Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The detection and measurement of pulmonary edema by the thermal-dye method appears to be accurate and reproducible under specified laboratory conditions. The ETV, which represents the difference in distribution volumes of the diffusible (thermal) indicator and the intravascular (green dye) indicator, should closely estimate the ELM (ETV = 0.984 ELM). Experimental measurements of ETV have shown a very good correlation with ELM, with a tendency for overestimation in normal lungs and underestimation in severely edematous lungs. In contrast to previous measurements using isotopic water methods, thermal-dye measurements have revealed that the estimation of ELM by ETV in severe edema (alveolar flooding) does not plateau. The limitations of the thermal-dye technique reflect the evenness of lung perfusion. Depending on their size and number, emboli produce perfusion defects and reduce ETV. Airway injury also reduces ETV, apparently by redistribution of blood flow. Alterations of ETV by hemodynamic factors suggest that reduction in perfusion pressure may be more significant than changes in flow, although more data are needed. Atelectasis without a reduction in blood flow does not decrease ETV. PEEP may increase ETV when lung injury is not uniform, perhaps by redistributing blood flow, and this maneuver may be useful in detecting underestimation of ELM. Position of the thermistor produces the greatest degree of variability by distorting the thermodilution curve and prolonging the MTT. This results in an increased ETV and an overestimation of ELM. In laboratory studies, the measurements of ETV can be validated by gravimetric analyses of lung water. Since this method of validation is not possible in clinical studies, measurements of ETV in patients must be interpreted in light of limitations demonstrated in the laboratory. Suggestions for avoiding the most common errors in measuring ETV are listed in Table 3.
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PMID:Thermodilution measurement of lung water. 390 46

Fumonisin B1 (FB1) is a mycotoxin produced by the fungus Fusarium verticillioides (formerly Fusarium moniliforme) and is found in diverse crops such as corn, wheat, and barley. Many diseases linked to FB1, such as porcine pulmonary edema, rat hepatic cancer, and equine leukoencephalomalacia, indicate a compromised immune system. The purpose of this study was to determine whether FB1 altered immunological responses in various cell populations of Single Comb White Leghorn chicks. Cells collected for this study were obtained from those immunological organs with well-defined responses (i.e., spleen, thymus, and blood). Cell populations were exposed to 5 to 50 microg/mL FB1 in vitro for 24 to 72 h, and viability and mitogenic response were evaluated. The effects of FB1 on the mitogenic response were evaluated in cell populations from the spleen and blood stimulated with the mitogens, lipopolysaccharide, concanavalin A, and pokeweed mitogen and in thymocytes stimulated with concanavalin A. The 3-(4,5-dimethylthazol-2-yl)-diphenyl-2H-tetrazolium bromide (MTT) reduction assay was used to assess viability and mitogenic response. Fumonisin B1 decreased spleen cell viability and mitogenic response, albeit the degree of decrease varied with mitogen and time of exposure. Fumonisin B1 increased number of viable thymic cells at 50 microg/mL but had no effect on the mitogenic response of thymocytes. Fumonisin B1 had no effect on blood lymphocyte viability or mitogenic response.
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PMID:The effects of fumonisin B1 on viability and mitogenic response of avian immune cells. 1677 70

Nanoparticles are now emerging as a novel class of autophagy activators. Functionalized single-walled carbon nanotubes (f-SWCNTs) are valuable nanomaterials in many industries. This article is designed to assess the autophagic response for f-SWCNTs exposure in vitro and in vivo. A few types of f-SWCNTs were screened in human lung adenocarcinoma A549 cells for the autophagic response and related pathways in vitro. Formation of autophagosomes and LC3-II upregulation were confirmed on the basis of electron microscopy and LC3 western blotting for COOH-CNT, but not for PABS-CNT and PEG-CNT. MTT assay showed marked increase in cell viability, when COOH-CNT was added to cells in the presence of autophagy inhibitor 3MA, ATG6 or TSC2 siRNA. Consistent with the involvement of the Akt-TSC1/2-mTOR pathway, the phosphorylation levels of mTOR, mTOR's substrate S6 and Akt were shown significantly decreased in A549 cells on treatment with COOH-CNT using western blotting. What's more, autophagy inhibitor 3MA significantly reduced the lung edema in vivo. In a word, COOH-CNT induced autophagic cell death in A549 cells through the AKT-TSC2-mTOR pathway and caused acute lung injury in vivo. Inhibition of autophagy significantly reduced COOH-CNT-induced autophagic cell death and ameliorated acute lung injury in mice, suggesting a potential remedy to address the growing concerns on the safety of nanomaterials.
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PMID:A functionalized single-walled carbon nanotube-induced autophagic cell death in human lung cells through Akt-TSC2-mTOR signaling. 2159 91