Application of Portable Air Purifiers for Mitigating COVID-19 in Large Public Spaces

This study investigated, using validated computational fluid dynamics techniques, the actual performance of portable air purifiers for reducing the infection risks of airborne respiratory diseases such as COVID-19, by properly installing air purifiers in complicated large public spaces of primary concern, such as restaurants and ballrooms. The research results reveal that portable air purifiers with HEPA filtration provide an effective solution to help mitigate virus-carrying parti-cles/droplets in large spaces where the central air conditioning system with HEPA filtration may not provide adequate dilution and/or effective ventilation. Deploying portable air purifier changes the local flow directions, and thus, reduces the cross-table airflows that may enhance the possibility of cross-infection. A field experiment was further conducted in a restaurant and a ballroom to verify the on-site performance. This study indicates that each space is unique in furniture, occupant and system layouts and capacities, and thus, requires individualized investigation of appropriate puri-fier number, capacities, and locations. Flexible solutions such as portable air purifiers are important and low-cost supplements to more elaborate solutions installed in central air systems.</p

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Privatising Australia's ports. by Keith Trace

tag=1 data=Privatising Australia's ports. by Keith Trace tag=2 data=Trace, Keith tag=3 data=Policy tag=4 data=7 tag=5 data=1 tag=6 data=Autumn 1991 tag=7 data=15-18. tag=8 data=PORTS & HARBOURS tag=10 data=The current reform of Australia's ports has barely begun to bring them up to international standards of efficiency. tag=11 data=1991/3/6 tag=12 data=91/0514 tag=13 data=CABThe current reform of Australia's ports has barely begun to bring them up to international standards of efficiency

TRACE AND NORM, II

Let L/K be a finite Galois extension, with Galois group G = Gal(L/K). We can express characteristic polynomials, traces, and norms for the extension L/K in terms of G. Theorem 1.1. When L/K is a finite Galois extension with Galois group G and α ∈ L, χα,L/K(X) = ∏ (X − σ(α)). In particular, TrL/K(α) = ∑ σ(α), σ∈G σ∈G NL/K(α) = ∏ σ(α). Proof. Let πα,K(X) be the minimal polynomial of α over K, so χ α,L/K(X) = πα,K(X) n/d, where n = [L: K] and d = [K(α) : K] = deg πα,K. From Galois theory, πα,K(X) = d∏ (X − σi(α)), i=1 where σ1(α),..., σd(α) are all the distinct values of σ(α) as σ runs over the Galois group. For each σ ∈ G, σ(α) = σi(α) for a unique i from 1 to d. Moreover, σ(α) = σi(α) if and only if σ ∈ σiH, where H = {τ ∈ G: τ(α) = α} = Gal(L/K(α)). Therefore as σ runs over G, the number σi(α) appears as σ(α) whenever σ is in the left coset σiH, so σi(α) occurs |H | times, and |H | = [L: K(α)] = [L: K]/[K(α) : K] = n/d. Therefore d∏ (X − σ(α)) = (X − σi(α)) n/d ()n/d d∏ = (X − σi(α)) = πα,K(X) n/d, σ∈G i=1 and that power of the minimal polynomial is the characteristic polynomial. Example 1.2. In Q ( √ d)/Q, where d is a nonsquare rational number, the two elements of the Galois group are σ(a + b √ d) = a + b √ d and σ(a + b √ d) = a − b √ d. Then i=1 σ∈

Strategies for Medical Research Institutes

This paper considers the strategies used by a group of 17 medical research institutes to ensure continued funding. The study was based on two financial years, 1989/90 and 1990/94. No correlations have been found between the income of the institutes and output as assessed by publications. Whilst such a link may exist for individuals and competitive grants, it is not seen at the organisational level. A positive correlation does exist between the size of the research team and output. The analysis of the 1989/90 financial year identified four distinct strategies by mapping the institutes in two dimensions: government sourced funding and private sourced funding. For government sourced funding the variable was the ratio of competitive grant funding to direct government funding. For private sourced funding the variable was the ratio of corporate sourced funds to public appeal funding. This analysis has been repeated for the 1993/94 financial year. In the four year intervening period, all of the institutes have adopted, or moved towards adopting, similar strategies. This may be explained by mimetic organisation theory. During this time all institutes increased their dependence on income from government sources, particularly competitive grants. Similarly there was a move by all institutes to increase the proportion of funding from corporate sources as opposed to public donations