gebhart/patrepeval huggingface dataset:
THEMULTIFUNCTIONALCAPSIDPROTEINS OFPLANTRNA VIRUSES (2001)

This article summarizes studies of viral coat (capsid) proteins (CPs) of RNA plant viruses. In addition, we discuss and seek to interpret the knowledge accumulated to data. CPs are named for their primary function; to encapsidate viral genomic nucleic acids. However, encapsidation is only one feature of an extremely diverse array of structural, functional, and ecological roles played during viral infection and spread. Herein, we consider the evolution of viral CPs and their multitude of interactions with factors encoded by the virus, host plant, or viral vector (biological transmission agent) that influence the infection and epidemiological facets of plant disease. In addition, applications of today's understanding of CPs in the protection of crops from viral infection and use in the manufacture of valuable compounds are considered.
Myeloid Suppressor Lines Inhibit T Cell Responses by an NO-Dependent Mechanism (2002)

CD11b(+)Gr-1(+) myeloid suppressor cells (MSC) accumulate in lymphoid organs under conditions of intense immune stress where they inhibit T and B cell function. We recently described the generation of immortalized MSC lines that provide a homogeneous source of suppressor cells for dissecting the mechanism of suppression. In this study we show that the MSC lines potently block in vitro proliferation of T cells stimulated with either mitogen or antigenic peptide, with as few as 3% of MSC cells causing complete suppression. Inhibition of mitogenic and peptide-specific responses is not associated with a loss in IL-2 production or inability to up-modulate the early activation markers, CD69 and CD25, but results in direct impairment of the three IL-2R signaling pathways, as demonstrated by the lack of Janus kinase 3, STAT5, extracellular signal-regulated kinase, and Akt phosphorylation in response to IL-2. Suppression is mediated by and requires NO, which is secreted by MSC in response to signals from activated T cells, including IFN-gamma and a contact-dependent stimulus. Experiments with inducible NO synthase knockout mice demonstrated that the inhibition of T cell proliferation by CD11b(+)Gr-1(+) cells in the spleens of immunosuppressed mice is also dependent upon NO, indicating that the MSC lines accurately represent their normal counterparts. The distinctive capacity of MSC to generate suppressive signals when encountering activated T cells defines a specialized subset of myeloid cells that most likely serve a regulatory function during times of heightened immune activity.
Patterns of cytokine secretion by autoreactive proteolipid protein-specific T cell clones during the course of multiple sclerosis. (1995)

To determine whether cytokine secretion patterns change with disease status in patients with multiple sclerosis (MS), we measured IFN-gamma, TNF-alpha beta, IL-4, IL-6, IL-10 and TGF-beta secretion in a panel of T cell clones (TCCs) specific for proteolipid protein (PLP) after stimulation with PLP peptides or polyclonal activators. During acute attack, the predominant pattern of cytokine secretion resembled that of murine Th1 cells; i.e, IFN-gamma and TNF-alpha beta, and appeared to be restricted to PLP-reactive TCCs. None of the TCCs isolated during acute attack produced TGF-beta in response to PLP, Con A, or anti-CD3 Ab. Half of these TCCs were, however, capable of TGF-beta secretion and mRNA expression upon stimulation with PMA and the calcium inonphore A23187, suggesting a possible defect in activation through the TCR/CD3 pathway. During remission in the same patients all but two PLP-TCCs showed patterns of cytokine secretion resembling that of murine Th0, Th1, and Th2 subsets. The levels of IL-10 secreted by these TCCs were significantly higher than those of TCCs isolated during acute attacks and those derived from normal subjects and patients with other noninflammatory neurologic diseases. Furthermore, 50% of these TCCs were capable of producing TGF-beta after Ag-specific or polyclonal stimulation. All TCCs isolated from control subjects exhibited a Th0 like secretion profile. These data indicate that different stages of disease in MS are characterized by different patterns of cytokine secretion by PLP-specific TCCs, suggesting a role for cytokines in clinical events during the course of MS.
Tumor Suppressor Genes in Breast Cancer (2005)

Tumor suppressor genes encode for proteins whose normal function is to inhibit cell transformation and whose inactivation is advantageous for tumor cell growth and survival. A variety of mechanisms result in the inactivation of tumor suppressor genes, including intragenic mutations, chromosomal deletions, and loss of expression by methylation-mediated transcriptional silencing or increased proteolysis. Tumor suppressor genes participate in a variety of critical and highly conserved cell functions, including regulation of the cell cycle and apoptosis, differentiation, surveillance of genomic integrity and repair of DNA errors, signal transduction, and cell adhesion. Tumor suppressor functions can be separated into 2 major categories: gatekeepers and caretakers. Gatekeepers directly inhibit tumor growth or promote tumor death. Inactivation of these genes contributes directly to cancer formation and progression. Among them, the p53 gene is the most well known. Located on chromosome band 17p13, p53 encodes a 53-kd multifunctional transcription factor that regulates the expression of genes involved in cell cycle control, apoptosis, DNA repair, and angiogenesis. In breast cancer, most studies have shown that p53 mutation or down-regulation is associated with adverse prognosis. Other tumor suppressor genes of interest in breast cancer include the retinoblastoma gene (pRb), PTEN, p16, nm23, and maspin.
The Use of N-Formylamino Acids in Peptide Synthesis (1958)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Use of N-Formylamino Acids in Peptide SynthesisJohn C. Sheehan and Ding-Djung H. YangCite this: J. Am. Chem. Soc. 1958, 80, 5, 1154–1158Publication Date (Print):March 1, 1958Publication History Published online1 May 2002Published inissue 1 March 1958https://pubs.acs.org/doi/10.1021/ja01538a036https://doi.org/10.1021/ja01538a036research-articleACS PublicationsRequest reuse permissionsArticle Views2671Altmetric-Citations317LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Prostacyclin Synthesis Induced in Vascular Cells by Interleukin-1 (1985)

Supernatants from cultures of human monocytes that had been stimulated with endotoxin or silica induced the synthesis of prostacyclin in endothelial and smooth muscle cells. The lymphokine mediating these effects on the cells of the blood vessel wall was identified as interleukin-1; interferons and interleukin-2 were inactive. Interleukin-1-induced prostacyclin synthesis represents a new aspect of the interaction between the immune system (as well as other tissues) and the vessel wall and may serve as a basis for the development of new strategies in antithrombotic therapy.
Interferon‐regulated chemokines as biomarkers of systemic lupus erythematosus disease activity: A validation study (2009)

Monitoring serum chemokine levels in SLE may improve the assessment of current disease activity, the prediction of future disease flares, and the overall clinical decision-making.
Mitogenic Responses of Vascular Smooth Muscle Cells to Lipid Peroxidation-derived Aldehyde 4-Hydroxy-trans-2-nonenal (HNE) (2006)

Products of lipid peroxidation such as 4-hydroxy-trans-2-nonenal (HNE) trigger multiple signaling cascades that variably affect cell growth, differentiation, and apoptosis. Because glutathiolation is a significant metabolic fate of these aldehydes, we tested the possibility that the bioactivity of HNE depends upon its conjugation with glutathione. Addition of HNE or the cell-permeable esters of glutathionyl-4-hydroxynonenal (GS-HNE) or glutathionyl-1,4-dihydroxynonene (GS-DHN) to cultures of rat aortic smooth muscle cells stimulated protein kinase C, NF-kappaB, and AP-1, and increased cell growth. The mitogenic effects of HNE, but not GS-HNE or GS-DHN, were abolished by glutathione depletion. Pharmacological inhibition or antisense ablation of aldose reductase (which catalyzes the reduction of GS-HNE to GS-DHN) prevented protein kinase C, NF-kappaB, and AP-1 stimulation and the increase in cell growth caused by HNE and GS-HNE, but not GS-DHN. The growth stimulating effect of GS-DHN was enhanced in cells treated with antibodies directed against the glutathione conjugate transporters RLIP76 (Ral-binding protein) or the multidrug resistance protein-2. Overexpression of RLIP76 abolished the mitogenic effects of HNE and its glutathione conjugates, whereas ablation of RLIP76 using RNA interference promoted the mitogenic effects. Collectively, our findings suggest that the mitogenic effects of HNE are mediated by its glutathione conjugate, which has to be reduced by aldose reductase to stimulate cell growth. These results raise the possibility that the glutathione conjugates of lipid peroxidation products are novel mediators of cell signaling and growth.
Fecal Microbiota and Metabolome of Children with Autism and Pervasive Developmental Disorder Not Otherwise Specified (2013)

This study aimed at investigating the fecal microbiota and metabolome of children with Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and autism (AD) in comparison to healthy children (HC). Bacterial tag-encoded FLX-titanium amplicon pyrosequencing (bTEFAP) of the 16S rDNA and 16S rRNA analyses were carried out to determine total bacteria (16S rDNA) and metabolically active bacteria (16S rRNA), respectively. The main bacterial phyla (Firmicutes, Bacteroidetes, Fusobacteria and Verrucomicrobia) significantly (P<0.05) changed among the three groups of children. As estimated by rarefaction, Chao and Shannon diversity index, the highest microbial diversity was found in AD children. Based on 16S-rRNA and culture-dependent data, Faecalibacterium and Ruminococcus were present at the highest level in fecal samples of PDD-NOS and HC children. Caloramator, Sarcina and Clostridium genera were the highest in AD children. Compared to HC, the composition of Lachnospiraceae family also differed in PDD-NOS and, especially, AD children. Except for Eubacterium siraeum, the lowest level of Eubacteriaceae was found on fecal samples of AD children. The level of Bacteroidetes genera and some Alistipes and Akkermansia species were almost the highest in PDD-NOS or AD children as well as almost all the identified Sutterellaceae and Enterobacteriaceae were the highest in AD. Compared to HC children, Bifidobacterium species decreased in AD. As shown by Canonical Discriminant Analysis of Principal Coordinates, the levels of free amino acids and volatile organic compounds of fecal samples were markedly affected in PDD-NOS and, especially, AD children. If the gut microbiota differences among AD and PDD-NOS and HC children are one of the concomitant causes or the consequence of autism, they may have implications regarding specific diagnostic test, and/or for treatment and prevention.
Epithelial-Mesenchymal Interactions in Cancer (1995)

Epithelial-mesenchymal transitions in development and tumor progression.- Regulation of scatter factor (hepatocyte growth factor) production by tumor-stroma interaction.- Regulation of HGF and HGFR gene expression.- The role of scatter factor and the c-met proto-oncogene in angiogenic responses.- Modulation of intercellular junctions of epithelia by scatter factor (hepatocyte growth factor).- The Met-HGF/SF autocrine signaling mechanism is involved in sarcomagenesis.- Tumor cell interactions with the vascular endothelium and their role in cancer metastasis.- Stimulation and regulation of tumor cell motility in invasion and metastasis.- Tumor-stromal cytokine interactions in ovarian neoplasms.- Keratinocyte growth factor as a cytokine that mediates mesenchymal-epithelial interaction.- Stromal-epithelial interaction in type IV collagenase expression and activation: The role in cancer metastasis.- Angiogenesis as a component of epithelial-mesenchymal interactions.- Mammary tumor fibroblasts are phenotypically distinct from non-tumor fibroblasts.- Fibroblast subpopulations as accelerators of tumor progression: The role of migration stimulating factor.
The Association of Measured Breast Tissue Characteristics with Mammographic Density and Other Risk Factors for Breast Cancer (2005)

All risk factors for breast cancer must ultimately exert their influence by an effect on the breast, and these findings suggest that, for some risk factors, this influence includes an effect on the number of cells and the quantity of collagen.
Bodenin: A novel murine gene expressed in restricted areas of the brain (1998)

A gene trap screen designed to isolate novel mouse genes involved in nervous system development was performed. Here, we describe the isolation and characterization of a novel gene, bodenin, which is expressed in restricted areas of the brain. beta-Galactosidase marker gene activity was detected in the embryo at the start of organogenesis (embryonic day 8.5; E8.5). Staining gradually became stronger until E12.5, when embryos exhibited widespread expression. In brains of newborn and adult mice, beta-galactosidase staining was confined predominantly to forebrain structures. Transcriptional activity was also observed in kidney, liver, lung, heart, skeletal muscle, and testes. Part of the trapped gene was isolated by 5'-rapid amplification of cDNA ends (5'-RACE). Isolation and sequencing of the complete cDNA revealed an unknown gene encoding a 200 amino acid protein. Comparison with published sequences showed 94% amino acid identity to a human integrin cytoplasmic domain-associated protein. Mice homozygous for the mutation were viable and did not exhibit any obvious abnormal phenotype. However, concealed phenotypic abnormalities cannot be excluded. The lack of readily visible abnormalities may also be due to functional compensation or to the production of low levels of wild-type protein in mice homozygous for the gene trap vector insertion. Nevertheless, the restricted expression of bodenin in the brain of newborn and adult mice suggests a role for this novel gene in the developing and mature central nervous system.
Overview of the applicability of H.264/MVC for real-time light-field applications (2014)

Several methods for compressing light-fields (LF) and multiview 3D video content have been proposed in the literature. The most widely accepted and standardized method is the Multi View Coding (MVC) extension of H.264, which is considered appropriate for use with stereoscopic and multiview 3D displays. In this paper we will focus on light-field 3D displays, outline typical use cases for such displays, analyze processing requirements for display-specific and display-independent light-fields, and see how these map to MVC as the underlying 3D video compression method. We also provide an overview of available MVC implementations, and the support these provide for multiview 3D video. Directions for future research and additional features supporting LF video compression are presented.
The second intron of the K-ras gene containsregulatory elements associated with mouse lung tumorsusceptibility. (1994)

We have previously demonstrated the preferential activation of the K-ras gene from the susceptible A/J parent in lung tumors from F1 mouse hybrids. In the present study, the mechanism of this observation is further investigated. Higher levels of expression of A/J K-ras allele were detected in lung adenomas (30 of 30) from the C3A mouse. In addition, three K-ras alleles, designated as susceptible (Ks), intermediate (Ki), or resistant (Kr), were identified by sequence analysis of the second intron of the K-ras gene from 32 strains of mice. These K-ras alleles are associated with differences in mouse lung tumor susceptibility. All Kr alleles have a tandem 37-bp direct repeat (nt 282-355) in the second intron of the K-ras gene. Ks and Ki alleles have only one copy of the 37-bp sequence (nt 282-318). Ks strains have three base variations at nt 288, 296, and 494, and Ki strains have two base variations at nt 288 and 494 in the second intron of the K-ras gene. Differential protein-binding patterns were observed in gel-mobility-shift experiments between the duplicated 37-bp sequence of the Kr allele and the single 37-bp sequence of the Ks and Ki alleles. DNase I footprinting assay revealed protein binding sites in the second intron of the K-ras gene that correspond to the tandem repeat sequences. Our data suggest that higher expression of the A/J allele relative to C3H allele may be responsible for the allele-specific activation of the K-ras gene in lung tumors from F1 hybrid mice.
Nanomaterials for Heterogeneous Combustion (2004)

Abstract Nanophase materials and nanocomposites, characterized by an ultra fine grain size (less than 100 nm) have attracted wide spread interest in recent years by virtue of their unusual mechanical, electrical, optical, magnetic, and energetic properties. Studies have shown that the thermal behavior of nano‐scaled materials is quite different from micron‐sized powders. Nanosized metallic and explosive powders have been used as solid propellant and explosive mixtures to increase efficiency. At the same time recent studies reveal that the presence of nanosized metals in propellants does not necessary translate into an increased burning rate and burning temperature. The reasons of this effect are far from being clear. This paper presents a new approach to the production of nanocomposites of some energetic materials – ammonium nitrite, cyclotrimethylene trinitramine (RDX), and aluminum – by the vacuum co‐deposition technique. The thermal behavior of the synthesized nanopowder and nanocomposites is investigated. A substantial difference in burning rate of RDX nanopowder has been found in comparison to micron‐sized material. Experimental results allow investigating the effects of nanosized materials on the combustion characteristics.
Atlas of Zeolite Structure Types (1988)

This is an expanded and updated version of the 1978 compilation, which defines and supplies a condensed characterization of the currently established zeolite structure types. New types of microporous solids, such as aluminophosphate molecule sieves based on tetrahedral frameworks, have expanded the field of zeolites and zeolite-like materials. The number of known and topologically distinct tetrahedral networks has risen to 64 and is expected to continue to increase at the rate of at least three per year. The numerous new materials and the advent of modern methods of structure solving, in particular powder techniques including ab initio structure determinations and Rietveld refinements, have made this rapid advance possible.
Prenatal diagnosis of myotonic dystrophy using fetal DNA obtained from maternal plasma. (2000)

Myotonic dystrophy (DM; MIM 160900) is an autosomal dominant disorder associated with expansion of an unstable CTG trinucleotide repeat in the 3′ untranslated region of the DM kinase gene (DMPK) on chromosome 19q13 (1). Patients are heterozygous for expanded alleles in the range of 50–4000 repeats (1). The molecular diagnosis of DM routinely is performed by analyzing the CTG number on genomic DNA extracted from various biological sources, including trophoblast cells sampled at 10–11 weeks of amenorrhea during the first trimester of pregnancy (2)(3). We evaluated the possibility of using maternal plasma for prenatal diagnosis of DM, by monitoring the pregnancy of an unaffected woman whose husband was affected by DM (70 CTG repeats).

All participants gave oral and written informed consent.

A blood sample (∼10 mL) was collected at 10 weeks of gestation before chorionic villus sampling (CVS) and was centrifuged at 3000 g for 10 min. Plasma was carefully removed from EDTA-containing tube and centrifuged again at 3000 …
Current Medical Diagnosis and Treatment 1986. (1986)

Current Medical Diagnosis and Treatment 2011 - Libros de Medicina - Medicina general - 85,50
Tissue pH Determination for the Detection of Metabolically Active, Inflamed Vulnerable Plaques Using Near-Infrared Spectroscopy: An in-vitro Feasibility Study (2004)

Detection of vulnerable plaques as the underlying cause of myocardial infarction is at the center of attention in cardiology. We have previously shown that infiltration of inflammatory cells in atherosclerotic plaques renders these plaques relatively hot and acidic, with substantial plaque temperature and pH variation. The objective of this investigation was to determine whether near-infrared diffuse reflectance spectroscopy (NIRS) could be used to non-destructively measure the tissue pH in atherosclerotic plaques. NIRS and tissue pH electrode measurements were taken on freshly excised carotid plaques maintained under physiological conditions. The coefficient of determination between NIRS and the pH microelectrode measurement was 0.75 using 17 different areas. The estimated accuracy of the NIRS measurement was 0.09 pH units. These results demonstrate the feasibility of using NIRS tissue pH in freshly excised atherosclerotic plaques in light of marked pH heterogeneity and warrants future in-vivo investigations on pH measurement of atherosclerotic plaques.
Directing osteogenic and myogenic differentiation of MSCs: interplay of stiffness and adhesive ligand presentation (2008)

The mechanical properties of the extracellular matrix (ECM) can exert significant influence in determining cell fate. Human mesenchymal stem cells (MSCs) grown on substrates with varying stiffness have been shown to express various cell lineage markers, without the use of toxic DNA demethylation agents or complex cocktails of expensive growth factors. Here we investigated the myogenic and osteogenic potential of various polyacrylamide gel substrates that were coated with covalently bound tissue-specific ECM proteins (collagen I, collagen IV, laminin, or fibronectin). The gel-protein substrates were shown to support the growth and proliferation of MSCs in a stiffness-dependent manner. Higher stiffness substrates encouraged up to a 10-fold increase in cell number over lower stiffness gels. There appears to be definitive interplay between substrate stiffness and ECM protein with regard to the expression of both osteogenic and myogenic transcription factors by MSCs. Of the 16 gel-protein combinations investigated, osteogenic differentiation was found to occur significantly only on collagen I-coated gels with the highest modulus gel tested (80 kPa). Myogenic differentiation occurred on all gel-protein combinations that had stiffnesses >9 kPa but to varying extents as ascertained by MyoD1 expression. Peak MyoD1 expression was seen on gels with a modulus of 25 kPa coated in fibronectin, with similar levels of expression observed on 80-kPa collagen I-coated gels. The modulation of myogenic and osteogenic transcription factors by various ECM proteins demonstrates that substrate stiffness alone does not direct stem cell lineage specification. This has important implications in the development of tailored biomaterial systems that more closely mimic the microenvironment found in native tissues.