gebhart/patrepeval huggingface dataset:
Potential Role of Protein Kinase B in Insulin-induced Glucose Transport, Glycogen Synthesis, and Protein Synthesis (1998)

Various biological responses stimulated by insulin have been thought to be regulated by phosphatidylinositol 3-kinase, including glucose transport, glycogen synthesis, and protein synthesis. However, the molecular link between phosphatidylinositol 3-kinase and these biological responses has been poorly understood. Recently, it has been shown that protein kinase B (PKB/c-Akt/Rac) lies immediately downstream from phosphatidylinositol 3-kinase. Here, we show that expression of a constitutively active form of PKB induced glucose uptake, glycogen synthesis, and protein synthesis in L6 myotubes downstream of phosphatidylinositol 3-kinase and independent of Ras and mitogen-activated protein kinase activation. Introduction of constitutively active PKB induced glucose uptake and protein synthesis but not glycogen synthesis in 3T3L-1 adipocytes, which lack expression of glycogen synthase kinase 3 different from L6 myotubes. Furthermore, we show that deactivation of glycogen synthase kinase 3 and activation of rapamycin-sensitive serine/threonine kinase by PKB in L6 myotubes might be involved in the enhancement of glycogen synthesis and protein synthesis, respectively. These results suggest that PKB acts as a key enzyme linking phosphatidylinositol 3-kinase activation to multiple biological functions of insulin through regulation of downstream kinases in skeletal muscle, a major target tissue of insulin.
Alzheimer disease in the United States (2010–2050) estimated using the 2010 census (2013)

The number of people in the United States with AD dementia will increase dramatically in the next 40 years unless preventive measures are developed.
Soluble derivatives of the β amyloid protein precursor in cerebrospinal fluid (1990)

We isolated and sequenced a soluble approximately 25 kDa amino-terminal derivative of the beta amyloid protein precursor (beta APP) that is readily detected in human cerebrospinal fluid (CSF). In CSF samples from 24 Alzheimer's disease (AD) patients and 12 controls, we then quantitated this approximately 25 kDa form as well as the approximately 125 and approximately 105 kDa derivatives that we previously identified. Our analysis shows (1) that, in AD, there is a significant decrease in the relative amount of the approximately 105 kDa form and a corresponding significant increase in the relative amount of the approximately 25 kDa form; (2) that these changes correlate with the mental status of the AD patients; and (3) that the same changes occur to a lesser extent in elderly as compared with young control patients. These observations indicate that processing of the beta APP changes in normal individuals as they age and to a greater extent in those who develop AD. The changes in beta APP derivatives that we have observed in CSF could have major implications because they may reflect fundamental mechanisms responsible for amyloid deposition and can be measured in living patients.
An efficient representation for irradiance environment maps (2001)

We consider the rendering of diffuse objects under distant illumination, as specified by an environment map. Using an analytic expression for the irradiance in terms of spherical harmonic coefficients of the lighting, we show that one needs to compute and use only 9 coefficients, corresponding to the lowest-frequency modes of the illumination, in order to achieve average errors of only 1%. In other words, the irradiance is insensitive to high frequencies in the lighting, and is well approximated using only 9 parameters. In fact, we show that the irradiance can be procedurally represented simply as a quadratic polynomial in the cartesian components of the surface normal, and give explicit formulae. These observations lead to a simple and efficient procedural rendering algorithm amenable to hardware implementation, a prefiltering method up to three orders of magnitude faster than previous techniques, and new representations for lighting design and image-based rendering.
Hantaviruses: Clinical, Microbiologic, and Epidemiologic Aspects (1995)

Hantaviruses comprise a genus of the family Bunyaviridae. Bunyaviruses are enveloped viruses with a negative-sense, tripartite RNA genome. Hantaviruses are etiologic agents for two acute and severe illnesses of man, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Each hantavirus is primarily associated with a single rodent host species or genus, and is transmitted to man through accidental inhalation or ingestion of virus-contaminated rodent excreta. The distribution of hantaviruses is worldwide. HFRS is caused by infection with Hantaan, Seoul, Dobrava/Belgrade, and Puumala hantaviruses, all of which are enzootic in murid rodents of Old World origin. HPS is caused by any of several hantavirus species associated with indigenous New World rodents of the subfamily Sigmodontinae, family Muridae. HFRS and HPS have numerous common epidemiologic, clinical, and laboratory characteristics. Common features include fever, myalgia, thrombocytopenia, neutrophilia, and a profound capillary leak syndrome associated with hypotension, decreased cardiac output, and shock. Worldwide, HPS is much less common than HFRS but is associated with a higher mortality rate. Recovery from hantavirus disease is generally complete, although chronic renal insufficiency may be a rare sequel of HFRS.
The New, New Portlanders (2011)

From Chinese laborers in the 1850s to Afghan refugees in the 2010s, immigrants have changed the economic and cultural life of the metroscape. A survey of the history of foreign immigration to Portland, and the agencies and organizations that have assisted newcomer integration in the region.
Thrombin Activation of Factor XI on Activated Platelets Requires the Interaction of Factor XI and Platelet Glycoprotein Ibα with Thrombin Anion-binding Exosites I and II, Respectively (2003)

Activation of factor XI (FXI) by thrombin on stimulated platelets plays a physiological role in hemostasis, providing additional thrombin generation required in cases of severe hemostatic challenge. Using a collection of 53 thrombin mutants, we identified 16 mutants with <50% of the wild-type thrombin FXI-activating activity in the presence of dextran sulfate. These mutants mapped to anion-binding exosite (ABE) I, ABE-II, the Na+-binding site, and the 50-insertion loop. Only the ABE-II mutants showed reduced binding to dextran sulfate-linked agarose. Selected thrombin mutants in ABE-I (R68A, R70A, and R73A), ABE-II (R98A, R245A, and K248A), the 50-insertion loop (W50A), and the Na+-binding site (E229A and R233A) with <10% of the wild-type activity also showed a markedly reduced ability to activate FXI in the presence of stimulated platelets. The ABE-I, 50-insertion loop, and Na+-binding site mutants had impaired binding to FXI, but normal binding to glycocalicin, the soluble form of glycoprotein Ibalpha (GPIb alpha). In contrast, the ABE-II mutants were defective in binding to glycocalicin, but displayed normal binding to FXI. Our data support a quaternary complex model of thrombin activation of FXI on stimulated platelets. Thrombin bound to one GPIb alpha molecule, via ABE-II on its posterior surface, is properly oriented for its activation of FXI bound to a neighboring GPI alpha molecule, via ABE-I on its anterior surface. GPIb alpha plays a critical role in the co-localization of thrombin and FXI and the resultant efficient activation of FXI.
Active Printed Materials for Complex (2014)

We propose a new design of complex self-evolving structures that vary over time due to environmental interaction. In conventional 3D printing systems, materials are meant to be stable rather than active and fabricated models are designed and printed as static objects. Here, we introduce a novel approach for simulating and fabricating self-evolving structures that transform into a predetermined shape, changing property and function after fabrication. The new locally coordinated bending primitives combine into a single system, allowing for a global deformation which can stretch, fold and bend given environmental stimulus.
Hydrolytic Degradation (2010)

This chapter contains sections titled: Introduction Degradation Mechanism Parameters for Hydrolytic Degradation Structural and Property Changes During Hydrolytic Degradation Applications of Hydrolytic Degradation Conclusions References
Structure of a free, unassociated alkyl-substituted .alpha.-sulfonyl carbanion: isolation and x-ray crystal structure analysis of the inclusive lithium cryptate (Me2CSO2Ph)(Li.cntdot.[2.1.1]cryptand) (1991)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTStructure of a free, unassociated alkyl-substituted .alpha.-sulfonyl carbanion: isolation and x-ray crystal structure analysis of the inclusive lithium cryptate (Me2CSO2Ph)(Li.cntdot.[2.1.1]cryptand)Hans Joachim Gais, Juergen Mueller, Juergen Vollhardt, and Hans J. LindnerCite this: J. Am. Chem. Soc. 1991, 113, 10, 4002–4003Publication Date (Print):May 1, 1991Publication History Published online1 May 2002Published inissue 1 May 1991https://pubs.acs.org/doi/10.1021/ja00010a058https://doi.org/10.1021/ja00010a058research-articleACS PublicationsRequest reuse permissionsArticle Views149Altmetric-Citations36LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Lineage Structure of the Human Antibody Repertoire in Response to Influenza Vaccination (2013)

The human antibody repertoire is one of the most important defenses against infectious disease, and the development of vaccines has enabled the conferral of targeted protection to specific pathogens. However, there are many challenges to measuring and analyzing the immunoglobulin sequence repertoire, including that each B cell's genome encodes a distinct antibody sequence, that the antibody repertoire changes over time, and the high similarity between antibody sequences. We have addressed these challenges by using high-throughput long read sequencing to perform immunogenomic characterization of expressed human antibody repertoires in the context of influenza vaccination. Informatic analysis of 5 million antibody heavy chain sequences from healthy individuals allowed us to perform global characterizations of isotype distributions, determine the lineage structure of the repertoire, and measure age- and antigen-related mutational activity. Our analysis of the clonal structure and mutational distribution of individuals' repertoires shows that elderly subjects have a decreased number of lineages but an increased prevaccination mutation load in their repertoire and that some of these subjects have an oligoclonal character to their repertoire in which the diversity of the lineages is greatly reduced relative to younger subjects. We have thus shown that global analysis of the immune system's clonal structure provides direct insight into the effects of vaccination and provides a detailed molecular portrait of age-related effects.
Thin-film silicon solar cells with efficient periodic light trapping texture (2007)

For solar cells based on thin-film microcrystalline (μc-Si:H) or amorphous silicon (a-Si:H) with absorber layers in the micrometer range, highly effective light trapping and an optimal incoupling of the entire sun spectrum are essential. To investigate and optimize both effects the wave propagation in thin-film silicon solar cells is modeled in three dimensions (3D) solving the Maxwell equations rigorously. A periodic nanostructured texture is investigated as an alternative to the common randomly rough texture. Inverted 3D pyramids with a periodicity of 850nm and structure height of 400nm show promising high quantum efficiencies close to the Tiedje limit.
Frequency offset compensation of pilot symbol assisted modulation in frequency flat fading (1997)

Pilot symbol assisted modulation (PSAM) is a practical technique in mobile digital communications since it can provide high performance in fading with large constellations and it has a simple implementation. Maintaining high performance with PSAM requires an accurate estimate of the transmitted carrier frequency. This paper examines model-based frequency estimation for mobile digital communications with PSAM. Maximum-likelihood estimators (MLE), which include the model for the fading, are derived and compared with those in an additive white Gaussian noise (AWGN) channel, and performance hounds are computed. Reduced complexity frequency estimators based on the MLE are derived and the performance is quantified by Monte-Carlo simulation.
“Non‐Fouling” Oligo(ethylene glycol)‐ Functionalized Polymer Brushes Synthesized by Surface‐Initiated Atom Transfer Radical Polymerization (2004)

The in‐situ synthesis of oligo(ethylene glycol)‐functionalized polymer brushes from a self‐assembled monolayer of an alkanethiol on gold that presents a tethered initiator by surface‐initiated atom transfer radical polymerization is reported. These polymer brushes exhibit no detectable adsorption of proteins, and are cell‐resistant for up to a month under typical cell culture conditions. The synthesis method is compatible with a range of patterning techniques from the nano‐ to the microscale, and enables the patterning of cells in a biologically relevant milieu over extended periods of time. Images of the brushes are shown on the inside front cover.
On the control dependence in the program dependence graph (1988)

The program dependence graph, PDG, is used to represent the data and control dependencies between the statements of some program. The data dependencies between the statements are fully understood and they correspond to the definition-use chain. On the other hand the concept of control dependence is not fully explored. In this paper we formalize and analyze the concept or control dependence and present algorithms to find directly the control dependence subgraph of PDG in Ο(N α(N)), where N is the number of statements in the program.
Immunity and immunopathology in dengue virus infections. (1992)

Dengue virus infections are a serious public health problem in tropical and subtropical areas of the world. Based on epidemiological data, it has been postulated that immune responses to dengue virus contribute to the pathogenesis of severe dengue illness, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Host immune responses are also important for controlling dengue virus infection. Therefore, dengue virus infections are an interesting model to explore the interactions between viruses and the immune system which result in immunopathology or recovery from infection. In this paper, we review immune responses to dengue viruses with an emphasis on the human T cell responses, and discuss possible roles of these immune responses in the control of dengue virus infection and in the pathogenesis of DHF/DSS.
Minimally modified low-density lipoprotein induces monocyte adhesion to endothelial connecting segment-1 by activating β1 integrin (1999)

We have shown previously that treatment of human aortic endothelial cells (HAECs) with minimally modified low-density lipoprotein (MM-LDL) induces monocyte but not neutrophil binding. This monocyte binding was not mediated by endothelial E-selectin, P-selectin, vascular cell adhesion molecule-I, or intercellular adhesion molecule-I, suggesting an alternative monocyte-specific adhesion molecule. We now show that moncytic alpha4beta1 integrins mediate binding to MM-LDL-treated endothelial cells. We present data suggesting that the expression of the connecting segment-1 (CS-1) domain of fibronectin (FN) is induced on the apical surface of HAEC by MM-LDL and is the endothelial alpha4beta1 ligand in MM-LDL-treated cells. Although the levels of CS-1 mRNA and protein were not increased, we show that MM-LDL treatment causes deposition of FN on the apical surface by activation of beta1integrins, particularly those associated with alpha5 integrins. Activation of beta1 by antibody 8A2 also induced CS-1-mediated monocyte binding. Confocal microscopy demonstrated the activated beta1 and CS-1colocalize in concentrated filamentous patches on the apical surface of HAEC. Both anti-CS-1 and an antibody to activated beta1 showed increased staining on the luminal endothelium of human coronary lesions with active monocyte entry. These results suggest the importance of these integrin ligand interactions in human atherosclerosis.
The Genetic Basis of Pheromone Evolution in Moths (2015)

Moth sexual pheromones are widely studied as a fine-tuned system of intraspecific sexual communication that reinforces interspecific reproductive isolation. However, their evolution poses a dilemma: How can the female pheromone and male preference simultaneously change to create a new pattern of species-specific attraction? Solving this puzzle requires us to identify the genes underlying intraspecific variation in signals and responses and to understand the evolutionary mechanisms responsible for their interspecific divergence. Candidate gene approaches and functional analyses have yielded insights into large families of biosynthetic enzymes and pheromone receptors, although the factors controlling their expression remain largely unexplored. Intra- and interspecific crosses have provided tantalizing evidence of regulatory genes, although, to date, mapping resolution has been insufficient to identify them. Recent advances in high-throughput genome and transcriptome sequencing, together with established techniques, have great potential to help scientists identify the specific genetic changes underlying divergence and resolve the mystery of how moth sexual communication systems evolve.
Cancer cells metabolically "fertilize" the tumor microenvironment with hydrogen peroxide, driving the Warburg effect (2011)

Previously, we proposed that cancer cells behave as metabolic parasites, as they use targeted oxidative stress as a "weapon" to extract recycled nutrients from adjacent stromal cells. Oxidative stress in cancer-associated fibroblasts triggers autophagy and mitophagy, resulting in compartmentalized cellular catabolism, loss of mitochondrial function, and the onset of aerobic glycolysis, in the tumor stroma. As such, cancer-associated fibroblasts produce high-energy nutrients (such as lactate and ketones) that fuel mitochondrial biogenesis, and oxidative metabolism in cancer cells. We have termed this new energy-transfer mechanism the "reverse Warburg effect." To further test the validity of this hypothesis, here we used an in vitro MCF7-fibroblast co-culture system, and quantitatively measured a variety of metabolic parameters by FACS analysis (analogous to laser-capture micro-dissection). Mitochondrial activity, glucose uptake, and ROS production were measured with highly-sensitive fluorescent probes (MitoTracker, NBD-2-deoxy-glucose, and DCF-DA). Interestingly, using this approach, we directly show that cancer cells initially secrete hydrogen peroxide that then triggers oxidative stress in neighboring fibroblasts. Thus, oxidative stress is contagious (spreads like a virus) and is propagated laterally and vectorially from cancer cells to adjacent fibroblasts. Experimentally, we show that oxidative stress in cancer-associated fibroblasts quantitatively reduces mitochondrial activity, and increases glucose uptake, as the fibroblasts become more dependent on aerobic glycolysis. Conversely, co-cultured cancer cells show significant increases in mitochondrial activity, and corresponding reductions in both glucose uptake and GLUT1 expression. Pre-treatment of co-cultures with extracellular catalase (an anti-oxidant enzyme that detoxifies hydrogen peroxide) blocks the onset of oxidative stress, and potently induces the death of cancer cells, likely via starvation. Given that cancer-associated fibroblasts show the largest increases in glucose uptake, we suggest that PET imaging of human tumors, with Fluoro-2-deoxy-D-glucose (F-2-DG), may be specifically detecting the tumor stroma, rather than epithelial cancer cells.
Recent Advances in Targeting the EGFR Signaling Pathway for the Treatment of Metastatic Colorectal Cancer (2017)

Outcomes for metastatic colorectal cancer (mCRC) patients have been improved by treatment with anti-epidermal growth factor receptor (anti-EGFR) antibodies, particularly when combined with predictive biomarkers to select patients lacking <i>RAS</i> mutations. New technologies such as liquid biopsy and next-generation sequencing have revealed that potential mechanisms of resistance to anti-EGFR therapies act through acquired mutations of <i>KRAS</i> and the <i>EGFR</i> ectodomain. Mutations in cross-talking molecular effectors that participate in downstream EGFR signaling are also negative predictors for anti-EGFR therapy. In the current review, we describe recent advances in anti-EGFR therapy and discuss new treatment strategies to target downstream RAS-MAPK signaling in mCRC.
Homocysteine–NMDA receptor‐mediated activation of extracellular signal‐regulated kinase leads to neuronal cell death (2009)

Hyperhomocysteinemia is an independent risk factor for stroke and neurological abnormalities. However, the underlying cellular mechanisms by which elevated homocysteine can promote neuronal death is not clear. In the present study we have examined the role of NMDA receptor-mediated activation of the extracellular signal-regulated kinase-mitogen-activated protein (ERK-MAP) kinase pathway in homocysteine-dependent neurotoxicity. The study demonstrates that in neurons l-homocysteine-induced cell death was mediated through activation of NMDA receptors. The study also shows that homocysteine-dependent NMDA receptor stimulation and resultant Ca2+ influx leads to rapid and sustained phosphorylation of ERK-MAP kinase. Inhibition of ERK phosphorylation attenuates homocysteine-mediated neuronal cell death thereby demonstrating that activation of ERK-MAP kinase signaling pathway is an intermediate step that couples homocysteine-mediated NMDA receptor stimulation to neuronal death. The findings also show that cAMP response-element binding protein (CREB), a pro-survival transcription factor and a downstream target of ERK, is only transiently activated following homocysteine exposure. The sustained activation of ERK but a transient activation of CREB together suggest that exposure to homocysteine initiates a feedback loop that shuts off CREB signaling without affecting ERK phosphorylation and thereby facilitates homocysteine-mediated neurotoxicity.