Browsing by Author "Hidalgo, P"

Now showing 1 - 4 of 4
  • Thumbnail Image
    Item
    Calibration of structural cracking models for asphalt pavements: HDM-4 case
    (NATL INST SCIENCE COMMUNICATION, 2003) de Solminihac, H; Hidalgo, P; Salgado, M; Altamira, A
    The HDM-4 (Highway Development Management) models used for pavement management activities must be adapted to specific conditions of the country or region where they are to be used by adjusting certain calibration factors. This work presents results obtained from the calibration of structural cracking models in HDM-4 version 1.1, and comparing the results from equivalent HDM-III models. The "windows" methodology is used to reconstruct the distress performance curve of a specific road category based on the observation of conditions of diverse roads with similar characteristics (such as traffic, pavement structural capacity and climatic conditions) but different ages. Also, recommendations are made for calibrating performance models, as well as for establishing calibration factors for asphalt pavement structural cracking models more appropriate for Chilean roads. Although the results of the HDM-III and HDM-4 calibrated models have similar values, the HDM-4 version 1.1 cracking models are recommended due to their operational advantages.
  • Thumbnail Image
    Item
    Glycoprotein Ib/IX complex is the target in rifampicin-induced immune thrombocytopenia
    (BLACKWELL SCIENCE LTD, 2000) Pereira, J; Hidalgo, P; Ocqueteau, M; Blacutt, M; Marchesse, M; Nien, Y; Letelier, L; Mezzano, D
    Thrombocytopenia is a major adverse effect of several drug treatments. Rifampicin has been recognized as a cause of immune thrombocytopenia during intermittent high-dose therapy. We characterized the antibody of a patient who presented with purpura and thrombocytopenia during treatment of tuberculosis with rifampicin. Drug-dependent binding of the antibody to platelets was demonstrated by flow cytometry. In a glycoprotein-specific immunoassay, the binding epitope of the IgG antibody was found in the glycoprotein Ib/IX complex, using four different monoclonal antibodies (mAbs) against various epitopes on the GPIb/IX complex, as well as mAbs against GPIIb/IIIa, GPIa/IIa and GPIV. By immunoprecipitation of biotin-labelled platelets, reactivity of the antibody with GPIb/IX was found only in the presence of the drug. These findings clearly demonstrate that rifampicin induces the formation of drug-dependent antibodies capable of causing thrombocytopenia. The binding site of the rifampicin-dependent antibody, located in the GPIb/IX complex, seems to be a favoured target for antibodies induced by different drugs.
  • Thumbnail Image
    Item
    Platelet membrane glycoprotein polymorphisms do not influence the clinical expressivity of von Willebrand disease type I
    (SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN, 2003) Pereira, J; Quiroga, T; Pereira, ME; Morales, M; Goycoolea, M; Hidalgo, P; Prieto, C; Mezzano, D
    Von Willebrand disease (VWD) is characterized by a significant variation in bleeding symptoms among patients with similar laboratory profiles and equivalent plasma levels of von Willebrand factor (VWF) activities. Considering the recent suggestion that platelet membrane glycoprotein polymorphisms (PltGPs) may play a role as modulators of thromboembolic or haemorrhagic diseases, we investigated the role of different PltGPs and GPVI content in the clinical expression of patients with VWD type 1. The diagnosis of VWD (n = 76) was based on laboratory findings (VWF:Ag, VWF:RCo, VWF:CB, FVIII:C, and multimer analysis), family and personal history of bleeding. All patients were interviewed using a standardized questionnaire, and classified into two categories: bleeders (unequivocal bleeding tendency, n = 53) and non bleeders (absence of bleeding symptoms, n = 23). PltGPs, HPA-1, 2 and 5 and C807T of GPla were determined by fluorophore-labelled hybridization probes on a LightCycler(TM). GPVI content was measured by western blotting.
  • Thumbnail Image
    Item
    Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis
    (WILEY, 2005) Palomo, I; Pereira, J; Alarcon, M; Diaz, G; Hidalgo, P; Pizarro, I; Jara, E; Rojas, P; Quiroga, G; Moore Carrasco, R
    Heparin-induced thrombocytopenia (HIT) type II is a serious complication of heparin therapy. It presents initially as thrombocytopenia, and is associated with thrombosis in 20-50% of the cases. HIT is related to the presence of heparin-induced antibodies (HIA), which show specificity for the PF4-heparin (PF4-H) complex. The Fc gamma RIIa receptor has been suggested to participate in the pathogenic mechanism of HIA. Since patients undergoing chronic hemodialysis (HD) are exposed repeatedly to heparin, we studied the prevalence of HIA and their eventual relationship with thrombocytopenia and/or thrombosis, and the possible participation of the Fc gamma RIIa polymorphism. We studied 207 patients with chronic renal failure (CRF) undergoing HID. As a control we included 130 blood donors and 28 patients with CRF without HID. The HIA patients were studied with the use of a PF4-H ELISA. Additionally, in some positive cases for the previous test, a C-14- serotonin release assay (C-14-SRA) was performed. The polymorphism Fc gamma RIIa H/R131 was studied by polymerase chain reaction (PCR) with allele-specific primers. Thirty-seven patients (17.9%) undergoing HD presented with HIA. The majority of these antibodies were IgG, IgM, and IgA. The HIA investigated presented specificity against the PF4-H complex, but not against PF4 alone (P < 0.001). Twelve out of 22 (54.5%) PF4-H antibodies were positive when tested with the C-14-SRA. The distribution of the Fc gamma RIIa polymorphism in patients and healthy controls was 42.6% and 41.6% for H/H131, 41% and 48.9% for the H/R131 isoform, and 16.4% and 9.5% for the R/R131 isoform, respectively. No statistically significant difference in the Fc gamma RIIa isoform distribution was found. Twenty-nine out of 156 patients (18.5%) presented thrombocytopenia, and 21/207 (12.4%) had thrombosis of the native vein arterio-venous fistula (AVF). We did not find any statistically significant between HIA and thrombocytopenia or thrombosis. An important proportion of patients with CRF undergoing HD developed HIA, but these cases were not associated with thrombocytopenia or thrombosis of AVF. The frequency of the Fc gamma RIIa polymorphism did not statistically differ between HIT type II and normal controls.