bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does Myelopathy Increase the Morbidity and Mortality of Elective Single-Level Anterior Cervical Discectomy and Fusion? An Updated Propensity-Matched Analysis of 3938 Patients From the American College of Surgeons National Surgical Quality Improvement Program Database
Authors: Alomari Safwan , Lubelski Daniel , Sacino Amanda N , Sciubba Daniel M , Bydon Ali 
Published: February 2021

Abstract

BACKGROUND
Myelopathy is thought to be associated with higher morbidity and mortality after anterior cervical discectomy and fusion (ACDF); however, the literature investigating this association has limitations.

OBJECTIVE
To investigate the influence of myelopathy on early perioperative complications of elective single-level ACDF.

METHODS
Patients who underwent ACDF between 2016 and 2018 were reviewed from the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database. Propensity score matching analysis was used.

RESULTS
Twenty percent of the cohort was myelopathic. These patients were significantly older, had more comorbidities, more likely to be functionally dependent, and to undergo emergency surgery when compared to the nonmyelopathic cohort. When 1969 myelopathic patients were 1:1 propensity matched with nonmyelopathic patients, there was no difference between the myelopathic and nonmyelopathic patients in incidence of postoperative intensive care unit admission or death. Patients in the myelopathic group were significantly more likely to have a nonhome discharge and less likely to be discharged on the first postoperative day. Myelopathic patients had a higher rate of return to operating room within the same admission (2.2%) as well as a higher unplanned readmission rate (4.2%). The total operation time (143 min) and average length of hospital stay (52 h) were significantly higher in the myelopathic group when compared to the nonmyelopathic group (117 min) and (33 h), respectively.

CONCLUSION
Patients with myelopathy who undergo elective single-level ACDF have higher risks of several perioperative events including longer operative time, longer hospital stay, higher return to operating room, and unplanned readmission rates, when compared to nonmyelopathic patients. On the other hand, myelopathic patients did not exhibit higher mortality rate.
Clinical utility of comprehensive genomic profiling in central nervous system tumors of children and young adults
Authors: Ji Jianling , Kaneva Kristiyana , Hiemenz Matthew C , Dhall Girish , Davidson Tom Belle , Erdreich-Epstein Anat , Hawes Debra , Hurth Kyle , Margol Ashley S , Mathew Anna J , Robison Nathan J , Schmidt Ryan J , Tran Hung N , Judkins Alexander R , Cotter Jennifer A , Biegel Jaclyn A 
Published: February 2021

Abstract

Background
Recent large-scale genomic studies have revealed a spectrum of genetic variants associated with specific subtypes of central nervous system (CNS) tumors. The aim of this study was to determine the clinical utility of comprehensive genomic profiling of pediatric, adolescent and young adult (AYA) CNS tumors in a prospective setting, including detection of DNA sequence variants, gene fusions, copy number alterations (CNAs), and loss of heterozygosity.

Methods
OncoKids, a comprehensive DNA- and RNA-based next-generation sequencing (NGS) panel, in conjunction with chromosomal microarray analysis (CMA) was employed to detect diagnostic, prognostic, and therapeutic markers. NGS was performed on 222 specimens from 212 patients. Clinical CMA data were analyzed in parallel for 66% (146/222) of cases.

Results
NGS demonstrated clinically significant alterations in 66% (147/222) of cases. Diagnostic markers were identified in 62% (138/222) of cases. Prognostic information and targetable genomic alterations were identified in 22% (49/222) and 18% (41/222) of cases, respectively. Diagnostic or prognostic CNAs were revealed by CMA in 69% (101/146) of cases. Importantly, clinically significant CNAs were detected in 57% (34/60) of cases with noncontributory NGS results. Germline cancer predisposition testing was indicated for 27% (57/212) of patients. Follow-up germline testing was performed for 20 patients which confirmed a germline pathogenic/likely pathogenic variant in 9 cases: TP53 (2), NF1 (2), SMARCB1 (1), NF2 (1), MSH6 (1), PMS2 (1), and a patient with 47,XXY Klinefelter syndrome.

Conclusions
Our results demonstrate the significant clinical utility of integrating genomic profiling into routine clinical testing for pediatric and AYA patients with CNS tumors.
Human Adenovirus 11 in 2 Renal Transplant Recipients: Suspected Donor-Derived Infection
Authors: Sherman Amy C , Lu Xiaoyan , Schneider Eileen , Langston Amelia , Ellis Carla L , Pastan Stephen , Bhatnagar Julu , Reagan-Steiner Sarah , Annambhotla Pallavi , Lindstrom Stephen , Mehta Aneesh , Pouch Stephanie M , Sexton Marybeth E 
Published: February 2021

Abstract

Background
Human adenovirus (HAdV) infections can lead to high mortality in solid organ transplant (SOT) recipients, with rare reports of donor-derived infection.

Methods
Two renal transplant recipients with HAdV-11 infection who received kidneys from the same donor are described. Whole-genome sequencing (WGS) was performed.

Results
WGS showed 100% nucleotide sequence identity for the 2 HAdV-11 isolates. The patients presented with distinct clinical syndromes, and both were treated with brincidofovir.

Conclusions
Donor-derived HAdV infection is presumed to be low; however, disseminated HAdV in SOT recipients can be severe, and clinicians should be aware of the clinical course and treatment options.
Disempowerment through the Backdoor: The Impact of Populist Parties on the National Parliament in Poland
Authors: Maatsch Aleksandra 
Published: February 2021

AbstractDo populist governments disempower parliaments? If so, which strategies do they employ to do it? The empirical analysis here concerns two legislative periods in Poland: T1 2011–2015 (centre-right coalition, populist actors in the opposition) and T2 2015–2018 (populist government). The article traces changes in formal rules regulating scrutiny and law-making but also how these rules were interpreted and exercised. The article addresses the following explanatory factors: position in government, strength of parliamentary formal provisions and the readiness of political actors to revise institutional competences. The article shows that although changes to formal parliamentary powers were minor, disempowerment of the legislative was profound. The outcome has actually been achieved through radical changes in parliamentary practices regarding both law-making and scrutiny.
Deconstructing and reconstructing joint hypermobility on an evo-devo perspective
Authors: Castori Marco 
Published: February 2021

Abstract
Joint hypermobility is a common characteristic in humans. Its non-casual association with various musculoskeletal complaints is known and currently defined “the spectrum”. It includes hypermobile Ehlers–Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD). hEDS is recognized by a set of descriptive criteria, while HSD is the background diagnosis for individuals not fulfilling these criteria. Little is known about the aetiopathogenesis of the spectrum. It may be interpreted as a complex trait according to the integration model. Particularly, the spectrum is common in the general population, affects morphology, presents extreme clinical variability and is characterized by marked sex bias without a clear Mendelian or hormonal explanation. Joint hypermobility and the other hEDS systemic criteria are intended as qualitative derivatives of continuous traits of normal morphological variability. The need for a minimum set of criteria for hEDS diagnosis implies a tendency to co-vary of these underlying continuous traits. In evolutionary biology, such a co-variation (i.e. integration) is driven by multiple forces, including genetic, developmental, functional and environmental/acquired interactors. The aetiopathogenesis of the spectrum may be resolved by a deeper understanding of phenotypic variability, which superimposes on normal morphological variability.
Association between socioeconomic status and longitudinal sleep quality patterns mediated by depressive symptoms
Authors: Lee Ga Bin , Kim Hyeon Chang , Jeon Ye Jin , Jung Sun Jae 
Published: February 2021

Abstract

Study Objectives
We aimed to examine whether associations between socioeconomic status (SES) and longitudinal sleep quality patterns are mediated by depressive symptoms.

Methods
We utilized data on 3347 participants in the Korean Genome and Epidemiology Study aged 40–69 years at baseline from 2001 to 2002 who were followed up for 16 years. A group-based modeling approach was used to identify sleep quality trajectories using the Pittsburgh Sleep Quality Index (years 2, 6, 8, 10, and 12). Educational attainment (college graduated or less), monthly household income (≥$2500 or less), and occupation (unemployed, manual labor, and professional labor) at baseline (year 0) were used for analyses. Depressive symptoms were assessed using Beck’s Depression Inventory at year 4. Associations between SES and sleep quality patterns were examined using a multinomial logistic regression model. The mediation effect of depressive symptoms was further examined using PROC CAUSALMED.

Results
We identified five distinct sleep quality trajectories: “normal-stable” (n = 1697), “moderate-stable” (n = 1157), “poor-stable” (n = 320), “developing to poor” (n = 84), and “severely poor-stable” (n = 89). Overall, associations between SES levels and longitudinal sleep patterns were not apparent after full adjustment for sociodemographic and lifestyle factors measured at baseline. Depressive symptoms, however, tended to fully mediate associations between SES levels and sleep quality patterns (odds ratio range for indirect effects of depressive symptoms: for education, 1.05-1.17; for income, 1.05-1.15).

Conclusion
A significant mediating role for depressive symptoms between SES levels and longitudinal sleep quality warrants consideration among mental healthcare professionals.
Restless sleep disorder in children with NREM parasomnias
Authors: Senel Gulcin Benbir , Kochan Kizilkilic Esra , Karadeniz Derya 
Published: February 2021

Abstract

Study objectives
Restless sleep disorder (RSD) is a newly defined sleep disorder in the pediatric age group. Here, we investigated the frequency of RSD and the sleep characteristics in children with NREM (non-rapid eye movements) parasomnias associated with RSD.

Methods
We analyzed all patients with NREM parasomnias for the last 1 year, and investigated the clinical and polysomnographic characteristics.

Results
Twenty-eight children with NREM parasomnias and age- and gender-matched 20 healthy children were analyzed. The diagnosis of RSD was made in eight children with NREM parasomnias (28.6%), and none of the children had RSD in controls (p = 0.008). The most common diagnosis among children with RSD was somnambulism (six children), but not significantly (p = 0.308). Sleep efficiency was lower in children with RSD than those without RSD (p = 0.033). In cyclic alternating pattern analysis (CAP), CAP rate, durations and the indices of phases A1, A2, and A3 were significantly higher in children with NREM parasomnias in compared to controls. CAP parameters between children with or without RSD; however, were similar, except for higher index of phase A3 in children with RSD, suggesting arousal reactions accompanying RSD.

Conclusions
We demonstrated that RSD was present in almost one third of the children with NREM parasomnias. Sleep quality was worse in children with NREM parasomnias and RSD. An increase in sleep instability compatible with NREM parasomnia was present, while an increased phase A3 in RSD was remarkable. RSD is associated with a worse sleep quality and increased arousals, and should be questioned in children with NREM parasomnias.
Effects of six weeks of chronic sleep restriction with weekend recovery on cognitive performance and wellbeing in high-performing adults
Authors: Smith Michael G , Wusk Grace C , Nasrini Jad , Baskin Pamela , Dinges David F , Roma Peter G , Basner Mathias 
Published: February 2021

AbstractChronic sleep loss is associated with escalating declines in vigilant attention across days of sleep restriction. However, studies exceeding 2 weeks of chronic sleep loss are scarce, and the cognitive performance outcomes assessed are limited. We assessed the effects of 6 weeks of chronic sleep restriction on a range of cognitive domains in 15 high-performing individuals (38.5 ± 8.2 years, 6 women) confined to small space in groups of 4. Sleep opportunities were limited to 5 h on weekdays and 8 h on weekends. Individual sleep–wake patterns were recorded with actigraphy. Neurobehavioral performance was assessed in evenings with Cognition, a computerized battery of ten tests assessing a range of cognitive domains. There were some small to moderate effects of increasing sleep debt relative to pre-mission baseline, with decreases in accuracy across cognitive domains (standardized β = –0.121, p = 0.001), specifically on tests of spatial orientation (β = –0.289, p = 0.011) and vigilant attention (β = –0.688, p &lt; 0.001), which were not restored by two nights of weekend recovery sleep. Cognitive and subjective decrements occurred despite occasional daytime napping in breach of study protocol, evening testing around the circadian peak, and access to caffeine before 14:00. Sensorimotor speed, spatial learning and memory, working memory, abstraction and mental flexibility, emotion identification, abstract reasoning, cognitive throughput, and risk decision making were not significantly affected by sleep debt. Taken together with modest lower subjective ratings of happiness and healthiness, these findings underline the importance of sufficient sleep, on both an acute and chronic basis, for performance in selected cognitive domains and subjective wellbeing in operationally relevant environments.
The Role of Hepatic Vagal Tone in Ozone-Induced Metabolic Dysfunction in the Liver
Authors: Colonna Catherine H , Henriquez Andres R , House John S , Motsinger-Reif Alison A , Alewel Devin I , Fisher Anna , Ren Hongzu , Snow Samantha J , Schladweiler Mette C , Miller Desinia B , Miller Colette N , Kodavanti Prasada Rao S , Kodavanti Urmila P 
Published: February 2021

AbstractAir pollution has been associated with metabolic diseases and hepatic steatosis-like changes. We have shown that ozone alters liver gene expression for metabolic processes through neuroendocrine activation. This study aimed to further characterize ozone-induced changes and to determine the impact of hepatic vagotomy (HV) which reduces parasympathetic influence. Twelve-week-old male Wistar-Kyoto rats underwent HV or sham surgery 5–6 days before air or ozone exposure (0 or 1 ppm; 4 h/day for 1 or 2 days). Ozone-induced lung injury, hyperglycemia, glucose intolerance, and increases in circulating cholesterol, triglycerides, and leptin were similar in rats with HV and sham surgery. However, decreases in circulating insulin and increased HDL and LDL were observed only in ozone-exposed HV rats. Ozone exposure resulted in changed liver gene expression in both sham and HV rats (sham &gt; HV), however, HV did not change expression in air-exposed rats. Upstream target analysis revealed that ozone-induced transcriptomic changes were similar to responses induced by glucocorticoid-mediated processes in both sham and HV rats. The directionality of ozone-induced changes reflecting cellular response to stress, metabolic pathways, and immune surveillance was similar in sham and HV rats. However, pathways regulating cell-cycle, regeneration, proliferation, cell growth, and survival were enriched by ozone in a directionally opposing manner between sham and HV rats. In conclusion, parasympathetic innervation modulated ozone-induced liver transcriptional responses for cell growth and regeneration without affecting stress-mediated metabolic changes. Thus, impaired neuroendocrine axes and parasympathetic innervation could collectively contribute to adverse effects of air pollutants on the liver.
Organophosphate Flame Retardants, Highly Fluorinated Chemicals, and Biomarkers of Placental Development and Disease During Mid-Gestation
Authors: Varshavsky Julia R , Robinson Joshua F , Zhou Yan , Puckett Kenisha A , Kwan Elaine , Buarpung Sirirak , Aburajab Rayyan , Gaw Stephanie L , Sen Saunak , Gao Songmei , Smith Sabrina Crispo , Park June-Soo , Zakharevich Igor , Gerona Roy R , Fisher Susan J , Woodruff Tracey J 
Published: February 2021

Abstract
Perfluoroalkyl and polyfluoroalkyl substances (PFASs) and organophosphate flame retardants (OPFRs) are chemicals that may contribute to placenta-mediated complications and adverse maternal-fetal health risks. Few studies have investigated these chemicals in relation to biomarkers of effect during pregnancy. We measured 12 PFASs and four urinary OPFR metabolites in 132 healthy pregnant women during mid-gestation and examined a subset with biomarkers of placental development and disease (n = 62). Molecular biomarkers included integrin alpha-1 (ITGA1), vascular endothelial-cadherin (CDH5), and matrix metalloproteinase-1 (MMP1). Morphological endpoints included potential indicators of placental stress and the extent of cytotrophoblast (CTB)-mediated uterine artery remodeling. Serum PFASs and urinary OPFR metabolites were detected in ∼50%–100% of samples. The most prevalent PFASs were perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), and perfluorooctane sulfonic acid (PFOS), with geometric mean (GM) levels of ∼1.3–2.8 (95% confidence limits from 1.2–3.1) ng/ml compared to ≤0.5 ng/ml for other PFASs. Diphenyl phosphate (DPhP) and bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) were the most prevalent OPFR metabolites, with GMs of 2.9 (95% CI: 2.5–3.4) and 3.6 (95% CI: 2.2–3.1) ng/ml, respectively, compared to &lt;1 ng/ml for bis(2-chloroethyl) phosphate (BCEP) and bis(1-chloro-2-propyl) phosphate (BCIPP). We found inverse associations of PFASs or OPFRs with ITGA1 or CDH5 immunoreactivity and positive associations with indicators of placental stress in multiple basal plate regions, indicating these chemicals may contribute to abnormal placentation and future health risks. Associations with blood pressure and lipid concentrations warrant further examination. This is the first study of these chemicals with placental biomarkers measured directly in human tissues and suggests specific biomarkers are sensitive indicators of exposure during a vulnerable developmental period.
Genome Sequence Resource of Phomopsis longicolla YC2-1, a Fungal Pathogen Causing Phomopsis Stem Blight in Soybean
Authors: Zhao Xiaolin , Zhang Zhichao , Zheng Sujiao , Ye Wenwu , Zheng Xiaobo , Wang Yuanchao 
Published: February 2021

Diaporthe-Phomopsis disease complex causes considerable yield losses in soybean production worldwide. As one of the major pathogens, Phomopsis longicolla T. W. Hobbs (syn. Diaporthe longicolla) is not only the primary agent of Phomopsis seed decay but is also one of the agents of Phomopsis pod and stem blight and Phomopsis stem canker. We performed both PacBio long-read sequencing and Illumina short-read sequencing and obtained a genome assembly for the strain P. longicolla YC2-1, which was isolated from soybean stem with Phomopsis stem blight disease. The 63.1 Mb genome assembly contains 87 scaffolds, with a minimum, maximum, and N50 scaffold length of 20 kb, 4.6 Mb, and 1.5 Mb respectively, and a total of 17,407 protein-coding genes. The high-quality data expand the genomic resource of P. longicolla species and will provide a solid foundation for a better understanding of their genetic diversity and pathogenic mechanisms. [Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
TRAPPC13 Is a Novel Target of Mesorhizobium amorphae Type III Secretion System Effector NopP
Authors: Liu Dongying , Luo Yantao , Zheng Xiaofeng , Wang Xinye , Chou Minxia , Wei Gehong 
Published: February 2021

Similar to pathogenic bacteria, rhizobia can inject effector proteins into host cells directly to promote infection via the type III secretion system (T3SS). Nodulation outer protein P (NopP), a specific T3SS effector of rhizobia, plays different roles in the establishment of multiple rhizobia-legume symbiotic systems. Mesorhizobium amorphae CCNWGS0123 (GS0123), which infects Robinia pseudoacacia specifically, secretes several T3SS effectors, including NopP. Here, we demonstrate that NopP is secreted through T3SS-I of GS0123 during the early stages of infection, and its deficiency decreases nodule nitrogenase activity of R. pseudoacacia nodules. A trafficking protein particle complex subunit 13–like protein (TRAPPC13) has been identified as a NopP target protein in R. pseudoacacia roots by screening a yeast two-hybrid library. The physical interaction between NopP and TRAPPC13 is verified by bimolecular fluorescence complementation and coimmunoprecipitation assays. In addition, subcellular localization analysis reveals that both NopP and its target, TRAPPC13, are colocalized on the plasma membrane. Compared with GS0123-inoculated R. pseudoacacia roots, some genes associated with cell wall remodeling and plant innate immunity down-regulated in ΔnopP-inoculated roots at 36 h postinoculation. The results suggest that NopP in M. amorphae CCNWGS0123 acts in multiple processes in R. pseudoacacia during the early stages of infection, and TRAPPC13 could participate in the process as a NopP target. [Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
Jasmine (Jasminum officinale L. var. grandiflorum) Flower Extracts Inhibit the Formation of Methylglyoxal Induced Advanced Glycation Endproducts
Authors: Tang Xiaodan , Cai Ang , Li Dongli , Dain Joel A. , Seeram Navindra P. , Ma Hang 
Published: February 2021

Our laboratory initiated a program to investigate the chemical constituents and biological activities of medicinal plants and functional foods grown in the Lingnan region (“South of the Nanling Mountains”; region of Guangdong, Guangxi, and Hainan provinces in China). Jasmine (Jasminum officinale L. var. grandiflorum) is one of these medicinal plants that has traditionally been used as a functional food and dried jasmine flowers are often consumed as a tea for numerous health beneficial effects. However, the inhibitory effects of jasmine on the formation of advanced glycation endproducts (AGEs) are unknown. Herein, we evaluated the anti‐glycation effects of jasmine flower extracts using an assay model of methylglyoxal‐induced glycation of human serum albumin at 37 °C for 14 days. Jasmine flowers were extracted with 90% aqueous ethanol to afford a crude ethanol extract (JFE). JFE then was subjected to partitioning sequentially with organic solvents including petroleum ether (PE), ethyl acetate (EA), and n‐butanol (BuOH) to obtain extracts including JFPE, JFEA, and JFBuOH, respectively. These extracts were evaluated for their anti‐glycation effects. JFEE, JFPE, JFEA, and JFBuOH (at concentrations at 250 and 500 μg/mL) inhibited the formation of AGEs by 33.3% and 54.7%, 24.1% and 41.6%, 18.0% and 47.7%, and 10.5 and 38.0%, respectively. The mechanisms of the inhibitory effects of jasmine flower extracts on the formation of AGEs are currently being investigated by our group.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.