gebhart/patrepeval huggingface dataset:
Real Bills Doctrine (2008)

The ‘real bills doctrine’ has its origin in banking developments of the 17th and 18th centuries. It received its first authoritative exposition in Adam Smith’s Wealth of Nations, was then repudiated by Thornton and Ricardo in the famous Bullionist Controversy, and was finally rehabilitated as the ‘law of reflux’ by Tooke and Fullarton in the currency–banking debate of the mid-19th century. Even now, echoes of the real bills doctrine reverberate in modern monetary theory.
A new model of trispecific antibody resulting the cytotoxicity directed against tumor cells. (2003)

Bispecific antibodies (BsAb) with specificity to both tumor cells and CD3 molecule were believed to be promising immunological tools for the therapy with minimal residual diseases by activating cytotoxic T cells. However, without costimulatory molecule CD28, the activated T cells tended to apoptosis. In order to kill tumor cells more efficiently, a recombinant multifunctional single-chain trispecific antibody (scTsAb), which contains anti-ovarian carcinoma (OC) scFv, anti-CD3 scFv and VH domain of anti-CD28 antibody, was constructed and expressed in E. coli BL21 Star strain. The scTsAb showed strong binding avidities to membrane antigen of SK-OV-3 cell, CD3 molecule on Jurkat cell, and recombinant CD28 antigen. It was further demonstrated that this scTsAb could activate peripheral blood T cells to elicit strong cytotoxicity against SK-OV-3 cells. This new type of recombinant scFv antibody set up a new technological platform for T cells based immunotherapy against cancer, especially with the failure on MHC antigen presentation or absence of costimulating signal.
Experimental model of calcium-containing renal stone formation in a rabbit. (1979)

An experimental method of calcium-containing renal stone formation was devised using a rabbit on normal diet. The stone formation was induced unilaterally, massively, and rapidly in an extremely high incidence by temporary obstruction of the upper urinary tract, but not by permanent obstruction. The contralateral kidney was used as a control. The initial stone formation was not solid but muddy and seemed to occur through massive crystal aggregation, resulting in concretion within a few weeks. We strongly suspect that the mechanism of this stone formation is crystal aggregation induced by temporary obstruction of the kidney. This animal model should contribute to the investigation of the process of crystal aggregation which is considered to be the most important factor in idiopathic calcium stone formation in man.
Investigation of Proximity Effects in a 6T SRAM Cell Using Three-Dimensional TCAD Simulations (2011)

In this paper, we study the impacts of proximity effects on the electrical characteristics I <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">d</sub> -V <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">g</sub> and the static noise margin of a six-transistor (6T) bulk complementary metal-oxide-semiconductor (MOS) static random access memory (SRAM) cell using 3-D process and device technology computer-aided design (TCAD) simulations. We show that when a 6T SRAM cell is simulated as a single continuous 3-D structure, effective stresses in channels are reduced due to close proximity of n-channel and p-channel MOS transistors in the cell with respect to simulations of transistors as discrete 3-D structures. Furthermore, we find that doping in channels of SRAM transistors is reduced by well proximity and implant shadowing. Stress and doping proximity effects have opposite contributions to device performance. We estimate the influence of proximity effects for typical 32-nm technology to be more than 10% for certain electrical cell characteristics. We thus conclude that, to accurately predict electrical cell behavior via TCAD simulations, the 6T SRAM cell should be a single continuous 3-D structure, instead of a set of six discrete transistors, which are simulated as individual 3-D devices and connected via a netlist.
A fully-autonomous integrated rf energy harvesting system for wearable applications (2013)

In this paper we introduce a complete system architecture of a textile-based rectenna loaded by a novel power management platform able to be autonomously activated by ambient RF energy harvesters. An integral design approach of the system blocks is carried out to provide the actual nonlinear behavior of the rectenna output, which is a function of the operating frequencies and power levels, as the DC-DC converter input. The RF properties of the textile rectenna are computed by nonlinear techniques with textile materials and antenna layout numerically characterized by means of EM simulations. A novel integrated power converter is adopted. It is equipped with a start-up circuit and an energy storage unit and it is designed by microelectronic technology. Energy autonomy of the entire system, including a battery-less activation is expected for RF available power levels as low as -15 dBm. The system operation is computed with the wearable rectenna recovering RF energy upon user request from GSM 900, GSM 1800 and WiFi sources
Collagen fibrils in vitro grow from pointed tips in the C- to N-terminal direction (1990)

Growth of collagen fibrils was examined in a system in which collagen monomers are generated by specific enzymic cleavage of type IpCcollagen with procollagen C-proteinase. Fibrils formed at 37 degrees C had highly tapered and symmetrical pointed tips. The pattern of cross-striations in the pointed tips indicated that all the molecules were oriented so that the N-termini were directed towards the tip. At 29 degrees C and 32 degrees C, the fibrils formed were thicker. One end of fibrils formed at 29 degrees C was blunt, and the other was pointed. Growth of the fibrils was exclusively from pointed tips. Occasionally a spear-like projection appeared at a blunted end. The spear-like projection then became a new pointed tip for growth in the opposite direction. The results suggested a model for fibril growth with at least three distinct binding sites for monomers. In the model, the pointed tip is the site with the highest affinity for the binding of monomers and most probably defines the critical concentration for fibril assembly. The main shaft of the fibril is a site with very low affinity for binding. The blunted end defines a low-affinity binding site where monomers can bind in opposite orientation to produce growth from a new pointed end.
SRC gene expression in human cancer: the role of transcriptional activation (2004)

Human pp60c-Src (or c-Src) is a 60 kDa nonreceptor tyrosine kinase encoded by the SRC gene and is the cellular homologue to the potent transforming v-Src viral oncogene. c-Src functions at the hub of a vast array of signal transduction cascades that influence cellular proliferation, differentiation, motility, and survival. c-Src activation has been documented in upwards of 50% of tumors derived from the colon, liver, lung, breast, and pancreas. Therefore, a major focus has been to understand the mechanisms of c-Src activation in human cancer. Early studies concentrated on post-translational mechanisms that lead to increased c-Src kinase activity, which often correlated with overexpression of c-Src protein. More recently, the discovery of an activating SRC mutation in a small subset of advanced colon tumors has been reported. In addition, elevated SRC transcription has been identified as yet another mechanism contributing significantly to c-Src activation in a subset of human colon cancer cell lines. Interestingly, histone deacetylase (HDAC) inhibitors, agents with well-documented anti-cancer activity, repress SRC transcription in a wide variety of human cancer cell lines. Analysis of the mechanisms behind HDAC inhibitor mediated repression could be utilized in the future to specifically inhibit SRC gene expression in human cancer.
Targeting the Mitochondria Activates Two Independent Cell Death Pathways in Ovarian Cancer Stem Cells (2011)

Cancer stem cells are responsible for tumor initiation and chemoresistance. In ovarian cancer, the CD44+/MyD88+ ovarian cancer stem cells are also able to repair the tumor and serve as tumor vascular progenitors. Targeting these cells is therefore necessary to improve treatment outcome and patient survival. The previous demonstration that the ovarian cancer stem cells are resistant to apoptotic cell death induced by conventional chemotherapy agents suggests that other forms of targeted therapy should be explored. We show in this study that targeting mitochondrial bioenergetics is a potent stimulus to induce caspase-independent cell death in a panel of ovarian cancer stem cells. Treatment of these cells with the novel isoflavone derivative, NV-128, significantly depressed mitochondrial function exhibited by decrease in ATP, Cox-I, and Cox-IV levels, and by increase in mitochondrial superoxide and hydrogen peroxide. This promotes a state of cellular starvation that activates two independent pathways: (i) AMPKα1 pathway leading to mTOR inhibition; and (ii) mitochondrial MAP/ERK kinase/extracellular signal-regulated kinase pathway leading to loss of mitochondrial membrane potential. The demonstration that a compound can specifically target the mitochondria to induce cell death in this otherwise chemoresistant cell population opens a new venue for treating ovarian cancer patients.
CRISPR-Edited Stem Cells in a Patient with HIV and Acute Lymphocytic Leukemia (2019)

The safety of CRISPR (clustered regularly interspaced short palindromic repeats)-based genome editing in the context of human gene therapy is largely unknown. <i>CCR5</i> is a reasonable but not absolutely protective target for a cure of human immunodeficiency virus type 1 (HIV-1) infection, because <i>CCR5</i>-null blood cells are largely resistant to HIV-1 entry. We transplanted CRISPR-edited <i>CCR5</i>-ablated hematopoietic stem and progenitor cells (HSPCs) into a patient with HIV-1 infection and acute lymphoblastic leukemia. The acute lymphoblastic leukemia was in complete remission with full donor chimerism, and donor cells carrying the ablated <i>CCR5</i> persisted for more than 19 months without gene editing-related adverse events. The percentage of CD4+ cells with <i>CCR5</i> ablation increased by a small degree during a period of antiretroviral-therapy interruption. Although we achieved successful transplantation and long-term engraftment of CRISPR-edited HSPCs, the percentage of <i>CCR5</i> disruption in lymphocytes was only approximately 5%, which indicates the need for further research into this approach. (Funded by the Beijing Municipal Science and Technology Commission and others; ClinicalTrials.gov number, NCT03164135.).
The Anti-Inflammatory Properties of Antithrombin III: New Therapeutic Implications (1998)

Antithrombin III (AT III) supplementation has proven to be effective in the treatment of disseminated intravascular coagulation. Administration of AT III is also useful for prevention of organ failure in animals challenged with endotoxin or bacteria and it increases the survival rate of such animals. Since inhibition of coagulation abnormalities failed to prevent organ failure in animals given bacteria, AT III may exert a therapeutic effect independent of its anticoagulant effect. This therapeutic mechanism of AT III has been explored using an animal model of septicemia. AT III prevented pulmonary vascular injury by inhibiting leukocyte activation in rats given endotoxin. This effect is mediated by the promotion of endothelial release of prostacyclin which inhibits leukocyte activation. Interaction of AT III with heparin-like glycosaminoglycans (GAGs) on the endothelial cell surface appears to be important for this effect. Heparin inhibits these therapeutic effects of AT III by preventing AT III from interacting with the cell surface heparin-like GAGs. This activity of AT III may explain why AT III prevents organ failure as well as coagulation abnormalities in patients with sepsis. This antiinflammatory activity of AT III may be useful for the treatment of organ failure such as in ischemia/reperfusion-induced organ dysfunction, in which activated leukocytes play a critical role.
New design of a VirtualGlove for grasping applications (2010)

Abstract Virtual gloves have received much attention in the field of virtual reality and computer simulations. They are considered to be essential tools for implementing any sort of hand‐based experiences in virtual environments. For applications with simpler motions, the accuracy of finger‐bending amount returned by these virtual gloves is not of primary interest. For grasping applications, however, inaccuracy in the bending amount results in unrealistic scenarios having discrepancies in the contact geometry for the hand and the object. In this study, we improve the measurements of bending amount by placing the bend sensors on the palm of the hand, where the objects are touched directly. Supporting evaluative data and design details are also discussed. © 2010 Wiley Periodicals, Inc.
A Novel Poly[2,6-(4-dialkylmethylenecyclopentadithiophene)] with “in-Plane” Alkyl Substituents (2006)

ADVERTISEMENT RETURN TO ISSUEPREVNoteA Novel Poly[2,6-(4-dialkylmethylenecyclopentadithiophene)] with "in-Plane" Alkyl SubstituentsTorsten W. Bünnagel, Frank Galbrecht, and Ullrich ScherfView Author Information Macromolecular Chemistry and Institute for Polymer Technology, Bergische Universität Wuppertal, Gaussstrasse 20, D-42119 Wuppertal, Germany Cite this: Macromolecules 2006, 39, 25, 8870–8872Publication Date (Web):November 9, 2006Publication History Received12 August 2006Revised2 October 2006Published online9 November 2006Published inissue 1 December 2006https://pubs.acs.org/doi/10.1021/ma0618530https://doi.org/10.1021/ma0618530brief-reportACS PublicationsCopyright © 2006 American Chemical SocietyRequest reuse permissionsArticle Views585Altmetric-Citations11LEARN 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 SUBJECTS:Alcohols,Alkyls,Monomers,Polymers,Substituents Get e-Alerts
Development of pancreatic enzyme microsphere technology and US findings with Pancrease in the treatment of chronic pancreatitis. (1989)

Enzyme replacement therapy is a vital aspect of the management of patients with chronic pancreatic insufficiency. However, pharmaceutical technology in the manufacture of enzyme products has advanced significantly only in the last decade. In the late 1970s, Johnson & Johnson scientists developed novel pH-sensitive enteric-coated microspheres of pancrelipase (Pancrease) that could be encapsulated for convenient administration. The increased efficiency of the formulation allowed lower daily doses than had been required with conventional enzyme products. In vitro studies indicate that the microspheres disintegrate at a pH appropriate for patients with cystic fibrosis and chronic pancreatitis. Clinical studies of Pancrease in chronic pancreatitis demonstrate a significant improvement in fecal fat excretion, fat utilization, stool weight, and stool frequency, as well as significant weight gain and improved quality of life of patients. Pancrease represents a major advance in the clinical management of chronic pancreatic insufficiency.
Effects of dietary supplementation of (β2‐adrenergic agonist clenbuterol on carcase characteristics and some metabolites in ducks (1994)

1. Ducks (622 in total) aged 25 d were given diets supplemented with clenbuterol (CL) at 0 (control), 0.5, 1, 2, 3 and 5 mg/kg for 25 d to investigate the effect of dietary CL on muscle and fat deposition and some metabolites in ducks. 2. The mass of the breast muscles was increased by 10 to 31%, while subcutaneous fat plus skin and abdominal fat pad were reduced by 8 to 23% and 20 to 37%, respectively, in the ducks supplemented 1 to 5 mg CL/kg diet. 3. Increased RNA:DNA ratios in the breast muscle, reduced uric acid and increased free fatty acid concentrations in the serum were observed in clenbuterol-fed ducks.
Active photonic lattices for high-coherent-power generation (2002)

Active photonic lattices (APLs) of large index step ((Delta) n&gt;=0.05 for spatial-mode stability) have been used, as early as 1988, for effective lateral-mode control in large-aperture (&gt;=100micrometers ) high-power coherent devices. Photonic-bandpass (PBP) structures, so called ROW arrays, have allowed stable, near-diffraction-limited beam operation to powers as high as 1.6W CW and 10W peak pulsed. Photonic-bandgap (PBG) structures, so called ARROW lasers, have provided up to 0.5W peak-pulsed stable, single-mode power and hold the potential for 1W CW reliable single-mode operation from apertures ~10micrometers wide. The solution for high efficiency surface emission, from 2nd order DFB/DBR lasers, in an othonormal, single-lobe beam pattern was found in 2000. That opens the way for the realization fo 2-D surface-emitting, 2nd order APLs for the stable generation of watts of CW single-lobe, single-mode power form large 2-D apertures.
SecA protein: autoregulated ATPase catalysing preprotein insertion and translocation across the Escherichia coli inner membrane (1993)

Recent insight into the biochemical mechanisms of protein translocation in Escherichia coli indicates that SecA ATPase is required both for the initial binding of preproteins to the inner membrane as well as subsequent translocation across this structure. SecA appears to promote these events by direct recognition of the preprotein or preprotein-SecB complex, binding to inner-membrane anionic phospholipids, insertion into the membrane bilayer and association with the preprotein translocator, SecY/SecE. ATP binding appears to control the affinity of SecA for the various components of the system and ATP hydrolysis promotes cycling between its different biochemical states. As a component likely to catalyse a rate-determining step in protein secretion, SecA synthesis is co-ordinated with the activity of the protein export pathway. This form of negative regulation appears to rely on SecA protein binding to its mRNA and repressing translation if conditions of rapid protein secretion prevail within the cell. A precise biochemical scheme for SecA-dependent catalysis of protein export and the details of secA regulation appear to be close at hand. The evolutionary conservation of SecA protein among eubacteria as well as the general requirement for translocation ATPases in other protein secretion systems argues for a mechanistic commonality of all prokaryotic protein export pathways.
Voltage-Gated Calcium Channels as Targets for the Treatment of Chronic Pain (2004)

This review focuses on the importance of voltage-gated calcium channels in modulating and controlling the function of peripheral and central neurons involved in nociceptive processing. We describe the different families of voltage-gated calcium channels that are expressed in pain pathway neurons, how the expression levels of calcium channel currents change in chronic pain conditions, and the validation of N-type, T-type, and P-type calcium channels as targets for the treatment of pain. The molecular mechanism of action is reviewed for the most prominent calcium channel-targeted drugs including gabapentin and ziconotide as well as antiepileptics administered off-label for the treatment of pain. We discuss how the major genetic, functional, and pharmacological differences between subtypes of neuronal calcium channels can be leveraged to identify new molecular targets and to discover and develop new therapeutic agents for the treatment of chronic pain syndromes.
Predicting Prostate Cancer Risk Through Incorporation of Prostate Cancer Gene 3 (2008)

New markers for prostate cancer can be incorporated into the Prostate Cancer Prevention Trial risk calculator by a novel approach. Incorporation of prostate cancer gene 3 improved the diagnostic accuracy of the Prostate Cancer Prevention Trial risk calculator.
RIBONUCLEASE P: Unity and Diversity in a tRNA Processing Ribozyme (1998)

Ribonuclease P (RNase P) is the endoribonuclease that generates the mature 5'-ends of tRNA by removal of the 5'-leader elements of precursor-tRNAs. This enzyme has been characterized from representatives of all three domains of life (Archaea, Bacteria, and Eucarya) (1) as well as from mitochondria and chloroplasts. The cellular and mitochondrial RNase Ps are ribonucleoproteins, whereas the most extensively studied chloroplast RNase P (from spinach) is composed solely of protein. Remarkably, the RNA subunit of bacterial RNase P is catalytically active in vitro in the absence of the protein subunit (2). Although RNA-only activity has not been demonstrated for the archael, eucaryal, or mitochondrial RNAs, comparative sequence analysis has established that these RNAs are homologous (of common ancestry) to bacterial RNA. RNase P holoenzymes vary greatly in organizational complexity across the phylogenetic domains, primarily because of differences in the RNase P protein subunits: Mitochondrial, archaeal, and eucaryal holoenzymes contain larger, and perhaps more numerous, protein subunits than do the bacterial holoenzymes. However, that the nonbacterial RNase P RNAs retain significant structural similarity to their catalytically active bacterial counterparts indicates that the RNA remains the catalytic center of the enzyme.
B-Cell Lymphoma and Myeloma Protection Induced by Idiotype Vaccination with Dendritic Cells Is Mediated Entirely by T Cells in Mice (2005)

Immunoglobulin idiotypes (Id) of malignant B cells are tumor-specific antigens that may be targeted for immunotherapy. Id-directed immunotherapy by immunization with autologous Id has been initiated in clinical trials to control residual disease in B-cell lymphoma and multiple myeloma. The effector mechanisms responsible for destruction of B-cell tumors are a controversial issue. The authors show that vaccination with Id-pulsed dendritic cells (DCs) or with soluble Id-KLH in adjuvant induced immune responses that eliminated both B-cell lymphoma and myeloma in tumor-bearing mice; however, the two vaccination regimens resulted in distinct immune responses. Whereas soluble Id plus adjuvant induced high levels of anti-Id antibodies, the Id-pulsed DCs did not induce anti-Id or any antitumor antibodies. Immunization with Id-pulsed DCs induced a significant increase in the frequency of Id-reactive T cells. Depletion studies in DC-vaccinated mice showed that the predominant effector cells responsible for tumor rejection were of the CD8 subset. The finding that DC-based Id vaccines elicit tumor protection, which is entirely based on cell-mediated effector mechanisms, is of particular importance for plasma cell tumors because these tumors do not express Id on the surface and hence do not bind anti-Id antibodies.