Browsing by Author "Palomo, I"

Now showing 1 - 5 of 5
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    Multiple conceptualizations of nature are key to inclusivity and legitimacy in global environmental governance
    (2020) Coscieme, L; Hyldmo, HD; Fernandez-Llamazares, A; Palomo, I; Mwampamba, TH; Selomane, O; Sitas, N; Jaureguiberry, P; Takahashi, Y; Lim, M; Barral, MP; Farinaci, JS; Diaz-Jose, J; Ghosh, S; Ojino, J; Alassaf, A; Baatuuwie, BN; Balint, L; Basher, Z; Boeraeve, F; Budiharta, S; Chen, RS; Desrousseaux, M; Dowo, G; Febria, C; Ghazi, H; Harmackova, ZV; Jaffe, R; Kalemba, MM; Lambini, CK; Lasmana, FPS; Mohamed, AAA; Niamir, A; Pliscoff, Patricio; Sabyrbekov, R; Shrestha, UB; Samakov, A; Sidorovich, AA; Thompson, L; Valle, M
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    Platelet aging in vivo is associated with activation of apoptotic pathways: Studies in a model of suppressed thrombopoiesis in dogs
    (SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN, 2002) Pereira, J; Soto, M; Palomo, I; Ocqueteau, M; Coetzee, LM; Astudillo, S; Aranda, E; Mezzano, D
    The mechanism(s) involved in the clearance of senescent platelets are largely unknown. We have recently demonstrated that platelet aging in vivo is associated with loss of membrane phospholipid asymmetry, a universal phenomenon in cells undergoing apoptosis. Thus, We postulated that senescent platelets may exhibit programmed cell death changes, which may trigger their removal from circulation. Since platelets contain the apoptosis machinery as well as mitochondria, a key organelle in the regulation of apoptosis, we studied the appearance of apoptotic-like changes during platelet aging in vivo. To investigate this, we assessed changes in mitochondrial membrane potential in circulating canine platelets during decline in platelet Count after suppression of thrombopoiesis by estradiol injection. a validated model to obtain circulating platelets of increasing mean ace. Phosphatidyl-serine (PS) exposure was determined by flow cytometry by binding of FITC-labeled annexin V. Mitochondrial Deltapsi was studied with the cationic lipophilic dye DIOC6 (3) and the J-aggregate-forming cation JC-1 and analysis by flow cytometry. The proportion of platelets with exposed PS rose significantly with age, from 2.88% before to 6.7%. 8 days after estradiol injection. By flow, cytometry it was demonstrated a significant decreased in DIOC6 (3) fluorescence (median fluorescence intensity 791 98 vs 567 1021 day 0 vs day 8 post injection of estradiol, respectively n:11; p<0.01), consistent with mitochondrial &UDelta;ψ collapse. JC-1 has the unique property of forming J-aggregates tinder high mitochondrial &UDelta;ψ (red fluorescence, FL2) whereas the monomeric form fluoresces in green (FL1). Aged platelets in vivo, loaded with JC-1, exhibited a significant increase in FL1/FL2 ratio (2.5&PLUSMN;1.7 vs 4.7&PLUSMN;1.6, day 0 vs day 8 post injection of estradiol, respectively n:13; p<0.05). confirming the mitochondrial Deltapsi alteration.
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    Platelet aging in vivo is associated with loss of membrane phospholipid asymmetry
    (F K SCHATTAUER VERLAG GMBH, 1999) Pereira, J; Palomo, I; Ocqueteau, M; Soto, M; Aranda, E; Mezzano, D
    The mechanism(s) involved in the clearance of senescent platelets are largely unknown. The loss of membrane phospholipid (PL) asymmetry, with phosphatidylserine (PS) exposure appears to be an important signal for the ingestion by macrophages of apoptotic nucleated cells and it has also been suggested as a signal for the removal of aged erythrocytes. Accordingly, it seems possible that the clearance of normal aged platelets from circulation might be triggered by PS exposure. To investigate this, we determined PS exposure in human aging platelets taking advantage of the relationship between platelet density and platelet age and in dog platelets in a model of platelet aging in vivo. PS exposure was determined in two experimental conditions: 1) human platelet density subpopulations obtained by centrifugation in arabinogalactan gradients; 2) circulating canine platelets during decline in platelet count after suppression of thrombopoiesis following estradiol injection. PS exposure was determined by flow cytometry after labeling the cells with FITC-conjugated annexin V. The proportion of human platelets with exposed PS was significantly higher in high density (HD) platelets compared to low density (LD) platelets (11.3 +/- 8.0% vs 5.2 +/- 3.7%; p < 0.05, respectively). In dogs, the proportion of cells with exposed PS rises dramatically with age, from 3.1 +/- 0.4% before to 17.7 +/- 12.3% ten days after estradiol injection. These findings suggest that platelet aging is associated with loss of phospholipid asymmetry and PS exposure on the outer leaflet of cell membrane, which may play an important role in the recognition and subsequent removal of senescent platelets.
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    Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)-infected Chilean patients
    (WILEY, 2003) Palomo, I; Alarcon, M; Sepulveda, C; Pereira, J; Espinola, R; Pierangeli, S
    Antiphospholipid (aPL) and antiplatelet (aPlt) antibodies, found in patients with autoimmune diseases, are also detected in infectious diseases. The purpose of this study was to examine the prevalence of these antibodies in HIV patients and to evaluate an association of these antibodies with thrombocytopenia and/or thrombosis. Sixty-three HIV-seropositive patients and 52 normal controls were studied. Anticardiolipin (aCL), anti-beta(2) glycoprotein I (anti-beta(2)GPI), and antiprothrombin (aPT) antibodies were determined and the lupus anticoagulant (LA) test was performed. Antiplatelet antibodies (aPlt) were also determined. Seven out of 63 (12.7%) HIV patients were positive for aCL, four of 63 (6.3%) for anti-beta(2)GPI, and five of 63 (7.9%) for aPT. No patients studied were LA positive. Six out of 63 (9.5%) patients were positive for aPlt. One of them showed weak reactivity for GPIb-IX. The platelet count of patients (202 +/- 63 x 10(3) platelets/muL) was significantly lower than in the controls (343+/-6 x 10(3) platelets/muL) (P<0.001). There was no correlation between the presence of aPL and/or aPlt and thrombocytopenia. Of the HIV-infected patients, 22.2% presented aPL and 9.4% aPlt antibodies. In this study, the presence of aPL and aPlt antibodies was not associated with the development of thrombosis and/or thrombocytopenia. (C) 2003 Wiley-Liss, Inc.
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    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.