[Pulmonary re-expansion in metastatic pleural effusions after thoracentesis: A pilot study]. / Échogénicité des pleurésies : facteur prédictif d'amélioration de la dyspnée ? Étude pilote concernant les pleurésies métastatiques.

INTRODUCTION: Metastatic pleural effusion is a cause of dyspnea. The American thoracic society has strongly suggested that studies evaluating thoracic ultrasonography as potentially predictive of improvment of dyspnea are needed. METHODS: We conducted a prospective monocentric observational study to assess chest ultrasound predictors of response to thoracentesis. Fifteen patients with metastatic pleural effusion were included. RESULTS: The initial mean VAS score was5 ± 2,9 cm. The majority of patients had pleural effusions equal to or greater than 5 intercostal spaces (EIC) in height, while 7 patients had an abnormal curvature of the hemidiaphragm (flattened or inverted). PRIMARY ENDPOINT: The volume removed was greater in the group with anechoic pleurisy compared to the group with sonographic septation, notwithstanding complex pleural effusion (non-septated, relatively hyperechoic, with some spots in the effusion). The patients with complex pleural effusions had an higher score of dyspnea. SECONDARY ENDPOINTS: The 7 patients with abnormal diaphragmatic curvature presented significant dyspnea with a pain score of approximately 7 and profuse pleurisy occupying 8 intercostal spaces in height. The effusions of those who could not normalize their curvature had a complex aspect and the volume removed was lower. CONCLUSIONS: The ultrasound characteristics of pleural effusions seem to be predictors of improvment of dyspnea after thoracentesis. The septated and complex aspects are probably predictors of non improvment of dyspnea.

Aminoisobutyric acid transport in soleus muscles of lean and gold thioglucose-obese mice.

The uptake of alpha-aminoisobutyric acid (AIB) was studied in soleus muscles isolated from lean and gold thioglucose-lesioned obese mice (GTG-obese), both in basal and in insulin-stimulated conditions. The basal (i.e., non-insulin-stimulated) influx of AIB was decreased in muscles of GTG-obese mice because of a decrease in the apparent Vmax of the transport system. In muscles from both types of mice, insulin stimulated AIB influx by increasing the apparent Vmax of transport; this effect was partially dependent on new protein synthesis. In muscles of GTG-obese mice, the effect of insulin was altered in two ways: the absolute value of the maximally insulin-stimulated AIB influx was lower than in muscles of lean controls, and the dose response of insulin-stimulated AIB influx was shifted to the right (half-maximally effective concentration, EC50 congruent to 1.7 nM) compared to that observed in muscles of lean animals (EC50 congruent to 0.7 nM). It is concluded that in muscles of obese mice a) amino acid transport per se is altered, and b) the sensitivity of this process to the stimulatory effect of insulin is markedly diminished.