proliferation, apoptosis, and differentiation in cancer cells. Our purpose was to identify several functional miRNAs as potential drug targets by using specific antisense-microRNA oligonucleotides (AMOs), and to study the inhibitory effects of these AMOs on A549 cell growth. miR-16, miR-21, miR-214, and miR-181a were selected as target candidates, based on which specific AMOs were designed, synthesized, and transfected into A549 cells. The viable cells were counted by using trypan blue dye exclusion assay. Apoptosis of A549 cells were determined flowcytometrically, and miR-21 expression levels in A549 cells were determined by real-time PCR. The results showed that AMO-miR-21, AMO-miR-16, and AMO-miR-181a inhibited A549 cell growth by inducing apoptosis and S-phase arrest. These inhibitory effects increased with dose and time. It was found that AMO-miR-21 down-regulated miR-21 expression in A549 cells. We conclude that miR-21, miR-16, and miR-181a are potential targets for lung cancer therapy, and specific AMOs can be a powerful technique for miRNA inhibition.
C5a promotes development of experimental lupus nephritis which can be blocked with a specific receptor antagonist (2005)

The MRL/lpr murine SLE model has widespread complement activation and deposition of complement fragments in affected tissues. The potent anaphylatoxin C5a has the potential to play a key role in the pathogenesis of lupus nephritis. We found that renal expression of C5aR mRNA and protein was significantly increased in MRL/lpr mice compared to control MRL/+ mice. To examine the role of C5a signaling through C5aR, a specific small molecule antagonist (a) of C5aR was administered continuously to MRL/lpr mice from 13 to 19 wks of age. Littermate controls were given vehicle alone. The progressive impairment in renal function exhibited in the control group was prevented by C5aRa treatment. Infiltration of neutrophils and macrophages into kidneys was significantly reduced in animals treated with C5aRa compared to controls. Furthermore, renal expression of IL-1beta and MIP-2 mRNA as well as the extent of apoptosis were significantly decreased with blockade of C5aR, indicating their dependence upon signals delivered through C5aR. Thus, pharmacological blockade of C5aR reduces disease manifestations in experimental lupus nephritis. These data support an important role for the C5a anaphylatoxin in lupus nephritis, and that blockade of C5aR represents a potentially viable treatment for human lupus nephritis.
Model Electrochemical Cell Study of Cut-Edge Corrosion Inhibition on Coil-Coated Steel Sheet by Chromate-, Phosphate-, and Calcium-Containing Pigments (2001)

Corrosion at cut edges is the most important failure mechanism of organic-coated, profiled galvanized steel architectural claddings. Currently, edge corrosion is generally controlled by the addition of strontium chromate in the paint primers; however, there is substantial interest in chromate replacements due to environmental reasons. This work describes an experimental study of inhibition with specific relevance to the cut-edge situation; essentially equivalent to a small galvanic cell between zinc and steel. Although chromate initially acts as an anodic inhibitor for Zinc corrosion at the cut edge, over a few hours of immersion, it was found to also strongly inhibit the steel cathode, hence reducing the cathodic protection current requirement on the zinc and thus acted as a mixed inhibitor in the cut-edge galvanic cell. Although individually, Zinc phosphate and calcium ion-exchanged silica pigments had relatively poor inhibition, they showed a strong synergistic effect. Thus, a mixture of the two compounds had comparable inhibitive efficiency to chromate. This was found to be due to a similar mixed inhibition mechanism as chromate. Thus, anodic inhibition of zinc was evident as well as strong cathodic inhibition on the steel due to the formation of a compact. thin film containing zinc, calcium, and phosphate species. © 2001 The Electrochemical Society. [DOI: 10.1149/1.1381072] All rights reserved.