bluuebunny/crossref_metadata_2025_split huggingface dataset:
Climate drives differences in the germination niche of a globally distributed invasive grass
Authors: Fletcher Rebecca A , Varnon Kayla M , Barney Jacob N 
Published: January 2020

Abstract

Aims
Exotic invasive species are often exposed to strong selection pressures in their new ranges that can often lead to substantial intraspecific variation. Population differentiation in the timing of life history events in response to climate gradients is thought to be an important mechanism facilitating the range expansion of many invasive species. For seed producing plants, the timing of seed germination determines the first environmental conditions experienced by newly emerged germinates, and can have important implications for the successful colonization, establishment and spread of invasive plants—though the role of germination in the success of invasive plants remains poorly understood.

Methods
We assessed the variation in seed germination dynamics among 10 populations of the invasive plant Johnsongrass (Sorghum halepense) across its North American distribution, capturing both a temperature and precipitation gradient, and whether that variation is associated with home climate. Seeds were exposed to a wide range of temperatures (11–48°C) and two water availability treatments.

Important Findings
We found that Johnsongrass seeds germinated across a wide range of temperatures, but there was substantial variation among populations in the proportion of seeds that germinated in response to both temperature and water availability. Evidence indicates that as Johnsongrass expanded its range from warmer climates into cooler climates, there was a concurrent shift in the germination temperature niche to cooler temperatures. Our results suggest that the germination of Johnsongrass seeds has adapted to home climate allowing this invader to maximize germination throughout its range, and that this may be an important contributing factor to its invasion into new environments.
The Wounded Male Body: Masculinity and Disability in Wartime and Post-WWI Italy
Authors: Salvante Martina 
Published: January 2020

Abstract
This article examines the variety of ways in which Italian soldiers responded to the experience of incurring a permanent physical disability during the First World War. It also describes the potentially unsettling presence of soldiers’ disabled bodies in Italian society, where they were perceived as being disruptive to cultural understandings of male embodiment and hegemonic masculinities. By analyzing different intimate and social exchanges, as well as emotional bonds, this article attempts to disentangle historically the intersection between masculinity and disability. In so doing, it will expose the implications of normative expectations of masculinity, the anxiety that arose from attempts to challenge these norms, and the relevance of context and life phase in understanding the impact of disability on male identity. Drawing on both theories of masculinity and literature on disability, this article will ultimately illustrate how and to what extent disabled veterans in post–First World War Italy negotiated and shaped their gendered identities. It will conclude by considering the role of Fascism in promoting a model of hegemonic masculinity, to which the war disabled could also conform.
“Will you still want me if I come back like Vincenzo Bellu?” “With only one arm? Of course, because they’ll give you the Order of Vittorio Veneto and I’ll be your lady! [. . .]” “I’m not joking. Would you still want me if I was a cripple? Deafened by a grenade or with no legs like Luigi Barranca?” “I’d want you back in any condition, as long as you’re still alive. [. . .]” “Maybe you can imagine having me back as a worm, but I’d rather die full of life ten times over than have to live ten years like a dead man. If that happens to me I shall do what Barranca did and shoot myself.”1
Surface, adhesiveness and virulence aspects of Candida haemulonii species complex
Authors: Ramos Lívia S , Oliveira Simone S C , Silva Laura N , Granato Marcela Q , Gonçalves Diego S , Frases Susana , Seabra Sergio H , Macedo Alexandre J , Kneipp Lucimar F , Branquinha Marta H , Santos André L S 
Published: January 2020

AbstractThe emerging opportunistic pathogens comprising the Candida haemulonii complex (C. haemulonii [Ch], C. duobushaemulonii [Cd] and C. haemulonii var. vulnera[Chv]) are notable for their intrinsic antifungal resistance. Different clinical manifestations are associated with these fungal infections; however, little is known about their biology and potential virulence attributes. Herein, we evaluated some surface properties of 12 clinical isolates of Ch (n = 5), Cd (n = 4) and Chv (n = 3) as well as their virulence on murine macrophages and Galleria mellonella larvae. Scanning electron microscopy demonstrated the presence of homogeneous populations among the species of the C. haemulonii complex, represented by oval yeasts with surface irregularities able to form aggregates. Cell surface hydrophobicity was isolate-specific, exhibiting high (16.7%), moderate (25.0%) and low (58.3%) hydrophobicity. The isolates had negative surface charge, except for one. Mannose/glucose- and N-acetylglucosamine-containing glycoconjugates were evidenced in considerable amounts in all isolates; however, the surface expression of sialic acid was poorly detected. Cd isolates presented significantly higher amounts of chitin than Ch and Chv. Membrane sterol and lipid bodies, containing neutral lipids, were quite similar among all fungi studied. All isolates adhered to inert surfaces in the order: polystyrene &gt; poly-L-lysine-coated glass &gt; glass. Likewise, they interacted with murine macrophages in a quite similar way. Regarding in vivo virulence, the C. haemulonii species complex were able to kill at least 80% of the larvae after 120 hours. Our results evidenced the ability of C. haemulonii complex to produce potential surface-related virulence attributes, key components that actively participate in the infection process described in Candida spp.
Are exoplanetesimals differentiated?
Authors: Bonsor Amy , Carter Philip J , Hollands Mark , Gänsicke Boris T , Leinhardt Zoë , Harrison John H D 
Published: January 2020

ABSTRACTMetals observed in the atmospheres of white dwarfs suggest that many have recently accreted planetary bodies. In some cases, the compositions observed suggest the accretion of material dominantly from the core (or the mantle) of a differentiated planetary body. Collisions between differentiated exoplanetesimalrrs produce such fragments. In this work, we take advantage of the large numbers of white dwarfs where at least one siderophile (core-loving) and one lithophile (rock-loving) species have been detected to assess how commonly exoplanetesimals differentiate. We utilize N-body simulations that track the fate of core and mantle material during the collisional evolution of planetary systems to show that most remnants of differentiated planetesimals retain core fractions similar to their parents, while some are extremely core rich or mantle rich. Comparison with the white dwarf data for calcium and iron indicates that the data are consistent with a model in which $66^{+4}_{-6}{{\ \rm per\ cent}}$ have accreted the remnants of differentiated planetesimals, while $31^{+5}_{-5}{{\ \rm per\ cent}}$ have Ca/Fe abundances altered by the effects of heating (although the former can be as high as $100{{\ \rm per\ cent}}$, if heating is ignored). These conclusions assume pollution by a single body and that collisional evolution retains similar features across diverse planetary systems. These results imply that both collisions and differentiation are key processes in exoplanetary systems. We highlight the need for a larger sample of polluted white dwarfs with precisely determined metal abundances to better understand the process of differentiation in exoplanetary systems.
Capital Accumulation and Structural Transformation*
Authors: Bustos Paula , Garber Gabriel , Ponticelli Jacopo 
Published: January 2020

AbstractSeveral scholars argue that high agricultural productivity can retard industrial development because it draws resources toward the comparative advantage sector, agriculture. However, agricultural productivity growth can increase savings and the supply of capital, generating an expansion of the capital-intensive sector, manufacturing. We highlight this mechanism in a simple model and test its predictions in the context of a large and exogenous increase in agricultural productivity due to the adoption of genetically engineered soy in Brazil. We find that agricultural productivity growth generated an increase in savings, but these were not reinvested locally. Instead, there were capital outflows from rural areas. Capital reallocated toward urban regions, where it was invested in the industrial and service sectors. The degree of financial integration affected the speed of structural transformation. Regions that were more financially integrated with soy-producing areas through bank branch networks experienced faster growth in nonagricultural lending. Within these regions, firms with preexisting relationships with banks receiving funds from the soy area experienced faster growth in borrowing and employment.
Cognitive Impairment and Diminished Neural Responses Constitute a Biomarker Signature of Negative Symptoms in Psychosis
Authors: Hudgens-Haney Matthew E , Clementz Brett A , Ivleva Elena I , Keshavan Matcheri S , Pearlson Godfrey D , Gershon Elliot S , Keedy Sarah K , Sweeney John A , Gaudoux Florence , Bunouf Pierre , Canolle Benoit , Tonner Françoise , Gatti-McArthur Silvia , Tamminga Carol A 
Published: January 2020

AbstractThe treatment of negative symptoms (NS) in psychosis represents an urgent unmet medical need given the significant functional impairment it contributes to psychosis syndromes. The lack of progress in treating NS is impacted by the lack of known pathophysiology or associated quantitative biomarkers, which could provide tools for research. This current analysis investigated potential associations between NS and an extensive battery of behavioral and brain-based biomarkers in 932 psychosis probands from the B-SNIP database. The current analyses examined associations between PANSS-defined NS and (1) cognition, (2) pro-/anti-saccades, (3) evoked and resting-state electroencephalography (EEG), (4) resting-state fMRI, and (5) tractography. Canonical correlation analyses yielded symptom-biomarker constructs separately for each biomarker modality. Biomarker modalities were integrated using canonical discriminant analysis to summarize the symptom-biomarker relationships into a “biomarker signature” for NS. Finally, distinct biomarker profiles for 2 NS domains (“diminished expression” vs “avolition/apathy”) were computed using step-wise linear regression. NS were associated with cognitive impairment, diminished EEG response amplitudes, deviant resting-state activity, and oculomotor abnormalities. While a connection between NS and poor cognition has been established, association to neurophysiology is novel, suggesting directions for future mechanistic studies. Each biomarker modality was related to NS in distinct and complex ways, giving NS a rich, interconnected fingerprint and suggesting that any one biomarker modality may not adequately capture the full spectrum of symptomology.
High separation anxiety trajectory in early childhood is a risk factor for sleep bruxism at age 7
Authors: Garmroudinezhad Rostami Elham , Touchette Évelyne , Huynh Nelly , Montplaisir Jacques , Tremblay Richard E , Battaglia Marco , Boivin Michel 
Published: January 2020

Abstract

Study Objectives
The evolution of sleep bruxism manifestations and their co-occurrence with separation anxiety in early childhood remain unclear. Our threefold aim was to: (1) describe developmental sleep bruxism trajectories in early childhood, (2) investigate co-occurrences between trajectories of sleep bruxism and separation anxiety, and (3) determine whether distinct trajectories of separation anxiety increase the risk of presenting sleep bruxism during the first year of elementary school.

Methods
This study is part of the Québec Longitudinal Study of Child Development. Sleep bruxism scores were assessed from age 1.5 to 7 years with the Self-Administered Questionnaire for Mother (n = 1946). Separation anxiety scores were measured from age 1.5 to 6 years with the Interviewer-Completed Computerized Questionnaire (n = 2045).

Results
We identified four sleep bruxism trajectories from age 1.5 to 6 years: High-Increasing sleep bruxism at age 1.5 (14.1%), High-Increasing sleep bruxism at age 4 (18.3%), Low-Persistent sleep bruxism (12.1%), and Never-Persistent sleep bruxism (55.5%); and four separation anxiety trajectories from age 1.5 to 6 years: Low-Persistent separation anxiety (60.2%), High-Increasing separation anxiety (6.9%), High-Decreasing separation anxiety (10.8%), and Low-Increasing separation anxiety (22.1%). Sleep bruxism and separation anxiety trajectories were weakly associated (X2 = 37.84, p &lt; 0.001). Compared with preschoolers belonging to the Low-Persistent separation anxiety trajectory, preschoolers in the High-Increasing separation anxiety trajectory had almost double the risk of presenting sleep bruxism at age 7 (95% CI = 1.25–3.22, p = 0.04).

Conclusion
When separation anxiety issues are detected in early childhood, it would be useful to target sleep bruxism during the first year of elementary school.
Developing preliminary blood metabolomics-based biomarkers of insufficient sleep in humans
Authors: Depner Christopher M , Cogswell Dasha T , Bisesi Paul J , Markwald Rachel R , Cruickshank-Quinn Charmion , Quinn Kevin , Melanson Edward L , Reisdorph Nichole , Wright Kenneth P 
Published: January 2020

AbstractStudy ObjectiveIdentify small molecule biomarkers of insufficient sleep using untargeted plasma metabolomics in humans undergoing experimental insufficient sleep.MethodsWe conducted a crossover laboratory study where 16 normal-weight participants (eight men; age 22 ± 5 years; body mass index &lt; 25 kg/m2) completed three baseline days (9 hours sleep opportunity per night) followed by 5-day insufficient (5 hours sleep opportunity per night) and adequate (9 hours sleep opportunity per night) sleep conditions. Energy balanced diets were provided during baseline, with ad libitum energy intake provided during the insufficient and adequate sleep conditions. Untargeted plasma metabolomics analyses were performed using blood samples collected every 4 hours across the final 24 hours of each condition. Biomarker models were developed using logistic regression and linear support vector machine (SVM) algorithms.ResultsThe top-performing biomarker model was developed by linear SVM modeling, consisted of 65 compounds, and discriminated insufficient versus adequate sleep with 74% overall accuracy and a Matthew’s Correlation Coefficient of 0.39. The compounds in the top-performing biomarker model were associated with ATP Binding Cassette Transporters in Lipid Homeostasis, Phospholipid Metabolic Process, Plasma Lipoprotein Remodeling, and sphingolipid metabolism.ConclusionWe identified potential metabolomics-based biomarkers of insufficient sleep in humans. Although our current biomarkers require further development and validation using independent cohorts, they have potential to advance our understanding of the negative consequences of insufficient sleep, improve diagnosis of poor sleep health, and could eventually help identify targets for countermeasures designed to mitigate the negative health consequences of insufficient sleep.
Cell cycle regulation and hematologic malignancies
Authors: Dai Yun , Jin Fengyan , Wu Wei , Kumar Shaji K. 
Published: January 2020

Abstract
A complex network precisely regulates the cell cycle through the G1, S, G2, and M phases and is the basis for cell division under physiological and pathological conditions. On the one hand, the transition from one phase to another as well as the progression within each phase is driven by the specific cyclin-dependent kinases (CDKs; e.g., CDK1, CDK2, CDK4, CDK6, and CDK7), together with their exclusive partner cyclins (e.g., cyclin A1, B1, D1–3, and E1). On the other hand, these phases are negatively regulated by endogenous CDK inhibitors such as p16ink4a, p18ink4c, p19ink4d, p21cip1, and p27kip1. In addition, several checkpoints control the commitment of cells to replicate DNA and undergo mitosis, thereby avoiding the passage of genomic errors to daughter cells. CDKs are often constitutively activated in cancer, which is characterized by the uncontrolled proliferation of transformed cells, due to genetic and epigenetic abnormalities in the genes involved in the cell cycle. Moreover, several oncogenes and defective tumor suppressors promote malignant changes by stimulating cell cycle entry and progression or disrupting DNA damage responses, including the cell cycle checkpoints, DNA repair mechanisms, and apoptosis. Thus, genes or proteins related to cell cycle regulation remain the main targets of interest in the treatment of various cancer types, including hematologic malignancies. In this context, advances in the understanding of the cell cycle regulatory machinery provide a basis for the development of novel therapeutic approaches. The present article summarizes the pathways as well as their genetic and epigenetic alterations that regulate the cell cycle; moreover, it discusses the various approved or potential therapeutic targets associated with the cell cycle, focusing on hematologic malignancies.
Hematopoietic stem cell metabolism and stemness
Authors: Huang Dan , Chen Chiqi , Xie Li , Yu Zhuo , Zheng Junke 
Published: January 2020

AbstractHematopoietic stem cells (HSCs) are considered to originate from the aorta-gonad-mesonephros, migrate into fetal liver for a rapid expansion, and eventually reside into a unique hypoxic bone marrow niche, where they maintain their homeostasis throughout their life span. HSCs have been widely used for the treatment of many begin or malignant hematopoietic disorders. However, the unavailability of sufficient amount of HSCs still impedes their applications in the clinic. It is urgent to understand how HSC stemness or cell fates are determined at different developmental stages. Although many intrinsic and extrinsic factors (niche components) have been identified in the regulation of HSC origination, expansion, migration, and localization, the underlying mechanisms remain largely unknown. In this article, we summarize current views on the metabolic profiles of HSCs and related regulatory networks, which shows that intrinsic metabolic regulation may be critical for the cell fate determinations of HSCs: HSCs utilize glycolysis as their major energy sources; mitochondrial respiration is also required for the homeostasis of HSCs; amino acids, lipids, or other nutrient metabolisms also have unique roles in sustaining HSC activities. Mechanistically, many important regulatory pathways, such as MEIS1/HIF1A, MYC, PPM1K/CDC20, and ROS signals, are identified to fine-tune the nutrient metabolisms and cell fate commitments in HSCs. Nevertheless, more effort is required for the optimization or establishment of sensitive and specific metabolic techniques/systems for the metabolism studies in HSCs with limited cell numbers and exploring the metabolic profiles and fundamental regulatory mechanisms of different types of nutrients at each developmental stage of HSCs.
Engineered human pluripotent stem cell-derived natural killer cells: the next frontier for cancer immunotherapy
Authors: Zhu Huang , Kaufman Dan S. 
Published: January 2020

Abstract
Adoptive immunotherapy using immune effector cells has revolutionized cancer treatments with approval of two autologous chimeric antigen receptor (CAR) T cell therapies by the US FDA. Clinical trials using natural killer (NK) cell-based adoptive immunotherapy have been shown to be safe and effective for treatment of multiple malignancies, especially acute myelogenous leukemia. However, most of these trails use primary NK cells isolated from peripheral or cord blood which can have donor-dependent variability and can be challenging to genetic engineer to improve antitumor functions, limiting the widespread use of this promising new therapy. NK cells can now be routinely produced from human pluripotent stem cells, both human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs). These pluripotent stem cells are homogenous, easy to genetically modify on a clonal level and can be used as unlimited source of NK cells, making them ideal population to develop standardized, off-the-shelf adoptive NK cell therapy products. In this review, we discuss recent advances of obtaining and expanding hESC and iPSC-derived NK cells and novel genetic engineering strategies that are being applied to improve their antitumor functions.
Temporal Relationship of Computed and Structured Diagnoses in Electronic Health Record Data
Authors: Schulz Wade L. , Young H. Patrick , Coppi Andreas , Mortazavi Bobak J. , Lin Zhenqiu , Jean Raymond A. , Krumholz Harlan M. 
Published: January 2020

AbstractThe electronic health record (EHR) holds the prospect of providing more complete and timely access to clinical information for studies, quality assessments, and quality improvement compared to other data sources, such as administrative claims. Our goal was to assess the completeness and timeliness of structured diagnoses in the EHR compared to computed diagnoses for hypertension (HTN), hyperlipidemia (HLD), and diabetes mellitus (DM). We determined the amount of time for a structured diagnosis to be recorded in the EHR from when an equivalent diagnosis could be computed from other structured data elements, such as vital signs and laboratory results. Using our local instance of EHR data in the PCORnet common data model (CDM) with encounters from January 1, 2012 through February 10, 2019, we identified patients with at least two observations above threshold separated by at least 30 days. The thresholds were outpatient blood pressure of ≥ 140/90 mmHg, any low-density lipoprotein ≥ 130 mg/dl, or any hemoglobin A1c ≥ 7%, respectively. The primary measure was the length of time between the computed diagnosis and the time at which a structured diagnosis could be identified within the EHR history or problem list. We found that 39.8% of those with HTN, 21.6% with HLD, and 1.0% with DM did not receive a corresponding structured diagnosis recorded in the EHR. For those who received a structured diagnosis, a mean of 389, 198, and 106 days elapsed before the patient had the corresponding diagnosis of HTN, HLD, or DM, respectively, recorded in the EHR. We identified a marked temporal delay between when a diagnosis can be computed or inferred and when an equivalent structured diagnosis is recorded within the EHR. These findings demonstrate the continued need for additional study of the EHR to avoid bias when using observational data and reinforce the need for computational approaches to identify clinical phenotypes.