bluuebunny/crossref_metadata_2025_split huggingface dataset:
Infectious Causes of Death: An Autopsy-Based Study of 546 Cases
Authors: Eshaghi Soudabeh , Sheybani Fereshte , Hedjazi Aria , Naderi HamidReza , Shirazinia Matin , Morovatdar Negar 
Published: February 2025

Abstract

Background
Diagnostic accuracy in cases of infectious diseases is crucial for appropriate patient management and public health interventions. This retrospective study aimed to evaluate the most common causes of death caused by infectious diseases and the rate of agreement between clinical diagnoses and autopsy findings in individuals diagnosed with infectious diseases in Mashhad, Iran.

Methods
Autopsy reports from March 2009 to February 2018 were analyzed for patients diagnosed with infectious diseases. Demographic data, clinical diagnoses, and autopsy results were collected and compared. Discrepancies between clinical and autopsy diagnoses were assessed, and potential predictors of diagnostic discrepancy were examined.

Results
Among 28 451 autopsied cases, 546 (1.9%) were diagnosed with infectious diseases. Pleuropulmonary infections were the most common cause of death (69.8%) as determined by autopsy, followed by bloodstream infections (14.1%) and intra-abdominal infections (10.0%). Discrepancies between clinical and autopsy diagnoses were identified in 22.4% of cases. Pleuropulmonary infections had the highest frequency of diagnostic discrepancies (29.1%), followed by central nervous system (CNS) infections (15.8%).

Conclusions
This study underscores the importance of autopsy in identifying diagnostic discrepancies and improving clinical practice in cases of infectious diseases. They also highlight the need for ongoing efforts to enhance diagnostic capabilities, particularly in challenging cases such as pleuropulmonary and CNS infections, to reduce the burden of misdiagnosis and improve patient outcomes.
A framework for sharing power in research teams and promoting justice in scientific publication
Authors: Cockle Kristina L , Cuatianquiz Lima Cecilia , Núñez Montellano María Gabriela , Bonaparte Eugenia Bianca , Zaffignani Daniela , Juncosa Polzella Agostina S , Radi Blas , Ferreira-Xavier Hipólito D , da Hora Jéssica S , Di Sallo Facundo G , Soto-Patiño Juliana , López Fernando G , Zulian Viviane , Miño Carolina I , Pérez Moira , Norris Andrea R , Schaufler María Laura ,   grupo ornitologíaS
Published: February 2025

Abstract
Many ornithologists seek tools to work more equitably with people from historically marginalized and exploited groups. We developed a process to promote collective construction of ornithological knowledge in the Special Feature series "Ecology and conservation of cavity nesters in the Neotropics'' for the journals Ornithology and Ornithological Applications. Colonialism produces systems that consecrate Eurocentric ideas from dominant nations (including Canada, USA, and countries of western Europe) and reinforce hierarchies of power between and within regions. Recognizing these systems, we proposed a Special Feature to support, highlight, and connect teams from Latin America, a region historically exploited by imperial powers. We adopted sociocracy, a governance model that promotes sharing of power, to create the proposal and organize the call for papers and to write a review and this Perspective article. We adopted and developed transparent, consent-based decision-making processes, including a process for determining authorship order. We crafted open invitations, used collective proposals (structured brainstorming), encouraged citation of work from regional journals, tested a system for manuscript submission and review in Spanish, and introduced mechanisms for multi-way feedback. This framework helped reduce some barriers commonly faced by historically marginalized authors, distribute power more equitably, and recognize a broader diversity of contributions to ornithology. Despite these efforts, several challenges remained. For example, the publishing interests of Ornithology, Ornithological Applications, and most high-impact ornithological journals are often poorly aligned with current research priorities in many parts of Latin America (e.g., reproductive biology of endangered species). We encourage scientists at all career stages, technicians, and non-academics to reflect on their citation politics (which sources they cite, and how their citation practice may unintentionally reproduce inequities), and to implement collective workflows that promote equitable sharing of power within research teams. Translated versions of this article are available in Supplementary Material 1 (Spanish) and Supplementary Material 2 (Portuguese).
Role of epigenetics in mangroves: Recent progress and future perspectives
Authors: Meera Suraj Prasannakumari , Kumar Ajay 
Published: February 2025

Abstract
Epigenetic modifications in plants involve heritable changes in gene expression patterns that are not due to changes in gene sequences. Unlike genetic adaptations, which are long-term evolutionary changes, epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNAs, act as adaptive responses and allow plants to better cope with environmental stresses. As mangroves are uniquely located between the land and sea and remain continuously exposed to varying salinity, submergence, and hypoxia stresses, it is expected that certain epigenetic mechanisms might help them withstand the impacts of recurring stress fluctuations. Therefore, understanding the role of epigenetic regulation in mangrove stress adaptations to the intertidal environment is crucial. Despite only few studies to date having investigated epigenetic responses in mangroves, they nonetheless provide important insights into this process on which to base future research. Here, we present an update on recent progress in mangrove epigenetic research and offer perspectives on the potential roles of various epigenetic players in mangrove adaptations to the intertidal environment.
Trends in the Burden of Epilepsy in China from 1990 to 2021 and Its Forecast until 2044: Based on the 2021 Global Burden of Disease Study
Authors: Fang Zhiyong , Wang Feng , Mei Zhen , Huang Xiaofen , Gao Lin , Zheng Lixian , Lin Yuanxiang , Hu Xuequn 
Published: February 2025

Abstract

Background
Epilepsy is one of the most prevalent neurological disorders, but no updated analysis of its burden in China.

Aims
This study provides the most up-to-date, comprehensive analysis of temporal trends and predicts future trends of idiopathic epilepsy in China.

Design
Secondary analysis based on the Global Burden of Disease (GBD).

Methods
GBD 2021 data were analyzed to estimate the incidence, prevalence, mortality, and Disability-Adjusted Life Years (DALYs) of epilepsy in China across different genders, age groups, and years. Joinpoint regression and decomposition analysis assessed temporal changes and the contributions of aging, population growth, and epidemiological changes to disease trends. The Bayesian Age-Period-Cohort (BAPC) model was used to predict age-standardized rates (ASRs) per 100,000 individuals until 2044.

Results
In 2021, the ASRs of incidence, prevalence, deaths, and DALYs for epilepsy in China were 28.2 (95% uncertainty interval [UI]: 19.0–37.9), 214.7 (150.1–278.6), 0.8 (0.7–1.0), and 101.4 (72.5–139.4) per 100,000 population, respectively. The incidence and prevalence rates were 26.1% and 13.4% higher than those in 1990, while deaths and DALYs decreased by 56.6% and 43.2%, respectively, compared to 1990. The highest burden was seen in the youngest and older adults, with men more affected than women. Predictions indicate rising incidence and prevalence rates by 2044, alongside declining mortality and disability rates.

Conclusion
Epilepsy poses a significant health burden in China, with increasing incidence and prevalence from 1990 to 2021, and projections indicating a continued rise through 2044. The disease burden also varies across genders, age groups, and time periods.
RFSoC receiver calibration system for 21-cm global spectrum experiments from space: the CosmoCube case
Authors: Zhu Jiacong , Acedo Eloy de Lera , Artuc Kaan , Chen Xuelei 
Published: February 2025

ABSTRACT
The CosmoCube project plans to deploy a global 21-cm spectrometer with 10–100 MHz observation band in a lunar orbit. The farside part of such an orbit, i.e. the part of orbit behind the Moon, offers an ideal site for accurately measuring the 21-cm signal from the dark ages, cosmic dawn, and epoch of reionization, as the effects of the Earth’s ionosphere, artificial radio frequency interference, and complex terrain and soil are all avoided. Given the limitations of a satellite platform, we propose a receiver calibration system design based on a radio frequency system-on-chip, consisting of a vector network analyser (VNA) subsystem, and a source switching subsystem. We introduce the measurement principle of the VNA, and discuss the effect of quantization error. The accuracy, stability, and trajectory noise of the VNA are tested in laboratory experiments. We also present the design of the source-switching subsystem, generating mock data sets, showing that the imperfect return loss, insertion loss, and isolation of surface-mounted microwave switches have a minimal effect on the sky foreground fitting residuals, which are within $\pm 10$ mK under optimal fitting condition. When all possible measurement errors in reflection coefficients and physical temperatures are taken into account, the foreground fitting residuals for the 50–90 MHz part of the spectrum remain around $\pm 20$ mK.
A systematic review and meta-analysis of group-based trajectory modeling of sleep duration across age groups and in relation to health outcomes
Authors: Wang Wei , Cheung Sing-Hang , Cheung Shu Fai , Sun Rong Wei , Hui C Harry , Ma Ho Yin Derek , Lau Esther Yuet Ying 
Published: February 2025

Abstract

Study Objectives
To shed light on understanding sleep duration trajectories (SDTs) using different classification methods and their outcomes, this study aimed to (1) identify common SDTs among different age groups, (2) investigate the alignment versus differences between SDTs identification by group-based trajectory modeling (GBTM) and clinical standards, and (3) examine the impacts of SDTs on health outcomes.

Methods
A systematic literature search from four databases yielded 34 longitudinal SDT studies with GBTM analyses spanning three or more data waves. Apart from the proportion meta-analysis, a three-level meta-analysis was conducted with 14 of the studies that examined the association between SDT groups and health outcomes. Assessment of study quality was performed using the Guidelines for Reporting on Latent Trajectory Studies checklist.

Results
Qualitative analysis identified four age-related SDT classes based on longitudinal trends: “persistent sleepers,” “increase sleepers,” “decrease sleepers,” and “variable sleepers.” Meta-analysis also showed differential proportions of “GBTM-defined shortest sleepers” across age groups and sample regions, as well as significant discrepancies in the prevalence of short sleep identified by clinical standards (=50% vs. 15% per GBTM). Overall, SDTs predicted emotional and behavioral outcomes, neurocognitive problems, and physical health (OR = 1.538, p &lt; 0.001), in GBTM-defined “short,” “fluctuating,” “long,” and “decreasing” sleepers as compared to the “adequate” group. The effects were stronger in adolescents and in datasets with more waves.

Conclusions
The identification of the GBTM-defined “short,” “fluctuating,” “long,” and “decreasing” SDT groups and their associations with various health outcomes supported longitudinal investigations, as well as the development of interventions focusing on both the length and stability of sleep durations, especially in younger populations. Study registration: PROSPERO registration number CRD42023412201.
Inhibition of proton sensor GPR68 suppresses endothelial dysfunction and acute lung injury caused by Staphylococcus aureus bacterial particles
Authors: Karki Pratap , Ke Yunbo , Zhang Chen‐Ou , Promnares Kamoltip , Li Yue , Williams Charles H. , Hong Charles C. , Birukov Konstantin G. , Birukova Anna A. 
Published: February 2025

AbstractLung bacterial infections, including hospital‐acquired pneumonia, remain a serious problem for public health. Endothelial cell (EC) exposure to heat‐killed Staphylococcus aureus (HKSA) represents a clinical scenario of high titers of killed bacterial particles present in the host after antibiotic therapy, which triggers inflammatory cascades, cytokine storms, and EC dysfunction leading to acute lung injury (ALI). GPR68 is a member of the proton‐sensing G protein‐coupled receptor family. Acting as a pH sensor, GPR68 becomes activated upon pH reduction and contributes to pathologic cell responses by activating ER stress and unfolded protein response. This study investigated the role of GPR68 in HKSA‐induced EC dysfunction and HKSA‐induced ALI. HKSA robustly increased GPR68 mRNA levels in human pulmonary EC and directly stimulated GPR68 activity. A selective GPR68 small molecule inhibitor, OGM‐8345, attenuated HKSA‐induced EC permeability and protected cell junction integrity. OGM‐8345 inhibited HKSA‐induced activation of inflammatory genes TNF‐α, IL‐6, IL‐8, IL‐1β, and CXCL5 and decreased cytokine secretion by HKSA‐challenged EC. Co‐treatment with the GPR68 activator Ogerin or medium acidification to pH 6.5 augmented HKSA‐induced EC dysfunction, which was rescued by OGM‐8345. Intratracheal HKSA injection increased vascular leak and lung inflammation in mice which were monitored by lung Evans blue extravasation, increased cell and protein count in bronchoalveolar lavage, and mRNA expression of inflammatory genes. ALI and barrier dysfunction was attenuated by OGM‐8345. We show for the first time the role of GPR68 in mediating HKSA‐induced lung injury and the strong potential for OGM‐8345 as a therapeutic treatment of bacterial pathogen‐induced ALI associated with tissue acidification.
Dual independent mechanisms underlying gut epithelial remodeling upon sugar substitute consumption
Authors: Seo Dong Woo , Hong Kyung Tae , Lee Jung Hoon , Lee Jun‐Seok , Jeong Yong Taek 
Published: February 2025

AbstractIntestinal epithelial cells (IECs) are dynamically regulated by luminal contents, including dietary ingredients, food additives, and microbiota‐derived metabolites. Although sugar substitutes are commonly used as food additives for their sweet taste and lower calorie content, there is limited experimental evidence regarding their potential to drive gut remodeling. In this study, we designed experimental models for short‐term consumption of erythritol, a natural sugar alcohol widely used as a sugar substitute, and investigated its effects on gut remodeling and the underlying mechanisms. Our findings indicate that erythritol consumption induces hyperplasia in tuft cells (TCs) and goblet cells (GCs), as well as enhances the activity of intestinal stem cells–increases in expression levels of leucine‐rich repeat containing G protein‐coupled receptor 5 (Lgr5), the key intestinal stem cell marker, in the number of proliferating stem cells, and facilitation of their differentiation into villi cells–while maintaining the number of Lgr5+ intestinal stem cells. Notably, the enhanced stem cell activity was observed even in Trpm5 knockout mice, suggesting that it is mechanistically independent of TC hyperplasia. Instead, we demonstrated the functional involvement of the gut microbiota, as antibiotic treatment abolished this effect, and fecal material transfer from erythritol‐consumed mice replicated the enhancement of stem cell activity in recipient mice. Furthermore, we identified acetate as the metabolite responsible for enhancing stem cell activity. These findings suggest the functional decoupling of TC hyperplasia and the enhancement of stem cell activity, providing a potential therapeutic avenue for gut epithelial diseases.
Alpha protein kinase 1 knockout mitigates microglial pyroptosis and cognition deficits in ADP‐heptose‐stimulated mice
Authors: Zou Xiao , Du Ou , Yang Yan‐Rong , Yang Yu‐Xin , Zheng Zi‐Xing , Li Meng‐Yang , Wu An‐Guo , Du Jun‐Rong 
Published: February 2025

AbstractMicroglial activation and pyroptosis are central to neuroinflammation and significantly contribute to cognitive decline associated with neurodegenerative diseases. Alpha protein kinase 1 (ALPK1) is recently identified as a critical mediator of inflammatory responses in response to ADP‐heptose (a pathogen‐associated molecular pattern). However, its specific role in microglial pyroptosis and cognitive dysfunction remains unclear. In this study, we investigated the effects of ALPK1 on cognitive function and pyroptosis in wild‐type (WT) and ALPK1 KO mice by intracerebroventricular administration of ADP‐heptose to induce neuroinflammation. Cognitive performance was evaluated using behavioral tests (the Y‐Maze, Morris Water Maze, and step‐down passive avoidance), while Western blot, immunofluorescence, transmission electron microscopy, and enzyme‐linked immunosorbent assay were used to evaluate the expression of pyroptosis markers such as NLRP3, Caspase‐1, and gasdermin D (GSDMD) in vivo and in vitro. Our results reveal that the absence of ALPK1 significantly attenuated ADP‐heptose‐induced cognitive deficits and neuronal injury, and inhibited the NLRP3/Caspase‐1/GSDMD pathway of pyroptosis and the secretion of pro‐inflammatory cytokines IL‐1β and IL‐18. Notably, ADP‐heptose‐stimulated conditioned media from primary microglial cells of ALPK1 KO mice significantly enhanced neuronal cell viability, suggesting a protective role for ALPK1 deficiency in supporting neuronal health. These findings suggest the pivotal role of ALPK1 in ADP‐heptose‐induced microglial pyroptosis and cognitive impairment, thereby highlighting its potential as a therapeutic target in neuroinflammatory disorders.
Targeted inhibition of menin promotes β‐catenin‐mediated GLP‐1 expression and improves glucose tolerance in high‐fat diet‐induced obese mice
Authors: Cao Xiaoru , Yu Ling , Zhang Qian , Cheng Zhaosi , Meng Haiyue , Wang Chenghao , Guo Zhitao , Guo Yinghao , Xin Guoshun , Wang Yue , Zhou Pingping , Luo Yakun , Sun Bin , Ma Jian 
Published: February 2025

AbstractGlucagon‐like peptide‐1 (GLP‐1), derived from enteroendocrine cells, is a pivotal hormone crucial for blood glucose regulation. Menin, encoded by the MEN1 gene and known for its tumor suppressor role, is abundantly expressed in the intestine. Previous research has demonstrated that acute Men1 excision reverses preexisting glucose intolerance in high‐fat diet‐fed mice. However, its impact on GLP‐1 expression in enteroendocrine cells has not been investigated. In the present study, both the knockdown of Men1 and the administration of the MI‐463 menin inhibitor increased GLP‐1 expression in glucose‐stimulated STC‐1 cells. Additionally, administering MI‐463 to obese mice significantly elevated GLP‐1 levels in both ileal epithelial cells and serum. Mechanistically, menin inhibition enhanced the nuclear accumulation of β‐catenin, allowing it to bind TCF7L2, thereby increasing glucagon gene (Gcg) transcription. Furthermore, compared with control mice, mice with intestinal epithelial cell‐specific Men1 knockdown exhibited significant improvements in glucose tolerance under fat challenge, which was correlated with elevated GLP‐1 levels. These findings suggest that menin‐mediated regulation of GLP‐1 expression may be an important mechanism through which menin inhibiton alleviates type 2 diabetes.
Diurnal variation in skeletal muscle mitochondrial function dictates time‐of‐day‐dependent exercise capacity
Authors: Khatri Subhash , Das Souparno , Singh Anshit , Ahmad Shabbir , Kashiv Mohit , Laxman Sunil , Kolthur‐Seetharam Ullas 
Published: February 2025

AbstractExercise impinges on almost all physiological processes at an organismal level and is a potent intervention to treat various diseases. Exercise performance is well established to display diurnal rhythm, peaking during the late active phase. However, the underlying molecular/metabolic factors and mitochondrial energetics that possibly dictate time‐of‐day exercise capacity remain unknown. Here, we have unraveled the importance of diurnal variation in mitochondrial functions as a determinant of skeletal muscle exercise performance. Our results show that exercise‐induced muscle metabolome and mitochondrial energetics are distinct at ZT3 and ZT15. Importantly, we have elucidated key diurnal differences in mitochondrial functions that are well correlated with disparate time‐of‐day‐dependent exercise capacity. Providing causal mechanistic evidence, we illustrate that loss of Sirtuin4 (SIRT4), a well‐known mitochondrial regulator, abrogates mitochondrial diurnal variation and consequently abolishes time‐of‐day‐dependent muscle output. Therefore, our findings unequivocally demonstrate the pivotal role of baseline skeletal muscle mitochondrial functions in dictating diurnal exercise capacity.
Cerebral palsy
Authors: Smigelski Garrett D. 
Published: February 2025

ABSTRACT
Cerebral palsy (CP) is an encompassing term for a group of permanent neurologic disorders of movement and posture commonly seen in early childhood and caused by abnormal brain development early in life. The cause of CP is unclear in the majority of patients affected and can be multifactorial, occurring in various time frames such as prenatal, intrapartum, and postpartum. Because CP is a clinical diagnosis, clinicians must have a strong understanding of the clinical presentation to ensure early diagnosis and improved outcomes for patients. This article reviews CP and describes advances in diagnosis and management; it also provides an overview of new treatments that are under investigation.