gebhart/patrepeval huggingface dataset:
Understanding the Mechanisms Involved in Shape Memory Starch: Macromolecular Orientation, Stress Recovery and Molecular Mobility (2011)

The effect of a deformation near and above the glass transition on macromolecular orientation, residual stress, and molecular mobility was investigated on amorphous stimuli-responsive starch. The recovery stress, linked to the residual stress in the temporary shape, evolves linearly with the macromolecular orientation. Increasing the deformation temperature decreases the residual stress and the macromolecular orientation. This also leads to a higher glass transition temperature induced by a decrease in molecular mobility. The local structures potentially involved in orientation and stress recovery and their behavior during deformation at different temperatures are discussed.
Inhibition of mucin glycosylation by aryl-N-acetyl-α-galactosaminides in human colon cancer cells (1989)

Specific inhibitors of the glycosylation of O-glycosidically linked glycoproteins have not previously been described. When tested for their effects on mucin glycosylation in a mucin-producing colon cancer cell line, LS174T, benzyl-, phenyl-, and p-nitrophenyl-N-acetyl-alpha-galactosaminide inhibited the formation of fully glycosylated mucin in a dose-dependent manner. Free aryl-oligosaccharides were found in the medium of treated cells labeled with [3H]glucosamine, [3H]galactose, [3H]fucose, [3H]mannosamine, or phenyl-alpha-[6-3H] N-acetylgalactosamine. UDP-Gal:GalNAc-beta 1,3-galactosyltransferase was inhibited by aryl-N-acetyl-alpha-galactosaminides but not by a number of other aryl-glycosides. Treatment with these inhibitors also causes reversible morphologic changes including formation of intercellular cysts. Aryl-N-acetyl-alpha-galactosaminides can be useful for the structural and functional studies of mucin macromolecules and other O-linked glycoproteins.
UK-1, a novel cytotoxic metabolite from Streptomyces sp. 517-02. I. Taxonomy, fermentation, isolation, physico-chemical and biological properties. (1993)

A new benzoxazole, UK-1, was isolated from the mycelial cake of an actinomycete strain 517-02. Based on morphological, cultural and physiological characteristics, strain 517-02 was seemed to be a close relative of Streptomyces morookaense. UK-1 showed potent cytotoxic activity against B16, HeLa and P388 cells and did not show any antimicrobial activity.
Translation of exogenous messenger RNA coding for nicotinic acetylcholine receptors produces functional receptors in Xenopus oocytes (1982)

Messenger RNA extracted from the electric organ of Torpedo was injected into Xenopus oocytes. This led to the synthesis and incorporation of functional acetylcholine receptors into the membrane of the oocyte. When activated by acetylcholine these Torpedo acetylcholine receptors in the oocyte membrane opened channels whose ionic permeability resembled that of nicotinic receptors in other cells.
Effect of Hydrogen Plasma Treatment on Formation of Amorphous Silicon Film Using Organosoluble Silicon Cluster as a Precursor (2000)

A novel process for the formation of amorphous silicon thin film by a coating technique using an organosoluble silicon cluster as a precursor was developed. The process of conversion of organic silicon film to inorganic silicon film was investigated by Raman and Fourier transform infrared (FT-IR) spectroscopies. Upon heat treatment of the precursor film, the disappearance of the organic substituent and the appearance of the transverse optical phonon band of amorphous silicon were observed in Raman spectra. The combination of heat and hydrogen plasma treatments of the thin film reduced the conversion temperature dramatically.
Molecular Cloning of F4/80-Like-Receptor, a Seven-Span Membrane Protein Expressed Differentially by Dendritic Cell and Monocyte-Macrophage Subpopulations (2001)

A novel dendritic cell (DC) surface molecule termed F4/80-like-receptor (FIRE) has been selected based on its differential expression between DC subsets. The gene encoding FIRE has been cloned and sequenced, and mAbs specific for FIRE have been produced. FIRE is a seven-transmembrane-spanning molecule with two epidermal growth factor-like domains in the extracellular region. It is a novel member of the epidermal growth factor/transmembrane-7 protein subfamily and shows similarity to the macrophage marker F4/80. FIRE is expressed by CD8- DC, but not by CD8+ DC, and it is down-regulated on DC activation. It is expressed by blood monocytes and by some tissue macrophages, but not by most macrophage cell lines or by lymphoid cells. FIRE is a useful marker of myeloid cells with a DC developmental potential.
Mesoderm induction by activin requires FGF-mediated intracellular signals (1994)

We have examined the role of FGF signaling during activin-mediated mesoderm induction in Xenopus. Using dominant inhibitory mutants of FGF signal transducers to disrupt the FGF-signaling pathway at the plasma membrane or in the cytosol prevents animal cap blastomeres from expressing several mesodermal markers in response to exogenous activin. Dominant inhibitory mutants of the FGF receptor, c-ras or c-raf inhibit the ability of activin to induce molecular markers of both dorsal and ventral mesoderm including Xbra, Mix1 and Xnot. Some transcriptional responses to activin such as goosecoid and Xwnt8 are inhibited less effectively than others, however, suggesting that there may differing requirements for an FGF signal in the responses of mesoderm-specific genes to activin induction. Despite the requirement for this signaling pathway during activin induction, downstream components of this pathway are not activated in response to activin, suggesting that activin does not signal directly through this pathway.
Numerical values (2012)

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A Total Synthesis of dl-Δ1-Tetrahydrocannabinol, the Active Constituent of Hashish1 (1965)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA Total Synthesis of dl-Δ1-Tetrahydrocannabinol, the Active Constituent of Hashish1R. Mechoulam and Y. GaoniCite this: J. Am. Chem. Soc. 1965, 87, 14, 3273–3275Publication Date (Print):July 1, 1965Publication History Published online1 May 2002Published inissue 1 July 1965https://pubs.acs.org/doi/10.1021/ja01092a065https://doi.org/10.1021/ja01092a065research-articleACS PublicationsRequest reuse permissionsArticle Views2969Altmetric-Citations286LEARN 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
Emerging therapeutic strategies for chronic pain (2000)

Chronic pain affects a high percentage of the general population. Traditional therapies based upon non-steroidal anti-inflammatory drugs (NSAIDs), opioids and co-analgesic therapies, such as antidepressant or anti-epileptic drugs, are often relatively ineffective in treating chronic pain. In addition, the low therapeutic indexes and, in particular, the often-intolerable side effect profiles of conventional compounds, limit their usefulness, especially in the elderly population. Despite intensive research, until recently there was little change in the classes of drugs available to treat chronic pain clinically. This was partly due to a failure to understand which physiological processes are important in mediating clinical chronic pain. Recently, however, greater understanding of the neurophysiology critical to chronic pain development has lead to the development of numerous alternative pharmacological strategies. This review article outlines the physiological processes occurring in chronic pain, highlights some of the approaches recently developed and mentions a number of drugs currently under development that aim to provide safer and more effective analgesia for chronic pain. These include COX-2 inhibitors, gabapentin, capsaicin, new opioid strategies, neurokinin-1 (NK-1) antagonists, cannabinoid receptor agonists, neuronal nitric oxide synthase (nNOS) inhibitors and NMDA receptor antagonists, as well as a number of other therapeutic strategies in development.
Accumulation of a unique mature B cell population in aged mice. (132.2) (2010)

Abstract Humoral immune responses and protective immunity are compromised in aged individuals, but the basis for this remains unclear. We have discovered a novel CD21/35-CD23-CD43-AA4.1-CD19+B220+ B cell population that gradually increases with age, expanding more than 5-fold in magnitude by 22 months of age. Despite sharing phenotypic features with mature follicular and marginal zone B cells, this novel subset is largely unresponsive to BCR, TLR or CD40 mediated stimulation. In addition, this population is markedly less reliant on the survival factor BLyS both in vitro and in vivo. The expansion of this unusual population does not reflect intrinsic features of cells derived from aged BM progenitors, but instead appears to be derived from a very small subset of FO B cells after exhaustive expansion. Together these findings reveal that primary B cell pools in aged individuals are increasingly populated by a unique population with the characteristics of “exhausted” B cells.
Effect of Grafting RGD and BMP-2 Protein-Derived Peptides to a Hydrogel Substrate on Osteogenic Differentiation of Marrow Stromal Cells (2008)

Osteogenic differentiation and mineralization of bone marrow stromal (BMS) cells depends on the cells’ interactions with bioactive peptides associated with the matrix proteins. The RGD peptides of ECM proteins interact with BMS cells through integrin surface receptors to facilitate cell spreading and adhesion. The BMP peptide corresponding to residues 73−92 of bone morphogenetic protein-2 promotes differentiation and mineralization of BMS cells. The objective of this work was to investigate the effects of RGD and BMP peptides, grafted to a hydrogel substrate, on osteogenic differentiation and mineralization of BMS cells. RGD peptide was acrylamide-terminated by reacting acrylic acid with the N-terminal amine group of the peptide to produce the functionalized Ac-GRGD peptide. The PEGylated BMP peptide was reacted with 4-carboxybenzenesulfonazide to produce an azide functionalized Az-mPEG-BMP peptide. Poly (lactide-co-ethylene oxide-co-fumarate) (PLEOF) macromer was cross-linked with Ac-GRGD peptide and propargyl acrylate to produce an RGD conjugated hydrogel. Az-mPEG-BMP peptide was grafted to the hydrogel by “click chemistry”. The RGD and BMP peptide density on the hydrogel surface was 1.62 ± 0.37 and 5.2 ± 0.6 pmol/cm2, respectively. BMS cells were seeded on the hydrogels and the effect of RGD and BMP peptides on osteogenesis was evaluated by measuring ALPase activity and calcium content with incubation time. BMS cells cultured on RGD conjugated, BMP peptide grafted, and RGD+BMP peptide modified hydrogels showed 3, 2.5, and 5-fold increase in ALPase activity after 14 days incubation. BMS cells seeded on RGD+BMP peptides modified hydrogel showed 4.9- and 11.8-fold increase in calcium content after 14 and 21 days, respectively, which was significantly higher than RGD conjugated or BMP grafted hydrogels. These results demonstrate that RGD and BMP peptides, grafted to a hydrogel substrate, act synergistically to enhance osteogenic differentiation and mineralization of BMS cells. These findings are potentially useful in developing engineered scaffolds for bone regeneration.
An Il12-Il2-Antibody Fusion Protein Targeting Hodgkin's Lymphoma Cells Potentiates Activation Of Nk And T Cells For An Anti-Tumor Attack (2012)

Successful immunotherapy of Hodgkin's disease is so far hampered by the striking unresponsiveness of lymphoma infiltrating immune cells. To mobilize both adoptive and innate immune cells for an anti-tumor attack we fused the pro-inflammatory cytokines IL2 and IL12 to an anti-CD30 scFv antibody in a dual cytokine fusion protein to accumulate both cytokines at the malignant CD30(+) Hodgkin/Reed-Sternberg cells in the lymphoma lesion. The tumor-targeted IL12-IL2 fusion protein was superior in activating resting T cells to amplify and secrete pro-inflammatory cytokines compared to targeted IL2 or IL12 alone. NK cells were also activated by the dual cytokine protein to secrete IFN-γ and to lyse target cells. The tumor-targeted IL12-IL2, when applied by i.v. injection to immune-competent mice with established antigen-positive tumors, accumulated at the tumor site and induced tumor regression. Data demonstrate that simultaneous targeting of two cytokines in a spatial and temporal simultaneous fashion to pre-defined tissues is feasible by a dual-cytokine antibody fusion protein. In the case of IL12 and IL2, this produced superior anti-tumor efficacy implying the strategy to muster a broader immune cell response in the combat against cancer.
Blocking NRG1 and Other Ligand-Mediated Her4 Signaling Enhances the Magnitude and Duration of the Chemotherapeutic Response of Non–Small Cell Lung Cancer (2013)

Although standard chemotherapies are commonly used to treat most types of solid tumors, such treatment often results in inadequate response to, or relapse after, therapy. This is particularly relevant for lung cancer because most patients are diagnosed with advanced-stage disease and are treated with frontline chemotherapy. By studying the residual tumor cells that remain after chemotherapy in several in vivo non-small cell lung cancer models, we found that these cells have increased levels of human epidermal growth factor receptor (HER) signaling due, in part, to the enrichment of a preexisting NRG1(HI) subpopulation. Neuregulin 1 (NRG1) signaling in these models can be mediated by either the HER3 or HER4 receptor, resulting in the differential activation of downstream effectors. Inhibition of NRG1 signaling inhibits primary tumor growth and enhances the magnitude and duration of the response to chemotherapy. Moreover, we show that inhibition of ligand-mediated Her4 signaling impedes disease relapse in cases where NRG1 inhibition is insufficient. These findings demonstrate that ligand-dependent Her4 signaling plays an important role in disease relapse.
Low-Dose Radiation Hypersensitivity in Human Tumor Cell Lines: Effects of Cell–Cell Contact and Nutritional Deprivation (2002)

The hyper-radiosensitivity at low doses recently observed in vitro in a number of cell lines is thought to have important implications for improving tumor radiotherapy. However, cell-cell contact and the cellular environment influence cellular radiosensitivity at higher doses, and they may alter hyper-radiosensitivity in vivo. To confirm this supposition, we investigated the effects of cell density, multiplicity and nutritional deprivation on low-dose hypersensitivity in vitro. Cell survival in the low-dose range (3 cGy to 2 Gy) was studied in cells of two human glioma (BMG-1 and U-87) and two human oral squamous carcinoma (PECA-4451 and PECA-4197) lines using a conventional macrocolony assay. The effects of cell density, multiplicity and nutritional deprivation on hyper-radiosensitivity/induced radioresistance were studied in cells of the BMG-1 cell line, which showed prominent hypersensitivity and induced radioresistance. The induction of growth inhibition, cell cycle delay, micronuclei and apoptosis was also studied at the hyper-radiosensitivity-inducing low doses. Hyper-radiosensitivity/induced radioresistance was evident in the cells of all four cell lines to varying extents, with maximum sensitivity at 10-30 cGy, followed by an increase in survival up to 50 cGy-1 Gy. Both the glioma cell lines had more prominent hyper-radiosensitivity than the two squamous carcinoma cell lines. Low doses inducing maximum hyper-radiosensitivity did not cause significant growth inhibition, micronucleation or apoptosis in BMG-1 cells, but a transient G(1)/S-phase block was evident. Irradiating and incubating BMG-1 cells at high density for 0 or 4 h before plating, as well as irradiating cells as microcolonies, reduced hyper-radiosensitivity significantly, indicating the role of cell-cell contact-mediated processes. Liquid holding of BMG-1 cells in HBSS + 1% serum during and after irradiation for 4 h significantly reduced hyper-radiosensitivity, suggesting that hyper-radiosensitivity may be due partly to active damage fixation processes at low doses. Therefore, our findings suggest that the damage-induced signaling mechanisms influenced by (or mediated through) cell-cell contact or the cellular environment, as well as the lesion fixation processes, play an important role in hyper-radiosensitivity. Further studies are required to determine the exact nature of the damage that triggers these responses as well as for evaluating the potential of low-dose therapy.
Monoclonal antibodies in myeloma. (2015)

The development of monoclonal antibodies (mAbs) for the treatment of disease goes back to the vision of Paul Ehrlich in the late 19th century; however, the first successful treatment with a mAb was not until 1982, in a lymphoma patient. In multiple myeloma, mAbs are a very recent and exciting addition to the therapeutic armamentarium. The incorporation of mAbs into current treatment strategies is hoped to enable more effective and targeted treatment, resulting in improved outcomes for patients. A number of targets have been identified, including molecules on the surface of the myeloma cell and components of the bone marrow microenvironment. Our review focuses on a small number of promising mAbs directed against molecules on the surface of myeloma cells, including CS1 (elotuzumab), CD38 (daratumumab, SAR650984, MOR03087), CD56 (lorvotuzumab mertansine), and CD138/syndecan-1 (BT062/indatuximab ravtansine).
Branched-chain amino acids in the treatment of chronic hepatic encephalopathy. (1982)

The therapeutic efficacy of orally administered branched-chain amino acids in patients with liver cirrhosis and chronic encephalopathy was examined in a double blind, randomised crossover study. Seven patients with manifest hepatic cirrhosis and encephalopathy of six months' duration or longer ingested 30 g branched-chain amino acids or placebo during two 14-day periods. Psychometric tests and electroencephalograms were used to evaluate cerebral function. Neither clinical observations nor psychometric testing or electroencephalogram indicated a significant difference in the patients' response to branched-chain amino acids as compared with placebo. In four patients given branched-chain amino acids for longer periods (five to 22 weeks), psychometric tests also remained unchanged. The plasma concentrations of these acids after oral intake increased significantly, demonstrating adequate absorption. Basal plasma amino acid concentrations were unchanged, however, after branched-chain amino acid therapy. No side-effects were seen, which indicates that these amino acids are well tolerated as an extra protein supply in patients with chronic hepatic encephalopathy. As compared with placebo, however, no effect of branched-chain amino acids on the encephalopathy could be detected.
Factors Affecting Pain Scores during Female Urethral Catheterization (2004)

Catheter size and lubricant type did not affect the severity of pain after urethral catheterization in women.
High performance low temperature polysilicon thin film transistor using ECR plasma thermal oxide as gate insulator (1994)

Electron cyclotron resonance (ECR) plasma thermal oxide has been investigated as a gate insulator for low temperature (/spl les/600/spl deg/C) polysilicon thin-film transistors based on solid phase crystallization (SPC) method. The ECR plasma thermal oxide films grown on a polysilicon film has a relatively smooth interface with the polysilicon film when compared with the conventional thermal oxide and it shows good electrical characteristics. The fabricated poly-Si TFT's without plasma hydrogenation exhibit field-effect mobilities of 80 (60) cm/sup 2//V/spl middot/s for n-channel and 69 (48) cm/sup 2//V/spl middot/s for p-channel respectively when using Si/sub 2/H/sub 6/(SiH/sub 4/) source gas for the deposition of active poly-Si films.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Egr-1-Induced Endothelial Gene Expression: A Common Theme in Vascular Injury (1996)

A number of pathophysiologically relevant genes, including platelet-derived growth factor B-chain (PDGF-B), are induced in the vasculature after acute mechanical injury. In rat aorta, the activated expression of these genes was preceded by a marked increase in the amount of the early-growth-response gene product Egr-1 at the endothelial wound edge. Egr-1 interacts with a novel element in the proximal PDGF-B promoter, as well as with consensus elements in the promoters of other genes induced by endothelial injury. This interaction is crucial for injury-induced PDGF-B promoter-dependent expression. Sp1, whose binding site in the PDGF-B promoter overlaps that of Egr-1, occupies this element in unstimulated cells and is displaced by increasing amounts of Egr-1. These findings implicate Egr-1 in the up-regulated expression of PDGF-B and other potent mediators in mechanically injured arterial endothelial cells.
Activity recognition via user-trace segmentation (2008)

A major issue of activity recognition in sensor networks is automatically recognizing a user's high-level goals accurately from low-level sensor data. Traditionally, solutions to this problem involve the use of a location-based sensor model that predicts the physical locations of a user from the sensor data. This sensor model is often trained offline, incurring a large amount of calibration effort. In this article, we address the problem using a goal-based segmentation approach, in which we automatically segment the low-level user traces that are obtained cheaply by collecting the signal sequences as a user moves in wireless environments. From the traces we discover primitive signal segments that can be used for building a probabilistic activity model to recognize goals directly. A major advantage of our algorithm is that it can reduce a significant amount of human effort in calibrating the sensor data while still achieving comparable recognition accuracy. We present our theoretical framework for activity recognition, and demonstrate the effectiveness of our new approach using the data collected in an indoor wireless environment.