gebhart/patrepeval huggingface dataset:
Oxidation-Reduction Potentials of Thiol-Dithio Systems: Thiourea-Formamidine Disulfide1 (1947)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTOxidation-Reduction Potentials of Thiol-Dithio Systems: Thiourea-Formamidine Disulfide1Paul W. Preisler and Louis BergerCite this: J. Am. Chem. Soc. 1947, 69, 2, 322–325Publication Date (Print):February 1, 1947Publication History Published online1 May 2002Published inissue 1 February 1947https://pubs.acs.org/doi/10.1021/ja01194a048https://doi.org/10.1021/ja01194a048research-articleACS PublicationsRequest reuse permissionsArticle Views898Altmetric-Citations94LEARN 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
Cytosine base editor 4 but not adenine base editor generates off-target mutations in mouse embryos (2020)

Deaminase base editing has emerged as a tool to install or correct point mutations in the genomes of living cells in a wide range of organisms. However, the genome-wide off-target effects introduced by base editors in the mammalian genome have been examined in only one study. Here, we have investigated the fidelity of cytosine base editor 4 (BE4) and adenine base editors (ABE) in mouse embryos using unbiased whole-genome sequencing of a family-based trio cohort. The same sgRNA was used for BE4 and ABE. We demonstrate that BE4-edited mice carry an excess of single-nucleotide variants and deletions compared to ABE-edited mice and controls. Therefore, an optimization of cytosine base editors is required to improve its fidelity. While the remarkable fidelity of ABE has implications for a wide range of applications, the occurrence of rare aberrant C-to-T conversions at specific target sites needs to be addressed.
Phosphomimetic Mutations Enhance Oligomerization of Phospholemman and Modulate Its Interaction with the Na/K-ATPase (2011)

Na/K-ATPase (NKA) activity is dynamically regulated by an inhibitory interaction with a small transmembrane protein, phospholemman (PLM). Inhibition is relieved upon PLM phosphorylation. Phosphorylation may alter how PLM interacts with NKA and/or itself, but details of these interactions are unknown. To address this, we quantified FRET between PLM and its regulatory target NKA in live cells. Phosphorylation of PLM was mimicked by mutation S63E (PKC site), S68E (PKA/PKC site), or S63E/S68E. The dependence of FRET on protein expression in live cells yielded information about the structure and binding affinity of the PLM-NKA regulatory complex. PLM phosphomimetic mutations altered the quaternary structure of the regulatory complex and reduced the apparent affinity of the PLM-NKA interaction. The latter effect was likely due to increased oligomerization of PLM phosphomimetic mutants, as suggested by PLM-PLM FRET measurements. Distance constraints obtained by FRET suggest that phosphomimetic mutations slightly alter the oligomer quaternary conformation. Photon-counting histogram measurements revealed that the major PLM oligomeric species is a tetramer. We conclude that phosphorylation of PLM increases its oligomerization into tetramers, decreases its binding to NKA, and alters the structures of both the tetramer and NKA regulatory complex.
The genome sequence of Bifidobacterium longum subsp. infantis reveals adaptations for milk utilization within the infant microbiome (2008)

Following birth, the breast-fed infant gastrointestinal tract is rapidly colonized by a microbial consortium often dominated by bifidobacteria. Accordingly, the complete genome sequence of Bifidobacterium longum subsp. infantis ATCC15697 reflects a competitive nutrient-utilization strategy targeting milk-borne molecules which lack a nutritive value to the neonate. Several chromosomal loci reflect potential adaptation to the infant host including a 43 kbp cluster encoding catabolic genes, extracellular solute binding proteins and permeases predicted to be active on milk oligosaccharides. An examination of in vivo metabolism has detected the hallmarks of milk oligosaccharide utilization via the central fermentative pathway using metabolomic and proteomic approaches. Finally, conservation of gene clusters in multiple isolates corroborates the genomic mechanism underlying milk utilization for this infant-associated phylotype.
Magnetic Resonance Imaging of the Breast (2001)

MRI of the breast is emerging as a valuable adjunct to mammography and sonography for specific clinical indications. Additional clinical studies that define indications, interpretation criteria, imaging parameters, and cost effectiveness are needed. A multi-institutional study designed to address these issues is in progress.
What Are They Blogging About? Personality, Topic and Motivation in Blogs (2009)

Personal weblogs (blogs), provide individuals with the opportunity to write freely and express themselves online in the presence of others. In such situations, what do bloggers write about, and what are their motivations for blogging? Using a large blog corpus annotated with the LIWC text analysis program, we examine the content of blogs to provide insight into the role of personality in motivation for blogging. As predicted, we find that highly Neurotic authors use blogs to serve a cathartic or auto-therapeutic function, and reflect mainly upon themselves and negative emotions. Highly Extraverted blog authors, as expected, use blogs to document their lives at a high level, and uniquely interact directly with the reader. Additionally Extraverts use blogs to vent both positive and negative emotions. Bloggers who are high scorers on the Openness trait are more concerned with leisure activities, although they are more evaluative than intellectual, whereas high Conscientiousness bloggers tend to report daily life – and work – around them. As in other contexts, expressing positive rather than negative emotions is associated with high Agreeableness, but that trait is associated with self reference to a greater degree in blogs than elsewhere. In general, findings are consistent with other contexts indicating that bloggers tend to adapt to the possibilities of the medium, rather than try to present themselves differently.
Analysis of CC chemokine and chemokine receptor expression in solid ovarian tumours (2001)

To understand the chemokine network in a tissue, both chemokine and chemokine receptor expression should be studied. Human epithelial ovarian tumours express a range of chemokines but little is known about the expression and localisation of chemokine receptors. With the aim of understanding chemokine action in this cancer, we investigated receptors for CC-chemokines and their ligands in 25 biopsies of human ovarian cancer. CC-chemokine receptor mRNA was generally absent from solid tumours, the exception being CCR1 which was detected in samples from 75% of patients. CCR1 mRNA localised to macrophages and lymphocytes and there was a correlation between numbers of CD8(+) and CCR1 expressing cells (P = 0.031). mRNA for 6 CC-chemokines was expressed in a majority of tumour samples. In a monocytic cell line in vitro, we found that CCR1 mRNA expression was increased 5-fold by hypoxia. We suggest that the CC-chemokine network in ovarian cancer is controlled at the level of CC-chemokine receptors and this may account for the phenotypes of infiltrating cells found in these tumours. The leukocyte infiltrate may contribute to tumour growth and spread by providing growth survival factors and matrix metalloproteases. Thus, CCR1 may be a novel therapeutic target in ovarian cancer.
Magnetic Effects in Chemical Reactions (1976)

The Review discusses in what elementary chemical reactions the intrinsic angular momentum of electrons and nuclei is conserved and in what reactions it is not conserved, how weak electron-nuclear magnetic interaction and an external magnetic field influence the conservation of angular momentum and what are the consequences of this effect, and what magnetic effects occur in chemical reactions, as well as the conditions for their development and detection. Conditions are formulated for the non-conservation of the intrinsic angular momentum of electrons and nuclei in chemical reactions. The bibliography contains 36 references.
Portal fibrosis and hepatic steatosis in morbidly obese subjects: A spectrum of nonalcoholic fatty liver disease (2004)

Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that can lead to hepatic fibrosis and cirrhosis. Portal fibrosis in the absence of NASH, called isolated portal fibrosis (IPF), has received less attention and has not been classified as a spectrum of NAFLD. The aims of this study were to determine the prevalence of IPF in subjects undergoing gastric bypass surgery, to identify biochemical variables associated with IPF, and to assess the metabolic syndrome as defined by the AdultTreatment Panel III criteria. We analyzed liver biopsies from 195 morbidly obese subjects after excluding all other causes of liver disease. The prevalence of fatty liver (FL) only, IPF, and NASH was 30.3%, 33.3%, and 36.4%, respectively. Several biochemical parameters significantly trended across the 3 groups, with IPF falling between FL and NASH. Hyperglycemia was the only metabolic parameter associated with NASH (OR, 5.4; 95% CI, 2.4-12; P < .0001) and IPF (OR, 2.8; 95% CI, 1.2-6.5; P = .01). Subjects with diabetes had the greatest risk for NASH (OR, 8; 95% CI, 3.3-19.7; P < .0001) and IPF (OR, 4.3; 95% CI, 1.6-11.6; P = .003). The metabolic syndrome was identified in 78.5% of subjects, and a significant trend for the number of metabolic criteria was observed across the spectrum of FL, IPF, and NASH. In conclusion, a significant subset of morbidly obese individuals has portal fibrosis in the absence of NASH that is associated with glycemic dysregulation. Therefore, IPF should be considered a spectrum of NAFLD that may prelude NASH in morbid obesity.
IL6 and CRPhaplotypes are associated with COPD risk and systemic inflammation: a case-control study (2009)

Our findings suggest that common genetic variation in CRP and IL6 genes may contribute to heterogeneity of COPD population associated with systemic inflammation.
Brain Plasticity and Stroke Rehabilitation (2000)

Neuronal connections and cortical maps are continuously remodeled by our experience. Knowledge of the potential capabilityof the brain to compensate for lesions is a prerequisite for optimal stroke rehabilitation strategies. Experimental focal cortical lesions induce changes in adjacent cortex and in the contralateral hemisphere. Neuroimaging studies in stroke patients indicate altered poststroke activation patterns, which suggest some functional reorganization. To what extent functional imaging data correspond to outcome data needs to be evaluated. Reorganization may be the principle process responsible for recovery of function after stroke, but what are the limits, and to what extent can postischemic intervention facilitate such changes? Postoperative housing of animals in an enriched environment can significantly enhance functional outcome and can also interact with other interventions, including neocortical grafting. What role will neuronal progenitor cells play in future rehabilitation-stimulated in situ or as neural replacement? And what is the future for blocking neural growth inhibitory factors? Better knowledge of postischemic molecular and neurophysiological events, and close interaction between basic and applied research, will hopefully enable us to design rehabilitation strategies based on neurobiological principles in a not-too-distant future.
Transfer of tissue factor from leukocytes to platelets is mediated by CD15 and tissue factor (2000)

Abstract We describe thrombogenic tissue factor (TF) on leukocyte-derived microparticles and their incorporation into spontaneous human thrombi. Polymorphonuclear leukocytes and monocytes transfer TF+particles to platelets, thereby making them capable of triggering and propagating thrombosis. This phenomenon calls into question the original dogma that vessel wall injury and exposure of TF within the vasculature to blood is sufficient for the occurrence of arterial thrombosis. The transfer of TF+ leukocyte-derived particles is dependent on the interaction of CD15 and TF with platelets. Both the inhibition of TF transfer to platelets by antagonizing the interaction CD15 with P-selectin and the direct interaction of TF itself suggest a novel therapeutic approach to prevent thrombosis.
The positive activator of cephamycin C and clavulanic acid production in Streptomyces clavuligerus is mistranslated in a bldA mutant The GenBank accession number for the sequence reported in this paper is AF436078. (2002)

In Streptomyces coelicolor bldA encodes the principal leucyl tRNA for translation of UUA codons and controls pigmented antibiotic production by the presence of TTA codons in the genes encoding the pathway-specific activators of actinorhodin and undecylprodigiosin biosynthesis. In Streptomyces clavuligerus the gene encoding the pathway-specific activator of both cephamycin C and clavulanic acid production, ccaR, also contains a TTA codon and was expected to exhibit bldA-dependence. A cloned S. clavuligerus DNA fragment containing a sequence showing 91% identity to the S. coelicolor bldA-encoded tRNA was able to restore antibiotic production and sporulation to bldA mutants of S. coelicolor and the closely related Streptomyces lividans. A null mutation of the bldA gene in S. clavuligerus resulted in the expected sporulation defective phenotype, but unexpectedly had no effect on antibiotic production. Transcript analysis showed no difference in the levels of ccaR transcripts in the wild-type and bldA mutant strains, ruling out any effect of elevated levels of the ccaR mRNA. Furthermore, when compared to the wild-type strain, the bldA mutant showed no differences in the levels of CcaR, suggesting that the single TTA codon in ccaR is mistranslated efficiently. The role of codon context in bldA dependence is discussed.
Identification, characterization, and comparative genomic distribution of the HERV-K (HML-2) group of human endogenous retroviruses (2011)

Our analysis has found and corrected several errors in the annotation of HML-2 elements in the human genome, including mislabeling of a newly identified group called HML-11. HML-elements have been implicated in a wide array of diseases, and characterization of these elements will play a fundamental role to understand the relationship between endogenous retrovirus expression and disease.
Tumor and metastasis suppression by the human RNASET2 gene (2005)

The region 6q27 from human chromosome 6 has been reported to contain one or more tumor suppressor genes on the basis of cytogenetic, molecular and functional studies. We have recently carried out a detailed analysis of a candidate gene from 6q27 to evaluate its putative role as a tumor suppressor gene involved in ovarian cancer pathogenesis. The RNASET2 gene was shown to behave as a class II tumor suppressor and abolish the tumorigenic potential of an ovarian cancer-derived cell line. In this study, we have started the cellular and biochemical characterization of RNASET2 and showed that it is a secreted glycoprotein. Moreover, we have extended our previous studies by evaluating the effect of RNASET2 on the metastatic behavior of the highly-invasive ovarian cancer cell line HEY3MET2. From such analysis, RNASET2 was found to significantly decrease the metastatic potential of this cell line in vivo. Moreover, RNASET2-mediated suppression of tumorigenesis and metastasis was not affected by a double point mutation targeted to the putative ribonuclease catalytic sites, suggesting that tumor suppression by RNASET2 is not mediated by its ribonuclease activity. The potential biological implications of this unexpected finding are discussed in relation to the current evolutionary models.
Phosphorylation of Arfaptin 2 at Ser260 by Akt Inhibits PolyQ-huntingtin-induced Toxicity by Rescuing Proteasome Impairment (2005)

Huntington disease (HD) is caused by an abnormal expanded polyglutamine repeat in the huntingtin protein. Insulin-like growth factor-1 is of particular interest in HD because it strongly inhibits polyQ-huntingtin-induced neurotoxicity. This neuroprotective effect involves the phosphorylation of huntingtin at Ser(421) by the prosurvival kinase Akt (Humbert, S., Bryson, E. A., Cordelieres, F. P., Connors, N. C., Datta, S. R., Finkbeiner, S., Greenberg, M. E., and Saudou, F. (2002) Dev. Cell 2, 831-837). Here, we report that Akt inhibits polyQ-huntingtin-induced toxicity in the absence of phosphorylation of huntingtin at Ser(421), suggesting that Akt also acts on other downstream effector(s) to prevent neuronal death in HD. We show that this survival effect involves the ADP-ribosylation factor-interacting protein arfaptin 2, the levels of which are increased in HD patients. Akt phosphorylated arfaptin 2 at Ser(260). Lack of phosphorylation of arfaptin 2 at this site substantially modified its subcellular distribution and increased neuronal death and intranuclear inclusions caused by polyQ-huntingtin. In contrast, arfaptin 2 had a neuroprotective effect on striatal neurons when phosphorylated by Akt. This effect is mediated through the proteasome, as phosphorylated arfaptin 2 inhibited the blockade of the proteasome induced by polyQ-huntingtin. This study points out a new mechanism by which Akt promotes neuroprotection in HD, emphasizing the potential therapeutic interest of this pathway in the disease.
Sound Retrieval and Ranking Using Sparse Auditory Representations (2010)

To create systems that understand the sounds that humans are exposed to in everyday life, we need to represent sounds with features that can discriminate among many different sound classes. Here, we use a sound-ranking framework to quantitatively evaluate such representations in a large-scale task. We have adapted a machine-vision method, the passive-aggressive model for image retrieval (PAMIR), which efficiently learns a linear mapping from a very large sparse feature space to a large query-term space. Using this approach, we compare different auditory front ends and different ways of extracting sparse features from high-dimensional auditory images. We tested auditory models that use an adaptive pole-zero filter cascade (PZFC) auditory filter bank and sparse-code feature extraction from stabilized auditory images with multiple vector quantizers. In addition to auditory image models, we compare a family of more conventional mel-frequency cepstral coefficient (MFCC) front ends. The experimental results show a significant advantage for the auditory models over vector-quantized MFCCs. When thousands of sound files with a query vocabulary of thousands of words were ranked, the best precision at top-1 was 73% and the average precision was 35%, reflecting a 18% improvement over the best competing MFCC front end.
Accurate latency-based congestion feedback for datacenters (2015)

The nature of congestion feedback largely governs the behavior of congestion control. In datacenter networks, where RTTs are in hundreds of microseconds, accurate feedback is crucial to achieve both high utilization and low queueing delay. Proposals for datacenter congestion control predominantly leverage ECN or even explicit in-network feedback (e.g., RCP-type feedback) to minimize the queuing delay. In this work we explore latency-based feedback as an alternative and show its advantages over ECN. Against the common belief that such implicit feed-back is noisy and inaccurate, we demonstrate that latency-based implicit feedback is accurate enough to signal a single packet’s queuing delay in 10 Gbps networks. DX enables accurate queuing delay measurements whose error falls within 1.98 and 0.53 microseconds us-ing software-based and hardware-based latency measure-ments, respectively. This enables us to design a new congestion control algorithm that performs fine-grained control to adjust the congestion window just enough to achieve very low queuing delay while attaining full utiliza-tion. Our extensive evaluation shows that 1) the latency measurement accurately reflects the one-way queuing de-lay in single packet level; 2) the latency feedback can be used to perform practical and fine-grained congestion control in high-speed datacenter networks; and 3) DX outperforms DCTCP with 5.33x smaller median queueing delay at 1 Gbps and 1.57x at 10 Gbps. 1
Formulation Of An Immunogenic Human Cytomegalovirus Vaccine: Responses In Mice (1995)

The immunogenicity of a vaccine formulation consisting of recombinant-derived human cytomegalovirus (HCMV) glycoprotein B (UL55) combined with a chemically defined adjuvant derived from saponin, QS-21, was evaluated in mice. The immune responses of mice given the gB/QS-21 formulation were compared with those induced by gB combined with either Freund's adjuvant or aluminum hydroxide. The gB/QS-21 combination induced higher levels of virus-binding antibodies and significantly higher levels of virus-neutralizing antibodies than gB combined with either Freund's adjuvant or aluminum hydroxide. Animals given gB/QS-21 exhibited IgG subclass switching and produced significant titers of virus-specific IgG2a antibodies. Furthermore, animals given gB/QS-21 produced antigen-specific cytotoxic spleen cells. Because of its immunogenicity, a subunit vaccine containing HCMV gB and QS-21 offers a potential approach to the immunoprophylaxis of HCMV disease.
Neuropeptides and appetite: contribution of neuropharmacological modeling. (1984)

It is now clear that a variety of neuropeptides interact with the more classically defined neurotransmitters to stimulate or inhibit feeding. An extensive peripheral peptide satiety system has been identified. Peptides involved in this system include cholecystokinin, bombesin, gastrin-releasing peptide, glucagon, somatostatin, and possibly thyrotropin-releasing hormone and calcitonin. Some of these peptides appear to inhibit feeding by activating ascending fibers in the vagus, whereas others exert their actions independent of the vagus. In addition, neuropeptides appear to play a role in producing the neuromodulatory effects of taste on appetite, and hormones from the endocrine system modulate neuropeptide effects on feeding. The central appetite regulatory system appears to be arranged in a cascade, with an interaction between dynorphin and dopamine producing a part of the feeding drive. This drive is held in check by a variety of neuropeptides including calcitonin, corticotropin-releasing factor, and bombesin. In turn, these peptides are modulated by a norepinephrine-alpha-aminobutyric acid (GABA) system. Neurotensin, serotonin, cyclohistidyl proline diketopiperazine, and the peripheral satiety system appear to modulate the norepinephrine-GABA disinhibitory system. By the judicious use of neuropharmacological modeling we have developed a model of the neurotransmitter interactions involved in appetite regulation that can act as a springboard for the design of future experiments to unravel the mysteries of appetite regulation.