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The paper presents the effects of the storm‐time prompt penetration electric fields (PPEF) and traveling atmospheric disturbances (TADs) on the total electron content (TEC), foF2 and hmF2 in the American sector (north and south) during the geomagnetic storm on 23–24 April 2023. The data show a poleward shift of the Equatorial Ionization Anomaly (EIA) crests to 18°N and 20°S in the evening of 23 April (attributed to eastward PPEF) and the EIA crests remaining almost in the same latitudes after the PPEF reversed westward. The thermospheric neutral wind velocity, foF2, hmF2, and TEC variations show that TADs from the northern and southern high latitudes propagating equatorward and crossing the equator after midnight on 23 April. The meridional keograms of ΔTEC show the TAD structures in the north/south propagated with phase velocity 470/485 m/s, wave length 4,095/4,016 km and period 2.42/2.30 hr, respectively. The interactions of the TADs also appear to modify the wind velocities in low latitudes. The eastward PPEF and equatorward TADs also favored the development of a clear/not so clear F3 layer in northern/southern regions of the equator. Plain Language Summary: The thermosphere‐ionosphere‐magnetosphere system is largely affected during events of geomagnetic storms. Its dynamics, mainly in the ionized environment, may impact modern lives by degradations in the satellite signals affecting, for example, all applications involving Global Navigation Satellite System. The thermosphere and ionosphere responses to the large geomagnetic storm of 23–24 April 2023 are analyzed here and the main discoveries are the unexpected spatial plasma density distribution over Boa Vista (MLat ≈ 8°N) due to resulting effects of a disturbed eastward electric field and traveling atmospheric disturbance (TAD). The interactions/interferences of TADs were able to explain the unexpected moment of the peak in thermospheric neutral wind speed measurements over the equatorial station, as well as all variations in ionospheric parameters (foF2, hmF2, and total electron content) recorded in pairs by seven Digisondes and GNSS receivers spread across Brazil. Key Points: Interactions of traveling atmospheric disturbances (TADs) cause unexpected thermospheric neutral wind speeds in the American equatorial and low‐latitude sectorsThe effects resulting from a disturbed electric field and TADs were able to produce anomalous electron density distribution at low latitudesThe variations in the ionospheric observational measurements recorded around 4 UT in Brazil on 24 April 2023 were explained by the passages of TADs [ABSTRACT FROM AUTHOR]

Drinking and related problems on the college campus have reached near epidemic levels. In order to address this trend, many colleges have launched alcohol prevention and intervention programs for college students. Unfortunately, most such programs are either not empirically validated or are plainly based on models that have shown poor efficacy. This overview of the college treatment literature describes the kinds of interventions that have shown the best success and offers directions for future studies. In general, educational and abstinence-based approaches show the least efficacy, while other types of skills, attitudinal and feedback-based interventions based on aspects of the social learning model appear to be more successful. In addition to employing those approaches that have shown empirical success, a re-examination of the role that alcohol plays in the larger campus culture is crucial. [ABSTRACT FROM AUTHOR]

Exposure to ozone causes decrements in pulmonary function, a response associated with alterations in lung lipids. Pulmonary lipid homeostasis is dependent on the activity of peroxisome proliferator activated receptor gamma (PPARγ), a nuclear receptor that regulates lipid uptake and catabolism by alveolar macrophages (AMs). Herein, we assessed the role of PPARγ in ozone-induced dyslipidemia and aberrant lung function in mice. Exposure of mice to ozone (0.8 ppm, 3 h) resulted in a significant reduction in lung hysteresivity at 72 h post exposure; this correlated with increases in levels of total phospholipids, specifically cholesteryl esters, ceramides, phosphatidylcholines, phosphorylethanolamines, sphingomyelins, and di- and triacylglycerols in lung lining fluid. This was accompanied by a reduction in relative surfactant protein-B (SP-B) content, consistent with surfactant dysfunction. Administration of the PPARγ agonist, rosiglitazone (5 mg/kg/day, i.p.) reduced total lung lipids, increased relative amounts of SP-B, and normalized pulmonary function in ozone-exposed mice. This was associated with increases in lung macrophage expression of CD36, a scavenger receptor important in lipid uptake and a transcriptional target of PPARγ. These findings highlight the role of alveolar lipids as regulators of surfactant activity and pulmonary function following ozone exposure and suggest that targeting lipid uptake by lung macrophages may be an efficacious approach for treating altered respiratory mechanics., (© The Author(s) 2023. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Introduction/aims: Riluzole is a glutamate inhibitor approved for the treatment of amyotrophic lateral sclerosis (ALS). There are scant data on factors associated with riluzole initiation and adherence. The goal of this study was to describe the use of riluzole at the Penn State Hershey Medical Center (PSHMC) ALS clinic., Methods: A retrospective medical record review of ALS patients seen at the PSHMC from January 2007 to December 2016. A timeline of riluzole use was established for each patient. Factors contributing to dose changes or discontinuations were recorded. Riluzole adherence was assessed using the proportion of days covered (PDC) calculated by the patient-reported length of riluzole use divided by total time from prescription to death/censor. Multivariable analysis was performed to evaluate the association of demography and clinical course with adherence., Results: Seven hundred twenty-three records were screened, with 508 (307 men, 201 women) meeting the criteria for inclusion. The median duration of riluzole use was 435 (range, 0-3773) days. The median PDC for the group was 64%. Those with higher initial overall function and slower rate of decline were more likely to have a larger PDC. No trends in patients' demographics, riluzole use, and tracheostomy-free survival were found over time., Discussion: A high rate of riluzole initiation and adherence was found in this sample. The most common reasons for dose modification were related to adverse effects, yet social-, economic-, and patient-related factors were also common. The characteristics of riluzole prescription and use have remained relatively unchanged in a single tertiary ALS center over the past 10 years., (© 2022 Wiley Periodicals LLC.)

To curb transmission of SARS-CoV-2 and preserve hospital resources, elective procedures were postponed in the United States, affecting patients previously scheduled for electrophysiology (EP) procedures. We aimed to understand patients' perceptions related to procedural postponements during the first wave of the SARS-CoV-2 pandemic. We performed a telephone survey between May 1-15 2020, of consecutive patients who experienced procedural postponement from March-April. Of 112 patients, 20% may have been lost to follow up and 12% lost interest in having their procedures done. The level of anxiety related to postponement was moderate to high in more than two thirds of patients., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2021.)

In this paper, we present a technique for dimensionality reduction in hyperspectral imaging during the data collection process. A four-channel hyperspectral imager using liquid crystal Fabry-Perot etalons has been built and used to verify this method for four applications: auroral imaging, plant study, landscape classification, and anomaly detection. This imager is capable of making measurements simultaneously in four wavelength ranges while being tunable within those ranges, and thus can be used to measure narrow contiguous bands in four spectral domains. In this paper, we describe the design, concept of operation, and deployment of this instrument. The results from preliminary testing of this instrument are discussed and are promising and demonstrate this instrument as a good candidate for hyperspectral imaging.

Recent improvements in high-throughput sequencing technologies underscore the pervasiveness of circular RNA (circRNA) expression in animal cells. CircRNAs are distinct from their linear counterparts because they lack the 5' caps and 3' tails that typically help determine the cellular fate of a transcript. However, due to the lack of free ends, circRNAs are impervious to exonucleases and thus can evade normal RNA turnover mechanisms. Most circRNAs are derived from protein-coding pre-mRNAs, via a mechanism called "back-splicing." Existing methods of circRNA expression thus typically involve genes that have been engineered to contain sequence elements that promote back-splicing. We recently uncovered an anciently conserved mechanism of RNA circularization in metazoans that involves splicing of tRNA introns. This splicing mechanism is completely independent from that of pre-mRNAs. In this chapter, we detail an orthogonal method that involves splicing of intron-containing tRNAs in order to produce circRNAs in vivo. We utilize fluorescence-based RNA reporters to characterize the expression, localization, and stability of these so-called tRNA intronic circular RNAs. Because tRNA biogenesis is essential for all cellular life, this method provides a means to express ultrastable, high-copy, circRNA effectors in a wide variety of metazoan cell types., (© 2016 Elsevier Inc. All rights reserved.)

Injury and inflammation in the gastric epithelium can cause disruption of the pathways that guide the differentiation of cell lineages, which in turn can cause persistent alterations in differentiation patterns, known as metaplasia. Metaplasia that occurs in the stomach is associated with increased risk for cancer. Methods for isolating distinct gastric epithelial cell populations would facilitate dissection of the molecular and cellular pathways that guide normal and metaplastic differentiation. Here, we identify alanyl aminopeptidase (CD13) as a specific surface marker of zymogenic chief cells (ZCs) in the gastric epithelium. We show that 1) among gastric epithelial cells alanyl aminopeptidase expression is confined to mature ZCs, and 2) its expression is lost en route to metaplasia in both mouse and human stomachs. With this new marker coupled with new techniques that we introduce for dissociating gastric epithelial cells and overcoming their constitutive autofluorescence, we are able to reliably isolate enriched populations of ZCs for both molecular analysis and for the establishment of ZC-derived ex vivo gastroid cultures., (Copyright © 2015 the American Physiological Society.)

A four channel hyperspectral imager using Liquid Crystal Fabry-Perot (LCFP) etalons has been built and tested. This imager is capable of making measurements simultaneously in four wavelength ranges in the visible spectrum. The instrument was designed to make measurements of natural airglow and auroral emissions in the upper atmosphere of the Earth and was installed and tested at the Poker Flat Research Range in Fairbanks, Alaska from February to April 2014. The results demonstrate the capabilities and challenges this instrument presents as a sensor for aeronomical studies.

The stem cell in the isthmus of gastric units continually replenishes the epithelium. Atrophy of acid-secreting parietal cells (PCs) frequently occurs during infection with Helicobacter pylori, predisposing patients to cancer. Atrophy causes increased proliferation of stem cells, yet little is known about how this process is regulated. Here we show that CD44 labels a population of small, undifferentiated cells in the gastric unit isthmus where stem cells are known to reside. Loss of CD44 in vivo results in decreased proliferation of the gastric epithelium. When we induce PC atrophy by Helicobacter infection or tamoxifen treatment, this CD44(+) population expands from the isthmus toward the base of the unit. CD44 blockade during PC atrophy abrogates the expansion. We find that CD44 binds STAT3, and inhibition of either CD44 or STAT3 signaling causes decreased proliferation. Atrophy-induced CD44 expansion depends on pERK, which labels isthmal cells in mice and humans. Our studies delineate an in vivo signaling pathway, ERK → CD44 → STAT3, that regulates normal and atrophy-induced gastric stem/progenitor-cell proliferation. We further show that we can intervene pharmacologically at each signaling step in vivo to modulate proliferation.

The p53 protein plays a central role in the prevention of tumorigenesis. Cellular stresses, such as DNA damage and aberrant oncogene activation, trigger induction of p53 that halts cellular proliferation and allows cells to be repaired. If cellular damage is beyond the capability of the repair mechanisms, p53 induces apoptosis or cell cycle arrest, preventing damaged cells from becoming cancerous. However, emerging evidence suggests that the function of p53 needs to be considered as isoform-specific. Here, we report that the expression profile of p53 can be shifted toward inhibitory p53 isoforms by the pathogenic bacterium Helicobacter pylori, which is known for its strong association with gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. We found that interaction of H. pylori with gastric epithelial cells, mediated via the cag pathogenicity island, induces N-terminally truncated Δ133p53 and Δ160p53 isoforms in human cells. Induction of an orthologous p53 isoform, Δ153p53, was also found in H. pylori-infected Mongolian gerbils. The p53 isoforms inhibit p53 and p73 activities, induce NF-κB, and increase survival of infected cells. Expression of Δ133p53, in response to H. pylori infection, is regulated by phosphorylation of c-Jun and activation of activator protein-1-dependent transcription. Together, these results provide unique insights into the regulation of p53 protein and may contribute to the understanding of tumorigenesis associated with H. pylori.

Background & Aims: Colonization of gastric mucosa by Helicobacter pylori leads to epithelial hyperproliferation, which increases the risk for gastric adenocarcinoma. One H pylori virulence locus associated with cancer risk, cag, encodes a secretion system that transports effectors into host cells and leads to aberrant activation of β-catenin and p120-catenin (p120). Peroxisome proliferator-activated receptor (PPAR)δ is a ligand-activated transcription factor that affects oncogenesis in conjunction with β-catenin. We used a carcinogenic H pylori strain to define the role of microbial virulence constituents and PPARδ in regulating epithelial responses that mediate development of adenocarcinoma., Methods: Gastric epithelial cells or colonies were co-cultured with the H pylori cag(+) strain 7.13 or cagE(-), cagA(-), soluble lytic transglycosylase(-), or cagA(-)/soluble lytic transglycosylase(-) mutants. Levels of PPARδ and cyclin E1 were determined by real-time, reverse-transcription polymerase chain reaction, immunoblot analysis, or immunofluorescence microscopy; proliferation was measured in 3-dimensional culture. PPARδ and Ki67 expression were determined by immunohistochemical analysis of human biopsies and rodent gastric mucosa., Results: H pylori induced β-catenin- and p120-dependent expression and activation of PPARδ in gastric epithelial cells, which were mediated by the cag secretion system substrates CagA and peptidoglycan. H pylori stimulated proliferation in vitro, which required PPARδ-mediated activation of cyclin E1; H pylori did not induce expression of cyclin E1 in a genetic model of PPARδ deficiency. PPARδ expression and proliferation in rodent and human gastric tissue was selectively induced by cag(+) strains and PPARδ levels normalized after eradication of H pylori., Conclusions: The H pylori cag secretion system activates β-catenin, p120, and PPARδ, which promote gastric epithelial cell proliferation via activation of cyclin E1. PPARδ might contribute to gastric adenocarcinoma development in humans., (Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.)

We demonstrate the use of a switchable circular-to-point converter (SCPC) device based on holographic polymer-dispersed liquid-crystal technology for application in lidar detection and optical telecommunication. A SCPC device converts the Fabry-Perot ring pattern into a single point or an array of points, while an external electrical field on the SCPC deactivates the conversion. Stacking different SCPC elements gives a random optical switch for applications in lidar detection and optical telecommunication. Two types of SCPC designs are analyzed and one is chosen and built for testing.

A total of 205 (113 male, 92 female) nonhospitalized recovering alcoholics with > 3 months of continuous abstinence from alcohol and drugs and relatively heavy tobacco dependence (Fagerstrom Tolerance Questionnaire score = 7.7; mean number of cigarettes per day, 26.8; mean number of years smoked, 24.4) were randomized to standard treatment (ST) American Lung Association quit program plus nicotine anonymous meetings (n = 70), behavioral counseling plus physical exercise (BEX; n = 72), or behavioral counseling plus nicotine gum (BNIC; n = 63). A 3 x 4 repeated measures design was used to evaluate the effectiveness of the interventions on smoking outcome at baseline, posttreatment, and 6- and 12-month follow-ups. Self-reported smoking status was verified with biochemical and informant report. Verified self-report indicated that significantly more smokers in BEX quit by posttreatment (60%) than in either BNIC (52%) or ST (31%), chi 2 (2, N = 205) = 17.85, p < .01, but not at the 6-month (29%, 27%, and 21%, respectively) or 12-month (27%, 27%, and 26%, respectively) follow-up. Only 4% (7 of 188) relapsed to alcohol or drugs. Alcohol relapse did not differ by treatment group or smoking status. Length of alcohol abstinence was not associated with smoking cessation outcome.