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There are some concerns about the use of Pseudomonas-based products as biocontrol agents because of the hemolytic activity shown by their metabolites. The effects of Pseudomonas lipodepsipeptides (LDPs) on mammals via ingestion and the LDP degradation during the digestion and intestinal permeability have not been evaluated. In this research, the susceptibility of different LDPs to degradation was assayed with enzymatic gastrointestinal digestion, and intestinal permeability to LDPs was investigated in an in vitro system based on an intestinal cell layer system. Results demonstrated that trypsin and chymotrypsin hydrolyze up to 50% of the various LDPs, and that proteolysis was further increased by pronase E treatment. A decrease in LDP hemolytic activity matched LDP degradation during the various steps of the digestion process. Moreover, it was shown that syringomycin E (SRE), the main known LDE was not able to cross the intestinal cell layer, suggesting that SRE does not reach the bloodstream in vivo. It was concluded that the Pseudomonas-based biocontrol products do not represent a serious risk for consumer health. In fact, LDPs possibly present on biocontrol-treated agricultural commodities would likely be partially digested by gastrointestinal enzymes and would not be absorbed at the intestinal level. [ABSTRACT FROM AUTHOR]

Leonardo Govoni,1 Raffaele L Dellaca,1 Oscar Peñuelas,2,3 Giacomo Bellani,4,5 Antonio Artigas,3,6 Miquel Ferrer,3,7 Daniel Navajas,3,8,9 Antonio Pedotti,1 Ramon Farré3,81TBM-Lab, Dipartimento di Bioingegneria, Politecnico di Milano University, Milano, Italy; 2Hospital Universitario de Getafe – CIBERES, Madrid, Spain; 3CIBER de Enfermedades Respiratorias, Bunyola, Spain; 4Department of Experimental Medicine, University of Milan, Bicocca, Italy; 5Department of Perioperative Medicine and Intensive Care, San Gerardo Hospital, Monza (MI), Italy; 6Critical Care Center, Sabadell Hospital, Corporació Sanitaria Universitaria Parc Tauli, Universitat Autonoma de Barcelona, CIBERES, Spain; 7Department of Pneumology, Hospital Clinic, IDIBAPS, Barcelona, Spain; 8Unitat de Biofísica i Bioenginyeria, Facultat de Medicina, Universidad de Barcelona-IDIBAPS, Barcelona, Spain; 9Institut de Bioenginyeria de Catalunya, Barcelona, SpainAbstract: Even if the performance of a given ventilator has been evaluated in the laboratory under very well controlled conditions, inappropriate maintenance and lack of long-term stability and accuracy of the ventilator sensors may lead to ventilation errors in actual clinical practice. The aim of this study was to evaluate the actual performances of ventilators during clinical routines. A resistance (7.69 cmH2O/L/s) – elastance (100 mL/cmH2O) test lung equipped with pressure, flow, and oxygen concentration sensors was connected to the Y-piece of all the mechanical ventilators available for patients in four intensive care units (ICUs; n = 66). Ventilators were set to volume-controlled ventilation with tidal volume = 600 mL, respiratory rate = 20 breaths/minute, positive end-expiratory pressure (PEEP) = 8 cmH2O, and oxygen fraction = 0.5. The signals from the sensors were recorded to compute the ventilation parameters. The average ± standard deviation and range (min–max) of the ventilatory parameters were the following: inspired tidal volume = 607 ± 36 (530–723) mL, expired tidal volume = 608 ± 36 (530–728) mL, peak pressure = 20.8 ± 2.3 (17.2–25.9) cmH2O, respiratory rate = 20.09 ± 0.35 (19.5–21.6) breaths/minute, PEEP = 8.43 ± 0.57 (7.26–10.8) cmH2O, oxygen fraction = 0.49 ± 0.014 (0.41–0.53). The more error-prone parameters were the ones related to the measure of flow. In several cases, the actual delivered mechanical ventilation was considerably different from the set one, suggesting the need for improving quality control procedures for these machines.Keywords: equipment and supplies, medical devices, intravenous, quality assurance, health care quality assessment, ventilator accuracy, ventilation error

Abstract Background The aim was to test the hypothesis that the blood serum of rats subjected to recurrent airway obstructions mimicking obstructive sleep apnea (OSA) induces early activation of bone marrow-derived mesenchymal stem cells (MSC) and enhancement of endothelial wound healing. Methods We studied 30 control rats and 30 rats subjected to recurrent obstructive apneas (60 per hour, lasting 15 s each, for 5 h). The migration induced in MSC by apneic serum was measured by transwell assays. MSC-endothelial adhesion induced by apneic serum was assessed by incubating fluorescent-labelled MSC on monolayers of cultured endothelial cells from rat aorta. A wound healing assay was used to investigate the effect of apneic serum on endothelial repair. Results Apneic serum showed significant increase in chemotaxis in MSC when compared with control serum: the normalized chemotaxis indices were 2.20 ± 0.58 (m ± SE) and 1.00 ± 0.26, respectively (p < 0.05). MSC adhesion to endothelial cells was greater (1.75 ± 0.14 -fold; p < 0.01) in apneic serum than in control serum. When compared with control serum, apneic serum significantly increased endothelial wound healing (2.01 ± 0.24 -fold; p < 0.05). Conclusions The early increases induced by recurrent obstructive apneas in MSC migration, adhesion and endothelial repair suggest that these mechanisms play a role in the physiological response to the challenges associated to OSA.

Abstract Background Cognitive impairment is one of the main consequences of obstructive sleep apnea (OSA) and is usually attributed in part to the oxidative stress caused by intermittent hypoxia in cerebral tissues. The presence of oxygen-reactive species in the brain tissue should be produced by the deoxygenation-reoxygenation cycles which occur at tissue level during recurrent apneic events. However, how changes in arterial blood oxygen saturation (SpO2) during repetitive apneas translate into oxygen partial pressure (PtO2) in brain tissue has not been studied. The objective of this study was to assess whether brain tissue is partially protected from intermittently occurring interruption of O2 supply during recurrent swings in arterial SpO2 in an animal model of OSA. Methods Twenty-four male Sprague-Dawley rats (300-350 g) were used. Sixteen rats were anesthetized and non-invasively subjected to recurrent obstructive apneas: 60 apneas/h, 15 s each, for 1 h. A control group of 8 rats was instrumented but not subjected to obstructive apneas. PtO2 in the cerebral cortex was measured using a fast-response oxygen microelectrode. SpO2 was measured by pulse oximetry. The time dependence of arterial SpO2 and brain tissue PtO2 was carried out by Friedman repeated measures ANOVA. Results Arterial SpO2 showed a stable periodic pattern (no significant changes in maximum [95.5 ± 0.5%; m ± SE] and minimum values [83.9 ± 1.3%]). By contrast, brain tissue PtO2 exhibited a different pattern from that of arterial SpO2. The minimum cerebral cortex PtO2 computed during the first apnea (29.6 ± 2.4 mmHg) was significantly lower than baseline PtO2 (39.7 ± 2.9 mmHg; p = 0.011). In contrast to SpO2, the minimum and maximum values of PtO2 gradually increased (p < 0.001) over the course of the 60 min studied. After 60 min, the maximum (51.9 ± 3.9 mmHg) and minimum (43.7 ± 3.8 mmHg) values of PtO2 were significantly greater relative to baseline and the first apnea dip, respectively. Conclusions These data suggest that the cerebral cortex is partially protected from intermittently occurring interruption of O2 supply induced by obstructive apneas mimicking OSA.

Purpose: Cardiac tissue engineering emerges as a promising alternative to current therapies addressed to myocardial infarction. In this context, we aimed to obtain and characterize myocardial bioprosthesis based on a decellularized matrix capable of being engrafted in damaged myocardium.Methods: Myocardial blocks (3x3 cm), differentiating epicardial, mesocardial and endocardial regions, were obtained from cadaveric porcine hearts (n=5) and decellularized using two different protocols: Protocol 1 (P1) combines chemical (ionic and non-ionic detergents), enzymatic (DNase) and physical (agitation) treatments, and Protocol 2 (P2) is based on a combination of chemical (non-ionic detergent, acid, hypotonic and hypertonic solutions), enzymatic (trypsin) and physical (agitation) procedures. Decellularization level was assessed histologically (Masson's Trichrome stain and immunohistochemistry) and molecularly (DNA quantification). The resulting acellular structure was examined by scanning electron microscopy. Extracellular matrix components were analyzed by immunohistochemistry and local matrix stiffness was determined by measuring the Young's modulus with atomic force microscopy. Biodegradability of decellularized matrices was evaluated in vitro with collagenase treatment.Results: Total absence of cells after decellularization was confirmed by Trichrome staining and immunohistochemistry. DNA content was significantly reduced in both protocols (P1: 86.0±1.7%, P2: 96.3±1.1%, compared to native tissue; p<0.001), with significant differences between them (p<0.001). Remarkably, integrity of matrix filaments was preserved due the presence of type-I collagen and elastin. Mechanical testing revealed no significant changes in stiffness of decellularized matrices when compared to native tissue (Native: 27.5±4.9, P1: 33.0±10.7, P2: 40.0±7.1 kPa; p=0.55). The biodegradability assay also confirmed complete degradation of matrices without differences among protocols (Weight loss: P1: 90.1±5.4%, P2: 93.8±5.1%; p=0.19). Finally, non-significant differences were found in epicardial, mesocardial and endocardial decellularized blocks in terms of cells removal, structural, proteical or mechanical characterization.Conclusions: Acellular myocardial matrices were successfully obtained by both decellularization protocols, preserving major structural components so as mechanical and biodegradability properties.Furthermore, trypsin-based protocol (P2) yielded less DNA residues which could contribute to prevent rejection. [ABSTRACT FROM PUBLISHER]