gebhart/patrepeval huggingface dataset:
CpG Oligodeoxynucleotides (2001)

Research Articles| October 03 2008 Purification and Desiccation of Salmonella-polysaccharides by Means of Repeated Alcohol-acetone Precipitation Subject Area: Further Areas , Oncology , Pathology and Cell Biology E. Engelbrecht E. Engelbrecht Institute of Hygiene, Section for Serology, Geneva Search for other works by this author on: This Site PubMed Google Scholar Pathologia et Microbiologia (1969) 34 (5): 273–281. https://doi.org/10.1159/000162171 Article history Received: September 02 1969 Published Online: October 03 2008 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation E. Engelbrecht; Purification and Desiccation of Salmonella-polysaccharides by Means of Repeated Alcohol-acetone Precipitation. Pathologia et Microbiologia 1 May 1969; 34 (5): 273–281. https://doi.org/10.1159/000162171 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPathobiology Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1969Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Rapid and quantitative detection of bloodSerratia marcescensby a real-time PCR assay: Its clinical application and evaluation in a mouse infection model (2005)

Large-scale nosocomial outbreaks of Serratia marcescens septicaemia in Japan have had a fatality rate of 20-60% within 48 h. As a countermeasure, a real-time PCR assay was constructed for the rapid diagnosis of S. marcescens septicaemia. This assay indeed detected S. marcescens in clinical blood specimens (at ca. 10(2)CFU ml(-1)), at a frequency of 0.5% in suspected cases of septicaemia. In mice, the assay provided estimates of blood S. marcescens levels at various infectious stages: namely, 10(7) to 10(8)CFU ml(-1) at a fatal stage (resulting in 100% death), 10(4)-10(5)CFU ml(-1) at a moderately fatal stage (resulting in 50% or more death), and <10(3)CFU ml(-1) at a mild stage (resulting in 100% survival), consistent with actual CFU measurements. Blood bacterial levels could be an important clinical marker that reflects the severity of septicaemia. The simultaneous detection of S. marcescens and the carbapenem resistance gene was also demonstrated.
Conformational changes in fibrinogen elicited by its interaction with platelet membrane glycoprotein GPIIb-IIIa. (1993)

The binding of fibrinogen to membrane glycoprotein GPIIb-IIIa on activated platelets leads to platelet aggregation. This interaction results in conformational changes in fibrinogen as evidenced by the expression of receptor-induced binding sites, RIBS, epitopes which are expressed by the bound but not the free ligand. In the present study, two RIBS epitopes have been localized. One sequence resides at gamma 112-119 and is recognized by mAb 9F9; the second is the RGDF sequence at A alpha 95-98 and is recognized by mAb 155B16. These epitopes are also exposed by adsorption of fibrinogen onto a plastic surface and digestion of the molecule by plasmin. Proteolytic exposure of the epitopes coincides with cleavage of the carboxyl-terminal aspects of the A alpha-chains to form fragment X2. The inaccessibility of the RGDF sequence at A alpha 95-98 in fibrinogen suggests that this sequence does not participate in the initial binding of the molecule to GPIIb-IIIa. The location of these RIBS epitopes suggests a model in which binding of fibrinogen to its receptor alters the conformation of the carboxyl-terminal aspects of the A alpha-chains, exposing the sequences which reside in the coiled-coil connector segments between the D and E domains of the molecule. These sequences may then serve as epitopes and may mediate unique functions of the receptor-bound molecule.
Investigating Causal Relations by Econometric Models and Cross-spectral Methods (1969)

There occurs on some occasions a difficulty in deciding the direction of causality between two related variables and also whether or not feedback is occurring. Testable definitions of causality and feedback are proposed and illustrated by use of simple two-variable models. The important problem of apparent instantaneous causality is discussed and it is suggested that the problem often arises due to slowness in recording information or because a sufficiently wide class of possible causal variables has not been used. It can be shown that the cross spectrum between two variables can be decomposed into two parts, each relating to a single causal arm of a feedback situation. Measures of causal lag and causal strength can then be constructed. A generalisation of this result with the partial cross spectrum is suggested.
Corticosteroid Suppression of VEGF-A in Infantile Hemangioma-Derived Stem Cells (2010)

In a murine model, dexamethasone inhibited the vasculogenic potential of stem cells derived from human infantile hemangioma. The corticosteroid also inhibited the expression of VEGF-A by hemangioma-derived stem cells, and silencing of VEGF-A expression in these cells inhibited vasculogenesis in vivo.
Determination of plasma electron-density distribution from the resonant frequencies of a parallel-plate cavity (1971)

A microwave resonant cavity method of plasma diagnostics is demonstrated for a parallel-plate cavity containing a cold, collisionless, and isotropic plasma. The method is extended to more general cavities and plasmas in the Appendix. The approach presented here differs from perturbational formulations in that assumptions about the perturbed fields are not made. The analysis gives an exact relation between the electron-density distribution and the resonant frequencies. Laboratory measurements of resonant frequencies then allow a spatially detailed computation of the electron-density distribution. Results are found to agree well with Langmuir probe measurements.
Computer-supported conflict resolution for collaborative facility designers (2003)

Fundamental in engineering design is the notion that collaboration is useful to reduce total project development time and increase design quality. A critical element of collaborative design is the resolution of conflict situations that result naturally from the interaction of cooperating designers, particularly when they are widely dispersed. A multi-approach method for computer-supported resolution of conflict situations in collaborative facility design is introduced. The method is based on social sciences theories used to solve human conflicts. FDL-CR, an extension of the Facility Description Language (FDL) with conflict resolution capabilities provided by the new tool, is the major development in this research. It provides fast identification of the conflict situation, diagnostics of conflict parameters, access to the conflict information by all conflicting parties and mechanisms for conflict resolution. The usefulness of FDL-CR is evaluated with a design case study where a neural-fuzzy inference system is developed to validate the conflict resolution method through the confrontation of conflicting parties. Computer-supported confrontation of conflicting parties was effective when other approaches, such as third-party mediation and persuasion, failed to provide conflict resolution. The new tool is viewed as an essential component of virtual design and manufacturing, and in general e-work.
Neuronal cell death in nervous system development, disease, and injury (Review) (2001)

Neuronal death is normal during nervous system development but is abnormal in brain and spinal cord disease and injury. Apoptosis and necrosis are types of cell death. They are generally considered to be distinct forms of cell death. The re-emergence of apoptosis may contribute to the neuronal degeneration in chronic neurodegenerative disease, such as amyotrophic lateral sclerosis and Alzheimer's disease, and in neurological injury such as cerebral ischemia and trauma. There is also mounting evidence supporting an apoptosis-necrosis cell death continuum. In this continuum, neuronal death can result from varying contributions of coexisting apoptotic and necrotic mechanisms; thus, some of the distinctions between apoptosis and necrosis are becoming blurred. Cell culture and animal model systems are revealing the mechanisms of cell death. Necrosis can result from acute oxidative stress. Apoptosis can be induced by cell surface receptor engagement, growth factor withdrawal, and DNA damage. Several families of proteins and specific biochemical signal-transduction pathways regulate cell death. Cell death signaling can involve plasma membrane death receptors, mitochondrial death proteins, proteases, kinases, and transcription factors. Players in the cell death and cell survival orchestra include Fas receptor, Bcl-2 and Bax (and their homologues), cytochrome c, caspases, p53, and extracellular signal-regulated protein kinases. Some forms of cell death require gene activation, RNA synthesis, and protein synthesis, whereas others forms are transcriptionally-translationally-independent and are driven by posttranslational mechanisms such as protein phosphorylation and protein translocation. A better understanding of the molecular mechanisms of neuronal cell death in nervous system development, injury and disease can lead to new therapeutic approaches for the prevention of neurodegeneration and neurological disabilities and will expand the field of cell death biology.
Identification of Gene Signatures and Molecular Markers for Human Lung Cancer Prognosis using an In vitro Lung Carcinogenesis System (2009)

Lung cancer continues to be a major deadly malignancy. The mortality of this disease could be reduced by improving the ability to predict cancer patients' survival. We hypothesized that genes differentially expressed among cells constituting an in vitro human lung carcinogenesis model consisting of normal, immortalized, transformed, and tumorigenic bronchial epithelial cells are relevant to the clinical outcome of non-small cell lung cancer (NSCLC). Multidimensional scaling, microarray, and functional pathways analyses of the transcriptomes of the above cells were done and combined with integrative genomics to incorporate the microarray data with published NSCLC data sets. Up-regulated (n = 301) and down-regulated genes (n = 358) displayed expression level variation across the in vitro model with progressive changes in cancer-related molecular functions. A subset of these genes (n = 584) separated lung adenocarcinoma clinical samples (n = 361) into two clusters with significant survival differences. Six genes, UBE2C, TPX2, MCM2, MCM6, FEN1, and SFN, selected by functional array analysis, were also effective in prognosis. The mRNA and protein levels of one these genes-UBE2C-were significantly up-regulated in NSCLC tissue relative to normal lung and increased progressively in lung lesions. Moreover, stage I NSCLC patients with positive UBE2C expression exhibited significantly poorer overall and progression-free survival than patients with negative expression. Our studies with this in vitro model have lead to the identification of a robust six-gene signature, which may be valuable for predicting the survival of lung adenocarcinoma patients. Moreover, one of those genes, UBE2C, seems to be a powerful biomarker for NSCLC survival prediction.
Protection against Anthrax Lethal Toxin Challenge by Genetic Immunization with a Plasmid Encoding the Lethal Factor Protein (2001)

The ability of genetic vaccination to protect against a lethal challenge of anthrax toxin was evaluated. BALB/c mice were immunized via gene gun inoculation with eucaryotic expression vector plasmids encoding either a fragment of the protective antigen (PA) or a fragment of lethal factor (LF). Plasmid pCLF4 contains the N-terminal region (amino acids [aa] 10 to 254) of Bacillus anthracis LF cloned into the pCI expression plasmid. Plasmid pCPA contains a biologically active portion (aa 175 to 764) of B. anthracis PA cloned into the pCI expression vector. One-micrometer-diameter gold particles were coated with plasmid pCLF4 or pCPA or a 1:1 mixture of both and injected into mice via gene gun (1 microg of plasmid DNA/injection) three times at 2-week intervals. Sera were collected and analyzed for antibody titer as well as antibody isotype. Significantly, titers of antibody to both PA and LF from mice immunized with the combination of pCPA and pCLF4 were four to five times greater than titers from mice immunized with either gene alone. Two weeks following the third and final plasmid DNA boost, all mice were challenged with 5 50% lethal doses of lethal toxin (PA plus LF) injected intravenously into the tail vein. All mice immunized with pCLF4, pCPA, or the combination of both survived the challenge, whereas all unimmunized mice did not survive. These results demonstrate that DNA-based immunization alone can provide protection against a lethal toxin challenge and that DNA immunization against the LF antigen alone provides complete protection.
The Acceleration of SOA Adoption in Singapore: Challenges and Issues (2008)

This paper addresses real challenges and ensuing issues facing the Singapore government in their endeavour to enhance global economic competitiveness through the adoption of innovative technologies development and usage; in this case, the acceleration of SOA. Key stakeholders have spearheaded a strategic and systematic project (called SOA1) to ensure that SOA is inculcated into the mainstream of businesses and industries. Outcomes, insights and lessons learned are presented along with a glimpse of the next phase of the SOA1 project (called Enterprise 2.0). IT Management complexities not accounted for in SOA1 and Enterprise 2.0 are examined with a call for empirical academic research in the areas of people and organisational behaviour within the context of SOA adoption and implementation.
Deflazacort Increases Laminin Expression and Myogenic Repair, and Induces Early Persistent Functional Gain in mdx Mouse Muscular Dystrophy (2000)

Deflazacort slows the progress of Duchenne muscular dystrophy (DMD) with fewer side effects than prednisone. In mdx mice, deflazacort treatment augments repair and growth of new muscle fibers. We tested the hypothesis that deflazacort improves muscle function and promotes repair by increasing myogenic cell proliferation and fiber differentiation. mdx mice (3.5 weeks old) were treated with deflazacort (1.2 mg/kg) or vehicle for 4 weeks. Forelimb grip strength was measured. After 4 weeks, the right tibialis anterior muscle (TA) was crush injured to induce synchronous regeneration. DNA was labeled using different markers 24 and 2 h before collecting tissues 4 days after injury. The expression of creatine kinase (CK) isoforms, laminin-2 (merosin) mRNA and protein, and proliferation by myogenic cells were measured and satellite cells were identified by immunolocalization of c-met receptor. Peak grip strength increased 15% within 10 days of treatment, and was maintained up to 6 weeks after the end of treatment in a second experiment. Expression of CK MM in the regenerating TA rose from 46% to 55% of total CK activity after deflazacort treatment. Satellite cells were more numerous and appeared earlier on new fibers, in concert with a threefold increase in proliferation by myogenin+ (but not MyoD+) myoblasts. alpha2-Laminin mRNA expression and protein increased 1.3-5.5-fold relative to MM CK in regenerating and dystrophic TA, respectively. These studies support the hypothesis that deflazacort promotes functional gains, myogenic differentiation, myoblast fusion, and laminin expression in regenerating dystrophic muscle. The potential to augment precursor specification, strength, and possible membrane stability may be useful in directing long-term benefits for DMD patients and short-term amplification of precursors prior to myoblast transfer.
A novel homeodomain-encoding gene is associated with a large CpG island interrupted by the myotonic dystrophy unstable (CTG)n repeat (1995)

Myotonic dystrophy (DM) is associated with a (CTG)n trinucleotide repeat expansion in the 3'-untranslated region of a protein kinase-encoding gene, DMPK, which maps to chromosome 19q13.3. Characterisation of the expression of this gene in patient tissues has thus far generated conflicting data on alterations in the steady state levels of DMPK mRNA, and on the final DMPK protein levels in the presence of the expansion. The DM region of chromosome 19 is gene rich, and it is possible that the repeat expansion may lead to dysfunction of a number of transcription units in the vicinity, perhaps as a consequence of chromatin disruption. We have searched for genes associated with a CpG island at the 3' end of DMPK. Sequencing of this region shows that the island extends over 3.5 kb and is interrupted by the (CTG)n repeat. Comparison of genomic sequences downstream (centromeric) of the repeat in human and mouse identified regions of significant homology. These correspond to exons of a gene predicted to encode a homeodomain protein. RT-PCR analysis shows that this gene, which we have called DM locus-associated homeodomain protein (DMAHP), is expressed in a number of human tissues, including skeletal muscle, heart and brain.
An artificial gastrocnemius for a transtibial prosthesis (2009)

A transtibial amputee does not have a functional gastrocnemius muscle, which affects the knee as well as the ankle joint. In this investigation, we developed a transtibial prosthesis comprising an artificial gastrocnemius mechanism as well as a powered ankle-foot device. A pilot study was conducted with a bilateral transtibial amputee walking at a self-selected speed. The trial compared muscle electromyography and metabolic cost data for the amputee while using the active gastrocnemius prosthesis and a conventional Flex-Foot prosthesis. The experimental data showed that the compensation for ankle-foot and gastrocnemius function offered by the active device resulted in a reduced metabolic cost for the amputee participant.
Colon-cancer cell variants producing regressive tumors in syngeneic rats, unlike variants yielding progressive tumors, attach to interstitial collagens through integrin α2β1 (1996)

Nine clones of tumor cells, derived from a single rat colon carcinoma, were analyzed for their adhesive properties and in vivo growth patterns. Four clones (denoted REG) gave rise to regressively growing tumors. Cells from the 4 REG clones attached significantly better to collagen types I and III than did cells from the 5 clones (denoted PRO) which grew progressively in vivo. In contrast, REG and PRO clones did not differ in their attachment to collagen type IV, laminin or fibronectin. The attachment of REG cells to collagen was dependent on Mg2+, but not Ca2+. Monospecific rabbit IgG to rat integrin beta 1-chain inhibited REG cell attachment to collagen, demonstrating involvement of a beta 1 integrin in this process. PRO and REG cells expressed an underglycosylated beta 1 chain (Mr approximately 105,000) that was somewhat smaller than beta 1-chains described previously on rat fibroblasts and hepatocytes (Mr approximately 115,000). Monoclonal IgG to rat integrin alpha 2 beta 1, but not to alpha 1 beta 1, readily inhibited REG cell attachment to collagen, demonstrating the involvement of integrin alpha 2 beta 1. However, beta 1 and alpha 2 integrin subunits were found in purified glycoproteins from both PRO and REG cells. This suggests that alpha 2 beta 1 integrin is expressed by both cell variants, but is functional as a collagen receptor on REG cells only. In this system of tumor-cell variants, the clear-cut differences in attachment to interstitial collagens of the 9 clones suggest a possible relationship between this attachment and the capacity to induce progressive or regressive tumors.
Neural Degeneration and Regeneration in Human Renal Transplants (1970)

Neural degeneration and regeneration were studied histologically with hematoxylin–eosin and Bodian stains in 33 human renal transplants. By the fifteenth day after transplantation few intact axons were recognizable, and by the twenty-sixth day, only axonal debris remained. As early as the twenty-eighth day, regenerating axons appeared distal to the graft's arterial anastomosis. Regenerating axons could be traced to the nerves accompanying the interlobular arteries, but the axon population did not reach the number observed in normal nerves of comparable size. Allografts and isografts exhibited comparable patterns of neural regeneration.
Normally incident resonant grating reflection filters for efficient narrow-band spectral filtering of finite beams (2001)

Resonant grating reflection filters operating at normal incidence are investigated. At normal incidence these structures are shown to have characteristics different from those of structures operated at oblique incidence. We show how higher-order diffraction within the structure laterally confines the incident energy about the point of incidence and results in a broadened angular selectivity. Multimode structures are shown to exhibit broader angular selectivities and narrower spectral linewidths than those of single-mode structures, achieving angular selectivities hundreds of times broader than what could be obtained at oblique incidence. When compared with that for oblique incidence, the increase in angular selectivity is shown to greatly improve the performance of these filters for spectrally filtering finite incident beams.