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Träfflista för sökning "WFRF:(Fernandez A. M.) srt2:(1997-1999)"

Sökning: WFRF:(Fernandez A. M.) > (1997-1999)

  • Resultat 1-11 av 11
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1.
  • Rakov, V. A., et al. (författare)
  • New insights into lightning processes gained from triggered-lightning experiments in Florida and Alabama
  • 1998
  • Ingår i: Journal of Geophysical Research - Atmospheres. - 2169-897X .- 2169-8996. ; 103:D12, s. 14117-14130
  • Tidskriftsartikel (refereegranskat)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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2.
  • Chen, Q, et al. (författare)
  • Identification of Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) as the rosetting ligand of the malaria parasite P. falciparum
  • 1998
  • Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 187:1, s. 15-23
  • Tidskriftsartikel (refereegranskat)abstract
    • Severe Plasmodium falciparum malaria is characterized by excessive sequestration of infected and uninfected erythrocytes in the microvasculature of the affected organ. Rosetting, the adhesion of P. falciparum–infected erythrocytes to uninfected erythrocytes is a virulent parasite phenotype associated with the occurrence of severe malaria. Here we report on the identification by single-cell reverse transcriptase PCR and cDNA cloning of the adhesive ligand P. falciparum erythrocyte membrane protein 1 (PfEMP1). Rosetting PfEMP1 contains clusters of glycosaminoglycan-binding motifs. A recombinant fusion protein (Duffy binding-like 1–glutathione S transferase; Duffy binding-like-1–GST) was found to adhere directly to normal erythrocytes, disrupt naturally formed rosettes, block rosette reformation, and bind to a heparin-Sepharose matrix. The adhesive interactions could be inhibited with heparan sulfate or enzymes that remove heparan sulfate from the cell surface whereas other enzymes or similar glycosaminoglycans of a like negative charge did not affect the binding. PfEMP1 is suggested to be the rosetting ligand and heparan sulfate, or a heparan sulfate–like molecule, the receptor both for PfEMP1 binding and naturally formed erythrocyte rosettes.
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  • Fernandez-Mateos, P, et al. (författare)
  • Point mutations and deletion responsible for the Bombay H null and the Reunion H weak blood groups.
  • 1998
  • Ingår i: Vox sanguinis. - 0042-9007. ; 75:1, s. 37-46
  • Tidskriftsartikel (refereegranskat)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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8.
  • Mannervik, B, et al. (författare)
  • An evolutionary approach to the design of glutathione-linked enzymes
  • 1998
  • Ingår i: CHEMICO-BIOLOGICAL INTERACTIONS. - : ELSEVIER SCI IRELAND LTD. - 0009-2797. ; 112, s. 15-21
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)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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9.
  • Richard, G., et al. (författare)
  • Multi Modal Verification for Teleservices and Security Applications (M2VTS)
  • 1999
  • Ingår i: IEEE International Conference on Multimedia Computing and Systems. - Los Alamitos : IEEE. - 0769502539 ; , s. 1061-1064
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)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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10.
  • Alvarez Fernandez, Marcia, et al. (författare)
  • Inhibition of mammalian legumain by some cystatins is due to a novel second reactive site
  • 1999
  • Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 274:27, s. 19195-19203
  • Tidskriftsartikel (refereegranskat)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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