What does it mean to be a 'picky eater'? A qualitative study of food related identities and practices.

Picky eaters are defined as those who consume an inadequate variety of food through rejection of a substantial amount of food stuffs that are both familiar and unfamiliar. Picky eating is a relatively recent theoretical concept and while there is increasing concern within public health over the lack of diversity in some children's diets, adult picky eaters remain an under researched group. This paper reports on the findings of a qualitative study on the routine food choices and practices of 26 families in Sandwell, West Midlands, UK. Photo elicitation and go-along interview data collection methods were used to capture habitual food related behaviours and served to describe the practices of nine individuals who self identified or were described as picky eaters. A thematic analysis revealed that those with the food related identity of picky eater had very restricted diets and experienced strong emotional and physical reactions to certain foods. For some this could be a distressing and alienating experience that hindered their ability to engage in episodes of social eating. Further research is needed to illuminate the specific practices of adult picky eaters, how this impacts on their lives, and how possible interventions might seek to address the challenges they face

Editorial: Sport and Community

© 2022 Rich, Jenkin, Millar, Sveinson and Sherry. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). https://creativecommons.org/licenses/by/4.0/Peer reviewe

Dynamic telomerase gene suppression via network effects of GSK3 inhibition

<b>Background</b>: Telomerase controls telomere homeostasis and cell immortality and is a promising anti-cancer target, but few small molecule telomerase inhibitors have been developed. Reactivated transcription of the catalytic subunit hTERT in cancer cells controls telomerase expression. Better understanding of upstream pathways is critical for effective anti-telomerase therapeutics and may reveal new targets to inhibit hTERT expression. <b>Methodology/Principal Findings</b>: In a focused promoter screen, several GSK3 inhibitors suppressed hTERT reporter activity. GSK3 inhibition using 6-bromoindirubin-3′-oxime suppressed hTERT expression, telomerase activity and telomere length in several cancer cell lines and growth and hTERT expression in ovarian cancer xenografts. Microarray analysis, network modelling and oligonucleotide binding assays suggested that multiple transcription factors were affected. Extensive remodelling involving Sp1, STAT3, c-Myc, NFκB, and p53 occurred at the endogenous hTERT promoter. RNAi screening of the hTERT promoter revealed multiple kinase genes which affect the hTERT promoter, potentially acting through these factors. Prolonged inhibitor treatments caused dynamic expression both of hTERT and of c-Jun, p53, STAT3, AR and c-Myc. <b>Conclusions/Significance</b>: Our results indicate that GSK3 activates hTERT expression in cancer cells and contributes to telomere length homeostasis. GSK3 inhibition is a clinical strategy for several chronic diseases. These results imply that it may also be useful in cancer therapy. However, the complex network effects we show here have implications for either setting

SECURING DATA PAYLOADS SENT FROM A CLIENT MACHINE WITH MINIMAL USER OR ADMINISTRATOR INTERACTION

Techniques are described herein for providing an extra layer of security for a Multi-Factor Authentication (MFA) application (e.g., a device health application) installed on a user’s machine to ensure that the data payload being sent to authentication servers came from the authenticating user’s machine. The application may be enrolled with a cryptographic keypair stored in the hardware of the user’s machine. The key may be used to sign health data payloads sent to the MFA servers

Decentralized Community Center: River's Bend Park

Report completed by students enrolled in ARCH 3250: Community Design and Public Interest Architecture, taught by James Wheeler, and LA 3002: Informants of Creating Landscape Space, taught by Jessica Rossi-Mastracci and Joe Favour, in Spring 2018.This project was completed as part of a year-long partnership between the City of Ramsey and the University of Minnesota's Resilient Communities Project (rcp.umn.edu). The goal of this project was to research and propose changes to Rivers' Bend Park in the City of Ramsey, in conjunction with a proposed greenway system, to maximize use of the site. Ramsey project lead Mark Riverblood collaborated with a team of students enrolled in James Wheeler's ARCH 3250 course. and Jessica Rossi-Mastracci and Joe Favour's LA 3002 course, to research the needs of the community and produce conceptual designs. A final student report from the project is available.This project was supported by the Resilient Communities Project (RCP), a program at the University of Minnesota whose mission is to connect communities in Minnesota with U of MN faculty and students to advance community resilience through collaborative, course-based projects. RCP is a program of the Center for Urban and Regional Affairs (CURA). More information at http://www.rcp.umn.edu

Effects of Lidocaine and Articaine on Neuronal Survival and Recovery

The local anesthetics lidocaine and articaine are among the most widely used drugs in the dentist’s arsenal, relieving pain by blocking voltage-dependent Naþ channels and thus preventing transmission of the pain signal. Given reports of infrequent but prolonged paresthesias with 4% articaine, we compared its neurotoxicity and functional impairment by screening cultured neural SH-SY5Y cells with formulations used in patients (2% lidocaine + 1:100,000 epinephrine or 4% articaine + 1:100,000 epinephrine) and with pure formulations of the drugs. Voltage-dependent sodium channels Na(v)1.2 and Na(v)1.7 were expressed in SH-SY5Y cells. To test the effects on viability, cells were exposed to drugs for 5 minutes, and after washing, cells were treated with the ratiometric Live/Dead assay. Articaine had no effect on the survival of SH-SY5Y cells, while lidocaine produced a significant reduction only when used as pure powder. To determine reversibility of blockage, wells were exposed to drugs for 5 minutes and returned for medium for 30 minutes, and the calcium elevation induced by depolarizing cells with a high-potassium solution was measured using the calcium indicator Fura-2. High potassium raised calcium in control SH-SY5Y cells and those treated with articaine, but lidocaine treatment significantly reduced the response. In conclusion, articaine does not damage neural cells more than lidocaine in this in vitro model. While this does not question the safety of lidocaine used clinically, it does suggest that articaine is no more neurotoxic, at least in the in vitro setting. © 2018 by the American Dental Society of Anesthesiology