gebhart/patrepeval huggingface dataset:
Scaling and Suppression of Anomalous Heating in Ion Traps (2006)

We measure and characterize anomalous motional heating of an atomic ion confined in the lowest quantum levels of a novel rf ion trap that features moveable electrodes. The scaling of heating with electrode proximity is measured, and when the electrodes are cooled from 300 to 150 K, the heating rate is suppressed by an order of magnitude. This provides direct evidence that anomalous motional heating of trapped ions stems from microscopic noisy potentials on the electrodes that are thermally driven. These observations are relevant to decoherence in quantum information processing schemes based on trapped ions and perhaps other charge-based quantum systems.
Molecular Interaction Studies Using Microscale Thermophoresis (2011)

Abstract The use of infrared laser sources for creation of localized temperature fields has opened new possibilities for basic research and drug discovery. A recently developed technology, Microscale Thermophoresis (MST), uses this temperature field to perform biomolecular interaction studies. Thermophoresis, the motion of molecules in temperature fields, is very sensitive to changes in size, charge, and solvation shell of a molecule and thus suited for bioanalytics. This review focuses on the theoretical background of MST and gives a detailed overview on various applications to demonstrate the broad applicability. Experiments range from the quantification of the affinity of low-molecular-weight binders using fluorescently labeled proteins, to interactions between macromolecules and multi-component complexes like receptor containing liposomes. Information regarding experiment and experimental setup is based on the Monolith NT.115 instrument (NanoTemper Technologies GmbH).
Liver Transduction with Recombinant Adeno-Associated Virus Is Primarily Restricted by Capsid Serotype Not Vector Genotype (2005)

We and others have recently reported highly efficient liver gene transfer with adeno-associated virus 8 (AAV-8) pseudotypes, i.e., AAV-2 genomes packaged into AAV-8 capsids. Here we studied whether liver transduction could be further enhanced by using viral DNA packaging sequences (inverted terminal repeats [ITRs]) derived from AAV genotypes other than 2. To this end, we generated two sets of vector constructs carrying expression cassettes embedding a gfp gene or the human factor IX (hfIX) gene flanked by ITRs from AAV genotypes 1 through 6. Initial in vitro analyses of gfp vector DNA replication, encapsidation, and cell transduction revealed a surprisingly high degree of interchangeability among the six genotypes. For subsequent in vivo studies, we cross-packaged the six hfIX variants into AAV-8 and infused mice via the portal vein with doses of 5 x 10(10) to 1.8 x 10(12) particles. Notably, all vectors expressed comparably high plasma hFIX levels within a dose cohort over the following 6 months, concurrent with the finding of equivalent vector DNA copy numbers per cell. Partial hepatectomies resulted in approximately 80% drops of hFIX levels and vector DNA copy numbers in all groups, indicating genotype-independent persistence of predominantly episomal vector DNA. Southern blot analyses of total liver DNA in fact confirmed the presence of identical and mostly nonintegrated molecular vector forms for all genotypes. We conclude that, unlike serotypes, AAV genotypes are not critical for efficient hepatocyte transduction and can be freely substituted. This corroborates our current model for AAV vector persistence in the liver and provides useful information for the future design and application of recombinant AAV.
Experimental reactivation of equid herpesvirus 1 (EHV 1) following the administration of corticosteroids (1985)

Eight ponies were experimentally infected with equid herpesvirus 1 (EHV 1) (subtype 1). All animals showed clinical and serological evidence of infection and virus was isolated from nasal swabs and leucocytes. These ponies were kept in isolation for a further three months during which time complement fixing antibody decreased at least four-fold. Following immunosuppression with dexamethasone and prednisolone subtype 1 virus was recovered from six of the eight animals within 14 days. Five of these six ponies were viraemic and three of them shed virus in nasal secretions; only four displayed significant rises in complement fixing antibody and only two in neutralising antibody. Clinical abnormalities were not detected during reactivation.
Analysis of gene expression in multiple sclerosis lesions using cDNA microarrays (1999)

In multiple sclerosis (MS) patients, a coordinated attack of the immune system against the primary constituents of oligodendrocytes and/or the myelin sheath of oligodendrocytes results in the formation of lesions in the brain and spinal cord. Thus far, however, a limited number of genes that potentially contribute to lesion pathology have been identified. Using cDNA microarray technology, we have performed experiments on MS tissue monitoring the expression pattern of over 5,000 genes and compared the gene expression profile of normal white matter with that found in acute lesions from the brain of a single MS patient. Sixty-two differentially expressed genes were identified, including the Duffy chemokine receptor, interferon regulatory factor-2, and tumor necrosis factor alpha receptor-2 among others. Thus, cDNA microarray technology represents a powerful new tool for the identification of genes not previously associated with the MS disease process.
Noncationic Peptides Obtained From Azurin Preferentially Enter Cancer Cells (2009)

Azurin, a member of the cupredoxin family of copper containing redox proteins, preferentially penetrates human cancer cells and exerts cytostatic and cytotoxic (apoptotic) effects with no apparent activity on normal cells. Amino acids 50 to 77 (p28) of azurin seem responsible for cellular penetration and at least part of the antiproliferative, proapoptotic activity of azurin against a number of solid tumor cell lines. We show by confocal microscopy and fluorescence-activated cell sorting that amino acids 50 to 67 (p18) are a minimal motif (protein transduction domain) responsible for the preferential entry of azurin into human cancer cells. A combination of inhibitors that interfere with discrete steps of the endocytotic process and antibodies for caveolae and Golgi-mediated transport revealed that these amphipathic, alpha-helical peptides are unique. Unlike the cationic cell-penetrating peptides, alpha-helical antennapedia-like, or VP22 type peptides, p18 and p28 are not bound by cell membrane glycosaminoglycans and preferentially penetrate cancer cells via endocytotic, caveosome-directed, and caveosome-independent pathways. Once internalized, p28, but not p18, inhibits cancer cell proliferation initially through a cytostatic mechanism. These observations suggest the azurin fragments, p18 and p28, account for the preferential entry of azurin into human cancer cells and a significant amount of the antiproliferative activity of azurin on human cancer cells, respectively.
Wider bandwidth with high transmission through waveguide bends in two-dimensional photonic crystal slabs (2002)

We demonstrate the use of a defect to improve the transmission property of waveguide bends in two-dimensional photonic crystal slabs. We show that high reflection in the two-dimensional photonic crystal slab previously reported is due to the fact that the waveguide is multimoded at the bend while it is single moded along the straight waveguide. By making the waveguide single moded at the bend, the transmission property can be significantly improved. An extension of more than twice of high-transmission bandwidth is achieved.
Control of Membrane Protein Topology by a Single C-Terminal Residue (2010)

The mechanism by which multispanning helix-bundle membrane proteins are inserted into their target membrane remains unclear. In both prokaryotic and eukaryotic cells, membrane proteins are inserted cotranslationally into the lipid bilayer. Positively charged residues flanking the transmembrane helices are important topological determinants, but it is not known whether they act strictly locally, affecting only the nearest transmembrane helices, or can act globally, affecting the topology of the entire protein. Here we found that the topology of an Escherichia coli inner membrane protein with four or five transmembrane helices could be controlled by a single positively charged residue placed in different locations throughout the protein, including the very C terminus. This observation points to an unanticipated plasticity in membrane protein insertion mechanisms.
Inverted Apical CD24 and Weak EZH2 Expressions Are Phenotypic Characteristics of Pure Invasive Micropapillary Carcinoma of the Breast (2013)

Invasive micropapillary carcinomas (IMPC) of the breast account for less than 2% of all breast cancers and have been recently described as luminal B carcinomas. CD24, CD44, ALDH1 and EZH2 are commonly used as stem-cell markers that display differential expression as a function of stage and molecular type, but their pattern of expression according to this rare histological type remains poorly defined and unknown for EZH2. We assessed expression of these markers in a series of 28 micropapillary breast carcinomas and compared the results with those obtained in a series of luminal A (27 cases) and B (34 cases) invasive carcinomas not otherwise specified (IC-NST). CD24 and CD44 were expressed in most cases. However, CD24 was expressed at the inverted apical membrane in 85% of invasive micropapillary carcinoma and at the apical pole of gland-forming cells in 45% of luminal A (p-val = 6.8 × 10－4) and 13% of luminal B cases (p-val = 1.1 × 10－7). ALDH1 was expressed in the stroma in most tumors, but in only 25%, 11% and 15% in epithelial cells of IMPC, luminal A and B IC-NST, respectively. Nuclear expression of EZH2 was not observed in luminal A tumors, and was detected in 35% (12/34) of luminal B carcinomas (p-val = 6.1 × 10－3) and only 4% (1/28) of invasive micropapillary carcinomas. This series shows that invasive micropapillary carcinomas harbor a CD24-positive inverted apical pole associated with weak EZH2 expression, phenotypical characteristics that distinguish this entity from other luminal carcinomas.
Long-range electron transfer in multisite metalloproteins (1989)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTLong-range electron transfer in multisite metalloproteinsHarry B. Gray and Bo G. MalmstroemCite this: Biochemistry 1989, 28, 19, 7499–7505Publication Date (Print):September 19, 1989Publication History Published online1 May 2002Published inissue 19 September 1989https://pubs.acs.org/doi/10.1021/bi00445a001https://doi.org/10.1021/bi00445a001research-articleACS PublicationsRequest reuse permissionsArticle Views365Altmetric-Citations127LEARN 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
Generation of hydrogen peroxide during brief oxygen‐glucose deprivation induces preconditioning neuronal protection in primary cultured neurons (2005)

Although reactive oxygen species (ROS) have been implicated in ischemic preconditioning (IPC)-induced neuronal protection, several key questions concerning ROS remain to be elucidated. The purpose of this study is to obtain direct evidence for the formation of specific ROS species generated by IPC, and to determine the specific species that is responsible for the observed neuronal protection. Primary cultured cortex neurons from rat embryos were preconditioned with 10 min of oxygen-glucose deprivation (OGD), which increased the intracellular levels of superoxide and hydrogen peroxide. This preconditioning markedly induced neuronal protection against 2-hr OGD stimuli. Preconditioning with exogenous ROS by the administration of xanthine/xanthine oxidase (X/XO), or hydrogen peroxide was also found to induce IPC-like neuronal protection. Administration of hydrogen peroxide scavengers, such as catalase, glutathione, or the thiol reductant N-(2-mercaptopriopionyl)-glycine, all reduced the increase in the intracellular hydrogen peroxide levels, which effectively eliminated IPC- or exogenous ROS-induced neuronal protection. In contrast, administration of the membrane-permeable superoxide dismutase mimic Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride was able to block the increase of intracellular superoxide levels during IPC, but did not abolish either IPC- or exogenous X/XO preconditioning-induced neuronal protection. These findings strongly suggest that IPC enhances the generation of superoxide, which is then converted to hydrogen peroxide, and that hydrogen peroxide is likely the main trigger involved in the mechanism of IPC-induced neuronal protection.
Monoclonal antibodies : production, engineering, and clinical application (1995)

1. Introduction 2. Production of monoclonal antibodies 3. Antigen-antibody interactions: how affinity and kinetics affect assay design and selection procedures 4. The production and characterisation of synthetic peptide-derived antibodies 5. Human monoclonal antibodies 6. Bispecific monoclonal antibodies 7. The production of antibodies using phage display libraries 8. Genetic manipulation of monoclonal antibodies 9. Monoclonal antibodies in diagnostic immunoassays 10A. Monoclonal antibodies in diagnostic pathology 10B. In vivo targeting of monoclonal antibodies for immunoscintigraphy and therapy of human malignancies 11A. Monoclonal antibodies in infectious disease: diagnosis 11B. Monoclonal antibodies in the prophyllaxis and therapy of infectious disease 12A. Monoclonal antibodies in transplantation: immunohistology 12B. Monoclonal antibodies in transplantation: experimental studies on in vivo immunosuppression 12C. Monoclonal antibodies in transplantation: prophyllaxis of graft-versus-host disease after bone marrow transplantation 12D. Monoclonal antibodies in transplantation: use as therapeutic agents in clinical organ transplantation 13. Monoclonal antibodies and the skin 14. Monoclonal antibodies in endocrinology 15. Monoclonal antibodies in rheumatology 16. Technical appendix.
[Reconstruction of bone using tissue engineering and nanoscale technology]. (2006)

Nd : YAG laser could produce nanoscale grooves on the FDBM surface. The nanoscale grooves are conductive to adherence, proliferation and matrix secretion of osteoblasts. Complexes by tissue engineering and nanoscale technology have some osteogenic abilities in vivo after implanted the animal model.
Embryonic Mortality in Domestic Species (1994)

This comprehensive text contains extensive literature citations summarizing available information on causes and possible therapies for reducing embryonic mortality in domestic farm species. Chapters devoted to the cause of embryonic mortality in swine, cattle, sheep (goats) and horses provide in-depth insight. Germinal chapters on fertilization failure, nutritional factors relating to embryonic loss and immunological aspects of embryonic loss are provided.
A Primate-dominant Third Glycosylation Site of the β2-Adrenergic Receptor Routes Receptors to Degradation during Agonist Regulation (2004)

beta(2)-adrenergic receptors (beta(2)AR) of all species are N-linked glycosylated at amino terminus residues approximately 6 and approximately 15. However, the human beta(2)AR has a potential third N-glycosylation site at ECL2 residue 187. To determine whether this residue is glycosylated and to ascertain function, all possible single/multiple Asn --> Gln mutations were made in the human beta(2) AR at positions 6, 15, and 187 and were expressed in Chinese hamster fibroblast cells. Substitution of Asn-187 alone or with Asn-6 or Asn-15 decreased the apparent molecular mass of the receptor on SDS-PAGE in a manner consistent with Asn-187 glycosylation. All receptors bound the agonist isoproterenol and functionally coupled to adenylyl cyclase. However, receptors without 187 glycosylation failed to display long term agonist-promoted down-regulation. In contrast, loss of Asn-6/Asn-15 glycosylation did not alter down-regulation. Cell surface distribution and agonist-promoted internalization of receptors and recruitment of beta-arrestin 2 were unaffected by the loss of 187 glycosylation. Furthermore, acutely internalized wild-type and Gln-187 receptors were both localized by confocal microscopy to early endosomes. During prolonged agonist exposure, wild-type beta(2)AR co-localized with lysosomes, consistent with trafficking to a degradation compartment. However, Gln-187 beta(2)AR failed to co-localize with lysosomes despite agonist treatments up to 18 h. Phylogenetic analysis revealed that this third glycosylation site is found in humans and other higher order primates but not in lower order primates such as the monkey. Nor is this third site found in rodents, which are frequently utilized as animal models. These data thus reveal a previously unrecognized beta(2)AR regulatory motif that appeared late in primate evolution and serves to direct internalized receptors to lysosomal degradation during long term agonist exposure.
Individual and combined effects of relaxin, estrogen, and progesterone in ovariectomized gilts. I. Effects on the growth, softening, and histological properties of the cervix. (1994)

Marked growth and softening of the uterine portion of the cervix occur during the last third of the 115-day gestation period in the gilt. These changes in the cervix are temporally correlated with elevated blood levels of relaxin, estrogen, and progesterone. We recently demonstrated that relaxin plays a major role in promoting both the growth and softening of the cervix that occur in pregnant gilts. The roles of estrogen and progesterone in these cervical changes remain poorly understood. Accordingly, this study determined the influence of relaxin, estrogen, and progesterone, individually and in combination, on cervical growth and softening in gilts. Fifteen days after ovariectomy, six to nine nonpregnant, sexually mature gilts were assigned to one of the following eight treatment groups: ovariectomized controls, relaxin treated, estrogen treated, progesterone treated, estrogen plus relaxin treated, progesterone plus relaxin treated, estrogen plus progesterone treated, and progesterone plus estrogen plus relaxin treated. Treatment was given for 10 days, with doses of relaxin (0.5 mg, four times daily), estradiol benzoate (1 mg, twice daily), and progesterone (50 mg, twice daily) selected to provide blood levels resembling those between days 100-110 of gestation. The growth, softening, and histological characteristics of the cervices were determined. Treatment with relaxin significantly increased the growth and softening and altered the histological characteristics of the uterine portion of the cervix in the absence of steroid treatment. Estrogen treatment alone increased cervical growth, but when given in combination with relaxin, estrogen did not augment relaxin's ability to increase either cervical growth or softening. Progesterone alone had little or no effect on the growth or softening of the uterine portion of the cervix. Unexpectedly, when given in combination with relaxin, progesterone augmented markedly relaxin's effects on softening and alteration of the histological characteristics of the cervix. In conclusion, this study is consistent with recent reports that relaxin promotes both the growth and softening of the cervix in the pig. Additionally, this study provides evidence that estrogen and relaxin act independently to promote the growth of the cervix in gilts, whereas progesterone acts in concert with relaxin to promote softening of the cervix and a reduction in the organization and density of cervical collagen fibers. This study provides evidence that relaxin, estrogen, and progesterone all very likely play important roles in the modifications of the cervix that occur during late pregnancy in the gilt.
Efficient image compression using directionlets (2007)

Directionlets are built as basis functions of critically sampled perfect-reconstruction transforms with directional vanishing moments imposed along different directions. We combine the directionlets with the space-frequency quantization (SFQ) image compression method, originally based on the standard two-dimensional wavelet transform. We show that our new compression method outperforms the standard SFQ as well as the state-of-the-art image compression methods, such as SPIHT and JPEG-2000, in terms of the quality of compressed images, especially in a low-rate compression regime. We also show that the order of computational complexity remains the same, as compared to the complexity of the standard SFQ algorithm.
Methods for detection of point mutations: performance and quality assessment. IFCC Scientific Division, Committee on Molecular Biology Techniques. (1997)

We give an overview of current methods for the detection of point mutations as well as small insertions and deletions in clinical diagnostics. For each method, the following characteristics are specified: (a) principle, (b) major modifications, (c) maximum fragment size that can be analyzed, (d) ratio and type of mutations that can be detected, (e) minimum ratio of mutant to wild-type alleles at which mutations can be detected, and (f) detection methods. Special attention is paid to the possibilities of quality assessment and the potential for standardization and automation.
Antitumor Activity of BRAF Inhibitor Vemurafenib in Preclinical Models of BRAF-Mutant Colorectal Cancer (2011)

The protein kinase BRAF is a key component of the RAS-RAF signaling pathway which plays an important role in regulating cell proliferation, differentiation, and survival. Mutations in BRAF at codon 600 promote catalytic activity and are associated with 8% of all human (solid) tumors, including 8% to 10% of colorectal cancers (CRC). Here, we report the preclinical characterization of vemurafenib (RG7204; PLX4032; RO5185426), a first-in-class, specific small molecule inhibitor of BRAF(V600E) in BRAF-mutated CRC cell lines and tumor xenograft models. As a single agent, vemurafenib shows dose-dependent inhibition of ERK and MEK phosphorylation, thereby arresting cell proliferation in BRAF(V600)-expressing cell lines and inhibiting tumor growth in BRAF(V600E) bearing xenograft models. Because vemurafenib has shown limited single-agent clinical activity in BRAF(V600E)-mutant metastatic CRC, we therefore explored a range of combination therapies, with both standard agents and targeted inhibitors in preclinical xenograft models. In a BRAF-mutant CRC xenograft model with de novo resistance to vemurafenib (RKO), tumor growth inhibition by vemurafenib was enhanced by combining with an AKT inhibitor (MK-2206). The addition of vemurafenib to capecitabine and/or bevacizumab, cetuximab and/or irinotecan, or erlotinib resulted in increased antitumor activity and improved survival in xenograft models. Together, our findings suggest that the administration of vemurafenib in combination with standard-of-care or novel targeted therapies may lead to enhanced and sustained clinical antitumor efficacy in CRCs harboring the BRAF(V600E) mutation.