Ozone-induced lung function decrements do not correlate with early airway inflammatory or antioxidant responses.

This study sought to clarify the early events occurring within the airways of healthy human subjects performing moderate intermittent exercise following ozone challenge. Thirteen healthy nonsmoking subjects were exposed in a single blinded, crossover control fashion to 0.2 parts per million (ppm) O3 and filtered air for 2 h, using a standard intermittent exercise and rest protocol. Lung function was assessed pre- and immediately post-exposure. Bronchoscopy was performed with endobronchial mucosal biopsies, bronchial wash (BW) and bronchoalveolar lavage (BAL) 1.5 h after the end of the exposure period. Respiratory tract lining fluid (RTLF) redox status was assessed by measuring a range of antioxidants and oxidative damage markers in BW and BAL fluid samples. There was a significant upregulation after O3 exposure in the expression of vascular endothelial P-selectin (p<0.005) and intercellular adhesion molecule-1 (p<0.005). This was associated with a 2-fold increase in submucosal mast cells (p<0.005) in biopsy samples, without evidence of neutrophilic inflammation, and a decrease in BAL fluid macrophage numbers (1.6-fold, p<0.005), with an activation of the remaining macrophage subset (2.5-fold increase in % human leukocyte antigen (HLA)-DR+ cells, p<0.005). In addition, exposure led to a 4.5-fold and 3.1-fold increase of reduced glutathione (GSH) concentrations, in BW and BAL fluid respectively (p<0.05), with alterations in urate and alpha-tocopherol plasma/RTLF partitioning ratios (p<0.05). Spirometry showed reductions in forced vital capacity (p<0.05) and forced expiratory volume in one second (p<0.01), with evidence of small airway narrowing using forced expiratory flow values (p<0.005). Evidence was found of O3-induced early adhesion molecule upregulation, increased submucosal mast cell numbers and alterations to the respiratory tract lining fluid redox status. No clear relationship was demonstrable between changes in these early markers and the lung function decrements observed. The results therefore indicate that the initial lung function decrements are not predictive of, or causally related to the O3-induced inflammatory events in normal human subjects.     

Symposium

This study aims to provide an estimate of women's risk of ovarian hyperstimulation syndrome (OHSS) when undergoing superovulation to donate eggs for research. This is an essential prerequisite for appropriate informed consent. In the absence of sufficiently large numbers of egg donors to assess the risk, comparative data was obtained from women undergoing the same superovulation protocol for in vitro fertilization (IVF) treatment. In this prospective study 339 women, who developed ≥20 follicles after superovulation in their first treatment cycle (total number of treatment cycles during the same period – 2417), were intensively monitored on five occasions, between human chorionic gonadotrophin and pregnancy test, according to our routine clinical protocol. Hospital admission was needed for 49 (14.5%) women, 13 (3.8%) needed intravenous fluids and 9 (2.7%) needed paracentesis. The admission rates were similar in pregnant and non-pregnant women (13.5% vs. 15%); the need for intravenous fluids and paracentesis were 3.2% vs. 2.3% and 6.3% vs. 2.3%, respectively. The peak increase in haematocrit occurred on Day 4 after hCG, and the mean day of hospital admission was Day 5. If an egg donor develops <20 follicles, she can be reassured that the risk of OHSS is very small (<0.1%). If ≥20 follicles develop, her risk of hospital admission due to OHSS is <15%. The absence of pregnancy in egg donors does not eliminate the risk of OHSS. Given the timescale of development of the haematological and biochemical abnormalities, egg donors who develop ≥20 follicles should be actively monitored for the first week after egg collection.     

juris PraxisKommentar SGB V.

Ohne Zusammenfassung     

Über den Gesamtsterin- und Ergosterinhaushalt während der Entwicklung des Organismus

Ohne ZusammenfassungMit 6 Textabbildungen.Dr.H. Hentschel ist am 21. XII. 1930 im Gefolge einer auf den von ihm geleiteten Krankenabteilungen der Klinik erworbenen Infektion verstorben. Der Unterfertigte wurde von den Angehörigen mit der Herausgabe des wissenschaftlichen Nachlasses betraut. Es handelte sich hauptsächlich um Protokolle über bereits abgeschlossene und noch laufende Experimente und Analysen sowie Entwürfe zu weiteren Studien über das im Titel genannte Thema, die in ihrer Gesamtheit als Habilitationsschrift publiziert werden sollten. Herr Dr. phil. et med.Hermann Mai hatte die Freundlichkeit, das verwertbare Material mit großer Sorgfalt zu sammeln, zu sichten, die Analysen zu Ende zu führen und die Ergebnisse in die vorliegende Form zu bringen. Herr Professor Dr.Fritz Laquer in Wuppertal-Vohwinkel steuerte vor und nachHentschels Tode zahlreiche Ergosterinbestimmungen bei und die Nothilfe der Deutschen Wissenschaft ansehnliche Beträge. Beiden wird im Namen des frühverstorbenen ausgezeichneten Forschers hierfür der ergebenste Dank ausgesprochen.M. Pfaundler.     

Befund einer eigenartigen fibro-myxomatösen Hyperplasie der Mitralis

Ohne ZusammenfassungMit 3 Abbildungen im Text.