bluuebunny/crossref_metadata_2025_split huggingface dataset:
Population‐ and community‐level rarity have opposing effects on pollinator visitation and seed set
Authors: Brown Kaitlyn S. , Gilbert Benjamin 
Published: March 2020

AbstractWhen can small, isolated populations overcome the negative consequences of rarity? Despite considerable effort to understand threats to rare species, few studies consider how community context alters these threats. Plant–pollinator interactions offer the opportunity to test the effect of community context on rare species success, as plant–pollinator dynamics are thought to be influenced by neighbouring plants, both through competition for pollinators (reducing success in small populations) and attraction of potential pollinators (increasing success in small populations). Here, we test these predictions by experimentally decoupling community‐level rarity (relative abundance) from population‐level rarity (population size) in experimental two‐species fragments.We created experimental plant communities varying independently in population rarity (population size) and community rarity (relative abundance) of two annual plant species. We isolated plant roots to eliminate resource competition. We then compared the effects of population size versus relative abundance on pollinator visitation rates and an estimate of seed production.Both species had greatest pollinator visitation in large populations, but the negative effects of population rarity on visitation were partially offset when the neighbouring species was more abundant—community rarity offset the impacts of population rarity for the most common group of pollinators, solitary bees. These visitation trends impacted seed production for one species. When at low relative abundance,Polanisia dodecandrahad higher seed set, matching increased visitation by solitary bees.Chamaecrista fasciculatashowed no change in seed production with population‐ or community‐level rarity.Synthesis.Our results suggest that the surrounding community can offset the negative effects of low absolute abundance on fitness when neighbouring species are more abundant, and may ultimately maintain diversity even in fragmented ecological communities.
Atractylenolide III reduces NLRP3 inflammasome activation and Th1/Th2 imbalances in both in vitro and in vivo models of asthma
Authors: Zhu Cuimin , Zhang Leguo , Liu Zhiming , Li Chen , Bai Yajie , Wang Linlin 
Published: March 2020

AbstractPaediatric asthma is a common inflammatory disease in children. Atractylenolide III is an active component of the Atractylodes rhizome, an herbal medicine that has been used as an asthma treatment. This study aimed to explore the effects and underlying mechanisms of atractylenolide III in IL‐4‐induced 16HBE cells and ovalbumin‐induced asthmatic mice. The results showed that IL‐4 stimulation significantly decreased, and atractylenolide III treatment increased, growth and apoptosis of 16HBE cells. In 16HBE cells, administration of atractylenolide III also significantly suppressed the IL‐4‐induced increases in the expression of cleaved caspase‐1; apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC); and nucleotide‐binding domain and leucine‐rich repeat protein 3 (NLRP3). Moreover, the numbers of total leukocytes, neutrophils, eosinophils, and macrophages significantly increased in ovalbumin‐induced mice, and then decreased after atractylenolide III treatment. In ovalbumin‐induced asthmatic mice, atractylenolide III treatment also significantly inhibited NLRP3 inflammasome activation and restored the Th1/Th2 balance. These results indicate that atractylenolide III reduced NLRP3 inflammasome activation and regulated the Th1/Th2 balance in IL‐4 induced 16HBE cells and ovalbumin‐induced asthmatic mice, suggesting it has a protective effect that may be useful in the treatment of paediatric asthma.
Toxic males: Density‐dependent male mating harassment can explain geographic parthenogenesis
Authors: Yamamichi Masato , Koizumi Ichiro 
Published: March 2020

AbstractUnderstanding evolutionary forces that maintain sexual reproduction has been a central question in evolutionary biology, because the well‐known “two‐fold” cost of sex demands an explanation, especially since asexual reproduction (vegetative reproduction and parthenogenesis) often arises by mutation and hybridization. Geographic parthenogenesis, where asexual reproduction by close relatives of sexual lineages tends to be found in “marginal” habitats, has been considered a key pattern for studying the maintenance of sex. Recent studies of sexually reproducing populations have revealed that mating attempts by males can be harmful to females due to sexual conflict. Where that occurs and where there is a mixture of both sexual and asexual females, if male mating harassment is more harmful to asexual females than to sexual females, this may prevent the invasion of rare asexuals. Here, we use a simple ecological model with density‐dependent male mating harassment to show how asexual reproduction can become prevalent in habitats when environmental conditions are poor (i.e., low carrying capacities). The maintenance of sex is possible in a bistable system where abundant males are so harmful that they prevent the invasion of rare asexuals. However, male density is not large enough to suppress asexuals and sex is lost when carrying capacities are low or when sex ratio is highly male‐biased. While previous theoretical studies employed a frequency‐dependent model to study male mating harassment, we demonstrate that density‐dependence may be important to explain the dynamics in low population densities where there is geographical parthenogenesis.
Quantifying sample completeness and comparing diversities among assemblages
Authors: Chao Anne , Kubota Yasuhiro , Zelený David , Chiu Chun‐Huo , Li Ching‐Feng , Kusumoto Buntarou , Yasuhara Moriaki , Thorn Simon , Wei Chih‐Lin , Costello Mark J. , Colwell Robert K. 
Published: March 2020

AbstractWe develop a novel class of measures to quantify sample completeness of a biological survey. The class of measures is parameterized by an order q ≥ 0 to control for sensitivity to species relative abundances. When q = 0, species abundances are disregarded and our measure reduces to the conventional measure of completeness, that is, the ratio of the observed species richness to the true richness (observed plus undetected). When q = 1, our measure reduces to the sample coverage (the proportion of the total number of individuals in the entire assemblage that belongs to detected species), a concept developed by Alan Turing in his cryptographic analysis. The sample completeness of a general order q ≥ 0 extends Turing's sample coverage and quantifies the proportion of the assemblage's individuals belonging to detected species, with each individual being proportionally weighted by the (q − 1)th power of its abundance. We propose the use of a continuous profile depicting our proposed measures with respect to q ≥ 0 to characterize the sample completeness of a survey. An analytic estimator of the diversity profile and its sampling uncertainty based on a bootstrap method are derived and tested by simulations. To compare diversity across multiple assemblages, we propose an integrated approach based on the framework of Hill numbers to assess (a) the sample completeness profile, (b) asymptotic diversity estimates to infer true diversities of entire assemblages, (c) non‐asymptotic standardization via rarefaction and extrapolation, and (d) an evenness profile. Our framework can be extended to incidence data. Empirical data sets from several research fields are used for illustration.
Medicaid expansion and infant mortality, revisited: A difference‐in‐differences analysis
Authors: Wiggins Alexandra , Karaye Ibraheem M. , Horney Jennifer A. 
Published: March 2020

AbstractObjectiveTo determine the association between Medicaid expansion and infant mortality rate (IMR) in the United States.Data SourcesState‐level aggregate data on US IMR, race, and sex were abstracted from the US Center for Disease Control and Prevention's Wide‐ranging Online Data for Epidemiologic Research.Study DesignThe association between Medicaid expansion and IMR adjusted for race and sex was assessed with multiple linear regression models using difference‐in‐differences estimation and Huber‐White robust standard errors.Principal FindingsDifference‐in‐differences regression found no association between Medicaid expansion status and change in national IMR from 2010 to 2017 (Coef. = 0.04; 95% CI: −0.39, 0.46). However, among Hispanics, the program was found to be associated with reduction in IMR (Diff‐in‐Diff Coef. = −0.53; 95% CI: −1.02, −0.03).ConclusionsOverall, the Affordable Care Act–induced Medicaid expansion was not associated with IMR reduction in expansion states relative to nonexpansion states. However, the program was associated with a significant IMR decline among Hispanics.
Proteomic signatures of in vivo muscle oxidative capacity in healthy adults
Authors: Adelnia Fatemeh , Ubaida‐Mohien Ceereena , Moaddel Ruin , Shardell Michelle , Lyashkov Alexey , Fishbein Kenneth W. , Aon Miguel A. , Spencer Richard G. , Ferrucci Luigi 
Published: March 2020

AbstractAdequate support of energy for biological activities and during fluctuation of energetic demand is crucial for healthy aging; however, mechanisms for energy decline as well as compensatory mechanisms that counteract such decline remain unclear. We conducted a discovery proteomic study of skeletal muscle in 57 healthy adults (22 women and 35 men; aged 23–87 years) to identify proteins overrepresented and underrepresented with better muscle oxidative capacity, a robust measure of in vivo mitochondrial function, independent of age, sex, and physical activity. Muscle oxidative capacity was assessed by 31P magnetic resonance spectroscopy postexercise phosphocreatine (PCr) recovery time (τPCr) in the vastus lateralis muscle, with smaller τPCr values reflecting better oxidative capacity. Of the 4,300 proteins quantified by LC‐MS in muscle biopsies, 253 were significantly overrepresented with better muscle oxidative capacity. Enrichment analysis revealed three major protein clusters: (a) proteins involved in key energetic mitochondrial functions especially complex I of the electron transport chain, tricarboxylic acid (TCA) cycle, fatty acid oxidation, and mitochondrial ABC transporters; (b) spliceosome proteins that regulate mRNA alternative splicing machinery, and (c) proteins involved in translation within mitochondria. Our findings suggest that alternative splicing and mechanisms that modulate mitochondrial protein synthesis are central features of the molecular mechanisms aimed at maintaining mitochondrial function in the face of impairment. Whether these mechanisms are compensatory attempt to counteract the effect of aging on mitochondrial function should be further tested in longitudinal studies.
miR‐155‐5p inhibition rejuvenates aged mesenchymal stem cells and enhances cardioprotection following infarction
Authors: Hong Yimei , He Haiwei , Jiang Guojun , Zhang Hao , Tao Wuyuan , Ding Yue , Yuan Dongsheng , Liu Jing , Fan Huimin , Lin Fang , Liang Xiaoting , Li Xin , Zhang Yuelin 
Published: March 2020

AbstractAging impairs the functions of human mesenchymal stem cells (MSCs), thereby severely reducing their beneficial effects on myocardial infarction (MI). MicroRNAs (miRNAs) play crucial roles in regulating the senescence of MSCs; however, the underlying mechanisms remain unclear. Here, we investigated the significance of miR‐155‐5p in regulating MSC senescence and whether inhibition of miR‐155‐5p could rejuvenate aged MSCs (AMSCs) to enhance their therapeutic efficacy for MI. Young MSCs (YMSCs) and AMSCs were isolated from young and aged donors, respectively. The cellular senescence of MSCs was evaluated by senescence‐associated β‐galactosidase (SA‐β‐gal) staining. Compared with YMSCs, AMSCs exhibited increased cellular senescence as evidenced by increased SA‐β‐gal activity and decreased proliferative capacity and paracrine effects. The expression of miR‐155‐5p was much higher in both serum and MSCs from aged donors than young donors. Upregulation of miR‐155‐5p in YMSCs led to increased cellular senescence, whereas downregulation of miR‐155‐5p decreased AMSC senescence. Mechanistically, miR‐155‐5p inhibited mitochondrial fission and increased mitochondrial fusion in MSCs via the AMPK signaling pathway, thereby resulting in cellular senescence by repressing the expression of Cab39. These effects were partially reversed by treatment with AMPK activator or mitofusin2‐specific siRNA (Mfn2‐siRNA). By enhancing angiogenesis and promoting cell survival, transplantation of anti‐miR‐155‐5p‐AMSCs led to improved cardiac function in an aged mouse model of MI compared with transplantation of AMSCs. In summary, our study shows that miR‐155‐5p mediates MSC senescence by regulating the Cab39/AMPK signaling pathway and miR‐155‐5p is a novel target to rejuvenate AMSCs and enhance their cardioprotective effects.
Efficacy of Er:YAG laser‐assisted direct pulp capping in permanent teeth with cariously exposed pulp: A pilot study
Authors: Wang Mengchen , Ma Lin , Li Qian , Yang Wendong 
Published: March 2020

AbstractDirect pulp capping is a minimally invasive method to preserve pulp integrity. We evaluated the treatment efficacy of Er:YAG laser irradiation combined with direct pulp capping for pulp exposure due to caries. A total of 21 patients with 22 teeth were enrolled in the conventional group (calcium hydroxide), and 24 patients with 25 teeth were enrolled in the laser‐assisted group (Er:YAG laser irradiation at settings of 10 Hz, 50 mJ; combined with calcium hydroxide). The cumulative success rate of the conventional group and the laser‐assisted group was 68.2% and 91.7% at 12 months, respectively. Results showed that the laser‐assisted procedure increased the survival time (β = 0.04, OR = 0.07), while proximal‐occlusal cavities in molars decreased the survival time (β = 0.03, OR = 12.5). Er:YAG lasers improve the effectiveness of conventional direct pulp capping (using Dycal) with limited side‐effects and can be applied clinically.
Eleven faces of coronavirus disease 2019
Authors: Dong Xiang , Cao Yi‐yuan , Lu Xiao‐xia , Zhang Jin‐jin , Du Hui , Yan You‐qin , Akdis Cezmi A. , Gao Ya‐dong 
Published: March 2020

AbstractBackground and aimsThe outbreak of coronavirus disease 2019 (COVID‐19) caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection has recently spread worldwide and been declared a pandemic. We aim to describe here the various clinical presentations of this disease by examining eleven cases.MethodsElectronic medical records of 11 patients with COVID‐19 were collected, and demographics, clinical manifestations, outcomes, key laboratory results, and radiological images are discussed.ResultsThe clinical course of the eleven cases demonstrated the complexity of the COVID‐19 profile with different clinical presentations. Clinical manifestations range from asymptomatic cases to patients with mild and severe symptoms, with or without pneumonia. Laboratory detection of the viral nucleic acid can yield false‐negative results, and serological testing of virus‐specific IgG and IgM antibodies should be used as an alternative for diagnosis. Patients with common allergic diseases did not develop distinct symptoms and severe courses. Cases with a pre‐existing condition of chronic obstructive pulmonary disease or complicated with a secondary bacterial pneumonia were more severe.ConclusionAll different clinical characteristics of COVID‐19 should be taken into consideration to identify patients that need to be in strict quarantine for the efficient containment of the pandemic.
Disorganization of claudin‐11 and dysfunction of the blood‐testis barrier during puberty in a cryptorchid rat model
Authors: Kato Taiki , Mizuno Kentaro , Nishio Hidenori , Moritoki Yoshinobu , Kamisawa Hideyuki , Kurokawa Satoshi , Nakane Akihiro , Maruyama Tetsuji , Ando Ryosuke , Hayashi Yutaro , Yasui Takahiro 
Published: March 2020

AbstractBackgroundCryptorchidism is known to impair spermatogenesis. The blood‐testis barrier (BTB) becomes defined in seminiferous tubules around puberty and provides a suitable environment for germ cells. Little is known about the BTB in undescended testes (UDT).ObjectivesTo determine the role of BTB during puberty in UDT using a non‐surgical cryptorchid rat model.Material and MethodsUnilateral cryptorchid male rats were intraperitoneally injected with non‐steroidal antiandrogen during intrauterine development; the testes were harvested at 4, 5, and 6 weeks after birth. Testicular histology, expression levels of the BTB proteins (claudin‐11, occludin, zonula occludens‐1), and apoptotic cells were evaluated by immunohistochemistry, Western blotting, and TUNEL assay. The functionality of the BTB was investigated by electron microscopy using the lanthanum tracer method.ResultsThe testicular histology of undescended testes 6 weeks after birth showed maturation arrest at the spermatocyte level. The BTB protein distributions were altered in the UDT, with a noticeable difference in claudin‐11(CLDN11) localization from 4 to 5 weeks after birth between control and UDT samples. BTB protein levels were similar. More apoptotic germ cells were detected in the adluminal compartment of tubules in the UDT than in the control testes. Electron microscopy showed that the lanthanum tracer was limited to the BTB of control testes, whereas it penetrated the BTB of UDT.DiscussionHere, loss of normal BTB function and impaired spermatogenesis were observed in UDT during puberty. CLDN11 is a pivotal tight junction protein belonging to the BTB. Tight junctions are considered as essential for normal spermatogenesis, and abnormal CLDN11 organization may cause UDT‐associated male infertility.ConclusionCLDN11 disorganization within the BTB may cause spermatogenic impairment, possibly by limiting the BTB function.
The development of an instrument to test pre‐service teachers’ beliefs consistent and inconsistent with self‐regulation theory
Authors: Darmawan I Gusti Ngurah , Vosniadou Stella , Lawson Michael J. , Van Deur Penny , Wyra Mirella 
Published: March 2020

BackgroundStudents are more effective when they employ appropriate strategies to regulate their learning processes and outcomes. However, many teachers do not provide, or provide very little, explicit instructions to promote this self‐regulated learning (SRL). This suggests that teachers’ belief systems may include beliefs that may be inconsistent with SRL.AimsThis paper reported the validation of the 78‐item Beliefs about Teaching and Learning (BALT) instrument designed to measure pre‐service teachers’ beliefs about learning and teaching with particular emphasis on SRL.SamplesOut of the 78 items included in the BALT instrument, 50 of them were administered in BALT 1 and 53 in BALT2 with 25 items administered in both surveys and were common to both instruments. The BALT 1 was administered to 430 pre‐service teachers. BALT 2 was administered to 366 pre‐service students.MethodsConfirmatory factor analysis and the Rasch model were used to investigate the unidimensionality of the scales and psychometric properties of the items. In addition, the summated rating scale procedure was used to create composite scores for the examination of the coexistence of beliefs both consistent and inconsistent with SRL.ResultsPre‐service teachers expressed high overall agreement with items related to beliefs consistent with SRL and low agreement with items related to beliefs inconsistent with SRL. However, many of them also indicated high agreement with items related to beliefs in Transmissive Teaching.ConclusionsThe study resulted in the development of a 58‐item instrument, which was balanced with respect to the inclusion of SRL‐consistent and SRL‐inconsistent items. This study also provided evidence for the coexistence of pre‐service teachers’ beliefs in Constructive Teaching and Transmissive Teaching.
Myelofibrosis biology and contemporary management
Authors: Gangat Naseema , Tefferi Ayalew 
Published: March 2020

SummaryMyelofibrosis is an enigmatic myeloproliferative neoplasm, despite noteworthy strides in understanding its genetic underpinnings. Driver mutations involving JAK2, CALR or MPL in 90% of patients mediate constitutive JAK‐STAT signaling which, in concert with epigenetic alterations (ASXL1, DNMT3A, SRSF2, EZH2, IDH1/2 mutations), play a fundamental role in disease pathogenesis. Aberrant immature megakaryocytes are a quintessential feature, exhibiting reduced GATA1 protein expression and secreting a plethora of pro‐inflammatory cytokines (IL‐1 ß, TGF‐ß), growth factors (b‐FGF, PDGF, VEGF) in addition to extra cellular matrix components (fibronectin, laminin, collagens). The ensuing disrupted interactions amongst the megakaryocytes, osteoblasts, endothelium, stromal cells and myofibroblasts within the bone marrow culminate in the development of fibrosis and osteosclerosis. Presently, prognostic assessment tools for primary myelofibrosis (PMF) are centered on genetics, with incorporation of cytogenetic and molecular information into the mutation‐enhanced (MIPSS 70‐plus version 2.0) and genetically‐inspired (GIPSS) prognostic scoring systems. Both models illustrate substantial clinical heterogeneity in PMF and serve as the crux for risk‐adapted therapeutic decisions. A major challenge remains the dearth of disease‐modifying drugs, whereas allogeneic transplant offers the chance of long‐term remission for some patients. Our review serves to synopsise current appreciation of the pathogenesis of myelofibrosis together with emerging management strategies.