gebhart/patrepeval huggingface dataset:
Disruption of the SRC-1 gene in mice suppresses breast cancer metastasis without affecting primary tumor formation (2008)

Steroid receptor coactivator-1 (SRC-1) is a coactivator for nuclear hormone receptors such as estrogen and progesterone receptors and certain other transcription factors such as Ets-2 and PEA3. SRC-1 expression in breast cancer is associated with HER2 and c-Myc expression and with reduced disease-free survival. In this study, SRC-1(-/-) mice were backcrossed with FVB mice and then cross-bred with MMTV-polyoma middle T antigen (PyMT) mice to investigate the role of SRC-1 in breast cancer. Although mammary tumor initiation and growth were similar in SRC-1(-/-)/PyMT and wild-type (WT)/PyMT mice, genetic ablation of SRC-1 antagonized PyMT-induced restriction of mammary ductal differentiation and elongation. SRC-1(-/-)/PyMT mammary tumors were also more differentiated than WT/PyMT mammary tumors. The intravasation of mammary tumor cells and the frequency and extent of lung metastasis were drastically reduced in SRC-1(-/-)/PyMT mice compared with WT/PyMT mice. Metastatic analysis of transplanted WT/PyMT and SRC-1(-/-)/PyMT tumors in SRC-1(-/-) and WT recipient mice revealed that SRC-1 played an intrinsic role in tumor cell metastasis. Furthermore, SRC-1 was up-regulated during mammary tumor progression. Disruption of SRC-1 inhibited Ets-2-mediated HER2 expression and PyMT-stimulated Akt activation in the mammary tumors. Disruption of SRC-1 also suppressed colony-stimulating factor-1 (CSF-1) expression and reduced macrophage recruitment to the tumor site. These results suggest that SRC-1 specifically promotes metastasis without affecting primary tumor growth. SRC-1 may promote metastasis through mediating Ets-2-mediated HER2 expression and activating CSF-1 expression for macrophage recruitment. Therefore, functional interventions for coactivators like SRC-1 may provide unique approaches to control breast cancer progression and metastasis.
Platelet-Erythrocyte Adhesion in Sickle Cell Disease (1999)

Thrombospondin on sRBC may mediate, at least in part, sRBC-platelet adhesion in sickle cell disease. The study of heterotypic cell-cell interactions is important in understanding the pathogenesis of vaso-occlusion in sickle cell disease.
Exendin-4 Improves Glycemic Control, Ameliorates Brain and Pancreatic Pathologies, and Extends Survival in a Mouse Model of Huntington's Disease (2008)

Targeting both peripheral and neuronal deficits, Ex-4 is an attractive agent for therapeutic intervention in Huntington's disease patients suffering from diabetes.
Respiratory Membrane Permeability and Bronchial Hyperreactivity in Patients with Stable Asthma: Effects of Therapy with Inhaled Steroids (1991)

In patients with stable asthma, we assayed plasma proteins in the bronchoalveolar lavage fluid to obtain information on plasma exudation into the airways. Fourteen nonsmoking patients with asthma who were in a stable period of their disease and eight nonsmoking healthy volunteers were studied. The ratios of the concentrations of albumin, ceruloplasmin (CP), and alpha-2-macroglobulin (A2M) between blood and epithelial lining fluid were calculated (cQalb, cQCP, and cQA2M). The cQalb was increased in the patients (Mann-Whitney U test, p less than 0.05). In 10 patients the bronchial hyperreactivity was assessed with histamine provocation tests. Significant relationships between the cQalb, cQCP, and cQA2M on the one hand and PC15 on the other hand were found (Spearman's rank correlation: r = -0.62, p less than 0.05; r = -0.61, p less than 0.05; r = -0.79, p less than 0.01, respectively). Fourteen patients were treated with two inhalations of 200 micrograms glucocorticosteroids per day in a 3-month prospective study. Three of them were excluded from further study because of an intercurrent exacerbation of asthmatic symptoms during therapy. In the 11 patients with stable asthma, the cQalb and cQA2M decreased after treatment with inhaled steroids (Wilcoxon's matched pairs signed rank test, p less than 0.03). Our results show that in patients with stable asthma, there is an increased plasma exudation into the airways, most likely caused by an increased respiratory membrane permeability. The plasma exudation correlated with the bronchial hyperreactivity to histamine, and it decreased after corticosteroid therapy.
Development of flow-cytometry-based miniature chemical fluid analysis system using fluorescent microbeads (1998)

We present a demonstration of an optical microfluidic system for rapid and simultaneous measurement of several fluid analytes in a microscale volume that is based on fluorescent indicators immobilized on polymer microbeads. The fluorescence properties of such 'reporter beads' can be a function of the concentration of an analyte, and can be monitored in a silicon microfabricated flow channel. The sizes of microbeads can be determined by the scattering signal, so this system can be used to analyze several analytes at the same time by using beads of different sizes that are sensitive to different analytes. The fluorescent indicator Carboxy-SNAFL 1 was immobilized on amino-functionalized polystyrene beads of 5 micrometer diameter. The intensities of two fluorescent peaks (at 560 nm and at 620 nm) were measured and their ratio was dependent on the pH value of the analyte. A 488 nm air-cooled argon laser was used to excite the fluorescent beads flowing through a microfabricated V-groove channel. Two miniature photomultiplier modules and interference filters were used to simultaneously measure both fluorescence intensities.
Asymmetric Magnetic Interference Patterns in 0-πJosephson Junctions (1998)

We examine the magnetic interference patterns of Josephson junctions with a region of 0 and of $\ensuremath{\pi}$ phase shift. Such junctions have recently been realized as $c$-axis YBCO-Pb junctions with a single twin boundary in YBCO. We show that in general the junction generates self-fields which introduces an asymmetry in the critical current under reversal of the magnetic field. Numerical calculations of these asymmetries indicate that they account well for unexplained features observed in single twin boundary junctions.
Germs Take a Bite Out of Antibiotics (2008)

As far as patients and doctors are concerned, bacteria are supposed to do one thing when they encounter antibiotics: drop dead. But a broad survey of soil microbes shows that numerous species devour even the most potent drugs. The craving for antibiotics is widespread across environments and bacterial groups, researchers report on page 100, fueling worries about the dwindling power of our main weapons against infections.
Stimulation of vaccinia topoisomerase I by nucleoside triphosphates. (1994)

The rate of relaxation of supercoiled DNA by purified vaccinia topoisomerase I is stimulated 20-fold by 5 mM ATP. A similar effect is elicited by GTP, CTP, UTP, dATP, and adenosine 5'-(beta, gamma-imido)triphosphate. ATP-mediated rate enhancement requires salt as a coactivator. ADP and inorganic pyrophosphate also stimulate relaxation 10-20-fold, whereas AMP and inorganic phosphate have little effect. A model for allosteric activation of topoisomerase by nucleotides is suggested.
Stability of thrombosis induced by electrocoagulation of rat middle cerebral artery. (1994)

The electrocoagulation process commonly used in experimental stroke studies may produce only a temporary occlusion of the rat middle cerebral artery.
Development of a user interface for MARIAN and CODER systems (1993)

The objective of this project is to implement a Graphical User Interface (GUI) for information storage and retrieval (lS&R) that will be easy to use, easy to maintain and easy to extend. The user interface implementation took advantage of the advanced object oriented GUI development environment provided by NeXTstep to provide an iconic interface that allows direct manipulation and supports mixed initiative dialogues. The GUI will be used in conjunction with a family of IS&R systems at Virginia Tech: CODER (COmposite Document Expert/effective/extended and Retrieval), a test-bed that is being developed to experiment with various intelligent information retrieval techniques, and MARIAN (Multiple Access and Retrieval Information with ANnotation), an advanced on-line public access library catalog system providing network access to all facets of bibliographic information.
Pleiotropic Effects of Tocotrienols and Quercetin on Cellular Senescence: Introducing the Perspective of Senolytic Effects of Phytochemicals (2016)

The possibility to target cellular senescence with natural bioactive substances open interesting therapeutic perspective in cancer and aging. Engaging senescence response is suggested as a key component for therapeutic intervention in the eradication of cancer. At the same time, delaying senescence or even promote death of accumulating apoptosis-resistant senescent cells is proposed as a strategy to prevent age related diseases. Although these two desired outcome present an intrinsic dichotomy, there are examples of promising natural compounds that appear to satisfy all the requirements to develop senescence- targeted health promoting nutraceuticals. Tocotrienols (T3s) and quercetin (QUE), albeit belonging to different phytochemical classes, display similar and promising effects "in vitro" when tested in normal and cancer cells. Both compounds have been shown to induce senescence and promote apoptosis in a multitude of cancer lines. Conversely, they display senescence delaying activity in primary cells and rejuvenating effects in senescent cells. More recently, QUE has been shown to display senolytic effects in some primary senescent cells, likely as a consequence of its inhibitory effects on specific anti-apoptotic genes (i.e. PI3K and other kinases). Senolytic activity has not been tested for T3s but part of metabolic and apoptotic pathways affected by these compounds in cancer cells overlap with those of QUE. This suggests that the rejuvenating effects of T3s and QUE on pre-senescent and senescent primary cells might be the net results of a senolytic activity on senescent cells and a selective survival of a sub-population of non-senescent cells in the culture. The meaning of this hypothesis in the context of adjuvant therapy of cancer and preventive anti-aging strategies with QUE or T3s is discussed.
Stable and controllable RNA interference: Investigating the physiological function of glutathionylated actin (2003)

RNA interference is an effective method to silence specific gene expression. Its application to mammalian cells, however, has been hampered by various shortcomings. Recently, it was reported that introduction of 22-bp double-stranded RNAs (dsRNAs) would specifically suppress expression of endogenous and heterogeneous genes in various mammalian cell lines. However, using this method, we failed to knock out proteins of interest effectively. Here we report the development of a stable and controllable method for generating dsRNA intracellularly. Tetracycline-responsive transactivator-containing cells were transfected with a vector capable of tetracycline-induced bidirectionally overexpressing sense and antisense RNA to form dsRNA in vivo. With this method, glutaredoxin, monitored by Western blot, was knocked out by overexpressing 290-base sense and antisense RNA in NIH 3T3 cells controlled by tetracycline or doxycycline. By using these glutaredoxin knocked-out cells, we have demonstrated that actin deglutathionylation plays a key role in growth factor-mediated actin polymerization, translocalization, and reorganization near the cell periphery.
Familial Hypercholesterolemia and Atherosclerosis in Cloned Minipigs Created by DNA Transposition of a Human PCSK9 Gain-of-Function Mutant (2013)

Lack of animal models with human-like size and pathology hampers translational research in atherosclerosis. Mouse models are missing central features of human atherosclerosis and are too small for intravascular procedures and imaging. Modeling the disease in minipigs may overcome these limitations, but it has proven difficult to induce rapid atherosclerosis in normal pigs by high-fat feeding alone, and genetically modified models similar to those created in mice are not available. D374Y gain-of-function mutations in the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene cause severe autosomal dominant hypercholesterolemia and accelerates atherosclerosis in humans. Using Sleeping Beauty DNA transposition and cloning by somatic cell nuclear transfer, we created Yucatan minipigs with liver-specific expression of human D374Y-PCSK9. D374Y-PCSK9 transgenic pigs displayed reduced hepatic low-density lipoprotein (LDL) receptor levels, impaired LDL clearance, severe hypercholesterolemia, and spontaneous development of progressive atherosclerotic lesions that could be visualized by noninvasive imaging. This model should prove useful for several types of translational research in atherosclerosis.
Wave attenuation attributes as flow unit indicators (2002)

In this article we present a model-based interpretation algorithm to predict attenuation signatures associated with a reservoir's structure and its intrinsic properties. Scattering losses are caused by multiple reflections associated with the impedance contrast between different reservoir boundaries. Intrinsic losses are due to the fluids in the reservoir, the rock fabric, and the anisotropy due to vertical fractures. Because amplitude data are sensitive to these reservoir characteristics, we calculate the wave attenuation response of the reservoir in the frequency range of surface seismic, VSP, crosswell seismic, and borehole sonic. A model of a plane wave traveling in a poroelastic multilayer earth medium allows us to include anisotropy. The multilayer part of the model simulates elastic scattering; the poroelastic part of the model simulates fluid-flow effects in the reservoir; and the anisotropic part of the model simulates reservoir fractures.
Measurement of enzyme E.deg.' values by optically transparent thin layer electrochemical cells (1975)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMeasurement of enzyme E.deg.' values by optically transparent thin layer electrochemical cellsWilliam R. Heineman, Barbara J. Norris, and John F. GoelzCite this: Anal. Chem. 1975, 47, 1, 79–84Publication Date (Print):January 1, 1975Publication History Published online1 May 2002Published inissue 1 January 1975https://pubs.acs.org/doi/10.1021/ac60351a001https://doi.org/10.1021/ac60351a001research-articleACS PublicationsRequest reuse permissionsArticle Views418Altmetric-Citations180LEARN 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
Mcl1 haploinsufficiency protects mice from Myc-induced acute myeloid leukemia (2010)

Antiapoptotic BCL2 family members have been implicated in the pathogenesis of acute myelogenous leukemia (AML), but the functional significance and relative importance of individual proteins (e.g., BCL2, BCL-XL, and myeloid cell leukemia 1 [MCL1]) remain poorly understood. Here, we examined the expression of BCL2, BCL-XL, and MCL1 in primary human hematopoietic subsets and leukemic blasts from AML patients and found that MCL1 transcripts were consistently expressed at high levels in all samples tested. Consistent with this, Mcl1 protein was also highly expressed in myeloid leukemic blasts in a mouse Myc-induced model of AML. We used this model to test the hypothesis that Mcl1 facilitates AML development by allowing myeloid progenitor cells to evade Myc-induced cell death. Indeed, activation of Myc for 7 days in vivo substantially increased myeloid lineage cell numbers, whereas hematopoietic stem, progenitor, and B-lineage cells were depleted. Furthermore, Mcl1 haploinsufficiency abrogated AML development. In addition, deletion of a single allele of Mcl1 from fully transformed AML cells substantially prolonged the survival of transplanted mice. Conversely, the rapid lethality of disease was restored by coexpression of Bcl2 and Myc in Mcl1-haploinsufficient cells. Together, these data demonstrate a critical and dose-dependent role for Mcl1 in AML pathogenesis in mice and suggest that MCL1 may be a promising therapeutic target in patients with de novo AML.
CCD and CMOS Imaging Array Technologies: Technology Review (1998)

This paper provides an overview of both CCD (charged coupled device) and CMOS (complimentary metal oxide semiconductor) imaging array technologies. CCDs have been in existence for nearly 30 years and the technology has matured to the point where very large, consistent (low numbers of defects) devices can now be produced. However, CCDs suffer from a number of drawbacks, including cost, complex power supplies and support electronics. CMOS imaging arrays, on the other hand, are still in their infancy, but are set to develop rapidly and offer a number of potential benefits over CCDs. This review provides an overview of both CCD and CMOS imaging technology, and includes explanations of how images are captured and read out from the imaging arrays. Also covered are issues such as performance characteristics, cost considerations and the future of imaging arrays. This review does not provide details of colour sensors, colour filter arrays and colour interpolation, etc., as these will be the subject of a separate report. Introduction to CCDs The Charged Coupled Device (CCD) was invented in 1970 by Willard Boyle and George
Cytokine involvement in dynorphin-induced allodynia (2000)

Dynorphin A is an endogenous opioid peptide, which has previously been shown to produce a long-lasting allodynia and hyperalgesia in mice, behavioral states consistent with signs of clinically observed neuropathic pain. This dynorphin-induced allodynia was used as a pharmacological, central model of neuropathic pain. In this study, we examined the involvement of the cytokine IL-1beta, the transcription factor nuclear factor kappa B (NF-kappaB), and de novo protein synthesis in the development of allodynia induced by intrathecal (i.t.) administration of dynorphin in male ICR mice. Pretreatment with the protein synthesis inhibitor cycloheximide (0. 3-85nmol), the NF-kappaB inhibitor pyrrolidinedithiocarbamate (PDTC) (0.001-1000pmol), the IL-1 receptor antagonist (IL-1ra) protein (0. 01-100ng), the caspase-1 inhibitor (YVAD) (0.1-300pmol), and the anti-inflammatory cytokine IL-10 (0.1-300ng) all dose-dependently reduced the induction of dynorphin-induced allodynia. Finally, IL-10 administered within the first 24h after the dynorphin insult prevented the development of chronic allodynia. These results demonstrate that the anti-inflammatory cytokines IL-10 and IL-1ra impede the development of dynorphin-induced allodynia. These results also suggest that production of new proteins through NF-kappaB activation is required for the induction of allodynia. We speculate that IL-1ra, IL-10, PDTC and cycloheximide interfere with the central pro-inflammatory cascade. Modulation of cytokine activity in the spinal cord may therefore prove to be an effective therapeutic strategy for the treatment of chronic pain.
Iodide management in formamidinium-lead-halide–based perovskite layers for efficient solar cells (2017)

The formation of a dense and uniform thin layer on the substrates is crucial for the fabrication of high-performance perovskite solar cells (PSCs) containing formamidinium with multiple cations and mixed halide anions. The concentration of defect states, which reduce a cell's performance by decreasing the open-circuit voltage and short-circuit current density, needs to be as low as possible. We show that the introduction of additional iodide ions into the organic cation solution, which are used to form the perovskite layers through an intramolecular exchanging process, decreases the concentration of deep-level defects. The defect-engineered thin perovskite layers enable the fabrication of PSCs with a certified power conversion efficiency of 22.1% in small cells and 19.7% in 1-square-centimeter cells.
Functional analysis of a liver-specific enhancer of the hepatitis B virus. (1991)

The liver-specific enhancer I of the human hepatitis B virus contains several regions of DNA-protein interaction. Located within this element are also the domains of a promoter controlling the synthesis of the X open reading frame. Functional domains of the enhancer I and the X gene promoter were identified using DNase I protection analysis, deletion mutagenesis, and cell transfections. A unique liver-specific interaction was identified within this element whose binding site includes a direct sequence repeat, 5'-AGTAAACAGTA-3'. The factor(s) binding to this sequence motif was purified by oligonucleotide-affinity chromatography. Binding of this factor appears to play a key role in determining the overall enhancer function. Additionally, the interaction of several purified factors is presented. Cotransfection of liver cells with expression vectors encoding transcriptional factors resulted in trans-activation of the promoter/enhancer function. Based on the results of genetic analysis a model outlining the functional domains of the enhancer/promoter region is presented.
In Vitro Selection of mRNA Display Libraries Containing an Unnatural Amino Acid (2002)

The incorporation of unnatural amino acid into selectable, amplifiable peptide and protein libraries expands the chemical diversity of such libraries, thus considerably facilitating the process of obtaining ligands with improved properties (affinity, specificity, and function), particularly against therapeutically interesting targets. Here, we report that biocytin, a biotin derivative of lysine, can be inserted into an mRNA−protein fusion molecule through amber stop codon suppression. We also demonstrate that templates containing the codon corresponding to the biocytin tRNA (a UAG stop codon) can be enriched by iterative cycles of selection against a streptavidin agarose matrix.
Massive Social Network Analysis: Mining Twitter for Social Good (2010)

Social networks produce an enormous quantity of data. Facebook consists of over 400 million active users sharing over 5 billion pieces of information each month. Analyzing this vast quantity of unstructured data presents challenges for software and hardware. We present GraphCT, a Graph Characterization Toolkit for massive graphs representing social network data. On a 128-processor Cray XMT, GraphCT estimates the betweenness centrality of an artificially generated (R-MAT) 537 million vertex, 8.6 billion edge graph in 55 minutes and a real-world graph (Kwak, et al.) with 61.6 million vertices and 1.47 billion edges in 105 minutes. We use GraphCT to analyze public data from Twitter, a microblogging network. Twitter's message connections appear primarily tree-structured as a news dissemination system. Within the public data, however, are clusters of conversations. Using GraphCT, we can rank actors within these conversations and help analysts focus attention on a much smaller data subset.