gebhart/patrepeval huggingface dataset:
Kinetic characterization of CMD-A2-Gd-DOTA as an intravascular contrast agent for myocardial perfusion measurement with MRI (2000)

Recent developments in magnetic resonance imaging (MRI) using specific contrast media allow the assessment of myocardial perfusion. The purpose of this study was to characterize the intravascular properties of a new macromolecular contrast agent, CMD-A2-Gd-DOTA, to evaluate myocardial perfusion. Two groups of isolated pig hearts perfused at various controlled flows were used. To demonstrate the intravascular properties of CMD-A2-Gd-DOTA, the agent was simultaneously injected with 99mTc-labeled red blood cells in five hearts (group 1). Tracer kinetics of both compounds were assessed by coronary sinus effluent sampling, radioactivity counting and concentration determination in samples for first-pass time curves measurements. Five other hearts (group 2) were studied using a two-slice turboFLASH sequence on a 1.5-T whole-body MRI in order to evaluate first-pass CMD-A2-Gd-DOTA signal intensity (SI) versus time curves. In group 1, for the studied flows ranging from 0.8 to 3.1 ml/min(-1) x g(-1), CMD-A2-Gd-DOTA showed first-pass concentration curves typical of an intravascular contrast agent. In group 2, MRI parameters, i.e., upslope and mean transit time of SI time curves correlated strongly with myocardial perfusion. Within the physiologic range of flows, CMD-A2-Gd-DOTA was able to demonstrate tracer kinetics for in vivo assessment of myocardial perfusion using MRI.
Photophysics of thiacarbocyanine dye in organic solvent (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTPhotophysics of thiacarbocyanine dye in organic solventDimitri Noukakis, Mark Van de Auweraer, Susanne Toppet, and Frans C. De SchryverCite this: J. Phys. Chem. 1995, 99, 31, 11860–11866Publication Date (Print):August 1, 1995Publication History Published online1 May 2002Published inissue 1 August 1995https://pubs.acs.org/doi/10.1021/j100031a012https://doi.org/10.1021/j100031a012research-articleACS PublicationsRequest reuse permissionsArticle Views331Altmetric-Citations78LEARN 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 Get e-Alerts
Glycoprotein B Subtyping of Cytomegalovirus (CMV) in the Vitreous of Patients with AIDS and CMV Retinitis (1998)

A 550-bp region of the cytomegalovirus (CMV) glycoprotein B (gB) gene was amplified by polymerase chain reaction (PCR) from 141 vitreous specimens of 120 patients with AIDS and CMV retinitis from three different metropolitan centers. The distribution of gB subtypes I, II, III, and IV were 19%, 43%, 12%, and 21%, respectively, based on restriction enzyme digestion patterns of PCR-amplified DNA. Two patients had simultaneous infection with two different gB subtypes. The ratio of gB subtypes was similar among the three geographically distinct patient populations. Two of 14 patients with bilateral vitreous specimens had different viral subtypes in each eye. In addition, different gB subtypes were observed in 1 of 6 patients with serial specimens. The ratio of different gB subtypes in the vitreous of patients with CMV retinitis is similar to that previously reported in the peripheral blood of patients with advanced AIDS.
Digital imaging of free calcium changes and of spatial gradients in growing processes in single, mammalian central nervous system cells. (1986)

Intracellular free calcium levels have been measured in cultured central nervous system (CNS) cells by using the fluorescent indicator fura-2 and digital imaging techniques. Cells were plated from rat embryo diencephalon (embryonic day 17 or 18), with nearly all of the cells surviving dissociation having undergone final mitosis within the previous 24 hr. The initially spherical cells were observed within the first 24 hr in culture when they were extending processes but had not established a network of fibers that would prevent the identification of the origin of a given fiber. Cells that were rapidly extending showed high Ca2+ levels in the regions of growth. Where processes had just emerged from the soma or where growth was proceeding from more than one pole, Ca2+ levels were uniform and estimated levels of 500 nM were commonly seen. In active growth cones distant from the soma, Ca2+ levels exceeded 200 nM, whereas the soma levels were in the 60-80 nM range. Nonextended and extended cells that had stalled had uniform Ca2+ levels in the range of 30-70 nM. The results show that high Ca2+ levels are at least a correlate of extension in CNS cells and that under some conditions the region of high calcium can be localized to a small part of the cell.
Dual DNA Staining Assessment of Bovine Sperm Viability Using SYBR‐14 and Propidium Iodide (1994)

A new membrane-permeant DNA stain, SYBR-14, was used in combination with propidium iodide (PI) to estimate the proportion of living sperm in bovine semen. The SYBR-14 stained living sperm while PI only stained degenerate cells that had lost their membrane integrity. Staining with SYBR-14 resulted in the nuclei of living sperm fluorescing bright green. Aliquots containing nearly all living bovine sperm were prepared using glass wool/Sephadex filtration to remove dead and damaged cells. A portion of this filtered sample was killed by unprotected freeze-thawing and used to provide mixed aliquots containing known ratios of living and dead sperm. Flow cytometry was used to assess the green and red fluorescence of these mixtures. The percentages of living sperm, as determined by the log of green fluorescence, were 85.1, 68.8, 39.8, 20.7, and 1.4 for ratios of 100:0, 75:25, 50:50, 25:75, and 0:100 of the filtered, killed mixtures. Also, bovine semen was diluted 1:60 in HEPES-0.1% bovine serum albumin and incubated for 0, 3, 6, and 24 hours at 36 degrees C to assess changes in cell viability. As cell death occurred during this incubation period, a relatively rapid transition of staining from green to red occurred as sperm died. Three replicates of cryopreserved sperm from six bulls were also examined using SYBR-14 and PI to assess the proportion of living and dead cells. Flow cytometric analyses of these samples, which had been processed and stored in homogenized milk, indicated that this stain combination was useful in assessing the quality of cryopreserved sperm. The combination of SYBR-14 and PI was determined to be an effective tool for assessing the viability of fresh or cryopreserved sperm.
Vulnerability-Specific Execution Filtering for Exploit Prevention on Commodity Software (2018)

Exploits for new vulnerabilities, especially when incorporated within a fast spreading worm, can compromise nearly all vulnerable hosts within a short amount of time. This problem demonstrates the need for fast defenses which can react to a new vulnerability quickly. In addition, a realistic defense system should (a) not require source code since in practice most vulnerable systems do not have source code access nor is there adequate time to involve the software vendor, (b) be accurate, i.e., have a negligible false positive rate and low false negative rate, and (c) be efficient, i.e., add little overhead to normal program execution. We propose vulnerability-specific execution-based filtering (VSEF) – a new approach for automatic defense which achieves a lower error rate and wider applicability than input filters and has better performance than full execution monitoring. VSEF is an execution-based filter which filters out attacks on a specific vulnerability based on the vulnerable program’s execution trace. We present VSEF, along with a system for automatically creating VSEF filters and a hardened program without access to source code. In our system, the time it takes to create the filter and generate the hardened program is negligible. The overhead of the hardened program is only a few percent in most cases. The false positive rate is zero in most cases, and the hardened program is resilient against polymorphic variants of exploits on the same vulnerability. VSEF therefore achieves the required performance, accuracy, and response speed requirements to defend against current fast-spreading exploits.
Molecular genetics of herpes simplex virus. VII. Characterization of a temperature-sensitive mutant produced by in vitro mutagenesis and defective in DNA synthesis and accumulation of gamma polypeptides (1981)

We report on the properties of a temperature-sensitive mutant produced by transfection of cells with intact DNA and a specific DNA fragment mutagenized with low levels of hydroxylamine. The plating efficiency of the mutant at 39 degrees C relative to that at 33.5 degrees C was 5 X 10(-6). The pattern of polypeptides produced at the nonpermissive temperature was similar to that seen with wild-type virus in infected cells treated with inhibitory concentrations of phosphonoacetic acid in that alpha and beta polypeptides were produced, whereas most gamma polypeptides were either reduced or absent. Consistently, the mutant did not make viral DNA, although temperature sensitivity of the viral DNA polymerase could not be demonstrated. Marker rescue studies with herpes simplex virus type 2 (HSV-2) DNA mapped the mutant in the L component within map positions 0.385 and 0.402 in the prototype (P) arrangement of the HSV-1 genome. Analysis of the recombinants permitted the mapping of the genes specifying infected cell polypeptides 36, 35, 37, 19.5, 11, 8, 2, 43, and 44, but only the infected cell polypeptide 8 of HSV-2 was consistently made by all recombinants containing demonstrable HSV-2 sequences. Marker rescue studies with cloned HSV-1 DNA fragments mapped the temperature-sensitive lesion within less than 10(3) base pairs between 0.383 and 0.388 map units. Translation of the RNA hybridizing to cloned HSV-1 DNA, encompassing the smallest region containing the mutation, revealed polypeptide 8 (128,000 molecular weight), which was previously identified as a beta polypeptide with high affinity for viral DNA, and a polypeptide (25,000 molecular weight) not previously identified in lysates of labeled cells.
Oxidative stress and redox regulation of lung inflammation in COPD (2006)

Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (c-Jun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-kappaB and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-kappaB-mediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of kappaB-alpha kinase or the enhanced recruitment and activation of transcriptional co-activators. Enhanced NF-kappaB-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression. Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity. The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/quercetin and reserveratol), specific spin traps, such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-kappaB activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells. Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.
HPK1 Influences Regulatory T Cell Functions (2020)

Hematopoietic progenitor kinase 1 (HPK1) is a negative regulator of TCR-initiated signal transduction. Both the <i>HPK1<sup>-/-</sup></i> mice and the genetically engineered mice with a point mutation that disrupts the catalytic activity of HPK1 possess enhanced antitumor immunity, especially when these mice are treated with anti-PD-L1 immune checkpoint Ab. Because CD4<sup>+</sup>FOXP3<sup>+</sup> regulatory T cells (Tregs) play an important role in suppressing tumor immunity, we investigated whether the loss of HPK1 expression could result in the reduction of Treg functions. We found that the number of <i>HPK1<sup>-/-</sup></i> Tregs is elevated relative to the number found in wild-type C57/BL6 mice. However, <i>HPK1<sup>-/-</sup></i> Tregs lack the ability to carry out effective inhibition of TCR-induced proliferative responses by effector T cells. Furthermore, <i>HPK1<sup>-/-</sup></i> Tregs respond to TCR engagement with an elevated and sustained Erk MAPK and p65/RelA NF-κB phosphorylation in comparison with wild-type Tregs. Also, a multiplex cytokine analysis of <i>HPK1<sup>-/-</sup></i> Tregs revealed that they demonstrate an aberrant cytokine expression profile when stimulated by anti-CD3ε and anti-CD28 crosslinking, including the uncharacteristic expression of IL-2 and antitumor proinflammatory cytokines and chemokines such as IFN-γ, CCL3, and CCL4. The aberrant <i>HPK1<sup>-/-</sup></i> phenotype observed in these studies suggests that HPK1 may play an important role in maintaining Treg functions with wider implications for HPK1 as a novel immunotherapeutic target.
Reduced conduction failure of the main axon of polymodal nociceptive C-fibres contributes to painful diabetic neuropathy in rats (2012)

Painful diabetic neuropathy is a common complication of diabetes mellitus and can affect many aspects of life and severely limit patients' daily functions. Signals of painful diabetic neuropathy are believed to originate in the peripheral nervous system. However, its peripheral mechanism of hyperalgesia has remained elusive. Numerous studies have accumulated that polymodal nociceptive C-fibres play a crucial role in the generation and conduction of pain signals and sensitization of which following injury or inflammation leads to marked hyperalgesia. Traditionally, the number of nociceptive primary afferent firings is believed to be determined at the free nerve endings, while the extended main axon of unmyelinated C-fibres only involves the reliable and faithful propagation of firing series to the central terminals. We challenged this classic view by showing that conduction of action potential can fail to occur in response to repetitive activity when they travel down the main axon of polymodal nociceptive C-fibres. Quantitative analysis of conduction failure revealed that the degree of conduction failure displays a frequency-dependent manner. Local administration of low threshold, rapidly activating potassium current blocker, α-dendrotoxin (0.5 nM) and persistent sodium current blocker, low doses of tetrodotoxin (<100 nM) on the main axon of C-fibres can reciprocally regulate the degree of conduction failure, confirming that conduction failure did occur along the main axon of polymodal nociceptive C-fibres. Following streptozotocin-induced diabetes, a subset of polymodal nociceptive C-fibres exhibited high-firing-frequency to suprathreshold mechanical stimulation, which account for about one-third of the whole population of polymodal nociceptive C-fibres tested. These high-firing-frequency polymodal nociceptive C-fibres in rats with diabetes displayed a marked reduction of conduction failure. Delivery of low concentrations of tetrodotoxin and Nav1.8 selective blocker, A-803467 on the main axon of C-fibres was found to markedly enhance the conduction failure in a dose-dependent manner in diabetic rats. Upregulated expression of sodium channel subunits Nav1.7 and Nav1.8 in both small dorsal root ganglion neurons and peripheral C-fibres as well as enhanced transient and persistent sodium current and increased excitability in small dorsal root ganglion neurons from diabetic rats might underlie the reduced conduction failure in the diabetic high-firing-frequency polymodal nociceptive C-fibres. This study shed new light on the functional capability in the pain signals processing for the main axon of polymodal nociceptive C-fibres and revealed a novel mechanism underlying diabetic hyperalgesia.
The Role of Blood Supply to Soft Tissue in the Healing of Diaphyseal Fractures (1972)

From the Department of Orthopaedic Surgery, Bristol Royal Infirmary, King's College Hospital, London
Gastroprotective Effects of L‐Lysine Salification of Ketoprofen in Ethanol‐Injured Gastric Mucosa (2014)

Ketoprofen L-lysine salt (KLS), a NSAID, is widely used for its analgesic efficacy and tolerability. L-lysine salification was reported to increase the solubility and the gastric absorption and tolerance of ketoprofen. Since the management of NSAIDs gastrotoxicity still represents a major limitation in prolonged therapies, mainly when gastric lesions are present, this study investigated the gastro-protective activity of L-lysine by using a well-established model of gastric mucosa injury, the ethanol-gastric injury model. Several evidences show that the damaging action of ethanol could be attributed to the increase of ROS, which plays a key role in the increase of lipid peroxidation products, including malonyldialdehyde and 4-hydroxy-2-nonenal. With the aim to unravel the mechanism of L-lysine gastroprotection, cellular MDA levels and 4-HNE protein adducts as markers of lipid peroxidation and a panel of key endogenous gastro-protective proteins were assayed. The data obtained indicate a gastroprotective effect of L-lysine on gastric mucosa integrity.
Oral creatine monohydrate supplementation improves brain performance: a double–blind, placebo–controlled, cross–over trial (2003)

Creatine supplementation is in widespread use to enhance sports-fitness performance, and has been trialled successfully in the treatment of neurological, neuromuscular and atherosclerotic disease. Creatine plays a pivotal role in brain energy homeostasis, being a temporal and spatial buffer for cytosolic and mitochondrial pools of the cellular energy currency, adenosine triphosphate and its regulator, adenosine diphosphate. In this work, we tested the hypothesis that oral creatine supplementation (5 g d(-1) for six weeks) would enhance intelligence test scores and working memory performance in 45 young adult, vegetarian subjects in a double-blind, placebo-controlled, cross-over design. Creatine supplementation had a significant positive effect (p < 0.0001) on both working memory (backward digit span) and intelligence (Raven's Advanced Progressive Matrices), both tasks that require speed of processing. These findings underline a dynamic and significant role of brain energy capacity in influencing brain performance.
Gene vaccination with naked plasmid DNA: mechanism of CTL priming. (1996)

The injection of naked plasmid DNA directly into the muscle cells of mice has been shown to induce potent humoral and cellular immune responses. The generation of a cytotoxic T lymphocyte (CTL) response after plasmid DNA injection may involve the presentation of the expressed antigen in the context of the injected myocytes' endogenous major histocompatibility (MHC)-encoded class I molecules or may use the MHC molecules of bone marrow-derived antigen presenting cells (APC) which are capable of providing co-stimulation as well. To resolve which cell type provides the specific restricting element for this method of vaccination we generated parent-->F1 bone marrow chimeras in which H-2bxd recipient mice received bone marrow that expressed only H-2b or H-2d MHC molecules. These mice were injected intramuscularly with naked plasmid DNA that encoded the nucleoprotein from the A/PR/8/34 influenza strain, which as a single antigen has epitopes for both H-2Db and H-2Kd. The resulting CTL responses were restricted to the MHC haplotype of the bone marrow alone and not to the second haplotype expressed by the recipient's myocytes. The role of somatic tissues that express protein from injected plasmids may be to serve as a reservoir for that antigen which is then transferred to the APC. Consequently, our data show that the mechanism of priming in this novel method for vaccination uses the MHC from bone marrow-derived APC, which are efficient at providing all of the necessary signals for priming the T cell.
Handbook of nucleoside synthesis (2001)

Foreword. Preface. Acknowledgments. Synthesis of Nucleosides. Introduction. Nucleoside Synthesis. Silyl-Hilbert-Johnson Reaction in the Presence of Friedel-Crafts Catalysts. Mechanism of Nucleoside Formation in the Presence of Friedel-Crafts Catalysts. Special Preparations. Miscellaneous Methods. Alternative Nucleoside-Forming Reactions. Experimental Conditions. Experimental Procedures. Tabular Survey. References. Index.
Type I collagen is thermally unstable at body temperature (2002)

Measured by ultra-slow scanning calorimetry and isothermal circular dichroism, human lung collagen monomers denature at 37 degrees C within a couple of days. Their unfolding rate decreases exponentially at lower temperature, but complete unfolding is observed even below 36 degrees C. Refolding of full-length, native collagen triple helices does occur, but only below 30 degrees C. Thus, contrary to the widely held belief, the energetically preferred conformation of the main protein of bone and skin in physiological solution is a random coil rather than a triple helix. These observations suggest that once secreted from cells collagen helices would begin to unfold. We argue that initial microunfolding of their least stable domains would trigger self-assembly of fibers where the helices are protected from complete unfolding. Our data support an earlier hypothesis that in fibers collagen helices may melt and refold locally when needed, giving fibers their strength and elasticity. Apparently, Nature adjusts collagen hydroxyproline content to ensure that the melting temperature of triple helical monomers is several degrees below rather than above body temperature.
Turbo source coding: a noise-robust approach to data compression (2003)

Summary form only given. All traditional data compression techniques, such as Huffman coding, the Lempel-Ziv algorithm, run-length limited coding, Tunstall coding and arithmetic coding are highly susceptible to residual channel errors and noise. We have previously proposed the use of parallel concatenated codes and iterative decoding for fixed-length to fixed-length source coding, i.e., turbo coding for data compression purposes. The work presented here extends these results and also considers the case when decompression must be done from compressed data corrupted by additive white Gaussian noise (AWGN).