gebhart/patrepeval huggingface dataset:
Linear vein–based arteriovenous malformations in children (2009)

A linear vein-based morphological pattern is common in pediatric AVMs and may recapitulate the embryological origins of the cerebral circulation. Surgical treatment in these cases can also be vein-based, through a narrow surgical corridor, which leads to minimal cortical disruption.
Duality between source coding and channel coding and its extension to the side information case (2003)

We explore the information-theoretic duality between source coding with side information at the decoder and channel coding with side information at the encoder. We begin with a mathematical characterization of the functional duality between classical source and channel coding, formulating the precise conditions under which the optimal encoder for one problem is functionally identical to the optimal decoder for the other problem. We then extend this functional duality to the case of coding with side information. By invoking this duality, we are able to generalize the result of Wyner and Ziv (1976) relating to no rate loss for source coding with side information from Gaussian to more arbitrary distributions. We consider several examples corresponding to both discrete- and continuous-valued cases to illustrate our formulation. For the Gaussian cases of coding with side information, we invoke geometric arguments to provide further insights into their duality. Our geometric treatment inspires the construction and dual use of practical coset codes for a large class of emerging applications for coding with side information, such as distributed sensor networks, watermarking, and information-hiding communication systems.
Characterization of MeCP2, a vertebrate DNA binding protein with affinity for methylated DNA (1992)

Methylated DNA in vertebrates is associated with transcriptional repression and inactive chromatin. Two activities have been identified, MeCP1 and MeCP2, which bind specifically to DNA containing methyl-CpG pairs. In this report we characterize MeCP2. We show that it is more abundant than MeCP1, is more tightly bound in the nucleus, and is distinguishable chromatographically. The two proteins share widespread expression in somatic mammalian cells, and barely detectable expression in early embryonic cells. DNAs containing thymidine which has a methyl group at position 5 are not ligands for the MeCPs. The possible role of MeCP2 in methylation-associated gene inactivation was tested in in vitro transcription extracts. Purified MeCP2 inhibited transcription from both methylated and nonmethylated DNA templates in vitro, probably due to the presence of nonspecific DNA binding domains within the protein. We hypothesise that MeCP2 normally binds methylated DNA in the context of chromatin, contributing to the long-term repression and nuclease-resistance of methyl-CpGs.
Ink-Jet Printing of Catalyst Patterns for Electroless Metal Deposition (1999)

ADVERTISEMENT RETURN TO ISSUEPREVNoteNEXTInk-Jet Printing of Catalyst Patterns for Electroless Metal DepositionPratik Shah, Yannis Kevrekidis, and Jay BenzigerView Author Information Department of Chemical Engineering, Princeton University, Princeton, New Jersey 08544-5263 Cite this: Langmuir 1999, 15, 4, 1584–1587Publication Date (Web):January 20, 1999Publication History Received20 July 1998Revised30 October 1998Published online20 January 1999Published inissue 1 February 1999https://pubs.acs.org/doi/10.1021/la9809123https://doi.org/10.1021/la9809123brief-reportACS PublicationsCopyright © 1999 American Chemical SocietyRequest reuse permissionsArticle Views1238Altmetric-Citations63LEARN 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 SUBJECTS:Copper,Deposition,Inkjet printing,Optical properties,Platinum Get e-Alerts
The Conformational Switch from the Factor X Zymogen to Protease State Mediates Exosite Expression and Prothrombinase Assembly (2008)

Zymogens of the chymotrypsin-like serine protease family are converted to the protease state following insertion of a newly formed, highly conserved N terminus. This transition is accompanied by active site formation and ordering of several surface loops in the catalytic domain. Here we show that disruption of this transition in factor X through mutagenesis (FXa(I16L) and FXa(V17A)) not only alters active site function, but also significantly impairs Na(+) and factor Va binding. Active site binding was improved in the presence of high NaCl or with saturating amounts of factor Va membranes, suggesting that allosteric linkage exists between these sites. In line with this, irreversible stabilization of FXa(I16L) with Glu-Gly-Arg-chloromethyl ketone fully rescued FVa binding. Furthermore, the K(m) for prothrombin conversion with the factor Xa variants assembled into prothrombinase was unaltered, whereas the k(cat) was modestly reduced (3- to 4-fold). These findings show that intramolecular activation of factor X following the zymogen to protease transition not only drives catalytic site activation but also contributes to the formation of the Na(+) and factor Va binding sites. This structural plasticity of the catalytic domain plays a key role in the regulation of exosite expression and prothrombinase assembly.
Schistosoma mansoni Worms Induce Anergy of T Cells via Selective Up-Regulation of Programmed Death Ligand 1 on Macrophages (2004)

Infectious pathogens can selectively stimulate activation or suppression of T cells to facilitate their survival within humans. In this study we demonstrate that the trematode parasite Schistosoma mansoni has evolved with two distinct mechanisms to suppress T cell activation. During the initial 4- to 12-wk acute stages of a worm infection both CD4(+) and CD8(+) T cells are anergized. In contrast, infection with male and female worms induced T cell anergy at 4 wk, which was replaced after egg laying by T cell suppression via a known NO-dependent mechanism, that was detected for up to 40 wk after infection. Worm-induced anergy was mediated by splenic F4/80(+) macrophages (Mphi) via an IL-4-, IL-13-, IL-10-, TGF-beta-, and NO-independent, but cell contact-dependent, mechanism. F4/80(+) Mphi isolated from worm-infected mice were shown to induce anergy of naive T cells in vitro. Furthermore, naive Mphi exposed to live worms in vitro also induced anergy in naive T cells. Flow cytometry on in vivo and in vitro worm-modulated Mphi revealed that of the family of B7 costimulatory molecules, only programmed death ligand 1 (PD-L1) was selectively up-regulated. The addition of inhibitory mAb against PD-L1, but not PD-L2, to worm-modulated Mphi completely blocked the ability of these cells to anergize T cells. These data highlight a novel mechanism through which S. mansoni worms have usurped the natural function of PD-L1 to reduce T cell activation during early acute stages of infection before the subsequent emergence of egg-induced T cell suppression in the chronic stages of infection.
L-Phenylalanine ammonia-lyase (maize, potato, and Rhodotorula glutinis). Studies of the prosthetic group with nitromethane (1975)

Highly purified enzyme (EC 4.1.3.5) from Rhodotorula glutinis was shown by sodium dodecyl sulfate gel electrophoresis to have subunits which if not identical are closely similar in molecular weight. Like the enzyme from maize and potato [Havir, E. A., and Hanson, K. R. (1973), Biochemistry 12, 1583] it is a tetramer of molecular weight similar to 4 times 83,000. Enzyme from all three sources inactivated and labeled at the active site with 14-CH3NO2 gave on HCl hydrolysis 14-CO2, H-14-CO2H, D- and L-[14-C]aspartic acid, and unidentified radioactive products. In addition, the labeled R. glutinis enzyme gave [1,2-14-C2]glycine. The formation of the first three products is compatible with the hypothesis that the electrophilic prosthetic group of the enzyme contains the dehydroalanine imine system greater than C equals to N minus C-alpha(equals to C-beta-H2)COminus and inactivation involves attack on C-beta. The second-order rate constants for CH3NO2 inactivation varied with pH as a simple titration curve. The pKa values calculated from the curves for the three enzymes differed and were lower than the pKa of CH3NO2 by at least 1 pH unit. Apparently the inactivation process is enzyme catalyzed. Both inactivation and addition of the substrate amino group may occur with attack on C-beta.
IC14, a CD14 specific monoclonal antibody, is a potential treatment for patients with severe sepsis (2001)

CD14 is a pattern recognition receptor for the bacterial cell wall components from Gram-positive and Gram-negative bacteria as well as mycobacteria. Binding of lipopolysaccharide (LPS) or other cell wall constituents to CD14 initiates signal transduction through the Toll-like receptors resulting in the release of pro-inflammatory cytokines and the initiation of the systemic inflammatory response. In rabbits and non-human primates, CD14 specific antibodies were shown to attenuate responses to LPS or Escherichia coli challenge including pro-inflammatory cytokine release, acute lung injury, hypotension and changes in lung, liver, spleen and adrenal gland morphology. In healthy human subjects, single doses of a chimeric CD14 antibody (IC14) have been shown to be well tolerated and result in a dose-related degree of saturation of CD14 receptors on monocytes and granulocytes. Pretreatment of healthy subjects with IC14 2 h prior to LPS resulted in an attenuation of the LPS-induced fever, clinical symptoms, and leukocyte activation and degranulation. IC14 inhibited the release of TNF-alpha, IL-6, and IL-10 and delayed the release of sTNFR(I) and IL-1ra. Further studies are in progress to characterize the safety and clinical pharmacology of IC14 in patients with severe sepsis.
The roles of SRA1 gene in breast cancer (2011)

The Steroid receptor RNA activator (SRA) gene has been implicated in estrogen receptor signaling pathw ay. First identified as a RNA coregulator, SRA had been shown to increase steroid receptor activity. SRA RNA exp ression is altered during breast tumorigenesis and its molecul ar role in underscoring these events has been sugge sted. The subsequent identification of molecules capable of b inding SRA, including RNA helicase p68, SRA stem-loop interacting RNA binding protein (SLIRP), and steroi dogenic factor 1 (SF1) indicates SRA function is no t exclusively limited to modulate steroid receptor activity. A re cent genome-wide expression analysis by depleting SRA in cancer cells has further expanded our understanding of a b roader biological role played by SRA. In addition, several RNA isoforms have been found to encode an endogenous protein (SRAP), which is well conserved among Chordata. Interestingly, SRAP also modulates steroid receptor activity and functions as a co-regulator in estrog en receptor signaling. The recent observation that a higher exp ression of SRAP protein is associated with poorer s urvival in breast cancer patients treated with tamoxifen, highlights the potential relevance of this protein in cancer. Together, the SRA1 gene encodes both functional RNA and protein (SRAP) products, making it a unique member amongst the growing population of steroid receptor co-regulators.
PMPA in perspective. (1995)

PMPA, an experimental anti-HIV drug, is a member of a new class of drugs called nucleotide analogs. PMPA gained attention when it was reported that it completely protected macaque monkeys from SIV (a virus closely related to HIV). No other potential treatment has been able to do this. It is difficult to tell how quickly nucleotide analogs can work because, for unknown reasons, viral loads show only modest reductions even when other information suggests that they may be working better than the viral loads imply. PMPA is undergoing standard animal toxicology tests in preparation for human trials. The first nucleotide analog likely to reach widespread human use is bis-POM PMEA, since it is already in human trials.
Pharmacodynamics, Pharmacokinetics, Safety, and Tolerability of Albiglutide, a Long-Acting Glucagon-Like Peptide-1 Mimetic, in Patients with Type 2 Diabetes (2008)

Albiglutide improved fasting plasma glucose and postprandial glucose with a favorable safety profile in subjects with type 2 diabetes. Albiglutide's long half-life may allow for once-weekly or less frequent dosing.
N-Terminal Deletion of Peptide:N-Glycanase Results in Enhanced Deglycosylation Activity (2009)

Peptide:N-glycanase catalyzes the detachment of N-linked glycan chains from glycopeptides or glycoproteins by hydrolyzing the beta-aspartylglucosaminyl bond. Peptide:N-glycanase in yeast binds to Rad23p through its N-terminus. In this study, the complex formed between Peptide:N-glycanase and Rad23p was found to exhibit enhanced deglycosylation activity, which suggests an important role for this enzyme in the misfolded glycoprotein degradation pathway in vivo. To investigate the role of this enzyme in this pathway, we made stepwise deletions of the N-terminal helices of peptide:N-glycanase. Enzymatic analysis of the deletion mutants showed that deletion of the N-terminal H1 helix (Png1p-DeltaH1) enhanced the deglycosylation activity of N-glycanase towards denatured glycoproteins. In addition, this mutant exhibited high deglycosylation activity towards native glycoproteins. Dynamic simulations of the wild type and N-terminal H1 deletion mutant implied that Png1p-DeltaH1 is more flexible than wild type Png1p. The efficient deglycosylation of Png1p-DeltaH1 towards native and non-native glycoproteins offers a potential biotechnological application.
Acid-induced Lung Injury: Protective Effect of Anti-interleukin-8 Pretreatment on Alveolar Epithelial Barrier Function in Rabbits (1999)

Although prior experimental work has demonstrated that anti-interleukin-8 (anti-IL-8) therapy reduces lung endothelial injury after acid instillation, there is no information regarding the effect of anti-IL-8 on the function of the alveolar epithelial barrier after acid-induced lung injury. Therefore, the primary objective of this study was to determine the effect of acid-induced lung injury on the function of the alveolar epithelium, and secondly to determine whether pretreatment with anti-IL-8 attenuates acid-induced injury to the lung epithelial barrier. Hydrochloric acid (pH = 1.5 in 1/3 normal saline) was instilled into the lungs of anesthetized, ventilated rabbits. Anti-IL-8 monoclonal antibody (2 mg/kg) or saline was given intravenously 5 min before acid instillation. Acid instillation into the distal airspaces caused an increase in the alveolar epithelial permeability to protein and an approximately 50% reduction in net alveolar fluid clearance. Because a decrease in net alveolar fluid clearance could be due to lung endothelial injury and increased fluid flux from the blood into the airspaces, additional experiments were carried out in which pulmonary blood flow was eliminated. In the absence of pulmonary blood flow, acid instillation led to a 50% decrease in net alveolar fluid clearance. Pretreatment with anti-IL-8 antibody significantly reduced the acid-mediated increase in bi-directional transport of protein across the alveolar epithelium and restored alveolar fluid clearance to normal. The results indicate that acid instillation causes injury to the alveolar epithelial barrier that can be distinguished from the injury to the lung endothelium. Furthermore, pretreatment with anti-IL-8 therapy prevents acid-induced alveolar epithelial injury, a finding of potential clinical importance.
Combinational Immunotherapy with Allo-DRibble Vaccines and Anti-OX40 Co-Stimulation Leads to Generation of Cross-Reactive Effector T Cells and Tumor Regression (2016)

It is well-known that vaccines comprising of irradiated whole tumor cells or tumor-derived heat shock proteins can generate tumor-specific immune responses. In contrast, we showed recently that vaccines composed of autophagosomes (DRibbles) derived from syngeneic sarcomas could induce cross-reactive T-cell responses and cross-protection against the tumor. This unusual property of DRibbles was related to the selective recruitment of defective ribosomal products (DRiPs) and other short-lived proteins (SLiPs) into autophagosomes via sequestosome (SQSTM1, p62) mediated association of ubiquitinated SLiPs to the autophagy gene product LC3. Here, we extend our observations to mammary carcinomas from mice of different genetic background. We demonstrated that combined of intranodal administration of autologous or allogeneic DRibbles together with anti-OX40 antibody led to robust proliferation, expansion, and differentiation of memory and effector T cells. We also showed that SLiPs is an excellent source of antigen for cross-priming of CD8<sup>+</sup> T-cells that recognize shared tumor antigens in the context of host MHC class I molecules. Thus, our results provide a strong basis for novel clinical trials that combine allogeneic "off-the-shelf" DRibble vaccines together with antibodies against co-stimulatory molecules.
Two glycosyltransferase genes, lgtF and rfaK, constitute the lipooligosaccharide ice (inner core extension) biosynthesis operon of Neisseria meningitidis (1996)

We have characterized an operon required for inner-core biosynthesis of the lipooligosaccharide (LOS) of Neisseria meningitidis. Using Tn916 mutagenesis, we recently identified the alpha-1,2-N-acetylglucosamine (GlcNAc) transferase gene (rfaK), which when inactivated prevents the addition of GlcNAc and alpha chain to the meningococcal LOS inner core (C. M. Kahler, R. W. Carlson, M. M. Rahman, L. E. Martin, and D. S. Stephens, J. Bacteriol. 178:1265-1273, 1996). During the study of rfaK, a second open reading frame (lgtF) of 720 bp was found upstream of rfaK. An amino acid sequence homology search of the GenBank and EMBL databases revealed that the amino terminus of LgtF has significant homology with a family of beta-glycosyltransferases involved in the biosynthesis of polysaccharides and O antigen of lipopolysaccharides. The chromosomal copy of lgtF was mutagenized with a nonpolar antibiotic resistance cassette to minimize potential polar effects on rfaK. Tricine sodium dodecyl sulfate-polyacrylamide gel electrophoresis and composition analysis of the LOS from the nonpolar lgtF mutant showed that this strain produced a truncated LOS structure which contained a LOS inner core of GlcNAc1Hep2KDO2lipid A but without the addition of lacto-N-neotetraose to HepI or glucose to HepII. These results and the amino acid homology with beta-glycosyltransferases suggest that lgtF encodes the UDP-glucose:LOS-beta-1,4-glucosyltransferase which attaches the first glucose residue to HepI of LOS. Reverse transcriptase PCR and primer extension analysis indicate that both lgtF and rfaK are cotranscribed as a polycistronic message from a promoter upstream of lgtF. This arrangement suggests that completion of the LOS inner core and the initiation of the alpha chain addition are tightly coregulated in N. meningitidis.
Effect of step-synchronized vibration stimulation of soles on gait in Parkinson's disease: a pilot study (2006)

Augmented sensory feedback improves parkinsonian gait steadiness in the short-term setting. Because the suprathreshold stimulation prevented blinding of subjects, the learning effect and increased attention can be a confounding factor underlying results. Long-term studies are needed to establish the clinical value of the S-VS.
TREM2-activating antibodies abrogate the negative pleiotropic effects of the Alzheimer's disease variant Trem2R47H on murine myeloid cell function (2018)

Triggering receptor expressed on myeloid cells 2 (TREM2) is an orphan immune receptor expressed on cells of myeloid lineage such as macrophages and microglia. The rare variant R47H TREM2 is associated with an increased risk for Alzheimer's disease, supporting the hypothesis that TREM2 loss of function may exacerbate disease progression. However, a complete knockout of the <i>TREM2</i> gene in different genetic models of neurodegenerative diseases has been reported to result in both protective and deleterious effects on disease-related end points and myeloid cell function. Here, we describe a <i>Trem2</i><sup>R47H</sup> transgenic mouse model and report that even in the absence of additional genetic perturbations, this variant clearly confers a loss of function on myeloid cells. The <i>Trem2</i><sup>R47H</sup> variant-containing myeloid cells exhibited subtle defects in survival and migration and displayed an unexpected dysregulation of cytokine responses in a lipopolysaccharide challenge environment. These subtle phenotypic defects with a gradation in severity across genotypes were confirmed in whole-genome RNA-Seq analyses of WT, <i>Trem2</i><sup>-/-</sup>, and <i>Trem2</i><sup>R47H</sup> myeloid cells under challenge conditions. Of note, TREM2-activating antibodies that boost proximal signaling abrogated survival defects conferred by the variant and also modulated migration and cytokine responses in an antibody-, ligand-, and challenge-dependent manner. In some instances, these antibodies also boosted WT myeloid cell function. Our studies provide a first glimpse into the boost in myeloid cell function that can be achieved by pharmacological modulation of TREM2 activity that can potentially be ameliorative in neurodegenerative diseases such as Alzheimer's disease.
Where do all the placentas go? (1994)

Re-examining the disposal of placentas as pathological waste is suggested by the author. Placentas can be reprocessed safely for the production of blood derivatives necessary for human treatment by following accepted infection control guidelines in collection, transportation and reprocessing in approved medical laboratories. Money can be saved by removing placentas from the pathological waste stream. Historically, infection control reasons have often been cited as the rationale for preventing changes in the perinatal area. It may be time for infection control teams, administrators and obstetrical staff to review the ethical, legal and infection control issues related to disposal of placentas.