1,721,002 research outputs found
Physical and biochemical properties of metallo-enzymes with elastolytic activity isolated from rat macrophages and platelets
Isolation and partial characterization of a proteinase with elastolytic activity from mouse blood leukocyte
Leukocyte elastase has been implicated in the etiology of pulmonary emphysema. Recently, two genetic models of emphysema have been described, in mouse, which may enhance our understanding of the pathogenesis of emphysema. We therefore sought to purify mouse leukocyte elastase in order to characterize its biochemical properties. Leukocyte enzyme has been purified by a two-step procedure involving salt extraction of granular fraction, followed by preparative isoelectric focusing on Sephadex G-75 Superfine. The enzyme hydrolyses elastin and synthetic substrates for elastase, even if to a different extent. Inhibition studies indicates that the enzyme is a serine proteinase. Mouse elastase has a single isoelectric point of 8.65 and it behaves on sodium dodecyl sulphate polyacrylamide gel electrophoresis as a major band (molecular weight 29,000) and two minor bands (molecular weight 27,000 and 25,800, respectively
Frazionamento e caratterizzazione, su gel poliacrilammide, di differenti forme di elastasi pancreatiche e leucocitarie del ratto con l'impiego di una nuova tecnica zimografica
Fisiopatologia polmonare
-Insufficienza respiratoria
-Polmoniti
-Broncopneumopatie ostruttive
-Pneumopatie restrittive
-Atelettasia
-Pneumotorac
Immunologia
-Cellule della rissposta immune
-Immunità naturale
-Immunità specifica umorale e cellulo-mediata
-Immunità specifica attiva e passiv
Mindfulness-based stress reduction program improves psychological well-being and blood pressure in an Italian context: potential mechanisms and benefits
Background: Chronic psychosocial stress may exacerbate inflammation and oxidative stress, potentially contributing to the aetiology of many lifestyle-related diseases, including elevation of blood pressure (BP) and increased cardiovascular risk. Mindfulness-based stress reduction (MBSR) improves psychological well-being, but few studies have investigated its effect on biological parameters related to stress. This study evaluated whether the MBSR program can lower stress and anxiety and improve some biological stress markers. Methods: This is a one-group pretest-posttest quasi-experimental design. We recruited 42 adult volunteers to partake in a standard 8-week MBSR program. The main outcomes were psychological well-being (perceived stress, anxiety and awareness) and stress-related biomarkers (systolic and diastolic BP, salivary cortisol, IL-6 and IL-8 levels, plasma carotenoids concentration). Results: MBSR decreased stress (p = 0.002) and anxiety (p = 0.05) and increased awareness (p = 0.01). MBSR also significantly lowered systolic and diastolic BP (p = 0.02; p = 0.001), cortisol (p = 0.01), and IL-6 and IL-8 pro-inflammatory cytokines (p = 0.02; p = 0.03), and enhanced carotenoids (p = 0.03). We found a strong positive correlation between Δ PSS and Δ STAI-Y1 (r = 0.62, p = 0.008), Δ STAI-Y1 and Δ IL8 (r = 0.74, p = 0.0007), and Δ PSS and Δ IL8 (r = 0.5, p = 0.04). Significant negative correlations were observed between Δ PSS and Δ MAAS (r = −0.77, p = 0.0003), Δ STAI-Y1 and Δ MAAS (r = −0.51, p = 0.04), and Δ MAAS and Δ IL8 (r = −0.68, p = 0.003). Conclusion: These preliminary data indicate that the MBSR program significantly improves all the analysed parameters. This program can help cope with stress and anxiety and lower BP by reducing nervous system activation and cortisol levels. By regulating cortisol levels, MBSR can lower inflammation and oxidative stress responses involved in many diseases, including hypertension. Further studies are needed to unravel the complex relationship between mindfulness and its effects on human health
Mindfulness based stress reduction (MBSR) program leads to a reduction in physiological evaluated stress
Background: Oxidative stress has complex interactions with our lifestyle habits that negatively affect our health. Increasing evidence suggests that chronic psychosocial stress enhances oxidative stress, which in turn may contribute to aging and aetiology of many
lifestyle-related degenerative diseases. Mindfulness practice is defined as “paying attention in an intentional and non-judgmental way to the present moment”. Past studies investigating the link between mindfulness and stress response demonstrated that Mindfulness-Based Stress Reduction (MBSR) program is an effective stress management technique which have beneficial effects on emotional and psychological responses to stressors. In contrast, there have been less studies of its effect on physiological parameters, such as oxidative stress. Methods: In this study, we evaluated the effectiveness of MBSR program on a sample of 42 people (age 30-66 years).
In particular, we analyzed blood pressure, plasma concentration of carotenoids and salivary cortisol levels, before (baseline) and after an MBSR training (8 weeks). Cortisol was measured by an Enzyme Immunoassay kit. Carotenoid concentration was evaluated by Raman spectroscopic technique. Levels of perceived stress, anxiety and awareness were assessed by Perceived Stress Scale, State Anxiety Inventory, and Mindful Attention Awareness Scale questionnaires, respectively. Student’s t was used for statistical analysis (P < 0.05). Results: Mindfulness practice significantly reduced salivary levels of cortisol (P < 0.01), blood pressure in hypertensive people (P < 0.01) and increases blood concentration of carotenoids (P < 0.05). An increase in awareness and a decrease in perceived stress and anxiety were also observed. All the parameters analysed showed a statistically significant improvement (P < 0.01). Conclusions: These preliminary data are a first indication that the MBSR program is an effective tool to ameliorate antioxidant defence (as indicated by carotenoids data) confirming positive effects on blood pressure and psychological outcomes. Further studies on pro-inflammatory cytokine levels and overall redox related mechanisms are needed to better evaluate MBSR systemic effects
F2-Isoprostanes as markers of oxidative stress and mediators of CCl4-induced liver fibrosis
INTRODUCTION: F2-isoprostanes are considered as the most reliable markers of OS in vivo and mediators of some important biological effects, such as the vasoconstriction of kidney glomerular arterioles. It is known that hepatic fibrosis induced by CCl4 may be linked to oxidative stress (OS). In previous studies, we demonstrated the role of isoprostanes as possible mediators of CCl4-induced hepatic fibrosis. Plasma levels of isoprostanes were found to be elevated in rat chronically treated with CCl4 and correlated with hepatic collagen content. We also demonstrated that in vitro isoprostanes induced a marked increase in DNA and collagen synthesis in cultured hepatic stellate cells (HSC), in the concentration range found in the in vivo studies (1-10 nM). It has been suggested that isoprostanes act through the activation of receptors analogous to those for tromboxane A2 (TxA2r). Thus, the possible occurrence of TxA2r on HSC was investigated. Binding studies with [3H]SQ29548 (a specific antagonist of TxA2r) and competition binding experiments with I-BOP (a specific agonist of TxA2r) demonstrated the existence of TxA2r in HSC and the involvement of TxA2r in Iso-evoked responses. We then examined which signal transduction pathways are set into motion by isoprostanes to exert their fibrogenic effects. METHODS: HSC were isolated from the rat liver and treated with 8-epi-PGE2the most represented isomer). Ins(1,4,5)P3 (IP3) and cAMP levels were determined by commercial kits. Activation of mitogen-activated protein kinases (MAPK) and cyclin 1 was assessed by Western blotting. Cell proliferation and collagen production were assessed by measuring the incorporation of 3H-thymidine and 3H-proline, respectively. RESULTS: 8-epi-PGE2 increased 4 times IP3 and affected cAMP production. The expression of cyclin D1, a molecule involved in cell proliferation, is also increased. Furthermore, 8-epi-PGE2 activated two classes of MAPK: extracellular signal-regulated kinase (ERK) and p38, which have been shown to influence cell proliferation and collagen gene expression. CONCLUSION: On the basis of these data, it is possible to hypothesize that one of the pathways activated by 8-epi-PGF2a is that of Gq/PKC. The binding of isoprostanes to TxA2r could stimulate downstream MAPK activation, via PKC. In particular, p38 is known to increase in HSC collagen production, while ERK is able to increase cyclin D1 expression and then cell proliferation. Thus, fibrogenic effects of isoprostanes in HSC are mediated through TxA2r binding by specific activation of these transduction pathways
- …
