gebhart/patrepeval huggingface dataset:
[Recent Advances in α-dystroglycanopathy]. (2011)

Fukuyama-type congenital muscular dystrophy (FCMD), muscle-eye-brain disease (MEB), and Walker-Warburg syndrome (WWS) are autosomal recessive disorders characterized by congenital muscular dystrophy with structural brain and eye abnormalities. Aberrant glycosylation of α-dystroglycan (α-DG) is a common pathomechanism of these disorders. In addition, genetic and glycobiological evidence has shown that abnormal glycosylation of α-DG is also seen in several forms of congenital and limb-girdle-type muscular dystrophies. These disorders are collectively called "α-dystroglycanopathy" and nowadays, this term is widely accepted because it is useful for illustrating a complicated genotype-phenotype correlation of these disorders. α-DG is a membrane-associated protein that interacts with extracellular matrix proteins such as laminin, and abnormal glycosylation of α-DG results in loss of its laminin-binding activity. A number of serine/threonine residues are present in the mucin-like domain of α-DG and are majorly composed of sugar chains. Among these glycans, an O-mannosyl tetrasaccharide (Neu5Ac-α2,3-Gal-β1,4-GlcNAc-β1,2-Man) is important for laminin-binding activity of α-DG. POMT1/2 and POMGnT1, protein products of causative genes of WWS and MEB, respectively, are enzymes that directly catalyze the biosynthesis of this glycan. Recent studies have suggested that a phosphodiester-linked structure on O-mannose is also important for the laminin-binding activity and that mutations in other causative genes of α-dystroglycanopathy, such as fukutin (originally identified as the gene responsible for FCMD) and LARGE, disrupt the post-phosphoryl structure. Here, we review the history of basic and clinical research on α-dystroglycanopathy and refine its clinical spectrum, which should be broadly extended. In addition, we reveal some progress in research on α-dystroglycanopathy including a novel disease mechanism and anti-sense oligonucleotide therapy for FCMD.
SCARF: a segmental conditional random field toolkit for speech recognition (2010)

This paper describes a new toolkit SCARF for doing speech recognition with segmental conditional random fields. It is designed to allow for the integration of numerous, possibly redundant segment level acoustic features, along with a complete language model, in a coherent speech recognition framework. SCARF performs a segmental analysis, where each segment corresponds to a word, thus allowing for the incorporation of acoustic features defined at the phoneme, multi-phone, syllable and word level. SCARF is designed to make it especially convenient to use acoustic detection events as input, such as the detection of energy bursts, phonemes, or other events. Language modeling is done by associating each state in the SCRF with a state in an underlying n-gram language model, and SCARF supports the joint and discriminative training of language model and acoustic model parameters. SCARF is available for download from http://research.microsoft.com/en-us/projects/scarf/
Conformational changes of phospholipid headgroups induced by a cationic integral membrane peptide as seen by deuterium magnetic resonance (1989)

Deuterium nuclear magnetic resonance (2H NMR) was used to study the interaction of a cationic amphiphilic peptide with pure DMPC membranes and with mixed bilayers of dimyristoylphosphatidylcholine (DMPC) and dimyristoylphosphatidylserine (DMPS). The choline and serine headgroups were selectively deuteriated at the alpha and beta positions. The amphiphilic peptide, with 20 leucine residues in the hydrophobic core and two cationic hydrophilic lysine residues at each end, spanned the lipid bilayer. Although 2H NMR experiments using DMPC with perdeuteriated fatty acyl chains showed that the average order parameter of the hydrophobic region was not significantly modified by the incorporation of the amphiphilic peptide, for either DMPC or DMPC/DMPS (5:1) bilayers, large perturbations of the quadrupolar splittings of the choline and serine headgroups were observed. The results obtained with the DMPC headgroup suggest that the incorporation of the cationic peptide in both DMPC and DMPC/DMPS (5:1) bilayers leads to a structural perturbation directly related to the net charge on the membrane surface. The magnitude of the observed effect seems to be similar to those observed previously with other cationic molecules [Seelig, J., MacDonald, P.M., & Scherer, P.G. (1987) Biochemistry 26, 7535-7541]. Two of the three quadrupolar splittings of the PS headgroup exhibited large variations in the presence of the amphiphilic peptide, while the third one remained unchanged. Our data have led us to propose a model describing the influence of membrane surface charges on headgroup conformation. In this model, the surface charge is represented as a uniform charge distribution. The electric field due to the charges produces a torque which rotates the polar headgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
Prefrontal cortex and executive function in young children: a review of NIRS studies (2013)

Executive function (EF) refers to the higher-order cognitive control process for the attainment of a specific goal. There are several subcomponents of EF, such as inhibition, cognitive shifting, and working memory. Extensive neuroimaging research in adults has revealed that the lateral prefrontal cortex plays an important role in EF. Developmental studies have reported behavioral evidence showing that EF changes significantly during preschool years. However, the neural mechanism of EF in young children is still unclear. This article reviews recent near-infrared spectroscopy (NIRS) research that examined the relationship between the development of EF and the lateral prefrontal cortex. Specifically, this review focuses on inhibitory control, cognitive shifting, and working memory in young children. Research has consistently shown significant prefrontal activation during tasks in typically developed children, but this activation may be abnormal in children with developmental disorders. Finally, methodological issues and future directions are discussed.
Synthetic Resins and Synthetic Rubbers (1942)

RETURN TO ISSUEPREVNewsNEXTSynthetic Resins and Synthetic RubbersP. O. POWERSView Author Information Armstrong Cork Co., Lancaster, Penna.Cite this: Chem. Eng. News 1942, 20, 8, 536–538Publication Date (Print):April 25, 1942Publication History Published online4 November 2010Published inissue 25 April 1942https://pubs.acs.org/doi/10.1021/cen-v020n008.p536https://doi.org/10.1021/cen-v020n008.p536newsACS PublicationsCopyright © 1942 AMERICAN CHEMICAL SOCIETYArticle Views3Altmetric-Citations3LEARN 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 options SUBJECTS:Organic polymers Get e-Alerts
Atorvastatin Inhibits Renal Crystal Retention in a Rat Stone Forming Model (2008)

The interactions between crystals and renal tubular cells are important factors in urolithiasis formation. Moreover, some reports have suggested the involvement of renal tubular cell injury in crystal-cell interaction processes. Atorvastatin, which is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, is prescribed to decrease high cholesterol levels, and it has anti-inflammation and anti-oxidization activities. Atorvastatin is also reported to control transforming growth factor-beta1 expression. We investigated whether atorvastatin can prevent renal tubular cell injury by oxalate and inhibit renal crystal retention.Ten-week-old specific pathogen-free male Sprague-Dawley rats were used. Atorvastatin (2 mg/kg) in 0.5% carboxymethyl cellulose was administered orally daily for 2 weeks. The rats were separated into 4 experimental groups, including group 1--water and 0.5% carboxymethyl cellulose daily, group 2--water and atorvastatin in 0.5% carboxymethyl cellulose daily, group 3--1% ethylene glycol dissolved in water, 0.5 mug vitamin D3 dissolved in 1 ml salad oil and 0.5% carboxymethyl cellulose daily, and group 4--1% ethylene glycol dissolved in water, 0.5 microg vitamin D3 dissolved in 1 ml salad oil and atorvastatin in 0.5% carboxymethyl cellulose daily. The ethylene glycol model of hyperoxaluria and the effect of atorvastatin treatment were analyzed in groups 1 to 4. Urine samples were collected every 24 hours in metabolic cages and analyzed immediately or stored at -70C until analysis. The rats were sacrificed after 2 weeks and the kidneys were removed for further examination. We measured urinary N-acetyl glucosaminidase levels as a biomarker of renal tubular cell injury and urinary 8-OHdG as a biomarker of oxidative stress in 24-hour urine samples. Removed kidneys were used for quantitative analysis of the superoxide dismutase level and the detection of apoptosis. Finally, we measured the amount of crystal deposits in renal tubular cells.Urinary N-acetyl glucosaminidase and 8-OHdG levels were decreased significantly by atorvastatin treatment in this stone forming rat model. Atorvastatin treatment increased the superoxide dismutase level and inhibited the degree of renal tubular cell N-acetyl glucosaminidase compared with stone forming control group 3. A decrease in renal crystal retention was noted when excised kidneys were evaluated following atorvastatin treatment.Atorvastatin was found to have inhibitory effects on the renal tubular cell injury and oxidative stress caused by oxalate and crystals. Atorvastatin inhibited renal crystal retention. We believe that atorvastatin could help prevent and treat renal crystal formation.
A Genetic Interaction between the Core and NS3 Proteins of Hepatitis C Virus Is Essential for Production of Infectious Virus (2011)

By analogy to other members of the Flaviviridae family, the hepatitis C virus (HCV) core protein is presumed to oligomerize to form the viral nucleocapsid, which encloses the single-stranded RNA genome. Core protein is directed to lipid droplets (LDs) by domain 2 (D2) of the protein, and this process is critical for virus production. Domain 1 (D1) of core is also important for infectious particle morphogenesis, although its precise contribution to this process is poorly understood. In this study, we mutated amino acids 64 to 75 within D1 of core and examined the ability of these mutants to produce infectious virus. We found that residues 64 to 66 are critical for generation of infectious progeny, whereas 67 to 75 were dispensable for this process. Further investigation of the defective 64 to 66 mutant (termed JFH1(T)-64-66) revealed it to be incapable of producing infectious intracellular virions, suggesting a fault during HCV assembly. Furthermore, isopycnic gradient analyses revealed that JFH1(T)-64-66 assembled dense intracellular species of core, presumably representing nucleocapsids. Thus, amino acids 64 to 66 are seemingly not involved in core oligomerization/nucleocapsid assembly. Passaging of JFH1(T)-64-66 led to the emergence of a single compensatory mutation (K1302R) within the helicase domain of NS3 that completely rescued its ability to produce infectious virus. Importantly, the same NS3 mutation abrogated virus production in the context of wild-type core protein. Together, our results suggest that residues 64 to 66 of core D1 form a highly specific interaction with the NS3 helicase that is essential for the generation of infectious HCV particles at a stage downstream of nucleocapsid assembly.
Hypoxia-Inducible Factor 1 Protects Hypoxic Astrocytes against Glutamate Toxicity (2012)

Stroke is a major neurological disorder characterized by an increase in the Glu (glutamate) concentration resulting in excitotoxicity and eventually cellular damage and death in the brain. HIF-1 (hypoxia-inducible factor-1), a transcription factor, plays an important protective role in promoting cellular adaptation to hypoxic conditions. It is known that HIF-1α, the regulatable subunit of HIF-1, is expressed by astrocytes under severe ischaemia. However, the effect of HIF-1 on astrocytes following Glu toxicity during ischaemia has not been well studied. We investigated the role of HIF-1 in protecting ischaemic astrocytes against Glu toxicity. Immunostaining with GFAP (glial fibrillary acidic protein) confirmed the morphological modification of astrocytes in the presence of 1 mM Glu under normoxia. Interestingly, when the astrocytes were exposed to severe hypoxia (0.1% O2), the altered cell morphology was ameliorated with up-regulation of HIF-1α. To ascertain HIF-1's protective role, effects of two HIF-1α inhibitors, YC-1 [3-(50-hydroxymethyl-20-furyl)-1-benzylindazole] and 2Me2 (2-methoxyoestradiol), were tested. Both the inhibitors decreased the recovery in astrocyte morphology and increased cell death. Given that ischaemia increases ROS (reactive oxygen species), we examined the role of GSH (reduced glutathione) in the mechanism for this protection. GSH was increased under hypoxia, and this correlated with an increase in HIF-1α stabilization in the astrocytes. Furthermore, inhibition of GSH with BSO (l-butathione sulfoximine) decreased HIF-1α expression, suggesting its role in the stabilization of HIF-1α. Overall, our results indicate that the expression of HIF-1α under hypoxia has a protective effect on astrocytes in maintaining cell morphology and viability in response to Glu toxicity.
Data acquisition and event filtering by using transputers (2002)

An experimental study of backward Lambda hyperon production is being carried out at the National Laboratory for High Energy Physics in Japan (KEK-PS). In the experiment, high-speed data acquisition associated with a sophisticated online event trigger is required. For the data acquisition, a CAMAC data acquisition system using a transputer and a transputer link has been developed. The data transfer speed achieved in this system is 220 Kbyte/s, which is a performance almost equal to that of the conventional system. For the event trigger, a detection of the Lambda hyperon's decay vertex is very important for selecting a Lambda event out of vast background events. An event selection algorithm has been developed by using a modified tree method. It has been confirmed that, under parallel processing using eight transputers, one can achieve the required performance of the event trigger, i.e., a processing speed of 100 events/s. It was concluded that data can be taken fairly well by the developed data acquisition system and that only interested data can be selected and stored efficiently by the developed algorithm.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
Syk Is Required for Monocyte/Macrophage Chemotaxis to CX3CL1 (Fractalkine) (2005)

CX3CL1 (fractalkine), the only member of the delta subclass of chemokines, is a known chemotactic factor for monocytes/macrophages as well as NK cells and T lymphocytes. In several pathologies, excessive production of CX3CL1 at specific sites leads primarily to monocyte/macrophage recruitment, which causes tissue and vascular damage. Despite their clinical relevance, the mechanisms underlying monocyte/macrophage chemotaxis to CX3CL1 remain poorly documented. The present report addresses this issue and identifies cell signaling crucial for this process. Using the murine monocyte/macrophage RAW cell line, we show that CX3CL1 treatment elicits a rapid and transient increase in F-actin and the formation of F-actin-enriched cell protrusions. CX3CL1 also triggers tyrosine phosphorylation of proteins localized in those protrusions. The protein tyrosine kinase Syk is activated upon CX3CL1 treatment, and reduction of Syk expression using RNA-mediated interference results in a specific and massive impairment of RAW cell migration to CX3CL1. Similar results are obtained using the Syk inhibitor, piceatannol. Cells with reduced Syk expression also exhibit a major defect in CX3CL1-induced cytoskeletal remodeling. These data suggest that in monocytes/macrophages, Syk is essential for proper reorganization of the actin cytoskeleton in response to CX3CL1 and is therefore required for cell chemotaxis to CX3CL1.
Structural study of monosubstituted β-cyclodextrins. Crystal structures of phenylthio-β-cyclodextrin and phenylsulphinyl-β-cyclodextrin and spectroscopic study of related compounds in aqueous solution (1987)

The crystal structures of two monosubstituted β-cyclodextrins which have bulky hydrophobic groups instead of primary hydroxy groups were determined by X-ray diffraction. These compounds consist of the host (cyclodextrin moieties) and guest parts (hydrophobic groups), and have the ability to act as both host and guest at the same time. The crystal structures were solved by using Patterson maps, rotation functions, and trial-and-error methods combined with a rigid-body least-squares technique. The structures were refined by using a block-diagonal least-squares method to R values of 0.14 and 0.13. Hydrophobic groups are intermolecularly included in the cyclodextrin cavity of another molecule, and novel helical polymers are formed by repetition of this intermolecular inclusion. A spectroscopic study confirmed that this intermolecular inclusion occurs in aqueous solution.
Genomic Strategies for Personalized Cancer Therapy (2007)

PL04-03 The ability to tailor cancer therapy to characteristics of the individual patient is key in achieving a successful outcome. We have made use of genomic data to develop a capacity to predict risk for individual patients and then combine this with a capacity to identify potential therapeutic options. An example can be seen in early stage lung cancer where the current standard of care for Stage 1A patients is surgery and observation with no indication of benefit from chemotherapy. Nevertheless, 25% of Stage IA patients will have a disease recurrence suggesting the need to identify individuals in this subgroup for more effective therapy. We developed gene expression profiles that could predict risk of recurrence, performing significantly better than previously described clinical prognostic factors. This predictive model was validated in two independent patient cohorts. Importantly, we show that this provides an opportunity to re-classify Stage IA patients to identify a subset of higher risk patients that might be appropriate for adjuvant chemotherapy. We have also developed a series of gene expression signatures that have the capacity to predict sensitivity to cytotoxic chemotherapeutics, including those used in the treatment of lung cancer. Making use of in vitro drug response data generated with the NCI-60 panel of cancer cell lines as well as other sources, coupled with baseline Affymetrix gene expression data, we developed genomic predictors of response and resistance. Many of these predictors have been validated with chemotherapeutic response data from patient samples, including a prospective breast neoadjuvant study, demonstrating a capacity to identify those patients most likely to respond to a given drug. Importantly, these predictions also accurately identify those patients likely to be resistant to current standard of care regimens emphasizing the importance of developing strategies for effective therapy of these individuals. One approach has made use of predictions of pathway deregulation in cancer cell lines that are shown to coincide with sensitivity to therapeutic agents that target components of the pathway, underscoring the potential for such pathway prediction to guide the use of targeted therapeutics. Finally, we have combined the chemotherapy predictive signatures with the signatures of oncogenic pathway deregulation to identify therapeutic strategies that make use of all available drugs, matched to the characteristics of the individual patient. We suggest that this approach provides a strategy towards the development of personalized treatment options for the individual patient.
Biochemical Oscillations and Cellular Rhythms (1996)

This book addresses the molecular bases of some of the most important biochemical rhythms known at the cellular level. Clarifying the mechanism of these oscillatory phenomena is of key importance for understanding the origin as well as the physiological function of these rhythms, and the conditions in which simple periodic behaviour transforms into complex oscillations including bursting and chaos. It will appeal to graduate students and researchers in a wide variety of fields. On the one hand, it will be of interest to life scientists such as biochemists, cell biologists, medical scientists, pharmacologists and chronobiologists. On the other hand, scientists studying nonlinear phenomena, including oscillations and chaos, in chemistry, physics, mathematics and mathematical biology will also find these ideas of value.
Low sulfur products from high sulfur crude oil (1981)

Four refining process schemes compared are similar except for the handling of the atmospheric resid. In this aspect, the following variations are used: (1) atmospheric resid hydrodesulfurization (HDS), vacuum distillation, delayed coking, and gas oil fluid catalytic cracking (FCC); (2) vacuum distillation, fluxcoking, FCC feed HDS, and gas oil FCC; (3) atmospheric resid HDS, and heavy oil catalytic cracking; and (4) atmospheric resid HDS, vacuum distillation, solvent deasphalting, and gas oil FCC. Comparison of product yields, product characteristics, and investment costs for the 4 refinery schemes are tabulated as are advantages and disadvantages of the scheme. No choice of schemes can be made from the data presented even though one had somewhat lower operating costs, because the products desired and the relative value placed on these products dictate the final choice of scheme. (BLM)
User behavior augmented software testing for user-centered GUI (2011)

User interface design plays an important role in software usability. In particular, the user human interaction in embedded systems and cyber-physical systems is a critical design challenge. GUI improves user experience for untrained users but, at the same time, brings great challenges to software testing. In 2002, Memon reported that up to 60% of the software testing are conducted against user interface. In the last decade, many automatic GUI testing approaches are proposed to address this challenge. In particular, model-based GUI testing mechanisms generate testing cases according to state transition diagram and software model. In this paper, we present the design and implementation for a user behavior augmented GUI test case generation mechanism. We define User Computer Interaction Hidden Markov Model (UCIHMM) to model user behaviors. With trained UCIHMMs, the developed algorithm generates test cases to emulate user computer interactions for various types of users. To evaluate the effectiveness and completeness of the developed mechanism, we conduct the experiments against an open source embedded software for hospital staffs. The results show that the developed mechanism allows the developers to discover the software flaws that model-based testing approaches fail to.
Determination of RhD Zygosity: Comparison of a Double Amplification Refractory Mutation System Approach and a Multiplex Real-Time Quantitative PCR Approach (2001)

Double ARMS and real-time quantitative PCR are alternative robust assays for the determination of RhD zygosity.