Disability and exertional dyspnea associated with chronic obstructive pulmonary disease has led to the development of rehabilitation programmes that aim to increase exercise tolerance and relief of dyspnea. To evaluate whether aerobic training (training groups P1 and P4), strength training (P2 and P5) or a combination of both (P4 and P6) is useful, 69 patients (44 m/25 f) with moderate to severe COPD were randomised to a three week inpatient training program. The training consisted of three weekly twenty minute exercise sessions without (P1 - P3) or with supplemental oxygen (P4 - P6) on a calibrated ergocycle (70 % W(max)) or three weekly sessions of 20 - 25 repetitions of 2 - 4 training series (40 % W(max)) or a combination of both. In general, the programme failed to demonstrate significant changes in lung function and arterial blood gases. Evaluation of exercise capacity via the six-minute-walking test (6MT) yielded a significant increase of the walking distance in all groups except P2 (60 - 83 m), The time to finish a test-set of daily activities (TAF) was reduced in all groups (5 - 58 sec) and reached significance in P1, P3, P5 and P6. After the 6MT, exertional dyspnea improved in all groups except P4 and was significant in P1 and P3; after the TAF, dyspnea again was reduced in all groups with a significant change in P2 and P5. These data support the hypotheses that a short term inpatient training programme is suitable to improve exercise-capacity and dyspnea. Patients with advanced disease (P4 - P6) show greater benefits with strength training (alone or in combination with aerobic training) while for patients with moderate disease (P1 - P3) aerobic training is favourable. These changes may translate into improved performance of daily activities and general well-being.
No abstract
The biosynthesis and secretion of M-type and Z-type «i-antitrypsin was studied in human monocytes. In monocytes of PiMM individuals a\-antitrypsin represented 0.08% of the newly synthesized proteins and 0.44% of the secreted proteins. Two molecular forms of a r antitrypsin could be identified: a 51-kDa intracellular form, susceptible to endoglucosaminidase H, thus representing the highmannose type precursor form and a 56-kDa form resistant to endoglucosaminidase H which was secreted into the medium. Inhibition of de novo glycosylation by tunicamycin impaired the secretion of M-type OL\-antitrypsin by about 75% whereas inhibition of oligosaccharide processing by the mannosidase II inhibitor swainsonine did not alter the secretion of Mtype c^-antitrypsin. «i-Antitrypsin secreted by human monocytes was functionally active as measured by complex formation with porcine pancreatic elastase. Even unglycosylated a r antitrypsin secreted by human monocytes treated with tunicamycin formed a complex with elastase. In monocytes of PiZZ individuals the secretion of a r antitrypsin was decreased. 72% of newly synthesized M-type «i-antitrypsin, but only 35% of newly synthesized Z-type a r antitrypsin were secreted during a labeling period of 3 h with [ 35 S]methionine.The 51-kDa form of Z-type «i-antitrypsin accumulated intracellularly, whereas the 56-kDa form was secreted. Inhibition of oligosaccharide processing by swainsonine did not alter the decreased secretion of Z-type a r antitrypsin, whereas inhibition of de novo glycosylation by tunicamycin blocked the secretion of Z-type «i-antitrypsin completely. Biosynthese und Sekretion von M-und Z-Typ-a r Antitrypsin in menschlichen Monozyten. Einflu von Inhibitoren der Glycosylierung und des Oligosaccharid-"Processings" auf Sekretion und FunktionZusammenfassung: Die Biosynthese von M-und ZTyp-a r Antitrypsin wurde in menschlichen Monozyten untersucht. In Monozyten von PiMM-Individuen stellte «i-Antitrypsin 0.08% der neu synthestisierten und 0.44% der sezernierten Proteine dar. Es konnten 2 molekulare Formen von a r Antitrypsin identifiziert werden: eine 51 kDa intrazellul re Form, die Endoglucosaminidase-H-spaltbar war und somit die Mannose-reiche Vorl uferform darstellte, und eine 56-kDa-Form, die nicht durch Endoglucosaminidase H gespalten werden konnte und die ins Medium sezerniert wurde. Hemmung der De-novo-Glycosylierung durch Tunicamycin hemmte die Sekretion von M-Typ-«i-Antitrypsin um etwa 75%, wohingegen eine Hemmung des Oligosaccharid-"Processings" durch den Mannosidase-II-Inhibitor Swainsonin die Sekretion von M-Typ-cxi-Antitrypsin nicht ver nderte. «i-Antitrypsin, das von menschlichen Monozyten sezerniert
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