bluuebunny/crossref_metadata_2025_split huggingface dataset:
Giant endometrial polyp in a post-menopausal woman: a rare case report from Nepal
Authors: Pokhrel Kailash Mani , Pokhrel Popular , Mulmi Utsha , Khanal Kapil , Panthi Anup , Aryal Suraj , Ghimire Asmita 
Published: February 2024

Introduction:
Endometrial polyps (EPs) result from the overgrowth of endometrial glands and stroma. Giant endometrial polyps, defined as those exceeding 4 cm, are rare, and their association with phytoestrogen (PE) intake is infrequently reported.

Case presentation:
The authors present a case of a giant endometrial polyp in a 59-year-old post-menopausal woman from Nepal. The patient presented with lower abdominal pain and a history of vaginal spotting. She was not under any drugs or medications, including hormones, but had a regular intake of PE-rich foods. Imaging revealed a giant endometrial polyp and a uterine fibroid. Total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH-BSO) were performed and histopathology examination confirmed the diagnosis of endometrial polyp and fibroid.

Discussion:
In our case, the patient’s increased age and PE-rich diet were identified as potential risk factors for the giant endometrial polyp. Giant endometrial polyps are rare, with limited cases reported to date, often associated with tamoxifen or raloxifene use. Phytoestrogens can exhibit oestrogenic effects, contributing to endometrial polyps. This case emphasizes the importance of further research to explain the relationship between phytoestrogen intake and giant endometrial polyps.

Conclusion:
Giant endometrial polyps are uncommon, and their association with phytoestrogen intake remains underexplored. Clinicians should consider dietary factors in history while evaluating endometrial polyps, and further research is necessary to explore the potential role of phytoestrogens in the development of giant endometrial polyps.
Glucagon-Like Peptide-1 Receptor Agonists During Electroconvulsive Therapy
Authors: Espinoza Randall T. , Antongiorgi Zarah 
Published: February 2024

Abstract
Glucagon-like peptide-1 receptor agonists are an emerging class of medications transforming the management of diabetes mellitus and obesity, two highly prevalent and chronic medical conditions associated with significant morbidity and posing serious public health concerns. Although generally well tolerated and relatively safe to use, case reports of patients taking these medications while undergoing elective procedures with general anesthesia describe a potential heightened risk of regurgitation and pulmonary aspiration of gastric contents, deriving from the delayed gastric emptying effect of these agents. Based on increased recognition of this risk, the American Society of Anesthesiologists convened a task force to review available data, resulting in the promulgation of a new procedural management guideline for patients on these drugs and undergoing elective procedures with general anesthesia. However, this guideline pertains mostly to procedures and situations that are distinct from electroconvulsive therapy (ECT). This case report describes the experience of a patient on semaglutide, a glucagon-like peptide-1 receptor agonist for obesity, undergoing ECT, provides a general overview of this novel drug class, identifies issues specific to ECT management, and suggests potential adaptations to patient care over different phases of ECT practice.
Endocrine flexibility can facilitate or constrain the ability to cope with global change
Authors: Taff Conor C. , Baldan Davide , Mentesana Lucia , Ouyang Jenny Q. , Vitousek Maren N. , Hau Michaela 
Published: February 2024

Global climate change has increased average environmental temperatures world-wide, simultaneously intensifying temperature variability and extremes. Growing numbers of studies have documented phenological, behavioural and morphological responses to climate change in wild populations. As systemic signals, hormones can contribute to orchestrating many of these phenotypic changes. Yet little is known about whether mechanisms like hormonal flexibility (reversible changes in hormone concentrations) facilitate or limit the ability of individuals, populations and species to cope with a changing climate. In this perspective, we discuss different mechanisms by which hormonal flexibility, primarily in glucocorticoids, could promote versus hinder evolutionary adaptation to changing temperature regimes. We focus on temperature because it is a key gradient influenced by climate change, it is easy to quantify, and its links to hormones are well established. We argue that reaction norm studies that connect individual responses to population-level and species-wide patterns will be critical for making progress in this field. We also develop a case study on urban heat islands, where several key questions regarding hormonal flexibility and adaptation to climate change can be addressed. Understanding the mechanisms that allow animals to cope when conditions become more challenging will help in predicting which populations are vulnerable to ongoing climate change.
This article is part of the theme issue ‘Endocrine responses to environmental variation: conceptual approaches and recent developments’.
Endocrine disruption in teleosts and amphibians is mediated by anthropogenic and natural environmental factors: implications for risk assessment
Authors: Kloas Werner , Stöck Matthias , Lutz Ilka , Ziková-Kloas Andrea 
Published: February 2024

Environmental variation in the Anthropocene involves several factors that interfere with endocrine systems of wildlife and humans, presenting a planetary boundary of still unknown dimensions. Here, we focus on chemical compounds and other impacts of anthropogenic and natural origins that are adversely affecting reproduction and development. The main sink of these endocrine disruptors (EDs) is surface waters, where they mostly endanger aquatic vertebrates, like teleost fish and amphibians. For regulatory purposes, EDs are categorized into EATS modalities (oestrogenic, androgenic, thyroidal, steroidogenesis), only addressing endocrine systems being assessable by validated tests. However, there is evidence that non-EATS modalities—and even natural sources, such as decomposition products of plants or parasitic infections—can affect vertebrate endocrine systems. Recently, the disturbance of natural circadian light rhythms by artificial light at night (ALAN) has been identified as another ED. Reviewing the knowledge about EDs affecting teleosts and amphibians leads to implications for risk assessment. The generally accepted WHO-definition for EDs, which focuses exclusively on ‘exogenous substances' and neglects parasitic infections or ALAN, seems to require some adaptation. Natural EDs have been involved in coevolutionary processes for ages without resulting in a general loss of biodiversity. Therefore, to address the ‘One Health’-principle, future research and regulatory efforts should focus on minimizing anthropogenic factors for endocrine disruption.
This article is part of the theme issue ‘Endocrine responses to environmental variation: conceptual approaches and recent developments’.
Glucocorticoids and land cover: a largescale comparative approach to assess a physiological biomarker for avian conservation
Authors: Alaasam Valentina J. , Behnke Tessa L. , Grant Avery R. , Ouyang Jenny Q. 
Published: February 2024

As humans alter landscapes worldwide, land and wildlife managers need reliable tools to assess and monitor responses of wildlife populations. Glucocorticoid (GC) hormone levels are one common physiological metric used to quantify how populations are coping in the context of their environments. Understanding whether GC levels can reflect broad landscape characteristics, using data that are free and commonplace to diverse stakeholders, is an important step towards physiological biomarkers having practical application in management and conservation. We conducted a phylogenetic comparative analysis using publicly available datasets to test the efficacy of GCs as a biomarker for large spatial-scale avian population monitoring. We used hormone data from HormoneBase (51 species), natural history information and US national land cover data to determine if baseline or stress-induced corticosterone varies with the amount of usable land cover types within each species' home range. We found that stress-induced levels, but not baseline, positively correlated with per cent usable land cover both within and across species. Our results indicate that GC concentrations may be a useful biomarker for characterizing populations across a range of habitat availability, and we advocate for more physiological studies on non-traditional species in less studied populations to build on this framework.This article is part of the theme issue ‘Endocrine responses to environmental variation: conceptual approaches and recent developments’.
Endocrine responses to environmental variation
Authors: Little Alexander G. , Seebacher Frank 
Published: February 2024

Hormones regulate most physiological functions and life history from embryonic development to reproduction. In addition to their roles in growth and development, hormones also mediate responses to the abiotic, social and nutritional environments. Hormone signalling is responsive to environmental changes to adjust phenotypes to prevailing conditions. Both hormone levels and receptor densities can change to provide a flexible system of regulation. Endocrine flexibility connects the environment to organismal function, and it is central to understanding environmental impacts and their effect on individuals and populations. Hormones may also act as a ‘sensor’ to link environmental signals to epigenetic processes and thereby effect phenotypic plasticity within and across generations. Many environmental parameters are now changing in unprecedented ways as a result of human activity. The knowledge base of organism–environmental interactions was established in environments that differ in many ways from current conditions as a result of ongoing human impacts. It is an urgent contemporary challenge to understand how evolved endocrine responses will modulate phenotypes in response to anthropogenic environmental impacts including climate change, light-at-night and chemical pollution. Endocrine responses play a central role in ecology, and their integration into conservation can lead to more effective outcomes.This article is part of the theme issue ‘Endocrine responses to environmental variation: conceptual approaches and recent developments’.
Fish reproduction in a warming world: vulnerable points in hormone regulation from sex determination to spawning
Authors: Lema Sean C. , Luckenbach J. Adam , Yamamoto Yoji , Housh Madeline J. 
Published: February 2024

Reproduction in fishes is sensitive to temperature. Elevated temperatures and anomalous ‘heat waves’ associated with climate change have the potential to impact fish reproductive performance and, in some cases, even induce sex reversals. Here we examine how thermal sensitivity in the hormone pathways regulating reproduction provides a framework for understanding impacts of warmer conditions on fish reproduction. Such effects will differ depending on evolved variation in temperature sensitivity of endocrine pathways regulating reproductive processes of sex determination/differentiation, gametogenesis and spawning, as well as how developmental timing of those processes varies with reproductive ecology. For fish populations unable to shift geographical range, persistence under future climates may require changes in temperature responsiveness of the hormone pathways regulating reproductive processes. How thermal sensitivity in those hormone pathways varies among populations and species, how those pathways generate temperature maxima for reproduction, and how rapidly reproductive thermal tolerances can change via adaptation or transgenerational plasticity will shape which fishes are most at risk for impaired reproduction under rising temperatures.
This article is part of the theme issue ‘Endocrine responses to environmental variation: conceptual approaches and recent developments’.
Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells
Authors: Gardner Jennifer J. , Cushen Spencer C. , Oliveira da Silva Reneé de Nazaré , Bradshaw Jessica L. , Hula Nataliia , Gorham Isabelle K. , Tucker Selina M. , Zhou Zhengyang , Cunningham Rebecca L. , Phillips Nicole R. , Goulopoulou Styliani 
Published: February 2024

ABSTRACTCirculating cell-free mitochondrial DNA (ccf-mtDNA) is an indicator of cell death, inflammation, and oxidative stress. ccf-mtDNA differs in pregnancies with placental dysfunction from healthy pregnancies and the direction of this difference depends on gestational age and method of mtDNA quantification. Reactive oxygen species (ROS) trigger release of mtDNA from non-placental cells; yet it is unknown whether trophoblast cells release mtDNA in response to oxidative stress, a common feature of pregnancies with placental pathology. We hypothesized that oxidative stress would induce cell death and release of mtDNA from trophoblast cells. BeWo cells were treated with antimycin A (10-320 μM) or rotenone (0.2-50 μM) to induce oxidative stress. A multiplex real-time quantitative PCR (qPCR) assay was used to quantify mtDNA and nuclear DNA in membrane bound, non-membrane bound, and vesicular-bound forms in cell culture supernatants and cell lysates. Treatment with antimycin A increased ROS (p<0.0001), induced cell necrosis (p=0.0004) but not apoptosis (p=0.6471) and was positively associated with release of membrane-bound and non-membrane bound mtDNA (p<0.0001). Antimycin A increased mtDNA content in exosome-like extracellular vesicles (vesicular-bound form; p=0.0019) and reduced autophagy marker expression (LC3A/B, p=0.0002; p62, p<0.001). Rotenone treatment did not influence mtDNA release or cell death (p>0.05). Oxidative stress induces release of mtDNA into the extracellular space and causes non-apoptotic cell death and a reduction in autophagy markers in BeWo cells, an establishedin vitromodel of human trophoblast cells. Intersection between autophagy and necrosis may mediate the release of mtDNA from the placenta in pregnancies exposed to oxidative stress.NEW & NOTEWORTHYThis is the first study to test whether trophoblast cells release mitochondrial DNA in response to oxidative stress and to identify mechanisms of release and biological forms of mtDNA from this cellular type. This research identifies potential cellular mechanisms that can be used in future investigations to establish the source and biomarker potential of circulating mitochondrial DNA in preclinical experimental models and humans.
Regulatory role of cholesterol in modulating actin dynamics and cell adhesive interactions in the trabecular meshwork
Authors: Wang Ting , Kimmel Hannah R C , Park Charles , Ryoo Hyeon , Liu Jing , Underhill Gregory H , Pattabiraman Padmanabhan P 
Published: February 2024

AbstractThe trabecular meshwork (TM) tissue plays a crucial role in maintaining intraocular pressure (IOP) homeostasis. Increased TM contractility and stiffness are directly correlated with elevated IOP. Although cholesterol is known to be a determinant of glaucoma occurrence and elevated IOP, the underlying mechanisms remain elusive. In this study, we used human TM (HTM) cells to unravel the effects of cholesterol on TM stiffness. We achieved this by performing acute cholesterol depletion with Methyl-β-cyclodextrin (MβCD) and cholesterol enrichment/replenishment with MβCD cholesterol complex (CHOL). Interestingly, cholesterol depletion triggered notable actin depolymerization and decreased focal adhesion formation, while enrichment/replenishment promoted actin polymerization, requiring the presence of actin monomers. Using a specific reporter of phosphatidylinositol 4,5-bisphosphate (PIP2), we demonstrated that cholesterol depletion decreases PIP2 levels on the cell membrane, whereas enrichment increases them. Given the critical role of PIP2 in actin remodeling and focal adhesion formation, we postulate that cholesterol regulates actin dynamics by modulating PIP2 levels on the membrane. Furthermore, we showed that cholesterol levels regulate integrin α5β1 and αVβ3 distribution and activation, subsequently altering cell-extracellular matrix (ECM) interactions. Notably, the depletion of cholesterol, as a major lipid constituent of the cell membrane, led to a decrease in HTM cell membrane tension, which was reversed upon cholesterol replenishment. Overall, our systematic exploration of cholesterol modulation on TM stiffness highlights the critical importance of maintaining appropriate membrane and cellular cholesterol levels for achieving IOP homeostasis.
Spatiotemporal Clusters of ERK Activity Coordinate Cytokine-induced Inflammatory Responses in Human Airway Epithelial Cells
Authors: DeCuzzi Nicholaus L. , Oberbauer Daniel P. , Chmiel Kenneth J. , Pargett Michael , Ferguson Justa M. , Murphy Devan , Zeki Amir A. , Albeck John G. 
Published: February 2024

ABSTRACTRATIONALESpatially coordinated ERK signaling events (“SPREADs”) transmit radially from a central point to adjacent cells via secreted ligands for EGFR and other receptors. SPREADs maintain homeostasis in non-pulmonary epithelia, but it is unknown whether they play a role in the airway epithelium or are dysregulated in inflammatory disease.OBJECTIVES(1) To characterize spatiotemporal ERK activity in response to pro-inflammatory ligands, and (2) to assess pharmacological and metabolic regulation of cytokine-mediated SPREADs.METHODSSPREADs were measured by live-cell ERK biosensors in human bronchial epithelial cell lines (HBE1 and 16HBE) and primary human bronchial epithelial (pHBE) cells, in both submerged and biphasic Air-Liquid Interface (ALI) culture conditions (i.e., differentiated cells). Cells were exposed to pro-inflammatory cytokines relevant to asthma and chronic obstructive pulmonary disease (COPD), and to pharmacological treatments (gefitinib, tocilizumab, hydrocortisone) and metabolic modulators (insulin, 2-deoxyglucose) to probe the airway epithelial mechanisms of SPREADs. Phospho-STAT3 immunofluorescence was used to measure localized inflammatory responses to IL-6.RESULTSPro-inflammatory cytokines significantly increased the frequency of SPREADs. Notably, differentiated pHBE cells display increased SPREAD frequency that coincides with airway epithelial barrier breakdown. SPREADs correlate with IL-6 peptide secretion and localized pSTAT3. Hydrocortisone, inhibitors of receptor signaling, and suppression of metabolic function decreased SPREAD occurrence.CONCLUSIONSPro-inflammatory cytokines modulate SPREADs in human airway epithelial cells via both secreted EGFR and IL6R ligands. SPREADs correlate with changes in epithelial barrier permeability, implying a role for spatiotemporal ERK signaling in barrier homeostasis and dysfunction during inflammation. The involvement of SPREADs in airway inflammation suggests a novel signaling mechanism that could be exploited clinically to supplement corticosteroid treatment for asthma and COPD.Brief SummaryCombining live-cell ERK biosensors with multiple human airway epithelial models, we demonstrate that pro-inflammatory cytokines cause spatiotemporally organized ERK signaling events called “SPREADs”, correlating with conditions that disrupt epithelial barrier function. Additionally, common anti-inflammatory treatments tocilizumab, gefitinib, and hydrocortisone suppress cytokine-induced SPREADs. These findings suggest that localized ERK signaling coordinates the innate immune response via spatially restricted cytokine release and regulation of airway barrier permeability.
Cabibbo suppressed hyperon production off nuclei induced by antineutrinos
Authors: Benitez Galan M. , Alvarez-Ruso L. , Rafi Alam M. , Ruiz Simo I. , Vicente Vacas M. J. 
Published: February 2024

In this work, we study the production of Σ and Λ hyperons in strangeness-changing ΔS=−1 charged-current interactions of muon antineutrinos on nuclear targets. At the nucleon level, besides quasielastic scattering, we consider the inelastic mechanism in which a pion is produced alongside the hyperon. Its relevance for antineutrinos with energies below 2 GeV is conveyed in integrated and differential cross sections. We observe that the distributions on the angle between the hyperon and the final lepton are clearly different for quasielastic and inelastic processes. Hyperon final-state interactions, modeled with an intranuclear cascade, lead to a significant transfer from primary produced Σ’s into final Λ’s. They also cause considerable energy loss, which is apparent in hyperon energy distributions. We have investigated Λ production off Ar40 in the conditions of the recently reported MicroBooNE measurement. We find that the Λπ contribution, dominated by Σ*(1385) excitation, accounts for about one third of the cross section.

Published by the American Physical Society
2024
Radiation from an oscillating dipole in the presence of photon-sector
CPT
and Lorentz violation
Authors: O’Connor Joshua , Altschul Brett 
Published: February 2024

We examine one of the standard loci for studying electromagnetic wave emission—the radiation from an oscillating electric dipole—in a model in which the electromagnetic sector is modified to include novel CPT- and Lorentz-violating propagation effects involving a preferred axial vector background. We evaluate the vacuum-birefringent radiation fields, including nonperturbative terms where appropriate. In general, the energy momentum carried by the fields in this model is known to have a complicated nonperturbative structure, which cannot be captured by naive power-series expansions in the components of the preferred background vector. However, we nevertheless find that at the lowest nontrivial orders, there are actually no modifications to the Larmor expressions for the energy-momentum emission.

Published by the American Physical Society
2024