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Introduction Respiratory mechanic is challenging for patients treated with veno-arterial Extracorporeal Membrane Oxygenation (VA ECMO). Whereas growing evidences were reported of changes in diaphragm thickness during mechanical ventilation (1,2), no study has reported an impact of VA ECMO settings on diaphragm effort. We hypothesized that ECMO settings influenced diaphragm thickening during ECMO weaning. We assessed diaphragm thickening fraction (TF) at the time of recovery from heart failure. Methods We conducted a nine-month prospective monocentric observational study. Adult patients ready for a first VA ECMO weaning trial, breathing spontaneously and hemodynamically stable at 2 l/min of VA ECMO flow were included. Sweep gas flow (SGF) was set for 15 min at 4 l/min, 2 l/min and 1 l/min with a 10 min return to baseline between each step (3). Mechanical ventilation when required was set at pressure support 7 cmH2O and positive end expiratory pressure 0cmH2O (PSV7 +ZEEP). Diaphragm ultrasound was used to assess TF at the end of each step. Demographic, left ventricle ejection fraction (LVEF) assessed through echocardiography and outcome data were collected. Results Thirty-seven patients were screened and 15 patients with VA ECMO were included. Ten patients were extubated, 5 were ventilated in PSV7+ZEEP. The baseline TF was 11% [4 – 15] at a SGF of 2.3 [2 - 4] l/min. TF was 6.3% [0 - 10] at 4 l/min, 13.3% [10 - 26] at 2 l/min and 26.7% [22 - 44] at 1 l/min (ANOVA, P Discussion Diaphragm TF was related with VA ECMO settings and LVEF at the time of the first assessment of patient weaning. Inappropriate ECMO settings lead to impaired diaphragm activity, which could consequently produce atelectasis, pulmonary complications or respiratory muscle fatigue.

Many intravenous (IV) drugs are required for complex and polypathologic critically ill ICU patients management. ICU nurses are daily confronted with drugs preparation and administration (solvent type and volume, infusion rate). They also have to deal with drugs physiochemical incompatibilities (PCI), especially as various IV medications are delivered via a single catheter lumen. PCI may induce a loss of drug efficiency, catheter thrombosis and embolism. Data about drugs PCI in ICU are scarce (1).

Introduction Sunitinib is a multikinase inhibitor active in various cancers types including renal cancers and endocrine tumors. The study analyzed the influence of the lean body mass (LBM) and of pharmacogenetic variants on the exposure to sunitinib and its active metabolite, SU12662, and on sunitinib toxicity and clinical activity. Materials and Methods Exposure to sunitinib and SU12662 was assessed on days 10 and 21 during the first treatment cycle. Acute toxicity was graded using the NCI 4.0 CTCAE ver. 4.0. The LBM and 14 common single nucleotide polymorphisms in the CYP3A4/3A5, NR1I2, NR1I3, ABCB1, and ABCG2 genes were analyzed according to the drug exposure at day 10. Determinants (including sunitinib exposure and pharmacogenetic variants) for toxicities were assessed, as well as the relationship between drug exposure and survival in renal cancer patients. Results Ninety-two patients (60 % with renal cancer) were assessable for pharmacokinetics, toxicity and survival, and 66 for genetic analysis. The LBM (p A) (p = 0.014) were two independent parameters accounting for the variability of composite (sunitinib + SU12662) exposure. Advanced age (OR = 1.47 [1.01–2.15], p = 0.048) and high sunitinib exposure (OR = 1.16 [1.05–1.28], p = 0.005) were independently associated with any grade ≥ 3 acute toxicity, and high SU12662 exposure was associated with grade ≥ 2 thrombocytopenia (OR = 1.27 [1.03–1.57], p = 0.028). A high composite area under the curve (AUC) >1,973 ng/mL∙h at day 21 was associated with a doubled survival (35.2 vs 16.7 months; log-rank p = 0.0051) in renal cancer patients. Conclusions This study indicates that LBM and drug monitoring may be helpful in the management of sunitinib-treated patients.

In this paper, we report the state-of-the-art results obtained in quasi-self-aligned (QSA) single polysilicon NPN bipolar transistors fabricated within a low-complexity 0.5-/spl mu/m CMOS process. Our devices demonstrate nearly ideal static characteristics and very good frequency performance. In fact, the obtained 30-GHz maximum f/sub T/ and 4.1 V breakdown voltage are comparable to the best reported results for single-poly self-aligned (SA) transistors. Some details of the technological process as well as statistical measurements performed on the different optimization splits are presented. The f/sub T/ and f/sub max/ on-wafer high-frequency measurements are discussed in terms of reproducibility, sensitivity to process parameters, and device geometry.

SAOS = Syndrome d'apnées obstructives du sommeil, CPAP = Continue positive airway pressure; This ancillary study, based on a cohort of 28 OSA patients, found no effect of Valsartan or CPAP on three inflammatory markers (CRPus, 11-TXB2, LTE4). The failure of CPAP to reduce these inflammatory biomarkers could be due to our population composition that mainly included overweight individuals, in whom obesity is a well known confounding factor associated to underlying inflammation. Valsartan is indicated in the treatment of essential hypertension. The decrease of cardiovascular risk which can be attributed to this molecule could be mainly due to its anti-hypertensive properties, and seems to be independent of potential anti-inflammatory effects. This lack of effect may be explained by the absence of PPAR-γ agonist property. A comparison between Valsartan and ARBs sharing this property, such as Irbesartan, on two matched groups could elucidate the underlying mechanism.; Cette étude ancillaire, portant sur une population de 28 patients SAOS, n'a pas retrouvé d'effet du Valsartan ou de la CPAP sur les trois marqueurs inflammatoires considérés (CRPus, 11-TXB2, LTE4). L'absence d'effet de la CPAP pourrait être attribuée à notre population majoritairement composée d'individus en surpoids, chez qui il a été démontré qu'un traitement efficace par CPAP ne permettait pas de normaliser le taux de marqueurs inflammatoires. Le Valsartan est quant à lui en premier lieu un anti-hypertenseur. L'amélioration du risque cardiovasculaire qu'il peut induire semble donc attribuable en premier lieu à ses effets normotenseurs, indépendamment d'éventuels effets sur l'inflammation, que notre étude n'a pas réussi à mettre en évidence. Cette absence d'effets anti-inflammatoires pourrait s'expliquer par l'absence de propriété agoniste PPAR-γ. Une comparaison entre le Valsartan et un ARA-II possédant cette propriété tel que l'Irbésartan sur deux groupes appariés en tous autres points pourrait permettre d'élucider le mécanisme sous-jacent.

A low cost high performance 0.5 /spl mu/m single-poly quasi self-aligned npn bipolar technology is described. The devices feature record f/sub T/ and f/sub max/ values of 30 GHz and 40 GHz respectively, with 4.2 V BV/sub CEO/ well into the range of performances usually covered by double-poly bipolar transistors.