gebhart/patrepeval huggingface dataset:
INDUCTION OF TOLERANCE-INDUCING ANTIGEN-PRESENTING CELLS IN BONE MARROW CULTURES IN VITRO USING MONOCLONAL ANTIBODIES TO CD200R (2004)

CD200 to CD200R interactions produce immunoregulation. We investigated whether the expression of CD200R on dendritic cell (DC) precursors affects their developmental fate. C57BL/6 bone marrow (BM) cells were cultured in vitro in the presence of (interleukin-4 + granulocyte-macrophage colony-stimulating activity) to generate allostimulatory DCs, which were in turn used to induce cytotoxic T-lymphocyte and cytokine production after culture with C3H responder spleen cells. Some marrow cultures included anti-CD200R antibodies. The inclusion of monoclonal antibodies in different isoforms of CD200R in the BM culture led to a generation of cells (tolerogenic DCs) that were unable to produce allostimulation in vitro with responder cells. Cells taken from these latter mixed leukocyte cultures (MLCs) now contained CD4(+)CD25(+) cells able to inhibit the antigen-specific MLC response of fresh C3H responder cells to stimulation with C57BL/6 cells, but not stimulation with BALB/c cells. Tolerogenic DCs, infused in vivo into mice receiving C57BL/6 skin grafts, produced antigen-specific decreased rejection of BL/6 allografts, not BALB/c allografts, compared with mice receiving control DCs (generated from BM in the absence of anti-CD200R). The induction of CD4(+)CD25(+) suppressor cells in MLCs using tolerogenic DCs from the initial BM cultures could be overcome by using limiting numbers of tolerogenic DCs and an excess of allostimulatory DCs derived from BM cultures maintained in the absence of anti-CD200R. These data indicate that anti-CD200R biases stem cells in BM toward the development of suppressive antigen-presenting cells, which can induce CD4(+)CD25(+) regulatory T cells. Tolerogenic DCs have the potential to modify graft acceptance in vivo.
Lamellar Domain Spacings of Diblock Copolymer/Homopolymer Blends and Conformations of Block Chains in Their Microdomains (1997)

Lamellar domain spacings (D) of blends of a styrene-2-vinylpyridine (SP) diblock copolymer and homopolymers corresponding to the block polymers (S and/or P), of which molecular weights are lower than that of the block polymer, were examined by small-angle X-ray scattering (SAXS), and the dimensions of block chains in the lamellae were investigated by small-angle neutron scattering (SANS). The D's for SP/S/P ternary and SP/S (or SP/P) binary blends increase with increasing the molecular weight of the homopolymers, MH, as well as the volume fraction of the homopolymers, ΦH, in the corresponding lamella. The variations of the D's with ΦH for the blends with homopolymers having different MH's reveal that homopolymers with higher MH are localized at the center of the corresponding lamella, while those with lower MH are distributed throughout the lamella. Moreover, the comparison between the D's for ternary and binary blends with homopolymers having equal MH's implies that the homopolymers in binary blends are more localized than those in ternary blends. In these ternary and binary blends the radii of gyration of styrene block chains along the direction parallel to lamellar interface are not much different from that for a pure diblock copolymer irrespective of ΦH as well as MH.
GISSD: Group I Intron Sequence and Structure Database (2007)

Group I Intron Sequence and Structure Database (GISSD) is a specialized and comprehensive database for group I introns, focusing on the integration of useful group I intron information from available databases and providing de novo data that is essential for understanding these introns at a systematic level. This database presents 1789 complete intron records, including the nucleotide sequence of each annotated intron plus 15 nt of the upstream and downstream exons, and the pseudoknots-containing secondary structures predicted by integrating comparative sequence analyses and minimal free energy algorithms. These introns represent all 14 subgroups, with their structure-based alignments being separately provided. Both structure predictions and alignments were done manually and iteratively adjusted, which yielded a reliable consensus structure for each subgroup. These consensus structures allowed us to judge the confidence of 20 085 group I introns previously found by the INFERNAL program and to classify them into subgroups automatically. The database provides intron-associated taxonomy information from GenBank, allowing one to view the detailed distribution of all group I introns. CDSs residing in introns and 3D structure information are also integrated if available. About 17 000 group I introns have been validated in this database; approximately 95% of them belong to the IC3 subgroup and reside in the chloroplast tRNA(Leu) gene. The GISSD database can be accessed at http://www.rna.whu.edu.cn/gissd/
Gallinacins: cysteine‐rich antimicrobial peptides of chicken leukocytes (1994)

We purified three homologous antimicrobial peptides ('gallinacins') from chicken leukocytes, examined their antimicrobial activity in vitro, and established their primary sequences by a combination of gas phase microsequencing and on-line LC-ESI-MS analysis of endo- and exoprotease peptide digests. The peptides contained 36-39 amino acid residues, were relatively cationic due to their numerous lysine and arginine residues, and each contained 3 intramolecular cystine disulfide bonds. Gallinacins showed primary sequence homology to the recently delineated beta-defensin family, heretofore found only in the respiratory epithelial cells and neutrophils of cattle, suggesting that beta-defensins originated at least 250 million years ago, before avian and mammalian lineages diverged. The 9 invariant residues (6 cysteines, 2 glycines and 1 proline) common to avian gallinacins and bovine beta-defensins are likely to constitute the essential primary structural motif of this ancient family of host-defense peptides.
CD97: a dedifferentiation marker in human thyroid carcinomas. (1997)

CD97 is a dimeric glycoprotein of Mr 75,000-85,000 and 28,000 belonging to a novel subfamily of seven-span transmembrane region leukocyte cell surface molecules. It is expressed abundantly in cells of hematopoietic origin. This is the first report demonstrating the expression of CD97 outside the hematopoetic system. CD97 was studied in normal human and neoplastic follicular epithelium of the thyroid and anaplastic (n = 3) and papillary (n = 1) thyroid carcinoma cell lines. In normal thyroid tissue (n = 11), no immunoreactivity of CD97 could be found, whereas in differentiated thyroid carcinomas (n = 10), CD97 expression was either lacking or low. Eleven of 12 undifferentiated anaplastic carcinomas revealed high CD97 presentation. CD97 was absent or only weakly present in patients with postoperative T1 tumors but increased greatly with the progression to postoperative T4 tumors. CD97 is clearly present in thyroid carcinoma cell lines but only at a very low level in normal human thyrocytes. Quantitation of CD97 cell surface expression levels revealed that C 643 and SW 1736 cells showed a two to four times higher specific antibody-binding capacity than did 8505 C and HTh 74 cells and a nearly 20 times higher specific antibody-binding capacity than normal thyrocytes. Phorbol 12-myristate 13-acetate treatment progressively caused a decrease of CD97 antigen expression in all cell lines to about 30% of their initial levels after 48 h. Immunohistochemical staining of SW 1736 cells revealed that CD97 is located in most of the cell compartments and suggested a CD97 internalization process after phorbol 12-myristate 13-acetate treatment. Semiquantitative reverse transcription-PCR showed a correlation of CD97 mRNA and cell surface CD97 expression level in the cell lines. SW 1736, HTh 74, and 8505 C cells apparently expressed CD97 with alternative glycosylation compared to peripheral lymphocytes, whereas most of the CD97 antigen presented on thyrocytes and C 643 cells had glycosylation sites resembling those of lymphocytes. The data suggest that CD97 expression may be a sensitive marker of dedifferentiation and of lymph node involvement in human thyroid tumors.
Ghrelin Prevents Cisplatin-Induced Mechanical Hyperalgesia and Cachexia (2007)

Complications induced by the chemotherapeutic agent cisplatin, such as neuropathy and cachexia, occur frequently, are often dose limiting, and have an impact on quality of life and survival in cancer patients. The recently discovered hormone ghrelin is a potent GH secretagogue with orexigenic and neuroprotective properties that may prevent or ameliorate these complications. The objective of this study was to determine the effects of ghrelin administration on mechanical hyperalgesia, anorexia, and cachexia induced by cisplatin. Adult male Sprague-Dawley rats were given cisplatin, ghrelin, ghrelin-cisplatin, or vehicle ip. Food intake and body weight were measured daily. Behavioral tests to assess the development of hyperalgesia were conducted by measuring mechanical and thermal sensitivity. Plasma ghrelin and IGF-I levels were also measured. Our results indicate that ghrelin coadministration inhibited the development of cisplatin-induced mechanical hyperalgesia, anorexia, and cachexia induced by cisplatin. Although ghrelin treatment had no effect on plasma IGF-I levels in control rats, it prevented the decrease in IGF-I levels induced by cisplatin. The attenuation of cisplatin-induced mechanical hyperalgesia induced by ghrelin was correlated with the prevention of cisplatin-induced lowering of IGF-I. In conclusion, ghrelin administration may be useful in the treatment or prevention of chemotherapy induced neuropathy and cachexia. Attenuation of mechanical hyperalgesia in the rat by the hormone ghrelin provides a unique model for elucidating the mechanisms involved, which are essential toward our understanding of these complications.
Role of surface morphology in wafer bonding (1991)

The strain patterns detected by x-ray topography in wafers bonded for silicon-on-insulator (SOI) technology were found related to the flatness nonuniformity of the original wafers. Local stresses due to the bonding process are estimated to be about 1×108 dynes/cm2. The stress is reduced about 100 times for the thin (0.5 μm) SOI films. Most of the wafer deformation occurs during room temperature mating of the wafers. The deformation is purely elastic even at 1200 °C. The magnitude of the stress appears insignificant for complimentary metal-oxide-semiconductor devices performance.
Effect of coronary sinus occlusion on coronary pressure-flow relations (1980)

We studied the effect of transient occlusion of the coronary sinus on the relationship between aortic pressure and circumflex coronary blood flow in open-chest anesthetized dog preparations during artificially prolonged diastoles. The coronary pressure-flow relation was linear, and flow stopped at an arterial pressure (Pf = 0) that always exceeded coronary venous pressure (Pcv). During reactive hyperemia, Pf = 0 was 31 mmHg when Pcv was 5 mmHg and increased to 52 mmHg when the coronary sinus was occluded (Pcv, 38 mmHg). Elevation of Pcv translated the coronary pressure-flow relation to a higher Pf = 0 without altering the slope of the relation. Pf = 0 increased by about two-thirds of the increase in Pcv. We found no evidence that there existed a level of Pcv below which changes in Pcv had no effect on the coronary pressure-flow relation. These data are not compatible with the existence of a vascular waterfall mechanism in the coronary circulation unless it is assumed that Pcv is one of the determinants of Pf = 0.
Thioredoxin Peroxidase Is a Novel Inhibitor of Apoptosis with a Mechanism Distinct from That of Bcl-2 (1997)

Thioredoxin peroxidase (TPx) is a member of a newly discovered family of proteins that are conserved from yeast to mammals and to which natural killer enhancing factor belongs. These proteins are antioxidants that function as peroxidases only when coupled to a sulfhydryl reducing system. The physiological function of TPx in cells is not yet known. Here we demonstrate that when the human TPx II, a member of this family, is stably overexpressed in Molt-4 leukemia cells, it protects from apoptosis induced by serum deprivation, ceramide, or etoposide. TPx II, like Bcl-2, is able to inhibit release of cytochrome c from mitochondria to cytosol, and it inhibits lipid peroxidation in cells. TPx II, unlike Bcl-2, could prevent hydrogen peroxide accumulation in cells, suggesting that it functions upstream of Bcl-2 in the protection from apoptosis and may be implicated as an endogenous regulator of apoptosis.
Dictionary of protein secondary structure: Pattern recognition of hydrogen‐bonded and geometrical features (1983)

Abstract For a successful analysis of the relation between amino acid sequence and protein structure, an unambiguous and physically meaningful definition of secondary structure is essential. We have developed a set of simple and physically motivated criteria for secondary structure, programmed as a pattern‐recognition process of hydrogen‐bonded and geometrical features extracted from x‐ray coordinates. Cooperative secondary structure is recognized as repeats of the elementary hydrogen‐bonding patterns “turn” and “bridge.” Repeating turns are “helices,” repeating bridges are “ladders,” connected ladders are “sheets.” Geometric structure is defined in terms of the concepts torsion and curvature of differential geometry. Local chain “chirality” is the torsional handedness of four consecutive C α positions and is positive for right‐handed helices and negative for ideal twisted β‐sheets. Curved pieces are defined as “bends.” Solvent “exposure” is given as the number of water molecules in possible contact with a residue. The end result is a compilation of the primary structure, including SS bonds, secondary structure, and solvent exposure of 62 different globular proteins. The presentation is in linear form: strip graphs for an overall view and strip tables for the details of each of 10.925 residues. The dictionary is also available in computer‐readable form for protein structure prediction work.
Oxidative Stress, Chromatin Remodeling and Gene Transcription in Inflammation and Chronic Lung Diseases (2003)

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-capital KJE, MacedonianB and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-kappaB/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and antiinflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.
Photon energy recovery for crosstalk correction in simultaneous 99mTc/201Tl imaging. (2000)

PER is quantitatively efficient to remove 99mTc crosstalk photons from 201Tl images for 99mTc/201Tl ratios ranging from 5:1 to 2:1.
Identification of a tumor necrosis factor-responsive element in the tumor necrosis factor alpha gene (1991)

The regulation by tumor necrosis factor alpha (TNF) of its own promoter has been investigated by transient transfection and nuclear protein binding assays. In human K652 erythroleukemia cells TNF produced an 8-10-fold activation of the human TNF promoter linked to the chloramphenicol acetyltransferase gene. The TNF-responsive element was localized to the -125 to -82 region by examining the TNF activation in 5'-deletion or site-directed mutants of the TNF promoter and by demonstrating that the -125 to -82 fragment confers TNF responsiveness to the thymidine kinase promoter. This region contains a palindrome, 5' TGAGCTCA 3', that resembles the consensus binding sequences for the transcription factors, activator protein-1 (AP-1), cyclic AMP-responsive element binding protein (CREB), and activation transcription factor (ATF). An internal deletion in the palindrome abolished the TNF responsiveness, whereas known AP-1 and CREB/ATF elements were unresponsive to TNF. In band shift analyses a nuclear factor from U937 cells specifically bound to the -125 to -82 TNF-responsive fragment in or near the palindromic sequence. Oligonucleotides containing AP-1 or CREB/ATF sites did not effectively compete for the binding, indicating that the U937 cell factor is different from these factors. Anti-c-fos antiserum did not affect binding of the U937 cell factor, whereas anti-c-jun antiserum did block its binding, indicating that either c-jun or a protein antigenically related to c-jun is a component of the factor. These results suggest that the TNF-responsive element is not activated by AP-1 or CREB in U937 cells and that a novel DNA binding factor is important for constitutive and inducible TNF gene expression.
Arabidopsis thaliana VTC4 Encodes L-Galactose-1-P Phosphatase, a Plant Ascorbic Acid Biosynthetic Enzyme (2006)

In plants, a proposed ascorbate (vitamin C) biosynthesis pathway occurs via GDP-D-mannose (GDP-D-Man), GDP-L-galactose (GDP-L-Gal), and L-galactose. However, the steps involved in the synthesis of L-Gal from GDP-L-Gal in planta are not fully characterized. Here we present evidence for an in vivo role for L-Gal-1-P phosphatase in plant ascorbate biosynthesis. We have characterized a low ascorbate mutant (vtc4-1) of Arabidopsis thaliana, which exhibits decreased ascorbate biosynthesis. Genetic mapping and sequencing of the VTC4 locus identified a mutation (P92L) in a gene with predicted L-Gal-1-P phosphatase activity (At3g02870). Pro-92 is within a beta-bulge that is conserved in related myo-inositol monophosphatases. The mutation is predicted to disrupt the positioning of catalytic amino acid residues within the active site. Accordingly, L-Gal-1-P phosphatase activity in vtc4-1 was approximately 50% of wild-type plants. In addition, vtc4-1 plants incorporate significantly more radiolabel from [2-(3)H]Man into L-galactosyl residues suggesting that the mutation increases the availability of GDP-L-Gal for polysaccharide synthesis. Finally, a homozygous T-DNA insertion line, which lacks a functional At3g02870 gene product, is also ascorbate-deficient (50% of wild type) and deficient in L-Gal-1-P phosphatase activity. Genetic complementation tests revealed that the insertion mutant and VTC4-1 are alleles of the same genetic locus. The significantly lower ascorbate and perturbed L-Gal metabolism in vtc4-1 and the T-DNA insertion mutant indicate that L-Gal-1-P phosphatase plays a role in plant ascorbate biosynthesis. The presence of ascorbate in the T-DNA insertion mutant suggests there is a bypass to this enzyme or that other pathways also contribute to ascorbate biosynthesis.
The effect of continuous G‐CSF application in human cyclic neutropenia: a model analysis (1995)

Human cyclic neutropenia (CN) is a rare haematological disorder characterized by oscillations of blood neutrophils at subnormal levels with a stable period of approximately 21 d. During the phase of severe neutropenia (neutrophils < 250 cells/microliters), which last 4-10 d, the patients are endangered by serious infections. Several authors report that continuous G-CSF application can elevate the blood neutrophils to such a level that the risk of infections is significantly reduced. Although the characteristic cycles are not eliminated by G-CSF, the period of the oscillations is shortened to 12-14 d. Based on a previously proposed computer-simulation model of human CN, the effects of continuous G-CSF application on CN are studied. It is shown how the known different cell-kinetic effects of G-CSF on granulopoiesis explain the clinical data in CN. The reduced length of the cycles emerges as a result of the transit time reduction of the post-mitotic granulopoietic cells by G-CSF. The measured increase of the neutrophil maxima is reproduced by the additional mitoses of the immature granulopoietic bone marrow cells induced by G-CSF. The slight elevation of the neutrophil nadirs can be attributed to a weak effect of G-CSF on the assumed underlying defect in CN (an abnormally small variance of the granulopoietic bone-marrow transit time).
Expression of the Met/HGF receptor in normal and neoplastic human tissues. (1991)

The MET oncogene encodes a transmembrane tyrosine kinase receptor. Recently, hepatocyte growth factor (HGF), a potent growth factor for hepatocytes involved in liver regeneration, has been proposed as a ligand. In this paper, the physiological role of the human Met/HGF receptor is investigated by studying its specific distribution in normal and neoplastic tissues. Northern blot analysis has shown that the MET gene is selectively expressed in several epithelial tissues. High levels of MET mRNA have been found in liver, gastrointestinal tract, thyroid and kidney. Western blot analysis has shown that the levels of the Met protein generally correspond to those of the mRNA. However, in the thyroid, where there is a high level of MET mRNA, the protein was barely detectable, suggesting translational or post-translational regulation. The protein was also detected in the brain. Normal or increased levels of MET mRNA and Met protein were consistently found in fresh samples of carcinomas as well as in epithelial tumor cell lines. In thyroid carcinomas of a specific histiotype the amount of Met protein, almost undetectable in the normal counterpart, was found to be increased more than 100-fold. The tissue distribution of the Met/HGF receptor indicates that this molecule is involved in growth control of epithelial cells other than hepatocytes and suggests that its increased expression may confer a growth advantage to neoplastic cells.