The design of medical laser surgery dermatology handpieces for radiation control and direct extraction of infectious laser generated plume

Surgical skin treatments such as; laser ablation, laser scalpels, hair removal, tattooed removal etc can all generate direct and secondary optical radiation hazards, however, because they are designed to intentionally destroy human tissue, they also generate gaseous and particulate emissions. This second family often referred to as; surgical smoke, surgical smoke plume and surgical fume, have now been identified as producing viable bio-active aerosols, these by-products now pose infectious hazards to the patient and staff of the operating room. Local extraction is sometimes used to try and reduce the airborne concentration of these byproducts though in virtually all cases the smell of the process is detectable by all. The optical radiation hazard usually dictates the wearing of protective eyewear to provide some level of personal protection. A major health concern to all medical and cosmetic facilities is that of infection control. Surgical smoke is usually overlooked as a source of infection within the operating environment and it has been known since the mid-1980s that the particulate can carry with it live pathogens from the patient which can now be in skin contact or respired by the operating staff. A paper presented by the authors in the Medical Session here at ILSC provides possibly the first quantitative analysis of the hazards the surgeon and other staff are subject to. This paper examines the practical limitations of the existing approaches and provides some simple practical control measures that provide complete radiation containment as well as enable complete particulate and gas extraction without any reliance on any form of personal protection for the patient and operating staff. These designs have now been tested and are shown to offer 100% effective plume extraction and radiation containment

Deciphering long-term records of natural variability and human impact as recorded in lake sediments: a palaeolimnological puzzle

Global aquatic ecosystems are under increasing threat from anthropogenic activity, as well as being exposed to past (and projected) climate change, however, the nature of how climate and human impacts are recorded in lake sediments is often ambiguous. Natural and anthropogenic drivers can force a similar response in lake systems, yet the ability to attribute what change recorded in lake sediments is natural, from that which is anthropogenic, is increasingly important for understanding how lake systems have, and will continue to function when subjected to multiple stressors; an issue that is particularly acute when considering management options for aquatic ecosystems. The duration and timing of human impacts on lake systems varies geographically, with some regions of the world (such as Africa and South America) having a longer legacy of human impact than others (e.g., New Zealand). A wide array of techniques (biological, chemical, physical and statistical) is available to palaeolimnologists to allow the deciphering of complex sedimentary records. Lake sediments are an important archive of how drivers have changed through time, and how these impacts manifest in lake systems. With a paucity of ‘real-time’ data pre-dating human impact, palaeolimnological archives offer the only insight into both natural variability (i.e., that driven by climate and intrinsic lake processes) and the impact of people. While there is a need to acknowledge complexity, and temporal and spatial variability when deciphering change from sediment archives, a palaeolimnological approach is a powerful tool for better understanding and managing global aquatic resources

Participant response to the survey.

<p>Participant response to the survey.</p

Attitudes of healthcare professionals about training for AF screening.

<p>Attitudes of healthcare professionals about training for AF screening.</p

Perceived role of healthcare professionals in future AF screening.

<p>Perceived role of healthcare professionals in future AF screening.</p

Additional file 1: of Genetics, sleep and memory: a recall-by-genotype study of ZNF804A variants and sleep neurophysiology

The Avon Longitudinal Study of Parents and Children. This file contains a description of the cohort used for the study, including details of participant recruitment and genotyping and imputation procedures. (PDF 72 kb

Supplemental Material - Variation in multimorbidity by sociodemographics and social drivers of health among patients seen at community-based health centers

Supplemental Material for Variation in multimorbidity by sociodemographics and social drivers of health among patients seen at community-based health centers by Wyatt P Bensken, Suparna M Navale, Brenda M McGrath, Nicole Cook, Yui Nishiike, Gretchen Mertes, Rose Goueth, Matthew Jones, Anna Templeton, Stephen J Zyzanski, Siran M Koroukian, and Kurt C Stange in Journal of Multimorbidity and Comorbidity</p

Additional file 1: of Heterogeneous ribonuclear protein A3 (hnRNP A3) is present in dipeptide repeat protein containing inclusions in Frontotemporal Lobar Degeneration and Motor Neurone disease associated with expansions in C9orf72 gene

Selected clinical, pathological and genetic details on cases studied. (XLSX 17 kb

Additional file 1: Figure S1. of Pathological tau deposition in Motor Neurone Disease and frontotemporal lobar degeneration associated with TDP-43 proteinopathy

α-synuclein (a-c) pathology in cingulate gyrus (a), CA2 region of hippocampus (b) and substantia nigra (c) and TDP-43 pathology in anterior horn cells of the spinal cord (d-f), with fine, particulate accumulations of TDP-43 (d,e) or skein-like structures (e,f) being present in affected cells in which the nucleus has been ‘cleared’ of its normal immunoreactivity. Immunoperoxidase, x400 microscope magnification. (DOCX 6504 kb

Additional file 2: of Pathological tau deposition in Motor Neurone Disease and frontotemporal lobar degeneration associated with TDP-43 proteinopathy

File S1. Clinical histories and neuropathological findings in patients #35 and 41. (DOCX 21 kb