gebhart/patrepeval huggingface dataset:
Anti-infective activity of apolipoprotein domain derived peptides in vitro: identification of novel antimicrobial peptides related to apolipoprotein B with anti-HIV activity (2010)

These data suggest that further antimicrobial peptides may be obtained using human apolipoprotein sequences, selecting regions with either amphipathic alpha-helical structure, or those linked to receptor-binding regions. The finding that an amphipathic alpha-helical region of apolipoprotein J has antiviral activity comparable with that for the previously reported apolipoprotein AI derived peptide 18A, suggests that full-length apolipoprotein J may also have such activity, as has been reported for full-length apolipoprotein AI. Although the strength of the anti-infective activity of the sequences identified was limited, this could be increased substantially by developing related mutant peptides. Indeed the apolipoprotein B-derived peptide mutants uncovered by the present study may have utility as HIV therapeutics or microbicides.
Genetic and biochemical characterization of the α and β components of a propionyl-CoA carboxylase complex of Streptomyces coelicolor A3(2) The GenBank accession numbers for the accA1, aacA2 and pccB sequences determined in this work are AF113603, AF113604 and AF113605, respectively. (1999)

Two genes, accA1 and accA2, with nearly identical nucleotide sequences were cloned from Streptomyces coelicolor A3(2). The deduced amino acid sequences of the product of these two genes showed high similarity to BcpA2 of Saccharopolyspora erythraea and other biotin-containing proteins from different organisms assumed to be the alpha subunit of a propionyl-CoA carboxylase. A gene, pccB, encoding the carboxyl transferase subunit of this enzyme complex was also characterized. Strains disrupted in accA1 did not show any change in acetyl- or propionyl-CoA carboxylase activity, whilst cell-free extracts of a pccB mutant strain contained a reduced level of propionyl-CoA carboxylase. No mutants in accA2 could be isolated, suggesting that the gene may be essential. Heterologous expression of accA1, accA2 and pccB in Escherichia col and in vitro reconstitution of enzyme activity confirmed that PccB is the beta subunit of a propionyl-CoA carboxylase and that either AccA1 or AccA2 could act as the alpha component of this enzyme complex. The fact that accA2 mutants appear to be inviable suggests that this gene encodes a biotinylated protein that might be shared with other carboxyl transferases essential for the growth of S. coelicolor.
Magnetic field-based SLAM method for solving the localization problem in mobile robot floor-cleaning task (2011)

In this paper we present a SLAM method based on indoor magnetic field anomalies and measure the acquired map quality in the context of the localization problem present in mobile robot floor-cleaning scenarios. According to our real-world robot experiments in different environments, it appears that most modern buildings have sufficient magnetic field variation to make the method applicable in mobile robot floor-cleaning tasks. We show that our method can be used to acquire maps that are accurate enough to be utilized in the robot coverage problem, thus reducing over-cleaning. We use Gaussian Processes to model the magnetic field and a Rao-Blackwellized Particle Filter to estimate the pose distribution of the robot. Because magnetic field anomalies are not correlated to typical features used in localization, our method can handle many situations in which other methods fail. The minimalistic sensory requirements of our method make it a very viable alternative for low-cost domestic robots.
Trazodone dosing regimen: experience with single daily administration. (1990)

Efficacy being constant, antidepressant choice is dictated by side effect profile, patient acceptance, and safety. Trazodone has been shown to be safe in overdose, and the side effect profile is mild, with sedation the most common side effect. Sleep electroencephalogram and clinical studies have shown trazodone effective in improving sleep in normal subjects, insomniac patients, and patients with major depression. Tolerance and rapid eye movement rebound on discontinuation do not occur. The 3- to 9-hour half-life of trazodone and its pharmacokinetics favors a dose weighted at bedtime. Studies comparing multiple daytime dosing to single dosing at bedtime have shown equal efficacy in relieving depression. At treatment onset, a single nighttime dose is more productive of sleep with less daytime drowsiness. These differences between single nighttime dosing and multiple daily dosing disappear with continued administration. Geriatric patients respond similarly. Trazodone is best dosed at 150 mg given predominantly (but not necessarily all) at bedtime and increased as needed to 200 to 300 mg for full antidepressant efficacy.
Development of a markerless gene knock-out system forMannheimia succiniciproducensusing a temperature-sensitive plasmid (2007)

A temperature-sensitive derivative of the Mannheimia varigena plasmid pMVSCS1 was constructed by hydroxylamine treatment for use in the development of a markerless gene knock-out system for Mannheimia succiniciproducens. The temperature-sensitive plasmid pMVSCS1-ts was stably maintained at 30 degrees C, but failed to replicate at 42 degrees C. DNA sequencing of the replication origin revealed a single base substitution as being responsible for its temperature sensitivity. The region of replication origin was amplified by PCR to construct an Escherichia coli-M. succiniciproducens shuttle vector pME19-ts to further examine the thermosensitivity. To make markerless mutants of M. succiniciproducens, the Cre-lox system with the variant lox66 and lox71 sites was used to prevent the instability caused by multiple loxP sites in the genome. The transient cre expression was carried out using the temperature-sensitive plasmid pCRX5, which was consequently cured after the verification of the markerless mutant by growing cells at 42 degrees C. For the demonstration of the markerless deletion of multiple genes using this method, the ldhA gene and the oadGAB operon of M. succiniciproducens encoding lactate dehydrogenase and oxaloacetate decarboxylase, respectively, were successfully deleted sequentially. This markerless deletion method should be useful for further metabolic engineering of M. succiniciproducens, which is a promising industrial bacterium for succinic acid production from renewable resources.
The response to levodopa in parkinson's disease: Imposing pharmacological law and order (1996)

Abstract The seemingly unpredictable response to levodopa in patients with Parkinson's disease can be understood as an interaction between several distinct pharmacological effects of levodopa. The most important are a short‐duration response with a half‐life of minutes to hours and a long‐duration response with a half‐life of days, superimposed on diurnal motor variation. A negative response characterized by brief worsening before and after the short‐duration response and dyskinesia accentuate the short‐duration response. These various responses are modified by disease progression and long‐term levodopa therapy. Pharmacodynamic modeling of the short‐duration response indicates that with time, the response becomes less graded and small changes in levodopa concentrations can produce big changes in response. In this setting, unpredictability arises from the variation in absorption and distribution of levodopa.
A Low-Noise Wide-BW 3.6-GHz Digital $\Delta\Sigma$ Fractional-N Frequency Synthesizer With a Noise-Shaping Time-to-Digital Converter and Quantization Noise Cancellation (2008)

A 3.6-GHz digital fractional-N frequency synthesizer achieving low noise and 500-kHz bandwidth is presented. This architecture uses a gated-ring-oscillator time-to-digital converter (TDC) with 6-ps raw resolution and first-order shaping of its quantization noise along with digital quantization noise cancellation to achieve integrated phase noise of less than 300 fs (1 kHz to 40 MHz). The synthesizer includes two 10-bit 50-MHz passive digital-to-analog converters for digital control of the oscillator and an asynchronous frequency divider that avoids divide-value delay variation at its output. Implemented in a 0.13-mum CMOS process, the prototype occupies 0.95-mm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> active area and dissipates 39 mW for the core parts with another 8 mW for the oscillator output buffer. Measured phase noise at 3.67 GHz carrier frequency is -108 and -150 dBc/Hz at 400 kHz and 20 MHz offset, respectively.
Sequence-Specific Packaging of DNA in Human Sperm Chromatin (1987)

The DNA in human sperm chromatin is packaged into nucleoprotamine (approximately 85%) and nucleohistone (approximately 15%). Whether these two chromatin fractions are sequence-specific subsets of the spermatozoon genome is the question addressed in this report. Sequence-specific packaging would suggest distinct structural and functional roles for the nucleohistone and nucleoprotamine in late spermatogenesis or early development or both. After removal of histones with 0.65M NaCl, exposed DNA was cleaved with Bam HI restriction endonuclease and separated by centrifugation from insoluble nucleoprotamine. The DNA sequence distribution of nucleohistone DNA in the supernatant and nucleoprotamine DNA in the pellet was compared by cloning size-selected single-copy sequences and by using the derived clones as probes of nucleohistone DNA and nucleoprotamine DNA. Two clones derived from nucleohistone DNA preferentially hybridized to nucleohistone DNA, and two clones derived from nucleoprotamine DNA preferentially hybridized to nucleoprotamine DNA, which demonstrated the existence of sequence-specific nucleohistone and nucleoprotamine components within the human spermatozoon.
Tumor-Induced Osteomalacia (2005)

Tumor-induced osteomalacia (TIO) is a rare paraneoplastic form of renal phosphate wasting that results in severe hypophosphatemia, a defect in vitamin D metabolism, and osteomalacia. This debilitating disorder is illustrated by the clinical presentation of a 55-year-old woman with progressive fatigue, weakness, and muscle and bone pain with fractures. After a protracted clinical course and extensive laboratory evaluation, tumor-induced osteomalacia was identified as the basis of her clinical presentation. In this article, the distinctive clinical characteristics of this syndrome, the advances in diagnosis of TIO, and new insights into the pathophysiology of this disorder are discussed.
EXPERIMENTS IN THE VERATROLE AND QUINOXALINE GROUPS (1947)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTEXPERIMENTS IN THE VERATROLE AND QUINOXALINE GROUPSJACOB EHRLICH and MARSTON TAYLOR BOGERTCite this: J. Org. Chem. 1947, 12, 4, 522–534Publication Date (Print):July 1, 1947Publication History Published online1 May 2002Published inissue 1 July 1947https://doi.org/10.1021/jo01168a006RIGHTS & PERMISSIONSArticle Views1359Altmetric-Citations29LEARN 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 InReddit PDF (1 MB) Get e-Alertsclose Get e-Alerts
Ion channel blockade attenuates aggregated alpha synuclein induction of microglial reactive oxygen species: relevance for the pathogenesis of Parkinson’s disease (2006)

Brain mononuclear phagocyte (perivascular macrophage and microglia, MG) inflammatory neurotoxins play a principal role in the pathogenesis of Parkinson's disease; chief among these are reactive oxygen species (ROS). We posit that aggregated, misfolded and oxidized alpha-synuclein (a major constituent of Lewy bodies), released or secreted from dying dopaminergic neurons, induces microglial ROS production that is regulated by ion channels and as such affects disease progression. To address this hypothesis, we performed patch clamp recordings of outward ionic currents in murine microglia and characterized their links to ROS production during alpha-synuclein stimulation. Aggregated nitrated alpha-synuclein induced ROS production in a dose-dependent manner that was inhibited by voltage-gated potassium current blockade, and to a more limited degree, by chloride current blockade. Interestingly, ROS produced in MG primed with tumor necrosis factor alpha and activated with phorbol myristate acetate was attenuated by voltage-gated potassium current blockade and more completely by chloride current blockade. In contrast, amyloid beta or cell membrane extract failed to induce microglial ROS production. Similar results were obtained using bone marrow-derived macrophages. The association of ROS production with specific plasma membrane ion currents provides a link between regulation of microglial ion transport and oxygen free radical production. Understanding these linkages may lead to novel therapeutics for Parkinson's disease where modulation of redox-related stress may slow disease progression.
Hydrophobicity of Amino Acid Residues in Globular Proteins (1985)

During biosynthesis, a globular protein folds into a tight particle with an interior core that is shielded from the surrounding solvent. The hydrophobic effect is thought to play a key role in mediating this process: nonpolar residues expelled from water engender a molecular interior where they can be buried. Paradoxically, results of earlier quantitative analyses have suggested that the tendency for nonpolar residues to be buried within proteins is weak. However, such analyses merely classify residues as either "exposed" or "buried." In the experiment reported in this article proteins of known structure were used to measure the average area that each residue buries upon folding. This characteristic quantity, the average area buried, is correlated with residue hydrophobicity.
Proteasome inhibitor PS‐341 induces growth arrest and apoptosis of non‐small cell lung cancer cells via the JNK/c‐Jun/AP‐1 signaling (2004)

Proteasome inhibitor PS-341 induces growth arrest and apoptosis of multiple myeloma (MM) cells via inactivation of NF-kappaB in vitro and has afforded some objective responses in individuals with relapsed, refractory MM. However, the activity of PS-341 against non-hematological malignancies remains to be fully elucidated. In this study, we found that PS-341 induced growth arrest and apoptosis of NCI-H520 and -H460 non-small cell lung cancer (NSCLC) cells in conjunction with markedly up-regulated levels of p21(waf1) and p53, and down-regulation of bcl-2 protein in these cells. Also, PS-341 caused phosphorylation of c-Jun NH(2)-terminal kinase (JNK) and c-Jun, and enhanced AP-1/DNA binding activities in these cells as measured by western blotting and enzyme-linked immunosorbent assay (ELISA), respectively. Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Thus, PS-341 might be useful for the treatment of individuals with NSCLC.
Screen content coding using non-square intra block copy for HEVC (2014)

To achieve high coding performance for screen content, the intra block copy (IntraBC) performs block matching within a limited area of the reconstructed samples inside the current picture. We further extend its notion from the unit of square coding unit (CU) to non-square prediction unit (PU) partitions. This design is then justified by theoretical and empirical analyses which reveal the same fact that blocks coded by IntraBC mode tend to enable more at smaller partition levels. Besides, the syntax design of the proposed method is fully aligned with that of inter partition modes. Therefore the architecture-wise change in video codec design can be minimized. The experimental results justify the effectiveness of the proposed mode for coding of screen content video. In particular, up to 19.5% rate reduction (with an average of 12.7%) relative to the HM-12.0+RExt-4.1 anchor can be achieved on top of the usage of CU-based IntraBC prediction.
Hepatitis C Virus Core Protein Interacts with 14-3-3 Protein and Activates the Kinase Raf-1 (2000)

Persistent hepatitis C virus (HCV) infection is a major cause of chronic liver dysfunction in humans and is epidemiologically closely associated with the development of human hepatocellular carcinoma. Among HCV components, core protein has been reported to be implicated in cell growth regulation both in vitro and in vivo, although mechanisms explaining those effects are still unclear. In the present study, we identified that members of the 14-3-3 protein family associate with HCV core protein. 14-3-3 protein bound to HCV core protein in a phosphoserine-dependent manner. Introduction of HCV core protein caused a substantial increase in Raf-1 kinase activity in HepG2 cells and in a yeast genetic assay. Furthermore, the HCV core-14-3-3 interaction was essential for Raf-1 kinase activation by HCV core protein. These results suggest that HCV core protein may represent a novel type of Raf-1 kinase-activating protein through its interaction with 14-3-3 protein and may contribute to hepatocyte growth regulation.
Allergy to bovine β‐lactoglobulin: specificity of immunoglobulin E generated in the Brown Norway rat to tryptic and synthetic peptides (1999)

These studies provide evidence that the immune system of the BN rat and humans - at least in the case of milk allergens - is recognizing similar protein allergens and indeed, at the molecular level, similar peptide epitopes.
Intestinal Targeting of Drugs: Rational Design Approaches and Challenges (2013)

Targeting drugs to the gastrointestinal tract has been and continues to be an active area of research. Gut-targeting is an effective means of increasing the local concentration of active substance at the desired site of action while minimizing concentrations elsewhere in the body that could lead to unwanted side-effects. Several approaches to intestinal targeting exist. Physicochemical property manipulation can drive molecules to large, polar, low absorption space or alternatively to lipophilic, high clearance space in order to minimize systemic exposure. Design of compounds that are substrates for transporters within the gastrointestinal tract, either uptake or efflux, or at the hepato-biliary interface, may help to increase intestinal concentration. Prodrug strategies have been shown to be effective particularly for colon targeting, and several different technology formulation approaches are currently being researched. This review provides examples of various approaches to intestinal targeting, and discusses challenges and areas in need of future scientific advances.
Dystrobrevin deficiency at the sarcolemma of patients with muscular dystrophy (1997)

Mutations in the genes encoding dystrophin or dystrophin-associated proteins are responsible for Duchenne muscular dystrophy or various forms of limb-girdle muscular dystrophies respectively. We have recently cloned the gene for the murine 87 kDa postsynaptic protein dystrobrevin, a dystrophin-associated protein. Anti-dystrobrevin antibodies stain the sarcolemma in normal skeletal muscle indicating that dystrobrevin co-localises with dystrophin and the dystrophin-associated protein complex. By contrast, dystrobrevin membrane staining is severely reduced in muscles of Duchenne muscular dystrophy patients, consistent with dystrobrevin being a dystrophin-associated protein. Interestingly, dystrobrevin staining at the sarcolemma is dramatically reduced in patients with limb-girdle muscular dystrophy arising from the loss of one or all of the sarcoglycan components. Normal dystrobrevin staining is observed in patients with other forms of limb-girdle muscular dystrophy where dystrophin and the rest of the dystrophin-associated protein complex are normally expressed and in other neuromuscular disorders. Our results show that dystrobrevin-deficiency is a generic feature of dystrophies linked to dystrophin and the dystrophin-associated proteins. This is the first indication that a cytoplasmic component of the dystrophin-associated protein complex may be involved in the pathogenesis of limb-girdle muscular dystrophy.
A Capsid-Modified Helper-Dependent Adenovirus Vector Containing the β-Globin Locus Control Region Displays a Nonrandom Integration Pattern and Allows Stable, Erythroid-Specific Gene Expression (2005)

Gene therapy for hemoglobinopathies requires efficient gene transfer into hematopoietic stem cells and high-level erythroid-specific gene expression. Toward this goal, we constructed a helper-dependent adenovirus vector carrying the beta-globin locus control region (LCR) to drive green fluorescent protein (GFP) expression, whereby the LCR-GFP cassette is flanked by adeno-associated virus (AAV) inverted terminal repeats (Ad.LCR-beta-GFP). This vector possesses the adenovirus type 35 fiber knob that allows efficient infection of hematopoietic cells. Transduction and vector integration studies were performed in MO7e cells, a growth factor-dependent CD34(+) erythroleukemic cell line, and in cord blood-derived human CD34(+) cells. Stable transduction of MO7e cells with Ad.LCR-beta-GFP was more efficient and less subject to position effects and silencing than transduction with a vector that did not contain the beta-globin LCR. Analysis of integration sites indicated that Ad.LCR-beta-GFP integration in MO7e cells was not random but tethered to chromosome 11, specifically to the globin LCR. More than 10% of analyzed integration sites were within the chromosomal beta-globin LCR. None of the Ad.LCR-beta-GFP integrations occurred in exons. The integration pattern of a helper-dependent vector that contained X-chromosomal stuffer DNA was different from that of the beta-globin LCR-containing vector. Infection of primary CD34(+) cells with Ad.LCR-beta-GFP did not affect the clonogenic capacity of CD34(+) cells. Transduction of CD34(+) cells with Ad.LCR-beta-GFP resulted in vector integration and erythroid lineage-specific GFP expression.