bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterizing food environments of hospitals and long-term care facilities in the Netherlands: a mixed methods approach
Authors: Wierda Joline J. , de Vet Emely , Troost Ellemijn , Poelman Maartje P. 
Published: January 2024

Abstract
Background
Hospitals and long-term care facilities, which are key institutions to serve health and well-being, have an important exemplary role in providing supportive food environments to encourage healthy and sustainable food choices. The objective of this study is to characterize the physical, socio-cultural, political and economic dimensions of the food environment for health care receivers, health workforce and visitors in healthcare settings, and make comparisons between the food environment of hospitals and long-term care facilities.

Methods
To characterize the food environment in healthcare settings, two sub-studies were conducted. In sub-study 1, semi-structured interviews were held with staff members (n = 46) representing 11 hospitals and 26 long-term care facilities (rehabilitation centres, nursing homes, institutions for people with intellectual disabilities and mental healthcare institutions). In sub-study 2, staff members audited the food environment in hospitals (n = 28) and long-term care facilities (n = 36) using a predefined checklist.

Results
The food environment in Dutch healthcare settings varies substantially between locations although noticeable differences between hospitals and long-term care facilities were identified. Hospitals and larger long-term care facilities featured more often restaurants and utilized central spaces for preparation of meals, while smaller long-term care facilities often operated as household-like settings. Type of healthcare shaped the socio-cultural food environment, with hospitals primarily emphasizing nutrition for fast recovery, while long-term care facilities more often as an instrument (i.e., to structure the day). Participants highlighted the importance of food policies and broad organizational support for realizing and regulating improvement of the food environment. Yet, long-term care facilities were less familiar with national guidelines for food environments compared to hospitals. Several economical aspects, like profit motives, strict budgets and contracts with external parties affected and shaped the food available within all healthcare settings.

Conclusions
This study characterized the food environment in Dutch healthcare settings. Disclosed differences between hospitals and long-term care facilities should be incorporated in strategies for a transition of the food environment. Future research should investigate the underlying mechanisms of the healthcare food environment attaining all healthcare stakeholders - health care receivers, staff and visitors - while prioritizing sustainability alongside healthiness.
Age-dependent inflammatory response is altered in an ex vivo model of bacterial pneumonia
Authors: Sommer Charline , Reamon-Buettner Stella Marie , Niehof Monika , Hildebrand Christina Beatrix , Braun Armin , Sewald Katherina , Dehmel Susann , Brandenberger Christina 
Published: January 2024

Abstract
Background
Aging is associated with an increased incidence and mortality of Pseudomonas aeruginosa-induced pneumonias. This might be partly due to age-dependent increases in inflammatory mediators, referred to as inflamm-aging and a decline in immune functions, known as immunosenescence. Still, the impact of dysregulated immune responses on lung infection during aging is poorly understood. Here, we aimed to mimic inflamm-aging using ex vivo precision-cut lung slices (PCLS) and neutrophils – as important effector cells of innate immunity – from young and old mice and investigated the influence of aging on inflammation upon infection with P. aeruginosa bacteria.

Methods
Murine PCLS were infected with the P. aeruginosa standard lab strain PAO1 and a clinical P. aeruginosa isolate D61. After infection, whole-transcriptome analysis of the tissue as well as cytokine expression in supernatants and tissue lysates were performed. Responses of isolated neutrophils towards the bacteria were investigated by quantifying neutrophil extracellular trap (NET) formation, cytokine secretion, and analyzing expression of surface activation markers using flow cytometry.

Results
Inflamm-aging was observed by transcriptome analysis, showing an enrichment of biological processes related to inflammation, innate immune response, and chemotaxis in uninfected PCLS of old compared with young mice. Upon P. aeruginosa infection, the age-dependent pro-inflammatory response was even further promoted as shown by increased production of cytokines and chemokines such as IL-1β, IL-6, CXCL1, TNF-α, and IL-17A. In neutrophil cultures, aging did not influence NET formation or cytokine secretion during P. aeruginosa infection. However, expression of receptors associated with inflammatory responses such as complement, adhesion, phagocytosis, and degranulation was lower in neutrophils stimulated with bacteria from old mice as compared to young animals.

Conclusions
By using PCLS and neutrophils from young and old mice as immunocompetent ex vivo test systems, we could mimic dysregulated immune responses upon aging on levels of gene expression, cytokine production, and receptor expression. The results furthermore reflect the exacerbation of inflammation upon P. aeruginosa lung infection as a result of inflamm-aging in old age.
Perspectives of primary care physicians in Spain on malaria: a cross-sectional survey and retrospective review of cases
Authors: Linares-Rufo Manuel , Bermudez-Marval Harold , García-Bertolín Carlos , Santos-Galilea Joaquín , Balsa-Vázquez Javier , Pérez-Tanoira Ramón , Santos-Larrégola Laura , Cuadros-González Juan , Rojo-Marcos Gerardo , Ramos-Rincón José-Manuel 
Published: January 2024

Abstract
Background
In Spain, the risk of imported malaria has increased in recent years due to the rise in international travel and migration. Little is known about the knowledge, information sources, clinical practice, and specific needs of primary care physicians (PCPs) concerning malaria despite the pivotal role played by these professionals in managing the health of tourists. The objective of this study was to assess the knowledge, attitudes, and practices of PCPs in Spain regarding malaria.

Methods
This research analyses data from (1) a cross-sectional nationwide survey assessing the knowledge and attitudes of PCPs regarding malaria, and (2) a retrospective review of 373 malaria cases appearing in primary care medical records (PCMRs) in the Madrid area over the past 15 years to determine how cases were documented, managed, or characterized in the primary care setting.

Results
The survey findings reveal a modest level of self-perceived familiarity with malaria (221/360, 57.6%), even though 32.8% of the practitioners reported having delivered care for confirmed or suspected cases of the disease, these practitioners had greater knowledge of malaria (80.4%) compared to physicians who reported not having delivered care for malaria (19.6%, p < 0.001). Ten percent of the survey participants did not know the name of the mosquito that transmits malaria, and only 40.7% would promptly request malaria testing for a traveller with symptoms after a trip to an endemic area. Responses provided by younger PCPs varied to a greater extent than those of their more experienced colleagues regarding prevention practices and patient management.
A review of PCMRs showed that only 65% of all patients were recorded as such. Among those registered, only 40.3% had a documented malaria episode, and of those, only 16.6% received proper follow-up. Only 23.7% of the patients with a PCMR had a record that specifically indicated travel to an endemic country or travel classified as visiting friends and relatives (VFR).

Conclusions
The findings of this study underscore the critical role of PCPs in the field of travel medicine, particularly given the increase in imported malaria cases. These results highlight the need for targeted training in travel medicine and the need to ensure optimal patient education in care settings.
Association of remnant cholesterol with decreased kidney function or albuminuria: a population-based study in the U.S.
Authors: He Xuan , Zou Renfang , Du Xiaoqiong , Li Kuo , Sha Dujuan 
Published: January 2024

Abstract
Background
Dyslipidemia is frequently exhibited in individuals with chronic kidney disease (CKD). Remnant cholesterol (RC), an emerging novel lipid marker, plays an elusive role in CKD progression. This study sought to investigate the association of RC with decreased kidney function or albuminuria in the general population of U.S.

Method
Data were retrieved from the continuous 2001 to 2018 cycle of the National Health and Nutrition Examination Survey (NHANES). Individuals aged between 18 and 70 years were included. RC was divided into quartiles. Albuminuria was defined by albumin-to-creatinine ratio (ACR) ≥30 mg/g, while reduced kidney function was described as an estimated glomerular filtration rate (eGFR) below 60 ml/min/1.73 m2. Using a multivariable regression model, the association of RC with decreased eGFR or albuminuria was examined. The dose‒response relationship between RC and eGFR or ACR was also investigated using a restricted cubic spline (RCS) model.

Results
A total of 1551 (10.98%) participants with impaired renal function or albuminuria were identified. After multivariate adjustment, RC was not significantly associated with kidney function decline or albuminuria (odds ratio (OR) 1.24, 95% confidence interval (95% CI): 0.95, 1.61). However, a significantly inverse correlation was observed between RC and eGFR in a dose‒response manner (β -2.12, 95% CI: -3.04, -1.21). This association remained consistent when stratifying data by gender, age, race, hypertension, diabetes and body mass index (BMI).

Conclusion
A higher RC was significantly correlated with a lower eGFR in the general population. The role of RC in predicting kidney outcomes needed further investigation in prospective studies.
Impact of feedback generation and presentation on self-monitoring behaviors, dietary intake, physical activity, and weight: a systematic review and meta-analysis
Authors: Krukowski Rebecca A. , Denton Andrea H. , König Laura M. 
Published: January 2024

AbstractSelf-monitoring of dietary intake, physical activity, and weight is a key strategy in behavioral interventions, and some interventions provide self-monitoring feedback to facilitate goal setting and promote engagement. This systematic review aimed to evaluate whether feedback increases intervention effectiveness, and which forms of feedback presentation (e.g., personalized vs. not personalized) and generation (i.e., human vs. algorithm-generated) are most effective. To achieve this aim, 5 electronic databases (PubMed/MEDLINE, Web of Science, CINAHL, PsycINFO, and Google Scholar) were searched in April 2022 and yielded 694 unique records, out of which 24 articles reporting on 19 studies were included (with a total of 3261 participants). Two reviewers independently screened titles and abstracts and then full texts and categorized articles as eligible or excluded according to the pre-registered criteria (i.e., availability of full text, peer reviewed manuscript in English; adult participants in a randomized controlled trial that included both self-monitoring and feedback; comparisons of different forms of feedback or comparisons of feedback vs. no feedback; primary outcomes of diet, physical activity, self-monitoring behavior, and/or weight). All included studies were assessed for methodological quality independently by two reviewers using the revised Cochrane risk-of-bias tool for randomized studies (version 2). Ten studies compared feedback to no feedback, 5 compared human- vs. algorithm-generated feedback, and the remaining 4 studies compared formats of feedback presentation (e.g., frequency, richness). A random effects meta-analysis indicated that physical activity interventions with feedback provision were more effective than physical activity interventions without feedback (d=0.29, 95% CI [0.16;0.43]). No meta-analysis could be conducted for other comparisons due to heterogeneity of study designs and outcomes. There were mixed results regarding which form of feedback generation and presentation is superior. Limitations of the evidence included in this review were: lack of details about feedback provided, the brevity of most interventions, the exclusion of studies that did not isolate feedback when testing intervention packages, and the high risk of bias in many studies. This systematic review underlines the importance of including feedback in behavioral interventions; however, more research is needed to identify most effective forms of feedback generation and presentation to maximize intervention effectiveness.Trial registration (PROSPERO)CRD42022316206.
TIMELESS promotes reprogramming of glucose metabolism in oral squamous cell carcinoma
Authors: Chen Yafan , Han Zhengyang , Zhang Le , Gao Caihong , Wei Jingyi , Yang Xuyuan , Han Yabing , Li Yunbo , Zhang Chunmei , Wei Yixin , Dong Jiaqi , Xun Wenxing , Sun Weifu , Zhang Taotao , Zhang Hui , Chen Jingtao , Yuan Peng 
Published: January 2024

Abstract
Background
Oral squamous cell carcinoma (OSCC), the predominant malignancy of the oral cavity, is characterized by high incidence and low survival rates. Emerging evidence suggests a link between circadian rhythm disruptions and cancer development. The circadian gene TIMELESS, known for its specific expression in various tumors, has not been extensively studied in the context of OSCC. This study aims to explore the influence of TIMELESS on OSCC, focusing on cell growth and metabolic alterations.

Methods
We analyzed TIMELESS expression in OSCC using western blot, immunohistochemistry, qRT-PCR, and data from The Cancer Genome Atlas (TCGA) and the Cancer Cell Line Encyclopedia (CCLE). The role of TIMELESS in OSCC was examined through clone formation, MTS, cell cycle, and EdU assays, alongside subcutaneous tumor growth experiments in nude mice. We also assessed the metabolic impact of TIMELESS by measuring glucose uptake, lactate production, oxygen consumption, and medium pH, and investigated its effect on key metabolic proteins including silent information regulator 1 (SIRT1), hexokinase 2 (HK2), pyruvate kinase isozyme type M2 (PKM2), recombinant lactate dehydrogenase A (LDHA) and glucose transporter-1 (GLUT1).

Results
Elevated TIMELESS expression in OSCC tissues and cell lines was observed, correlating with reduced patient survival. TIMELESS overexpression enhanced OSCC cell proliferation, increased glycolytic activity (glucose uptake and lactate production), and suppressed oxidative phosphorylation (evidenced by reduced oxygen consumption and altered pH levels). Conversely, TIMELESS knockdown inhibited these cellular and metabolic processes, an effect mirrored by manipulating SIRT1 levels. Additionally, SIRT1 was positively associated with TIMELESS expression. The expression of SIRT1, HK2, PKM2, LDHA and GLUT1 increased with the overexpression of TIMELESS levels and decreased with the knockdown of TIMELESS.

Conclusion
TIMELESS exacerbates OSCC progression by modulating cellular proliferation and metabolic pathways, specifically by enhancing glycolysis and reducing oxidative phosphorylation, largely mediated through the SIRT1 pathway. This highlights TIMELESS as a potential target for OSCC therapeutic strategies.
ChemR23 signaling ameliorates brain injury via inhibiting NLRP3 inflammasome-mediated neuronal pyroptosis in ischemic stroke
Authors: Liu Lan , Zhang Jiawei , Lu Kaili , Zhang Yaxuan , Xu Xiaofeng , Deng Jiangshan , Zhang Xiaojie , Zhang Haibing , Zhao Yuwu , Wang Xiuzhe 
Published: January 2024

Abstract
Background
Inflammatory response has been recognized as a pivotal pathophysiological process during cerebral ischemia. ChemR23 signaling is involved in the pathophysiology of various inflammatory diseases. Nevertheless, the role of ChemR23 signaling in ischemic stroke remains largely unknown.

Methods
Permanent ischemic stroke mouse model was accomplished by middle cerebral artery occlusion (MCAO). Resolvin E1 (RvE1) or chemerin-9 (C-9), the agonists of ChemR23, were administered by intracerebroventricular (i.c.v) injection before MCAO induction. Then, analysis of neurobehavioral deficits and brain sampling were done at Day 1 after MCAO. The brain samples were further analyzed by histological staining, immunofluorescence, RNA sequencing, ELISA, transmission electron microscope, and western blots. Furthermore, oxygen–glucose deprivation (OGD) was employed in SH-SY5Y to mimic MCAO in vitro, and ChemR23 signaling pathway was further studied by overexpression of ChemR23 or administration of related agonists or antagonists. Analysis of cell death and related pathway markers were performed.

Results
ChemR23 expression was upregulated following MCAO. Under in vitro and in vivo ischemic conditions, ChemR23 deficiency or inhibition contributed to excessive NLRP3-mediated maturation and release of IL-1β and IL-18, as well as enhanced cleavage of GSDMD-N and neuronal pyroptosis. These influences ultimately aggravated brain injury and neuronal damage. On the other hand, ChemR23 activation by RvE1 or C-9 mitigated the above pathophysiological abnormalities in vivo and in vitro, and overexpression of ChemR23 in SH-SY5Y cells also rescued OGD-induced neuronal pyroptosis. Blockade of NLRP3 mimics the protective effects of ChemR23 activation in vitro.

Conclusion
Our data indicated that ChemR23 modulates NLRP3 inflammasome-mediated neuronal pyroptosis in ischemic stroke. Activation of ChemR23 may serve as a promising potential target for neuroprotection in cerebral ischemia.
iPSC-derived PSEN2 (N141I) astrocytes and microglia exhibit a primed inflammatory phenotype
Authors: Sullivan Michael A. , Lane Samuel D. , McKenzie André D. J. , Ball Sarah R. , Sunde Margaret , Neely G. Gregory , Moreno Cesar L. , Maximova Alexandra , Werry Eryn L. , Kassiou Michael 
Published: January 2024

Abstract
Background
Widescale evidence points to the involvement of glia and immune pathways in the progression of Alzheimer’s disease (AD). AD-associated iPSC-derived glial cells show a diverse range of AD-related phenotypic states encompassing cytokine/chemokine release, phagocytosis and morphological profiles, but to date studies are limited to cells derived from PSEN1, APOE and APP mutations or sporadic patients. The aim of the current study was to successfully differentiate iPSC-derived microglia and astrocytes from patients harbouring an AD-causative PSEN2 (N141I) mutation and characterise the inflammatory and morphological profile of these cells.

Methods
iPSCs from three healthy control individuals and three familial AD patients harbouring a heterozygous PSEN2 (N141I) mutation were used to derive astrocytes and microglia-like cells and cell identity and morphology were characterised through immunofluorescent microscopy. Cellular characterisation involved the stimulation of these cells by LPS and Aβ42 and analysis of cytokine/chemokine release was conducted through ELISAs and multi-cytokine arrays. The phagocytic capacity of these cells was then indexed by the uptake of fluorescently-labelled fibrillar Aβ42.

Results
AD-derived astrocytes and microglia-like cells exhibited an atrophied and less complex morphological appearance than healthy controls. AD-derived astrocytes showed increased basal expression of GFAP, S100β and increased secretion and phagocytosis of Aβ42 while AD-derived microglia-like cells showed decreased IL-8 secretion compared to healthy controls. Upon immunological challenge AD-derived astrocytes and microglia-like cells showed exaggerated secretion of the pro-inflammatory IL-6, CXCL1, ICAM-1 and IL-8 from astrocytes and IL-18 and MIF from microglia.

Conclusion
Our study showed, for the first time, the differentiation and characterisation of iPSC-derived astrocytes and microglia-like cells harbouring a PSEN2 (N141I) mutation. PSEN2 (N141I)-mutant astrocytes and microglia-like cells presented with a ‘primed’ phenotype characterised by reduced morphological complexity, exaggerated pro-inflammatory cytokine secretion and altered Aβ42 production and phagocytosis.
Commonly disrupted pathways in brain and kidney in a pig model of systemic endotoxemia
Authors: Olney Kimberly C. , de Ávila Camila , Todd Kennedi T. , Tallant Lauren E. , Barnett J. Hudson , Gibson Katelin A. , Hota Piyush , Pandiane Adithya Shyamala , Durgun Pinar Cay , Serhan Michael , Wang Ran , Lind Mary Laura , Forzani Erica , Gades Naomi M. , Thomas Leslie F. , Fryer John D. 
Published: January 2024

AbstractSepsis is a life-threatening state that arises due to a hyperactive inflammatory response stimulated by infection and rarely other insults (e.g., non-infections tissue injury). Although changes in several proinflammatory cytokines and signals are documented in humans and small animal models, far less is known about responses within affected tissues of large animal models. We sought to understand the changes that occur during the initial stages of inflammation by administering intravenous lipopolysaccharide (LPS) to Yorkshire pigs and assessing transcriptomic alterations in the brain, kidney, and whole blood. Robust transcriptional alterations were found in the brain, with upregulated responses enriched in inflammatory pathways and downregulated responses enriched in tight junction and blood vessel functions. Comparison of the inflammatory response in the pig brain to a similar mouse model demonstrated some overlapping changes but also numerous differences, including oppositely dysregulated genes between species. Substantial changes also occurred in the kidneys following LPS with several enriched upregulated pathways (cytokines, lipids, unfolded protein response, etc.) and downregulated gene sets (tube morphogenesis, glomerulus development, GTPase signal transduction, etc.). We also found significant dysregulation of genes in whole blood that fell into several gene ontology categories (cytokines, cell cycle, neutrophil degranulation, etc.). We observed a strong correlation between the brain and kidney responses, with significantly shared upregulated pathways (cytokine signaling, cell death, VEGFA pathways) and downregulated pathways (vasculature and RAC1 GTPases). In summary, we have identified a core set of shared genes and pathways in a pig model of systemic inflammation.