36 research outputs found

    Critical discussion of Daniel C. Dennett, The Intentional Stance.

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    Daniel Dennett spends a good bit of time defending the possibility of a compromise position on the reality of beliefs and desires. It will be claimed that a puzzle remains in the interpretation of Dennett's position. In earlier works one finds a theme, which we can call 'near-fatalism', which has not been integrated with the kind of middle ground he describes. But the near-fatalism theme is dropped in later work. Is it because it is felt to be incompatible with that middle ground compromise? It is not obviously so

    History of malaria treatment as a predictor of subsequent subclinical parasitaemia: A cross-sectional survey and malaria case records from three villages in Pailin, western Cambodia

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    Background: Treatment of the sub-clinical reservoir of malaria, which may maintain transmission, could be an important component of elimination strategies. The reliable detection of asymptomatic infections with low levels of parasitaemia requires high-volume quantitative polymerase chain reaction (uPCR), which is impractical to conduct on a large scale. It is unknown to what extent sub-clinical parasitaemias originate from recent or older clinical episodes. This study explored the association between clinical history of malaria and subsequent sub-clinical parasitaemia. Methods: In June 2013 a cross-sectional survey was conducted in three villages in Pailin, western Cambodia. Demographic and epidemiological data and blood samples were collected. Blood was tested for malaria by high-volume qP

    Plasmodium malariae in Bangladesh

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    We describe a 32-year-old Bangladeshi male presenting with severe malaria caused by a mono-infection with Plasmodium malariae. Rosetting of infected and uninfected erythrocytes, a putative virulence factor in falciparum malaria, was observed in the blood slide. Severe disease caused by P. malariae is extremely rare. The patient made a rapid recovery with intravenous quinine treatment

    Pathogenesis of Plasmodium falciparum anaemia: metabolic modifications and signalling in red blood cells exposed to ferric protoporphyrin IX or malaria pigment

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    The pathogenesis of severe anaemia in children with P.falciparum (P.f.) malaria, has not been clarified, yet. Increased level of oxidation and signs of accelerated senescence have been demonstrated in human red blood cells co-cultured, but not infected by P.f (URBC)(Omodeo et al Blood, 2003). In addition, URBC show a marked decrease in cell deformability -a major determinant of microcirculatory obstruction and increased splenic clearance - and higher sensitivity to haemolysis. We have shown that ferric protoporphyrin IX (FP) and to a lesser extent beta haematin (BH,the synthetic haemozoin) contribute to URBC damage by reducing RBC deformability and inducing lipid and thiol oxidation of proteins leading to membrane destabilization and RBC lysis. This is counteracted by the reducing agent N-acetylcysteine (NAC) (Omodeo et al, Europ.J.Haematol, 2005). Here we report that FP, but not BH induce a dose- and time-dependent tyrosine phosphorylation (P-Tyr) (tyr 8 and 21) of Band 3, due to the oxidation of critical thiol groups of the membrane phosphatase PTP1B. The activity of glyceraldehyde 3 phosphate dehydrogenase and aldolase, two glycolytic enzymes bound to the cytosolic terminus of Band 3, is also increased. Moreover, treatment with FP leads to phosphatidylserine (PS) exposure as confirmed by annexin binding and enhanced sensitivity of RBC to phospholipase A2. FP-induced Band 3 P-Tyr and PS exposure may lead to earlier recognition and uptake of RBC by macrophages contributing to malaria anaemia. The capability of NAC of preventing FP-induced Band 3 phosphorylation is in agreement with the beneficial effects of NAC in clinical practice as adjunctive treatment in severe malaria anaemia and other RBC dysfunctions

    A new lead in malaria

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