1,721,106 research outputs found
Cor Pulmonale
No full textPer cor Pulmonale si intende l'ingrandimento del ventricolo destro che consegue a patologie del parenchima polmonare causanti l'ipertensione nel piccolo circolo. Il capitolo affronta fisiopatologia, eziopatogenesi, clinica, diagnosi e terapia di tale condizione
Role of cardiovascular magnetic resonance in acute and chronic ischemic heart disease
Full text linkCardiovascular magnetic resonance (CMR) is a multi-parametric, multi-planar, non-invasive imaging technique, which allows accurate determination of biventricular function and precise myocardial tissue characterization in a one-stop-shop technique, free from the use of ionizing radiations. Though CMR has been increasingly applied over the last two decades in every-day clinical practice, its widest application has been in the assessment of ischemic cardiomyopathy.</p
Surfactant protein A (SP-A) interacts with serum lipoproteins entering the airways
No full textSerum lipoproteins may enter the airways and appear in the sputum (chylophtysis) when the lymphatic circulation is impaired by inflammation, neoplasm, or by an abnormal proliferation of smooth muscle cells. While analyzing the bronchoalveolar lavage fluid of a patient with chylophtysis, we noticed that surfactant could not be separated from contaminating lipoproteins, and we speculated that surfactant components may interact with lipoproteins entering the airways. To clarify this point, we immobilized SP-A on microtiter wells and incubated it with 125I-VLDL. We found that SP-A binds VLDL. The binding is time and concentration dependent, is inhibited by excess VLDL and by liposomes (dipalmitoyl phosphatidylcholine: egg phosphatidylcholine: phosphatidylglycerol: cholesterol, 50:25:15:10), is increased by 5 mM Ca++, is unaffected by surfactant proteins B and C, or by methyl mannoside, and is greatly decreased if SP-A is alkylated and reduced before immobilization. Furthermore, we found that soluble SP-A increases the degradation of VLDL by alveolar macrophages collected from normal subjects, and favors the binding of VLDL to surfactant membranes. We conclude that SP-A affects the catabolism of serum lipoproteins entering the airways
Different pathways of degradation of SP-A and saturated phosphatidylcholine by alveolar macrophages
No full textAlveolar macrophages degrade surfactant protein (SP) A and saturated phosphatidycholine [dipalmitoylphosphatidylcholine (DPPC)]. To clarify this process, using rabbit alveolar macrophages, we analyzed the effect of drugs known to affect phagocytosis, pinocytosis, clathrin-mediated uptake, caveolae, the cytoskeleton, lysosomal pH, protein kinase C, and phosphatidylinositol 3-kinase (PI3K) on the degradation of SP-A and DPPC. We found the following: 1) SP-A binds to the plasma membrane, is rapidly internalized, and then moves toward degradative compartments. Uptake could be clathrin mediated, whereas phagocytosis, pinocytosis, or the use of caveolae are less likely. An intact cytoskeleton and an acidic milieu are necessary for the degradation of SP-A. 2) Stimulation of protein kinase C increases the degradation of SP-A. 3) PI3K influences the degradation of SP-A by regulating both the speed of internalization and subsequent intracellular steps, but its inhibition does not prevent SP-A from reaching the lysosomal compartment. 4) The degradation of DPPC is unaffected by most of the treatments able to influence the degradation of SP-A. Thus it appears that DPPC is degraded by alveolar macrophages through mechanisms very different from those utilized for the degradation of SP-A
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