Left-Sided Double-Lumen Tube vs EZ-Blocker for One-Lung Ventilation in Thoracic Surgery: A Systematic Review and Meta-Analysis.

Background. The EZ-Blocker is the newest generation of bronchial blocker and offers a potential alternative to left-sided double lumen tubes for lung isolation and one-lung ventilation during thoracic surgery. Methods. Databases were searched for randomized controlled trials comparing left-sided double lumen tube to the EZ-Blocker for one-lung ventilation during thoracic surgery. The time for placement, incidence of intraoperative displacement, and surgeons' rating of lung collapse quality were designated as coprimary outcomes. The safety profiles of the two devices, including the incidence of airway trauma and post-extubation discomfort were also examined. Results. Six randomized controlled trials (495 patients) were analyzed. Compared to the EZ-Blocker, the left-sided double lumen tube was faster to place by a weighted mean difference of [95% CI] of -61.24 seconds [-102.48, -20.00] (P = .004) and was much less likely to become displaced during lung isolation with an odds ratio [95% CI] of .56 [.34, .91] (P = .02). The left-sided double lumen tube and the EZ-Blocker provided similar surgeon-rated quality of lung isolation. Although the left-sided double lumen tube caused a greater degree of post-extubation sore throat, there was a similar incidence of carinal trauma and post-extubation hoarseness compared to the EZ-Blocker. Conclusion. Our analysis suggests that the left-sided double lumen tube can be placed more quickly and is less prone to intraoperative displacement compared to the EZ-Blocker; the quality of lung collapse is similar. Thus, evidence appears to support the continued utilization of the left-sided double lumen tube for routine thoracic surgery requiring one-lung ventilation.

The amyotrophic lateral sclerosis-linked protein TDP-43 regulates interleukin-6 cytokine production by human brain pericytes.

Amyotrophic lateral sclerosis (ALS) is a fatal movement disorder involving degeneration of motor neurons through dysfunction of the RNA-binding protein TDP-43. Pericytes, the perivascular cells of the blood-brain, blood-spinal cord, and blood-CSF barriers also degenerate in ALS. Indeed, pericytes are among the earliest cell types to show gene expression changes in pre-symptomatic animal models of ALS. This suggests that pericyte degeneration precedes neurodegeneration and may involve pericyte cell-autonomous TDP-43 dysfunction. Here we determined the effect of TDP-43 dysfunction in human brain pericytes on interleukin 6 (IL-6), a critical secreted inflammatory mediator reported to be regulated by TDP 43. Primary human brain pericytes were cultured from biopsy tissue from epilepsy surgeries and TDP-43 was silenced using siRNA. TDP-43 silencing of pericytes stimulated with pro-inflammatory cytokines, interleukin-1ß or tumour necrosis factor alpha, robustly suppressed the induction of IL-6 transcript and protein. IL-6 regulation by TDP-43 did not involve the assembly of TDP-43 nuclear splicing bodies, and did not occur via altered splicing of IL6. Instead, transcriptome-wide analysis by RNA-Sequencing identified a poison exon in the IL6 destabilising factor HNRNPD (AUF1) as a splicing target of TDP-43. Our data support a model whereby TDP-43 silencing favours destabilisation of IL6 mRNA, via enhanced AU-rich element-mediated decay by HNRNP/AUF1. This suggests that cell-autonomous deficits in TDP-43 function in human brain pericytes would suppress their production of IL-6. Given the importance of the blood-brain and blood-spinal cord barriers in maintaining motor neuron health, TDP-43 in human brain pericytes may represent a cellular target for ALS therapeutics.

Daylight exposure modulates bacterial communities associated with household dust.

BACKGROUND: Microbial communities associated with indoor dust abound in the built environment. The transmission of sunlight through windows is a key building design consideration, but the effects of light exposure on dust communities remain unclear. We report results of an experiment and computational models designed to assess the effects of light exposure and wavelengths on the structure of the dust microbiome. Specifically, we placed household dust in replicate model "rooms" with windows that transmitted visible, ultraviolet, or no light and measured taxonomic compositions, absolute abundances, and viabilities of the resulting bacterial communities. RESULTS: Light exposure per se led to lower abundances of viable bacteria and communities that were compositionally distinct from dark rooms, suggesting preferential inactivation of some microbes over others under daylighting conditions. Differences between communities experiencing visible and ultraviolet light wavelengths were relatively minor, manifesting primarily in abundances of dead human-derived taxa. Daylighting was associated with the loss of a few numerically dominant groups of related microorganisms and apparent increases in the abundances of some rare groups, suggesting that a small number of microorganisms may have exhibited modest population growth under lighting conditions. Although biological processes like population growth on dust could have generated these patterns, we also present an alternate statistical explanation using sampling models from ecology; simulations indicate that artefactual, apparent increases in the abundances of very rare taxa may be a null expectation following the selective inactivation of dominant microorganisms in a community. CONCLUSIONS: Our experimental and simulation-based results indicate that dust contains living bacterial taxa that can be inactivated following changes in local abiotic conditions and suggest that the bactericidal potential of ordinary window-filtered sunlight may be similar to ultraviolet wavelengths across dosages that are relevant to real buildings.