[Invasive mechanical ventilation in COPD and asthma]. / Ventilación mecánica invasiva en EPOC y asma.

COPD and asthmatic patients use a substantial proportion of mechanical ventilation in the ICU, and their overall mortality with ventilatory support can be significant. From the pathophysiological standpoint, they have increased airway resistance, pulmonary hyperinflation, and high pulmonary dead space, leading to increased work of breathing. If ventilatory demand exceeds work output of the respiratory muscles, acute respiratory failure follows. The main goal of mechanical ventilation in this kind of patients is to improve pulmonary gas exchange and to allow for sufficient rest of compromised respiratory muscles to recover from the fatigued state. The current evidence supports the use of noninvasive positive-pressure ventilation for these patients (especially in COPD), but invasive ventilation also is required frequently in patients who have more severe disease. The physician must be cautious to avoid complications related to mechanical ventilation during ventilatory support. One major cause of the morbidity and mortality arising during mechanical ventilation in these patients is excessive dynamic pulmonary hyperinflation (DH) with intrinsic positive end-expiratory pressure (intrinsic PEEP or auto-PEEP). The purpose of this article is to provide a concise update of the most relevant aspects for the optimal ventilatory management in these patients.

Design of an accurate wireless data logger for vibration analysis with Android interface.

In this work a new accurate wireless data logger using the Android interface was developed to monitor vibrations at low-cost. The new data logger is completely autonomous and extremely reduced in size. This instrument enables data collection wirelessly and the ability to display it on any tablet or smartphone with operating system Android. The prototype allows the monitoring of any industrial system with minimal investment in material and installation costs. The data logger is capable of making 12.8 kSPS enough to sample up to 5 kHz signals. The basic specification of the data logger includes a high resolution 1-axis piezoelectric accelerometer with a working range of ±30 G. In addition to the acceleration measurements, temperature can also be recorded. The data logger was tested during a 6-month period in industrial environments. The details of the specific hardware and software design are described. The proposed technology can be easily transferred to many other areas of industrial monitoring.

The chimeric FUS/TLS-CHOP fusion protein specifically induces liposarcomas in transgenic mice.

The characteristic t(12;16)(q13;p11) chromosomal translocation, which leads to gene fusion that encodes the FUS-CHOP chimeric protein, is associated with human liposarcomas. The altered expression of FUS-CHOP has been implicated in a characteristic subgroup of human liposarcomas. We have introduced the FUS-CHOP transgene into the mouse genome in which the expression of the transgene is successfully driven by the elongation factor 1alpha (EF1alpha) promoter to all tissues. The consequent overexpression of FUS-CHOP results in most of the symptoms of human liposarcomas, including the presence of lipoblasts with round nuclei, accumulation of intracellular lipid, induction of adipocyte-specific genes and a concordant block in the differentiation program. We have demonstrated that liposarcomas in the FUS-CHOP transgenic mice express high levels of the adipocyte regulatory protein PPARgamma, whereas it is not expressed in embryonic fibroblasts from these animals following induction to differentiation toward the adipocyte lineage, indicating that the in vitro system does not really reflect the in vivo situation and the developmental defect is downstream of PPARgamma expression. No tumors of other tissues were found in these transgenic mice despite widespread activity of the EF1alpha promoter. This establishes FUS-CHOP overexpression as a key determinant of human liposarcomas and provide the first in vivo evidence for a link between a fusion gene created by a chromosomal translocation and a solid tumor.