Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-one patients with falciparum malaria were studied prospectively to determine the plasma concentrations of the lysosomal proteinase, polymorphonuclear leucocyte elastase (PMN-elastase) and their relationship to disease severity. The patients were divided into 3 groups; severe (parasitaemia > 5%) or vital organ dysfunction (n = 23), moderate (parasitaemia 1%-5% without complications) (n = 15), and mild (parasitaemia < 1%) (n = 23). The mean plasma PMN-elastase level in 10 healthy Thai volunteers was 49.5 (SD = 21.6) ng/ml (range 33-65 ng/ml). Plasma PMN-elastase concentrations on admission were elevated (> 2 x SD above normal) in all patients with severe malaria and were above 100 ng/ml in 86.6% and 65% of the moderately severe and mild patients respectively. PMN-elastase levels during the first 3 hospital days were significantly higher in severe malaria compared with the other 2 groups (P = < 0.001-0.013). The levels decreased as the patients became afebrile and aparasitaemic. Admission plasma concentrations of PMN-elastase correlated directly with bilirubin (rs = 0.50, P < 0.001), serum glutamic oxalacetic transaminase (rs = 0.54, P0.001), parasite count (rs = 0.62, P < 0.001), blood urea nitrogen (rs = 0.54, P < 0.001) and inversely with antithrombin III activity (rs = 0.54, P < 0.001) and the platelet count (rs = 0.58, P < 0.001). Polymorphonuclear leucocyte activation may contribute to the pathogenesis of severe malaria.
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PMID:Polymorphonuclear leucocyte elastase in Plasmodium falciparum malaria. 128 9

We have examined the possible risk factors for poor prognosis in cerebral malaria in 61 Nigerian children in an area of high malaria transmission. The level of coma, decerebrate rigidity, hypoglycaemia, and high urea levels were indicators of poor prognosis. Pyrexia, vomiting, and anaemia did not influence prognosis. Post-mortem findings suggest gross cerebral oedema and raised intracranial pressure in 4 of 7 cases with petechial haemorrhages and small focal necrosis (Durck's granuloma).
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PMID:Prognostic risk factors and post mortem findings in cerebral malaria in children. 147 13

The previously described Plasmodium falciparum blood stage antigen, 5.1 (also referred to as exp-1) was expressed at a high level in Escherichia coli. Saimiri monkeys immunised with purified recombinant antigen 5.1 were partially protected from P. falciparum blood stage parasite challenge. The gene coding for 5.1 was combined with DNA coding for an (Asn-Ala-Asn-Pro)19 sequence (abbreviated (NANP)19 in the one-letter amino acid code). To facilitate purification of the recombinant protein, DNA coding for a hexahistidine (His6) sequence was introduced at the 5' end of the gene (proteins containing His6 have high affinity for Ni(2+)-chelate columns even in the presence of 6 M guanidine HCl). The recombinant protein, His6-5.1-(NANP)19 with an apparent molecular size of 40 kDa could be highly purified by a combination of 4 steps: (1) release and solubilization of the recombinant fusion protein from E. coli in the presence of 6 M guanidine-HCl; (2) precipitation of over 60% of the bacterial proteins by the addition of ammonium sulphate to 50% saturation; (3) affinity chromatography on a Ni(2+)-chelate column in the presence of 6 M guanidine-HCl; (4) adsorption onto a cation exchange resin in the presence of 6 M urea, and elution with an increasing NaCl gradient. Compared with the previously tested tetanus toxoid-(NANP)3 malaria vaccine, this protein elicits an anti-(NANP)n response which more closely resembles that evoked by native sporozoites. The recombinant vaccine also induces the production of antibodies against the blood stages of the malaria parasite.
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PMID:A Plasmodium falciparum malaria vaccine candidate which contains epitopes from the circumsporozoite protein and a blood stage antigen, 5.1. 171 16

Methods were developed for the production of clinical grade malaria vaccine candidates expressed in E. coli by recombinant DNA technologies. The essential features of the purification protocol consist of (1) mechanical breakage of host cells and solubilization of the recombinant proteins in 6 M guanidine hydrochloride; (2) ammonium sulfate fractionation; (3) affinity chromatography on a Ni(2+)-chelate gel in the presence of 6 M guanidine hydrochloride; and (4) ion exchange chromatograph on a Phospho Ultrogel column in the presence of 6 M urea. The use of undesirable chemicals (PMSF, DFP, TFA, acetonitrile, etc.) was avoided rather than demonstrating their complete removal after the purification steps. Testing of chromatographic fractions for host-cell proteins and the elimination of fractions with E. coli protein content was found necessary to obtain a final product that contained less than 0.01% of host derived proteins. The recombinant proteins were renatured either from 8 M urea or from 6 M guanidine hydrochloride by increasing the pH to 10.5 in the presence of glycine and EDTA, reduction with DTT, dilution to a protein concentration below 1 mg.ml-1, and dialysis against 0.9% NaCl. The method presented here can be tailor-fit, with minor modification, for the purification of almost any recombinant protein and the final product satisfies current regulations concerning the production of clinically acceptable therapeutic products.
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PMID:Preparation of clinical grade proteins produced by recombinant DNA technologies. 194 Mar 92

A total of 740 consecutive children aged between 6 months and 12 years who presented with acute encephalopathic illnesses during a three year period were assessed both clinically and by laboratory investigations. Cerebrospinal fluid was examined for the presence of cells or other abnormal substances, and any organisms were cultured. Blood examination included white cell count and estimations of haemoglobin, urea, glucose, and electrolyte concentrations and serum alanine aminotransferase and aspartate aminotransferase. A firm diagnosis was established in 278 patients (38%). Pyogenic meningitis (n = 134), measles encephalopathy (n = 38), and electrolyte imbalance (n = 23) were important causes in this group, cerebral malaria (n = 4) was uncommon and there were no cases of Reye's syndrome. The diagnoses of the remaining 462 were combined under the heading 'acute unexplained encephalopathy'. Altogether 394 of the 462 patients underwent virological investigations for arboviruses and 92 (23%) had one or more indicators of Japanese encephalitis. No other arboviruses could be isolated. Throat swabs from 187 patients with acute unexplained encephalopathy were studied on monkey kidney tissue cell lines of which 14 were positive (8%). These were identified as adenovirus, parainfluenza, influenza, poliomyelitis, Coxsackie, and echovirus; in two cases the virus was untypable. Japanese encephalitis is an important cause of acute childhood encephalopathy in this region. Clinical features of the illness may be mimicked by several disorders which require specific treatment. Thirty four of the 92 died (37%).
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PMID:Virological investigations of acute encephalopathy in India. 203 25

The course of malarial infection was compared in pregnant mice inoculated with Plasmodium berghei at different stages of gestation. When 12-14 wk old, pregnant BALB/c mice were inoculated with 1 x 10(6) of P. berghei NK65-infected red cells at gestation day 0, 2, 4, 6, 8, 10, 12, 14 or 16, the mice inoculated on gestation days 6-12 expired 6.5 days after inoculation compared to 9.5 days in non-pregnant mice. Parasitemia in these pregnant mice increased rapidly on day 4 after inoculation and anemia also developed earlier on day 5. However, the degree of parasitemia and anemia in the terminal stage of infection in these pregnant mice was milder than that of non-pregnant controls. Blood urea nitrogen increased at the terminal stage although the degree of increase in mice inoculated on gestation days 6-10 was comparatively small. Pregnant malarial mice died earlier with less physiological changes than non-pregnant controls. It was concluded that pregnancy makes the host susceptible to physiological changes caused by malaria.
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PMID:Influence of pregnancy on the course of malaria in mice infected with Plasmodium berghei. 219 52

The permeability properties of the human red cell membrane to various solutes are altered by malarial infection. In the present work we show that the permeability of the red cell membrane to water is also affected by the intraerythrocytic growth of the malaria parasite Plasmodium falciparum, whereas urea permeability appears unchanged. The data from infected cells show decreases in membrane surface area, cell volume, the osmotically active water fraction (Weff), and osmotic water permeability (Pf) as measured by stopped-flow spectroscopy. On the other hand, the data suggest an increase in diffusive water permeability (Pd) in infected cells with no change in urea permeability when measured by the continuous flow method. The decreased Pf/Pd ratio of infected cell membranes and its implications in the geometry of the red cell membrane water channel or pore are discussed.
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PMID:Water and urea transport in human erythrocytes infected with the malaria parasite Plasmodium falciparum. 219 24

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

Schizonts of the malaria parasite Plasmodium falciparum synthesize a 195 kDa surface glycoprotein (gp195) that is processed into several smaller products including one of 83 kDa, which, in the case of the Camp strain, is sequentially processed into 73 and 67 kDa products. gp195 and its processing intermediates larger than 83 kDa were not precipitated from culture supernates, but the 83 and 73 kDa products were precipitated by three monoclonal antibodies (McAbs). The 83 and 73 kDa products were affinity purified from culture supernates by adsorbing to McAb 7B2 coupled to Affigel 10 and eluting either with 0.2 N acetic acid, pH 2.8, or with 3 M potassium isothiocyanate (KSCN). The epitope recognized by McAb 7B2 was denatured by acid elution but could be regenerated by treating with 8 M urea followed by dialysis. The implications of renaturing antigens to regenerate epitopes should be considered in studies on the purification, function and immunogenicity of malaria antigens.
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PMID:Characterization of gp195 processed products purified from Plasmodium falciparum culture supernates. 244 21

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
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PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24


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