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Query: UMLS:C0024530 (malaria)
44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective survey was carried out on adult medical admissions to Kamuzu Central Hospital, Lilongwe, Malawi during the period January to December 1986, and results compared with those obtained in Queen Elizabeth Central Hospital, Blantyre in 1973. There were 4700 admissions which was more than twice the number seen in Blantyre. However, the age distribution, the pattern of disease and the overall hospital mortality were similar. Infections (malaria, pneumonia, tuberculosis, gastroenteritis/dysentery and meningitis) were the most common cause of admission, and the major causes of death were still tuberculosis, pneumonia and meningitis. Smoking related diseases were uncommon, and there was no documented case of ischaemic heart disease. The reasons for the importance of periodic surveys, such as the present study, are discussed.
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PMID:Medical admissions to Kamuzu Central Hospital, Lilongwe, Malawi in 1986: comparison with admissions to Queen Elizabeth Central Hospital, Blantyre in 1973. 229 37

We performed a series of studies to examine the sequential development of nephritis during murine malaria infections and to define the role of DNA-binding antibodies in the associated pathology. Serum levels of these antibodies were assessed throughout acute and chronic malaria infections. Increased levels of double-stranded DNA- and single-stranded DNA-binding antibodies were initially detected in mice infected with Plasmodium vinckei or Plasmodium yoelii nigeriensis during the middle stages of infection, and these levels were maintained until death. Infection with the more chronic organism Plasmodium berghei clone RC also resulted in increased single-stranded DNA-binding antibody titers, which fluctuated as the infection progressed. All three species caused kidney damage and dysfunction, as assessed by changes in morphology, blood urea nitrogen, and excreted albumin; this damage correlated with the extent of parasitemia and was observed before the levels of DNA-binding antibodies were detectably elevated in the serum. However, the results of immunohistochemical studies demonstrated that DNA-binding monoclonal antibodies bound ex vivo to glomeruli within kidneys prepared from mice at late stages of infection, after the initial damage had been incurred. Our findings suggest how DNA-binding antibodies could contribute to the kidney pathology associated with both malaria and certain autoimmune diseases, such as systemic lupus erythematosus.
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PMID:Role of DNA-binding antibodies in kidney pathology associated with murine malaria infections. 236 56

Infections with the human malaria parasite Plasmodium falciparum are characterized by sequestration of erythrocytes infected with mature forms of the parasite. Sequestration of infected erythrocytes appears to be critical for survival of the parasite and to mediate immunopathological abnormalities in severe malaria. A leukocyte differentiation antigen (CD36) was previously suggested to have a role in sequestration of malaria-infected erythrocytes. CD36 was purified from platelets, where it is known as GPIV, and was shown to be a receptor for binding of infected erythrocytes. Infected erythrocytes adhered to CD36 immobilized on plastic; purified CD36 exhibited saturable, specific binding to infected erythrocytes; and purified CD36 or antibodies to CD36 inhibited and reversed binding of infected erythrocytes to cultured endothelial cells and melanoma cells in vitro. The portion of the CD36 molecule that reverses cytoadherence may be useful therapeutically for rapid reversal of sequestration in cerebral malaria.
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PMID:Identification of a platelet membrane glycoprotein as a falciparum malaria sequestration receptor. 268 26

Infection with Plasmodium falciparum induces marked disturbances in normal immunoregulatory functions. Antigen-specific immunosuppression is a feature of acute malaria and has been linked to activation of CD8+ T suppressor cells. Among immune adults, cell-mediated immune responses to malaria antigens are extremely variable when measured in vitro, and there is no obvious relation between responsiveness and resistance to clinical disease. In this study, when CD8+ cells were removed from peripheral blood mononuclear cell preparations obtained from individuals who responded poorly to a soluble malaria antigen preparation, both lymphoproliferation and gamma interferon production were significantly enhanced, but responses to other soluble antigens and mitogen were unaffected. No effect of CD8+ cell depletion was seen in individuals whose undepleted mononuclear cells gave a high response to the malaria antigen. This suggests that for some malaria-exposed individuals, CD8+ cells activated in vitro by exposure to malaria antigens suppress other cellular responses and may obscure the presence of potentially protective immune mechanisms.
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PMID:CD8+ T cells inhibit Plasmodium falciparum-induced lymphoproliferation and gamma interferon production in cell preparations from some malaria-immune individuals. 252 21

Infections with the human malaria Plasmodium falciparum are characterized by the retention of parasitized erythrocytes in tissue capillaries and venules. Erythrocytes containing trophozoites and schizonts attach to the endothelial cells that line these vessels by means of structurally identifiable excrescences present on the surface of the infected cell. Such excrescences, commonly called knobs, are visible by means of scanning or transmission electron microscopy. The biochemical mechanisms responsible for erythrocyte adherence to the endothelial cell are still undefined. In an attempt to identify the cytoadhesive molecule on the surface of the infected cell, we have prepared monoclonal antibodies to knob-bearing erythrocytes infected with the FCR-3 strain of P. falciparum. One of these monoclonal antibodies, designed 4A3, is an IgM that reacts (by means of immunofluorescence) with the surface of unfixed erythrocytes bearing mature parasites of the knobby line; it does not react with knobless lines or uninfected erythrocytes. By immunoelectron microscopy the monoclonal antibody 4A3 was localized to the knob region. In an in vitro cytoadherence assay, the monoclonal antibody partially blocked the binding of knob-bearing cells (FCR-3 strain) to formalin-fixed amelanotic melanoma cells. The monoclonal antibody was used to immunoprecipitate a protein from extracts of knobby erythrocytes that had been previously surface iodinated. By a two-dimensional peptide mapping technique, the antigen recognized by the monoclonal antibody was found to be structurally related to band 3 protein, the human erythrocyte anion transporter.
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PMID:Characterization of a modified red cell membrane protein expressed on erythrocytes infected with the human malaria parasite Plasmodium falciparum: possible role as a cytoadherent mediating protein. 264 11

Parasitaemias and loss of natural antibody to Plasmodium falciparum were studied in 104 infants in a highly endemic area of Papua New Guinea. There were 4 cases of congenital infection. Most infants lost malaria-specific immunoglobulin G (IgG) between 4 and 7 months (median = 21 weeks). 73% of heavy infections developed in infants without detectable antimalarial IgG. Infections in the presence of antimalarial IgG were asymptomatic and had scanty parasitaemias.
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PMID:A seroepidemiological study to evaluate the role of passive maternal immunity to malaria in infants. 269 54

Burkitt's lymphoma is characterized by particular epidemiological features. It is a frequent childhood tumor in children in tropical Africa and occurs at a much lesser frequency all over the world. Chromosomal translocation affecting the long arm of chromosome 8 (band 8q24) and one of the chromosomes carrying the immunoglobulin loci (chromosomes 2, 14 or 22) are regularly observed in Burkitt's lymphoma, regardless of whether the tumor occurred in high or low incidence areas. The prevalence of Burkitt's lymphoma in Africa appears to be related to two factors: holo- or hyperendemic malaria and presence of Epstein-Barr virus genomes in the tumor cells. We present a model of pathogenesis, in which stimulation of B cells by malaria is the primary event in the development of the disease. The risk of the chromosomal translocation should be increased by increasing the number of new B cells generated per time. According to our model, the translocation leads to constitutive c-myc activation and makes the cells responsive to growth factors without inducing proliferation on its own. Infection of a translocation-carrying cell with EBV may provide an additional growth advantage and drive the cell further towards a fully malignant state.
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PMID:[Chromosome translocations and Epstein-Barr virus in Burkitt's lymphoma]. 282 99

Malaria sporozoite infection rates in a mixed species group of 244 Anopheles gambiae Giles sensu lato and 115 An.funestus Giles wild female mosquitoes were compared using three methods to determine cut-off absorbance values for positivity of a Plasmodium falciparum Welch enzyme-linked immunosorbent assay (ELISA). Positive controls were based on P.falciparum circumsporozoite protein. As negative controls, four wild male Anopheles were included on each microtitre plate; tests were repeated on four consecutive days for each plate. Infection rates were estimated at 13.1-22.8% using the mean absorbance value of negative controls plus three standard deviations, 11.7-12.8% using double the mean and 12.5-13.6% using the fixed cut-off value of 0.20 (allowing for 20% variation in negative control absorbance values). Observed agreement for positivity or negativity among samples tested four times was 98.6% for the 2 x mean method, 97.2% for the fixed cut-off 0.20 value, but only 82.7% for the mean + 3 SD method. It was concluded that the 2x mean cut-off method is most reliable for field studies. P.falciparum sporozoite rates of 12.2% in An.funestus and 11.9% in An.gambiae s.l. were thus determined on the basis of the 2x mean cut-off method. This comparative evaluation demonstrates that vector infectivity rates can be seriously over-estimated from sporozoite ELISA tests, by as much as 87% in one case considered here, depending on the absorbance cut-off method applied for negative controls.
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PMID:ELISA absorbance cut-off method affects malaria sporozoite rate determination in wild Afrotropical Anopheles. 298 Jan 82

Acute infections caused by the murine malarial parasite Plasmodium chabaudi adami are resolved by antibody-independent mechanisms of immunity. The fact that athymic nude mice developed high-grade unrelenting malaria and died when infected with this parasite suggested a significant role for T lymphocytes. Using adoptive transfer techniques, we demonstrated that spleen cells from either nonimmune or immune donor BALB/c mice eventually suppressed P. chabaudi adami infections in histocompatible recipient nude mice in a dose-dependent manner. Infections in recipients of "immune" spleen cells were less severe, demonstrating a depressed peak parasitemia and a shortened duration of patent infection, than was observed in recipients of normal spleen cells. Also, when sufficient numbers of immune spleen cells were transferred, the second wave of parasitemia (characteristic of this infection in nonimmune mice) failed to occur. T lymphocytes mediated protection in recipient mice, since T-cell-enriched, but not B-cell-enriched, spleen cell fractions suppressed P. chabaudi adami infections in nude mice. Protection was best achieved with T cells that bore the L3T4 phenotype. Patent parasitemias developed in all recipient mice, suggesting that the grafted cells did not limit parasite growth directly but achieved this end by activating other as yet unidentified inhibiting cell systems.
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PMID:T-cell immunity in murine malaria: adoptive transfer of resistance to Plasmodium chabaudi adami in nude mice with splenic T cells. 308 29

Cell-mediated immunity to malaria may involve macrophages, the monokines that mediate endotoxicity, and reactive oxygen species. Since interferon-gamma activates macrophages to release reactive oxygen species, and tumor necrosis factor-alpha (TNF-alpha) helps both to mediate endotoxicity and to induce leukocytes to secrete reactive oxygen, we monitored the effects of administering recombinant forms of these cytokines on Plasmodium chabaudi adami infections in mice. We also fed infected mice a diet containing 0.75% butylated hydroxyanisole, a scavenger of free radicals. Infections were suppressed by daily i.p. injections of 5 x 10(4) U of recombinant mouse interferon-gamma from day -1 or by recombinant human TNF released from i.p. osmotic pumps at the rate of 6 x 10(3) U/hr. Degenerate intraerythrocytic parasites (crisis forms) were evident much sooner in the course of the suppressed infections, and parasitemias fell correspondingly earlier. The butylated hydroxyanisole diet, in contrast, enhanced the infections. In these mice crisis forms were seen later, and at higher parasitemias, than they normally occur. These observations are consistent with the concept that T cell-dependent, macrophage-derived mediators are central to the type of malarial immunity that kills parasites inside circulating red cells. They also suggest, but do not prove, that both TNF and reactive oxygen species are involved, and that the role of TNF may be more indirect, although no less important, than that of reactive forms of oxygen.
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PMID:Inhibition of murine malaria (Plasmodium chabaudi) in vivo by recombinant interferon-gamma or tumor necrosis factor, and its enhancement by butylated hydroxyanisole. 311 10


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