gebhart/patrepeval huggingface dataset:
Antiviral activity of natural and semisynthetic polysaccharides on the early steps of rubella virus infection (1997)

The natural and semisynthetic carbohydrates scleroglucan, locust bean gum, tamarind gum (glyloid) and its three sulphate derivatives (GP4311, GP4327 and GP4324), glycogen and its two sulphate derivatives (GP4427 and GP4435), alginic acid and dextran sulphate, were investigated for their inhibitory effect on rubella virus (RV) infection of Vero cells. The neutral polymer scleroglucan and two highly negatively charged compounds, glyloid sulphate 4324 and dextran sulphate, had the highest inhibitory effect on RV antigen synthesis. The antiviral properties of active molecules appears to be dependent on the shape of the macromolecule and/or on the electric charge, while saccharide units play a minor role. The results indicated that polysaccharides blocked a step in virus replication subsequent to virus attachment, such as internalization and/or uncoating. Confirmation that the inhibitory activity of the compounds was directed at the early steps of RV multiplication, was that none of the polysaccharides had any effect on infection initiated by transfection of cells with RVRNA.
<title>Matching performance requirements with technology: an applications approach to vibration isolation</title> (1992)

An integrated solutions approach to frequently encountered vibration problems is most useful in solving real-world problems. By ''amalgamating'' several levels of vibration control--in the form of both new designs and existing technologies--one is able to create a foundation upon which a variety of requirements can be met. The combination of time-proven damping of optical bench tops and a novel technological advance involving a new damping technology for pneumatic isolators, leads to enhanced performance of passive isolation systems.
Tangles and plaques in nondemented aging and ?preclinical? Alzheimer's disease (1999)

The distribution and density of neurofibrillary tangles and amyloid plaques was studied in a unique series of cases whose premortem cognitive status had been assessed with the Clinical Dementia Rating (CDR), including 39 nondemented cases (CDR = 0; age, 51-88 years), 15 very mildly demented cases (CDR = 0.5), and 8 severely demented (CDR = 3) cases. The initial formation of tangles and plaques in healthy aging appeared to be independent of each other. Tangles were found in all the nondemented cases, especially in hippocampal and parahippocampal areas; the average tangle concentration increased exponentially with age. In contrast, plaques were absent in some brains up to age 88, and the earliest plaque formation in other cases occurred in the neocortex, in patches of diffuse plaques. Widely distributed neuritic as well as diffuse plaques throughout neocortex and limbic structures characterized a further group of nondemented cases. In these cases there was also a substantial increase over other nondemented cases, both in the number of tangles and in the rate of increase in tangles with age, suggesting an interaction between amyloid and neurofibrillary change at this stage. Such cases closely resemble CDR = 0.5 cases, and it is proposed they represent "preclinical" Alzheimer's disease.
Molecular pathogenesis of liver fibrosis. (2009)

Hepatic fibrosis is the final common pathway for most chronic liver diseases. The cell responsible for hepatic fibrosis appears to be the activated myofibroblast. The myofibroblast may be derived from quiescent hepatic stellate cells, epithelial to mesenhymal transition, or derived from bone marrow precursors. Studies in primary cultures of myofibroblasts and in mouse models of hepatic fibrosis have revealed several common pathophysiological mechanisms. Hepatic fibrosis is strongly associated with oxidative stress, increased transforming growth factor beta, hepatocyte death, and chronic inflammation. Finally, the reversal of fibrosis depends upon the elimination of the activated myofibroblast.
Isoflurane Activates PKC and Ca2+-Calmodulin-dependent Protein Kinase II via MAP Kinase Signaling in Cultured Vascular Smooth Muscle Cells (2002)

ERK1/2 signaling is downstream of PKC and CaMKII activated by isoflurane in vascular smooth muscle cells.
Synthetic peptides from the N-terminal regions of CD200 and CD200R1 modulate immunosuppressive and anti-inflammatory effects of CD200-CD200R1 interaction (2005)

A series of 15-mer peptides were synthesized defining continuous sequences of the extracellular region of the murine and human CD200 molecule. In addition, peptides mapping to the presumptive CDR1, CDR2 and CDR3 of the human and mouse CD200R1 molecules were synthesized. The ability of these various molecules to block the interaction of CD200 with CD200R1 was studied in a competitive ELISA using plate-bound CD200R1Fc and biotinylated CD200Fc, and by FACS using FITC-conjugated CD200Fc binding to 24-h LPS-activated adherent cells. Results from these data were compared with the functional ability of the same peptides to suppress the inhibition of generation of allo-specific CTL in vitro following inclusion of CD200Fc in mixed leukocyte culture reactions. Peptides defining discrete regions in the N terminal regions of CD200 and CD200R1 were functionally active in these different assays. Moreover, infused in vivo, the same mouse-specific peptides suppressed protection from graft rejection afforded by injection of soluble immunosuppressive CD200Fc. Used alone in vitro, these peptides enhanced alloimmunity.
IL-10 regulates plasmacytoid dendritic cell response to CpG-containing immunostimulatory sequences (2003)

Immunostimulatory sequences (ISS) are short oligonucleotides containing unmethylated cytosine-phosphate-guanine (CpG) dinucleotides that stimulate innate immune responses through Toll-like receptor-9 on B cells and plasmacytoid dendritic cell (PDC) precursors. The anti-inflammatory cytokine interleukin (IL)-10 is predicted to be a potent inhibitor of many of the activities described for ISS, and this may impact the use of ISS in disease states characterized by elevated IL-10. As the activities of ISS on PDCs are central to many clinical applications of ISS, we have studied the effects of IL-10 on PDC stimulation by 3 distinct classes of ISS. IL-10 inhibited cytokine production and survival of ISS-activated PDCs; however, IL-12 induction was much more sensitive to inhibition than interferon (IFN)-alpha induction. Within the PDC population are cells that respond to ISS by producing either IL-12 or IFN-alpha but not both cytokines. IL-12-producing PDCs require costimulation through CD40 and appear more mature than IFN-alpha-producing PDCs. The 3 distinct classes of ISS differed with respect to induction of PDC maturation and T-cell priming capacity. IL-10 regulated PDC activation but did not inhibit the subsequent T-cell-priming ability of PDCs already activated by ISS.
Antibodies as Tools to Study the Structure of Membrane Proteins: The Case of the Nicotinic Acetylcholine Receptor (1996)

The nicotinic acetylcholine receptor is the prototype of the ionotropic receptor superfamily of proteins, which includes the closely related gamma- aminobutyric acid type A and glycine receptors, and more distantly related serotonin type-3 and glutamate receptors. Several models of the transmembrane topology of the nicotinic acetylcholine receptor subunits were originally proposed based on hydropathy analysis of their deduced amino acid sequences. Antibodies specific to different epitopes of the nicotinic acetylcholine receptor have proven to be valuable probes for examining the validity of those models. Despite important caveats, a viable model for the transmembrane structure and functional topology of the nicotinic acetylcholine receptor subunits has been obtained from the antibody mapping studies. This model, and the associated methodological shortcomings and obstacles that were overcome in the process of its formulation, can legitimately be extended to other members of the ionotropic receptor superfamily and to other membrane proteins as well.
Identification of novel gene expression targets for the Ras association domain family 1 (RASSF1A) tumor suppressor gene in non-small cell lung cancer and neuroblastoma. (2003)

RASSF1A is a recently identified 3p21.3 tumor suppressor gene. The high frequency of epigenetic inactivation of this gene in a wide range of human sporadic cancers including non-small cell lung cancer (NSCLC) and neuroblastoma suggests that RASSF1A inactivation is important for tumor development. Although little is known about the function of RASSF1A, preliminary data suggests that it may have multiple functions. To gain insight into RASSF1A functions in an unbiased manner, we have characterized the expression profile of a lung cancer cell line (A549) transfected with RASSF1A. Initially we demonstrated that transient expression of RASSF1A into the NSCLC cell line A549 induced G(1) cell cycle arrest, as measured by propidium iodide staining. Furthermore, annexin-V staining showed that RASSF1A-expressing cells had an increased sensitivity to staurosporine-induced apoptosis. We then screened a cDNA microarray containing more than 6000 probes to identify genes differentially regulated by RASSF1A. Sixty-six genes showed at least a 2-fold change in expression. Among these were many genes with relevance to tumorigenesis involved in transcription, cytoskeleton, signaling, cell cycle, cell adhesion, and apoptosis. For 22 genes we confirmed the microarray results by real-time RT-PCR and/or Northern blotting. In silico, we were able to confirm the majority of these genes in other NSCLC cell lines using published data on gene expression profiles. Furthermore, we confirmed 10 genes at the RNA level in two neuroblastoma cell lines, indicating that these RASSF1A target genes have relevance in non-lung cell backgrounds. Protein analysis of six genes (ETS2, Cyclin D3, CDH2, DAPK1, TXN, and CTSL) showed that the changes induced by RASSF1A at the RNA level correlated with changes in protein expression in both non-small cell lung cancer and neuroblastoma cell lines. Finally, we have used a transient assay to demonstrate the induction of CDH2 and TGM2 by RASSF1A in NSCLC cell lines. We have identified several novel targets for RASSF1A tumor suppressor gene both at the RNA and the protein levels in two different cellular backgrounds. The identified targets are involved in diverse cellular processes; this should help toward understanding mechanisms that contribute to RASSF1A biological activity.
Recognition-Directed Supramolecular Assemblies of Metal Complexes of Terpyridine Derived Ligands with Self-Complementary Hydrogen Bonding Sites (2000)

The synthesis and X-ray structures of three metal complexes with terpyridine-derived ligands that contain amino-pyrimidine and amino-pyrazine moieties are presented. They have been designed in view of directing their self-assembly into specific supramolecular arrays through molecular recognition interactions. The solid-state structures indeed reveal extensive hydrogen-bonded networks. The Co complex 4a with PF6- counterions builds a two-dimensional infinite interwoven grid through strong double hydrogen bonds (d(N-H-N) =2.918-3.018 A) between the amino groups and the N atoms of the rings, with all H-bonding sites saturated. Changing the anions to BF4- in 4b leads to a similar infinite but partially broken grid with a quarter of the H-bonding sites unsaturated (d(N-H-N)=2.984-3.206 A). In the case of the Zn complex 12 with triflate anions, half of the hydrogen bonds are formed. Only one of the two orthogonal ligands has hydrogen bonds (d(N-H-N) = 3.082, 3.096 A) to the neighbouring complexes and thus builds linear, supramolecular, polymeric chains. These structural differences are mainly attributed to crystal-packing effects caused by the different anions. The data presented here may also be regarded as a prototype for the generation of organised arrays through sequential self-assembly processes.
Impact Resistance of Cement and Gypsum Plaster Nanomodified by Water-Soluble Fullerenols (2013)

The synthesis of cement and gypsum plaster nanomodified by water-soluble fullerenols was performed. The experimental data demonstrates an extreme increase in the specific impact resistance of nanomodified samples compared with nonmodified.
Fast Light, Slow Light (2002)

Get PDF Email Share Share with Facebook Tweet This Post on reddit Share with LinkedIn Add to CiteULike Add to Mendeley Add to BibSonomy Get Citation Copy Citation Text Raymond Y. Chiao and Peter W. Milonni, "Fast Light, Slow Light," Optics & Photonics News 13(6), 26-30 (2002) Export Citation BibTex Endnote (RIS) HTML Plain Text Citation alert Save article
Expression of Facilitative Glucose Transporter Isoforms in Human Brain Tumors (1993)

The expression of facilitative glucose transporter (GLUT) isoforms in human astrocytic tumors was examined. Reverse transcriptase-polymerase chain reaction of a surgically biopsied glioblastoma was carried out using the degenerative oligonucleotide primers corresponding to the sequences of the human facilitative glucose transporter family, and polymerase chain reaction products were hybridized with human GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5 cDNA probes. The results showed that a biopsied glioblastoma expressed GLUT1, GLUT3, and GLUT4 glucose transporter genes. Northern blot analysis of total RNA (10 micrograms) from a biopsied glioblastoma showed the transcripts of only GLUT1 and GLUT3, suggesting that the expression of insulin-responsive glucose transporter GLUT4 mRNA is relatively low. Immunoblot analysis of biopsied glioblastoma tissues by polyclonal antibodies against the C-terminal synthetic peptides of GLUT1, GLUT3, and GLUT4 showed a single band of each polypeptide. However, elevated expression of GLUT1 and GLUT3 glucose transporters was not observed in the glioblastoma. Astrocytic tumor tissues (n = 14) were also examined immunohistochemically. Reactive products for GLUT1 were observed in the luminal surface of capillaries in all cases, whereas tumor cells were positive for GLUT1 in only two of 14 cases. GLUT3 was positive in astrocytic tumor cells in all cases. Three of 14 cases expressed the GLUT4 protein, which was localized in the cytoplasm of tumor cells. These results suggest that the facilitative glucose transport may be altered in astrocytic tumor cells and thus display a significant change in glucose metabolism.
Extracting Haplotypes from Diploid Organisms (2006)

Each diploid organism has two alleles at every gene locus. In sexual organisms such as most plants, animals and fungi, the two alleles in an individual may be genetically very different from each other. DNA sequence data from individual alleles (called a haplotype) can provide powerful information to address a variety of biological questions and guide many practical applications. The advancement in molecular technology and computational tools in the last decade has made obtaining large-scale haplotypes feasible. This review summarizes the two basic approaches for obtaining haplotypes and discusses the associated techniques and methods. The first approach is to experimentally obtain diploid sequence information and then use computer algorithms to infer haplotypes. The second approach is to obtain haplotype sequences directly through experimentation. The advantages and disadvantages of each approach are discussed. I then discussed a specific example on how the direct approach was used to obtain haplotype information to address several fundamental biological questions of a pathogenic yeast. With increasing sophistication in both bioinformatics tools and high-throughput molecular techniques, haplotype analysis is becoming an integrated component in biomedical research.
Impact of leucocyte‐depleted blood components on the haematological recovery and prognosis of patients with acute myeloid leukaemia (1993)

Use of leucocyte-depleted blood components reduces refractoriness to platelet transfusions, but the cost-effectiveness of this policy has been in doubt. We retrospectively analysed data of 115 patients with acute myeloid leukaemia (AML), treated according to a standardized cytostatic protocol. Fifty patients had received standard (STD) platelet concentrates (PCs) and red blood cell concentrates (RBCs). Sixty-five patients had received leucocyte-depleted (L-D) components, with fewer than one million leucocytes per unit. Refractory patients (22% of the STD group and 3% of the L-D group) were excluded from further observations. There were no differences between the groups during the first cytostatic treatment period. Thereafter, significantly fewer PCs and RBCs were transfused to the L-D group. In the L-D group, granulocytopenia (< 0.5 x 10(9)/l) and thrombocytopenia (< 50 x 10(9)/l) were shorter, the lowest leucocyte counts were higher, serious infections were less common (44% v 59%), and the patients spent fewer days in hospital. The median relapse-free survival (RFS) was longer in the L-D group than in the STD group. We conclude that leucocyte depletion of blood components has favourable effects on the recovery of haematopoiesis, consumption of blood components, occurrence of serious infections, and relapse-free survival in AML.
FZD6is a novel gene for human neural tube defects (2011)

Neural tube defects (NTDs) are severe malformations of the central nervous system, affecting 1 of 1,000 live births. Mouse models were instrumental in defining the signaling pathways defective in NTDs, including the planar cell polarity (PCP), also called noncanonical Frizzled/Disheveled pathway. Based on the highly penetrant occurrence of NTDs in double Fzd3/Fzd6(-/-) mutant mice, we investigated the role of the human orthologues, FZD3 and FZD6, by resequencing a cohort of 473 NTDs patients and 639 ethnically matched controls. While we could not demonstrate a significant contribution of FZD3 gene, we identified five rare FZD6 variants that were absent in all controls and predicted to have a functional effect by computational analysis: one de novo frameshift mutation (c.1843_1844insA), three missense changes (p.Arg405Gln, p.Arg511Cys p.Arg511His), and one substitution (c.*20C>T) affecting the 3'-untranslated region (UTR) of the gene. The overall rate of predicted deleterious variants of FZD6 was 5.1-fold higher in cases compared to controls, resulting in a significantly increased NTDs mutation burden. This study demonstrates that rare nonsynonymous variants in FZD6 may contribute to NTDs in humans and enlarges the spectrum of mutations that link PCP pathway to NTDs.
Vaccinia virus strains Lister, USSR and Evans express soluble and cell-surface tumour necrosis factor receptors. (1999)

Poxviruses encode a broad range of proteins that interfere with host immune functions such as soluble versions of cytokine receptors. Soluble virus tumour necrosis factor receptors (vTNFRs) were described originally in myxoma and Shope fibroma viruses. Cowpox virus (CPV) encodes three vTNFRs (CrmB, CrmC and CrmD). The genes equivalent to CrmB and CrmC in vaccinia virus (VV) Copenhagen are mutated and are named B28R/C22L and A53R, respectively. CrmD was identified recently in CPV and ectromelia virus but the gene is absent in VV Copenhagen. We have tested for expression of soluble binding activity for human TNF in cultures infected with 18 orthopoxviruses and have found that TNFRs are mostly absent but are produced by VV strains Lister, USSR and Evans, by the CPV elephantpox and by camelpox virus. Interestingly, we also found TNFR activity on the surface of cells infected with VV Lister, USSR and Evans. Sequence analysis of the relevant regions in VV Lister identified an intact A53R gene and an inactive B28R gene. Expression of VV Lister A53R in baculovirus and VV Western Reserve demonstrated that gene A53R encodes an active soluble vTNFR of 22 kDa. Expression and characterization of recombinant vTNFRs from VV Lister (A53R) and CPV (CrmB and CrmC) showed a similar binding specificity, with each receptor binding TNF from man, mouse and rat, but not human lymphotoxin-alpha. Lastly, the VV Lister and CPV vTNFRs bind human TNF with high affinity and prevent the binding of TNF to cellular receptors.
Adeno-Associated Virus-Vectored Gene Therapy for Retinal Disease (2005)

Recombinant adeno-associated viral (AAV) vectors have become powerful gene delivery tools for the treatment of retinal degeneration in a variety of animal models that mimic corresponding human diseases. AAV vectors possess a number of features that render them ideally suited for retinal gene therapy, including a lack of pathogenicity, minimal immunogenicity, and the ability to transduce postmitotic cells in a stable and efficient manner. In the sheltered environment of the retina, AAV vectors are able to maintain high levels of transgene expression in the retinal pigmented epithelium (RPE), photoreceptors, or ganglion cells for long periods of time after a single treatment. Each cell type can be specifically targeted by choosing the appropriate combination of AAV serotype, promoter, and intraocular injection site. The focus of this review is on examples of AAV-mediated gene therapy in those animal models of inherited retinal degeneration caused by mutations directly affecting the interacting unit formed by photoreceptors and the RPE. In each case discussed, expression of the therapeutic gene resulted in significant recovery of retinal structure and/or visual function. Because of the key role of the vasculature in maintaining a healthy retina, a summary of AAV gene therapy applications in animal models of retinal neovascular diseases is also included.
Salmonella strain secreting active listeriolysin changes its intracellular localization (1995)

We describe the construction of an attenuated Salmonella dublin aroA strain which secretes via the Escherichia coli hemolysin secretion machinery an active hybrid cytolysin consisting of listeriolysin from Listeria monocytogenes and the C-terminal secretion signal of E. coli hemolysin. This hemolytic S. dublin strain is partially released into the cytoplasm of the host cell following uptake by J774 macrophage cells, whereas the nonhemolytic control S. dublin aroA strain remains in the phagosome.
Meta‐analyses of human gut microbes associated with obesity and IBD (2014)

Recent studies have linked human gut microbes to obesity and inflammatory bowel disease, but consistent signals have been difficult to identify. Here we test for indicator taxa and general features of the microbiota that are generally consistent across studies of obesity and of IBD, focusing on studies involving high‐throughput sequencing of the 16S rRNA gene (which we could process using a common computational pipeline). We find that IBD has a consistent signature across studies and allows high classification accuracy of IBD from non‐IBD subjects, but that although subjects can be classified as lean or obese within each individual study with statistically significant accuracy, consistent with the ability of the microbiota to experimentally transfer this phenotype, signatures of obesity are not consistent between studies even when the data are analyzed with consistent methods. The results suggest that correlations between microbes and clinical conditions with different effect sizes (e.g. the large effect size of IBD versus the small effect size of obesity) may require different cohort selection and analysis strategies.
Basic concepts of hematopoiesis and the hematopoietic growth factors (1989)

Clinical Pharmacology and Therapeutics (1989) 46, 250–256; doi:10.1038/clpt.1989.135