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- Richard, G., et al.
(author)
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Multi Modal Verification for Teleservices and Security Applications (M2VTS)
- 1999
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In: IEEE International Conference on Multimedia Computing and Systems. - Los Alamitos : IEEE. - 0769502539 ; , s. 1061-1064
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Conference paper (other academic/artistic)abstract
- This paper presents the European ACTS project M2VTS which stands for Multi Modal Verification for Teleservices and Security Applications. The primary goal of this project is to address the issue of secured access to local and centralised services in a multimedia environment. The main objective is to extend the scope of application of network-based services by adding novel and intelligent functionalities, enabled by automatic verification systems combining multimodal strategies (secured access based on speech, image or other information). The objectives of the project are also to show that limitations of individual technologies (speaker verification, frontal face authentication, profile identification,...) can be overcome by relying on multi-modal decisions (combination or fusion of these technologies).
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| 4. |
- Rakov, V. A., et al.
(author)
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New insights into lightning processes gained from triggered-lightning experiments in Florida and Alabama
- 1998
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In: Journal of Geophysical Research - Atmospheres. - 2169-897X .- 2169-8996. ; 103:D12, s. 14117-14130
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Journal article (peer-reviewed)abstract
- Analyses of electric and magnetic fields measured at distances from tens to hundreds of meters from the ground strike point of triggered lightning at Camp Blanding, Florida, and at 10 and 20 m at Fort McClellan, Alabama, in conjunction with currents measured at the lightning channel base and with optical observations, allow us to make new inferences on several aspects of the lightning discharge and additionally to verify the recently published “two-wave†mechanism of the lightning M component. At very close ranges (a few tens of meters or less) the time rate of change of the final portion of the dart leader electric field can be comparable to that of the return stroke. The variation of the close dart leader electric field change with distance is somewhat slower than the inverse proportionality predicted by the uniformly charged leader model, perhaps because of a decrease of leader charge density with decreasing height associated with an incomplete development of the corona sheath at the bottom of the channel. There is a positive linear correlation between the leader electric field change at close range and the succeeding return stroke current peak at the channel base. The formation of each step of a dart-stepped leader is associated with a charge of a few millicoulombs and a current of a few kiloamperes. In an altitude-triggered lightning the downward negative leader of the bidirectional leader system and the resulting return stroke serve to provide a relatively low-impedance connection between the upward moving positive leader tip and the ground, the processes that follow likely being similar to those in classical triggered lightning. Lightning appears to be able to reduce, via breakdown processes in the soil and on the ground surface, the grounding impedance which it initially encounters at the strike point, so at the time of channel-base current peak the reduced grounding impedance is always much lower than the equivalent impedance of the channel. At close ranges the measured M-component magnetic fields have waveshapes that are similar to those of the channel-base currents, whereas the measured M-component electric fields have waveforms that appear to be the time derivatives of the channel-base current waveforms, in further confirmation of the “two-wave†M-component mechanism.
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| 6. |
- Alvarez Fernandez, Marcia, et al.
(author)
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Inhibition of mammalian legumain by some cystatins is due to a novel second reactive site
- 1999
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In: Journal of Biological Chemistry. - 1083-351X. ; 274:27, s. 19195-19203
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Journal article (peer-reviewed)abstract
- We have investigated the inhibition of the recently identified family C13 cysteine peptidase, pig legumain, by human cystatin C. The cystatin was seen to inhibit enzyme activity by stoichiometric 1:1 binding in competition with substrate. The Ki value for the interaction was 0.20 nM, i.e. cystatin C had an affinity for legumain similar to that for the papain-like family C1 cysteine peptidase, cathepsin B. However, cystatin C variants with alterations in the N-terminal region and the "second hairpin loop" that rendered the cystatin inactive against cathepsin B, still inhibited legumain with Ki values 0.2-0.3 nM. Complexes between cystatin C and papain inhibited legumain activity against benzoyl-Asn-NHPhNO2 as efficiently as did cystatin C alone. Conversely, cystatin C inhibited papain activity against benzoyl-Arg-NHPhNO2 whether or not the cystatin had been incubated with legumain, strongly indicating that the cystatin inhibited the two enzymes with non-overlapping sites. A ternary complex between legumain, cystatin C, and papain was demonstrated by gel filtration supported by immunoblotting. Screening of a panel of cystatin superfamily members showed that type 1 inhibitors (cystatins A and B) and low Mr kininogen (type 3) did not inhibit pig legumain. Of human type 2 cystatins, cystatin D was non-inhibitory, whereas cystatin E/M and cystatin F displayed strong (Ki 0.0016 nM) and relatively weak (Ki 10 nM) affinity for legumain, respectively. Sequence alignments and molecular modeling led to the suggestion that a loop located on the opposite side to the papain-binding surface, between the alpha-helix and the first strand of the main beta-pleated sheet of the cystatin structure, could be involved in legumain binding. This was corroborated by analysis of a cystatin C variant with substitution of the Asn39 residue in this loop (N39K-cystatin C); this variant showed a slight reduction in affinity for cathepsin B (Ki 1.5 nM) but >>5,000-fold lower affinity for legumain (Ki >>1,000 nM) than wild-type cystatin C.
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| 10. |
- Fernandez-Mateos, P, et al.
(author)
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Point mutations and deletion responsible for the Bombay H null and the Reunion H weak blood groups.
- 1998
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In: Vox sanguinis. - 0042-9007. ; 75:1, s. 37-46
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Definition of the molecular basis of the Reunion and the Bombay red cell and salivary H-deficient phenotypes. METHODS: Sequence and expression of FUT1 and FUT2 genes from H-deficient individuals. Family segregation analysis of the mutations responsible for the fucosyltransferase defects of H, secretor and Lewis systems. RESULTS: The Indian red cell H null Bombay phenotype depends on a new mutation of the FUT1 gene. T725-->G changing Leu242-->Arg. Their salivary nonsecretor phenotype is secondary to a complete deletion of the FUT2 gene. The red cell H weak Reunion phenotype depends on another new mutation of FUT1, C349-->T which induces a change of His117-->Tyr. Their salivary nonsecretor phenotype is due to the known Caucasian inactivating mutation G428-->A. CONCLUSION: Single prevalent FUT1 and FUT2 point mutations and a deletion are responsible for the Indian Bombay H null and the Reunion H weak phenotypes found on Reunion island. This is in contrast with other H-deficient phenotypes where sporadic nonprevalent inactivating mutations are the rule.
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| 11. |
- Fernandez, V, et al.
(author)
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Small, clonally variant antigens expressed on the surface of the Plasmodium falciparum-infected erythrocyte are encoded by the rif gene family and are the target of human immune responses
- 1999
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In: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 190:10, s. 1393-1403
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Journal article (peer-reviewed)abstract
- Disease severity in Plasmodium falciparum infections is a direct consequence of the parasite's efficient evasion of the defense mechanisms of the human host. To date, one parasite-derived molecule, the antigenically variant adhesin P. falciparum erythrocyte membrane protein 1 (PfEMP1), is known to be transported to the infected erythrocyte (pRBC) surface, where it mediates binding to different host receptors. Here we report that multiple additional proteins are expressed by the parasite at the pRBC surface, including a large cluster of clonally variant antigens of 30–45 kD. We have found these antigens to be identical to the rifins, predicted polypeptides encoded by the rif multigene family. These parasite products, formerly called rosettins after their identification in rosetting parasites, are prominently expressed by fresh isolates of P. falciparum. Rifins are immunogenic in natural infections and strain-specifically recognized by human immune sera in immunoprecipitation of surface-labeled pRBC extracts. Furthermore, human immune sera agglutinate pRBCs digested with trypsin at conditions such that radioiodinated PfEMP1 polypeptides are not detected but rifins are detected, suggesting the presence of epitopes in rifins targeted by agglutinating antibodies. When analyzed by two-dimensional electrophoresis, the rifins resolved into several isoforms in the pI range of 5.5–6.5, indicating molecular microheterogeneity, an additional potential novel source of antigenic diversity in P. falciparum. Prominent polypeptides of 20, 22, 76–80, 140, and 170 kD were also detected on the surfaces of pRBCs bearing in vitro–propagated or field-isolated parasites. In this report, we describe the rifins, the second family of clonally variant antigens known to be displayed by P. falciparum on the surface of the infected erythrocyte.
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| 12. |
- Mannervik, B, et al.
(author)
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An evolutionary approach to the design of glutathione-linked enzymes
- 1998
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In: CHEMICO-BIOLOGICAL INTERACTIONS. - : ELSEVIER SCI IRELAND LTD. - 0009-2797. ; 112, s. 15-21
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Journal article (other academic/artistic)abstract
- Studies of protein structure provide information about principles of protein design that have come into play in natural evolution. This information can be exploited in the redesign of enzymes for novel functions. The glutathione-binding domain of glutathi
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| 13. |
- Perlmann, P, et al.
(author)
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Immunoglobulin E, a pathogenic factor in Plasmodium falciparum malaria
- 1997
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In: Infection and immunity. - : American Society for Microbiology. - 0019-9567 .- 1098-5522. ; 65:1, s. 116-121
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Journal article (peer-reviewed)abstract
- Most children and adults living in areas where the endemicity of Plasmodium falciparum malaria is high have significantly elevated levels of both total immunoglobulin E (IgE) and IgE antimalarial antibodies in blood. This elevation is highest in patients with cerebral malaria, suggesting a pathogenic role for this immunoglobulin isotype. In this study, we show that IgE elevation may also be seen in severe malaria without cerebral involvement and parallels an elevation of tumor necrosis factor alpha (TNF). IgE-containing serum from malaria immune donors was added to tissue culture plates coated with rabbit anti-human IgE antibodies or with P. falciparum antigen. IgE-anti-IgE complexes as well as antigen-binding IgE antibodies induced TNF release from peripheral blood mononuclear cells (PBMC). Nonmalaria control sera with no IgE elevation induced significantly less of this cytokine, and the TNF-inducing capacity of malaria sera was also strongly reduced by passing them over anti-IgE Sepharose columns. The cells giving rise to TNF were adherent PBMC. The release of this cytokine probably reflects cross-linking of their low-affinity receptors for IgE (CD23) by IgE-containing immune complexes known to give rise to monocyte activation via the NO transduction pathway. In line with this, adherent monocytic cells exposed to IgE complexes displayed increased expression of CD23. As the malaria sera contained IgG anti-IgE antibodies, such complexes probably also play a role in the induction of TNF in vivo. Overproduction of TNF is considered a major pathogenic mechanism responsible for fever and tissue lesions in P. falciparum malaria. This overproduction is generally assumed to reflect a direct stimulation of effector cells by certain parasite-derived toxins. Our results suggest that IgE elevation constitutes yet another important mechanism involved in excessive TNF induction in this disease.
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