gebhart/patrepeval huggingface dataset:
The Impact of Psoriasis on Psychosocial Life Domains (1997)

Living with a chronic disease, such as psoriasis, is likely to have psychological as well as social implications. Hence, knowledge about the impact of psoriasis on patients' life situation is important for designing and selecting suitable health care programmes for this group of patients. A review of studies published between 1983 and 1995 shows that there are some common factors as regards the psychological distress and social and functional limitations this group of patients has to deal with. However, it is difficult to compare the findings on the psychosocial impact of psoriasis owing to the differences in methods, study design and patient samples. This suggests that further research is needed. A holistic perspective that includes patients' quality of life may represent a fruitful approach.
Chondroitin sulfate proteoglycan with neurite-inhibiting activity is up-regulated following peripheral nerve injury (1998)

Numerous findings support the possibility that highly sulfated proteoglycans are inhibitory molecules which, at high concentration relative to growth-promoting signals, may regulate or guide axonal growth. Although most studies implicate sulfated proteoglycans in the poor regenerative capacity of the central nervous system, inhibitory proteoglycans also may play an important role in the successful regeneration of axons within peripheral nerve. Cultured rat schwannoma and Schwann cells produce chondroitin sulfate proteoglycan (CSPG) which binds to and inhibits the neurite-promoting activity of laminin [Muir et al. (1989) J. Cell Biol. 109:2353]. In the present study, we found a similar neurite-inhibiting activity associated with CSPG isolated from normal adult rat sciatic nerve. Following nerve crush injury, this inhibitory activity was increased sevenfold in regenerating nerve distal to the injury. This increase was largely attenuated by in vivo administration of the proteoglycan synthesis inhibitor beta-D-xyloside. In normal adult nerve, immunolabeling for CSPG core protein was concentrated in slender bands surrounding axon-Schwann cell units and within nodes of Ranvier. Following nerve crush injury, immunolabeling of CSPG and laminin became more intense in distal nerve and CSPG increased within endoneurium and surrounding nerve sheaths. Embryonic dorsal root ganglionic neurons cultured on longitudinal nerve sections extended neurites along the exposed surfaces of Schwann cell basal lamina. The length of neurites was increased 58% on normal nerve sections pretreated with chondroitinase. Even though laminin levels were elevated in basal lamina of injured nerve, neuritic growth on sections of injured nerve was not significant increased unless sections were pretreated with chondroitinase. These results indicate that inhibitory CSPG is up-regulated in injured nerve and plays a role in regulating axonal regeneration.
Role of a disintegrin and metalloprotease 10 in Staphylococcus aureus α-hemolysin–mediated cellular injury (2010)

Staphylococcus aureus alpha-hemolysin (Hla), a potent cytotoxin, plays an important role in the pathogenesis of staphylococcal diseases, including those caused by methicillin-resistant epidemic strains. Hla is secreted as a water-soluble monomer that undergoes a series of conformational changes to generate a heptameric, beta-barrel structure in host membranes. Structural maturation of Hla depends on its interaction with a previously unknown proteinaceous receptor in the context of the cell membrane. It is reported here that a disintegrin and metalloprotease 10 (ADAM10) interacts with Hla and is required to initiate the sequence of events whereby the toxin is transformed into a cytolytic pore. Hla binding to the eukaryotic cell requires ADAM10 expression. Further, ADAM10 is required for Hla-mediated cytotoxicity, most notably when the toxin is present at low concentrations. These data thus implicate ADAM10 as the probable high-affinity toxin receptor. Upon Hla binding, ADAM10 relocalizes to caveolin 1-enriched lipid rafts that serve as a platform for the clustering of signaling molecules. It is demonstrated that the Hla-ADAM10 complex initiates intracellular signaling events that culminate in the disruption of focal adhesions.
Effect of Cardioactive Drugs on Action Potential Generation and Propagation in Embryonic Stem Cell-Derived Cardiomyocytes (2007)

Extracellular recordings of spontaneous electrical activity in contracting cardiac clusters differentiated from murine embryonic stem cells enable to study electrophysiological features of this in-vitro cardiac-like tissue as well as effects of pharmacological compounds on its chronotropy and electrical conduction. To test if the microelectrode array (MEA) system could serve as a basis for development of a pharmacological screening tool for cardioactive drugs, we used spontaneously beating outgrowths of three-dimensional ES cell aggregates ("embryoid bodies", EBs) plated onto substrate-integrated MEAs. The effects of the L-type Ca(2+) channel antagonist verapamil and Na(+) and K(+) channel blockers (tetrodotoxin, 4-aminopyridine, and sparfloxacin) on the deduced interrelated cardiac network function were investigated. Application of 10(-6) M verapamil led to arrhythmic spiking with a burst-like pattern; at a higher concentration (10(-5) M) the drug caused a sustained negative chronotropy up to complete stop of beating. In the presence of tetrodotoxin a conduction block was observed. Since modulation of K(+) channel activity can cause anti- or proarrhythmic effects, the influence of K(+) channel blockers, namely 4-aminopyridine and sparfloxacin, was investigated. 4-aminopyridine (2x10(-3) M) significantly stabilized beating frequency, while the field potential duration (FPD) was concentration-dependently prolonged up to 2.7-fold. Sparfloxacin (3x10(-6) M) stabilized the beating frequency as well. At a higher concentration of sparfloxacin (3x10(-5) M), a significant prolongation of the spike duration was registered; application of the drug caused also early afterdepolarizations. The results demonstrate a suitability of the studied in-vitro cardiac cell model for pharmacological drug testing in cardiovascular research.
Parametric Trojans for Fault-Injection Attacks on Cryptographic Hardware. (2014)

We propose two extremely stealthy hardware Trojans that facilitate fault-injection attacks in cryptographic blocks. The Trojans are carefully inserted to modify the electrical characteristics of predetermined transistors in a circuit by altering parameters such as doping concentration and dopant area. These Trojans are activated with very low probability under the presence of a slightly reduced supply voltage (0.001 for 20% Vdd reduction). We demonstrate the effectiveness of the Trojans by utilizing them to inject faults into an ASIC implementation of the recently introduced lightweight cipher PRINCE. Full circuit-level simulation followed by differential cryptanalysis demonstrate that the secret key can be reconstructed after around 5 fault-injections. Keywords-fault-based cryptanalysis, fault injection, hardware Trojans
Synthesis of C-3 ureido steroids (1967)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis of C-3 ureido steroidsAkira Yagi, Julia Liang, and David K. FukushimaCite this: J. Org. Chem. 1967, 32, 3, 713–718Publication Date (Print):March 1, 1967Publication History Published online1 May 2002Published inissue 1 March 1967https://pubs.acs.org/doi/10.1021/jo01278a046https://doi.org/10.1021/jo01278a046research-articleACS PublicationsRequest reuse permissionsArticle Views66Altmetric-Citations6LEARN 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
A mouse model of myosin binding protein C human familial hypertrophic cardiomyopathy. (1998)

Familial hypertrophic cardiomyopathy can be caused by mutations in genes encoding sarcomeric proteins, including the cardiac isoform of myosin binding protein C (MyBP-C), and multiple mutations which cause truncated forms of the protein to be made are linked to the disease. We have created transgenic mice in which varying amounts of a mutated MyBP-C, lacking the myosin and titin binding domains, are expressed in the heart. The transgenically encoded, truncated protein is stable but is not incorporated efficiently into the sarcomere. The transgenic muscle fibers showed a leftward shift in the pCa2+-force curve and, importantly, their power output was reduced. Additionally, expression of the mutant protein leads to decreased levels of endogenous MyBP-C, resulting in a striking pattern of sarcomere disorganization and dysgenesis.
Transgenic animal models for study of the pathogenesis of Huntington&rsquo;s disease and therapy (2015)

Huntington's disease (HD) is caused by a genetic mutation that results in polyglutamine expansion in the N-terminal regions of huntingtin. As a result, this polyQ expansion leads to the misfolding and aggregation of mutant huntingtin as well as age-dependent neurodegeneration. The genetic mutation in HD allows for generating a variety of animal models that express different forms of mutant huntingtin and show differential pathology. Studies of these animal models have provided an important insight into the pathogenesis of HD. Mouse models of HD include transgenic mice, which express N-terminal or full-length mutant huntingtin ubiquitously or selectively in different cell types, and knock-in mice that express full-length mutant Htt at the endogenous level. Large animals, such as pig, sheep, and monkeys, have also been used to generate animal HD models. This review focuses on the different features of commonly used transgenic HD mouse models as well as transgenic large animal models of HD, and also discusses how to use them to identify potential therapeutics. Since HD shares many pathological features with other neurodegenerative diseases, identification of therapies for HD would also help to develop effective treatment for different neurodegenerative diseases that are also caused by protein misfolding and occur in an age-dependent manner.
Site-directed mutagenesis of human thioredoxin. Identification of cysteine 74 as critical to its function in the “early pregnancy factor” system. (1993)

Thioredoxin has been identified as a key component of the "early pregnancy factor" system, a system of components present in pregnancy sera which expresses a lymphocyte modifying activity in an assay known as the rosette inhibition assay. Although thioredoxin alone is inactive, addition of thioredoxin to lymphocytes in combination with nonpregnancy sera or platelet-activating factor results in a positive response. We have changed several amino acids of human thioredoxin by site-directed mutagenesis to investigate the residues required for this cooperative function. Conversion of the two active site residues (cysteines 32 and 35) to serines results in a protein devoid of classical redox activity; however, this protein retained its ability to cooperate with non-pregnancy sera or platelet-activating factor in the rosette inhibition assay. Vertebrate thioredoxins contain an additional conserved pair of cysteine residues in the C-terminal portion of the protein. Changing both to serines resulted in no change in redox activity but completely abolished function in the rosette inhibition assay. Further study revealed this function was solely dependent on cysteine 74 as conversion of only cysteine 74 to serine abolished function, whereas replacement of only cysteine 70 with serine had no effect. The nonfunctional mutants counteracted the action of pregnancy serum in the assay strongly supporting the hypothesis that thioredoxin is an integral part of the early pregnancy factor system with residue cysteine 74 having an important role.
An Efficient and Fast Block Size Decision Exploiting Boundary Information on Inner Block for H.264/AVC Intra Prediction (2008)

H.264/AVC, the newest video coding standard, offers an intra prediction with various block sizes and various prediction modes for luma component and chroma component. Due to this new feature, H.264/AVC offers a considerably higher improvement in coding efficiency compared to other compression standards such as MPEG-2, MPEG-4, H.263. However, the computational complexity of H.264/AVC is drastically increased because of the various modes. In this paper, we propose an efficient and fast algorithm to decide block size between 16×16 block and 4×4 block for the computational complexity reduction in the intra prediction of H.264/AVC. The proposed algorithm uses boundary difference values of sub-block, which has 8×8 size, in a macroblock for intra prediction. The boundary differences of inner center block represent the moving patterns of macroblock. Thus, if the value of the differences is smaller than threshold value, this macroblock is selected by 16×16 intra prediction mode. Otherwise, this is selected by 4×4 intra prediction mode. The boundary pixel values' differences of the inner center 8×8 block in 16×16 macroblock are correlated to the smoothness of macroblock. The experimental results show that the proposed algorithm saved on the average 22.9% encoding time without any significant PSNR losses.
Regulation of the expression of the cell‐cycle gene ftsZ by DicF antisense RNA. Division does not require a fixed number of FtsZ molecules (1992)

We show that the 53-nucleotide RNA molecule encoded by gene dicF blocks cell division in Escherichia coli by inhibiting the translation of ftsZ mRNA. Such a role for dicF had been predicted on the basis of the complementarity of DicF RNA with the ribosome-binding region of the ftsZ mRNA. An analysis of ftsZ expression at its chromosomal locus, and of an ftsZ-lacZ translational fusion controlled by promoters ftsZ1p and ftsZ2p only, indicates that ftsZ is not autoregulated. Partial inhibition of FtsZ synthesis leads to increased cell size. However, the number of FtsZ molecules per cell can be reduced threefold without affecting the division rate significantly. Our results suggest that septation is not triggered by a fixed number of newly synthesized FtsZ molecules per cell.
Validation of the Critical-Care Pain Observation Tool in Adult Patients (2006)

The Critical-Care Pain Observation Tool showed that no matter their level of consciousness, critically ill adult patients react to a noxious stimulus by expressing different behaviors that may be associated with pain. Therefore, the tool could be used to assess the effect of various measures for the management of pain.
Creating Air-Stable Supported Lipid Bilayers by Physical Confinement Induced by Phospholipase A2 (2014)

Supported lipid bilayer platforms have been used for various biological applications. However, the lipid bilayers easily delaminate and lose their natural structure after being exposed to an air-water interface. In this study, for the first time, we demonstrated that physical confinement can be used instead of chemical modifications to create air-stable membranes. Physical confinement was generated by the obstacle network induced by a peripheral enzyme, phospholipase A2. The enzyme and reacted lipids could be washed away from the obstacle network, which was detergent-resistant and strongly bonded to the solid support. On the basis of these properties, the obstacle framework on the solid support was reusable and lipid bilayers with the desired composition could be refilled and formed in the region confined by the obstacle framework. The results of fluorescence recovery after photobleaching (FRAP) indicate that the diffusivities of the lipid bilayers before drying and after rehydration were comparable, indicating the air stability of the physically confined membrane. In addition, we observed that the obstacles could trap a thin layer of water after the air-water interface passed through the lipid bilayer. Because the obstacles were demonstrated to be several times higher than a typical lipid membrane on a support, the obstacles may act as container walls, which can trap water above the lipid membrane. The water layer may have prevented the air-water interface from directly contacting the lipid membrane and, therefore, buffered the interfacial force, which could cause membrane delamination. The results suggest the possibility of using physical confinement to create air-stable membranes without changing local membrane rigidity or covering the membrane with protecting molecules.
A bovine papillomavirus E1-related protein binds specifically to bovine papillomavirus DNA (1991)

The E1 open reading frame of bovine papillomavirus (BPV) was expressed as a RecA-E1 fusion protein in Escherichia coli. The bacterially expressed RecA-E1 protein exhibited sequence-specific DNA binding activity; strong binding to the region from nucleotides 7819 to 93 on the BPV genome (designated region A) and weak binding to the adjacent region from nucleotides 7457 to 7818 (region B) were observed. The interaction between the BPV-derived RecA-E1 protein and region A appeared to be highly specific for BPV DNA, as no comparable binding was detected with heterologous papillomavirus DNAs. Binding to region A was eliminated by digestion of region A at the unique HpaI site, which suggests that the RecA-E1 binding site(s) was at or near the HpaI recognition sequence. Binding to region B but not region A was observed when nuclear extracts from ID13 cells were used as a source of E1 proteins. The absence of region A binding by ID13 extracts may reflect a negative regulation of E1 DNA binding activity.
Detection of hazardous gases and vapors: pattern recognition analysis of data from an electrochemical sensor array (1986)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDetection of hazardous gases and vapors: pattern recognition analysis of data from an electrochemical sensor arrayJoseph R. Stetter, Peter C. Jurs, and Susan L. RoseCite this: Anal. Chem. 1986, 58, 4, 860–866Publication Date (Print):April 1, 1986Publication History Published online1 May 2002Published inissue 1 April 1986https://pubs.acs.org/doi/10.1021/ac00295a047https://doi.org/10.1021/ac00295a047research-articleACS PublicationsRequest reuse permissionsArticle Views731Altmetric-Citations121LEARN 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
GRAFT-VERSUS-HOST DISEASE PREVENTION IN ALLOGENEIC BONE MARROW TRANSPLANTATION FROM HISTOCOMPATIBLE SIBLINGS A PILOT STUDY USING IMMUNOTOXINS FOR T CELL DEPLETION OF DONOR BONE MARROW (1987)

Seventeen patients, ages 7-53 years were transplanted with histocompatible bone marrow that had been depleted of T lymphocytes by ex vivo immunotoxin (IT) treatment. Twelve patients had high-risk acute leukemias, and five had chronic myelogenous leukemia. No other graft-vs.-host disease (GVHD) prophylaxis was used. A mixture of three anti-T-cell monoclonal antibodies conjugated to ricin were used in this study: TA-1, UCHT-1 (anti-CD3), and T101 (anti-CD5). The mean number of bone marrow cells infused was 1.5 X 10(8) mononuclear cells/kg recipient weight. Thirteen of the 17 patients demonstrated complete and sustained engraftment. Four patients experienced autologous marrow recovery and/or graft rejection. Compared with an historical group of leukemic patients who received GVHD prophylaxis with methotrexate alone or combinations of methotrexate, and prednisone plus antithymocyte globulin, (ATG) or OKT3, the IT patients with stable engraftment demonstrated shorter time to recovery of leukocytes greater than or equal to 1000mm3 for three consecutive days (median, 20 days vs. 26 days, P = .03). The recovery of total lymphocytes, B and T cell subsets, and T cell function by day 28 was highly variable, but similar, for patients in both the IT-treated group and historical controls. Four patients (ages 13, 18, 21, and 38) developed grade II skin GVHD, but none had severe GVHD. Eight of the 13 patients with durable engraftment have had posttransplant leukemic relapse. Currently only four patients remain alive; two have not relapsed posttransplant, while the other two achieved remission following posttransplant relapse. We conclude that severe GVHD was not observed in this small series with ex vivo T cell depletion for GVHD prophylaxis, and that favorable recovery of hematologic and lymphocytic function was demonstrated for cases where primary engraftment was sustained. A larger randomized controlled study will be needed to establish whether T cell depletion of donor bone marrow with IT can significantly reduce GVHD, and/or improve disease-free survival.
Correction of ADA-SCID by Stem Cell Gene Therapy Combined with Nonmyeloablative Conditioning (2002)

Hematopoietic stem cell (HSC) gene therapy for adenosine deaminase (ADA)-deficient severe combined immunodeficiency (SCID) has shown limited clinical efficacy because of the small proportion of engrafted genetically corrected HSCs. We describe an improved protocol for gene transfer into HSCs associated with nonmyeloablative conditioning. This protocol was used in two patients for whom enzyme replacement therapy was not available, which allowed the effect of gene therapy alone to be evaluated. Sustained engraftment of engineered HSCs with differentiation into multiple lineages resulted in increased lymphocyte counts, improved immune functions (including antigen-specific responses), and lower toxic metabolites. Both patients are currently at home and clinically well, with normal growth and development. These results indicate the safety and efficacy of HSC gene therapy combined with nonmyeloablative conditioning for the treatment of SCID.