On this month’s episode of the Arsenal Women Arsecast, Tim is joined by author, broadcaster and journalist Dr. Carrie Dunn, Carrie is an expert and academic on all things women’s sport and is the author of two books about the Lionesses- Roar of the Lionesses (2016) and Pride of the Lionesses (2019)- which you can by here https://www.pitchpublishing.co.uk/shop/pride-lionesses – or from your local bookstore if they are still delivering- they would probably appreciate the business right now!

Tim talks to Carrie about role modelling in women’s football, players in the women’s game are called upon to be role models, especially for young girls and to help increase participation in the sport. Many players see this as a privilege and an important responsibility- but to what extent is it fair? Is this just invisible labour we blithely place on female athletes?

Then Tim talks to Gunners defender Louise Quinn, who is a patron for lots of initiatives geared towards increasing participation in sport for young girls. Louise talks about why she believes in the power of role modelling and about her female role models when she was growing up. Tim also talks to Louise about how her and her teammates are handling training in times of quarantine and social distancing in response to the COVID-19 pandemic.

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As COVID-19 spreads worldwide, leaders are relying on mathematical models to make public health and economic decisions. A new model developed by Princeton and Carnegie Mellon researchers improves tracking of epidemics by accounting for mutations in diseases. Now, the researchers are working to apply their model to allow leaders to evaluate the effects of countermeasures to epidemics before they deploy them.

This is a frightening thought but I may be the most photographed person in all of China In my first few days here I kept catching people taking pictures of me on the sly and when I looked at them I noticed them waving but thought they wanted me to

We develop a multi-risk SIR model (MR-SIR) where infection, hospitalization and fatality rates vary between groups—in particular between the “young”, “the middle-aged” and the “old”. Our MR-SIR model enables a tractable quantitative analysis of optimal policy similar to those already developed in the context of the homogeneous-agent SIR models. For baseline parameter values for the COVID-19 pandemic applied to the US, we find that optimal policies differentially targeting risk/age groups significantly outperform optimal uniform policies and most of the gains can be realized by having stricter lockdown policies on the oldest group. For example, for the same economic cost (24.3% decline in GDP), optimal semi–targeted or fully-targeted policies reduce mortality from 1.83% to 0.71% (thus, saving 2.7 million lives) relative to optimal uniform policies. Intuitively, a strict and long lockdown for the most vulnerable group both reduces infections and enables less strict lockdowns for the lower-risk groups. We also study the impacts of social distancing, the matching technology, the expected arrival time of a vaccine, and testing with or without tracing on optimal policies. Overall, targeted policies that are combined with measures that reduce interactions between groups and increase testing and isolation of the infected can minimize both economic losses and deaths in our model.

Model-car building is one of the old-school hobbies enjoying a resurgence during the pandemic lockdown. Haven't done that in a while? Here's where to find a kit and what to look for.

A model predicts COVID-19 deaths in the U.S. will drop to zero by June. Another suggests without a vaccine, the coronavirus will be with us for years.

Looking through Sunday's Image section, reader Katherine Wertheim of Ventura felt something was missing.

A decade in the making, Tyra Banks' modeling utopia, ModelLand, 'will emulate a fantasy version of the modeling world.' The park opens in Santa Monica in May.

Tesla's stock price sank Thursday after Consumer Reports blasted the reliability of the company's new Model 3 sedan and dropped it from a list of recommended vehicles.

Three years after he promised to sell an all-electric Model 3 mass-market sedan for $35,000 before incentives, Elon Musk may finally be coming through.

Buyers who order the new lower-cost "standard-range" $35,000 Tesla Model 3 electric car and expect to receive it in two to four weeks might be in for a surprise.

Panasonic is freezing plans to expand its role as Tesla's electric car battery supplier, a move that raises new questions about demand for Tesla's Model 3 — and the company's future.

The Tesla Model 3 remained the bestselling electric car in the United States last month by far, according to estimates from website Inside EVs.

Tesla's sales of its Model 3 perked up in the U.S. in May, according to estimates from the website InsideEVs, after a round of price cuts.

Peer-to-peer car sharing seems strange but turns out to be easy, if a bit expensive.

Compartir el coche de persona a persona parece extraño, pero es fácil, aunque un poco caro

A tribute to Tony- and Emmy-winner Shirley Knight, an exemplar of Method who learned from the best of the Actor Studio stars.

To portray his on-screen hype man, Dave "Lil Dicky" Burd turned to his real-life hype man: Davionte "GaTa" Ganter.

CAR TAX changes and grants for those purchasing brand new fully electric vehicles means there's "never been a better time" to switch, according to an EV expert.

A Texas woman wanted to control her Tesla Model 3. So she implanted part of the vehicle's valet key in her arm.

Protease-activated receptor 2 (PAR-2) is activated by secreted proteases from immune cells or fungi. PAR-2 is normally expressed basolaterally in differentiated nasal ciliated cells. We hypothesized that epithelial remodeling during diseases characterized by cilial loss and squamous metaplasia may alter PAR-2 polarization. Here, using a fluorescent arrestin assay, we confirmed that the common fungal airway pathogen Aspergillus fumigatus activates heterologously-expressed PAR-2. Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI–H520 squamous cells increased intracellular calcium levels and granulocyte macrophage–colony-stimulating factor, tumor necrosis factor α, and interleukin (IL)-6 secretion. RPMI 2650 cells cultured at an air–liquid interface (ALI) responded to apically or basolaterally applied PAR-2 agonists. However, well-differentiated primary nasal epithelial ALIs responded only to basolateral PAR-2 stimulation, indicated by calcium elevation, increased cilia beat frequency, and increased fluid and cytokine secretion. We exposed primary cells to disease-related modifiers that alter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid deficiency, at concentrations and times that altered epithelial morphology without causing breakdown of the epithelial barrier to model early disease states. These altered primary cultures responded to both apical and basolateral PAR-2 stimulation. Imaging nasal polyps and control middle turbinate explants, we found that nasal polyps, but not turbinates, exhibit apical calcium responses to PAR-2 stimulation. However, isolated ciliated cells from both polyps and turbinates maintained basolateral PAR-2 polarization, suggesting that the calcium responses originated from nonciliated cells. Altered PAR-2 polarization in disease-remodeled epithelia may enhance apical responses and increase sensitivity to inhaled proteases.

1 April 2020

RK Tangirala
Nov 1, 1995; 36:2320-2328
Articles

The DOCK-D (dedicator of cytokinesis D) family proteins are atypical guanine nucleotide exchange factors that regulate Rho GTPase activity. The family consists of Zizimin1 (DOCK9), Zizimin2 (DOCK11), and Zizimin3 (DOCK10). Functions of the DOCK-D family proteins are presently not well-explored, and the role of the DOCK-D family in neuroinflammation is unknown. In this study, we generated three mouse lines in which DOCK9 (DOCK9−/−), DOCK10 (DOCK10−/−), or DOCK11 (DOCK11−/−) had been deleted and examined the phenotypic effects of these gene deletions in MOG35–55 peptide-induced experimental autoimmune encephalomyelitis, an animal model of the neuroinflammatory disorder multiple sclerosis. We found that all the gene knockout lines were healthy and viable. The only phenotype observed under normal conditions was a slightly smaller proportion of B cells in splenocytes in DOCK10−/− mice than in the other mouse lines. We also found that the migration ability of macrophages is impaired in DOCK10−/− and DOCK11−/− mice and that the severity of experimental autoimmune encephalomyelitis was ameliorated only in DOCK10−/− mice. No apparent phenotype was observed for DOCK9−/− mice. Further investigations indicated that lipopolysaccharide stimulation up-regulates DOCK10 expression in microglia and that microglial migration is decreased in DOCK10−/− mice. Up-regulation of C–C motif chemokine ligand 2 (CCL2) expression induced by activation of Toll-like receptor 4 or 9 signaling was reduced in DOCK10−/− astrocytes compared with WT astrocytes. Taken together, our findings suggest that DOCK10 plays a role in innate immunity and neuroinflammation and might represent a potential therapeutic target for managing multiple sclerosis.

A new study from University of Michigan climate researchers concludes that some of the latest-generation climate models may be overly sensitive to carbon dioxide increases and therefore project future warming that is unrealistically high.

To imagine earth without greenhouse gases in its atmosphere is to turn the familiar blue marble into a barren lump of rock and ice on which the average surface temperature hovers around -18ºC. Such a planet would not receive less of the sunlight which is the ultimate source of all Earth's warmth. But when the energy it absorbed from the sunlight was re-emitted as infrared radiation, as the laws of physics require, it would head unimpeded back out into space.

A lone developer from the company that provided aerodynamic analysis for the cars in the PlayStation game Gran Turismo has applied the tooling to demonstrate the spread of germs with and without wearing a mask

N. O. Malykh and I. S. Postevoy
Theor. Probability and Math. Statist. 99 (2020), 189-198.
Abstract, references and article information

S. S. Lohvinenko and K. V. Ralchenko
Theor. Probability and Math. Statist. 99 (2020), 149-168.
Abstract, references and article information

A. G. Kukush and O. O. Chernova
Theor. Probability and Math. Statist. 99 (2020), 125-135.
Abstract, references and article information

Yu. V. Kozachenko and I. V. Rozora
Theor. Probability and Math. Statist. 99 (2020), 113-124.
Abstract, references and article information

A. V. Ivanov and I. K. Matsak
Theor. Probability and Math. Statist. 99 (2020), 91-99.
Abstract, references and article information

O. D. Borysenko and D. O. Borysenko
Theor. Probability and Math. Statist. 99 (2020), 67-75.
Abstract, references and article information

Bin Li and Jieqiong Shen
Proc. Amer. Math. Soc. 148 (2020), 2565-2578.
Abstract, references and article information

Below, Mac Hyman, Tulane University, talks about types of mathematical models--their strengths and weaknesses--the data that we currently have and what we really need, and what models can tell us about a possible second wave.

At the beginning of the video, he thanks the mathematics community for its work, and near the end says, "Our mathematical community is really playing a central role in helping to predict the spread, and help mitigate this epidemic, and prioritize our efforts. …Do not underestimate the power that mathematics can have in helping to mitigate this epidemic—-we have a role to play."

See the full set of videos on modeling COVID-19 and see media coverage of mathematics' role in modeling the pandemic.

Fabry disease is a heritable lipid disorder caused by the low activity of α-galactosidase A and characterized by the systemic accumulation of globotriaosylceramide (Gb3). Recent studies have reported a structural heterogeneity of Gb3 in Fabry disease, including Gb3 isoforms with different fatty acids and Gb3 analogs with modifications on the sphingosine moiety. However, Gb3 assays are often performed only on the selected Gb3 isoforms. To precisely determine the total Gb3 concentration, here we established two methods for determining both Gb3 isoforms and analogs. One was the deacylation method, involving Gb3 treatment with sphingolipid ceramide N-deacylase, followed by an assay of the deacylated products, globotriaosylsphingosine (lyso-Gb3) and its analogs, by ultra-performance LC coupled to tandem MS (UPLC-MS/MS). The other method was a direct assay established in the present study for 37 Gb3 isoforms and analogs/isoforms by UPLC-MS/MS. Gb3s from the organs of symptomatic animals of a Fabry disease mouse model were mainly Gb3 isoforms and two Gb3 analogs, such as Gb3(+18) containing the lyso-Gb3(+18) moiety and Gb3(−2) containing the lyso-Gb3(−2) moiety. The total concentrations and Gb3 analog distributions determined by the two methods were comparable. Gb3(+18) levels were high in the kidneys (24% of total Gb3) and the liver (13%), and we observed Gb3(−2) in the heart (10%) and the kidneys (5%). These results indicate organ-specific expression of Gb3 analogs, insights that may lead to a deeper understanding of the pathophysiology of Fabry disease.

(University of Córdoba) The University of Cordoba participated in the first shaping of a hydrological model on a basin scale as a global model to advance in world hydrological predictions.

(University of Colorado at Boulder) What can researchers do when their mathematical models of the spread of infectious diseases don't match real-world data? One research team is working on a solution.

(University of Maryland) Many historians have claimed the Justinianic Plague (c. 541-750 CE) killed half of the population of Byzantine (Eastern Roman) Empire. New historical research and mathematical modeling challenge the death rate and severity of this first plague pandemic, named for Emperor Justinian I.

(American Society of Agronomy) Researchers develop soil-gas diffusivity model based on two agricultural soils.

(Penn State) A new process to harness multiple disease models for outbreak management has been developed by an international team of researchers. The team will immediately implement the process to help inform policy decisions for the COVID-19 outbreak.

Mary de Groot
Jan 1, 2010; 23:18-25
From Research to Practice