bluuebunny/crossref_metadata_2025_split huggingface dataset:
Availability of Pediatric Emergency Care Coordinators in US Emergency Departments in 2018
Authors: Boggs Krislyn M. , Espinola Janice A. , Sullivan Ashley F. , Li Joyce , Auerbach Marc , Hasegawa Kohei , Samuels-Kalow Margaret E. , Camargo Carlos A. 
Published: April 2023

Objectives
In 2007, the US Institute of Medicine recommended that every emergency department (ED) appoint pediatric emergency care coordinators (PECCs). Despite this recommendation, our national surveys showed that few (17%) US EDs reported at least 1 PECC in 2015. This number increased slightly to 19% in 2016 and 20% in 2017. The current study objectives were to determine the following: percent of US EDs with at least 1 PECC in 2018, factors associated with availability of at least 1 PECC in 2018, and factors associated with addition of at least 1 PECC between 2015 and 2018.

Methods
In 2019, we conducted a survey of all US EDs to characterize emergency care in 2018. Using the National ED Inventory-USA database, we identified 5514 EDs open in 2018. This survey collected availability of at least 1 PECC in 2018. A similar survey was administered in 2016 and identified availability of at least 1 PECC in 2015.

Results
Overall, 4781 (87%) EDs responded to the 2018 survey. Among 4764 EDs with PECC data, 1037 (22%) reported having at least 1 PECC. Three states (Connecticut, Massachusetts, and Rhode Island) had PECCs in 100% of EDs. The EDs in the Northeast and with higher visit volumes were more likely to have at least 1 PECC in 2018 (all P < 0.001). Similarly, EDs in the Northeast and with higher visit volumes were more likely to add a PECC between 2015 and 2018 (all P < 0.05).

Conclusions
The availability of PECCs in EDs remains low (22%), with a small increase in national prevalence between 2015 and 2018. Northeast states report a high PECC prevalence, but more work is needed to appoint PECCs in all other regions.
Overlapping Intravelar Veloplasty Improves the Speech Outcomes in Submucous Cleft Palate
Authors: Lee Seo Koo , Nam Seung Min , Cha Han Gyu , Jung Se A. , Choi Chang Yong , Park Eun Soo 
Published: April 2023

Background
Submucous cleft palate (SMCP) is a subgroup of cleft palate that can present as velopharyngeal insufficiency due to muscle displacement. The pharyngeal flap and Furlow palatoplasty have been introduced to correct SMCP patient with velopharyngeal insufficiency. However, pharyngeal flap and Furlow palatoplasty can occur various complications. We consider the overlapping intravelar veloplasty (IVVP) can overcome these complications. Therefore, we present the speech outcomes of overlapping IVVP for the treatment of patients with SMCP.

Methods
We retrospectively reviewed 12 patients with SMCP underwent overlapping IVVP between April 2016 and October 2018. The patients who underwent speech evaluation, nasometry, and nasoendoscopy before and after surgery and who were followed up for >18 months were enrolled in this study

Results
The average age of the patients was 5 years (range, 3–11 years) and the postoperative follow-up period ranged from 18 to 24 months (mean, 20 months). The preoperative perceptual speech evaluation was moderate and the postoperative evaluation was normal (P < 0.01). The preoperative and postoperative nasalance scores obtained using a nasometer were 37.00 and 12.50, respectively, (P < 0.01). Preoperative and postoperative velopharyngeal movements were grades 3 and 0, respectively, (P < 0.01).

Conclusions
Our study showed that overlapping IVVP could provide successful correction of velopharyngeal insufficiency in patients with SMCP, including relatively old patients.
Extracellular release of damaged mitochondria induced by pre-hematopoietic stem cell transplant conditioning exacerbates graft-versus-host disease
Authors: Vijayan Vijith , Yan Hao , Lohmeyer Juliane K. , Prentiss Kaylin A. , Patil Rachna V. , Barbarito Giulia , Lopez Ivan , Elezaby Aly , Peterson Kolten , Baker Jeanette , Ostberg Nicolai P. , Bertaina Alice , Negrin Robert S. , Mochly-Rosen Daria , Weinberg Kenneth , Haileselassie Bereketeab 
Published: April 2023

AbstractDespite therapeutic advancements, GVHD is a major complication of HSCT. In current models of GVHD, tissue injury induced by cytotoxic conditioning regimens, along with translocation of microbes expressing Pathogen Associated Molecular Patterns (PAMPs), result in activation of host antigen-presenting cells (APC) to stimulate alloreactive donor T lymphocytes. Recent studies have demonstrated that in many pathologic states, tissue injury results in the release of mitochondria from the cytoplasm to the extracellular space. We hypothesized that extracellular mitochondria, which are related to archaebacteria, could also trigger GVHD by stimulation of host APC. We found that clinically relevant doses of radiation or busulfan induced extracellular release of mitochondria by various cell types, including cultured intestinal epithelial cells. Conditioning-mediated mitochondrial release was associated with mitochondrial damage and impaired quality control but did not affect the viability of the cells. Extracellular mitochondria directly stimulated host APCs to express higher levels of MHC-II, co-stimulatory CD86, and pro-inflammatory cytokines, resulting in increased donor T cell activation, and proliferation in mixed lymphocyte reactions. Analyses of plasma from both experimental mice and a cohort of children undergoing HSCT demonstrated that conditioning induced extracellular mitochondrial releasein vivo. In mice undergoing MHC mismatched HSCT, administration of purified syngeneic extracellular mitochondria increased host APC activation and exacerbated GVHD. Our data suggests that pre-HSCT conditioning results in extracellular release of damaged mitochondria which increase alloreactivity and exacerbate GVHD. Therefore, decreasing the extracellular release of damaged mitochondria following conditioning could serve as a novel strategy for GVHD prevention.
Aspiration thrombectomy for patients with stroke and late onset to treatment: a subset analysis of the COMPLETE registry
Authors: Hassan Ameer E. , Fifi Johanna T. , Zaidat Osama O. ,   COMPLETE Study Investigators
Published: April 2023

AbstractBackgroundThe purpose of this study was to report the safety and performance of aspiration thrombectomy for patients with acute ischemic stroke (AIS) due to anterior circulation large vessel occlusion (LVO) and late onset to treatment.MethodsThis is a retrospective subset analysis of a global prospective multicenter registry (COMPLETE) that enrolled adults with AIS due to LVO and a pre-stroke modified Rankin Scale score (mRS) of 0 or 1 who were treated with aspiration thrombectomy with the Penumbra System. This subset analysis included all patients in the registry who had anterior circulation LVO, an Alberta Stroke Program Early CT Score of at least 6, and late onset to treatment (>6 hours from stroke onset to puncture).ResultsOf the 650 patients in the COMPLETE registry, 167 were included here. The rate of successful revascularization at the end of the procedure was 83.2% (139/167), the rate of good functional outcome (mRS 0-2) at 90 days was 55.4% (87/157), and the all-cause mortality rate at 90 days was 14.4% (24/167). No device-related serious adverse events (SAEs) occurred.Procedure-related SAEs occurred in 9 patients (5.4%) within 24 hours and in 12 patients (7.2%) overall. No significant difference was detected between the outcomes of patients with an onset to puncture time of greater than 6 hours and less than or equal to 12 hours and the outcomes of patients with an onset to puncture time of greater than 12 hours.ConclusionsFor patients with AIS due to anterior circulation LVO and with late onset to treatment, aspiration thrombectomy with the Penumbra System appears to be safe and effective. The rates of good functional outcome and all-cause mortality from this study compared favorably with those rates from the medical management arms of the DAWN and DEFUSE-3 studies.RegistrationURL:https://www.clinicaltrials.gov; Unique identifier:NCT03464565.
Single-cell RNA-sequencing of PBMCs from SAVI patients reveals disease-associated monocytes with elevated integrated stress response
Authors: de Cevins Camille , Delage Laure , Batignes Maxime , Riller Quentin , Luka Marine , Remaury Anne , Sorin Boris , Fali Tinhinane , Masson Cécile , Hoareau Bénédicte , Meunier Catherine , Parisot Mélanie , Zarhrate Mohammed , Pérot Brieuc P. , García-Paredes Víctor , Carbone Francesco , Canard Luc , Boussard Charlotte , Crickx Etienne , Guillemot Jean-Claude , Frémond Marie-Louise , Neven Bénédicte , Boldina Galina , Augé Franck , Alain Fischer , Didier Michel , Rieux-Laucat Frédéric , Ménager Mickael M. 
Published: April 2023

AbstractGain-of-function mutations inSTING1, which encodes the Stimulator of Interferon Gene (STING), result in a severe autoinflammatory disease termed STING-associated vasculopathy with onset in infancy (SAVI). Although elevated type I interferon (IFN) production is thought to be the leading cause of the symptoms observed in patients, STING can induce a set of pathways, which roles in the onset and severity of SAVI, remain to be elucidated. To address this point, we compared a single-cell RNA sequencing (scRNA-seq) dataset of peripheral blood mononuclear cells (PBMCs) from SAVI patients to a dataset of healthy PBMCs treated with recombinant IFN-β. We revealed a loss of mucosal associated invariant T cells and CD56brightnatural killer cells in SAVI patients, not observed in IFN-β-treated PBMC. Patients’ T cells present markers of early activation, associated with markers of senescence and apoptosis. Inferring cell-to-cell communication from scRNA-seq predicted monocytes as potential drivers of this T cell phenotype. Furthermore, scRNA-seq clustering identified a patient-specific subset of monocytes, expressing a strong integrated stress response (ISR), and highCCL3,CCL4andIL-6. It also pinpointed to a patient with lower ISR, allowing us to identify a secondary mutation in PERK, recently shown to be activated by STING to trigger the ISR. Finally, based on the identification of this patient-specific subset of monocytes and the exploration of IFN-β stimulated PBMCs from healthy donors, we developed a strategy to propose a transcriptomic signature specific of STING activation and independent of type I IFN response. Altogether, these results provide a deeper understanding of SAVI at the cellular and molecular levels.
Mapping of the gene network that regulates glycan clock of ageing
Authors: Frkatović-Hodžić Azra , Miškec Karlo , Mijakovac Anika , Nostaeva Arina , Sharapov Sodbo Z. , Landini Arianna , Haller Toomas , van den Akker Erik , Sharma Sapna , Cuadrat Rafael R. C. , Mangino Massimo , Li Yong , Keser Toma , Rudman Najda , Štambuk Tamara , Pučić-Baković Maja , Trbojević-Akmačić Irena , Gudelj Ivan , Štambuk Jerko , Pribić Tea , Radovani Barbara , Tominac Petra , Fischer Krista , Beekman Marian , Wuhrer Manfred , Gieger Christian , Schulze Matthias B. , Wittenbecher Clemens , Polasek Ozren , Hayward Caroline , Wilson James F. , Spector Tim D. , Köttgen Anna , Vučković Frano , Aulchenko Yurii S. , Vojta Aleksandar , Krištić Jasminka , Klarić Lucija , Zoldoš Vlatka , Lauc Gordan 
Published: April 2023

AbstractGlycans are an essential structural component of Immunoglobulin G (IgG) that modulate its structure and function. However, regulatory mechanisms behind this complex posttranslational modification are not well known. Previous genome-wide association studies (GWAS) identified 29 genomic regions involved in regulation of IgG glycosylation, but only a few were functionally validated. One of the key functional features of IgG glycosylation is the addition of galactose (galactosylation). We performed GWAS of IgG galactosylation (N=13,705) and identified 16 significantly associated loci, indicating that IgG galactosylation is regulated by a complex network of genes that extends beyond the galactosyltransferase enzyme that adds galactose to IgG glycans. Gene prioritization identified 37 candidate genes. Using a recently developed CRISPR/dCas9 system we manipulated gene expression of candidate genes in thein vitroIgG expression system. Up- and downregulation of three genes,EEF1A1, MANBAandTNFRSF13B, changed the IgG glycome composition, which confirmed that these three genes are involved in IgG galactosylation in thisin vitroexpression system.
Non-obese lipedema patients show a distinctly altered Quantitative Sensory Testing profile with high diagnostic potential
Authors: Dinnendahl Rebecca , Tschimmel Dominik , Löw Vanessa , Cornely Manuel , Hucho Tim 
Published: April 2023

AbstractBackgroundLipedema is a widespread severe chronic disease affecting mostly women. Characterized by painful bilateral fat accumulation in extremities sparing hands and feet, objective measurement-based diagnosis is currently missing. We tested for characteristic psychometric and/or sensory alterations including pain and for their potential for medical routine diagnostic.MethodsPain-psychometry were assessed using the German Pain Questionnaire. Sensory sensitivity toward painful and non-painful stimuli was characterized in non-obese lipedema patients and matched controls using the validated QST-protocol of the German Research Network on Neuropathic Pain.ResultsLipedema patients showed no overt psychometric abnormalities. Pain was reported as somatic rather than psychosomatic-aversive. All QST measurements were normal, but the pressure pain threshold (PPT) was twofold reduced and the vibration detection threshold (VDT) was two and a half times increased. Both thresholds were selectively altered at the affected thigh but not the unaffected hand. ROC-analysis of the combination of PPT and VDT of thigh versus hand into a PVTH-score shows high sensitivity and specificity, categorizing correctly 96.5% of the participants as lipedema patients or healthy controls. Bayesian inference analysis corroborated the diagnostic potential of a combined PVTH score.ConclusionWe propose to assess PPT and VDT at the painful thigh and the pain-free hand. Combination in a PVTH-score may allow a convenient lipedema diagnosis early during disease development.Trial RegistrationGerman Clinical Trials Register (DRKS00030509)FundingThe project was funded by the DFG (459479161).
Complete genome sequences of the species type strainsSinorhizobium garamanticumLMG 24692TandSinorhizobium numidicumLMG 27395Tand CIP 109850T
Authors: Kaur Sabhjeet , Espinosa-Sáiz Daniel , Velázquez Encarna , Menéndez Esther , diCenzo George C 
Published: April 2023

AbstractThe genusSinorhizobiumcomprises rhizobia that fix nitrogen in symbiosis with legumes. To support taxonomic studies of this genus and of rhizobia more broadly, we report complete genome sequences and annotations for the species type strainsSinorhizobium garamanticumLMG 24692TandSinorhizobium numidicumLMG 27395Tand CIP 109850T. Average nucleotide identity and core-genome phylogenetic analyses confirm thatS. garamanticumandS. numidicumrepresent distinct species.
Association between SARS-CoV-2 and metagenomic content of samples from the Huanan Seafood Market
Authors: Bloom Jesse D. 
Published: April 2023

ABSTRACTThe role of the Huanan Seafood Market in the early SARS-CoV-2 outbreak remains unclear. Recently the Chinese CDC released data from deep sequencing of environmental samples collected from the market after it was closed on January-1-2020 (Liu et al. 2023a). Prior to this release, Crits-Christophet al. (2023) analyzed data from a subset of the samples. Both studies concurred that the samples contained genetic material from a variety of species, including some like raccoon dogs that are susceptible to SARS-CoV-2. However, neither study systematically analyzed the relationship between the amount of genetic material from SARS-CoV-2 and different animal species. Here I implement a fully reproducible computational pipeline that jointly analyzes the number of reads mapping to SARS-CoV-2 and the mitochondrial genomes of chordate species across the full set of samples. I validate the presence of genetic material from numerous species, and calculate mammalian mitochondrial compositions similar to those reported by Crits-Christophet al. (2023). However, the number of SARS-CoV-2 reads is not consistently correlated with reads mapping to non-human susceptible species. For instance, 14 samples have >20% of their chordate mitochondrial material from raccoon dogs, but only one of these samples contains any SARS-CoV-2 reads, and that sample only has 1 of∼200,000,000 reads mapping to SARS-CoV-2. Instead, SARS-CoV-2 reads are most correlated with reads mapping to various fish, such as catfish and largemouth bass. These results suggest that while metagenomic analysis of the environmental samples is useful for identifying animals or animal products sold at the market, co-mingling of animal and viral genetic material is unlikely to reliably indicate whether any animals were infected by SARS-CoV-2.
Capsular polysaccharide-mediated protein loading onto extracellular membrane vesicles of a fish intestinal bacterium,Shewanella vesiculosaHM13
Authors: Kamasaka Kouhei , Kawamoto Jun , Tsudzuki Taiku , Liu Yuying , Imai Tomoya , Ogawa Takuya , Kurihara Tatsuo 
Published: April 2023

ABSTRACTBacterial extracellular membrane vesicles (EMVs) play various physiologically important roles mediated by cargo proteins. However, our understanding of the molecular mechanism underlying cargo loading onto EMVs is limited. In this study, we analyzed the mechanism of cargo protein loading onto EMVs from a fish intestinal Gram-negative bacterium,Shewanella vesiculosaHM13. This strain secretes EMVs carrying a major cargo protein, P49. Near the P49 gene, we found genes having homology to genes involved in protein secretion and surface polysaccharide-chain synthesis. Among them, the deletion of genes encoding homologs of a flippase involved in bacterial extracellular polysaccharide synthesis (HM3343), phosphoethanolamine transferase (HM3344), and glycerophosphodiester phosphodiesterase (HM3345) resulted in the loss of capsular polysaccharide (CPS) of EMVs. We conducted anin vitroP49 loading assay onto P49-free EMVs to examine whether P49 was loaded onto the EMVs via its interaction with the CPS of the EMVs. We found that purified P49 was loaded onto EMVs harboring CPSin vitro, whereas it was not loaded onto EMVs from the mutants lacking CPS production due to the loss of HM3343, HM3344, and HM3345. Transmission electron microscopy of EMVs loaded with P49in vitroandin vivoshowed spherical nanoparticles around the EMVs, whereas such particles were not observed for EMVs without loaded P49, implying that P49 constitutes those particles on the surface of EMVs. These results indicate that P49 is loaded onto EMVs via its interaction with the CPS of EMVs.IMPORTANCEElucidating the mechanisms of cargo loading onto bacterial extracellular membrane vesicles (EMVs) is important to understand their biogenesis and to develop their applications. Here, we show that the major cargo protein of EMVs from a fish intestinal Gram-negative bacterium,Shewanella vesiculosaHM13, is loaded onto EMVs through its interaction with capsular polysaccharide (CPS) of EMVs. Genes involved in CPS synthesis were also identified. To our knowledge, there have been no reports describing the cargo protein-loading mechanism in which CPS serves as the protein-binding scaffold for EMVs. Thus, this study represents a new mode of protein loading onto EMVs. The results deepen our understanding of cargo loading onto EMVs and would contribute to development of their applications.
Regional Prevalence of Hypertension Among People Diagnosed with Diabetes in Africa, A Systematic Review and Meta-analysis
Authors: Hinneh Thomas , Akyirem Samuel , Bossman Irene Fosuhemaa , Lambongang Victor , Ofori-Aning Patriot , Ogungbe Oluwabunmi , Commodore Mensah Yvonne 
Published: April 2023

AbstractBackgroundHypertension and diabetes share common pathophysiological mechanisms and hence have a high likelihood of co-occurring. The co-existence of hypertension and diabetes increases cardiovascular disease risk and healthcare spending. This review aimed to estimate the burden of hypertension among people with diabetes in African countries.MethodsThis review was registered in the International Prospective Register of Systematic Reviews (CRD42021256221). We searched PubMed, Embase, and Hinari databases to identify peer-reviewed articles which provided data on the prevalence of hypertension in people diagnosed with diabetes in Africa. Studies included in the review used different diagnostic criteria and thresholds for hypertension and diabetes diagnosis. We quantified the prevalence of hypertension using random-effects models. We applied generalized linear mixed models with logit transformation to compute regional and overall pooled prevalence and estimate heterogeneity (I2).ResultsOut of 3810 studies retrieved from various sources, 41 met the inclusion criteria with sample sizes ranging from 80 - 116726. The mean age was 58 (± 11) years and 56% were women. The pooled prevalence of hypertension in people diagnosed with diabetes was 58.1% [95% CI: 52.0% - 63.2%]. By African region, Central Africa had the highest hypertension prevalence; 77.6% [95% CI: 53.0% - 91.4%], South Africa 69.1% [95% CI: 59.8% - 77.1%;], North Africa 63.4% [95% CI: 37.1% - 69.1%;], West Africa 51.5% [95% CI: 41.8% - 61.1%] and East Africa 53.0% [95% CI: 45.8% - 59.1%]. Increasing age, being overweight/obese, being employed, longer duration of diabetes, urban residence, and male sex were associated with a higher likelihood of hypertension diagnosis (p-values<0.005).ConclusionThe high prevalence of hypertension among people with diabetes in Africa, highlights the critical need for an integrated differentiated service delivery to improve and strengthen primary care and prevent cardiovascular disease. Findings from this meta-analysis may inform the delivery of interventions to prevent premature cardiovascular disease deaths among persons in African countries.
Analysis of DNA transposition by DNA transposases in human cells
Authors: Bigot Yves , Yamada Makiko , Mueller Helen , Morell Victor , Alves Sabine , Lecomte Thierry , Kentsis Alex 
Published: April 2023

AbstractThis manuscript discusses the recent report “Cognate restriction of transposition bypiggyBac-like proteins” inNucleic Acids Researchby Beckermann et al and related recent publications about the inability to detect DNA transposition activity of human domesticated DNA transposase PGBD5. Measuring DNA transposition activity of transposases in human cells, where these enzymes can act on endogenous genomic substrates and induce DNA damage, is complicated by these and other cellular responses. Possible reasons for the discordant findings of Beckermann et al with prior independent reports of PGBD5 DNA transposition by Helou et al and Henssen et al and specific details of experimental methods in human cells are presented. In particular, by using independent experiments that reproduce PGBD5-mediated genomic integration, we demonstrate how supraphysiologic and ectopic overexpression of PGBD5 can cause DNA damage and cell death, and artifactual loss of apparent activity in clonogenic transposition reporter assays. While PGBD5 can support apparent DNA transposition, its cellular activity predominantly involves double-strand DNA breaks, deletions and other DNA rearrangements. We discuss the implications of this phenomenon for the interpretation of experimental assays and activities of domesticated DNA transposases.