bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantifying carbon stocks in shifting cultivation landscapes under divergent management scenarios relevant to REDD+
Authors: Borah Joli R. , Evans Karl L. , Edwards David P. 
Published: July 2018

AbstractShifting cultivation dominates many tropical forest regions. It is expanding into old‐growth forests, and fallow period duration is rapidly decreasing, limiting secondary forest recovery. Shifting cultivation is thus a major driver of carbon emissions through deforestation and forest degradation, and of biodiversity loss. The impacts of shifting cultivation on carbon stocks have rarely been quantified, and the potential for carbon‐based payments for ecosystem services (PES), such as REDD+, to protect carbon in shifting cultivation landscapes is unknown. We present empirical data on aboveground carbon stocks in old‐growth forest and shifting cultivation landscapes in northeast India, a hotspot of threatened biodiversity. We then model landscape‐level carbon stocks under business‐as‐usual scenarios, via expansion into the old‐growth forest or decreasing fallow periods, and intervention scenarios in which REDD+ is used to either reduce deforestation of primary or secondary forest or increase fallow period duration. We found substantial recovery of carbon stocks as secondary forest regenerates, with a 30‐yr fallow storing about one‐half the carbon of an old‐growth forest. Business‐as‐usual scenarios led to substantial carbon loss, with an 80% reduction following conversion of old‐growth forest to a 30‐yr shifting cultivation cycle and, relative to a 30‐yr cultivation landscape, a 70% reduction when switching to a 5‐yr cultivation cycle. Sparing old‐growth forests from deforestation using protected areas and intensifying cropping in the remaining area of shifting cultivation is the most optimal strategy for carbon storage. In areas lacking old‐growth forest, substantial carbon stocks accumulate over time by sparing fallows for permanent forest regeneration. Successful implementation of REDD+ in shifting cultivation landscapes can help avert global climate change by protecting forest carbon, with likely co‐benefits for biodiversity.
The effect of multiple biotic interaction types on species persistence
Authors: García‐Callejas David , Molowny‐Horas Roberto , Araújo Miguel B. 
Published: July 2018

AbstractNo species can persist in isolation from other species, but how biotic interactions affect species persistence is still a matter of inquiry. Is persistence more likely in communities with higher proportion of competing species, or in communities with more positive interactions? How do different components of community structure mediate this relationship? We address these questions using a novel simulation framework that generates realistic communities with varying numbers of species and different proportions of biotic interaction types within and across trophic levels. We show that when communities have fewer species, persistence is more likely if positive interactions—such as mutualism and commensalism—are prevalent. In species‐rich communities, the disproportionate effect of positive interactions on persistence is diluted and different combinations of biotic interaction types can coexist without affecting persistence significantly. We present the first theoretical examination of how multiple‐interaction networks with varying architectures relate to local species persistence, and provide insight about the underlying causes of stability in communities.
Metabolic wiring of murine T cell and intraepithelial lymphocyte maintenance and activation
Authors: Veldhoen Marc , Blankenhaus Birte , Konjar Špela , Ferreira Cristina 
Published: July 2018

AbstractAdaptive immunity critically depends on cell migration combined with clonal selection and rapid expansion of rare lymphocytes recognising their cognate antigen in secondary lymphoid organs. It has since become apparent that large populations of T cells are maintained in tissues, which do not migrate throughout the body and do not require clonal expansion. Murine intraepithelial lymphocytes (IELs), located in the skin and small intestines, are maintained in a state of semi‐activation, in marked contrast to the quiescent condition naive and memory lymphocytes are kept in. The poised activation state of IELs, their location in the top layers of barrier organs and close bidirectional interactions with epithelial cells suggests IELs are part of a sophisticated strategy of immune‐surveillance and compartmentalisation of immune responses. Recent murine studies have reemphasised the influence of metabolism in T‐cell activation and differentiation, with different metabolic make up of naive, effector and memory T cells. Here we highlight and discuss some of the current insights on immunometabolism of IELs, with emphasis on novel data contrasting how IELs may be maintained in a semi‐activated state and may become fully functional compared with conventional T cells.
Uricase Based Enzymatic Biosensor for Non‐invasive Detection of Uric Acid by Entrapment in PVA‐SbQ Polymer Matrix
Authors: RoyChoudhury Sohini , Umasankar Yogeswaran , Hutcheson Joshua D. , Lev‐Tov Hadar A. , Kirsner Robert S. , Bhansali Shekhar 
Published: July 2018

AbstractIn this work, an electrochemical approach using uricase (UOx) as an enzyme to detect uric acid (UA) for wound monitoring has been reported. UOx was entrapped in poly (vinyl alcohol) N‐methyl‐4(4’‐formylstyryl) pyridinium methosulfate acetal (PVA‐SbQ), a cationic polymer matrix. The polymer‐enzyme ratio for immobilization was calculated as 53.2 μg cm−2 : 0.25 U cm−2. UA was detected both optically as well as electrochemically. A redox electron shuttle, ferrocene carboxylic acid (FCA) was used to facilitate electron transfer. Entrapped UOx provided improved response to UA detection compared to physisorbed UOx. Sensor response was linear in the physiologically relevant ranges between 12 and 100 μM. The entrapped UOx biosensor was stable for 48 h and maintained 90 % activity until 5 days. This entrapped biosensor was used for UA measurements in biofluids of sweat and wounds. The sensor demonstrated a recovery of ∼102–107 %. These results show that entrapment of UA in such a polymer matrix is a preferred approach for UA measurements under physiological conditions.
Interest rate risk in long‐dated commodity options positions: To hedge or not to hedge?
Authors: Cheng Benjamin , Nikitopoulos Christina Sklibosios , Schlögl Erik 
Published: July 2018

AbstractWe empirically assess hedging interest rate risk beyond the conventional delta, gamma, and vega hedges in long‐dated crude oil options positions. Using factor hedging in a model featuring stochastic interest rates and stochastic volatility, interest rate hedges consistently provide an improvement beyond delta, gamma, and vega hedges. Under high interest rate volatility and/or when a rolling hedge is used, combining interest rate and delta hedging improves performance by up to four percentage points over the common hedges of gamma and/or vega. Thus, contrary to common practice, hedging interest rate risk should have priority over these “second‐order” hedges.
Astroglia contribute to the pathogenesis of spinocerebellar ataxia Type 1 (SCA1) in a biphasic, stage‐of‐disease specific manner
Authors: Kim Joo Hyun , Lukowicz Abigail , Qu Wenhui , Johnson Andrea , Cvetanovic Marija 
Published: July 2018

AbstractSpinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin‐1 (ATXN1) gene. SCA1 is characterized by balance and coordination deficits due to the predominant loss of Purkinje neurons in the cerebellum. We previously demonstrated that cerebellar astrogliosis beings during the early stages of SCA1, prior to onset of motor deficits and loss of Purkinje neurons. We communicate here that cerebellar astrogliosis contributes to SCA1 pathogenesis in a biphasic, stage of disease dependent manner. We modulated astrogliosis by selectively reducing pro‐inflammatory transcriptional regulator nuclear factor κ‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling in astroglia via a Cre‐lox mouse genetic approach. Our results indicate that inhibition of astroglial NF‐κB signaling, prior to motor deficit onset, exacerbates disease severity. This is suggestive of a neuroprotective role mediated by astroglia during early stage SCA1. In contrast, inhibition of astroglial NF‐κB signaling during late stage of disease ameliorated motor deficits, indicating a potentially harmful role of astroglia late in SCA1. These results indicate that astrogliosis may have a critical and dual role in disease. If so, our results imply that anti‐inflammatory astroglia‐based therapeutic approaches may need to consider disease progression to achieve therapeutic efficacy.
Incidence and severity of head injury hospitalisations in Australian children over a 10‐year period
Authors: Bierbaum Mia , Lystad Reidar P. , Curtis Kate , Mitchell Rebecca 
Published: July 2018

AbstractIssue addressedChild head injuries can cause life‐long disability and are a major cause of mortality globally. The incidence and impact of child head injuries in Australia is unknown. This study aimed to quantify the incidence, characteristics and treatment cost and to identify factors associated with the severity of hospitalisations of head injuries in Australian children.MethodsLinked hospitalisation and mortality data were used to retrospectively examine hospitalisation trends for head injury in children aged ≤16 years and associated factors, in Australia, from 1 July 2002 to 30 June 2012.ResultsThere were 164 126 hospitalisations of children for head injury during the 10‐year period, commonly male (65.5%), or aged ≤5 years (48.3%). The incidence among children aged <1 year and 1‐5 years significantly increased by 1.7% (95% CI 0.9‐2.6; P < 0.0001) and 1.5% (95% CI 1.1‐1.9; P < 0.0001) annually during the study period, respectively. The most common injury mechanisms across all age groups were falls (45.2%) and road trauma (16.0%). Head injury hospitalisations cost $468.9 million, with the higher costs found for children aged 11‐16 years, and for the most severe injuries.ConclusionHead injury hospitalisations cost the Australian health system close to half a billion dollars over a 10‐year period, with the most serious injuries resulting in lifelong health implications.So what?Targeted health promotion strategies such as the promotion of helmet wearing during scooter use, the introduction of cycleways, and impact absorbing surfaces on playgrounds, need to be implemented to reduce the occurrence of head injuries in children.
Prediction of Consumptive Use Under Different Soil Moisture Content and Soil Salinity Conditions Using Artificial Neural Network Models
Authors: Qi Yanbing , Huo Zailin , Feng Shaoyuan , Adeloye Adebayo J. , Dai Xiaoqin 
Published: July 2018

AbstractThe response of the water use of crops to soil moisture and salinity is complex to quantify using traditional field experiments. Based on field experimental data for 2 years, artificial neural network (ANN) models with five inputs including soil moisture content, total salt content, plant height, leaf area index and crop reference evapotranspiration (ET0) were developed to estimate daily actual evapotranspiration (ET). The models were later used to simulate the response of crop water consumption to soil moisture and salinity stresses at different growth stages. The results showed that the ANN model has a high precision with root mean squared error of 0.41 and 0.52 mm day‐1, relative error of 19.6 and 25.6%, and coefficient of determination of 0.87 and 0.79 for training and testing samples, respectively. Furthermore, the simulation results showed that the seed corn ET is sensitive to soil salt stress at all growth stages, although the salinity threshold at which the impact becomes felt and the extent of the impact vary for the different growth stages, with the booting and tasseling stages being the most robust. The study offers a more direct approach of evaluating actual crop evapotranspiration by considering explicitly water and salinity stresses. © 2018 John Wiley & Sons, Ltd.
Long‐noncoding RNA Atrolnc‐1 promotes muscle wasting in mice with chronic kidney disease
Authors: Sun Lijing , Si Meijun , Liu Xinyan , Choi Jong Min , Wang Yanlin , Thomas Sandhya S. , Peng Hui , Hu Zhaoyong 
Published: July 2018

AbstractBackgroundChronic kidney disease (CKD) is commonly associated with cachexia, a condition that causes skeletal muscle wasting and an unfavourable prognosis. Although mechanisms leading to cachexia have been intensively studied, the advance of biological knowledges and technologies encourages us to make progress in understanding the pathogenesis of this disorder. Long noncoding RNAs (lncRNAs) are defined as >200 nucleotides RNAs but lack the protein‐coding potential. LncRNAs are involved in the pathogenesis of many diseases, but whether they functionally involve in muscle protein loss has not been investigated.MethodsWe performed lncRNA array and identified an lncRNA, which we named Atrolnc‐1, remarkably elevated in atrophying muscles from mice with cachexia. We examined how overexpression or knockdown of Atrolnc‐1 could influence muscle protein synthesis and degradation. We also examined whether inhibition of Atrolnc‐1 ameliorates muscle wasting in mice with CKD.ResultsWe documented that Atrolnc‐1 expression is continuously increased in muscles of mice with fasting (5.4 fold), cancer (2.0 fold), or CKD (5.1 fold). We found that depressed insulin signalling stimulates the transcription factor C/EBP‐α binding to the promoter of Atrolnc‐1 and promotes the expression of Atrolnc‐1. In cultured C2C12 myotubes, overexpression of Atrolnc‐1 increases protein degradation (0.45±0.03 vs. 0.64±0.02, *p<0.05); Atrolnc‐1 knockdown significantly reduces the rate of protein degradation stimulated by serum depletion (0.61±0.03 vs. 0.47±0.02, *p<0.05). Using mass spectrometry and a lncRNA pull‐down assay, we identified that Atrolnc‐1 interacts with A20 binding inhibitor of NF‐κB‐1 (ABIN‐1). The interaction impairs function, resulting in enhanced NF‐κB activity plus MuRF‐1 transcription. This response is counteracted by CRISPR/dCas9 mediated overexpression. In muscles from normal mice, overexpression of Atrolnc‐1 stimulates a 2.7‐fold increase in MuRF‐1 expression leading to myofibers atrophy. In contrast, Atrolnc‐1 knockdown attenuates muscle wasting by 42% in mice with CKD via suppression of NF‐κB activity and MuRF‐1 expression.ConclusionsOur findings provide evidence that lncRNAs initiates the pathophysiological process of muscle wasting. The interaction between Atrolnc‐1 and NF‐κB signalling modulates muscle mass and proteolysis in CKD and perhaps other catabolic conditions.
Purkinje cell COX deficiency and mtDNA depletion in an animal model of spinocerebellar ataxia type 1
Authors: Ripolone Michela , Lucchini Valeria , Ronchi Dario , Fagiolari Gigliola , Bordoni Andreina , Fortunato Francesco , Mondello Stefania , Bonato Sara , Meregalli Mirella , Torrente Yvan , Corti Stefania , Comi Giacomo P. , Moggio Maurizio , Sciacco Monica 
Published: July 2018

AbstractSpinocerebellar ataxias (SCAs) are a genetically heterogeneous group of cerebellar degenerative disorders, characterized by progressive gait unsteadiness, hand incoordination, and dysarthria. Ataxia type 1 (SCA1) is caused by the expansion of a CAG trinucleotide repeat in the SCA1 gene resulting in the atypical extension of a polyglutamine (polyQ) tract within the ataxin‐1 protein. Our main objective was to investigate the mitochondrial oxidative metabolism in the cerebellum of transgenic SCA1 mice. SCA1 transgenic mice develop clinical features in the early life stages (around 5 weeks of age) presenting pathological cerebellar signs with concomitant progressive Purkinje neuron atrophy and relatively little cell loss; this evidence suggests that the SCA1 phenotype is not the result of cell death per se, but a possible effect of cellular dysfunction that occurs before neuronal demise. We studied the mitochondrial oxidative metabolism in cerebellar cells from both homozygous and heterozygous transgenic SCA1 mice, aged 2 and 6 months. Histochemical examination showed a cytochrome‐c‐oxidase (COX) deficiency in the Purkinje cells (PCs) of both heterozygous and homozygous mice, the oxidative defect being more prominent in older mice, in which the percentage of COX‐deficient PC was up to 30%. Using a laser‐microdissector, we evaluated the mitochondrial DNA (mtDNA) content on selectively isolated COX‐competent and COX‐deficient PC by quantitative Polymerase Chain Reaction and we found mtDNA depletion in those with oxidative dysfunction. In conclusion, the selective oxidative metabolism defect observed in neuronal PC expressing mutant ataxin occurs as early as 8 weeks of age thus representing an early step in the PC degeneration process in SCA1 disease.
Brain structural changes associated with aberrant functional responses to the Valsalva maneuver in heart failure
Authors: Song Xiaopeng , Roy Bhaswati , Fonarow Gregg C. , Woo Mary A. , Kumar Rajesh 
Published: July 2018

AbstractHeart failure (HF) patients show inability to regulate autonomic functions in response to autonomic challenges. The autonomic deficits may stem from brain tissue injury in central autonomic regulatory areas, resulting from ischemic and hypoxic processes accompanying the condition. However, the direct evaluation of correlations between brain structural injury and functional timing and magnitude of neural signal patterns within affected areas, which may lead to impaired autonomic outflow, is unclear. In this study, we evaluate neural responses to the Valsalva maneuver with blood oxygen level‐dependent functional magnetic resonance imaging in 29 HF patients and 35 control subjects and brain structural changes using diffusion tensor imaging‐based mean diffusivity in a subsample of 19 HF and 24 control subjects. HF showed decreased neural activation in multiple autonomic and motor control areas, including cerebellum cortices, vermis, left insular, left putamen, and bilateral postcentral gyrus. Structural brain changes emerged in similar autonomic, as well as cognitive and mood regulation areas. Functional MRI responses in cerebellum and insula in HF subjects are delayed or decreased in magnitude to the challenge. The impaired functional responses of insular and cerebellar sites are correlated with the severity of tissue changes. These results indicate that the functions of insular and cerebellar regions, sites that are involved in autonomic regulation, are compromised, and that autonomic deficits in these areas have brain structural basis for impaired functions. Our study enhanced our understanding of brain structural and functional alterations underlying impaired autonomic regulations in HF subjects.
The role of 5‐hydroxymethylcytosine in mitochondria after ischemic stroke
Authors: Ji Feng , Zhao Chenyu , Wang Bin , Tang Yan , Miao Zhigang , Wang Yongxiang 
Published: July 2018

Abstract5‐Hydroxymethylcytosine (5hmC) exists in DNA, RNA, and mitochondrial DNA (mtDNA) and plays an important role in many diseases. Specifically, 5hmC is involved in promoting gene expression, and this process is regulated by Tet enzymes. In this study, we identified that there is no difference in male mice and female mice at first; then we examined the levels of 5hmC in mtDNA and explored the relationship among 5hmC, mitochondrial gene expression and ATP production after acute brain ischemia. The abundance of mtDNA 5hmC was increased at 1 d and peaked at 2 d after ischemic injury, whereas that of mtDNA 5mC was unchanged. Furthermore, increased mitochondrial Tet2 expression was found to be responsible for the increase in mtDNA 5hmC. Tet2 inhibition decreased the mtDNA 5hmC abundance and increased the ATP levels in mitochondria, suggesting an association between the cellular ATP levels and mtDNA 5hmC abundance. We also demonstrated that mtDNA 5hmC increased the mRNA levels of mitochondrial genes after ischemia/reperfusion (I/R) injury.
Comparative estimation of sulfiredoxin levels between chronic periodontitis and healthy patients – A case‐control study
Authors: Ramesh Asha , Varghese Sheeja , Jayakumar Nadathur D. , Malaiappan Sankari 
Published: July 2018

AbstractBackgroundGrowing evidence suggests that oxidative stress forms a key component in the etiopathogenesis of periodontitis. Studies have shown potential antioxidants responsible for combating the pro‐oxidants which stress the periodontium. But, peroxiredoxin‐sulfiredoxin system is the least explored in periodontal disease.MethodsA case‐control study was conducted on 30 participants who fulfilled the inclusion criteria from the Department of Periodontics, Saveetha Dental College and Hospital, Chennai, India. The patients were divided into two groups: 1) Group A‐ healthy controls (n = 18), 2) Group B‐ patients with generalized chronic periodontitis (n = 17). Following clinical examination, gingival tissue samples were procured from both the groups and subjected to protein quantification by Lowry method. The samples with adequate protein concentration (n = 30) from the two groups were further analyzed by enzyme‐linked immunosorbent assay for estimation of sulfiredoxin levels.ResultsSulfiredoxin levels were significantly higher in the gingival tissues of chronic periodontitis patients (171.20 ± 16.97 ng/mL) than in healthy controls (131.20 ± 22.87) with P < 0.001. Also, the levels of sulfiredoxin in gingival tissue of periodontitis patients positively correlated with site‐specific probing depth (r = 0.67; P = 0.007) and clinical attachment level (r = 0.55; P = 0.035).ConclusionsThe present study was a novel attempt to estimate the levels of sulfiredoxin which was significantly elevated in the diseased sites of patients with chronic periodontitis. Future studies are required to probe the role of sulfiredoxin in the etiopathogenesis of periodontal disease.
Survival rates of hybrid rough surface implants and their alveolar bone level alterations
Authors: Lee Chun‐Teh , Tran Duong , Jeng Ming‐Dih , Shen Yi‐Tung 
Published: July 2018

AbstractBackgroundThe design of hybrid surface implants takes advantage of characteristics of two different textures to improve clinical outcomes. To date, there are limited numbers of studies reporting the clinical results of hybrid surface implants. This study aimed to assess hybrid surface implants with two different rough textures in regard to survival, marginal bone level change, and biological complications.MethodsRetrospective review of dental records was conducted for 161 patients who had 460 hybrid surface implants to analyze survival rate. These implants had the dual sandblasted and anode oxidized surface. Sixty patients with 192 implants who had consecutive radiographs taken at specific time points and complete clinical examinations were included in the comprehensive analysis. The associations between patient‐ and implant‐related characteristics, and clinical results were analyzed by log‐rank test, Cox regression, and linear regression analysis.ResultsCumulative survival at 12, 36, and 60 months after placement was 97.4%, 96.4%, and 95.8%, respectively. The average marginal bone level change from baseline to the last visit was 0.31 ± 0.68 mm and 0.34 ± 0.77 mm at the mesial and distal sites, respectively. Prevalence of peri‐implantitis was 0.5% at the implant level and 1.7% at the patient level. Implant site was associated with implant failure (P = 0.03). Smoking habit, history of periodontitis, and implant site were significantly associated with marginal bone level change (P = 0.001, < 0.001, 0.01, respectively).ConclusionsHybrid rough surface implants had high survival rate, stable bone level, and low prevalence of biological complications. This surface design demonstrated promising clinical outcomes. More studies are needed to further support the clinical advantages of hybrid surface implants.