Explore the vast range of titles available.

Abstract Assisted/supported modes of mechanical ventilation offer significant advantages over controlled modes in terms of ventilator muscle function/recovery and patient comfort (and sedation needs). However, assisted/supported breaths must interact with patient demands during all three phases of breath delivery: trigger, target, and cycle. Synchronous interactions match ventilator support with patient demands; dyssynchronous interactions do not. Dyssynchrony imposes high pressure loads on ventilator muscles, promoting muscle overload/fatigue and increasing sedation needs. On current modes of ventilation there are a number of features that can monitor and enhance synchrony. These include adjustments of the trigger variable, the use of pressure versus fixed flow targeted breaths, and a number of manipulations of the cycle variable. Clinicians need to know how to use these modalities and monitor them properly, especially understanding airway pressure and flow graphics. Future strategies are emerging that have theoretical appeal but they await good clinical outcome studies before they become commonplace.

Abstract Background Plasma microbial cell-free DNA (mcfDNA) sequencing can establish the etiology of multiple infectious syndromes by identifying microbial DNA in plasma. However, data are needed to define the clinical scenarios where this tool offers the highest clinical benefit. Methods We conducted a prospective multicenter observational study that evaluated the impact of plasma mcfDNA sequencing compared with usual care testing among adults with hematologic malignancies. This is a secondary analysis of an expanded cohort that evaluated the clinical utility of plasma mcfDNA sequencing across prespecified and adjudicated outcomes. We examined the percentage of participants for whom plasma mcfDNA sequencing identified a probable cause of pneumonia or clinically relevant nonpneumonia infection. We then assessed potential changes in antimicrobial therapy based on plasma mcfDNA sequencing results and the potential for early mcfDNA testing to avoid bronchoscopy and its associated adverse events. Results Of 223 participants, at least 1 microbial detection by plasma mcfDNA sequencing was adjudicated as a probable cause of pneumonia in 57 (25.6%) and a clinically relevant nonpneumonia infection in 88 (39.5%). A probable cause of pneumonia was exclusively identified by plasma mcfDNA sequencing in 23 (10.3%) participants. Antimicrobial therapy would have changed for 41 (18.4%) participants had plasma mcfDNA results been available in real time. Among the 57 participants with a probable cause of pneumonia identified by plasma mcfDNA sequencing, bronchoscopy identified no additional probable cause of pneumonia in 52 (91.2%). Conclusions Plasma mcfDNA sequencing could improve management of both pneumonia and other concurrent infections in immunocompromised patients with suspected pneumonia.

The purpose of the study was to identify the predictors of short-term mortality in patients undergoing percutaneous dilatational tracheostomy (PDT). Retrospective analysis of data pertaining to adult patients who underwent PDT between July 2005 and June 2008 in an urban, academic, tertiary care medical center was done. Clinical and demographic data were analyzed for 483 patients undergoing PDT via multivariate logistic regression. Mortality data were examined at in-hospital, 14, 30, and 180 days postprocedure. Overall mortality rates were 11% at 14 days, 19% at 30 days, and 40% at 180 days. In-hospital mortality was 30%. Patients undergoing PDT have significant short-term mortality with 11% dying within 14 days and an in-hospital mortality rate of 30%. We identified an index diagnosis of ventilator-associated pneumonia and trauma to be associated with a higher survival rate, whereas older age, oncological diagnosis, cardiogenic shock, and ventricular-assist devices were associated with higher mortality. There is significant heterogeneity in both underlying diagnosis and patient outcomes, and these factors should be considered when deciding to perform this procedure and discussed with patients/family members to provide a realistic expectation of potential prognosis.

Ethanol's action on the brain likely reflects altered function of key ion channels such as glutamatergic N-methyl-D-aspartate receptors (NMDARs). In this study, we determined how expression of a mutant GluN1 subunit (F639A) that reduces ethanol inhibition of NMDARs affects ethanol-induced behaviors in mice. Mice homozygous for the F639A allele died prematurely while heterozygous knock-in mice grew and bred normally. Ethanol (44 mM; ∼0.2 g/dl) significantly inhibited NMDA-mediated EPSCs in wild-type mice but had little effect on responses in knock-in mice. Knock-in mice had normal expression of GluN1 and GluN2B protein across different brain regions and a small reduction in levels of GluN2A in medial prefrontal cortex. Ethanol (0.75-2.0 g/kg; i.p.) increased locomotor activity in wild-type mice but had no effect on knock-in mice while MK-801 enhanced activity to the same extent in both groups. Ethanol (2.0 g/kg) reduced rotarod performance equally in both groups but knock-in mice recovered faster following a higher dose (2.5 g/kg). In the elevated zero maze, knock-in mice had a blunted anxiolytic response to ethanol (1.25 g/kg) as compared to wild-type animals. No differences were noted between wild-type and knock-in mice for ethanol-induced loss of righting reflex, sleep time, hypothermia or ethanol metabolism. Knock-in mice consumed less ethanol than wild-type mice during daily limited-access sessions but drank more in an intermittent 24 h access paradigm with no change in taste reactivity or conditioned taste aversion. Overall, these data support the hypothesis that NMDA receptors are important in regulating a specific constellation of effects following exposure to ethanol.

This study reports on type: variety-mode classification, digital stereomicroscopy, petrography, neutron activation analysis, and previously published reports and characterizes production and distribution of Mars Orange Paste Ware in the Middle Preclassic-period Maya Lowlands. The sample consists of 2028 sherds of Mars Orange Paste Ware from Holtun, Guatemala, and 4105 sherds reported from sites in Central Belize and Peten Guatemala. The combined data suggest Mars Orange Paste Ware was a “short-distance” trade ware produced in the northeastern Maya Lowlands and distributed from Central Belize to the west. En este estudio se informa sobre la tipología, estereomicroscopía digital, petrografía, análisis de activación por neutrones e informes publicados anteriormente sobre la vajilla Mars Naranja, con el objetivo de caracterizar su producción e intercambio en las Tierras Bajas Mayas durante el periodo Preclásico medio. La muestra considerada comprende 2.028 tiestos de la vajilla Mars Naranja de Holtun, Guatemala, y 4.105 tiestos procedentes de sitios en Belice central y Petén, Guatemala. La combinación de datos sugiere que la vajilla Mars Naranja fue un bien de intercambio de “corta distancia” producido en el noreste de las Tierras Bajas Mayas y distribuido desde el centro de Belice hacia el oeste.

Evidence from a large number of preclinical studies suggests that chronic exposure to drugs of abuse, such as psychostimulants or ethanol induces changes in glutamatergic transmission in key brain areas associated with reward and control of behavior. These changes include alterations in the expression of ionotropic glutamate receptors including N-methyl-D-aspartate receptors (NMDAR) that are important for regulating neuronal activity and synaptic plasticity. NMDA receptors are inhibited by ethanol and reductions in NMDA-mediated signaling are thought to trigger homestatic responses that limit ethanol's effects on glutamatergic transmission. Following repeated exposures to ethanol, these homeostatic responses may become unstable leading to an altered glutamatergic state that contributes to the escalations in drinking and cognitive deficits observed in alcohol-dependent subjects. An important unanswered question is whether ethanol-induced changes in NMDAR expression are modulated by the intrinsic sensitivity of the receptor to ethanol. In this study, we examined the effects of ethanol on NMDAR subunit expression in cortical (orbitofrontal, medial prefrontal), striatal (dorsal and ventral striatum) and limbic (dorsal hippocampus, basolateral amygdala) areas in mice genetically modified to express ethanol-resistant receptors (F639A mice). These mice have been previously shown to drink more ethanol than their wild-type counterparts and have altered behavioral responses to certain actions of ethanol. Following long-term voluntary drinking, F639A mice showed elevations in GluN2A but not GluN1 or GluN2B expression as compared to wild-type mice. Mice treated with repeated injections with ethanol (2-3.5 g/kg; i.p.) showed changes in NMDAR expression that varied in a complex manner with genotype, brain region, subunit type and exposure protocol all contributing to the observed response. F639A mice, but not wild-type mice, showed enhanced motor activity following repeated ethanol injections and this was associated with differences in NMDAR subunit expression across brain regions thought to be involved in drug sensitization. Overall, while the results of the study suggest that NMDARs with reduced sensitivity to ethanol favor the development of locomotor sensitization, they also show that intrinsic ethanol sensitivity is not the sole determinant underlying changes in NMDAR expression following repeated exposures to ethanol.