Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 72 (1994), S. 269-276 
    ISSN: 1432-1440
    Keywords: Emphysema ; Alveolar macrophage ; Elastase ; Smoking
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Current concepts of pathomechanisms leading to acquired emphysema suggest that alveolar macrophages (AM) activated by cigarette smoking may cause an elastase/antielastase imbalance localized to the microenvironment formed by phagocytes and lung tissue. A functional cell assay was used to evaluate the cell-associated elastinolytic activity of AM. AM were obtained by bronchoalveolar lavage from patients with emphysema and from patients with non obstructive chronic pulmonary diseases (non-COPD) and cultured under serum-free conditions in direct contact with 3H-labeled elastin particles. Elastinolytic activity was calculated from the released radioactivity in culture supernatants and expressed as micrograms of 3H-elastin degraded × 10−5 AM × 72 h−1. AM of patients with emphysema had significantly higher elastinolytic activity compared to that of non-COPD patients (median: 10.8 versus 4.1 μg; P 〈 0.01). Further differentiation of patients revealed the lowest median activity in sarcoidosis (2.3 μg). In respect to smoking habits there was a major difference between smokers with and those without emphysema; AM of smokers with emphysema degraded more than twice the amount of elastin than smokers in the non-COPD group (median:11 versus 3.9 μg, P = 0.01). From these data we conclude that AM-derived elastinolytic proteases may be involved in the destruction of lung elastin, which is thought to be the key event occurring in the pathogenesis of pulmonary emphysema.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1433-0385
    Keywords: Key words: Bronchogenic carcinoma ; Residual disease ; Bronchial resection margin ; Prognosis. ; Schlüsselwörter: Bronchialcarcinom ; Residualtumor ; Bronchusresektionsrand ; Prognose.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Nach Lungenresektion und ipsilateraler Lymphknotendissektion wegen Bronchialcarcinoms verblieb in 88 von 2464 Fällen (3,6 %) mikroskopisch Residualtumor (R1) am zentralen Bronchusresektionsrand. Sieben Patienten entwickelten eine Insuffizienz der Bronchusnaht, 2 weitere eine Nachblutung bzw. eine Herzluxation (Morbidität 8,0 %). Die Hospitalletalität betrug 16,6 %. Todesursachen waren Bronchusnahtinsuffizienz (n = 7), Arrosionsblutung (n = 4), respiratorische Insuffizienz (n = 1) und Pleuraempyem (n = 1). Eine postoperative Bestrahlung wurde bei 43 Patienten durchgeführt. Die mediane Überlebenszeit aller Patienten nach R1-Resektion war 16 Monate gegenüber 37 Monaten nach R0-Resektion (p 〈 0,001). Die Überlebenszeit war unabhängig von Tumorstadium und -histologie, Lokalisation des Residualtumors in der Bronchuswand und einer Nachbestrahlung. Inkomplette Resektionen sind durch intraoperativen Schnellschnitt zu verifizieren. Sofern funktionell vertretbar, sollte in den Stadien I und II eine Nachresektion (R0) angestrebt werden; auch in den Stadien III a und III b ist bei R0-Resektion ein statistisch signifikanter Überlebensvorteil gegenüber R1-Resektion zu verzeichnen, jedoch weniger deutlich als in niedrigeren Stadien.
    Notes: Summary. Residual tumor (R1) was proven at the proximal bronchial resection margin in 88 (3.6 %) of 2464 cases of lung cancer following lung resection and standard lymph node dissection. Postoperative complications (8 %) were: fistula of the bronchial suture line (n = 7), bleeding (n = 2) and heart luxation (n = 1). The in-hospital mortality was 16.6 %. Causes of death were: bronchial fistula (n = 7), erosion of the pulmonary artery (n = 4), respiratory failure (n = 1), and empyema (n = 1). Forty-three patients received postoperative radiation therapy. Median survival of all patients following incomplete resection was 16 months, compared to 37 months following complete resection (P 〈 0.001). Length of survival was independent of tumor stage, histology, site of infiltration and postoperative radiation. In conclusion, in resection for lung cancer clear margins should be verified by intraoperative frozen section. In the case of residual tumor at the bronchial resection margin, wider resection is mandatory in stage I and II if the patient meets the functional criteria. Even in stage III a and III b prognosis is significantly better after complete resection than R1-resection; the difference, however, is smaller than in lower stages.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...