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Forced expiratory volume in 1 s (FEV 1 ) detection of exercise-induced bronchoconstriction (EIB) to identify asthma has good specificity but rather low sensitivity. The aim was to test whether sensitivity may be improved by measuring respiratory resistance (RRS) by the forced oscillation technique (FOT). Forty-seven asthmatic and 50 control children (5-12 y) were studied before and after running 6 min on a treadmill. RRS in inspiration (RRSi) and expiration (RRSe), FEV 1 and RRSi response to a deep inhalation (DI) were measured before and after exercise. In asthmatics versus controls, exercise induced significantly larger increases in RRSi (p Ͻ 0.001) and larger decreases in FEV 1 (p ϭ 0.004). Asthmatics but not controls showed more bronchodilation by DI after exercise (p ϭ 0.02). At specificity Ͼ0.90, sensitivity was 0.53 with 25% increase RRSi and 0.45 with 27% increase RRSe or 5% decrease FEV 1 . It is concluded that the FOT improves sensitivity of exercise challenge, and the RRSi response to DI may prove useful in identifying the mechanism of airway obstruction. (Pediatr Res 68: 537-541, 2010) E xercise-induced bronchoconstriction (EIB) is closely linked to airway inflammation and unlikely to develop in healthy children (1), so that detecting airway hyperresponsiveness to exercise in the lung function laboratory is considered highly specific of asthma, i.e. it is associated with low rate of false-positive responses. A limitation is the rather low sensitivity of the test (2,3). EIB has been identified in primary school children by changes in forced expiratory volume in 1 s (FEV 1 ) or peak expiratory flow, and decision levels were mostly based on the former parameter (3). Respiratory resistance (RRS) measured by the forced oscillation technique (FOT) offers an alternative assessment of airway caliber, the time variations of which may be characterized for instance using a single excitation frequency (4). Computing RRS separately in inspiration and expiration (RRSi and RRSe, respectively) rather than over the whole breathing cycle may be of interest because the upper airways, which may represent a confounding factor in assessing the intrathoracic airways, are known to contribute differently to airway mechanics in inspiration and expiration (5,6). Furthermore, the RRS change in relation to volume history, more specifically the bronchomotor alteration that follows a deep inhalation (DI), has potential relevance in identifying the mechanism of EIB (7-9). Indeed, stretching the acutely contracted bronchial smooth muscle promotes bronchial wall relaxation, which in turn could be taken as an indicator of the magnitude of the airway response (10). To the best of our knowledge, a systematic analysis of diagnostic value of single-frequency RRS has not been performed during case-control identification of EIB in the lung function laboratory at school age.Therefore, the aim of this study was to assess the value of the FOT in identifying EIB in asthmatic children. More specifically, RRSi and RRSe and the change in...

BACKGROUND In a previous work, we demonstrated with flow cytometry (FCM) methods that accumulation of human cyclin B1 in leukemic cell lines begins during the G1 phase of the cell cycle (Viallard et al., Exp Cell Res 247:208‐219, 1999). In the present study, FCM was used to compare the localization and the kinetic patterns of cyclin B1 expression in Jurkat leukemia cell line and phytohemagglutinin (PHA)‐stimulated normal T lymphocytes. METHODS Cell synchronization was performed in G1 with sodium n‐butyrate, at the G1/S transition with thymidine and at mitosis with colchicine. Cells (leukemic cell line Jurkat or PHA‐stimulated human T‐lymphocytes) were stained for DNA and cyclin B1 and analyzed by FCM. Western blotting was used to confirm certain results. RESULTS Under asynchronous growing conditions and for both cell populations, cyclin B1 expression was essentially restricted to the G2/M transition, reaching its maximal level at mitosis. When the cells were synchronized at the G1/S boundary by thymidine or inside the G1 phase by sodium n‐butyrate, Jurkat cells accumulated cyclin B1 in both situations, whereas T lymphocytes expressed cyclin B1 only during the thymidine block. The cyclin B1 fluorescence kinetics of PHA‐stimulated T lymphocytes was strictly similar when considering T lymphocytes blocked at the G1/S phase transition by thymidine and in exponentially growing conditions. These FCM results were confirmed by Western blotting. The detection of cyclin B1 by Western blot in cells sorted in the G1 phase of the cell cycle showed that cyclin B1 was present in the G1 phase in leukemic T cells but not in normal T lymphocytes. Cyclin B1 degradation was effective at mitosis, thus ruling out a defective cyclin B1 proteolysis. CONCLUSIONS We found that the leukemic T cells behaved quite differently from the untransformed T lymphocytes. Our data support the notion that human cyclin B1 is present in the G1 phase of the cell cycle in leukemic T cells but not in normal T lymphocytes. Therefore, the restriction point from which cyclin B1 can be detected is different in the two models studied. We hypothesize that after passage through a restriction point differing in T lymphocytes and in leukemic cells, the rate of cyclin B1 synthesis becomes constant in the S and G2/M phases and independent from the DNA replication cycle. Cytometry 39:117–125, 2000 © 2000 Wiley‐Liss, Inc.

Background:In a previous work, we demonstrated with flow cytometry (FCM) methods that accumulation of human cyclin B1 in leukemic cell lines begins during the G 1 phase of the cell cycle (Viallard et al., Exp Cell Res 247: 208-219, 1999). In the present study, FCM was used to compare the localization and the kinetic patterns of cyclin B1 expression in Jurkat leukemia cell line and phytohemagglutinin (PHA)-stimulated normal T lymphocytes. Methods: Cell synchronization was performed in G 1 with sodium n-butyrate, at the G 1 /S transition with thymidine and at mitosis with colchicine. Cells (leukemic cell line Jurkat or PHA-stimulated human T-lymphocytes) were stained for DNA and cyclin B1 and analyzed by FCM. Western blotting was used to confirm certain results. Results: Under asynchronous growing conditions and for both cell populations, cyclin B1 expression was essentially restricted to the G 2 /M transition, reaching its maximal level at mitosis. When the cells were synchronized at the G 1 /S boundary by thymidine or inside the G 1 phase by sodium n-butyrate, Jurkat cells accumulated cyclin B1 in both situations, whereas T lymphocytes expressed cyclin B1 only during the thymidine block. The cyclin B1 fluorescence kinetics of PHA-stimulated T lymphocytes was strictly similar when considering T lymphocytes blocked