gebhart/patrepeval huggingface dataset:
Activation of the C4 and C2 components of complement by a proteinase in serum bactericidal factor, Ra reactive factor (1993)

Ra-reactive factor (RaRF) is a C-dependent bactericidal factor that binds specifically to LPS of Ra chemotype strains of Salmonella and kills the bacteria by triggering the C cascade. In the present study, we investigated the components of mouse RaRF that activate C4 and C2. The RaRF bound to LPS-coated E, and activated the C4 on the surface of E, causing the C4 to bind to the cells. Diisopropyl fluorophosphate (DFP) bound to RaRF and inhibited its ability to activate C4 and C2. Cleavage of the alpha-chain of C4 by RaRF generated a polypeptide with a size similar to that of the alpha'-chain of C4b, which is known to be a product of the cleavage of C4 by C1s subcomponent of C1. A fraction with the ability to activate C4 and C2 was separated from RaRF by gel-permeation chromatography in the presence of EDTA and acetonitrile. This fraction contained a DFP-binding polypeptide with an apparent m.w. of 100,000. This polypeptide is not the C1s in mouse C1 because the sizes of this polypeptide and of the fragments produced by its reduction were different from those of DFP-binding proteinases in mouse C1. These results indicate that mouse RaRF contains a C1s-like serine proteinase that is capable of activating C4 and, probably, C2.
Culture and Nutrition of Some Apochlorotic Diatoms of the Genus Nitzschia (1967)

SUMMARY Three distinct species of the genus Nitzschia, lacking chloroplasts and therefore obligately heterotrophic, were isolated in pure culture from various marine shores. The organisms reproduced rapidly in a defined medium based on an artificial sea water supplemented with mineral nutrients, thiamine and cobalamin. Lactate or succinate served as sole organic carbon source for all three species; two of the species also used glucose or glutamate. Two of the species were identified as N. putrida Benecke and N. leucosigma Benecke, respectively. The third organism appears to be a new species, here named N. alba.
The C terminus of mouse ornithine decarboxylase confers rapid degradation on dihydrofolate reductase. Support for the pest hypothesis (1991)

Several years ago, we proposed that polypeptide regions rich in proline (P), glutamic acid (E), serine (S), and threonine (T) (PEST) target intracellular proteins for destruction (Rogers, S., Wells, R., and Rechsteiner, M. (1986) Science 234, 364-368). To test the PEST hypothesis, we have produced chimeric proteins in which the N or C terminus of mouse dihydrofolate reductase is extended by the PEST-containing C terminus of mouse ornithine decarboxylase. Oligonucleotides encoding the 37 C-terminal residues of mouse ornithine decarboxylase (mODC) or equivalent lengths of dissimilar amino acids were inserted at appropriate sites in a dihydrofolate reductase (DHFR) expression vector. The various fusion proteins were expressed in Escherichia coli and purified to homogeneity by enzyme affinity chromatography. All purified fusion proteins exhibited similar abilities to convert dihydrofolate to tetrahydrofolate, thereby demonstrating that the attachment of peptide extensions to either terminus did not prevent the proper folding of DHFR. Metabolic stabilities of the radioiodinated fusion proteins were assayed in rabbit reticulocyte lysate or Xenopus egg extract. Proteolysis was found to be energy-dependent with mODC-DHFR fusion proteins being degraded from 2 to almost 40-fold faster than the parental DHFR molecule or DHFR fusion proteins bearing non-PEST extensions. Deletion of most of the PEST region from the mODC extension resulted in a significantly more stable fusion protein. Rapid proteolysis of DHFR proteins containing intact mODC extensions provides support for the PEST hypothesis.
Role of 5-Lipoxygenase Products of Arachidonic Acid in Cell-to-Cell Interaction Between Macrophages and Natural Killer Cells in Rat Spleen (1991)

In the present study we performed experiments to reveal the role of 5-lipoxygenase products of arachidonic acid in cell-to-cell interaction between rat peritoneal macrophages and spleen natural killer (NK) cells. Peritoneal macrophages were found to significantly enhance NK cell activity. It was found that the enhancing activity of macrophages was significantly inhibited by the ingestion of highly purified eicosapentaenoic acid-ethyl ester (EPA-E). But direct cytotoxic action of macrophage on target cells (YAC-1) was unchanged by the ingestion of EPA-E. In addition, the depressed enhancing activity of EPA-enriched macrophages (EPA macrophages) was partially, but significantly, restored by the addition of either 10(-10) M leukotriene B4 (LTB4) or 10(-12) M 5-hydroperoxyeicosatetraenoic acid (5-HPETE). The partial restoring effect of 10(-10) M LTB4 was further significantly enhanced by the addition of 5-HPETE. In contrast 5-hydroxyeicosatetraenoic acid (5-HETE) had no modulatory effect on the depressed activity of EPA macrophages. LTB4, 5-HPETE, and 5-HETE had no direct effect on NK cell activity itself. Significantly less amounts of LTB4 and 5-HETE were produced in EPA macrophages as compared with that in control macrophages. The present study indicates that macrophage modulatory action on NK cells can be partly mediated by LTB4 and 5-HPETE, which are produced in macrophages.
Host Defense Mechanisms Triggered by Microbial Lipoproteins Through Toll-Like Receptors (1999)

The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.
FLUTE - File Delivery over Unidirectional Transport (2004)

à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.
Increasing Epithelial Junction Permeability Enhances Gene Transfer to Airway Epithelia In Vivo (2000)

Gene transfer to airway epithelia is the most direct approach for treating the progressive lung disease associated with cystic fibrosis. However, the transduction efficiency is poor when viral vectors are applied to the mucosal surface. We reported previously that gene transfer via the apical surface of human airway epithelia in vitro was improved by formulating vectors with ethyleneglycol-bis-(2-aminoethyl ether)- N,N,N',N'-tetraacetic acid (EGTA) in a hypotonic buffer. First, we investigated the mechanism for this enhancement. When 100-nm fluorescent beads were applied to the apical surface in the presence of EGTA, paracellular deposition of the particles was noted. Transmission electron microscopy verified that the epithelial junction complex was disrupted under these conditions. The Ca(2+) chelators EGTA, 1,2-bis (2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA), and ethylenediaminetetraacetic acid all caused a rapid, reversible drop in transepithelial resistance and facilitated gene transfer with retrovirus or adenovirus in vitro. When Ca(2+) chelators were applied to rabbit tracheal epithelia or human nasal epithelia in vivo, the transepithelial voltage decreased, and amiloride sensitivity was lost, suggesting that epithelial junctions opened. Importantly, this novel formulation enhanced both retroviral- and adenoviral-mediated gene transfer to rabbit tracheal epithelia in vivo. This technique may have applications for vector or drug delivery to airway epithelia and other polarized cells.
The Role of Kalirin9 in p75/Nogo Receptor-mediated RhoA Activation in Cerebellar Granule Neurons (2008)

p75 and the Nogo receptor form a signaling unit for myelin inhibitory molecules, with p75 being responsible for RhoA activation. Because p75 lacks the GDP/GTP exchange factor domain, it has remained unclear how p75 activates RhoA. Here, we report that Kalirin9, a dual RhoGEF, binds p75 directly and regulates p75-Nogo receptor-dependent RhoA activation and neurite inhibition in response to myelin-associated glycoprotein. The region of p75 that Kalirin9 binds includes its mastoparan-like fifth helix, which was shown to recruit RhoGDI-RhoA. As predicted from the presence of a shared binding site, we found that Kalirin9 competes with RhoGDI for p75 binding in a dose-dependent manner in vitro. In line with these data, myelin-associated glycoprotein addition to cerebellar granule neurons resulted in a reduction in the association of Kalirin9 with p75, and a simultaneous increase in the binding of RhoGDI to p75. These results reveal a mechanism by which the fifth helix of p75 regulates RhoA activation.
Medical Service Utilization by Veterans Seeking Help for Posttraumatic Stress Disorder (2002)

OBJECTIVE: Posttraumatic stress disorder (PTSD) has been associated with higher rates of health complaints and medical conditions diagnosed by physicians, yet research examining the relationship between PTSD and health care utilization has been limited. This study compared the health service use of veterans with PTSD to that of help-seeking veterans without PTSD. The relationship between severity of PTSD and service utilization was also examined. METHOD: Data were collected from 996 veterans seeking an evaluation at a Veterans Affairs (VA) Medical Center specialty PTSD clinic in the southeastern United States between March 1992 and September 1998. Data included sociodemographic characteristics, severity of PTSD, and disability status. The outcome variable, VA health service utilization, was prospectively assessed 1 year from the date of the initial PTSD assessment. RESULTS: Although the use of VA mental health services by patients with PTSD was substantial (a median of seven clinic stops), these patients used more services in general physical health clinics that provided predominantly nonmental health services (a median of 18 clinic stops). Negative binomial regression models revealed that younger veterans with PTSD had greater health care utilization than those without PTSD who also sought services. Greater severity of PTSD was related to higher rates of mental and physical health service use among veterans without a service-connected disability. CONCLUSIONS: PTSD is associated with substantial health service use. The results highlight the importance of increased collaboration between primary care and mental health specialists, given that patients with PTSD are more likely to receive treatment in nonmental health clinics.
The role of IL-1 in the pathogenesis of heart disease (2009)

Interleukin (IL)-1 consists of two distinct ligands, IL-1alpha and IL-1beta, with indistinguishable biological activities that signal through the IL-1 type I receptor (IL-1RI). A naturally occurring IL-1 receptor antagonist (IL-1Ra) binds to IL-1RI without initiating signal transduction and prevents IL-1 signaling, competitively inhibiting IL-1-mediated responses. Emerging evidence suggests that the balance between IL-1 agonists and antagonists plays an essential role in a variety of cardiovascular conditions. IL-1 may play a role in atherothrombotic disease by promoting the formation of atheromatous lesions, enhancing vascular inflammation, and triggering plaque destabilization. Following myocardial infarction, IL-1 critically regulates the inflammatory response and is involved in the development of adverse remodeling by enhancing expression of matrix metalloproteinases. IL-1 signaling may also be an essential mediator in the pathogenesis of heart failure by suppressing cardiac contractility, promoting myocardial hypertrophy, and inducing cardiomyocyte apoptosis. The present review summarizes current available data showing the significant role of IL-1 signaling in heart disease and raising the possibility that IL-1 inhibitors (such as anakinra, a nonglycosylated recombinant human IL-1Ra) may be clinically useful agents in patients with certain cardiovascular conditions.
Examination of chlamydial glycolipid with monoclonal antibodies: cellular distribution and epitope binding. (1991)

A chlamydial glycolipid antigen (GLXA) is shed into the medium of C. trachomatis-infected cell cultures. This study screened monoclonal antibodies (mAb), prepared in different laboratories by immunization with embryonated egg propagated elementary bodies (EB), for their ability to bind with infected cells and to react with purified GLXA isolated from supernatants of infected McCoy cells. The fluorescent antibody (FA) staining pattern exhibited by a number of mAb indicated that they bound antigen present within the inclusion and at the inner membrane surface of infected cells; the observed pattern differs significantly from the distribution seen when anti-lipopolysaccharide (LPS) (mAb) were used. The staining pattern observed by immunofluorescence was confirmed and extended by ultrastructure studies of immunogold-labelled, infected human endometrial gland epithelial cells (HEGEC) and a human endometrial carcinoma-derived cell line (RL95-2). Additionally, the immunoelectron microscope studies revealed binding within the inclusion and on reticulate bodies, within the cell cytoplasm and at the surface of infected cells. The specificity of the reactive mAb, examined by molecular shift chromatography and isolated, affinity-purified GLXA, indicated that two mAb of the IgG isotype recognized an antigen which had been purified from tissue culture supernatants by affinity chromatography using an IgM mAb. The results suggest that GLXA is an important determinant whose role and function during in vitro and in vivo infections deserves further analyses.
Induction of the mesendoderm in the zebrafish germ ring by yolk cell-derived TGF-β family signals and discrimination of mesoderm and endoderm by FGF (1999)

The endoderm forms the gut and associated organs, and develops from a layer of cells which emerges during gastrula stages in the vertebrate embryo. In comparison to mesoderm and ectoderm, little is known about the signals which induce the endoderm. The origin of the endoderm is intimately linked with that of mesoderm, both by their position in the embryo, and by the molecules that can induce them. We characterised a gene, zebrafish gata5, which is expressed in the endoderm from blastula stages and show that its transcription is induced by signals originating from the yolk cell. These signals also induce the mesoderm-expressed transcription factor no tail (ntl), whose initial expression coincides with gata5 in the cells closest to the blastoderm margin, then spreads to encompass the germ ring. We have characterised the induction of these genes and show that ectopic expression of activin induces gata5 and ntl in a pattern which mimics the endogenous expression, while expression of a dominant negative activin receptor abolishes ntl and gata5 expression. Injection of RNA encoding a constitutively active activin receptor leads to ectopic expression of gata5 and ntl. gata5 is activated cell-autonomously, whereas ntl is induced in cells distant from those which have received the RNA, showing that although expression of both genes is induced by a TGF-beta signal, expression of ntl then spreads by a relay mechanism. Expression of a fibroblast growth factor (eFGF) or a dominant negatively acting FGF receptor shows that ntl but not gata5 is regulated by FGF signalling, implying that this may be the relay signal leading to the spread of ntl expression. In embryos lacking both squint and cyclops, members of the nodal group of TGF-beta related molecules, gata5 expression in the blastoderm is abolished, making these factors primary candidates for the endogenous TGF-beta signal inducing gata5.
Quenching and enhancement of single-molecule fluorescence under metallic and dielectric tips (2000)

We report on fluorescence experiments by apertureless near-field optical microscopy. We develop a simple model that demonstrates the importance of non-radiative transfer and that takes into account the dependence of non-radiative transfer on tip geometry. This process is in competition with field enhancement and it is a key process to understand the observed fluorescence enhancement factors. The analysis of the different factors involved in the global fluorescence enhancement or quenching leads to new strategies to reach resolution down to a few nanometers by apertureless fluorescence microscopy.
Cost structure analysis and reference model for scaleable network services (1996)

The BOURBON (AC001) project seeks to address the issue of providing cost effective, scaleable access to advanced services for SMEs in the wider context of Europe and the information society. The project will ultimately demonstrate scaleable solutions that will allow SME based users access to services and applications in advanced communications. The SMEs involved in the project are in the toolmaking, publishing, software and graphics arts industries among others. SMEs are very sensitive to the costs of services offered. That was a result of the RACE BRITEUR project carried out in 1994-1995. Marketing costs of network services are usually higher to the SMEs than to residential users or big corporates. Therefore cost structure of the services should be studied and analyzed in order to evaluate, develop and offer scaleable network services to the SMEs. The main service selection criteria for SME should be benefits rather than price. The BOURBON project and especially testbeds of BOURBON in different countries offers a great opportunity to develop and study cost structure of scaleable SME services in Europe and produce cost analysis for the services. SMEs can benefit from the cost structure information from this project. Also, operators and service providers can develop services that fit to the SME needs economically and can produce services cost efficiently. This paper addresses the initial work performed concerning cost structures in the BOURBON project. (9 pages)
Irinophore C, a Novel Nanoformulation of Irinotecan, Alters Tumor Vascular Function and Enhances the Distribution of 5-Fluorouracil and Doxorubicin (2008)

Irinophore C treatment improves the vascular function of the tumor, thereby reducing tumor hypoxia and increasing the delivery and accumulation of a second drug. Reducing hypoxia would enhance radiotherapy, whereas improving delivery of a second drug to the tumor should result in higher cell kill.
Analysis of nuclear pore protein p62 glycosylation (1995)

Glycoprotein components of the nuclear pore are essential for nuclear transport and are modified by both glycosylation and phosphorylation. The function and control of these post-translational modifications are poorly understood. Glycosylation of the major rat nuclear pore glycoprotein, p62, was examined in vitro using recombinant p62 as a substrate. Rat p62 was expressed in Escherichia coli and purified to near homogeneity. Kinetic analysis using a partially purified mammalian transferase suggests that the recombinant protein is an excellent substrate (Km = 0.30 microM) for the transfer of GlcNAc from UDP-GlcNAc (Km = 1.8 microM). Localization of the sites of O-linked GlcNAc glycosylation of rat p62 was performed by a combination of deletion analysis of in vitro translation products and by immunoprecipitation of [14C]GlcNAc-labeled proteolytic fragments. The amino terminus of rat p62 is poorly glycosylated with no O-linked GlcNAc sites between Lys22 and Lys97; the carboxyl terminus has one known glycosylation site at Ser471. The majority of the glycosylation sites in rat p62 are likely to occur on the six clustered Ser residues in the central Ser/Thr-rich region from Ser270 to Thr294. A synthetic peptide derived from this region is a good substrate for O-GlcNAc addition (Km = 30 microM) and a potent competitive inhibitor of p62 glycosylation (Ki = 15 microM). It is proposed that this Ser/Thr-rich domain functions as a linker region between the amino-terminal beta-pleated sheet and the carboxyl terminal alpha-helical domains. O-Glycosylation and phosphorylation of this linker region could provide a dynamic means of altering the conformation of p62 during nuclear pore assembly and disassembly.
Cytokine expression in chronic inflammatory disease (1995)

In chronic inflammatory diseases, typified by rheumatoid arthritis, we speculated that upregulation and/or disregulation of cytokine production in inflamed tissue might contribute both directly and/or indirectly to the pathology in the synovial joint tissue. This chapter summarises studies performed principally by our own group over the last 9 years or so, but also by others in the field who have investigated the expression of cytokines in RA. From our studies we identified one particular cytokine, tumour necrosis factor alpha (TNF alpha) as an important, 'pivotal', molecule in the disease process. This concept has led to the initiation and completion of the first successful clinical trials in RA patients to verify this hypothesis, using a neutralising antibody to TNF alpha.
PPARgamma: from adipose tissue to the atherosclerotic plaque (1998)

Journal Article PPARgamma: from adipose tissue to the atherosclerotic plaque Get access J V Lopez-Liuchi, J V Lopez-Liuchi Division d’Endocrinologie et Diabétologie, Département de Médecine Interne, Hôpital Universitaire de Genève, Rue Micheli-du-Crest 24, 1211 Geneva 14, Switzerland Search for other works by this author on: Oxford Academic Google Scholar C A Meier C A Meier Division d’Endocrinologie et Diabétologie, Département de Médecine Interne, Hôpital Universitaire de Genève, Rue Micheli-du-Crest 24, 1211 Geneva 14, Switzerland Correspondence should be addressed to C A Meier Search for other works by this author on: Oxford Academic Google Scholar European Journal of Endocrinology, Volume 139, Issue 4, Oct 1998, Pages 363–364, https://doi.org/10.1530/eje.0.1390363 Published: 01 October 1998
Light Enables a Very High Efficiency of Carbon Storage in Developing Embryos of Rapeseed (2005)

The conversion of photosynthate to seed storage reserves is crucial to plant fitness and agricultural production, yet quantitative information about the efficiency of this process is lacking. To measure metabolic efficiency in developing seeds, rapeseed (Brassica napus) embryos were cultured in media in which all carbon sources were [U-14C]-labeled and their conversion into CO2, oil, protein, and other biomass was determined. The conversion efficiency of the supplied carbon into seed storage reserves was very high. When provided with 0, 50, or 150 micromol m(-2) s(-1) light, the proportion of carbon taken up by embryos that was recovered in biomass was 60% to 64%, 77% to 86%, and 85% to 95%, respectively. Light not only improved the efficiency of carbon storage, but also increased the growth rate, the proportion of 14C recovered in oil relative to protein, and the fixation of external 14CO2 into biomass. Embryos grown at 50 micromol m(-2) s(-1) in the presence of 5 microM 1,1-dimethyl-3-(3,4-dichlorophenyl) urea (an inhibitor of photosystem II) were reduced in total biomass and oil synthesis by 3.2-fold and 2.8-fold, respectively, to the levels observed in the dark. To explore if the reduced growth and carbon conversion efficiency in dark were related to oxygen supplied by photosystem II, embryos and siliques were cultured with increased oxygen. The carbon conversion efficiency of embryos remained unchanged when oxygen levels were increased 3-fold. Increasing the O2 levels surrounding siliques from 21% to 60% did not increase oil synthesis rates either at 1,000 micromol m(-2) s(-1) or in the dark. We conclude that light increases the growth, efficiency of carbon storage, and oil synthesis in developing rapeseed embryos primarily by providing reductant and/or ATP.