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)

Malaria remains an important health problem in tropical countries like Brazil. Thrombocytopenia is the most common hematological disturbance seen in malarial infection. Oxidative stress (OS) has been implicated as a possible mediator of thrombocytopenia in patients with malaria. This study aimed to investigate the role of OS in the thrombocytopenia of Plasmodium vivax malaria through the measurement of oxidant and antioxidant biochemical markers in plasma and in isolated platelets. Eighty-six patients with P. vivax malaria were enrolled. Blood samples were analyzed for total antioxidant and oxidant status, albumin, total protein, uric acid, zinc, magnesium, bilirubin, total thiols, glutathione peroxidase (GPx), malondialdehyde (MDA), antibodies against mildly oxidized low-density lipoproteins (LDL-/nLDL ratio) and nitrite/nitrate levels in blood plasma and GPx and MDA in isolated platelets. Plasma MDA levels were higher in thrombocytopenic (TCP) (median 3.47; range 1.55-12.90 micromol/L) compared with the non-thrombocytopenic (NTCP) patients (median 2.57; range 1.95-8.60 micromol/L). Moreover, the LDL-/nLDL autoantibody ratio was lower in TCP (median 3.0; range 1.5-14.8) than in NTCP patients (median 4.0; range 1.9-35.5). Finally, GPx and MDA were higher in the platelets of TPC patients. These results suggest that oxidative damage of platelets might be important in the pathogenesis of thrombocytopenia found in P. vivax malaria as indicated by alterations of GPx and MDA.
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PMID:The role of platelet and plasma markers of antioxidant status and oxidative stress in thrombocytopenia among patients with vivax malaria. 1894 18

Ca(2+) channels regulate many crucial processes within cells and their abnormal activity can be damaging to cell survival, suggesting that they might represent attractive therapeutic targets in pathogenic organisms. Parasitic diseases such as malaria, leishmaniasis, trypanosomiasis and schistosomiasis are responsible for millions of deaths each year worldwide. The genomes of many pathogenic parasites have recently been sequenced, opening the way for rational design of targeted therapies. We analyzed genomes of pathogenic protozoan parasites as well as the genome of Schistosoma mansoni, and show the existence within them of genes encoding homologues of mammalian intracellular Ca(2+) release channels: inositol 1,4,5-trisphosphate receptors (IP(3)Rs), ryanodine receptors (RyRs), two-pore Ca(2+) channels (TPCs) and intracellular transient receptor potential (Trp) channels. The genomes of Trypanosoma, Leishmania and S. mansoni parasites encode IP(3)R/RyR and Trp channel homologues, and that of S. mansoni additionally encodes a TPC homologue. In contrast, apicomplexan parasites lack genes encoding IP(3)R/RyR homologues and possess only genes encoding TPC and Trp channel homologues (Toxoplasma gondii) or Trp channel homologues alone. The genomes of parasites also encode homologues of mammalian Ca(2+) influx channels, including voltage-gated Ca(2+) channels and plasma membrane Trp channels. The genome of S. mansoni also encodes Orai Ca(2+) channel and STIM Ca(2+) sensor homologues, suggesting that store-operated Ca(2+) entry may occur in this parasite. Many anti-parasitic agents alter parasite Ca(2+) homeostasis and some are known modulators of mammalian Ca(2+) channels, suggesting that parasite Ca(2+) channel homologues might be the targets of some current anti-parasitic drugs. Differences between human and parasite Ca(2+) channels suggest that pathogen-specific targeting of these channels may be an attractive therapeutic prospect.
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PMID:Identification of intracellular and plasma membrane calcium channel homologues in pathogenic parasites. 2202 73

Thyroid cancer is the most common endocrine malignant tumor in the world, and its incidence is increasing. Although the mortality rate of thyroid cancer is low, its persistence/recurrence rate is high. In addition, some patients with thyroid cancer fail to respond to radiation. Therefore, it is urgent need to develop a novel treatment for thyroid cancer. Parthenolide (PTL), a traditional Chinese medicine Tanacetum parthenium extract, has shown encouraging effects in anti-tumor, anti-inflammatory and anti-malaria. However, it is unclear whether PTL has an anti-thyroid cancer effect and its possible mechanism of action. In the recent years, metabonomics has been widely used in tumors research to explore the pharmacological mechanism of drugs, but few studies used metabonomics to investigate the pharmacological effects of PTL in thyroid tumors. In order to comprehensively reveal the mechanism and effects of PTL on anti-thyroid tumors, metabonomics combined cell biological research methods were conducted. The results showed that PTL promote apoptosis of thyroid cancer cells (TPC-1) in a concentration-dependent manner. The metabolic differences between the PTL group and the control group were compared by metabonomics, and 31 potential metabolites were identified. These metabolites were mainly involved in the tricarboxylic acid cycle, amino acid metabolism, choline metabolism and lipid metabolism. These results implied that PTL may inhibit the proliferation and development of thyroid carcinoma by accelerating oxidation emergency response, inhibiting adenosine triphosphate (ATP) synthesis and metabolic imbalance. The results of this study revealed that PTL can be an effective and potential drug for the treatment of thyroid cancer.
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PMID:Metabonomic study of the intervention effects of Parthenolide on anti-thyroid cancer activity. 3250 11