bluuebunny/crossref_metadata_2025_split huggingface dataset:
Searching for the signature of fast radio burst by Swift/XRT X-ray afterglow light curve
Authors: Shen Hsien-chieh , Sakamoto Takanori , Serino Motoko , Sato Yuri 
Published: June 2024

Abstract
A new type of cosmological transient, dubbed fast radio bursts (FRBs), was recently discovered. The source of FRBs is still unknown. One possible scenario of an FRB is the collapse of a spinning supra-massive neutron star. Zhang (2014, ApJ, 780, L21) suggests that the collapse can happen shortly (hundreds to thousands of seconds) after the birth of supra-massive neutron stars. The signatures can be visible in X-ray afterglows of long and short gamma-ray bursts (GRBs). For instance, a sudden drop (decay index steeper than $-3$ to $-9$) from a shallow decay (decay index shallower than $-1$) in the X-ray afterglow flux can indicate such an event. We selected the X-ray afterglow light curves with a steep decay after the shallow decay phase from the Swift/XRT GRB catalog. We analyzed when the decay index changed suddenly by fitting these light curves to double power-law functions and compared them with the onset of FRBs. We found that none of our GRB samples match the onset of FRBs.
Mutual funds’ strategic voting on environmental and social issues
Authors: Michaely Roni , Ordonez-Calafi Guillem , Rubio Silvina 
Published: June 2024

Abstract
Environmental and social (ES) funds in non-ES families must balance incorporating the stakeholders’ interests they advertise and maximizing shareholder value favored by their families. We find that these funds support ES proposals that are far from the majority threshold, while opposing them when their vote is more likely to be pivotal. This strategy results in a high average support for ES proposals, seemingly consistent with their fiduciary responsibilities, while opposing contested ES proposals. This greenwashing strategy is driven by ES funds in non-ES families who cater to institutional investors. Indeed, these funds experience lower inflows when providing low average support for ES proposals. This strategic voting is not exhibited in governance proposals, nor by ES funds in ES families or by non-ES funds in non-ES families, reinforcing the notion of strategic voting to accommodate family preferences while appearing to meet the fiduciary responsibilities of the funds.
Effects of human umbilical cord mesenchymal stem cell-derived exosomes in the rat osteoarthritis models
Authors: Yang Huanfeng , Zhou Yiqin , Ying Bi , Dong Xuhui , Qian Qirong , Gao Shaorong 
Published: June 2024

Abstract
Mesenchymal stem cells (MSCs) offer great potential for treatment of osteoarthritis (OA) by promoting articular cartilage regeneration via paracrine secretion of exosomes; however, the underlying mechanisms are not fully understood. This study aimed to explore the therapeutic effects of exosomes secreted by human umbilical cord-derived MSCs (hUC-MSCs) in rat models of OA and reveal the underlying mechanisms. UC-MSCs and UC-MSC-exosomes were prepared and identified by transmission electron microscopy and flow cytometry. IL-1β-induced OA chondrocytes and the operation and collagenase-induced OA rat models were established. The results of micro-computed tomography, histology, and immunohistochemistry showed that UC-MSC-exosomes promoted cartilage regeneration in OA rats. ELISA results showed that the levels of synovial fluid cytokines, TNF-α, IL-1β, and IL-6, were lower in exosome therapy group than control group in both OA rat models. Exosome treatment significantly downregulated the expression of MMP-13 and ADAMTS-5 in chondrocytes stimulated by IL-1β, and upregulated collagen II expression. These findings suggest that hUC-MSC-exosomes offer a promising option for the therapy for OA.
Comparison of Catheter Malposition Between Left and Right Ultrasound-Guided Infraclavicular Subclavian Venous Catheterizations: A Randomized Controlled Trial*
Authors: Shin Kyung Won , Park Seyong , Jo Woo-Young , Choi Seungeun , Kim Yoon Jung , Park Hee-Pyoung , Oh Hyongmin 
Published: June 2024

OBJECTIVES:
Catheter malposition after subclavian venous catheterization (SVC) is not uncommon and can lead to serious complications. This study hypothesized that the left access is superior to the right access in terms of catheter malposition after ultrasound-guided infraclavicular SVC due to the asymmetry of the bilateral brachiocephalic veins.

DESIGN:
Parallel-armed randomized controlled trial.

SETTING:
A tertiary referral hospital in Korea.

PATIENTS:
Patients 20–79 years old who were scheduled to undergo SVC under general anesthesia.

INTERVENTIONS:
Patients were randomly assigned to either the left (n = 224) or right (n = 225) SVC group. The primary outcome measure was the overall catheter malposition rate. The secondary outcome measures included catheter malposition rates into the ipsilateral internal jugular and contralateral brachiocephalic veins, other catheterization-related complications, and catheterization performance.

MEASUREMENTS AND MAIN RESULTS:
The catheter malposition rate was lower (10 [4.5%] vs. 31 [13.8%], p = 0.001), especially in the ipsilateral internal jugular vein (9 [4.0%] vs. 24 [10.7%], p = 0.007), in the left SVC group than in the right SVC group. In the left SVC group, catheterization success rates on the first pass (88 [39.3%] vs. 65 [28.9%], p = 0.020) and first-catheterization attempt (198 [88.4%] vs. 181 [80.4%], p = 0.020) were higher whereas times for vein visualization (30 s [18–50] vs. 20 s [13–38], p < 0.001) and total catheterization (134 s [113–182] vs. 132 s [103–170], p = 0.034) were longer. There were no significant differences in other catheterization performance and catheterization-related complications between the two groups.

CONCLUSIONS:
These findings strengthen the rationale for choosing the left access over the right access for ultrasound-guided infraclavicular SVC.
Newborn Dried Blood Spot Folate in Relation to Maternal Self-reported Folic Acid Intake, Autism Spectrum Disorder, and Developmental Delay
Authors: Schmidt Rebecca J. , Goodrich Amanda J. , Delwiche Lora , Hansen Robin L. , Simpson Claire L. , Tancredi Daniel , Volk Heather E. 
Published: June 2024

Background:
Maternal folic acid intake has been associated with decreased risk for neurodevelopmental disorders including autism spectrum disorder (ASD). Genetic differences in folate metabolism could explain some inconsistencies. To our knowledge, newborn folate concentrations remain unexamined.

Methods:
We measured folate in archived newborn dried blood spots of children from the CHARGE (Childhood Autism Risks from Genetics and the Environment) case–control study who were clinically confirmed at 24–60 months to have ASD (n = 380), developmental delay (n = 128), or typical development (n = 247). We quantified monthly folic acid intake from maternally-reported supplements and cereals consumed during pregnancy and 3 months prior. We assessed associations of newborn folate with maternal folic acid intake and with ASD or developmental delay using regression. We stratified estimates across maternal and child MTHFR genotypes.

Results:
Among typically developing children, maternal folic acid intake in prepregnancy and each pregnancy month and prepregnancy prenatal vitamin intake were positively associated with newborn folate. Among children with ASD, prenatal vitamin intake in pregnancy months 2–9 was positively associated with newborn folate. Among children with developmental delay, maternal folic acid and prenatal vitamins during the first pregnancy month were positively associated with neonatal folate. Associations differed by MTHFR genotype. Overall, neonatal folate was not associated with ASD or developmental delay, though we observed associations with ASD in children with the MTHFR 677 TT genotype (odds ratio: 1.76, 95% CI = 1.19, 2.62; P for interaction = 0.08).

Conclusion:
Maternal prenatal folic acid intake was associated with neonatal folate at different times across neurodevelopmental groups. Neonatal folate was not associated with reduced ASD risk. MTHFR genotypes modulated these relationships.
A critical review of health and financial implications of obesity during the COVID-19 pandemic
Authors: Hussain Syed Sadam , Loh Hanyou , Paul Tanya , Paul Tashvin , Njideaka-Kevin Temiloluwa , Bhandari Sushmita , Kumar Harendra , Karam Alvina , Metu Chiamaka , Shupe Ginger , Ferrer Gerardo F. , Katwal Shailendra 
Published: June 2024

The COVID-19 was reported in Wuhan, China, in December 2019. There is a link between increased mortality and obese individuals with the disease. The disease has been claimed to have disproportionately affected non-Hispanic blacks and Hispanics. The rise in food accessibility and the drop in the relative cost of junk food items are the two most significant changes in dietary patterns. Around the world, 2.8 million people die from being overweight or obese, and those with more body fat also have a higher risk of diabetes (44%) and heart disease (23%). Obesity weakens the immune system because adipose cells infiltrate the bone marrow, spleen, and thymus. Obesity was substantially more common among COVID-19 patients who were hospitalized than those who were not hospitalized. Over 900 000 adults in the United States are hospitalized due to a COVID-19 infection. Hospitalizations in 271 700 (30.2%) cases have been attributed to obesity. Obese patients may be experiencing reduced thoracic expansion following bariatric surgery. Less tracheal collapse and air-trapping at end-expiration chest computed tomography (CT) were observed post-surgery, and patients reported reduced dyspnea. COVID-19 is estimated to cost the European Union €13.9 billion in secondary care, with 76% of that cost attributed to treatment for overweight and obese individuals. The average price per hospitalized patient also increased with increasing BMI. Screening for obesity, preventive measures, and recommendations for healthy lifestyle changes should be of the utmost importance to decrease both the health and financial implications of COVID-19.
Mortality and Associated Risk Factors Among People Living With HIV With Kaposi Sarcoma: A5263/AMC066 and A5264/AMC067
Authors: Chagomerana Maganizo B. , Moser Carlee B. , Kang Minhee , Umbleja Triin , Hughes Michael D. , Campbell Thomas B. , Krown Susan E. , Borok Margaret Z. , Samaneka Wadzanai , Ngongondo McNeil , Nyirenda Mulinda , Langat Deborah C. , Hoagland Brenda , Burger Henriette , Busakhala Naftali , Njiru Evangeline , Mwelase Noluthando , Mngqibisa Rosie , Hosseinipour Mina C. 
Published: June 2024

Background:
AIDS-related Kaposi sarcoma (AIDS-KS) remains a leading cause of morbidity and mortality among people living with HIV in Africa. Mortality among people with AIDS-KS on antiretroviral therapy remains high compared with people on antiretroviral therapy who do not have AIDS-KS.

Setting:
People living with HIV with Kaposi sarcoma (KS) who participated in 2 randomized trials (A5263/AMC066 [advanced stage] and A5264/AMC067 [mild-to-moderate stage]) conducted by AIDS Clinical Trials Group/AIDS Malignancy Consortium in low- and middle-income countries.

Methods:
We estimated mortality rates over the trial period. Cox proportional hazards regressions were used to identify baseline characteristics associated with mortality and compared mortality rates between participants who had KS progression within 12 weeks of treatment initiation (early progression of KS [KS-PD]) and those who did not.

Results:
Of the 329 and 189 eligible participants in A5263/AMC066 and A5264/AMC067, 71 (21.6%) and 24 (12.7%) died, respectively. In both trials, hypoalbuminemia was associated with increased hazards of death compared with normal albumin; A5263/AMC066: mild hypoalbuminemia (adjusted hazard ratio [aHR] = 3.01; 95% CI: 1.42 to 6.29), moderate hypoalbuminemia (aHR = 5.11; 95% CI: 2.54 to 10.29), and severe hypoalbuminemia (aHR = 14.58; 95% CI: 6.32 to 35.60), and A5264/AMC067: mild hypoalbuminemia (aHR = 5.66; 95% CI: 1.90 to 16.93) and moderate hypoalbuminemia (aHR = 7.02; 95% CI: 2.57 to 19.15). The rate of death was higher among participants who had early KS-PD than those without early KS-PD in A5263/AMC066 (HR = 5.09; 95% CI: 1.71 to 15.19) but not in A5264/AMC067 (HR = 1.74; 95% CI: 0.66 to 4.62).

Conclusions:
Albumin measurements may be used to identify individuals at higher risk of death after initiating KS treatment and for evaluation of interventions that can reduce AIDS-KS mortality.
Incidental Detection of Lipomatous Hypertrophy of the Interventricular Septum on FDG PET/CT
Authors: Kumar Suraj , Mittal Bhagwant Rai , Kumar Rajender , Singh Harmandeep , Mohindra Satyawati 
Published: June 2024

AbstractCardiac lipomatous hypertrophy is a rare benign condition almost exclusively involving the interatrial septum. Interventricular septum involvement is seldom noted, with only a few documented case reports demonstrating the finding on various modalities such as ECHO, CT, and MRI. FDG PET can be a surrogate marker for lipomatous hypertrophy of the interventricular septum. Here, we describe a case of incidentally detected lipomatous hypertrophy of the interventricular septum on FDG PET/CT in a patient with squamous cell carcinoma of the oropharynx.
Atypical Presentation of Splenic Tissue Mimicking Neuroendocrine Tumor Relapse
Authors: Guarneri Andrea , Rufini Vittoria , Schinzari Giovanni , Rindi Guido , Leccisotti Lucia 
Published: June 2024

Abstract
A 61-year-old man underwent splenopancreasectomy for a 3-cm neuroendocrine tumor of the body of the pancreas (G2, pT1 pN0, Ki67 3%). Five months after surgery 68Ga-DOTATOC PET/CT showed increased radiotracer uptake in a solid tissue of the splenic fossa, possibly referring to a splenosis nodule. After 19 months, a further 68Ga-DOTATOC PET/CT showed a significant functional and dimensional increase of the previously detected tissue and the appearance of a new finding in the left lateral abdominal wall. In the suspicion of neuroendocrine tumor relapse, the patient underwent surgical excision of the documented lesions. Histology showed splenosis in both nodules.
Negative density dependence characterizes mutualistic interactions between birds and fruiting plants across latitudes
Authors: Carlo Tomás A. , Messeder João Vitor S. , Espíndola Wálter D. , Vizzachero Benjamin S. , Boyer Brady W. , Hernández-Mejía Jacqueline , Torres-Páucar E. Adrián , Fontanella Antonio , Pizo Marco A. , Amico Guillermo , Salinas Letty , Arana César , Morán-López Teresa , Morales Juan M. 
Published: June 2024

Negative density dependence (NDD) in biotic interactions of interference such as plant–plant competition, granivory and herbivory are well-documented mechanisms that promote species’ coexistence in diverse plant communities worldwide. Here, we investigated the generality of a novel type of NDD mechanism that operates through the mutualistic interactions of frugivory and seed dispersal among fruit-eating birds and plants. By sampling community-wide frugivory interactions at high spatial and temporal resolution in Pennsylvania, Puerto Rico, Peru, Brazil and Argentina, we evaluated whether interaction frequencies between birds and fruit resources occurred more often (selection), as expected, or below expectations (under-utilization) set by the relative fruit abundance of the fruit resources of each plant species. Our models considered the influence of temporal scales of fruit availability and bird phylogeny and diets, revealing that NDD characterizes frugivory across communities. Irrespective of taxa or dietary guild, birds tended to select fruits of plant species that were proportionally rare in their communities, or that became rare following phenological fluctuations, while they mostly under-utilized abundant fruit resources. Our results demonstrate that negative density-dependence in frugivore–plant interactions provides a strong equalizing mechanism for the dispersal processes of fleshy-fruited plant species in temperate and tropical communities, likely contributing to building and sustaining plant diversity.
This article is part of the theme issue 'Diversitydependence of dispersal: interspecific interactions determine spatial dynamics'.
Deployment and transcriptional evaluation of nitisinone, an FDA-approved drug, to control bed bugs
Authors: Sterkel M. , Tompkin J. , Schal C. , Guerra L. M. , Pessoa G. C. D. , Oliveira P. L. , Benoit J. B. 
Published: June 2024

AbstractBed bugs are blood-feeders that rapidly proliferate into large indoor infestations. Their bites can cause allergies, secondary infections and psychological stress, among other problems. Although several tactics for their management have been used, bed bugs continue to spread worldwide wherever humans reside. This is mainly due to human-mediated transport and their high resistance to several classes of insecticides. New treatment options with novel modes of action are required for their control. In this study, we evaluated the use of nitisinone (NTBC), an FDA-approved drug, for bed bug control in an insecticide-susceptible (HH) and an insecticide-resistant (CIN) population. Although NTBC was lethal to both populations when administered orally or applied topically in very low doses, we observed a slight but significant resistance in the CIN population. Transcriptomic analysis in both populations indicated that NTBC treatment elicited a broad suppression of genes associated with RNA post-transcriptional modifications, translation, endomembrane system, protein post-translational modifications and protein folding. The CIN population exhibited higher ATP production and xenobiotic detoxification. Feeding studies on a mouse model highlight that NTBC could be used as a control method of bed bugs by host treatment. The results demonstrate that NTBC can be used as a new active ingredient for bed bug control by topical or oral treatment and shed light on the molecular mechanisms of suppressed tyrosine metabolism following NTBC treatment.
Cortical inhibitory parvalbumin interneurons exhibit metabolic specializations coordinated by PGC-1α that are lost in rodents and humans after traumatic brain injury
Authors: Quiñones Sadi , Wang Jason C , Kim Elliot , Bottom-Tanzer Samantha , Armbruster Moritz , Macêdo Jéssica K A , Hawkinson Tara , Ribas Roberto , Singh Pankaj K. , Wu Lei , Cantrell Alex R , Kumar Parveen , George Joshy , Tai Albert , Whalen Michael , McConnell Michael J , Sun Ramon C , Gentry Matthew S , Dulla Chris G 
Published: June 2024

AbstractParvalbumin-positive interneurons (PV-INs) regulate neuronal and circuit activity, and their dysfunction is observed across neurological conditions, including traumatic brain injury (TBI), epilepsy, Alzheimer’s disease, and schizophrenia. PV-INs are particularly vulnerable to cell loss, potentially due to their increased metabolic demands arising from their uniquely high level of electrical activity, which render them susceptible to metabolic pressure. Here, we use single-nucleus RNA-sequencing (snRNAseq) data from a rodent model of TBI, as well as human TBI data, and demonstrate PV-INs have unique metabolic specializations that are lost after injury and can be rescued byin vivotreatment with the glycolytic inhibitor, 2-deoxyglucose. We generated a novel PV-IN transcriptional identity module comprised primarily of genes encoding specialized ion channels, metabolic enzymes, and synaptic machinery, that identifies heterogenous subsets of injury-associated PV-INs with loss of PV-IN transcriptional identity. We show that changes in metabolic specialization are coupled to changes in transcriptional identity in PV-INs and implicate the PV-IN-enriched transcriptional co-activator,Ppargc1a, as a key driver of PV-IN transcriptional metabolic dysfunction. We also identify a family of long non-coding RNAs enriched in this subset of transcriptionally dysfunctional PV-INs that negatively correlates with PV-IN metabolic specialization. Lastly, we utilize these tools to interrogate a published human TBI snRNAseq data set and find nearly identical changes, underscoring the importance of PV-IN metabolic dysfunction in the pathology of TBI.
Epigenomic programming of peripheral monocytes determines their transcriptional response to the tumor microenvironment
Authors: Kiss Máté , Halasz Laszlo , Hadadi Eva , Berger Wilhelm K. , Tzerpos Petros , Poliska Szilard , Kancheva Daliya , Debraekeleer Ayla , Brughmans Jan , Elkrim Yvon , Martens Liesbet , Saeys Yvan , Daniel Bence , Czimmerer Zsolt , Laoui Damya , Nagy Laszlo , Van Ginderachter Jo A. 
Published: June 2024

AbstractClassical monocytes are recruited to tumors and undergo transcriptional reprogramming resulting in tumor-promoting functions. Epigenomic features, such as post-translational modification of histones and chromatin accessibility, are key determinants of transcription factor binding and thereby play an important role in determining transcriptional responses to the tissue environment. It is unknown to what extent the epigenetic landscape of peripheral monocytes is rewired by cancer and how this could shape their transcriptional response upon recruitment to the tumor microenvironment. Here we used a combination of genome-wide assays for mRNA expression, chromatin accessibility and multiple histone modifications (H3K4me1, H3K4me3, H3K27ac) in a mouse model to investigate changes in the epigenomic landscape of peripheral monocytes. We then linked these epigenetic alterations to gene expression changes in monocytes occurring in the periphery or during tumor infiltration. We found that the distal tumor caused extensive remodeling of both H3K4me3+promoters and H3K4me1+enhancers in peripheral monocytes. Specifically, this involved the repression of interferon-responsive promoters and enhancers as well as the establishment of enhancers harboring binding motifs for transcription factors downstream of inflammatory and cytokine signaling pathways. The enhancers altered in the periphery could be linked to sustained gene expression changes which were less likely to be reversed in the tumor microenvironment. In addition, genes activated upon tumor infiltration showed prior epigenetic priming in peripheral monocytes. Overall, these results indicate that the epigenomic landscape of peripheral monocytes is altered in response to a distal tumor, and this could shape the transcriptional response of monocytes when they encounter microenvironmental signals upon infiltrating the tumor.