bluuebunny/crossref_metadata_2025_split huggingface dataset:
If you're happy and you know it: Associations between emotion, social context, and food choices in college freshmen
Authors: Ashurst Jessica , van Woerden Irene , Bruening Meg 
Published: November 2023

BACKGROUNDA lack of evidence exists on how food choices are related to emotional and social contexts, particularly for college freshmen who are still developing eating habits as they transition into adulthood. Ecological momentary assessments (EMAs) repeatedly assess what participants are doing at a particular moment, providing real‐time data on eating behaviors with mobile technology that does not require participants to leave their environment or reflect on past behaviors. By understanding these relationships in the context of when and why the behaviors are occurring, we can better promote healthy eating in this vulnerable population.OBJECTIVETo determine the association of negative, positive, and ambivalent emotions on food choices (fruits/vegetables, pizza, and sweet/salty snacks). We also examined the relationship of social context (alone vs. with others) on food choices.METHODSCollege freshmen (n=1078; 64% female; 52% non‐white) residing in campus dormitories completed up to 14 mobile‐based EMAs during the fall semester of 2015 as part of SPARC (Social impact of Physical Activity and nutRition in College), a larger, longitudinal study assessing the nutrition and physical activity choices of students. Of the completed EMAs, 2754 surveys (n=678 students; 70% female; 51% non‐white) had data on food choices, emotion (positive and negative), and social context. Mixed effects logistic regression models examined the relationship between food choices, emotions, and social context of eating, adjusting for sociodemographics, and clustering of students within dorms.RESULTSReporting happiness was positively associated with fruits/vegetables (OR=1.2, 95% CI: 1.0–1.4) and sweet/salty snacks (OR=1.5, 95% CI: 1.2–1.8) (p<0.05). Students who reported feeling meh were likely to report eating pizza (OR=1.3, 95%CI=1.0–1.7;p<0.05). Feeling sad was not associated with any food choices. Eating alone was positively associated with fruits and vegetables (OR=1.2, 95% CI: 1:1.4) and negatively associated pizza intake (OR=0.8, 95% CI: 0.7–0.9), above and beyond emotional state (p<0.05).CONCLUSIONSEmotional status was related to both healthy and unhealthy food choices. Students who eat alone were more likely to make healthier food choices. Interventions targeting college freshmen should consider how emotional and social contextual factors impact food choices.Support or Funding InformationThe Social impact of Physical Activity and nutRition in College study (1DP5OD017910‐01; PI: Bruening) was funded by the NIH Office of the Director and the Office of Behavioral and Social Sciences Research. Content expressed herein are the sole responsibility of the authors, and may not reflect official views held by the NIH.
Twist1 Phosphorylation Contributes to Pulmonary Fibrosis through Angiopoietin‐Tie2 Signaling
Authors: Mammoto Akiko , Jiang Amanda , Jiang Elisabeth , Mammoto Tadanori 
Published: November 2023

Idiopathic pulmonary fibrosis is a chronic and progressive lung disease, in which microvessel remodeling is deregulated. However, the mechanism by which deregulated angiogenesis contributes to the pathogenesis of pulmonary fibrosis remains unclear. Here we show that phosphorylation of a transcription factor, Twist1, controls angiogenesis through the angiopoietin‐Tie2 pathway and mediates fibrotic foci formation and pathological angiogenesis in a bleomycin‐induced mouse pulmonary fibrosis model. Twist1 knockdown decreases Tie2 expression and attenuates angiopoietin1‐induced endothelial cell (EC) sprouting in vitro. Angiogenesis is also inhibited in fibrin gel implanted on Tie2‐specific Twist1 conditional knockout (Tie2‐Twist1KO) mouse lung in vivo. Inhibition of Twist1 phosphorylation at the Serine 42 (Ser42) residue by treating ECs with a mutant construct (Twist1S42A) decreases Tie2 expression and attenuates angiogenesis in vitro and in vivo. Bleomycin treatment increases Twist1 Ser42 phosphorylation levels and expression of angiopoietin‐2 and Tie2, and induces fibrotic foci formation and increases blood vessel density in the mouse lung, while these effects are attenuated in Tie2‐Twist1KO mice. These results indicate that Twist1 Ser42 phosphorylation mediates bleomycin‐induced pulmonary fibrosis through angiopoietin‐Tie2 signaling.Support or Funding InformationBoston Children's Hospital career development award
Surface Topography During Neural Stem Cell Differentiation Regulates Cell Migration and Cell Morphology
Authors: Czeisler Catherine , Short Aaron , Stocker Ben , Cronin James , Lannutti John , Winter Jessica , Otero Jose Javier 
Published: November 2023

We sought to determine the contribution of scaffold topography to the migration and morphology of neural stem cells by mimicking features of scaffolds found in vivo. We mimicked two types of CNS scaffolds encountered by neural stem cells during development in vitro by constructing different diameter electrospun polycaprolactone (PCL) fiber mats, a substrate that we have shown to be topographically similar to brain scaffolds. We compared the effects of large fibers (made to mimic blood vessel topography) with those of small diameter fibers (made to mimic radial glial process topography) on the migration and differentiation of neural stem cells. Neural stem cells showed differential migratory and morphological reactions with laminin in different topographical contexts. We demonstrate, for the first time, that neural stem cell biological responses to laminin are dependent on topographical context. Topography‐induced cell morphology changes were inhibited by nocodazole, but not by cytochalasin‐D or ROCK‐inhibitor, suggesting that microtubule function is necessary for topography‐induced morphology changes. We propose that the physical structure of distinct scaffolds induces unique signaling cascades that regulate migration and morphology in embryonic neural progenitor cells.Support or Funding InformationBS acknowledges Pelotonia Foundation Undergraduate Research Fellowship. AS acknowledges The Ohio State University/Metro High School Graduate Teaching Assistant Fellowship. The project described was supported by Award Number Grant 8UL1TR000090‐05, from the National Center for Advancing Translational Sciences. The content is solely the responsibility of the authors and does not necessarily represent official views of the National Center for Advancing Translational Sciences or the National Institutes of Health. This work was sponsored by and represents activity of The Ohio State University Center for Regenerative Medicine and Cell Based Therapies (regenerativemedicine.osu.edu).
Neuropilin 2 Deficiency Prolongs Skin Inflammation and Edema
Authors: Bielenberg Diane Renee , Mucka Patrick , Levonyak Nicholas , Geretti Elena , Zwaans Bernadette M.M. , Li Xiaoran , Adini Irit , Klagsbrun Michael , Adam Rosalyn M 
Published: November 2023

The vasculature is involved in the progression and resolution of inflammation. Blood and lymphatic capillaries express vascular endothelial growth factor (VEGF) receptors that regulate fluid flow into and out of the interstitium. Neuropilin 2 (Nrp2), a unique receptor that binds VEGF‐A, VEGF‐C/D or semaphorin 3F (SEMA3F) ligands, is expressed by the endothelium during development but downregulated after birth. Mice lacking Nrp2 are viable into adulthood without signs of edema. Herein, we investigated the expression and function of Nrp2 in a model of acute inflammation. Immunoblotting and X‐gal staining of Nrp2+/LacZ mice showed increased Nrp2 or b‐galactosidase activity in the endothelium following delayed‐type hypersensitivity (DTH) reactions. Nrp2−/− mice exhibited massive tissue swelling, prolonged lymphedema, and delayed resolution after DTH compared to wild‐type mice. Vascular permeability was two‐fold higher in inflamed blood vessels in Nrp2‐deficient mice compared to Nrp2‐intact littermates. Histological examination revealed a lack of superficial lymphatic capillaries in Nrp2‐mutant mice. Addition of exogenous SEMA3F protein inhibited VEGFA‐induced vascular permeability in wild‐type mice. In summary, Nrp2 deficiency increased blood vessel permeability and decreased lymphatic vessel drainage during inflammation. Taken together our data suggest that Nrp2 is upregulated in the endothelium to modulate inflammation‐induced tissue swelling and resolve post‐inflammatory edema.Support or Funding InformationVascular Biology Program, Boston Children's Hospital; NCI and NIDDK under award numbers CA118732, CA155728 (D.R.B.), CA037392 (M.K.), and DK65298 (R.M.A.).
Transdifferentiation of Chondrocytes to Osteoblasts during Bone Fracture Healing
Authors: Marcucio Ralph , Hu Diane , Yang Frank , Bahney Chelsea , Miclau Theodore 
Published: November 2023

For more than 150 years, dogma has been that cartilage is replaced by bone during endochondral ossification. This is thought to be true during development and this process is recapitulated during repair of fractured bones. During endochondral ossification mesenchymal cells condense and differentiate into chondrocytes. The chondrocytes mature, become hypertrophic, and induce vascular invasion of the cartilage matrix. The currently accepted model states that chondrocytes undergo apoptosis and osteoblast progenitor cells are delivered to the cartilage by the invading vasculature to replace the cartilage with bone. However, recent data from our laboratory indicates that this model is incorrect. Chondrocytes undergo a transformation during bone fracture healing to become osteoblasts that make the new bone matrix. This process occurs in a region that we named “the transition zone” that is located adjacent to the invading vasculature. Chondrocytes located in the transition have two fates. Some of the chondrocytes die, while others re‐enter the cell cycle, switch off the chondrogenic program, activate the molecular program associated with pluripotency, activate the molecular program associated with osteogenesis, and synthesize new bone matrix via perilacunar remodeling, possibly in response to signals from the invading vasculature. Others have recognized this process in many contexts. In fact, in the early to middle 1800's metaplasia of cartilage to bone was considered to be the mechanism of bone formation. Our data support this model and indicate that the main process of bone formation is by direct transformation of chondrocytes to osteoblasts during bone fracture healing.Support or Funding InformationNIH: NIAMS: F32AR062469 to C.B., R01‐AR057344 to T.M., NIA: R01‐AG046282 to R.M. MTF Junior Investigator Award to C.B.
Exploring Cranial Functional Morphology and Evolution through the Jaws of Alligators
Authors: Holliday Casey M 
Published: November 2023

Among all of the extraordinary examples of vertebrate cranial adaptation, few are as iconic as the heads of alligators and their crocodilian relatives. Despite their inclusion in centuries of paleontological, anatomical and experimental work, these underutilized model organisms remain fonts of discovery in biomechanics, physiology, development and evolution. Although their remarkable feeding behaviors and familiar cranial shapes underlie many lines of inquiry, few studies have focused on the role of various cranial articulations within the feeding apparatus. Here I present a series of recent projects investigating the alligator and crocodyliform feeding apparatus with a focus on cranial articulations incorporating multiple lines of evidence combining anatomical techniques, imaging, mechanical testing, computational modeling and the fossil record. This comprehensive research program has built a solid foundation necessary for testing hypotheses of skeletal tissue regulation, adaptive plasticity, cranial kinesis, and ecomorphology in not only crocodilians, but other vertebrate clades. For example, comparative anatomical methods reveal the mandibular symphysis to be a complicated syndesmosis surrounding a synchondrosis formed by fused Meckel's cartilages, which grows throughout life. Morphometric approaches quantify how the characteristic Class 3 symphyseal plate increases in complexity during ontogeny and varies among other crocodylian species. Mechanical testing reveals how the symphysis is capable of withstanding such extreme bite forces. 3D visualization illustrates how jaw musculature changes orientation during gape cycles, ontogeny and evolution. Finally, biomechanical modeling accurately predicts how muscles and feeding forces load the symphysis and other cranial joints during different feeding behaviors. Results stemming from these Alligator projects have undeniably shed light on crocodyliform and suchian function, ecology and evolution, but more importantly, they have inspired new interdisciplinary collaborations investigating broader topics in vertebrate evolution including homoplasy in beak evolution, thermoregulatory adaptations of the temporal region, and the origin of the mammalian temporomandibular joint. Therefore, crocodilians are more than just ‘living fossils’ but instead are a gateway to new exploration of the complex patterns and processes underlying vertebrate evolution.Support or Funding InformationThis work was funded by NSF IOS 1457319, Missouri Research Board, Missouri Research Council, and the Department of Pathology and Anatomical Sciences.
Molecular Switches In Proteasome Assembly : Tales Of The Tails And Chaperones
Authors: Park Soyeon 
Published: November 2023

In the proteasome, the proteolytic 20S core particle (CP) associates with the 19S regulatory particle (RP) to degrade polyubiquitinated proteins. Six ATPases (Rpt1‐Rpt6) of the RP form a hexameric Rpt ring and interact with the heptameric α ring (α1–α7) of the CP via the Rpt C‐terminal tails individually binding to the α subunits. Importantly, the Rpt6 tail has been suggested to be crucial for RP assembly. Here, we show that the interaction of the CP and Rpt6 tail promotes a CP‐Rpt3 tail interaction, and that they jointly mediate proteasome activation via opening the CP gate for substrate entry. The Rpt6 tail forms a novel relationship with the Nas6 chaperone, which binds to Rpt3 and regulates the CP‐Rpt3 tail interaction, critically influencing cell growth and turnover of polyubiquitinated proteins. CP‐Rpt6 tail binding promotes the release of Nas6 from the proteasome. Based on disulfide crosslinking that detects cognate α3‐Rpt6 tail and α2‐Rpt3 tail interactions in the proteasome, decreased α3‐Rpt6 tail interaction facilitates robust α2‐Rpt3 tail interaction that is also strongly ATP‐dependent. Together, our data support the reported role of Rpt6 during proteasome assembly, and suggest that its function switches from anchoring for RP assembly into promoting Rpt3‐dependent activation of the mature proteasome.Support or Funding InformationThis study was supported by the University of Colorado start‐up fund and Boettcher Web‐Warring Biomedical Research Award to S.P.
Trans‐Translation As A Target For Novel Antibiotics
Authors: Keiler Kenneth 
Published: November 2023

The trans‐translation pathway rescues ribosomes stalled at the end of mRNAs in bacteria. This pathway is required for viability or virulence in many species, but is not targeted by existing antibiotics. Using a high‐throughput screen, we identified compounds that inhibit trans‐translation but not protein synthesis. These compounds are not toxic to eukaryotic cells, but inhibit growth of a broad spectrum of bacterial species, including Staphylococcus aureus, Bacillus anthracis, Shigella flexneri, Mycobacterium tuberculosis, and Francisella tularensis, both in vitro and during ex vivo infection. Chemical cross‐linking was used to determine the molecular targets of these compounds in bacteria. One family of inhibitors was found to bind to the base of helix 89 in 23S rRNA, a site that is not bound by other antibiotics. These data validate trans‐translation as a target for antibiotic development and provide new insights into the early steps of ribosome rescue pathways.Support or Funding InformationThis work was supported by grants GM068720 and AI111692 from the National Institutes of Health.
Transcriptional Control of Lipid Homeostasis
Authors: Totonoz Peter 
Published: November 2023

Control of lipid abundance and organization is essential for life. Dysregulation of lipid homeostasis is linked to common diseases, including diabetes, obesity, and atherosclerosis. Our long‐term goal is to understand the mechanisms whereby lipids control gene expression and impact the development of metabolic disease. We have used the transcriptional program controlled by the lipid‐activated nuclear receptor LXR as a Rosetta stone to uncover fundamental mechanisms involved in lipid metabolism and inflammation potential opportunities for drug development. LXR signaling is critical for the maintenance of cellular and systemic cholesterol balance in mammals. LXRs coordinately regulate the expression of a battery of target genes involved in the uptake, efflux, transport and elimination of sterols. The LXR pathway is an important counterpoint to the SREBP pathway, which regulates lipid synthesis, and there are multiple mechanisms for crosstalk and integration. LXR target genes are highly represented in GWAS for plasma lipid levels and coronary artery disease, underscoring the relevance of LXR signaling for human biology. Recent work has focused on three key mediators of LXR action: Idol–which controls lipoprotein receptor activity, and Lpcat3 and Abca1–which control membrane composition. Delineation of these pathways has revealed new regulatory concepts and brought insights with implications beyond the field of lipid metabolism.Support or Funding InformationNIH‐NHLBI NATIONAL HEART, LUNG, AND BLOOD INSTITUT
Transcription And The Maintenance Of Genome Stability
Authors: Svejstrup Jesper Q , Williamson Laura , Saponaro Marco , Boeing Stefan , Mitter Richard , Kelly Gavin 
Published: November 2023

Over the last decade it has become increasingly evident that transcription is closely integrated with other DNA‐related processes, such as chromatin dynamics, DNA replication and repair. Indeed, the essential process of expressing genes comes at a cost: the movement of RNA polymerases through chromatin is associated with significant genome instability. RNA Polymerase II stalling, arrest, and/or backtracking ‐ collectively referred to as transcription stress ‐ thus generates a cellular response akin to the DNA damage response, and constantly needs to be contended with to avoid DNA damage. The factors and mechanisms involved in suppressing transcription‐associated genome instability remain poorly understood. Conversely, DNA damage itself, such as that induced by UV‐irradiation, also greatly affects transcription. Indeed, UV‐damage triggers rapid reduction in global RNA synthesis and changes to mRNA splicing, but the molecular details and underlying mechanisms again remain unclear. In this talk, our recent advances in understanding the interface between transcription and the maintenance of genome integrity will be outlined.Support or Funding InformationSupported by grants from the ERC and the Francis Crick Institute
Endocytosis Separates EGF Receptors From Endogenous Fluorescently Labeled HRas and Prevents Receptor Signaling to MAP Kinases in Endosomes
Authors: Sorkin Alexander , Pinilla‐Macua Itziar 
Published: November 2023

Signaling from epidermal growth factor receptor (EGFR) to extracellular‐stimuli‐regulated protein kinase 1/2 (ERK1/2) is proposed to be transduced not only from the cell surface but also from endosomes, although the role of endocytosis in this signaling pathway is controversial. Ras is the only membrane‐anchored component in the EGFR‐ERK signaling axis, and therefore, its location determines intracellular sites of downstream signaling. However, Ras localization was studied predominantly in overexpression systems. Hence we labeled endogenous HRas with mVenus fluorescent protein using genome‐editing in HeLa cells. mVenus‐HRas was primarily located at the plasma membrane, and in small amounts in tubular recycling endosomes and associated vesicles. EGF stimulation resulted in fast but transient activation of mVenus‐HRas. While EGF:EGFR complexes were rapidly accumulated in endosomes together with the Grb2 adaptor, no mVenus‐HRas was detected in these endosomes. Interestingly, the activities of MEK1/2 and ERK1/2 remained high beyond the point of the physical separation of HRas from EGF:EGFR complexes and down‐regulation of Ras activity. Paradoxically, this sustained MEK1/2 and ERK1/2 activation was dependent on the active EGFR kinase. Cell‐surface biotinylation and selective inactivation of surface EGFRs suggested that a small fraction of active EGFRs remaining in the plasma membrane is responsible for continuous signaling to MEK1/2 and ERK1/2. We propose that under physiological conditions of cell stimulation, EGFR endocytosis serves to spatially separate EGFR‐Grb2 complexes and Ras, thus terminating Ras‐mediated signaling. However, sustained minimal activation of Ras by a small pool of active EGFRs in the plasma membrane is sufficient for extending MEK1/2 and ERK1/2 activities.Support or Funding InformationThis work was supported by NCI CA089151 grant.