gebhart/patrepeval huggingface dataset:
Cross-Linked Micelles (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCross-Linked MicellesF. M. Menger and Alexey V. EliseevCite this: Langmuir 1995, 11, 6, 1855–1857Publication Date (Print):June 1, 1995Publication History Published online1 May 2002Published inissue 1 June 1995https://pubs.acs.org/doi/10.1021/la00006a005https://doi.org/10.1021/la00006a005research-articleACS PublicationsRequest reuse permissionsArticle Views441Altmetric-Citations25LEARN 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
Forecasting and Scheduling for Past-Model Replacement Parts (1971)

All-time requirements forecasting and the translation of these forecasts, via a dynamic inventory model, into production schedules are effective tools for controlling manufacturing, inventory and obsolescence costs of past-model replacement parts. Traditional forecasting rules and steady-state EOQ models prove inappropriate for the special problems posed by the demand decay characteristics of all service parts. A new forecasting technique, based on the principle of estimating sales requirements for all-time into the future, is described along with a dynamic inventory model for ordering production runs. Together, these techniques—developed for implementation by an American auto manufacture—provide results superior to those of other, more traditional, procedures. An inventory review system for achieving model implementation is also discussed.
Transcriptionally Active Polymerase Chain Reaction (TAP) (2002)

An approach is described for making transcriptionally active PCR (TAP) fragments that were used directly in in vitro and in vivo expression experiments. TAP fragments encoding reporter genes were amplified in 1 day using typical PCR methodology and were expressed in cultured cells and in mice at levels comparable with a widely used cytomegalovirus promoter-based plasmid expression vector. Following intramuscular injection, a TAP fragment encoding hepatitis B surface antigen (HBsAg) induced anti-HBsAg antibody titers comparable with those induced by supercoiled plasmid encoding the same antigen. Epitope-tagged TAP fragments were generated and transfected into cells for rapid, high throughput immunocytochemical analysis of the tagged gene products. TAP fragments were also transferred directly into expression vectors by in vivo homologous recombination without conventional cloning, affording a high throughput cloning approach that does not require restriction enzyme digestion, ligations, or thymidine adenine complementation cloning. The methodology has been adapted to a robotic work station enabling the high throughput generation of transcriptionally active genes at the rate of more than 400 different genes per day. This technology offers a practical approach to directly utilize genome sequence data to generate functional proteomes.
Induction of a cellular immune response to a foreign antigen by a recombinant Listeria monocytogenes vaccine (1992)

A recombinant strain of Listeria monocytogenes that stably and constitutively expresses Escherichia coli beta-galactosidase was used as a live vaccine vector. BALB/c mice were immunized orally or parenterally with the recombinant L. monocytogenes, and their cellular and humoral immune responses to beta-galactosidase were measured. Spleen cells taken 1 week after oral inoculation or 5 weeks after oral or parenteral inoculation (with a boost at 4 weeks) showed beta-galactosidase-specific CTL responses. The CTL line derived from mice immunized i.p. was also shown to be class I restricted and Thy-1.2+, CD8+, and TCR alpha beta+. All mice immunized with the recombinant L. monocytogenes had positive delayed-type hypersensitivity responses to heat-killed L. monocytogenes, but only 15% had a positive delayed-type hypersensitivity reaction to beta-galactosidase. Individual serum samples from mice immunized i.p. or i.v. were tested for antibody to beta-galactosidase. Approximately 11% had low positive titers for beta-galactosidase antibodies. These results demonstrate that both oral and parenteral immunization with recombinant L. monocytogenes results in a cellular immune response to the foreign protein, which is primarily a specific CD8+ CTL response.
Axonal Elongation into Peripheral Nervous System "Bridges" After Central Nervous System Injury in Adult Rats (1981)

The origin, termination, and length of axonal growth after focal central nervous system injury was examined in adult rats by means of a new experimental model. When peripheral nerve segments were used as "bridges" between the medulla and spinal cord, axons from neurons at both these levels grew approximately 30 millimeters. The regenerative potential of these central neurons seems to be expressed when the central nervous system glial environment is changed to that of the peripheral nervous system.
A General and Efficient Catalyst System for a Wacker-Type Oxidation Using TBHP as the Terminal Oxidant: Application to Classically Challenging Substrates (2009)

Utilizing the rapidly synthesized Quinox ligand and commercially available aqueous TBHP, a Wacker-type oxidation has been developed, which efficiently converts the traditionally challenging substrate class of protected allylic alcohols to the corresponding acyloin products. Additionally, the catalytic system is general for several other substrate classes, converting terminal olefins to methyl ketones, with short reaction times. The system is scalable (20 mmol) and can be performed with a reduced catalyst loading of 1 mol%. Enantioenriched substrates undergo oxidation with complete retention of enantiomeric excess.
Role of critical thiol groups on the matrix surface of the adenine nucleotide translocase in the mechanism of the mitochondrial permeability transition pore (2002)

Opening of the mitochondrial permeability transition pore (MPTP) is sensitized to [Ca(2+)] by oxidative stress (diamide) and phenylarsine oxide (PAO). We have proposed that both agents cross-link two thiol groups on the adenine nucleotide translocase (ANT) involved in ADP and cyclophilin-D (CyP-D) binding. Here, we demonstrate that blocking Cys(160) with 80 microM eosin 5-maleimide (EMA) or 500 microM N-ethylmaleimide (NEM) greatly decreased ADP inhibition of the MPTP. The ability of diamide, but not PAO, to block ADP inhibition of the MPTP was antagonized by treatment of mitochondria with 50 microM NEM to alkylate matrix glutathione. Binding of detergent-solubilized ANT to a PAO-affinity matrix was prevented by pre-treatment of mitochondria with diamide, EMA or PAO, but not NEM. EMA binding to the ANT in submitochondrial particles (SMPs) was prevented by pre-treatment of mitochondria with either PAO or diamide, implying that both agents modify Cys(160). Diamide and PAO pre-treatments also inhibited binding of solubilized ANT to a glutathione S-transferase-CyP-D affinity column, both effects being blocked by 100 microM EMA. Intermolecular cross-linking of adjacent ANT molecules via Cys(57) by copper phenanthroline treatment of SMPs was abolished by pre-treatment of mitochondria with diamide and PAO, but not with EMA. Our data suggest that PAO and diamide cause intramolecular cross-linking between Cys(160) and Cys(257) directly (not antagonized by 50 microM NEM) or using glutathione (antagonized by 50 microM NEM) respectively. This cross-linking stabilizes the "c" conformation of the ANT, reducing the reactivity of Cys(57), while enhancing CyP-D binding to the ANT and antagonizing ADP binding. The two effects together greatly sensitize the MPTP to [Ca(2+)].
Y-12 Groundwater Protection Program Groundwater and Surface Water Sampling and Analysis Plan (CY2020) (2019)

This plan provides a description of the groundwater and surface water quality monitoring activities planned for calendar year (CY) 2020 at the U.S. Department of Energy Y-12 National Security Complex (Y-12) that will be managed by the Y-12 Groundwater Protection Program (GWPP). The following sections of this report provide details regarding the CY 2020 groundwater and surface water monitoring activities. Section 2 describes the monitoring locations in each regime and the processes used to select the sampling locations. A description of the field measurements and laboratory analytes is provided in Section 3. Sample collection methods and procedures are described in Section 4, and Section 5 lists the documents cited for more detailed operational and technical information.
Variant Alzheimer's disease with spastic paraparesis and cotton wool plaques is caused by PS-1 mutations that lead to exceptionally high amyloid-? concentrations (2000)

We describe 3 new families affected by Alzheimer's disease with spastic paraparesis. In affected individuals, including the earliest known patient with this clinical syndrome, neuropathological examination revealed large "cotton wool" plaques similar to those we have previously described in a Finnish family. In the families in which DNA was available, presenilin-1 mutations were observed. Transfection of cells with these mutant genes caused exceptionally large increases in secreted Abeta42 levels. Furthermore, brain tissue from individuals with this syndrome had very high amyloid-beta concentrations. These findings define the molecular pathogenesis of an important subgroup of Alzheimer's disease and have implications for the pathogenesis of the disease in general.
Systems for orthogonal self-assembly of electroactive monolayers on Au and ITO: an approach to molecular electronics (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSystems for orthogonal self-assembly of electroactive monolayers on Au and ITO: an approach to molecular electronicsTimothy J. Gardner, C. Daniel Frisbie, and Mark S. WrightonCite this: J. Am. Chem. Soc. 1995, 117, 26, 6927–6933Publication Date (Print):July 1, 1995Publication History Published online1 May 2002Published inissue 1 July 1995https://pubs.acs.org/doi/10.1021/ja00131a015https://doi.org/10.1021/ja00131a015research-articleACS PublicationsRequest reuse permissionsArticle Views2230Altmetric-Citations196LEARN 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
Real-Time Cellular Exometabolome Analysis with a Microfluidic-Mass Spectrometry Platform (2015)

To address the challenges of tracking the multitude of signaling molecules and metabolites that is the basis of biological complexity, we describe a strategy to expand the analytical techniques for dynamic systems biology. Using microfluidics, online desalting, and mass spectrometry technologies, we constructed and validated a platform well suited for sampling the cellular microenvironment with high temporal resolution. Our platform achieves success in: automated cellular stimulation and microenvironment control; reduced non-specific adsorption to polydimethylsiloxane due to surface passivation; real-time online sample collection; near real-time sample preparation for salt removal; and real-time online mass spectrometry. When compared against the benchmark of "in-culture" experiments combined with ultraperformance liquid chromatography-electrospray ionization-ion mobility-mass spectrometry (UPLC-ESI-IM-MS), our platform alleviates the volume challenge issues caused by dilution of autocrine and paracrine signaling and dramatically reduces sample preparation and data collection time, while reducing undesirable external influence from various manual methods of manipulating cells and media (e.g., cell centrifugation). To validate this system biologically, we focused on cellular responses of Jurkat T cells to microenvironmental stimuli. Application of these stimuli, in conjunction with the cell's metabolic processes, results in changes in consumption of nutrients and secretion of biomolecules (collectively, the exometabolome), which enable communication with other cells or tissues and elimination of waste. Naïve and experienced T-cell metabolism of cocaine is used as an exemplary system to confirm the platform's capability, highlight its potential for metabolite discovery applications, and explore immunological memory of T-cell drug exposure. Our platform proved capable of detecting metabolomic variations between naïve and experienced Jurkat T cells and highlights the dynamics of the exometabolome over time. Upregulation of the cocaine metabolite, benzoylecgonine, was noted in experienced T cells, indicating potential cellular memory of cocaine exposure. These metabolomics distinctions were absent from the analogous, traditional "in-culture" UPLC-ESI-IM-MS experiment, further demonstrating this platform's capabilities.
Serum Amyloid A (1989)

Acute response after traumatic events was studied in serial serum samples of 21 patients over a period of 13 days. Among the various biochemical and hematologic parameters, serum amyloid A (SAA) exhibited the most striking changes, with a pattern similar to that of the tissue marker creatine-P kinase (CPK). Maximal SAA level was detected 3–4 days after onset of the event, and reached 216 ± 41 SEM gm/ml (normal range <2 gm/ml), while maximal CPK level was detected on the same day and reached 530 ± 242 SEM IU/L (normal range 24–195 IU/L). Fibrinogen, leucocytes, platelets, albumin, alkaline phosphatase (AP), and calcium (Ca) each showed its own typical pattern of change. Fever did not develop. Comparison of SAA levels after various acute events suggests that damage to the myocardium is the most powerful stimulus for SAA induction, followed by traumatic events, arthritis, viral infections, and malignant diseases. It seems therefore that although acute response is considered a generalized reaction, it is not completely independent of the localized events which induce it. Among the known parameters, SAA is the most sensitive marker for monitoring the intensity of events.
BindingDB Entry 50022536: Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase. (2025)

The epidermal growth factor receptor (EGFR) is overexpressed in a significant percentage of carcinomas and contributes to the malignant phenotype. CP-358,774 is a directly acting inhibitor of human EGFR tyrosine kinase with an IC50 of 2 nM and reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM. This inhibition is selective for EGFR tyrosine kinase relative to other tyrosine kinases we have examined, both in assays of isolated kinases and whole cells. At doses of 100 mg/kg, CP-358,774 completely prevents EGF-induced autophosphorylation of EGFR in human HN5 tumors growing as xenografts in athymic mice and of the hepatic EGFR of the treated mice. CP-358,774 inhibits the proliferation of DiFi human colon tumor cells at submicromolar concentrations in cell culture and blocks cell cycle progression at the G1 phase. This inhibitor produces a marked accumulation of retinoblastoma protein in its underphosphorylated form and accumulation of p27KIP1 in DiFi cells, which may contribute to the cell cycle block. Inhibition of the EGFR also triggers apoptosis in these cells as determined by formation of DNA fragments and other criteria. These results indicate that CP-358,774 has potential for the treatment of tumors that are dependent on the EGFR pathway for proliferation or survival.
Design, Mechanism of Action, Bioavailability and Therapeutic Effects of Mn Porphyrin-Based Redox Modulators (2012)

Based on aqueous redox chemistry and simple in vivo models of oxidative stress, Escherichia coli and Saccharomyces cerevisiae, the cationic Mn(III) N-substituted pyridylporphyrins (MnPs) have been identified as the most potent cellular redox modulators within the porphyrin class of drugs; their efficacy in animal models of diseases that have oxidative stress in common is based on their high ability to catalytically remove superoxide, peroxynitrite, carbonate anion radical, hypochlorite, nitric oxide, lipid peroxyl and alkoxyl radicals, thus suppressing the primary oxidative event. While doing so MnPs could couple with cellular reductants and redox-active proteins. Reactive species are widely accepted as regulators of cellular transcriptional activity: minute, nanomolar levels are essential for normal cell function, while submicromolar or micromolar levels impose oxidative stress, which is evidenced in increased inflammatory and immune responses. By removing reactive species, MnPs affect redox-based cellular transcriptional activity and consequently secondary oxidative stress, and in turn inflammatory processes. The equal ability to reduce and oxidize superoxide during the dismutation process and recently accumulated results suggest that pro-oxidative actions of MnPs may also contribute to their therapeutic effects. All our data identify the superoxide dismutase-like activity, estimated by log k(cat)O2-*), as a good measure for the therapeutic efficacy of MnPs. Their accumulation in mitochondria and their ability to cross the blood-brain barrier contribute to their remarkable efficacy. We summarize herein the therapeutic effects of MnPs in cancer, central nervous system injuries, diabetes, their radioprotective action and potential for imaging. Few of the most potent modulators of cellular redox-based pathways, MnTE2-PyP5+, MnTDE-2-ImP5+, MnTnHex-2-PyP5+ and MnTnBuOE-2-PyP5+, are under preclinical and clinical development.
Lymphoid thyroiditis following immunization with group A streptococcal vaccine. (1978)

Severe lymphoid thyroiditis and associated hypothyroidism occurred in all of 7 male and 4 female F(7) derivatives (seventh generation) of rats immunized in each generation against Group A streptococci. This evidence of thyroiditis produced by immunization against a nonthyroidal antigen suggests that some cases of Hashimoto's thyroiditis in humans may result from nonspecific immune responses.
Effect of Silicon Oxidation on Long-Term Cell Selectivity of Cell-Patterned Au/SiO2Platforms (2006)

Cellular patterning on silicon platforms is the basis for development of integrated cell-based biosensing devices, for which long-term cell selectivity and biostability remain a major challenge. We report the development of a silicon-based platform in a metal-insulator format capable of producing uniform and biostable cell patterns with long-term cell selectivity. Substrates patterned with arrays of gold electrodes were surface-engineered such that the electrodes were activated with fibronectin to mediate cell attachment and the silicon oxide background was passivated with PEG to resist protein adsorption and cell adhesion. Three types of oxide surfaces, i.e., native oxide, dry thermally grown oxide, and wet thermally grown oxide, were produced to illustrate the effect of oxide state of the surface on long-term cell selectivity. Results indicated that the cell selectivity over time differed dramatically among three patterned platforms and the best cell selectivity was found on the dry oxide surface for up to 10 days. Surface analysis results suggested that this enhancement in cell selectivity may be related to the presence of additional, more active oxide states on the dry oxide surface supporting the stability of PEG films and effectively suppressing the cell adhesion. This research offers a new strategy for development of stable and uniform cell-patterned surfaces, which is versatile for immobilization of silane-based chemicals for preparation of biostable interfaces.
Biochemical and antitumor effects of 5,8-dideazaisopteroylglutamate, a unique quinazoline inhibitor of thymidylate synthase. (1983)

Abstract The effects of 5,8-dideazaisopteroylglutamate ( N -[ p -{[(2-amino-4-hydroxy-6-quinazolinyl)amino]methyl}benzoyl]-l-glutamic acid) (IAHQ) on thymidylate synthase and dihydrofolate reductase have been examined as a biochemical basis for the anticancer activity of IAHQ in several tumor systems. IAHQ, when administered at 85 mg/kg on Days 2 and 10 after tumor implantation, delayed the growth of methotrexate-resistant Colon Tumor 38 and resulted in 6 of 20 tumor-free animals at 90 days. IAHQ was also active against human colon adenocarcinoma (HCT-8), murine L1210, P388, L5178Y leukemias, and Walker 256 rat carcinoma in tissue culture, requiring concentrations of 0.5, 5, 5, 5, and 5 µm, respectively, to inhibit cell growth 50% compared to untreated cells. Several lines of evidence indicate that, unlike methotrexate, IAHQ exerts its effects via inhibition of thymidylate synthase. Thymidine alone protected HCT-8 cells from IAHQ cytotoxicity. CCRF-CEM human leukemic cells 75-fold resistant to IAHQ showed no cross-resistance to methotrexate. Although IAHQ was a more potent inhibitor of dihydrofolate reductase [K i slope (K i s), 0.7 µm] than thymidylate synthase (K i s 5 µm), the possible poly-γ-glutamyl metabolite of IAHQ, 5,8-dideazaisopteroyl-γ-l-glutamyl-γ-l-glutamyl-l-glutamic acid, is a better inhibitor of thymidylate synthase (K i s 0.09 µm) than dihydrofolate reductase (K i s 0.7 µm). Significant binding of IAHQ and 5,8-dideazaisopteroyl-γ-l-glutamyl-γ-l-glutamyl-l-glutamic acid to thymidylate synthase required the presence of deoxyuridylate. IAHQ and, to a greater extent, 5,8-dideazaisopteroyl-γ-l-glutamyl-γ-l-glutamyl-l-glutamic acid stimulated binding of deoxyuridylate to one site on thymidylate synthase with dissociation constants for deoxyuridylate in the ternary complexes of 1.2 and 0.041 µm, respectively. These data indicate that the biochemical basis for the antitumor effects of IAHQ is probably its intracellular conversion to poly-γ-glutamyl metabolites, which inhibit thymidylate synthase via quinazoline-deoxyuridylate-enzyme ternary complex formation.