gebhart/patrepeval huggingface dataset:
Soil-Structure Interaction (2023)

<p class="MDPI31text" style="text-indent: 0cm;">It is crucial that scientists and engineers develop their expertise and capability through research and practice to quantify the interaction of infrastructure with the surroundings and the ground upon which they are founded. Therefore, the engineering concept &lsquo;soil&ndash;structure interaction&rsquo; forms an integral part of delivering successful project outcomes. As the Lead and Honorary Editor for this Special Issue, Soil&ndash;Structure Interaction, I cordially invited the submission of esteemed articles related to recent projects, research, or case studies. These articles detail how geosciences (soil, rock, ground water, geochemistry, geology, hydrogeology, surface run-off, rain, wind, and temperature) directly interact with and impact the performance of human-made structures, buildings, or infrastructure through the following aspects: <p class="MDPI31text">i) Underground construction; ii) Innovative ground improvement methods; iii) Geological explorations and interpretation; iv) Instrumentation and field observational method; v) Use of artificial intelligence or algorithms; vi) Forensic engineering or inverse-analysis methods; vii) Geophysical methods for soil or rock characterization; viii) Advancement in laboratory and field testing of geomaterials; ix) Advancement in numerical analysis; x) Advancement in multi-disciplinary design theories, codes of practice, and engineering education.
Efficiencies and Mechanisms of Nuclear Reprogramming (2010)

The differentiated state of somatic cells is highly stable, but it can be experimentally reversed. The resulting cells can then be redirected into many different pathways. Nuclear reprogramming has been achieved by nuclear transfer to eggs, cell fusion, and overexpression of transcription factors. The mechanisms of nuclear reprogramming are not understood, but some insight into them is provided by comparing the efficiencies of different reprogramming strategies. Here, we compare these efficiencies by describing the frequency and rapidity with which reprogramming is induced and by the proportion of cells and level of expression in which reprogramming is achieved. We comment on the mechanisms that lead to successful somatic-cell reprogramming and on those that resist in helping to maintain the differentiated state of somatic cells.
Insulin-Like Growth Factor Receptor-1 as an Anti-Cancer Target: Blocking Transformation and Inducing Apoptosis (2002)

IGF-IR (Insulin-like growth factor receptor 1) is a tetrameric glycoprotein composed of two alpha and two beta subunits. The alpha subunit localizes extra-cellularly for ligand binding, whereas the beta subunit consists of transmembrane chains and a cytoplasmic tyrosine kinase domain for enzymatic activity. IGF-IR ligands, IGF-I and IGF-II, are mitogens and survival factors for many cancer cells. Binding of ligands to the IGF-IR initiates a cascade of events leading to activation of signal transduction pathways, mainly MAPK and PI-3K pathways, to stimulate proliferation/mitogenesis, to induce neoplastic transformation, to inhibit apoptosis, and to promote angiogenesis and metastasis. It has been shown that the presence of IGF-IR was required for transformation induced by many oncogenes and over-expression or constitutive activation of IGF-IR gave rise to transformed phenotypes. Significantly, over-expression of IGF-IR was observed in multiple human cancers including carcinomas of breast, lung, colon, and prostate. Patients with IGF-IR positive cancers had a worse prognosis in some cases. Furthermore, down-regulation or functional inactivation of IGF-IR sensitized tumor cells to apoptosis and reversed tumor cell phenotype. Thus, IGF-IR appears to be a promising cancer target. Indeed, a variety of approaches aimed at targeting IGF-IR have been utilized to prove the concept, or are being developed for potential anticancer therapies. These include targeting functional IGF-IR on cell surface, targeting ligand/receptor interaction, targeting receptor expression and functions, and targeting receptor kinase activity. Cancer patients could eventually benefit from the development of these specific IGF-IR antagonists.
Restoration of renal response to atrial natriuretic factor in experimental low-output heart failure (1989)

The renal response to atrial natriuretic factor (ANF) has been shown to be blunted in several experimental models of acute and chronic congestive heart failure. The mechanism responsible for this blunted response has been postulated to be activation of the renin-angiotensin system with associated potent antinatriuretic effects and/or the reduction in renal perfusion pressure (RPP) characteristic of heart failure. The present study was designed to examine the relative role of these two factors in mediating the blunted response to ANF in a model of acute low output heart failure produced by thoracic inferior vena cava constriction (TIVCC) in the anesthetized dog. TIVCC was produced in five groups of dogs. In group 1, ANF was infused after TIVCC to document the blunted natriuretic response. In group 2, ANF was infused after TIVCC in the presence of blockade of intrarenal angiotensin II (ANG II) by the intrarenal infusion of saralasin (Sar) at a dose without systemic effects. In group 3, ANF was infused after TIVCC in the presence of restoration of RPP by infusion of ANG II at a dose titrated to restore RPP to the level present before TIVCC. In group 4, ANF was infused in the presence of restoration of RPP with ANG II and blockade of intrarenal ANG II with Sar. Group 5 served as an additional control group where the effect of ANG II and Sar in TIVCC was examined in the absence of ANF. Restoration of RPP but not blockade of intrarenal ANG II resulted in a restoration of the response of sodium excretion and glomerular filtration rate to ANF. ANG II plus Sar in the absence of ANF did not produce a natriuresis. We conclude that RPP, more than intrarenal ANG II, modulates the blunted renal response to ANF observed in this model of acute low-output heart failure.
Studies on the Aroma of Five Fresh Tomato Cultivars and the Precursors of cis- and trans-4,5-Epoxy-(E)-2-Decenals and Methional (2008)

Three tasty (BR-139, FA-624, and FA-612) and two less tasty (R-144 and R-175) fresh greenhouse tomato cultivars, which significantly differ in their flavor profiles, were screened for potent odorants using aroma extract dilution analysis (AEDA). On the basis of AEDA results, 19 volatiles were selected for quantification in those 5 cultivars using gas chromatography−mass spectrometry (GC-MS). Compounds such as 1-penten-3-one, (E,E)- and (E,Z)-2,4-decadienal, and 4-hydroxy-2,5-dimethyl-3(2H)-furanone (Furaneol) had higher odor units in the more preferred cultivars, whereas methional, phenylacetaldehyde, 2-phenylethanol, or 2-isobutylthiazole had higher odor units in the less preferred cultivars. Simulation of the odor of the selected tomato cultivars by preparation of aroma models and comparison with the corresponding real samples confirmed that all important fresh tomato odorants were identified, that their concentrations were determined correctly in all five cultivars, and that differences in concentration, especially of the compounds mentioned above, make it possible to distinguish between them and are responsible for the differential preference. To help elucidate formation pathways of key odorants, labeled precursors were added to tomatoes. Biogenesis of cis- and trans-4,5-epoxy-(E)-2-decenals from linoleic acid and methional from methionine was confirmed.
Measuring the photon number parity in a cavity: from light quantum jumps to the tomography of non-classical field states (2007)

The photon number parity is a binary observable playing an important role in the description of the non-classical features of light. In microwave experiments, this observable can be measured by using a single Rydberg atom evolving in a two dimension space and interacting dispersively with a field stored in one or two cavities. The procedure, based on atomic interferometry, maps the field parity (+ 1 or − 1) onto the states of the two-level atom. By performing repeated measurements of the field parity, it is possible to observe field quantum jumps, to reconstruct the complete Wigner function of an arbitrary field and to study how it evolves due to decoherence.
Anticorps anti-neuronaux et affections du système nerveux central : apport diagnostique et intérêt physiopathologique (2000)

Des anticorps reagissant avec des antigenes du systeme nerveux central ont ete mis en evidence dans plusieurs affections neurologiques. Les plus connus sont les differents anticorps associes aux syndromes neurologiques paraneoplasiques (anticorps anti-Hu, Yo, Ri, amphiphysine, Tr, CV2 et Ta). Ces anticorps qui sont pour certains d'entre eux specifiques d'un type de cancer et d'un type de syndrome neurologique sont des outils diagnostiques precieux pour le clinicien. Ils ont contribue a l'hypothese que les syndromes neurologiques paraneoplasiques mettaient en jeu une auto-immunite croisee entre des antigenes tumoraux et des antigenes du systeme nerveux. Cependant, il est peu vraisemblable qu'ils soient par eux-memes pathogenes. Les anticorps anti-canaux calciques voltage dependants associes au syndrome de Lambert-Eaton qui n'est paraneoplasique que dans 60 p. 100 des cas s'observent aussi en cas d'atrophie cerebelleuse paraneopiasique. Les anticorps anti-GAD surviennent au cours du syndrome de l'homme raide non paraneoplasique et dans certaines atrophies cerebelleuses progressives. Des anticorps reagissant avec differents types de recepteurs au glutamate ont ete detectes dans differentes affections neurologiques dont l'encephalite de Rasmussen. Enfin on a decrit des anticorps au cours d'affections diverses telles que la sclerose laterale amyotrophique, la choree de Sydenham ou le syndrome de Gilles de la Tourette. La signification des anticorps observes en dehors du contexte des syndromes paraneoplasiques n'est pas a l'heure actuelle etablie mais les anticorps anti-GAD associes a des atrophies cerebelleuses progressives et des polyendocrinopathies autoimmunes pourraient temoigner du caractere autoimmun de certains processus neurologiques d'allure degenerative affectant le systeme nerveux central.
Test data decompression for multiple scan designs with boundary scan (1998)

The paper presents an efficient scheme to compress and decompress in parallel deterministic test patterns for circuits with multiple scan chains. It employs a boundary-scan-based environment for high quality testing with flexible trade-offs between test data volume and test application time while achieving a complete fault coverage for any fault model for which test cubes are obtainable. It also reduces bandwidth requirements, as all test cube transfers involve compressed data. The test patterns are generated by the reseeding of a two-dimensional hardware structure which is comprised of a linear feedback shift register (LFSR), a network of exclusive-or (XOR) gates used to scramble the bits of test vectors, and extra feedbacks which allow including internal scan flip-flops into the decompressor structure to minimize the area overhead. The test data decompressor operates in two modes: pseudorandom and deterministic. In the first mode, the pseudorandom pattern generator (PRPG) is used purely as a generator of test vectors. In the latter case, variable-length seeds are serially scanned through the boundary-scan interface into the PRPG and parts of internal scan chains and, subsequently, a decompression is performed in parallel by means of the PRPG and selected scan flip-flops interconnected to form the decompression device. Extensive experiments with the largest ISCAS' 89 benchmarks show that the proposed technique greatly reduces the amount of test data in a cost effective manner.
Induction of monocyte migration by recombinant macrophage colony-stimulating factor. (1988)

Human recombinant macrophage-CSF (M-CSF) induced migration across polycarbonate or nitrocellulose filters of human peripheral blood monocytes. Checkerboard analysis of M-CSF-induced migration, performed by seeding different cytokine concentrations above and below the filter, revealed that the locomotory response involved chemotaxis, though some gradient-independent augmentation of migration occurred. Polymixin B did not affect M-CSF chemotaxis and M-CSF was active on monocytes from the LPS-unresponsive mouse strain C3H/HeJ. These findings rule out a contribution of minute endotoxin contamination, below the sensitivity of the Limulus assay, in M-CSF chemotaxis. Rabbit anti-M-CSF antibodies inhibited the chemotactic activity of recombinant M-CSF, thus further indicating that the M-CSF molecule was indeed responsible for chemotaxis. M-CSF preparations encoded by 224 or 522 amino acid cDNA clones were equally effective in inducing monocyte migration. Recombinant M-CSF did not elicit a migratory response in large granular lymphocytes and in endothelial cells under conditions in which appropriate reference attractants were active. A modest stimulation of migration of polymorphonuclear leukocytes, inhibitable by antibodies, was observed at high cytokine concentrations (10 to 100 times higher than those required for monocyte locomotion). The maximal polymorphonuclear leukocytes response evoked by M-CSF was small compared to that evoked by reference chemoattractants or to that evoked by the same cytokine in monocytes. Hence, M-CSF is a potent chemoattractant for mononuclear phagocytes and exerts its action preferentially on cells of the monocyte-macrophage lineage. M-CSF, produced locally by activated macrophages, may play a role in the selective recruitment from the blood compartment of mononuclear phagocytes to amplify resistance against certain noxious agents.
Treatment of Prion Disease with Heterologous Prion Proteins (2015)

Prion diseases such as Creutzfeldt-Jakob disease in humans, bovine spongiform encephalopathy in cattle, and scrapie in sheep are fatal neurodegenerative diseases for which there is no effective treatment. The pathology of these diseases involves the conversion of a protease sensitive form of the cellular prion protein (PrPC) into a protease resistant infectious form (PrPsc or PrPres). Both in vitro (cell culture and cell free conversion assays) and in vivo (animal) studies have demonstrated the strong dependence of this conversion process on protein sequence homology between the initial prion inoculum and the host's own cellular prion protein. The presence of non-homologous (heterologous) proteins is often inhibitory to this conversion process. We hypothesize that the presence of heterologous prion proteins from one species might therefore constitute an effective treatment for prion disease in another species. To test this hypothesis, we infected mice intracerebrally with murine adapted RML-Chandler scrapie and treated them with heterologous prion protein (purified bacterially expressed recombinant hamster prion protein) or vehicle alone. Treated animals demonstrated reduced disease associated pathology, decreased accumulation of protease-resistant disease-associated prion protein, with delayed onset of clinical symptoms and motor deficits. This was concomitant with significantly increased survival times relative to mock-treated animals. These results provide proof of principle that recombinant hamster prion proteins can effectively and safely inhibit prion disease in mice, and suggest that hamster or other non-human prion proteins may be a viable treatment for prion diseases in humans.
Phage Display Based Cloning of Proteins Interacting with the Cytoplasmic Tail of Membrane Immunoglobulins (2002)

The reduced quantity and quality of serum immunoglobulins (sIgs) in mutant mice expressing truncated cytoplasmic tails of IgE and IgG1 indicate an active role for the cytoplasmic domains of mIgG1 and mIgE. We used phage display technology to identify candidate proteins able to interact with the cytoplasmic tail of mIgE. Using a murine cDNA B cell library displayed on the surface of phage as prey and the 28 amino acid long cytoplasmic tail of IgE as bait, we isolated phage encoding the murine hematopoietic progenitor kinase 1 (HPK1). Surface plasmon resonance analysis measurements confirmed affinity of HPK1 to the mIgE cytoplasmic tail and revealed association to other immunoglobulin isotypes as well. Immunoprecipitation experiments, using lysates from two B cell lines expressing nitrophenyl (NP) specific mIgE molecules showed co-precipitation of IgE and HPK1. The interaction of HPK1 with the cytoplasmic domains of membrane immunoglobulins indicate an active role of the tails as part of an isotype specific signal transduction, independent from the Igalpha/Igbeta heterodimers, and may represent a missing link to upstream regulatory elements of HPK1 activation.
'Sneeze syncope', basilar invagination and Arnold-Chiari type I malformation. (1976)

Syncope precipitated by sneezing in an adult male associated with an Arnold-Chiari type I malformation and basilar invagination presents a clinical problem in the differential diagnosis and pathological anatomy of Valsalva-related syncope. An abnormally acute clivoaxial angle, small foramen magnum, and type I Arnold-Chiari malformation appear to be a combination of features intolerant of Valsalva-induced changes in cerebral volume, brain-stem position, CSF fluid dynamics, or blood vessel relationships. Proposed mechanisms of pressure transmission to the area of intracranial pathology are discussed.
Stable target-sensitive immunoliposomes (1992)

Interaction of immunoliposomes composed of dioleoylphosphatidylethanolamine (DOPE) (80%), dioleoylphosphatidic acid (DOPA) (20%), and a small amount of specific antibody with Herpes Simplex virus (HSV) were studied by detecting the immune-dependent lysis of liposomes. DOPA was used as the principal stabilizer of the immunoliposomes. Antibodies conjugated with N-glutarylphosphatidylethanolamine or oxidized GM1 served as the target-specific ligands of immunoliposomes. These immunoliposomes (d = 160-180 nm) were stable for at least one month when stored at 4 degrees C. However, they undergo a rapid aggregation and lysis reaction in the presence of a membrane-bound target such as intact HSV virions. We have also employed epitope peptide-containing liposomes (target liposomes) to mimic the virus and showed that the immunoliposomes could be aggregated and lysed by the target liposomes in an antigen-dependent manner. Immunoliposome lysis could be accelerated by increasing the incubation temperature to 60-70 degrees C. No immunoliposome lysis was observed if the target liposomes were absent, indicating the prolonged stability of the immunoliposomes. Liposome lysis was always accompanied by liposome aggregation. However, the aggregation-induced liposome destabilization is unique to the HII phase-forming lipids such as DOPE. DOPC-containing immunoliposomes did not lyse despite the fact that massive liposome aggregation had taken place.
Subcutaneous Abdominal Adipose Tissue Subcompartments: Potential Role in Rosiglitazone Effects (2008)

Abdominal visceral tissue (VAT) and subcutaneous adipose tissue (SAT), comprised of superficial-SAT (sSAT) and deep-SAT (dSAT), are metabolically distinct. The antidiabetic agents thiazolidinediones (TZDs), in addition to their insulin-sensitizing effects, redistribute SAT suggesting that TZD action involves adipose tissue depot-specific regulation. We investigated the expression of proteins key to adipocyte metabolism on differentiated first passage (P1) preadipocytes treated with rosiglitazone, to establish a role for the diverse depots of abdominal adipose tissue in the insulin-sensitizing effects of TZDs. Adipocytes and preadipocytes were isolated from sSAT, dSAT, and VAT samples obtained from eight normal subjects. Preadipocytes (P1) left untreated (U) or treated with a classic differentiation cocktail (DI) including rosiglitazone (DIR) for 9 days were evaluated for strata-specific differences in differentiation including peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and lipoprotein lipase (LPL) expression, insulin sensitivity via adiponectin and glucose transport-4 (GLUT4), glucocorticoid metabolism with 11 beta-hydroxysteroid dehydrogenase type-1 (11 beta HSD1), and alterations in the adipokine leptin. While depot-specific differences were absent with the classic differentiation cocktail, with rosiglitazone sSAT had the most potent response followed by dSAT, whereas VAT was resistant to differentiation. With rosiglitazone, universal strata effects were observed for PPAR-gamma, LPL, and leptin, with VAT in all cases expressing significantly lower basal expression levels. Clear dSAT-specific changes were observed with decreased intracellular GLUT4. Specific sSAT alterations included decreased 11 beta HSD1 whereas secreted adiponectin was potently upregulated in sSAT with respect to dSAT and VAT. Overall, the subcompartments of SAT, sSAT, and dSAT, appear to participate in the metabolic changes that arise with rosiglitazone administration.
Targeting human CD27 with an agonist antibody stimulates T-cell activation and antitumor immunity (2014)

CD27 is an important co-stimulatory receptor of T cells that can potentially be exploited for immunotherapy. We developed a human IgG1 antibody that targets human CD27, and demonstrated its immunostimulatory and antineoplastic activity in various preclinical models. Currently, the antibody (1F5, CDX-1127) is being tested in patients affected by advanced malignancies.
Requirements for hyaluronic acid binding by CD44: a role for the cytoplasmic domain and activation by antibody. (1992)

The CD44-negative T lymphoma AKR1 (CD44.2 genotype) was transfected with a CD44.1 cDNA. The intact cDNA conferred on the transfected cells the ability to bind hyaluronic acid (HA) both from solution and immobilized on culture plates. It also conferred a CD44-dependent and hyaluronidase-sensitive increase in adhesion to a lymph node endothelial cell line. A mutant cDNA which codes for a CD44 molecule lacking most of the cytoplasmic domain of CD44 was also transfected into AKR1, and cell sorting was used to select transfectants expressing levels of cell surface CD44 expression comparable with the line transfected with the wild-type CD44 cDNA. The cells transfected with the mutant construct bound fluoresceinated HA from solution very poorly, but did adhere to immobilized HA, though less well than cells transfected with the wild-type construct. This result indicates that the cytoplasmic domain of CD44 is necessary for binding of HA from solution but is not required for binding to immobilized HA, although it may contribute to adhesion following ligand recognition. A monoclonal antibody (mAb), IRAWB 14, which reacts with CD44 on all CD44+ cells dramatically induced HA binding by some CD44+ cell lines that did not constitutively bind HA. The transfectant expressing a CD44 molecule with a truncated cytoplasmic domain could be induced by this antibody to bind fluoresceinated-HA from solution. Splenic T cells did not bind fluoresceinated HA constitutively. In the presence of the IRAWB 14 mAb, virtually all CD44+ splenic T cells bound HA. Induction was immediate and occurred equally well at room temperature and at 4 degrees C, indicating that the new HA-binding activity was due to preexistent CD44 molecules. These results are compatible with an antibody-induced activation of CD44 by either a conformational change in the CD44 molecule or a change in the distribution of CD44 molecules on the cell surface.