gebhart/patrepeval huggingface dataset:
METROPOLE-3D: a three-dimensional electromagnetic field simulator for EUV masks under oblique illumination (2003)

Conventional lithography techniques have been losing their ability to easily support continuous shrinking of feature sizes, especially when the pattern half-pitch is <60 nm. EUV lithography is one of the leading contenders to replace these conventional techniques. Because the EUV mask structure is many times thicker than the illumination wavelength, scalar Fraunhofer diffraction calculations cannot describe the scattering of light from the EUV masks with enough accuracy. In this paper, we present a rigorous 3-D electromagnetic field simulator for EUV masks. The simulator is based on a 3-D waveguide method developed to calculate the characteristics of the light scattered from nonplanar EUV masks. A typical EUV mask contains as many as 80 reflective layers in addition to the absorbing layers, and we have developed a fast method to calculate the scattering matrix of the reflective layers. Also, based on the existing numerical techniques, we can describe the light scattering in the absorbing layers with complex index of refraction. The simulator has been recently modified to handle oblique illumination conditions, and this is the focus of our paper. Aerial images are calculated in the image plane of a typical EUV stepper, and a threshold resist model is used to predict the printed pattern size. We will first compare our work with published results on dense and isolated lines. Then, we will describe the results of our calculations for two-dimensional patterns (e.g., contacts and islands) under oblique illumination. The typical simulation time is less than 10 hours on a desktop workstation for two-dimensional patterns.
Manganese(III) and manganese(IV) corroles: synthesis, spectroscopic, electrochemical and X-ray structural characterization (2005)

The synthesis, spectroscopic characterization and electrochemistry of four Mn(III) and Mn(IV) octaethylcorroles are reported and the potentials of the Mn(III) / Mn(IV) and Mn(IV) / Mn(III) processes examined as a function of the axial ligand. The investigated compounds are represented as ( OEC ) Mn , ( OEC ) MnCl , ( OEC ) Mn ( py ) and ( OEC ) Mn ( C 6 H 5 ) where OEC is the trianion of octaethylcorrole. The first one-electron oxidation of ( OEC ) Mn III and ( OEC ) Mn III ( py ) in PhCN or pyridine containing 0.1 M TBAP leads to the facile formation of a Mn(IV) species while the first one-electron reduction of ( OEC ) Mn IV Cl and ( OEC ) Mn IV ( C 6 H 5 ) in the same two solvents leads to the Mn(III) corrole. All other redox reactions occur at the corrole macrocycle to give π-cation radicals or π-anion radicals and there is no evidence for electrogeneration of a compound with a Mn(II) oxidation state as is the case for manganese(III) porphyrins which are all easily reduced to the Mn(II) state in nonaqueous media. The products of each Mn(III)/Mn(IV) redox reaction were characterized by UV-visible and/or ESR spectroscopy and the structures of ( OEC ) MnCl , ( OEC ) Mn ( py ) and ( OEC ) Mn ( C 6 H 5 ) were determined by single-crystal X-ray diffraction.
Power efficient router architecture for wireless Network-on-Chip (2016)

Wireless Networks-on-Chip (WNoCs) offer the most promising solution to overcome limitations of conventional Networks-on-Chip (NoCs) for long distance communications in future many-core processors. Detailed investigations of NoC with wireless interfaces (WIs) highlight their many benefits. But, static power consumption associated with WI components and routers, in general, is considerably high. By selectively turning off unused/ rarely used routers, static power consumption can be reduced. Additionally, in WNoCs with broadcast-capable antennas, only a single active wireless communication is allowed and many WIs remain inactive for longer duration and dissipate static power. To avoid this, we propose power-efficient fine-grained router architecture (FGRA) to keep power consumption to minimum. We also minimize wake-up latency by using an approach to wake-up a power-gated transceiver whenever signal is detected at its receiving antenna. We also propose non-blocking bypass channel (NBBC) to bypass power-gated routers and minimize routing latency and contention. We evaluate our proposed router design in presence of real and synthetic traffic patterns. FGRA saves up to 88.76% (per base router) and 62.50% (per WI) of static power as compared to regular architecture with 2.42% area overhead. Based on the utilization, FGRA also reduces overall network power consumption by 37.20% on average with negligible performance degradation. Design considerations for augmenting existing NoCs with these power-gated routers and corresponding overheads are also presented.
Multiple factors required for accurate initiation of transcription by purified RNA polymerase II. (1980)

A soluble extract prepared from human cells (KB S-100) has been recently shown to direct accurate transcription initiation by purified RNA polymerase II at the major late promoter of adenovirus 2. We have fractionated this extract by chromatography on phosphocellulose, DEAE-cellulose, and DNA-cellulose, and have identified four components that are required for the active and selective initiation of transcription by RNA polymerase II at this promoter. One of these components seems to act by suppressing random, but not selective, transcription by RNA polymerase II. All but one of these components have been shown to be chromatographically distinct from the factors involved in directing selective transcription by RNA polymerase III.
New Chemical Clues for Broomrape-Sunflower Host−Parasite Interactions: Synthesis of Guaianestrigolactones (2009)

A comparative structure-activity relationship (SAR) study has been conducted with several guaianolide sesquiterpene lactones (SLs) as inducers of the germination of sunflower broomrape (Orobanche cumana) seeds. Compounds were selected and synthesized to study the influence of the lactone-enol-gamma-lactone moiety on the selectivity of SLs toward the stimulation of sunflower broomrape germination. The results clearly illustrate that SLs are recognized only by O. cumana, while the introduction of a strigol-like second lactone moiety in the guaianolide backbone results in the loss of specificity and hence the germination of other broomrape species. We have named this new class of compounds guaianestrigolactones (GELs).
Expression and Functional Characterization of the Cancer-related Serine Protease, Human Tissue Kallikrein 14 (2006)

Human tissue kallikrein 14 (KLK14) is a novel extracellular serine protease. Clinical data link KLK14 expression to several diseases, primarily cancer; however, little is known of its (patho)-physiological role. To functionally characterize KLK14, we expressed and purified recombinant KLK14 in mature and proenzyme forms and determined its expression pattern, specificity, regulation, and in vitro substrates. By using our novel immunoassay, the normal and/or diseased skin, breast, prostate, and ovary contained the highest concentration of KLK14. Serum KLK14 levels were significantly elevated in prostate cancer patients compared with healthy males. KLK14 displayed trypsin-like specificity with high selectivity for P1-Arg over Lys. KLK14 activity could be regulated as follows: 1) by autolytic cleavage leading to enzymatic inactivation; 2) by the inhibitory serpins alpha1-antitrypsin, alpha2-antiplasmin, antithrombin III, and alpha1-antichymotrypsin with second order rate constants (k(+2)/Ki) of 49.8, 23.8, 1.48, and 0.224 microM(-1) min(-1), respectively, as well as plasminogen activator inhibitor-1; and 3) by citrate and zinc ions, which exerted stimulatory and inhibitory effects on KLK14 activity, respectively. We also expanded the in vitro target repertoire of KLK14 to include collagens I-IV, fibronectin, laminin, kininogen, fibrinogen, plasminogen, vitronectin, and insulin-like growth factor-binding proteins 2 and 3. Our results indicate that KLK14 may be implicated in several facets of tumor progression, including growth, invasion, and angiogenesis, as well as in arthritic disease via deterioration of cartilage. These findings may have clinical implications for the management of cancer and other disorders in which KLK14 activity is elevated.
Synergistic Transcriptional Activation of HumanAcyl-coenzyme A: Cholesterol Acyltransterase-1 Gene by Interferon-γ and All-trans-Retinoic Acid THP-1 Cells (2001)

Acyl-coenzyme A:cholesterol acyltransferase (ACAT) is an intracellular enzyme involved in cellular cholesterol homeostasis and in atherosclerotic foam cell formation. Human ACAT-1 gene contains two promoters (P1 and P7), each located in a different chromosome (1 and 7) (Li, B. L., Li, X. L., Duan, Z. J., Lee, O., Lin, S., Ma, Z. M., Chang, C. C., Yang, X. Y., Park, J. P., Mohandas, T. K., Noll, W., Chan, L., and Chang, T. Y. (1999) J. Biol Chem. 274, 11060-11071). Interferon-gamma (IFN-gamma), a cytokine that exerts many pro-atherosclerotic effects in vivo, causes up-regulation of ACAT-1 mRNA in human blood monocyte-derived macrophages and macrophage-like cells but not in other cell types. To examine the molecular nature of this observation, we identified within the ACAT-1 P1 promoter a 159-base pair core region. This region contains 4 Sp1 elements and an IFN-gamma activated sequence (GAS) that overlaps with the second Sp1 element. In the monocytic cell line THP-1 cell, the combination of IFN-gamma and all-trans-retinoic acid (a known differentiation agent) enhances the ACAT-1 P1 promoter but not the P7 promoter. Additional experiments showed that all-trans-retinoic acid causes large induction of the transcription factor STAT1, while IFN-gamma causes activation of STAT1 such that it binds to the GAS/Sp1 site in the ACAT-1 P1 promoter. Our work provides a molecular mechanism to account for the effect of IFN-gamma in causing transcriptional activation of ACAT-1 in macrophage-like cells.
Attomolar Detection of a Cancer Biomarker Protein in Serum by Surface Plasmon Resonance Using Superparamagnetic Particle Labels (2010)

Signal amplifiers: Superparamagnetic particle–antibody conjugates were used to detect a cancer biomarker in serum by surface plasmon resonance (SPR) at an unprecedented low level of 10 fg mL−1 (ca. 300 aM). Ultrahigh sensitivity is facilitated by enhanced mass and refractive index from aggregates of 1 μm magnetic particles on the SPR chip. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Reactive oxygen species, but not Ca2+overloading, trigger pH- and mitochondrial permeability transition-dependent death of adult rat myocytes after ischemia-reperfusion (2006)

We investigated the role of pH, reactive oxygen species (ROS), Ca2+, and the mitochondrial permeability transition (MPT) in pH-dependent ischemia-reperfusion injury to adult rat myocytes. Myocytes were incubated in anoxic Krebs-Ringer-HEPES buffer at pH 6.2 for 3 h to simulate ischemia. To simulate reperfusion, myocytes were reoxygenated at pH 6.2 or 7.4 for 2 h. Some myocytes were treated with MPT blockers (cyclosporin A and N-methyl-4-isoleucine cyclosporin) and antioxidants (desferal, diphenylphenylene diamine, and 2-mercaptopropionyl glycine). Mitochondrial membrane potential, inner membrane permeabilization, and ROS formation were imaged with tetramethylrhodamine methyl ester, calcein, and chloromethyldichlorofluorescein diacetate, respectively. For Ca2+ imaging, myocytes were coloaded with rhod-2 and fluo-4 to evaluate mitochondrial and cytosolic Ca2+, respectively. After 10 min of reperfusion at pH 7.4, calcein redistributed across the mitochondrial inner membrane, an event preceded by mitochondrial ROS formation and accompanied by hypercontracture, mitochondrial depolarization, and then cell death. Acidotic reperfusion, antioxidants, and MPT blockers each prevented the MPT, depolarization, hypercontraction, and cell killing. Antioxidants, but neither MPT blockers nor acidotic reperfusion, inhibited ROS formation after reperfusion. Furthermore, anoxic reperfusion at pH 7.4 prevented cell death. Both mitochondrial and cytosolic Ca2+ increased during ischemia but recovered in the first minutes of reperfusion. Mitochondrial and cytosolic Ca2+ overloading again occurred late after reperfusion. This late Ca2+ overloading was blocked by MPT inhibition. Intramitochondrial Ca2+ chelation by cold loading/warm incubation of BAPTA did not prevent cell death after reperfusion. In conclusion, mitochondrial ROS, together with normalization of pH, promote MPT onset and subsequent myocyte death after reperfusion. In contrast, Ca2+ overloading appears to be the consequence of bioenergetic failure after the MPT and is not a factor promoting MPT onset.
Genetically Encoded FRET Probe for PKC Activity Based on Pleckstrin (2004)

We developed a probe for investigating protein kinase C (PKC) activity in living cells. The probe is based on a fragment of pleckstrin enclosed by two FRET-capable fluorophores. PKC activity modulation was reliably followed by FRET change in vitro and in vivo. The probe responds quickly to PKC activation by phorbol ester. FRET changes were reversible when PKC inhibitors were administered. Stimulation of cellular signaling pathways using histamine or bradykinin triggered PKC in a physiologically relevant way.
Effect of immunization with pneumolysin on survival time of mice challenged with Streptococcus pneumoniae (1983)

The role of the cytolytic toxin pneumolysin in the pathogenicity of Streptococcus pneumoniae was investigated. Pneumolysin was purified to homogeneity and used to immunize mice. When these mice were subsequently challenged via the nasal route with virulent S. pneumoniae, they survived significantly longer than control mice. The mean survival times were 5.52 and 2.48 days for immunized and control mice, respectively. This work provides direct evidence for the involvement of pneumolysin in pneumococcal pathogenicity.
MOVING BLOCK SYSTEM WTIH CONTINUOUS TRAIN DETECTION UTILIZING TRAIN SHUNTING IMPEDANCE OF TRACK CIRCUIT (1989)

Moving block system, which is able to shorten train interval, gives a large merit of reducing the train headway. To shorten train interval, it is necessary to detect train positions continuously. We describe a method of continuous train detection utilizing the train shunting impedance of track circuit, and the error in train detection which is likely to happen when using this method. We also describe the moving block system utilizing this method.
Is the Amyloid Hypothesis of Alzheimer's disease therapeutically relevant? (2012)

The conventional view of AD (Alzheimer's disease) is that much of the pathology is driven by an increased load of β-amyloid in the brain of AD patients (the 'Amyloid Hypothesis'). Yet, many therapeutic strategies based on lowering β-amyloid have so far failed in clinical trials. This failure of β-amyloid-lowering agents has caused many to question the Amyloid Hypothesis itself. However, AD is likely to be a complex disease driven by multiple factors. In addition, it is increasingly clear that β-amyloid processing involves many enzymes and signalling pathways that play a role in a diverse array of cellular processes. Thus the clinical failure of β-amyloid-lowering agents does not mean that the hypothesis itself is incorrect; it may simply mean that manipulating β-amyloid directly is an unrealistic strategy for therapeutic intervention, given the complex role of β-amyloid in neuronal physiology. Another possible problem may be that toxic β-amyloid levels have already caused irreversible damage to downstream cellular pathways by the time dementia sets in. We argue in the present review that a more direct (and possibly simpler) approach to AD therapeutics is to rescue synaptic dysfunction directly, by focusing on the mechanisms by which elevated levels of β-amyloid disrupt synaptic physiology.
Bloqueio Atrioventricular Paroxístico como Causa de Síncope em Crianças sem Cardiopatia Congênita (2008)

Histórico: A síncope causada por bloqueio atrioventricular (AV) paroxístico, definido como bloqueio de segundo ou terceiro grau transitório, raramente é relatada em pacientes pediátricos sem cardiopatias congênitas. Métodos: Realizou-se uma revisao do banco de dados de arritmias da nossa instituiçao, de janeiro de 1988 a janeiro de 2007, para identificar todos os pacientes com menos de 18 anos de idade com anatomia cardíaca normal e episódios de síncope associados a bloqueio AV paroxístico. Informaçoes demográficas e clínicas foram coletadas. Resultados: Foram identificados seis pacientes, cinco do sexo feminino, com idade média de 9,3 ± 4,4 anos, que haviam sofrido episódios de síncope durante 5,6 ± 3,3 anos, em média, antes do diagnóstico (Tabela 1). Todos foram submetidos a exame físico, eletrocardiograma e ecocardiograma. Os resultados dos exames laboratoriais, inclusive para doença de Lyme, foram negativos. Nenhum deles recebia medicaçao capaz de interferir na conduçao AV nodal. Cinco dos seis episódios relatados foram atípicos para síncope vasovagal (com exceçao do paciente 6). Todos os pacientes tiveram bloqueio AV paroxístico documentado em monitor cardíaco ou gravador de Holter de 24 horas, registrado durante a síncope em pacientes internados. Houve manutençao ou aceleraçao do ritmo sinusal durante os episódios de síncope em todos os pacientes (ritmo atrial médio de 107 ± 37 bpm). Os seis pacientes receberam o implante de marcapasso transvenoso permanente, com a resoluçao dos sintomas durante um acompanhamento médio de 5,2 ± 6,3 anos. Conclusao: O bloqueio AV paroxístico é um achado raro em pacientes pediátricos, mas deve ser considerado uma etiologia possível naqueles que apresentam episódios atípicos de síncope vasovagal. A terapia utilizando marcapassos preveniu novas ocorrências em todos os seis pacientes.
The role of infectious agents in urogenital cancers (2012)

Since the late 1990s, infectious agents have been thought to play a role in the pathogenesis of approximately 15% of cancers. It is now widely accepted that infection of stomach tissue with the bacteria Helicobacter pylori is an important cause of stomach adenocarcinoma. In addition, oncogenic viruses, such as papilloma viruses, herpes viruses, and hepadnaviruses are strongly associated with increased risk of cervical cancer, lymphomas, liver cancer, amongst others. However, in the scientific community the percentage of cancers caused by pathogens is believed to be far higher than 15%. A significant volume of data collected to date show an association between infectious agents and urogenital cancers. These agents include Chlamydia trachomatis, Neisseria gonorrhoea, Mycoplasma genitalium and certain viruses that have been implicated in ovarian cancer. Other pathogens include the hepatitis C and Epstein-Barr viruses, which are potentially involved in kidney cancer. In addition, infections with Schistosoma haematobium, the human papillomavirus, and human polyomaviruses are strongly associated with an increased risk of urinary bladder cancer. This article reviews publications available to date on the role of infectious agents in urogenital cancers. A greater understanding of the role of such agents could aid the identification of novel methods of urogenital cancer treatment.
Developmental and morphological regulation of clathrin-mediated endocytosis inTrypanosoma brucei (2001)

Essentially all macromolecular communication between Trypanosoma brucei and its host is confined to vesicular trafficking events occurring at or around the flagellar pocket. The vertebrate stage bloodstream form trypomastigote exhibits an extremely high rate of endocytosis required for nutrient uptake and probably also evasion of the host immune system. However, the rate of endocytosis is very low in the procyclic vector parasite, indicating that endocytosis is subject to a marked level of developmental regulation. Previous ultrastructural studies and crude biochemical fractionations have indicated the presence of coated pits and vesicles that are analogous to clathrin coats in the bloodstream form, but not in the procyclic. However, a definitive description of the components of this coat and its molecular function in T. brucei has remained elusive. We describe the molecular cloning and initial characterisation of components of the T. brucei endocytic coats: clathrin heavy chain (TbCLH) and a beta-adaptin (TbAPbeta1). TbCLH is markedly upregulated in the bloodstream form compared with the procyclic, whereas TbAPbeta1 is subject to more limited developmental regulation. We generated antisera against both proteins and show that the clathrin coat is tightly associated with the flagellar pocket in both major life stages. However, in bloodstream parasites TbCLH is also extensively distributed throughout the posterior end of the cell on numerous large vesicular and tubular structures. By cryo-immuno EM, clathrin is localised to collecting tubules at the flagellar pocket and is also associated with the trans-Golgi network. These EM data confirm that the electron dense coats reported on trypanosome vesicles and tubules contain clathrin. The TbAPbeta1 exhibits an atypical distribution relative to previously characterised adaptins, associating not only with the trans-Golgi but also with other tubular-vesicular elements. Localisation of TbAPbeta1 is also subject to developmental regulation. These data describe major endocytic coat proteins in T. brucei for the first time, and indicate stage-specific expression of the clathrin heavy chain. Modulation of clathrin expression is likely to be an important factor in the developmental regulation of endocytosis and recycling in the African trypanosome.
The Virtual Brain: a simulator of primate brain network dynamics (2013)

We present The Virtual Brain (TVB), a neuroinformatics platform for full brain network simulations using biologically realistic connectivity. This simulation environment enables the model-based inference of neurophysiological mechanisms across different brain scales that underlie the generation of macroscopic neuroimaging signals including functional MRI (fMRI), EEG and MEG. Researchers from different backgrounds can benefit from an integrative software platform including a supporting framework for data management (generation, organization, storage, integration and sharing) and a simulation core written in Python. TVB allows the reproduction and evaluation of personalized configurations of the brain by using individual subject data. This personalization facilitates an exploration of the consequences of pathological changes in the system, permitting to investigate potential ways to counteract such unfavorable processes. The architecture of TVB supports interaction with MATLAB packages, for example, the well known Brain Connectivity Toolbox. TVB can be used in a client-server configuration, such that it can be remotely accessed through the Internet thanks to its web-based HTML5, JS, and WebGL graphical user interface. TVB is also accessible as a standalone cross-platform Python library and application, and users can interact with the scientific core through the scripting interface IDLE, enabling easy modeling, development and debugging of the scientific kernel. This second interface makes TVB extensible by combining it with other libraries and modules developed by the Python scientific community. In this article, we describe the theoretical background and foundations that led to the development of TVB, the architecture and features of its major software components as well as potential neuroscience applications.