Cleared to Land: Pilot Visual Detection of Small Unmanned Aircraft During Final Approach

Sighting reports of unmanned aircraft systems (UAS) by pilots, air traffic controllers, and other aviation stakeholders have continued to rise since the Federal Aviation Administration (FAA) began tracking in 2014. In 2018, the FAA received 2,307 such reports, with 22.8% (n = 526) occurring during the final approach phase of flight. The threat of a midair collision between a manned aircraft and UAS is heightened during the final approach phase of flight, as the aircraft transitions from higher-altitude airspace to the low-altitude arena, now shared with drones. Absent UAS sense and avoid systems, pilots are forced to rely on visual senses and scanning techniques to ensure the approach path remains clear of UAS incursions. This research evaluated the effectiveness of pilot visual detection of a multirotor UAS during five approach to landing scenarios in which an unmanned aircraft created an incursion into the approach path. During the scripted approach scenarios, the UAS either remained stationary or maneuvered laterally. Both aircraft and UAS were separated by established vertical safety margins and protocols to avoid an actual collision. Overall, participants detected the UAS during 30% of the approaches. The static UAS was only detected during 13.6% of the approaches, at a mean range of 647 ft. The detection rate improved to 50% when the drone was in motion, with a mean detection range of 1,593 ft. Vector data was calculated to determine the detection angle of UAS sightings, with the majority of successful detections occurring within 5˚ laterally and 10˚ vertically of center. Qualitative comments were solicited from the participants and evaluated for trends. Forty percent of the participants indicated that moving UAS are easier to spot. Other trends related to UAS contrast, object misidentification, and detection aspect angle were also identified by the participants. The authors emphasized that based on the recorded detection distance, pilots would only have a limited margin of error to successfully execute evasive maneuvers, based on the FAA’s Recommended Minimum Reaction Time Required for Evasion criteria. Full-text will be available October 30, 2019 at approximately 10:00 AM Eastern

Alterations in Platelet Function and Cell-Derived Microvesicles in Recently Menopausal Women: Relationship to Metabolic Syndrome and Atherogenic Risk

A woman’s risk for metabolic syndrome (MS) increases at menopause, with an associated increase in risk for cardiovascular disease. We hypothesized that early menopause-related changes in platelet activity and concentrations of microvesicles derived from activated blood and vascular cells provide a mechanistic link to the early atherothrombotic process. Thus, platelet functions and cellular origin of blood-borne microvesicles in recently menopausal women (n = 118) enrolled in the Kronos Early Estrogen Prevention Study were correlated with components of MS and noninvasive measures of cardiovascular disease [carotid artery intima medial thickness (CIMT), coronary artery calcium (CAC) score, and endothelial reactive hyperemic index (RHI)]. Specific to individual components of the MS pentad, platelet number increased with increasing waist circumference, and platelet secretion of ATP and expression of P-selectin decreased with increasing blood glucose (p = 0.005) and blood pressure (p < 0.05), respectively. Waist circumference and systolic blood pressure were independently associated with monocyte- and endothelium-derived microvesicles (p < 0.05). Platelet-derived and total procoagulant phosphatidylserine-positive microvesicles, and systolic blood pressure correlated with CIMT (p < 0.05), but not with CAC or RHI. In summary, among recently menopausal women, specific platelet functions and concentrations of circulating activated cell membrane-derived procoagulant microvesicles change with individual components of MS. These cellular changes may explain in part how menopause contributes to MS and, eventually, to cardiovascular disease

Plankton community respiration and bacterial metabolism in a North Atlantic Shelf Sea during spring bloom development (April 2015)

Spring phytoplankton blooms are important events in Shelf Sea pelagic systems as the increase in carbon production results in increased food availability for higher trophic levels and the export of carbon to deeper waters and the sea-floor. It is usually accepted that the increase in phytoplankton abundance and production is followed by an increase in plankton respiration. However, this expectation is derived from field studies with a low temporal sampling resolution (5–15 days). In this study we have measured the time course of plankton abundance, gross primary production, plankton community respiration, respiration of the plankton size classes (>0.8 µm and 0.2–0.8 µm) and bacterial production at ≤5 day intervals during April 2015 in order to examine the phasing of plankton autotrophic and heterotrophic processes. Euphotic depth-integrated plankton community respiration increased five-fold (from 22 ± 4 mmol O2 m−2 d−1 on 4th April to 119 ± 4 mmol O2 m−2 d−1 on 15th April) at the same time as gross primary production also increased five-fold, (from 114 ± 5 to 613 ± 28 mmol C m−2 d−1). Bacterial production began to increase during the development of the bloom, but did not reach its maximum until 5 days after the peak in primary production and plankton respiration. The increase in plankton community respiration was driven by an increase in the respiration attributable to the >0.8 µm size fraction of the plankton community (which would include phytoplankton, microzooplankton and particle attached bacteria). Euphotic depth-integrated respiration of the 0.2–0.8 µm size fraction (predominantly free living bacteria) decreased and then remained relatively constant (16 ± 3 – 11 ± 1 mmol O2 m−2 d−1) between the first day of sampling (4th April) and the days following the peak in chlorophyll-a (20th and 25th April). Recent locally synthesized organic carbon was more than sufficient to fulfil the bacterial carbon requirement in the euphotic zone during this productive period. Changes in bacterial growth efficiencies (BGE, the ratio of bacterial production to bacterial carbon demand) were driven by changes in bacterial production rates increasing from 0.8 µm during the development of the spring bloom, followed 5 days later by a peak in bacterial production. In addition, the size fractionated respiration rates and high growth efficiencies suggest that free living bacteria are not the major producers of CO2 before, during and a few days after this shelf sea spring phytoplankton bloom.The Leverhulme Trust | Ref. RPG-2017-089UK Natural Environment Research Council (NERC) | Ref. NE/K00168X/1UK Natural Environment Research Council (NERC) | Ref. NE/ K001884/1UK Natural Environment Research Council (NERC) | Ref. NE/K002058/1UK Natural Environment Research Council (NERC) | Ref. NE/K001701/

Inequality in Beijing: A Spatial Multilevel Analysis of Perceived Environmental Hazard and Self-Rated Health

Environmental pollution is a major problem in China, subjecting people to significant health risk. However, surprisingly little is known about how these risks are distributed spatially or socially. Drawing upon a large-scale survey conducted in Beijing in 2013, we examine how environmental hazards and health, as perceived by residents, are distributed at fine (sub-district) scale in urban Beijing, and investigate association between hazards, health and geographical context. A Bayesian spatial multilevel logistic model is developed to account for spatial dependence in unobserved contextual influences (‘neighbourhood effects’) on health. Results reveal robust associations between exposure to environmental hazards and health. A unit decrease on a 5-point Likert scale in exposure is associated with increases of 15.2% (air pollution), 17.5% (noise) and 9.3% (landfills) in the odds of reporting good health, with marginal groups including migrant workers reporting greater exposure. Health inequality is also evident, and associated with age, income, educational attainment and housing characteristics. Geographical context (neighbourhood features like local amenity) also plays a role in shaping the social distribution of health inequality. Results are discussed in the context of developing environmental justice policy within a Chinese social market system that experiences tension between its egalitarian roots and its pragmatic approach to tackling grand public policy challenges

Monocytes regulate the mechanism of T-cell death by inducing Fas-mediated apoptosis during bacterial infection.

Monocytes and T-cells are critical to the host response to acute bacterial infection but monocytes are primarily viewed as amplifying the inflammatory signal. The mechanisms of cell death regulating T-cell numbers at sites of infection are incompletely characterized. T-cell death in cultures of peripheral blood mononuclear cells (PBMC) showed 'classic' features of apoptosis following exposure to pneumococci. Conversely, purified CD3(+) T-cells cultured with pneumococci demonstrated necrosis with membrane permeabilization. The death of purified CD3(+) T-cells was not inhibited by necrostatin, but required the bacterial toxin pneumolysin. Apoptosis of CD3(+) T-cells in PBMC cultures required 'classical' CD14(+) monocytes, which enhanced T-cell activation. CD3(+) T-cell death was enhanced in HIV-seropositive individuals. Monocyte-mediated CD3(+) T-cell apoptotic death was Fas-dependent both in vitro and in vivo. In the early stages of the T-cell dependent host response to pneumococci reduced Fas ligand mediated T-cell apoptosis was associated with decreased bacterial clearance in the lung and increased bacteremia. In summary monocytes converted pathogen-associated necrosis into Fas-dependent apoptosis and regulated levels of activated T-cells at sites of acute bacterial infection. These changes were associated with enhanced bacterial clearance in the lung and reduced levels of invasive pneumococcal disease

Sprint interval and sprint continuous training increases circulating CD34+ cells and cardio-respiratory fitness in young healthy women

The improvement of vascular health in the exercising limb can be attained by sprint interval training (SIT). However, the effects on systemic vascular function and on circulating angiogenic cells (CACs) which may contribute to endothelial repair have not been investigated. Additionally, a comparison between SIT and sprint continuous training (SCT) which is less time committing has not been made

Intestinal function and transit associate with gut microbiota dysbiosis in cystic fibrosis

Background: Most people with cystic fibrosis (pwCF) suffer from gastrointestinal symptoms and are at risk of gut complications. Gut microbiota dysbiosis is apparent within the CF population across all age groups, with evidence linking dysbiosis to intestinal inflammation and other markers of health. This pilot study aimed to investigate the potential relationships between the gut microbiota and gastrointestinal physiology, transit, and health. Study design: Faecal samples from 10 pwCF and matched controls were subject to 16S rRNA sequencing. Results were combined with clinical metadata and MRI metrics of gut function to investigate relationships. Results: pwCF had significantly reduced microbiota diversity compared to controls. Microbiota compositions were significantly different, suggesting remodelling of core and rarer satellite taxa in CF. Dissimilarity between groups was driven by a variety of taxa, including Escherichia coli, Bacteroides spp., Clostridium spp., and Faecalibacterium prausnitzii. The core taxa were explained primarily by CF disease, whilst the satellite taxa were associated with pulmonary antibiotic usage, CF disease, and gut function metrics. Species-specific ordination biplots revealed relationships between taxa and the clinical or MRI-based variables observed. Conclusions: Alterations in gut function and transit resultant of CF disease are associated with the gut microbiota composition, notably the satellite taxa. Delayed transit in the small intestine might allow for the expansion of satellite taxa resulting in potential downstream consequences for core community function in the colon

A cardinal role for cathepsin D in co-ordinating the host-mediated apoptosis of macrophages and killing of pneumococci

The bactericidal function of macrophages against pneumococci is enhanced by their apoptotic demise, which is controlled by the anti-apoptotic protein Mcl-1. Here, we show that lysosomal membrane permeabilization (LMP) and cytosolic translocation of activated cathepsin D occur prior to activation of a mitochondrial pathway of macrophage apoptosis. Pharmacological inhibition or knockout of cathepsin D during pneumococcal infection blocked macrophage apoptosis. As a result of cathepsin D activation, Mcl-1 interacted with its ubiquitin ligase Mule and expression declined. Inhibition of cathepsin D had no effect on early bacterial killing but inhibited the late phase of apoptosis-associated killing of pneumococci in vitro. Mice bearing a cathepsin D-/- hematopoietic system demonstrated reduced macrophage apoptosis in vivo, with decreased clearance of pneumococci and enhanced recruitment of neutrophils to control pulmonary infection. These findings establish an unexpected role for a cathepsin D-mediated lysosomal pathway of apoptosis in pulmonary host defense and underscore the importance of apoptosis-associated microbial killing to macrophage function

Platelet factor XIII-A regulates platelet function and promotes clot retraction and stability.

Factor XIII (FXIII) is an important proenzyme in the hemostatic system. The plasma-derived enzyme activated FXIII cross-links fibrin fibers within thrombi to increase their mechanical strength and cross-links fibrin to fibrinolytic inhibitors, specifically α2-antiplasmin, to increase resistance to fibrinolysis. We have previously shown that cellular FXIII (factor XIII-A [FXIII-A]), which is abundant in the platelet cytoplasm, is externalized onto the activated membrane and cross-links extracellular substrates. The contribution of cellular FXIII-A to platelet activation and platelet function has not been extensively studied. This study aims to identify the role of platelet FXIII-A in platelet function. We used normal healthy platelets with a cell permeable FXIII inhibitor and platelets from FXIII-deficient patients as a FXIII-free platelet model in a range of platelet function and clotting tests. Our data demonstrate that platelet FXIII-A enhances fibrinogen binding to the platelet surface upon agonist stimulation and improves the binding of platelets to fibrinogen and aggregation under flow in a whole-blood thrombus formation assay. In the absence of FXIII-A, platelets show reduced sensitivity to agonist stimulation, including decreased P-selectin exposure and fibrinogen binding. We show that FXIII-A is involved in platelet spreading where a lack of FXIII-A reduces the ability of platelets to fully spread on fibrinogen and collagen. Our data demonstrate that platelet FXIII-A is important for clot retraction where clots formed in its absence retracted to a lesser extent. Overall, this study shows that platelet FXIII-A functions during thrombus formation by aiding platelet activation and thrombus retraction in addition to its antifibrinolytic roles