The coupling of wave drift and wind velocity profiles

The Stokes drift velocity profile due to Toba\u27s equilibrium wave spectrum is shown to consist of a surface constant shear layer, an intermediate logarithmic layer and a deep exponentially decaying tail. On identifying the logarithmic layer with a wall boundary layer (which is justified a posteriori by showing that the major part of the energy dissipation by wave breaking occurs in the roughness sublayer), for a range of directionality (p) of the wave spectrum ½–2, Toba\u27s constant (α) lies in the range 0.12–0.10 in good agreement with data. The roughness length for water (z0) of this profile has the Charnock form, z0 = au2*g–1 in which u* is the friction velocity in air, g is the acceleration of gravity and a is a constant of order unity determined by the condition that momentum transfer by wave breaking just supports the wind stress, and using this formula the transition from smooth to intermediate flow at which rippling commences is quite well estimated. The velocity profiles in air and water with respect to z0, are predicted from a similarity hypothesis to have the formsu′ = u* (γ + 1/κ ln z/z0) u = w* (γ − 1/κ ln z/z0) z \u3e z0where z is the distance from the sea surface, u′ and u are respectively the velocities in air and water, κ is Von Karman\u27s constant, w* is the friction velocity in water, γw* is the Stokes surface drift velocity, and γu* is a wave speed centered in the equilibrium range. Observations in the open sea indicate that γ ∼ 12. An alternate pair of profiles, also predicted from the similarity hypothesis, is,u′ = us + u*/κ ln z/z′0 u = us − w*/κ ln z/z′0 z \u3e z′0where z′0 is the roughness length for air, and us ∼ 2γw* is the surface current. Observations suggest that small surface drifters travel at speeds intermediate between γw* and 2γw

Fluticasone propionate — an update on preclinical and clinical experience

AbstractFluticasone propionate (FP) is a novel androstane glucocorticoid with potent anti-inflammatory activity which has been effectively used, intransasally, as therapy for seasonal and allergic perennial rhinitis. When taken by the inhaled route, FP has shown significant therapeutic efficacy in the management of asthma. Fluticasone propionate is a highly lipophilic molecule with good uptake, binding and retention characteristics in human lung tissue. Fluticasone propionate has high glucocorticoid receptor selectivity and affinity, demonstrating rapid receptor association and slow receptor dissociation. In vitro, FP has been shown to potently inhibit T lymphocyte proliferation, cytokine generation, tumour necrosis factor alpha (TNF-α)-induced adhesion molecule expression, interleukin-5-induced eosinophilia, mucosal oedema and toluene 2,4-diisocyanate-induced mast cell proliferation, while promoting secretory leucocyte protease inhibitor production and eosinophil apoptosis. In human studies, FP has demonstrated marked vasoconstrictor potency in normal subjects and inhibited antigen-induced mucosal platelet activating factor/eicosanoid production, T lymphocytes and CD25+ cells in patients with rhinitis. Biopsy data from mild asthmatics demonstrate FP-associated reduction in CD3, CD4, CD8 and CD25 cells, with an accompanying reduction in eosinophil and mast cell markers. Clinical studies have evaluated lung function, bronchial reactivity, exacerbation rates and oral corticosteroid-sparing effect. Results show that FP has at least twice the clinical potency of beclomethasone dipropionate and budesonide. This appears to be achieved without an accompanying increase in systemic effects, suggesting a therapeutic index which may be higher than other currently available inhaled corticosteroids

The New Zealand semi-diurnal tide

Data on the semi-diurnal tide around the coast of New Zealand, and on neighbouring islands are summarized, and interpreted using World, and a large scale, numerical models, and an analytical island-shelf model. The island-shelf model consists of a circular island (representing New Zealand) surrounded by a parabolic shelf, and a deep ocean of co~stant depth...

Cobimetinib and trametinib inhibit platelet MEK but do not cause platelet dysfunction

The MEK inhibitors cobimetinib and trametinib are used in combination with BRAF inhibitors to treat metastatic melanoma but increase rates of hemorrhage relative to BRAF inhibitors alone. Platelets express several members of the MAPK signalling cascade including MEK1 and MEK2 and ERK1 and ERK2 but their role in platelet function and haemostasis is ambiguous as previous reports have been contradictory. It is therefore unclear if MEK inhibitors might be causing platelet dysfunction and contributing to increased hemorrhage. In the present study we performed pharmacological characterisation of cobimetinib and trametinib in vitro to investigate potential for MEK inhibitors to cause platelet dysfunction. We report that whilst both cobimetinib and trametinib are potent inhibitors of platelet MEK activity, treatment with trametinib did not alter platelet function. Treatment with cobimetinib results in inhibition of platelet aggregation, integrin activation, alpha-granule secretion and adhesion but only at suprapharmacological concentrations. We identified that the inhibitory effects of high concentrations of cobimetinib are associated with off-target inhibition on Akt and PKC. Neither inhibitor caused any alteration in thrombus formation on collagen under flow conditions in vitro. Our findings demonstrate that platelets are able to function normally when MEK activity is fully inhibited, indicating MEK activity is dispensable for normal platelet function. We conclude that the MEK inhibitors cobimetinib and trametinib do not induce platelet dysfunction and are therefore unlikely to contribute to increased incidence of bleeding reported during MEK inhibitor therapy

Protective Coverall Design Development and Testing

The purpose of this study was to improve the design and function of a disposable, level-one protective coverall for a Fortune 500 company. This research used the design process in conjunction with product benchmarking, on-site observational studies, user feedback, 3D body scan technology, fit tests, and expert evaluation to develop a coverall that is superior to the company\u27s current offering

A survey of occupational therapists on a new tool for sensory processing

Occupational therapy is the leading profession with regard to supporting children who experience difficulties with occupations as a result of sensory processing differences. However, there are mixed reports with regard to the efficacy of various sensory interventions and approaches, leaving little clear guidance for occupational therapists supporting children with these difficulties. The Sensory Form is a planning tool developed in 2017 to guide occupational therapists in their professional reasoning for assessment and intervention of sensory processing differences. To date, no research has been conducted on its use. Researchers introduced the tool to 20 occupational therapists with relevant experience and conducted an online survey of their perceptions about The Sensory Form. Findings were analysed using descriptive statistics and qualitative content analysis. Therapists reported that they found the tool acceptable for use, described key strengths and weaknesses of The Sensory Form, and outlined changes to improve the tool. The Sensory Form may have an application in guiding the practice of therapists supporting children with sensory processing differences. Further development of associated resources may be warranted

Histologic Evaluation of Periodontal Implants in a Biologically “Closed” Model

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141262/1/jper0110.pd

Effectiveness of Subgingival Scaling and Root Planing: Single Versus Multiple Episodes of Instrumentation

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142277/1/jper0367.pd

Poor statistical reporting, inadequate data presentation and spin persist despite Journal awareness and updated Information for Authors

Sound reporting of research results is fundamental to good science. Unfortunately, poor reporting is common and does not improve with editorial educational strategies. We investigated whether publicly highlighting poor reporting at a journal can lead to improved reporting practices. We also investigated whether reporting practices that are required or strongly encouraged in journal Information for Authors are enforced by journal editors and staff. A 2016 audit highlighted poor reporting practices in the Journal of Neurophysiology. In August 2016 and 2018, the American Physiological Society updated the Information for Authors, which included the introduction of several required or strongly encouraged reporting practices. We audited Journal of Neurophysiology papers published in 2019 and 2020 (downloaded through the library of the University of New South Wales) on reporting items selected from the 2016 audit, the newly introduced reporting practices, and items from previous audits. Summary statistics (means, counts) were used to summarize audit results. In total, 580 papers were audited. Compared to results from the 2016 audit, several reporting practices remained unchanged or worsened. For example, 60% of papers erroneously reported standard errors of the mean, 23% of papers included undefined measures of variability, 40% of papers failed to define a statistical threshold for their tests, and when present, 64% of papers with p-values between 0.05 and 0.1 misinterpreted them as statistical trends. As for the newly introduced reporting practices, required practices were consistently adhered to by 34 to 37% of papers, while strongly encouraged practices were consistently adhered to by 9 to 26% of papers. Adherence to the other audited reporting practices was comparable to our previous audits. Publicly highlighting poor reporting practices did little to improve research reporting. Similarly, requiring or strongly encouraging reporting practices was only partly effective. Although the present audit focused on a single journal, this is likely not an isolated case. Stronger, more strategic measures are required to improve poor research reporting