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Historical review of piscine trypanosomiasis115Tait A. 1980. Evidence for diploidy and mating in Mastacembelus armatus in Maharashtra, India. Archtrypanosomes. Nature 283:536-538. Protistenkd 133:111-124.Tanabe M. 1925. Studies on the haemoflagellate of the loach, Warsi A and Fattohy ZI. 1976. Trypanosoma acanthobramaeMisgurus anguillicaudatus. Kitasato Arch Exp Med 6:121- n.sp. from freshwater fish Acanthobrama marmid (Heckel)138. (Family: Cyprinidae) from the river Tigris, Iraq. Curr SciTandon RS. 1986. Biochemical changes in fish (Wallago attu)215:838-839.infected with Trypanosoma. Ind J Parasitol 10: 87-91.Wita I and Ovcharenko M. 1997. Wystepowanie SwidrowcowTrypanosoma crasii we kewi ploci Rutilus rutilus I LinaTandon RS and Chandra S. 1977a. Physiology of host parasiteTinca tinca. Wiad Parazytol 43:385-392.relationship: Effects on serum alkaline phosphatase levelsof fish hosts parasitized by trypanosomes. Zeit Parasitenkd Wita I, Karbowiak G and Jezewski W. 2001. Wystepowanie52:195-198. Swidrowcow Rodzaju Trypanosoma U Leszcza Abramisbrama W Jeziorach Goslawskim I Goplo. Wiad ParazytolTandon RS and Chandra S. 1977b. Studies on ecophysiology offish parasites: Effect of trypanosomes on the serumcholesterol levels of fishes. Zeit Parasitenkd 52:199-202.Tandon RS and Joshi BD. 1973. Studies on the physiopathologyof blood of freshwater fishes infected with two new forms oftrypanosomes. Z Wiss Zool Leipzig 185: 207-221.Valentin GG. 1841. Ube rein Entozoon in Blute Von, Salmafario. Arch Anat Physiol 435.47:383-387.Woo PTK. 1969. The haematocrit centrifuge for the detectionof trypanosomes in blood. Can J Zool 47:921-923.Woo PTK. 1981a. Trypanosoma danilewskyi: A newmultiplication process for Trypanosoma (Protozoa:Kinetoplastida). J Parasitol 67:522-526.Woo PTK. 1981b. Acquired immunity against Trypanosomadanilewskyi in gold fish Carassius auratus. ParasitologyrdVan Duijin C. 1973. Diseases of fish. 3 ed. Thomas, 83:343-346.Springfield. Illinois.Woo PTK. 1995. Fish diseases and disorders. CABWahul MA. 1986a. Three new trypanosomes from water fishes International UK. pp 808.of the genus Mystus from Maharashtra (India). Ind JParasitol 10:217-227.Woo PTK Wehnert SD and Rodgers D. 1983. The susceptibilityof fishes to haemoflagellates at different ambientWahul MA. 1986b. Morphology of three new trypanosomes temperatures. Parasitology 87:385-392.from fresh water fishes of the genus Puntius. ArchProtistenkd.132:101-111.Yatindra and Mathur BN. 1986. Studies on Trypanosomaseenghali var. nov. sophorae from Puntius sophore. Curr SciWahul MA. 1987. Studies on the morphology of three new 55: 471-473.species of trypanosomes from the fresh water fish
Journal of Parasitic Diseases: December 2006, Vol. 30, No. 2, 116–124ReviewJ P DMalaria and macrophages: cellular and molecular basisof pathogenesis and immune protectionPrati Pal SinghNational Institute of Pharmaceutical Education and Research, S. A. S. Nagar.ABSTRACT. The roles of macrophages (MØs) in the pathogenesis and resolution of malariainfection is well known. However, the mechanisms of plasmodium-infected erythrocytes (IE)interaction with MØs leading to their internalization, factors that interfere with MØ-IEinteraction, the details of the factors and the mechanism(s) which activate MØs for augmentedphagocytosis of IE, the fate of IE ingested by MØs, and the nature and functions of variouscytokines generated by IE-ingested MØs, remain poorly understood. The Fc-receptors, and not thecomplement receptors, appear to mediate the attachment and internalization of IE by MØs.Immune-complexes (ICs) formed during acute malaria may inhibit the phagocytosis of IE early inthe infection, but, over time, may induce changes in MØs which result in the enhanced phagocytosisof IE. In cultures of splenocytes from animals immune to malaria, IE-containing MØs presentantigens to sensitized T-cells, which, in turn, elaborate lymphokines (LKs); these LKs are thoughtto activate MØs for enhanced phagocytosis of IE. Neutralizing concentrations of monoclonalantibodies against mouse interferon-gamma (IFN-γ) and interleukin-4 (IL-4) blocked the MØactivating activity of these LKs, which indicate that IFN-γ and IL-4, plausibly present in these LKpreparations, were responsible for the observed MØ activation. Both plasmodial components andintact IE can activate MØs and monocytes to produce colony-stimulating factors (CSFs), de novo, ina lipopolysaccharide-independent manner. Chloroquine, a lysosomotropic drug, inhibited theplasmodial antigen-induced production of CSFs by MØs. Purified human C-reactive protein(CRP) stimulated rhesus monkey (Macaca mulatta) blood monocyte-derived MØs for enhancedphagocytosis of Plasmodium fragile-IE, in vitro. These observations suggest that MØ-IE interactionand subsequent erythrophagocytosis constitute important steps in the pathogenesis and protectiveimmunity to malaria, and detailed molecular studies are warranted to understand the role(s) ofMØs in both parasite clearance and disease-causing mechanisms in malaria, which may be usefulfor the development of anti-disease and/or anti-parasite vaccine(s) against malaria.Keywords: C-reactive protein, cytokines, infected-erythrocytes, macrophages, malaria,phagocytosisINTRODUCTIONAt the end of 2004, 3.2 billion people in 107 countriesand territories lived in malaria transmission risk areas,and each year an estimated 300–500 million clinicalCorrespondence: Prof. Prati Pal Singh, National Institute ofPharmaceutical Education and Research, Sector-67, S. A. S.Nagar-160 062, India. E-mail: drppsingh2002@yahoo.commalaria cases and > 1 million falciparum malariadeaths occur (WHO, 2005). The four species of theprotozoan parasite that cause human malarias are:Plasmodium falciparum, P. vivax, P. malariae and P.ovale. Whereas, P. falciparum causes the most severeform of malaria, P. vivax, characterized by relapses, isnot fatal; together they cause 95% of world malaria.The parasite and vector resistance to anti-malarial
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J P DAUTHOR INDEX (2006)Agrawal, MC
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J P DLIST OF REFEREES (2006)Dr. S.
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