gebhart/patrepeval huggingface dataset:
Human Prostate Cancer: A Direct Role for Oestrogens (2007)

We have studied the response to oestrogen and expression of oestrogen receptors in responsive LNCaP and androgen non-responsive PC3 human prostate cancer cell lines. Growth of LNCaP cells is significantly stimulated by physiological concentrations of oestradiol; this growth increase appears to be comparable to that induced by either testosterone or dihydrotestosterone. In contrast, oestradiol significantly inhibits the proliferation of PC3 cells. We also present novel evidence for functional oestrogen binding in LNCaP cells. This evidence was first obtained by means of radioligand binding assays and was further corroborated using: (a) immunocytochemical analysis of oestrogen and progesterone receptors; (b) reverse transcriptase polymerase chain reaction of oestrogen receptor mRNAs; and (c) immunofluorescence of the 27 kDa heat shock protein (Hsp27), which has been reported to be a marker of functional oestrogen receptors. There appeared to be significantly and consistently lower levels of oestrogen receptor expressed in PC3 cells than in LNCaP cells. The observation that oestradiol-induced growth of LNCaP cells is completely reversed by the pure anti-oestrogen ICI 182,780 clearly implies that the biological response of these cells to oestradiol is mediated mainly via its own receptor. On the other hand, use of a neutralizing antibody against transforming growth factor (TGF)-beta 1 results in a remarkable increase in the growth of PC3 cells; this effect is almost completely abolished after the addition of oestradiol. This suggests that the oestradiol-induced growth inhibition may be mediated by TGF-beta 1. These results suggest that the current model for hormone-dependence of human prostatic carcinoma should be revised. This is of special concern, because recent data indicate that prostate cancer has become the most prevalent cancer and the second principal cause of cancer death in western countries.
Phi 29 DNA polymerase active site. Mutants in conserved residues Tyr254 and Tyr390 are affected in dNTP binding. (1992)

Phi 29 DNA polymerase shares with other alpha-like DNA polymerases several regions of amino acid similarity. Among them, the two conserved regions characterized by the amino acid motifs "D-NSLYP" and "K--NS(L/V)YG," regions 1 and 2a, respectively, according to Blanco et al. (Blanco, L., Bernad, A., Blasco, M. A. and Salas, M. (1991) Gene (Amst.) 100, 27-38) have been proposed to be part of the polymerization active site of alpha-like DNA polymerases. One phi 29 DNA polymerase mutant in residue Tyr254, located in conserved region 1, and two mutants in residue Tyr390, located in conserved region 2a, have been characterized. The three phi 29 DNA polymerase mutant proteins were affected in polymerization when Mg(2+)-dNTPs were used as substrate. However, when the substrate was Mn(2+)-dNTP, mutants behaved as the wild-type phi 29 DNA polymerase. Mutant Tyr254 to Phe (Y254F) was strongly affected in the protein-primed initiation step of phi 29 DNA replication showing a decreased affinity for Me(2+)-dATP, the initiating nucleotide. Furthermore, the analysis of the template-independent deoxynucleotidylation of the TP by Y254F mutant polymerase is consistent with a change in the relative affinity for dNTPs. On the other hand, mutants Y390F and Y390S were found to be hypersensitive to the dNTP analogs 2-(p-n-butylanilino)dATP and N2-(p-n-butyl-phenyl)dGTP. The results obtained indicate that residues Tyr254 and Tyr390 are involved, directly or indirectly, in Me(2+)-dNTP binding.
A novel key establishment scheme for wireless sensor networks based on complex network synchronization (2011)

As a low-consumption, low-cost, distributed self-organized network, wireless sensor network communicates as a self-similar, small-world and scale-free complex network. Based on the defects analysis of digital communication and sufficientnecessary condition of analog signal synchronization, we proposed a novel key distribution scheme in this paper. While some performance analyses as well as some prospects are also given in the end.
SiGe HBT technology: a new contender for Si-based RF and microwave circuit applications (1998)

The silicon-germanium heterojunction bipolar transistor (SiGe HBT) is the first practical bandgap-engineered device to be realized in silicon. SiGe HBT technology combines transistor performance competitive with III-V technologies with the processing maturity, integration levels, yield, and hence, cost commonly associated with conventional Si fabrication. In the ten-and-one-half years since the first demonstration of a functional transistor, SiGe HBT technology has emerged from the research laboratory, entered manufacturing on 200-mm wafers, and is poised to enter the commercial RF and microwave market. State-of-the-art SiGe HBT's can deliver: (1) f/sub T/ in excess of 50 GHz; (2) f/sub max/ in excess of 70 GHz; (3) minimum noise figure below 0.7 dB at 2.0 GHz; (4) 1/f noise corner frequencies below 500 Hz; (5) cryogenic operation; (6) excellent radiation hardness; (7) competitive power amplifiers; and (8) reliability comparable to Si. A host of record-setting digital, analog, RF, and microwave circuits have been demonstrated in the past several years using SiGe HBT's, and recent work on passives and transmission lines on Si suggest a migratory path to Si-based monolithic microwave integrated circuits (MMIC's) is possible. The combination of SiGe HBT's with advanced Si CMOS to form an SiGe BiCMOS technology represents a unique opportunity for Si-based RF system-on-a-chip solutions. This paper reviews state-of-the-art SiGe HBT technology and assesses its potential for current and future RF and microwave systems.
Building and Optimizing a Virus-specific T Cell Receptor Library for Targeted Immunotherapy in Viral Infections (2014)

Restoration of antigen-specific T cell immunity has the potential to clear persistent viral infection. T cell receptor (TCR) gene therapy can reconstitute CD8 T cell immunity in chronic patients. We cloned 10 virus-specific TCRs targeting 5 different viruses, causing chronic and acute infection. All 10 TCR genetic constructs were optimized for expression using a P2A sequence, codon optimization and the addition of a non-native disulfide bond. However, maximum TCR expression was only achieved after establishing the optimal orientation of the alpha and beta chains in the expression cassette; 9/10 TCRs favored the beta-P2A-alpha orientation over alpha-P2A-beta. Optimal TCR expression was associated with a significant increase in the frequency of IFN-gamma+ T cells. In addition, activating cells for transduction in the presence of Toll-like receptor ligands further enhanced IFN-gamma production. Thus, we have built a virus-specific TCR library that has potential for therapeutic intervention in chronic viral infection or virus-related cancers.
Dominant-negative inhibition of Flk-1 suppresses the growth of many tumor types in vivo. (1996)

Angiogenesis, the sprouting of new blood vessels from existing vessels, occurs in many physiological and pathological processes, including embryonic development, wound healing, and tumor growth. It is required for tumor growth because new blood vessel formation is necessary for tumors to expand beyond a minimum volume. Several growth factor receptor tyrosine kinases have been implicated in angiogenesis, including receptors for epidermal, fibroblast, and platelet-derived growth factors, as well as the receptors Flk-1/KDR, Flt-1 Tek/Tie-2, and Tie-1. Endothelial cells in the vessels of tumors express Flk-1/KDR, a receptor for vascular endothelial growth factor. Flk-1 was previously shown to play a role in angiogenesis and tumor formation of s.c. xenografts of C6 glioma cells using dominant-negative methodology. We now demonstrate that Flk-1 seems to be generally involved in the growth of a wide range of solid tumors, including mammary, ovarian, and lung carcinoma, as well as glioblastoma. Furthermore, survival times in rats bearing intracerebral tumors were prolonged using the same dominant-negative methodology. The involvement of Flk-1 in a variety of tumor types suggests an important role for Flk-1 in tumor angiogenesis.
Security & Scalability of Content-Centric Networking (2010)

By suggesting radical changes to the current Internet, approaches to clean-slate architectures run the risk of introducing new opportunities for attacks. These attacks can range from new forms of denial-of-service to attacks against other users’ privacy. In this thesis, we analyse the architecture proposed by Content-Centric Networking from a security perspective. One security-critical feature of Content-Centric Networking is the introduction of general-purpose caches that are shared by a small number of users. We show how attackers can leverage these caches to monitor what content its users are retrieving. More generally, we argue that there is a tradeoff between network efficiency and user privacy. Countermeasures against cache-based privacy attacks need to carefully explore this tradeoff.
Rule-based Machine Learning Methods for Functional Prediction (1995)

We describe a machine learning method for predicting the value of a real-valued function, given the values of multiple input variables. The method induces solutions from samples in the form of ordered disjunctive normal form (DNF) decision rules. A central objective of the method and representation is the induction of compact, easily interpretable solutions. This rule-based decision model can be extended to search efficiently for similar cases prior to approximating function values. Experimental results on real-world data demonstrate that the new techniques are competitive with existing machine learning and statistical methods and can sometimes yield superior regression performance.
Congenital Adrenal Hyperplasia (1987)

(Second of Two Parts)Molecular Genetics of 21-Hydroxylase DeficiencyIt has been demonstrated that the HLA-linked defect in 21-hydroxylase deficiency involves a structural gene for the corresponding cytochrome P450 (P450c21). A bovine cDNA clone was isolated that encoded part of this enzyme (i.e., "complementary DNA," corresponding to the messenger RNA for P450c21, linked to sequences that allowed this DNA to replicate autonomously in bacteria).52 DNA samples were extracted from leukocytes obtained from normal persons and from patients with 21-hydroxylase deficiency who carried the characteristic HLA haplotype A3;Bw47:DR7. These samples were analyzed with use of Southern blot hybridization.4, 53 For this analysis, . . .
‘Touchdown’ PCR to circumvent spurious priming during gene amplification (1991)

Journal Article 'Touchdown' PCR to circumvent spurious priming during gene amplification Get access R.H. Don, R.H. Don Centre for Molecular Biology and Biotechnology, The University of QueenslandBrisbane Queensland 4072, Australia Search for other works by this author on: Oxford Academic PubMed Google Scholar P. T. Cox, P. T. Cox * Centre for Molecular Biology and Biotechnology, The University of QueenslandBrisbane Queensland 4072, Australia *To whom correspondence should be addressed Search for other works by this author on: Oxford Academic PubMed Google Scholar B.J. Wainwright, B.J. Wainwright Centre for Molecular Biology and Biotechnology, The University of QueenslandBrisbane Queensland 4072, Australia Search for other works by this author on: Oxford Academic PubMed Google Scholar K. Baker, K. Baker Centre for Molecular Biology and Biotechnology, The University of QueenslandBrisbane Queensland 4072, Australia Search for other works by this author on: Oxford Academic PubMed Google Scholar J. S. Mattick J. S. Mattick Centre for Molecular Biology and Biotechnology, The University of QueenslandBrisbane Queensland 4072, Australia Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 19, Issue 14, 25 July 1991, Page 4008, https://doi.org/10.1093/nar/19.14.4008 Published: 25 July 1991 Article history Received: 04 April 1991 Published: 25 July 1991
Idiopathic noncirrhotic portal hypertension (2011)

Idiopathic noncirrhotic portal hypertension (INCPH) is characterized by an increased portal venous pressure gradient in the absence of a known cause of liver disease and portal vein thrombosis. In contrast to the high prevalence of this disorder in India, INCPH is a rare disease in the Western world. The etiology of INCPH can be divided in five categories: chronic infections, exposure to medication or toxins, thrombophilia, immunological disorders, and genetic disorders. Multifactorial etiology can also be encountered. Chronic abdominal infection is incriminated as the most important etiological factor in Eastern patients and thrombophilia in Western patients. The majority of patients with INCPH initially present with signs or complications of portal hypertension (mainly variceal bleeding and splenomegaly). These patients usually have preserved liver function. Liver function impairment occurs mainly in the context of intercurrent conditions. Patients with INCPH are often clinically and radiologically misdiagnosed as liver cirrhosis, so that a liver biopsy is indispensable to discriminate cirrhosis from INCPH. Histopathological characteristics of INCPH are heterogeneous, demonstrating overlap between several pathological entities (e.g., hepatoportal sclerosis, nodular regenerative hyperplasia, and incomplete septal cirrhosis). Even though hemodynamical changes in INCPH patients are not comparable to those in cirrhotics, prophylaxis and treatment of variceal bleeding are recommended to be similar. Anticoagulation therapy must be considered only in patients who develop portal vein thrombosis. INCPH has been considered a disorder with a relatively benign disease course. However, liver failure, hepatic encephalopathy, and hepatopulmonary syndrome can occur and are considered indications for liver transplantation.
Tyro3 Family-Mediated Cell Entry of Ebola and Marburg Viruses (2006)

Filoviruses, represented by the genera Ebolavirus and Marburgvirus, cause a lethal hemorrhagic fever in humans and in nonhuman primates. Although filovirus can replicate in various tissues or cell types in these animals, the molecular mechanisms of its broad tropism remain poorly understood. Here we show the involvement of members of the Tyro3 receptor tyrosine kinase family-Axl, Dtk, and Mer-in cell entry of filoviruses. Ectopic expression of these family members in lymphoid cells, which otherwise are highly resistant to filovirus infection, enhanced infection by pseudotype viruses carrying filovirus glycoproteins on their envelopes. This enhancement was reduced by antibodies to Tyro3 family members, Gas6 ligand, or soluble ectodomains of the members. Live Ebola viruses infected both Axl- and Dtk-expressing cells more efficiently than control cells. Antibody to Axl inhibited infection of pseudotype viruses in a number of Axl-positive cell lines. These results implicate each Tyro3 family member as a cell entry factor in filovirus infection.
High-Strength Aluminum-Based Composite Materials Reinforced by Microstructures and Nanostructures (Mini Review) (2019)

This mini review is devoted to analysis of the latest advances in the development of aluminum-based composite materials (CMs) reinforced by microstructures and nanostructures. The fabrication methods of CMs, various reinforcing additives (Al2O3, AlN, SiC, CuO, B4C, Li3N, C, and BN), and their morphological types (nanotubes, nanoplates, microparticles, and nanoparticles), as well as the structure and properties of CMs, are considered. The importance of theoretical modeling methods for studying the strength of interfaces in CMs is shown.
Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. (1997)

Induction of protein kinase C (PKC) pathway in the vascular tissues by hyperglycemia has been associated with many of the cellular changes observed in the complications of diabetes. Recently, we have reported that the use of a novel, orally effective specific inhibitor of PKC beta isoform (LY333531) normalized many of the early retinal and renal hemodynamics in rat models of diabetes. In the present study, we have characterized a spectrum of biochemical and molecular abnormalities associated with chronic changes induced by glucose or diabetes in the cultured mesangial cells and renal glomeruli that can be prevented by LY333531. Hyperglycemia increased diacylglycerol (DAG) level in cultured mesangial cells exposed to high concentrations of glucose and activated PKC alpha and beta1 isoforms in the renal glomeruli of diabetic rats. The addition of PKC beta selective inhibitor (LY333531) to cultured mesangial cells inhibited activated PKC activities by high glucose without lowering DAG levels and LY333531 given orally in diabetic rats specifically inhibited the activation of PKC beta1 isoform without decreasing PKC alpha isoform activation. Glucose-induced increases in arachidonic acid release, prostaglandin E2 production, and inhibition of Na+-K+ ATPase activities in the cultured mesangial cells were completely prevented by the addition of LY333531. Oral feeding of LY333531 prevented the increased mRNA expression of TGF-beta1 and extracellular matrix components such as fibronectin and alpha1(IV) collagen in the glomeruli of diabetic rats in parallel with inhibition of glomerular PKC activity. These results suggest that the activation of PKC, predominately the beta isoform by hyperglycemia in the mesangial cells and glomeruli can partly contribute to early renal dysfunctions by alteration of prostaglandin production and Na+-K+ ATPase activity as well as the chronic pathological changes by the overexpression of TGF-beta1 and extracellular matrix components genes.
Targeting the DNA Damage Response in Cancer (2009)

ADVERTISEMENT RETURN TO ISSUEPREVReviewNEXTTargeting the DNA Damage Response in CancerMats Ljungman*View Author Information Division of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109* Phone: (734) 764-3330. Fax: (734) 763-1581. E-mail: [email protected]Cite this: Chem. Rev. 2009, 109, 7, 2929–2950Publication Date (Web):June 22, 2009Publication History Received6 February 2009Published online22 June 2009Published inissue 8 July 2009https://doi.org/10.1021/cr900047gCopyright © 2009 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views7608Altmetric-Citations106LEARN 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 InReddit Read OnlinePDF (814 KB) Get e-AlertsSUBJECTS:Cancer,Cells,Genetics,Inhibitors,Peptides and proteins Get e-Alerts
Effects of Demineralized Bone Matrix on Tendon-Bone Healing in an Intra-articular Rodent Model (2012)

Introduction of osteoinductive DBM at the tendon-bone interface during ACL reconstructive surgery may improve short-term outcomes.
Performance measurement of dynamically compiled Java executions (1999)

Article Performance measurement of dynamically compiled Java executions Share on Authors: Tia Newhall University of Wisconsin Madison, Madison, WI University of Wisconsin Madison, Madison, WIView Profile , Barton P. Miller University of Wisconsin Madison, Madison, WI University of Wisconsin Madison, Madison, WIView Profile Authors Info & Claims JAVA '99: Proceedings of the ACM 1999 conference on Java GrandeJune 1999 Pages 42–50https://doi.org/10.1145/304065.304093Online:01 June 1999Publication History 7citation430DownloadsMetricsTotal Citations7Total Downloads430Last 12 Months4Last 6 weeks0 Get Citation AlertsNew Citation Alert added!This alert has been successfully added and will be sent to:You will be notified whenever a record that you have chosen has been cited.To manage your alert preferences, click on the button below.Manage my AlertsNew Citation Alert!Please log in to your account Save to BinderSave to BinderCreate a New BinderNameCancelCreateExport CitationPublisher SiteGet Access
Folding-Based Electrochemical Biosensors: The Case for Responsive Nucleic Acid Architectures (2010)

Biomolecular recognition is versatile, specific, and high affinity, qualities that have motivated decades of research aimed at adapting biomolecules into a general platform for molecular sensing. Despite significant effort, however, so-called "biosensors" have almost entirely failed to achieve their potential as reagentless, real-time analytical devices; the only quantitative, reagentless biosensor to achieve commercial success so far is the home glucose monitor, employed by millions of diabetics. The fundamental stumbling block that has precluded more widespread success of biosensors is the failure of most biomolecules to produce an easily measured signal upon target binding. Antibodies, for example, do not change their shape or dynamics when they bind their recognition partners, nor do they emit light or electrons upon binding. It has thus proven difficult to transduce biomolecular binding events into a measurable output signal, particularly one that is not readily spoofed by the binding of any of the many potentially interfering species in typical biological samples. Analytical approaches based on biomolecular recognition are therefore mostly cumbersome, multistep processes relying on analyte separation and isolation (such as Western blots, ELISA, and other immunochemical methods); these techniques have proven enormously useful, but are limited almost exclusively to laboratory settings. In this Account, we describe how we have refined a potentially general solution to the problem of signal detection in biosensors, one that is based on the binding-induced "folding" of electrode-bound DNA probes. That is, we have developed a broad new class of biosensors that employ electrochemistry to monitor binding-induced changes in the rigidity of a redox-tagged probe DNA that has been site-specifically attached to an interrogating electrode. These folding-based sensors, which have been generalized to a wide range of specific protein, nucleic acid, and small-molecule targets, are rapid (responding in seconds to minutes), sensitive (detecting sub-picomolar to micromolar concentrations), and reagentless. They are also greater than 99% reusable, are supported on micrometer-scale electrodes, and are readily fabricated into densely packed sensor arrays. Finally, and critically, their signaling is linked to a binding-specific change in the physics of the probe DNA, and not simply to adsorption of the target onto the sensor head. Accordingly, they are selective enough to be employed directly in blood, crude soil extracts, cell lysates, and other grossly contaminated clinical and environmental samples. Indeed, we have recently demonstrated the ability to quantitatively monitor a specific small molecule in real-time directly in microliters of flowing, unmodified blood serum. Because of their sensitivity, substantial background suppression, and operational convenience, these folding-based biosensors appear potentially well suited for electronic, on-chip applications in pathogen detection, proteomics, metabolomics, and drug discovery.