Clinical and functional baseline findings do not predict the response to PRP in COPD. The greater efficacy in patients with BMI>25 or with PaO(2)<60mmHg may be due to a greater deconditioning in overweight patients, and to a larger room for improvement in hypoxemic patients.
Thiol methyltransferase (EC 2.1.1.9, TMT) activity was measured with 2-mercaptoethanol in the microsomal fraction of 12 placenta and 31 fetal and 33 adult liver specimens. TMT activity (nmol/min incubation/mg protein; mean ± SD) was 0.61 ± 0.25 (placenta), 0.74 ± 0.45 (fetal liver), and 4.51 ± 2.29 (adult liver). TMT activity was also measured in extrahepatic tissues and it was about one order of magnitude lower in fetal lungs, kidney and intestine as compared with the fetal liver. A similar distribution pattern was also observed in adult tissues except that in the kidney TMT activity was one third of the hepatic one. Studies of enzyme kinetics showed that fetal and adult hepatic TMT obeyed non-Michaelis-Menten kinetics when 2-mercaptoethanol was the varying substrate. Average values of Km for the higher and lower affinity phases were 0.03 and 14.05 mmol/l, respectively (fetal liver) and 0.005 and 14.57 mmol/l, respectively (adult liver). This paper shows that TMT develops prenatally and its distribution pattern is consistent with that of other microsomal enzymes, being preferentially associated with the liver both in the human fetus and in adult subject.
Chronic obstructive pulmonary disease (COPD) is a complex condition in which systemic inflammation plays a role in extrapulmonary manifestations, including cardiovascular diseases: interleukin (IL)-6 has a role in both COPD and atherogenesis. The 2011 GOLD document classified patients according to FEV1, symptoms, and exacerbations history, creating four groups, from A (less symptoms/low risk) to D (more symptoms/high risk). Extracellular vesicles (EV) represent potential markers in COPD: nevertheless, no studies have explored their value in association to both disease severity and inflammation. We conducted a pilot study to analyze circulating endothelial-(E) and monocyte-derived (M) EV levels in 35 COPD patients, who were grouped according to the 2011 GOLD document; the relationship between EV and plasmatic markers of inflammation was analyzed. We found a statistically significant trend for increasing EEV, MEV, IL-6, from group A to D, and a significant correlation between EEV and IL-6. The associations between both EEV and MEV and disease severity, and between EEV and IL-6, suggest a significant interplay between pulmonary disease and inflammation, with non-respiratory cells (endothelial cells and monocytes) involvement, along with the progression of the disease. Thus, EV might help identify a high-risk population for extrapulmonary events, especially in the most severe patients.
1 The activities of microsomal glucuronyltransferase and thiomethyltransferase, and those of cytosolic sulphotransferase, acetyltransferase, glutathione transferase and thiomethyltransferase were measured in abnormal (cirrhosis and chronic hepatitis) and normal livers. 2 Glucuronyltransferase and sulphotransferase were investigated with 2-naphthol and ethinyloestradiol as substrates. p-Aminobenzoic acid, benzo(a)pyrene-4,5-epoxide and 2-mercaptoethanol were the substrates of acetyltransferase, glutathione transferase and thiomethyltransferase, respectively.3 Enzyme activities are expressed as nmol min-1 incubation mg-1 protein and the averages (± s.d.) are given. With 2-naphthol as substrate, the glucuronyltransferase activity was 6.55 ± 4.10 (abnormal liver, n = 33) and 7.81 ± 4.02 (normal liver, n = 26) (NS); whereas sulphotransferase activity was 0.28 ± 0.18 (abnormal liver, n = 35) and 0.68 ± 0.43 (normal liver, n = 26) (P < 0.01). Glucuronyltransferase activity towards ethinyloestradiol was 102.5 ± 56.9 (abnormal liver, n = 30) and 107 ± 59.9 (normal liver, n = 26) (NS), whereas sulphotransferase activity was 57.2 ± 36.0 (abnormal liver, n = 35) and 122 ± 67.6 (normal liver, n = 28) (P < 0.01). Acetyltransferase activity was 0.84 ± 0.83 (abnormal liver, n = 35) and 3.84 ± 1.65 (normal liver, n = 26) (P < 0.01). Glutathione transferase activity was 0.83 ± 0.68 (abnormal liver, n = 35) and 2.90 ± 1.59 (normal liver, n = 25) (P < 0.01) and thiomethyltransferase activity was 1.00 ± 0.69 (abnormal liver, n = 34) and 3.99 ± 1.49 (normal liver, n = 25) (P < 0.01). 4 Liver disease lowers the activities towards the substrates studied of sulphotransferase, acetyltransferase, glutathionetransferase and thiomethyltransferase but not that of glucuronyltransferase. Thus, overall hepatic conjugating capacity is decreased in liver injury. However, enzyme activity is substrate dependent and it is not possible to extrapolate the results for other compounds.
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