bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mendelian randomization evidence for lung function mediates the association between childhood allergies (age <16 years) and essential hypertension
Authors: Long Yu-Hang , She Jun-Sen , Guo Fei , Zhou Bo-Kang , Fang Chen , Hu Yi-Zhi , Gao Ling , Huang He-Feng 
Published: December 2024

Objective:
This study aimed to investigate the influence of lung function on the relationship between allergies and hypertension, thereby elucidating significant potential mechanisms from a genetic standpoint. We investigated the causal relationship between childhood allergies (age <16 years) and essential hypertension and identified and quantified the role of lung function (forced vital capacity [FVC] and forced expiratory volume in the first second/forced vital capacity [FEV1/FVC]) as potential mediators.

Methods:
Using data from a genome-wide association study and the Fenn Genn consortium, a two-sample Mendelian randomization (MR) analysis of genetically predicted childhood allergies (7128 cases and 211,703 controls) and essential hypertension (116,714 cases and 1,032,659 controls) was performed. Furthermore, we used two-step MR to quantify the effect of lung function-mediated childhood allergies on essential hypertension. The FVC and FEV1/FV sample size was 371, 898.

Results:
Childhood allergies were associated with increased odds of developing essential hypertension (odds ratio [OR] = 1.0900, 95% confidence interval [CI] = 1.0034–1.1842, P = 0.0414). No strong evidence that genetically predicted essential hypertension affected childhood allergy risk was identified (OR = 1.0631, 95% CI = 0.9829–1.1498, P = 0.1264). The proportion of genetically predicted childhood allergies mediated only by FVC was 5.67% (95% CI, 5.13%–5.73%).

Conclusion:
A causal relationship between childhood allergies and essential hypertension was identified, with a proportion of the effect mediated by FVC. Therefore, implementing early interventions in children with allergies is imperative to mitigate the long-term risk of developing hypertension. Further research is required to identify additional risk factors as potential mediators.
Predictors of healthy days at home: Benchmarking long-term outcomes in geriatric trauma
Authors: Castillo-Angeles Manuel , Zogg Cheryl K. , Smith Charlotte B. , Etheridge James C. , Wu Christine , Jarman Molly P. , Nitzschke Stephanie , Askari Reza , Cooper Zara , Salim Ali , Havens Joaquim M. 
Published: December 2024

BACKGROUND
Quality benchmarking has recently evolved from a historical focus on short-term morbidity and mortality as the key metrics to assessing long-term outcomes. Long-term quality metrics have been shown to provide a more complete assessment of geriatric trauma care. Among these metrics, patients' average number of healthy days at home (HDAH) proports to be a useful administrative claims-based marker of patient functional status. Our goal was to determine the predictors of HDAH among injured older adults.

METHODS
Medicare inpatient claims (2014–2015) were used to identify all geriatric trauma patients. Patients' number of HDAH was measured from the date of discharge and calculated as the total sum of patients' time during that period less any time spent in the hospital or emergency department, step-down/rehabilitation/nursing care, home health, or after death within a 365-period after index admission. Controlling for demographic, injury severity, and hospital-level characteristics, multivariable regression analyses were performed to identify the factors associated with increased HDAH.

RESULTS
We included 772,109 geriatric trauma patients. The mean age was 82.15 years (SD, 8.49 years), 68.3% were female, and 91.6% were White. The median HDAH was 351 days (interquartile range, 351–355 days). After adjusted analysis, age, Black race, Charlson Comorbidity Index (CCI), and care at a level 3/nontrauma center were associated with fewer HDAH within 365 days after discharge.

CONCLUSION
This study suggests that higher level trauma centers provide more HDAH after index admission for injured older adults. Future studies should focus on correlating HDAH with more granular but less readily accessible quality of life metrics.

LEVEL OF EVIDENCE
Prognostic and Epidemiological; III.
Caloric restriction: A potential approach for mitigating neuronal damage: Lesson from cellular model of Alzheimer disease
Authors: Sharma Apoorv , Bhardwaj Monika , Kumar Vijay , Islam Asimul , Prakash Hridayesh 
Published: December 2024

AbstractAlzheimer’s disease is a neurodegenerative disorder and characterized by amyloid beta accumulation, synaptic dysfunction, and oxidative stress, lacks effective therapies. Caloric restriction mimetics such as fisetin and chlorogenic acid, natural polyphenols with antioxidant and autophagy-inducing properties, show promise in mitigating age-related diseases. This study investigates their neuroprotective effects against amyloid beta induced toxicity in differentiated human neuroblastoma SHSY5Y cells. Amyloid beta exposure disrupted redox homeostasis, impaired autophagy, induced mitochondrial dysfunction, and exacerbating neuronal degeneration. Fisetin and chlorogenic acid treatments reversed these deleterious effects by restoring redox balance, suppressing reactive oxygen species and upregulating critical antioxidant enzymes like SOD1, GSR, and catalase. These compounds also attenuated amyloid beta induced mitophagy via reduced PINK1 expression and restored mitochondrial fusion by upregulating Mfn2. Autophagy-related pathways were significantly modulated, evidenced by increased AMPK and decreased mTOR mRNA levels, alongside elevated expression of ATG101, ATG13, ULK1, P62 and reduced ATG5 levels. Docking studies also revealed binding of fisetin and CGA within the binding pockets of AMPK and FKBP12 supporting their interaction. Furthermore, fisetin and CGA improved synaptic integrity by upregulating PSD95 and synaptophysin and reducing acetylcholinesterase expression. These findings highlight their potential in ameliorating amyloid beta induced neuronal toxicity through autophagy activation, synaptic preservation, and mitochondrial function enhancement. While this study demonstrates the transcriptional impact and binding affinities of these caloric restriction mimetics further translational and biophysical analyses are required to elucidate their mechanisms and confirm their therapeutic viability. This research underscores the potential of fisetin and CGA as neuroprotective agents, offering promising therapeutic avenues for combating related Alzheimer’s disease neuropathies.Abstract Figure
Enhanced Subjective Performance Achievement in Wind Instrument Playing through Positive Memory Recall: Effects of Sympathetic Activation and Emotional Valence
Authors: Watanabe Aiko , Kondoh Sotaro , Samma Tomohiro , Fujii Shinya 
Published: December 2024

AbstractControlling physiological and psychological states before a performance is essential for professional musicians to realize their full potential. However, the characteristics of the optimal pre-performance state remain unclear. While an increase in sympathetic nervous system activity is typically observed before performance, when associated with anxiety, it can degrade the performance quality. This study examined whether recalling positive autobiographical performance memories enhances subjective performance achievement, accompanied by increased emotional arousal, valence, and autonomic nervous system activity. Thirty-six professional wind instrument players participated in the study. Prior to performing musical pieces, participants engaged in one of three conditions: (1) recalling positive autobiographical memories, (2) recalling negative autobiographical memories, or (3) imagining routine pre-performance activities (no-memory condition). During the memory recall phase, heart rate was measured. After each performance, participants rated their subjective arousal, valence, and performance achievement. We calculated the heart rate variability indices, specifically SD1 (reflecting parasympathetic nervous system activity) and SD2/SD1 (reflecting sympathetic nervous system activity). The results showed that performance achievement, arousal, and valence were significantly higher in the positive than in the negative condition. Our path analysis further revealed that an increase in SD2/SD1 did not directly predict performance achievement; instead, it was associated with an increase in emotional valence, which in turn led to improved performance. These findings suggest that recalling positive performance memories activates sympathetic nervous system activity and fosters positive emotions, thereby enhancing the performance achievement of professional musicians.
A Brain Reward Circuit Inhibited By Next-Generation Weight Loss Drugs
Authors: Godschall Elizabeth N. , Gungul Taha Bugra , Sajonia Isabelle R. , Buyukaksakal Aleyna K. , Ogilvie Sophia , Keeler Austin B. , Zhang YuChen , Deutsch Tyler C. J. , Shi Yu , Conley Nicholas J. , Webster Addison N. , Calhan O. Yipkin , Akkoub Amani , Malik Karan , West Kaleigh I. , Karthikeyan Arun , van Gerven Grace , Patel Manoj K. , Campbell John N. , Deppmann Christopher D. , Güler Ali D. 
Published: December 2024

AbstractGlucagon-like peptide-1 receptor agonists (GLP1RAs) effectively reduce body weight and improve metabolic outcomes, yet established peptide-based therapies require injections and complex manufacturing. Small-molecule GLP1RAs promise oral bioavailability and scalable manufacturing, but their selective binding to human versus rodent receptors has limited mechanistic studies. The neural circuits through which these emerging therapeutics modulate feeding behavior remain undefined, particularly in comparison to established peptide-based GLP1RAs. Here, we developed humanized GLP1R mouse models to investigate how small- molecule GLP1RAs influence feeding behavior. Integrating genetic manipulations, calcium imaging, and behavior profiling, we discovered that these compounds regulate both homeostatic and hedonic feeding through parallel neural circuits. Beyond engaging canonical hypothalamic and hindbrain networks that control metabolic homeostasis, GLP1RAs recruit a discrete population of Glp1r-expressing neurons in the central amygdala, which selectively suppress the consumption of palatable foods by reducing dopamine release in the nucleus accumbens. Stimulating these central amygdalar neurons curtail hedonic feeding, whereas targeted deletion of the receptor in this cell population specifically diminishes the anorectic efficacy of GLP1RAs for reward-driven intake. These findings reveal a dedicated neural circuit through which small molecule GLP1RAs modulate reward processing, suggesting broad therapeutic potential in conditions of dysregulated dopamine signaling including substance use disorder and binge eating.
A Commander-independent function of COMMD3 in endosomal trafficking
Authors: Squiers Galen T. , Wan Chun , Gorder James , Puscher Harrison , Shen Jingshi 
Published: December 2024

ABSTRACTEndosomal recycling is a branch of intracellular membrane trafficking that retrieves endocytosed cargo proteins from early and late endosomes to prevent their degradation in lysosomes. A key player in endosomal recycling is the Commander complex, a 16-subunit protein assembly that cooperates with other endosomal factors to recruit cargo proteins and facilitate the formation of tubulo-vesicular carriers. While the crucial role of Commander in endosomal recycling is well established, its molecular mechanism remains poorly understood. Here, we genetically dissected the Commander complex using unbiased genetic screens and comparative targeted mutations. Unexpectedly, our findings revealed a Commander-independent function for COMMD3, a subunit of the Commander complex, in endosomal recycling. COMMD3 regulates a subset of cargo proteins independently of the other Commander subunits. The Commander-independent function of COMMD3 is mediated by its N-terminal domain (NTD), which binds and stabilizes ADP- ribosylation factor 1 (ARF1), a small GTPase regulating endosomal recycling. Mutations disrupting the COMMD3-ARF1 interaction diminish ARF1 expression and impair COMMD3- dependent cargo recycling. These data provide direct evidence that Commander subunits can function outside the holo-complex and raise the intriguing possibility that components of other membrane trafficking complexes may also possess functions beyond their respective complexes.
How does Gloger’s rule predict near- and mid-infrared radiation in birds?
Authors: Lee Thomas , Barrett Meghan , Pilon Laurent , Shultz Allison J. , McGlynn Terrence P 
Published: December 2024

AbstractAnimal coloration has diverse functions such as camouflage, communication, thermoregulation, protection from UV damage and more, and can be shaped by environmental selective pressures. Some climactic selective pressures are strong enough to produce consistent patterns in many species across large-scale geographic gradients. One pattern in endothermic animals is Gloger’s rule, which predicts that populations in hot, humid areas will be darker than those in cool, dry areas. This pattern has been demonstrated in several species across latitudinal gradients and is expected to relate to the selective effects of both local thermoregulatory pressures and humidity. However, shortwave radiation from sunlight extends beyond the visible spectrum [400-700 nm] into the near-infrared; thus, thermal pressures often result in changes in surface reflectance characteristics beyond the visible [e.g., 700-2500 nm]. Further, heat exchange with the environment extends into the mid-infrared, including MIR heat loss through the atmospheric transmission window [7.5 - 14 um]. Here, we examine both UV-NIR absorption and MIR emittance in five species of birds that have been shown to follow, or not follow, Gloger’s rule. We show that NIR absorption varies by species and population in ways that correspond to their habitat and thermoregulatory strategies. MIR emittance, by contrast, was very stable across both species and populations but differed across populations of Northern Bobwhites. We conclude by highlighting the importance of extending coloration research into the NIR and MIR. Further consideration of infrared radiation is necessary for a complete view of animals’ phenotypic diversity and possible responses to thermal challenge.
Chronic Behavioral and Seizure Outcomes following Experimental Traumatic Brain Injury and ComorbidKlebsiella pneumoniaeLung Infection in Mice
Authors: Rewell Sarah S. J. , Shad Ali , Chen Lingjun , Chu Erskine , Wang Jiping , Chen Ke , O’Brien Terence J. , Li Jian , Casillas Espinosa Pablo M. , Semple Bridgette D. 
Published: December 2024

ABSTRACTTraumatic brain injury (TBI) is a leading cause of long-term disability, and infections such as pneumonia represent a common and serious complication for TBI patients in the acute and subacute post-injury period. While the acute effects of infections have been documented, their long-term consequences on neurological and behavioral recovery as well as the potential precipitation of seizures after TBI remain unclear. This study aimed to investigate the chronic effects ofKlebsiella pneumoniaeinfection following TBI, focusing on post-traumatic seizure development and neurobehavioral changes. Using a mouse model, we assessed the long-term effects of TBI andK. pneumoniaeinfection both in isolation and in combination. We found that, while infection withK. pneumoniaeresulted in loss of body weight and increased mortality compared to vehicle-inoculated mice, there was no additional mortality in TBI animals. Further, although TBI alone induced chronic hyperactivity and reduced anxiety-like behaviors,K. pneumoniaelung infection had no lasting effect on these long-term outcomes. Thirdly, while TBI resulted in both spontaneous and evoked seizures long-term post-injury, early post-injuryK. pneumoniaeinfection did not affect late onset seizure susceptibility. Together with recent findings on acute outcomes in this combined insult model of TBI andK. pneumoniaeinfection, this study suggests thatK. pneumoniaedoes not significantly alter long-term neurobehavioral outcomes or the development of post-traumatic epilepsy. This research highlights the need to further explore the interplay between additional immune insults such as infection that may influence long-term recovery.
Percutaneous assessment of the relationship between Homologous and Non-homologous bones of Upper and Lower limbs among Ghanaian tertiary students
Authors: Okwan Daniel Kobina , Abaidoo Chrissie Stansie , Robertson Juliet , Bempah Samuel Kwadwo Peprah , Wepeba Pet-Paul , Asante Thomas Kwaku , Obeng Priscilla , Domfeh Ethel Akua Achiaa , Afriyie Sarah Owusu 
Published: December 2024

AbstractBackgroundNatural disasters and accidents may result in loss of some part of the upper and or lower limbs. In such situations, there is the need to design appropriate best fit prostheses for such victims. There is the need to have sex-and side-specific models that can be applied conveniently to design appropriate prosthesis for maximum benefit to the patient.AimTherefore, this study was designed to determine the relationship between homologous and non-homologous bones of upper and lower limbs among Ghanaians using a percutaneous approach.MethodologyEthical approval for this cross-sectional study was sought from the Committee on Human Research, Publication and Ethics, KNUST and 242 participants were sampled via a purposive sampling technique after seeking their consent.ResultsMales significantly recorded greater percutaneous long bones for both the upper and lower limbs than the female participants. With the exception of radial length among the females, for both sexes bilateral asymmetry was observed in the remaining percutaneous limb dimensions where the upper limb parameters were greater on the left side than the right side, but showed right dominance for the lower limb parameters. Although several useful equations were derived, most of them utilized humeral length in the prediction of lower limb length estimation.ConclusionFindings of the present study are useful for the biological profiling of humans with dismembered body parts involved in various disasters such as automobile accidents. The formulae derived would be useful for the design of appropriate prostheses. This study has also reaffirmed the existence of sexual and bilateral dimorphism in body dimensions.
Octadecanoids as emerging lipid mediators in cnidarian-dinoflagellate symbiosis
Authors: Botana Marina T. , Lewis Robert E. , Quaranta Alessandro , Salamin Olivier , Revol-Cavalier Johanna , Oakley Clint A. , Feussner Ivo , Hamberg Mats , Grossman Arthur R. , Suggett David J. , Weis Virginia M. , Wheelock Craig E. , Davy Simon K. 
Published: December 2024

AbstractOxylipin signaling has been suggested as a potential mechanism for the inter-partner recognition and homeostasis regulation of cnidarian-dinoflagellate symbiosis, which maintains the ecological viability of coral reefs. Here we assessed the effects of symbiosis and symbiont identity on a model cnidarian, the sea anemoneExaiptasia diaphana, using mass spectrometry to quantify octadecanoid oxylipins (i.e.,18-carbon-derived oxygenated fatty acids). A total of 84 octadecanoids were reported, and distinct stereospecificity was observed for the synthesis ofR-andS-enantiomers for symbiont-free anemones and free-living cultured dinoflagellate symbionts, respectively. Symbiont-derived 13(S)-hydroxy-octadecatetraenoic acid (13(S)- HOTE) linked to a 13S-lipoxygnase was translocated to the host anemone with a 32-fold increase, suggesting it as a biomarker of symbiosis and as a potential agonist of host receptors that regulate inflammatory transcription. Only symbiosis with the native symbiontBreviolum minutumdecreased the abundance of pro-inflammatory 9(R)-hydroxy-octadecadienoic acid (9(R)-HODE) in the host. In contrast, symbiosis with the non-native symbiontDurusdinium trenchiiwas marked by higher abundance of autoxidation-derived octadecanoids, corroborating previous evidence for cellular stress in this association. The putative octadecanoid signaling pathways reported here suggest foundational knowledge gaps that can support the bioengineering and selective breeding of more optimal host-symbiont pairings to enhance resilience and survival of coral reefs.
Could Quantum-Mediated Bacterial Signaling Explain Adaptive Mutation?
Authors: Ross Patrick 
Published: December 2024

AbstractThe phenomenon of adaptive mutation in bacteria presents several challenges to classical models of evolution, particularly regarding the observed coordination of mutation patterns across populations. Here, we examine statistical evidence from evolved Escherichia coli populations showing mutation enrichment up to 256-fold above background rates in key metabolic genes, with remarkable temporal stability that appears to transcend known bacterial communication mechanisms. We propose a theoretical framework suggesting that bacteria may utilize quantum coherent oscillations, potentially mediated through synchronized membrane potential fluctuations, to achieve this degree of coordination in adaptive mutation. Building on Sprouffske et al.’s findings that high mutation rates can limit adaptive evolution in E. coli, we examined mutation patterns in four key metabolic genes (pykF, topA, cspC, and rpoC) previously identified as targets of selection. While Sprouffske found that extremely high mutation rates impaired adaptation, our analysis reveals that these genes show non-random enrichment patterns (p < 1.76×10-34 for pykF) that maintain remarkable temporal stability across multiple timepoints. Recent advances in quantum biology have demonstrated sustained quantum coherence in biological systems, we present a model for how quantum-mediated bacterial signaling could potentially contribute to adaptive mutation. The framework makes several experimentally testable predictions about mutation patterns, population dynamics, and coherence times in bacterial populations under stress conditions. While substantial experimental validation remains necessary, this work provides specific approaches for investigating potential quantum contributions to bacterial adaptation, with implications for understanding evolutionary mechanisms and bacterial stress responses.