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

Apoptosis mediated by Fas/FasL has been implicated in pulmonary disorders. However, little is known about the relationship between Fas and FasL in the process of lung injury during malaria infection. Paraffin-embedded lung tissues from malaria patients were divided into two groups: those with pulmonary edema (PE) and those without pulmonary edema (non-PE). Normal lung tissues were used as the control group. Cellular expression of Fas, FasL, and the markers of apoptotic caspases, including cleaved caspase-3 and cleaved caspase-8 in the lung tissues were investigated by the immunohistochemistry (IHC) method. Semi-quantitative analysis of IHC staining revealed that cellular expression of Fas, FasL, cleaved caspase-8, and cleaved caspase-3 were significantly increased in the lungs of patients with PE compared with the lungs of patients with non-PE and control groups (all P < 0.05). In addition, significant positive correlations were obtained between Fas and apoptosis (rs = 0.937, P < 0.001) and FasL and apoptosis (rs = 0.808, P < 0.001). Significant positive correlations were found between Fas and FasL expression (rs = 0.827, P < 0.001) and between cleaved caspase-8 and cleaved caspase-3 expression (rs = 0.823, P < 0.001), which suggests that Fas-dependent initiator and effector caspases, including cleaved caspase-8 and caspase-3, are necessary for inducing apoptosis in the lungs of patients with severe P. falciparum malaria. The Fas/FasL system and downstream activation of caspases are important mediators of apoptosis and may be involved in the pathogenesis of pulmonary edema in severe P. falciparum malaria patients. The proper regulation of the Fas/FasL pathway can be a potential treatment for pulmonary complications in falciparum malaria patients.
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PMID:Enhanced expression of Fas and FasL modulates apoptosis in the lungs of severe P. falciparum malaria patients with pulmonary edema. 2661 8

Kidney injury molecule-1 (KIM-1) is a specific histological biomarker for diagnosing early acute kidney injury which is markedly up-regulated in the proximal tubular cells in acute and chronic tubular injury. KIM-1 expression is poorly defined in the renal tubules of malaria patients. This present study aimed to determine KIM-1 expression as a specific biomarker for acute tubular damage and to identify matrix metalloproteinase-3 (MMP-3) as a mediator for KIM-1 shedding. Paraffin-embedded kidney tissues from autopsies of malaria patients were obtained from the Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, Thailand. The kidney tissues were divided into 2 groups: those with acute kidney injury (AKI) (n = 10 cases) and those with non-AKI (n = 10 cases). Ten normal kidney tissues were used as a control group. The expression of KIM-1 and MMP-3 was examined by immunohistochemical staining. KIM-1 and MMP-3 expressions were strongly expressed in the proximal tubular cells in all kidney tissues from severe Plasmodium falciparum malaria with histological changes showing acute tubular damage. The mean intensity and total score of KIM-1 and MMP-3 expressions were significantly increased in proximal tubules of AKI group compared to non-AKI and control groups (all P < 0.001). There was a significant positive correlation of total score of KIM-1 expression and the parameters of kidney function for AKI, including serum creatinine (Cr) and blood urea nitrogen (BUN). In addition, strong positive correlations were found between total score of KIM-1 expression and proximal tubular necrosis and MMP-3 expression. The study supports the potential role of KIM-1 as a specific biomarker for renal proximal tubular damage in malarial AKI, and indicates that the process of KIM-1 shedding might be stimulated by MMP-3.
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PMID:Increased expression of kidney injury molecule-1 and matrix metalloproteinase-3 in severe Plasmodium falciparum malaria with acute kidney injury. 3196 33