An investigation into pilot and system response to critical in-flight events. Volume 1: Executive summary

Critical in-flight events (CIFE) that threaten the aircraft were studied. The scope of the CIFE was described and defined with emphasis on characterizing event development, detection and assessment; pilot information requirements, sources, acquisition, and interpretation, pilot response options, decision processed, and decision implementation and event outcome. Detailed scenarios were developed for use in simulators and paper and pencil testing for developing relationships between pilot performance and background information as well as for an analysis of pilot reaction decision and feedback processes. Statistical relationships among pilot characteristics and observed responses to CIFE's were developed

An investigation into pilot and system response to critical in-flight events. Volume 2: Appendix

Materials relating to the study of pilot and system response to critical in-flight events (CIFE) are given. An annotated bibliography and a trip summary outline are presented, as are knowledge surveys with accompanying answer keys. Performance profiles of pilots and performance data from the simulations of CIFE's are given. The paper and pencil testing materials are reproduced. Conditions for the use of the additive model are discussed. A master summary of data for the destination diversion scenario is given. An interview with an aircraft mechanic demonstrates the feasibility of system problem diagnosis from a verbal description of symptoms and shows the information seeking and problem solving logic used by an expert to narrow the list of probable causes of aircraft failure

Parenchymal and vascular Aβ-deposition and its effects on the degeneration of neurons and cognition in Alzheimer's disease

The deposition of the amyloid β-protein (Aβ) is one of the pathological hallmarks of Alzheimer's disease (AD). Aβ-deposits show the morphology of senile plaques and cerebral amyloid angiopathy (CAA). Senile plaques and vascular Aβ-deposits occur first in neocorti-cal areas. Then, they expand hierarchically into further brain regions. The distribution of Aβ plaques throughout the entire brain, thereby correlates with the clinical status of the patients. Imaging techniques for Aβ make use of the hierarchical distribution of Aβ to distinguish AD patients from non-AD patients. However, pathology seen in AD patients represents a late stage of a pathological process starting 10–30 years earlier in cognitively normal individuals. In addition to the fibrillar amyloid of senile plaques, oligomeric and monomeric Aβ is found in the brain. Recent studies revealed that oligomeric Aβ is presumably the most toxic Aβ-aggregate, which interacts with glutamatergic synapses. In doing so, dendrites are presumed to be the primary target for Aβ-toxicity. In addition, vascular Aβ-deposits can lead to capillary occlusion and blood flow disturbances presumably contributing to the alteration of neurons in addition to the direct neurotoxic effects of Aβ. All these findings point to an important role of Aβ and its aggregates in the neurodegenerative process of AD. Since there is already significant neuron loss in AD patients, treatment strategies aimed at reducing the amyloid load will presumably not cure the symptoms of dementia but they may stop disease progression. Therefore, it seems to be necessary to protect the brain from Aβ-toxicity already in stages of the disease with minor neuron loss before the onset of cognitive symptoms

Alzheimer's - Looking beyond plaques

Mounting evidence shows that inflammation plays a critical role in causing Alzheimer’s disease. Over the last few decades we have gone from a situation where inflammation was generally believed to have no role in the disease to the current picture where chronic activation of IL-1 inflammation has been shown to account for many of the hallmarks of the disease. This review is a personal account of the quest to prove that inflammation plays a critical role in causing Alzheimer’s disease

Perispinal etanercept: Potential as an Alzheimer therapeutic

Tumor necrosis factor-alpha (TNF) is one of a number of systemic and immunomodulating cytokines that generally act to promote acute-phase reactions but can drive degenerative changes when chronically elevated. Traditional focus on TNF has been directed at these inflammation-related functions. Of particular relevance to intersections between neuroinflammation and neurodegeneration is the ability of TNF to increase expression of interleukin-1 (IL-1), which in turn increases production of the precursors necessary for formation of amyloid plaques, neurofibrillary tangles, and Lewy bodies. More recent data have revealed that TNF, one of the few gliotransmitters, has strikingly acute effects on synaptic physiology. These complex influences on neural health suggest that manipulation of this cytokine might have important impacts on diseases characterized by glial activation, cytokine-mediated neuroinflammation, and synaptic dysfunction. Toward such manipulation in Alzheimer's disease, a six-month study was conducted with 15 probable-Alzheimer patients who were treated weekly with perispinal injection of Etanercept, an FDA-approved TNF inhibitor that is now widely used for treatment of rheumatoid arthritis and other systemic diseases associated with inflammation. The results demonstrated that perispinal administration of etanercept could provide sustained improvement in cognitive function for Alzheimer patients. Additionally, the authors were impressed by the striking rapidity with which these improvements occurred in the study patients. An example of this rapid improvement is presented in this issue as a case report by Tobinick and Gross. Such rapid gain of function inspires speculation about the role of gliotransmission or other equally rapid synaptic events in the relationship of TNF to Alzheimer-impacted neurophysiology. Because of the inability of large molecules such as etanercept to cross the blood brain barrier following conventional systemic administration, it is likely that the more direct drug delivery system pioneered by Tobinick also contributed to the effectiveness of the treatment. If so, this system could be useful in drug delivery to the brain in other neural disorders, as well as in animal research studies, many of which currently employ delivery strategies that inflict damage to neural cells and thus engender neuroinflammatory responses

A study of ASRS reports involving general aviation and weather encounters

Consideration is given to the nature and characteristics of problems involving dissemination of weather information, use of this information by pilots, its adequacy for the purpose intended, the ability of the air traffic control system to cope with weather related incidents, and the various aspects of pilot behavior, aircraft equipment, and NAVAIDS affecting flights in which weather figures. It is concluded from the study that skill and training deficiencies of general aviation pilots are not major factors in weather related occurrences, nor is lack of aircraft equipment. Major problem causes are identified with timely and easily interpreted weather information, judgement and attitude factors of pilots, and the functioning of the air traffic control system

Two-fluid dynamics for a Bose-Einstein condensate out of local equilibrium with the non-condensate

We extend our recent work on the two-fluid hydrodynamics of a Bose-condensed gas by including collisions involving both condensate and non-condensate atoms. These collisions are essential for establishing a state of local thermodynamic equilibrium between the condensate and non-condensate. Our theory is more general than the usual Landau two-fluid theory, to which it reduces in the appropriate limit, in that it allows one to describe situations in which a state of complete local equilibrium between the two components has not been reached. The exchange of atoms between the condensate and non-condensate is associated with a new relaxational mode of the gas.Comment: 4 pages, revtex, 1 postscript figure, Fig.1 has been correcte

Systematic review of the current status of cadaveric simulation for surgical training

Background: There is growing interest in and provision of cadaveric simulation courses for surgical trainees. This is being driven by the need to modernize and improve the efficiency of surgical training within the current challenging training climate. The objective of this systematic review is to describe and evaluate the evidence for cadaveric simulation in postgraduate surgical training. Methods: A PRISMA‐compliant systematic literature review of studies that prospectively evaluated a cadaveric simulation training intervention for surgical trainees was undertaken. All relevant databases and trial registries were searched to January 2019. Methodological rigour was assessed using the widely validated Medical Education Research Quality Index (MERSQI) tool. Results: A total of 51 studies were included, involving 2002 surgical trainees across 69 cadaveric training interventions. Of these, 22 assessed the impact of the cadaveric training intervention using only subjective measures, five measured impact by change in learner knowledge, and 23 used objective tools to assess change in learner behaviour after training. Only one study assessed patient outcome and demonstrated transfer of skill from the simulated environment to the workplace. Of the included studies, 67 per cent had weak methodology (MERSQI score less than 10·7). Conclusion: There is an abundance of relatively low‐quality evidence showing that cadaveric simulation induces short‐term skill acquisition as measured by objective means. There is currently a lack of evidence of skill retention, and of transfer of skills following training into the live operating theatre

Funding free and universal access to Journal of Neuroinflammation

Journal of Neuroinflammation is an Open Access, online journal published by BioMed Central. Open Access publishing provides instant and universal availability of published work to any potential reader, worldwide, completely free of subscriptions, passwords, and charges. Further, authors retain copyright for their work, facilitating its dissemination. Open Access publishing is made possible by article-processing charges assessed "on the front end" to authors, their institutions, or their funding agencies. Beginning November 1, 2004, the Journal of Neuroinflammation will introduce article-processing charges of around US$525 for accepted articles. This charge will be waived for authors from institutions that are BioMed Central members, and in additional cases for reasons of genuine financial hardship. These article-processing charges pay for an electronic submission process that facilitates efficient and thorough peer review, for publication costs involved in providing the article freely and universally accessible in various formats online, and for the processes required for the article's inclusion in PubMed and its archiving in PubMed Central, e-Depot, Potsdam and INIST. There is no remuneration of any kind provided to the Editors-in-Chief, to any members of the Editorial Board, or to peer reviewers; all of whose work is entirely voluntary. Our article-processing charge is less than charges frequently levied by traditional journals: the Journal of Neuroinflammation does not levy any additional page or color charges on top of this fee, and there are no reprint costs as publication-quality pdf files are provided, free, for distribution in lieu of reprints. Our article-processing charge will enable full, immediate, and continued Open Access for all work published in Journal of Neuroinflammation. The benefits from such Open Access will accrue to readers, through unrestricted access; to authors, through the widest possible dissemination of their work; and to science and society in general, through facilitation of information availability and scientific advancement

Down\u27s syndrome, neroinflammation, and Alzheimer neuropathogenesis

Down syndrome (DS) is the result of triplication of chromosome 21 (trisomy 21) and is the prevailing cause of mental retardation. In addition to the mental deficiencies and physical anomalies noted at birth, triplication of chromosome 21 gene products results in the neuropathological and cognitive changes of Alzheimer\u27s disease (AD). Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that this chromosome 21 gene product was a principal neuropathogenic culprit in AD as well as DS. The discovery of neuroinflammatory changes, including dramatic proliferation of activated glia overexpressing a chromosome 2 gene product--the pluripotent immune cytokine interleukin-1 (IL-1)--and a chromosome 21 gene product--S100B--in the brains of fetuses, neonates, and children with DS opened the possibility that early events in Alzheimer pathogenesis were driven by cytokines. The specific chromosome 21 gene products and the complexity of the mechanisms they engender that give rise to the neuroinflammatory responses noted in fetal development of the DS brain and their potential as accelerators of Alzheimer neuropathogenesis in DS are topics of this review, particularly as they relate to development and propagation of neuroinflammation, the consequences of which are recognized clinically and neuropathologically as Alzheimer\u27s disease