Fistules bronchiques postpneumonectomies : facteurs prédictifs

Yena, Sadio; Doddoli, Christophe; Doumbia, Seydou; D’Journo, Xavier Benoit; Aragon, Adrian; M, Mondini; Marghli, A.; Thomas, Philippe; Giudicelli, R; Sangaré, D; Soumaré, S; Fuentès, P.

doi:10.1016/j.anchir.2005.08.005

Cited by 13 publications

(5 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To our knowledge, this study is the first to demonstrate effects of a selective GPER agonist, G-1, on coronary artery SMC differentiation, proliferation and migration, and to propose key mediators of this response. Previous studies indicate that GPER activation promotes cancer cell proliferation and migration primarily by producing connective tissue growth factor in a human breast cancer cell line SKBr3 [32], [33]. In addition, tamoxifen, an ERα antagonist but GPER agonist, induces abnormal endometrial thickening and cell proliferation [34], [35].…”

Section: Discussionmentioning

confidence: 99%

Activation of GPER Induces Differentiation and Inhibition of Coronary Artery Smooth Muscle Cell Proliferation

Fen

Szynkarski

et al. 2013

PLoS ONE

View full text Add to dashboard Cite

BackgroundVascular pathology and dysfunction are direct life-threatening outcomes resulting from atherosclerosis or vascular injury, which are primarily attributed to contractile smooth muscle cells (SMCs) dedifferentiation and proliferation by re-entering cell cycle. Increasing evidence suggests potent protective effects of G-protein coupled estrogen receptor 1 (GPER) activation against cardiovascular diseases. However, the mechanism underlying GPER function remains poorly understood, especially if it plays a potential role in modulating coronary artery smooth muscle cells (CASMCs).Methodology/Principal FindingsThe objective of our study was to understand the functional role of GPER in CASMC proliferation and differentiation in coronary arteries using from humans and swine models. We found that the GPER agonist, G-1, inhibited both human and porcine CASMC proliferation in a concentration- (10−8 to 10−5 M) and time-dependent manner. Flow cytometry revealed that treatment with G-1 significantly decreased the proportion of S-phase and G2/M cells in the growing cell population, suggesting that G-1 inhibits cell proliferation by slowing progression of the cell cycle. Further, G-1-induced cell cycle retardation was associated with decreased expression of cyclin B, up-regulation of cyclin D1, and concomitant induction of p21, and partially mediated by suppressed ERK1/2 and Akt pathways. In addition, G-1 induces SMC differentiation evidenced by increased α-smooth muscle actin (α-actin) and smooth muscle protein 22α (SM22α) protein expressions and inhibits CASMC migration induced by growth medium.ConclusionGPER activation inhibits CASMC proliferation by suppressing cell cycle progression via inhibition of ERK1/2 and Akt phosphorylation. GPER may constitute a novel mechanism to suppress intimal migration and/or synthetic phenotype of VSMC.

show abstract

Section: Discussionmentioning

confidence: 99%

Activation of GPER Induces Differentiation and Inhibition of Coronary Artery Smooth Muscle Cell Proliferation

Fen

Szynkarski

et al. 2013

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Empyema and BPF are among the commonly declared postoperative complications, especially in the presence of chronic inflammatory lung disease and right pneumonectomy, with an incidence of 2 to 16% and 0.8 to 15%, respectively. [1][2][3][17][18][19][20] Management depends on the time and extent of the complication, general condition of the patient, and experience of the center; and includes closed drainage, thoracoplasty, fenestration, thoracoscopic debridement, and fibrinolysis for empyema; 9,21-24 and transthoracic, transpericardial repair, omentoplasty, and glue application for BPF. 3,[24][25][26] The technique for bronchial closure and preference of chest tube drainage are the controversial topics with respect to the correlation with postpneumonectomy complications.…”

Section: Discussionmentioning

confidence: 99%

Childhood Pneumonectomies: Two Decades' Experience of a Referral Center

et al. 2012

View full text Add to dashboard Cite

Correct selection of indications, careful preoperative preparation with eradication of infection, meticulous performance of surgical and anesthetic techniques, early detection and management of complications, and long-term follow-up including pulmonary rehabilitation are essential parameters to reduce morbidity and mortality rates in childhood pneumonectomy. Better compensatory lung growth and improvement in development after the operation will facilitate better health and improved life quality in children.

show abstract

“…Thus, 29 (0.39%) studies [9,14–41] (involving 70,111 patients) were deemed eligible after a comprehensive literature search. Of these 29 studies, 3 articles [9,16,22] presented data for both OS and postoperative pulmonary complications rate, 19 articles [15,17–20,23,24,26,28–30,32–37,39,40] reported OS only, 7 articles [14,21,25,27,31,38,41] reported the postoperative pulmonary complications rate only. Figure 1 shows the process involved in the assessment of the studies and in accordance to the process highlighted in the figure the studies were identified, those of them that fulfilled the conditions detailed earlier were included and those that did not were excluded.…”

Section: Resultsmentioning

confidence: 99%

“…Ten studies [9,14,16,21,22,25,27,31,38,41] were included to assess the association between COPD and risk of pulmonary complications, as bronchopleural fistula (BPF), pneumonia, prolonged air leakage, prolonged mechanical ventilation, and empyema in patients undergoing lung cancer surgery. Eight studies [9,14,16,21,22,25,27,31] reported a frequency of BPF; 5 [9,16,22,38,41] reported pneumonia; 3 [16,38,41] reported prolonged air leakage; 3 [9,16,22] reported prolonged mechanical ventilation; 3 [9,22,38] reported empyema.…”

Section: Resultsmentioning

confidence: 99%