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)

Mung bean nuclease was found to cut the genomic DNA of the malaria parasite Plasmodium at positions before and after genes but not within gene-coding regions. This cleavage, which had nearly the preciseness of a restriction nuclease, required controlled conditions in the presence of formamide. Southern blot analysis showed that the coding areas for Plasmodium actin, circumsporozoite protein, histidine-rich protein, ribosomal RNA's, and tubulin are each cleaved from genomic DNA to yield a single major band on an agarose gel. DNA sequence data on several clones of mung bean nuclease cleavage products containing the gene for the circumsporozoite protein of Plasmodium falciparum confirmed that cleavage sites are before and after genes. Recognition and cleavage of DNA did not seem to be related to any primary sequence but may be related to structural features of the DNA duplex that demarcate genes. Mung bean nuclease-cleaved DNA could be inserted directly into a lambda expression vector, yielding a representative but small gene bank of intact gene fragments.
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PMID:Mung bean nuclease cleaves Plasmodium genomic DNA at sites before and after genes. 633 Aug 99

We have determined the N-terminal amino acid sequence of the first 25 amino acids of the histidine-rich protein (HisRP) isolated from granules of the avian malaria parasite Plasmodium lophurae. The protein was purified from cytoplasmic granules and shown to be 65.2 mol % histidine, close to the previously described value of 73 mol % histidine (Kilejian (1974) J. Biol. Chem. 249, 4650-4655). Ten of the first 25 residues were histidine, five of which formed the sequence His-His-His-His-His (positions 14-18). Also notable was the presence of eight acidic residues within the N-terminal 25 residues. HisRP contained no detectable carbohydrate. When the HisRP was biosynthetically labeled in cultured infected erythrocytes, incorporation of [3H]His greatly exceeded [3H]Ile. Labeled HisRP was not solubilized with 1% w/v Triton X-100 but could be solubilized with greater than or equal to 1% w/v sodium dodecyl sulfate. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis the [3H]His labeled protein migrated as a doublet (Mr 53 000 and 50 000). Only one of these bands (Mr 53 000) comigrated with the Coomassie Blue stained protein isolated by the acid-extraction procedure from purified granules. The amino acid composition of HisRP and presence of five contiguous histidine residues in the sequence studied here suggests that other sequences of several contiguous histidine residues must exist in this molecule.
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PMID:N-terminal amino acid sequence of the histidine-rich protein from Plasmodium lophurae. 648 6

The histidine-rich protein (HRP) of the avian malaria parasite Plasmodium lophurae contains 70% histidine. It is found in dense cytoplasmic granules and during the erythrocytic cycle it accumulates to represent 10% of the dry weight of the parasite. In the present work the HRP mRNA was studied by in vitro translation and by the use of a polyhistidine oligonucleotide probe. The HRP mRNA contains 2,000-2,100 nucleotides encoding a protein with an apparent molecular weight of 50,000. In addition a HRP of molecular weight 35,000-40,000 is also produced in vitro, probably as a result of proteolytic cleavage of the molecular weight 50,000 polypeptide which corresponds to in vivo labeled and purified HRP. The HRP represents a much larger proportion of the in vitro products synthesized in the homologous cell-free system compared to the rabbit reticulocyte system, and it reflects more closely the pattern of protein synthesis seen in vivo. In addition, HRP mRNA is more abundant in polysomes isolated from young parasites than in polysomes from mature schizonts. These results indicate that the HRP accumulates as a result of amplified translation of its mRNA at certain stages of its erythrocytic cycle.
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PMID:In vitro translation and characterization of a unique histidine-rich protein mRNA in the avian malaria parasite Plasmodium lophurae. 657 48

The capacity of macrophages activated in vivo and in vitro to kill Plasmodium yoelii was investigated. Macrophages activated by BCG-, Con A-, or malaria-induced lymphokines (LK) were cultured with P. yoelii-parasitized erythrocytes (PE). In some experiments, effector and target cells were separated by a 0.45-micron filter. Parasite viability was assessed a) in vivo by injection of mice and quantitative detection of parasites by RIA or b) in vitro by the incorporation of 3H amino acids into parasite proteins. Activated macrophages killed target PE in a dose-dependent manner by elaborating a membrane-permeable soluble factor(s). The addition of small amounts of immune serum augmented the killing of the parasites. LK-activated macrophages underwent an oxidative burst upon the phagocytosis of PE as evidenced by the accumulation of reduced formazan in the NBT assay. The magnitude of the oxidative response corresponded to the number of parasites that were ingested. The phagocytosis-induced oxidative burst was necessary for subsequent killing of Plasmodium. Parasites incubated in microchambers separated from macrophages by a 0.45-micron filter were susceptible to H2O2 released by LK-activated macrophages incubated with PMA, opsonized zymosan, or P. yoelii antigen. Inhibition of protein synthesis by parasites exposed to products of activated macrophages was abrogated by preincubating macrophages with catalase but not with SOD, mannitol, or histidine. These results suggest that phagocytosis-associated oxidative mechanisms mediate the destruction of the malaria parasite. Hence, cell-mediated as well as antibody-dependent mechanisms cooperate in the immune response against malaria.
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PMID:Oxidative killing of the intraerythrocytic malaria parasite Plasmodium yoelii by activated macrophages. 669 Jun 6

Osler's influence in haematology was twofold: as an original observer both in the laboratory and the ward, and his encouragement of the establishment of clinical laboratories with the consequent development of clinical and laboratory haematologists. In 1870, when Osler entered McGill Medical School at the age of 21, he was already an experienced microscopist from his school days, but now his interest shifted from pond life to parasites and clinical microscopy. His post-graduate year with Burdon-Sanderson was to have been a study of leucocyte function, but instead came his research on platelets, continued and expanded when he returned to Montreal in 1874, together with much of his laboratory haematology--his comprehensive studies of pernicious anaemia and work on leukaemia, Hodgkin's disease etc. The move to Philadelphia in 1884 saw the establishment of a clinical laboratory, work on malaria, arsenic in anaemia and the blood disease chapter for Pepper's System. At Baltimore he had a rewarding clinical microscopy department, distinct from Welch's Institute, and this is the period, continued at Oxford, of Osler's accounts of clinical syndromes--polycythaemia, telangiectasia, mastocytosis and 'splenic anaemia'.
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PMID:Osler's influence on haematology. 703 26

Some of the problems caused by malaria, which places a huge roadblock in front of economic progress in the Third World, may be solved by a new vaccine created by Dr. Manuel Patarroyo, a Columbian physician and researcher. "Imagine how things would be if Canadians had malaria," he says. "Episodes last 10 days, then there are 10 days of recovering. This leaves only 10 days each month in which to do some productive work. Then imagine killing the population of Toronto each year, and you can see the huge toll in terms of the number of yearly deaths globally from malaria." His discovery also raises the issue of "intellectual racism" because of criticism of Patarroyo's methods by Western scientists. Patarroyo, meanwhile, turned down a $60-million offer for his vaccine, and instead donated the patent to the World Health Organization.
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PMID:Creation of first malaria vaccine raises troubling questions about "intellectual racism". Interview by Kirsteen MacLeod. 749 94

The case is recounted of a child who was admitted to hospitals several times over a period of 8 years on account of fictitious illnesses invented by his mother. The first occurred when he was 3.5 years old in January 1984. His mother, a nurse, gave a history of intermittent fever for 3 months, loss of appetite and weight. He had been treated with ampicillin, chloramphenicol, and procaine penicillin. No abnormality was detected and his weight at 15.5 kg was appropriate for his age. No fever was recorded throughout 2 weeks in hospital, but he was given chloroquine for possible malaria and then discharged. At follow-up 6 months later, the mother complained of his wheezing. On examination he was normal and had gained 3.8 kg since discharge. The possibility of vernal conjunctivitis plus asthma was entertained and he was then placed on ketotiphen prophylaxis. There was an uneventful follow-up for 6 months. 5 years later in March 1990, his mother related that he had been treated from 22 January 1988 to 21 November 1989 for tuberculosis with streptomycin, isoniazid, rifampicin, and ethambutol. He was also treated with digoxin and Esidrex-K for suspected rheumatic carditis, after which at the University Teaching Hospital, Enugu, he was investigated from 11 April 1989 to 10 August 1989 and found to be normal. One year later in August 1991 she went to one of the authors complaining about polydypsia, polyphagia, and polyuria. Examination had revealed nothing of note. A clinical assessment for diabetes mellitus found the urine specific gravity persistently at 1.010. He was therefore put on carbamazepine (Tegretol) 100 mg t.i.d. After review by a pediatric nephrologist, the child was declared normal. During this visit, the mother and child were interviewed separately. He believed he was ill because his mother said so. A diagnosis of Munchausen syndrome by proxy was made. The mother was referred back to her doctor to arrange for psychiatric care. In Munchausen syndrome, patients fabricate a variety of symptoms and evidence of illness that have no organic basis. Munchausen syndrome by proxy is a form of child abuse, difficult to diagnose, that could result in death. It is more prevalent in affluent countries with sophisticated medical facilities. Its rarity in developing countries may contribute to the difficulty of detection.
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PMID:Munchausen syndrome by proxy: an experience from Nigeria. 750 55

Immobilized metal-ion affinity partitioning (IMAP) is shown to be useful as a preliminary screening test and for the separation of different cell populations based upon recognition of the differences in the proteins on cell surfaces. The feasibility of using IMAP to segregate a spectrum of normal human cells (red blood cells, lymphocytes and fibroblasts) from their counterpart pathological cells has been demonstrated. A clear segregation between normal and sickle-cell anemia red blood cells (RBC), or malaria (Plasmodium vivax) infected RBCs was obtained. Further, the partition differences were found to depend on the nature and the concentrations of metal used. Cells from breast cancer and those from the lung adenocarcinoma showed differences in their partition pattern as compared to normal fibroblasts when PEG-IDA-M(II) was added to the phase system. Maximum differences between the three cell populations were observed in the presence of 10% PEG-IDA-Ni(II). Normal lymphocytes and Burkitt's lymphoma cells (Raji and Namalwa cell lines) were shown to partition differently in the presence of PEG-IDA-M(II) in the phase system. Normal lymphocytes could be distinguished from the Burkitt's lymphoma cell lines in all three phases (top, interface and bottom), in the presence of 10% PEG-IDA-Ni(II) in the system. These differences in the partition behavior could mainly be attributed to the density, surface exposure and micro-environment of histidine residues of cell membrane-associated proteins. These data, along with those obtained for normal and pathological human cells show that IMAP could be a simple and versatile tool for the segregation and study of cells.
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PMID:Segregation of normal and pathological human red blood cells, lymphocytes and fibroblasts by immobilized metal-ion affinity partitioning. 759 55

Falciparum malaria is the most hazardous form of malaria. Its high degree of parasitemia interferes with vital functions of most organs and is directly responsible for its high rate of mortality and morbidity. Quinine and other antimalarial drugs are relatively slow acting and not always effective due to the growing resistance developed by Plasmodium toward these drugs. Another emergency modality, which would remove the parasitic burden quickly and effectively, is thus much needed. We present a case of a 51-year-old sailor, who was admitted to the hospital because of complicated falciparum malaria. His situation deteriorated rapidly into a desparate stage, despite the various intensive treatments and quinine. He soon developed a systemic inflammatory response syndrome manifested as cerebral malaria, renal failure, acute respiratory distress syndrome and disseminated intravascular coagulation. An emergency blood exchange reversed the situation dramatically, and the patient recovered completely. It is recommended that any doctor, both in endemic and in non endemic areas, dealing with blood transfusions or infectious diseases, should be acquainted with this lifesaving modality, regardless of the controversy still surrounding this subject.
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PMID:Blood exchange [correction of exchance]-a rescue procedure for complicated falciparum malaria. 772 67

We have constructed a second generation malaria transmission-blocking vaccine candidate based on Pfs25, the predominate surface protein of Plasmodium falciparum zygotes, to overcome potential production problems with the original construct. Four modifications were made: (1) addition of the last cysteine residue of the fourth epidermal growth factor like-domain of Pfs25; (2) mutagenesis of asparagine-linked glycosylation sites with glutamine rather than alanine; (3) addition of a six histidine tag at the carboxy-terminus for highly efficient purification of recombinant protein on nickel-NTA agarose; and (4) fermentation that combines continuous glucose fed-batch methodology with pH-controlled glucose addition and a terminal ethanol feed. The resulting product, TBV25H (Transmission-Blocking Vaccine based on Pfs25 with a Histidine tag), appears to be a more potent antigen and immunogen than the original construct, and the fermentation and post-fermentation processing methodology easily lend themselves to technology transfer to the ultimate users, newly industrialized countries.
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PMID:Production, purification and immunogenicity of a malaria transmission-blocking vaccine candidate: TBV25H expressed in yeast and purified using nickel-NTA agarose. 776 8


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