bluuebunny/crossref_metadata_2025_split huggingface dataset:
Choice of Irrigation Water Management Practice Affects Indian Summer Monsoon Rainfall and Its Extremes
Authors: Devanand Anjana , Huang Maoyi , Ashfaq Moetasim , Barik Beas , Ghosh Subimal 
Published: August 2019

AbstractThere is an emerging understanding toward the importance of land‐atmosphere interactions in the monsoon system, but the effects of specific land and water management practices remain unclear. Here, using regional process‐based experiments, we demonstrate that monsoon precipitation is sensitive to the choice of irrigation practices in South Asia. Experiments with realistic representation of unmanaged irrigation and paddy cultivation over north‐northwest India exhibit an increase in the late season terrestrial monsoon precipitation and intensification of widespread extreme events over Central India, consistent with changes in observations. Such precipitation changes exhibit substantially different spatial patterns in experiments with a well‐managed irrigation system, indicating that increase in unmanaged irrigation might be a factor driving the observed changes in the intraseasonal monsoon characteristics. Our findings stress the need for accurate representation of irrigation practices to improve the reliability of earth system modeling over South Asia.
All‐Sky Imaging Observations and Modeling of Bright 630‐nm Airglow Structures Associated With MSTIDs
Authors: Martinis C. , Yokoyama T. , Nishioka M. 
Published: August 2019

AbstractAn all‐sky imager at El Leoncito Observatory (−31.8°, 69.3°W, 18.2° magnetic latitude) is used to study 630.0‐nm airglow emissions related to medium‐scale traveling ionospheric disturbances (MSTIDs). On the night of 6 December 2007 an unusual event consisting of bright bands propagating northwestward was observed. Enhancements in total electron content from ground‐based Global Positioning System receivers were observed collocated with the bright airglow bands. A regional Global Positioning System‐derived total electron content map matches the direction of motion, scale size, and location of these bright bands. Model results including F region coupling with E region structures reproduce the characteristics of the bright bands. Specific conditions in the E region must exist in order to observe these unusual MSTIDs consisting of propagating bright bands only.
How Accurately Can We Model Magma Reservoir Failure With Uncertainties in Host Rock Rheology?
Authors: Zhan Y. , Gregg P. M. 
Published: August 2019

AbstractForecasting the onset of a volcanic eruption from a closed system requires understanding its stress state and failure potential, which can be investigated through numerical modeling. However, the lack of constraints on model parameters, especially rheology, may substantially impair the accuracy of failure forecasts. Therefore, it is essential to know whether large variations and uncertainties in rock properties will preclude the ability of models to predict reservoir failure. A series of two‐dimensional, axisymmetric models are used to investigate sensitivities of brittle failure initiation to assumed rock properties. The numerical experiments indicate that the deformation and overpressure at failure onset simulated by elastic models will be much lower than the viscoelastic models, when the timescale of pressurization exceeds the viscoelastic relaxation time of the host rock. Poisson's ratio and internal friction angle have much less effect on failure forecasts than Young's modulus. Variations in Young's modulus significantly affect the prediction of surface deformation before failure onset when Young's modulus is < 40 GPa. Longer precursory volcano‐tectonic events may occur in weak host rock (E < 40 GPa) due to well‐developed Coulomb failure prior to dike propagation. Thus, combining surface deformation with seismicity may enhance the accuracy of eruption forecast in these situations. Compared to large and oblate magma systems, small and prolate systems create far less surface uplift prior to failure initiation, suggesting that more frequent measurements are necessary.
Parametric Controls on Vegetation Responses to Biogeochemical Forcing in the CLM5
Authors: Fisher Rosie A. , Wieder William R. , Sanderson Benjamin M. , Koven Charles D. , Oleson Keith W. , Xu Chonggang , Fisher Joshua B. , Shi Mingjie , Walker Anthony P. , Lawrence David M. 
Published: August 2019

AbstractFuture projections of land carbon uptake in Earth System Models are affected by land surface model responses to both CO2 and nitrogen fertilization. The Community Land Model, Version 5 (CLM5), contains a suite of modifications to carbon and nitrogen cycle representation. Globally, the CLM5 has a larger CO2 response and smaller nitrogen response than its predecessors. To improve our understanding of the controls over the fertilization responses of the new model, we assess sensitivity to eight parameters pertinent to the cycling of carbon and nitrogen by vegetation, both under present‐day conditions and with CO2 and nitrogen fertilization. The impact of fertilization varies with both model parameters and with the balance of limiting factors (water, temperature, nutrients, and light) in the pre‐fertilization model state. The model parameters that impact the pre‐fertilization state are in general not the same as those that control fertilization responses, meaning that goodness of fit to present‐day conditions does not necessarily imply a constraint on future transient projections. Where pre‐fertilization state has low leaf area, fertilization‐induced increases in leaf production amplify the model response to the initial fertilization via further increases in photosynthesis. Model responses to CO2 and N fertilization are strongly impacted by how much plant communities can increase their rates of nitrogen fixation and also directly affected by costs of N extraction from soil and stoichiometric flexibility. Illustration of how parametric flexibility impacts model outputs should help inform the interpretation of carbon‐climate feedbacks estimated by in fully coupled Earth system model simulations.
Estimation of Ionospheric Critical Plasma Frequencies From GNSS‐TEC Measurements Using Artificial Neural Networks
Authors: Otugo Vivian , Okoh Daniel , Okujagu Charity , Onwuneme Sylvester , Rabiu Babatunde , Uwamahoro Jean , Habarulema John Bosco , Tshisaphungo Mpho , Ssessanga Nicholas 
Published: August 2019

AbstractThis paper describes a new neural network‐based approach to estimate ionospheric critical plasma frequencies (f0F2) from Global Navigation Satellite Systems (GNSS)‐vertical total electron content (TEC) measurements. The motivation for this work is to provide a method that is realistic and accurate for using GNSS receivers (which are far more commonly available than ionosondes) to acquire f0F2 data. Neural networks were employed to train vertical TEC and corresponding f0F2 observations respectively obtained from closely located GNSS receivers and ionosondes in various parts of the globe. Available data from 52 pairs of ionosonde‐GNSS receiver stations for the 17‐year period from 2000 to 2016 were used. Results from this work indicate that the relationship between f0F2 and TEC is mostly affected by the seasons, followed by the level of solar activity, and then the local time. Geomagnetic activity was the least significant of the factors investigated. The relationship between f0F2 and TEC was also shown to exhibit spatial variation; the variation is less conspicuous for closely located stations. The results also show that there is a good correlation between the f0F2 and TEC parameters. The f0F2/TEC ratio was generally observed to be lower during enhanced ionospheric ionizations in the day time and higher during reduced ionospheric ionizations in the nights and early mornings. The analysis of errors shows that the model developed in this work (known as the NNT2F2 model) can be used to estimate the f0F2 from GNSS‐TEC measurements with accuracies of less than 1 MHz. The new approach described in this paper to obtain f0F2 based on GNSS‐TEC data represents an important contribution in space weather prediction.
Association of norepinephrine transporter methylation with in vivo NET expression and hyperactivity–impulsivity symptoms in ADHD measured with PET
Authors: Sigurdardottir H. L. , Kranz G. S. , Rami-Mark C. , James G. M. , Vanicek T. , Gryglewski G. , Berroterán-Infante N. , Kautzky A. , Hienert M. , Traub-Weidinger T. , Mitterhauser M. , Wadsak W. , Hartmann A. M. , Hacker M. , Rujescu D. , Kasper S. , Lanzenberger R. 
Published: August 2019

AbstractAttention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder with a robust genetic influence. The norepinephrine transporter (NET) is of particular interest as it is one of the main targets in treatment of the disorder. As ADHD is a complex and polygenetic condition, the possible regulation by epigenetic processes has received increased attention. We sought to determine possible differences in NET promoter DNA methylation between patients with ADHD and healthy controls. DNA methylation levels in the promoter region of the NET were determined in 23 adult patients with ADHD and 23 healthy controls. A subgroup of 18 patients with ADHD and 18 healthy controls underwent positron emission tomography (PET) with the radioligand (S,S)-[18F]FMeNER-D2 to quantify the NET in several brain areas in vivo. Analyses revealed significant differences in NET methylation levels at several cytosine–phosphate–guanine (CpG) sites between groups. A defined segment of the NET promoter (“region 1”) was hypermethylated in patients in comparison with controls. In ADHD patients, a negative correlation between methylation of a CpG site in this region and NET distribution in the thalamus, locus coeruleus, and the raphe nuclei was detected. Furthermore, methylation of several sites in region 1 was negatively associated with the severity of hyperactivity–impulsivity symptoms. Our results point to an epigenetic dysregulation in ADHD, possibly due to a compensatory mechanisms or additional factors involved in transcriptional processing.
Mechanisms and treatment of late-life depression
Authors: Alexopoulos George S. 
Published: August 2019

AbstractDepression predisposes to medical illnesses and advances biological aging indicated by shorter telomere length, accelerated brain aging and advanced epigenetic aging. Medical illnesses also increase the risk of late-life depression. The reciprocal relationships of depression with aging-related and disease-related processes have generated pathogenetic hypotheses and provided treatment targets. Targeting risk factors of vascular disease in mid-life is a logical approach in prevention of vascular depression. The depression-executive dysfunction and the vascular depression syndromes have clinical presentations and neuroimaging findings consistent with frontostriatal abnormalities. Dopamine D2/3agonists are effective in depression of Parkinson’s disease and their efficacy needs to be assessed in these two syndromes. Computerized cognitive remediation targeting functions of the cognitive control network may improve both executive functions and depressive symptoms of late-life major depression. Significant progress has been made in neurostimulation treatments in depressed younger adults. TMS targeting deep structures responsible for mood regulation is well tolerated by older adults and its efficacy in syndromes of late-life depression needs to be studied. Efficacious psychotherapies for late-life depression exist, but are underutilized in part because of their complexity. Streamlined, stepped psychotherapies targeting behaviors assumed to result from dysfunction of brain networks implicated in late-life depression can be easy to learn and have potential for dissemination. However, their effectiveness needs further investigation. Depression increases the risk of dementing disorders. Antidepressants are rather ineffective in treating depression of demented patients, but long-term use of antidepressants may reduce the risk of dementia. However, confirmation studies are needed.
Sustained Akt signaling in articular chondrocytes causes osteoarthritis via oxidative stress-induced senescence in mice
Authors: Xie Jing , Lin Jingting , Wei Min , Teng Yan , He Qi , Yang Guan , Yang Xiao 
Published: August 2019

AbstractOsteoarthritis (OA) is an age-related disorder that is strongly associated with chondrocyte senescence. The causal link between disruptive PTEN/Akt signaling and chondrocyte senescence and the underlying mechanism are unclear. In this study, we found activated Akt signaling in human OA cartilage as well as in a mouse OA model with surgical destabilization of the medial meniscus. Genetic mouse models mimicking sustained Akt signaling in articular chondrocytes viaPTENdeficiency driven by eitherCol2a1-CreorCol2a1-CreERT2developed OA, whereas restriction of Akt signaling reversed the OA phenotypes inPTEN-deficient mice. Mechanistically, prolonged activation of Akt signaling caused an accumulation of reactive oxygen species and triggered chondrocyte senescence as well as a senescence-associated secretory phenotype, whereas chronic administration of the antioxidant N-acetylcysteine suppressed chondrocyte senescence and mitigated OA progression inPTEN-deficient mice. Therefore, inhibition of Akt signaling by PTEN is required for the maintenance of articular cartilage. Disrupted Akt signaling in articular chondrocytes triggers oxidative stress-induced chondrocyte senescence and causes OA.
miR-425 deficiency promotes necroptosis and dopaminergic neurodegeneration in Parkinson’s disease
Authors: Hu Yong-Bo , Zhang Yong-Fang , Wang Hao , Ren Ru-Jing , Cui Hai-Lun , Huang Wan-Ying , Cheng Qi , Chen Hong-Zhuan , Wang Gang 
Published: August 2019

AbstractA major hallmark of Parkinson’s disease (PD) is the degeneration of dopaminergic neurons in the substantia nigra, and the causative mechanism is thought to be the activation of programmed neuronal death. Necroptosis is a regulated process of cell death triggered by RIPK1. Although the pathophysiology of PD has been studied extensively, the cellular mechanism underlying dopaminergic neuron death remains unclear. In this study, we detected a specific miRNA, miR-425, in response to MPTP toxicity and dopaminergic degeneration. In MPTP-treated mice, we observed necroptosis activation and miR-425 deficiency in the substantia nigra, which is correlated with dopaminergic neuron loss. This miRNA targeted RIPK1 transcripts and promoted the phosphorylation of MLKL and necroptosis. Similarly, in the brains of PD patients, miR-425 deficiency and necroptosis activation were also confirmed in dopaminergic neuron. Furthermore, we found that genetic knockdown of miR-425 aggravated MPTP-induced motor deficits and dopaminergic neurodegeneration via early upregulation of necroptotic genes. Intracerebral miR-425 mimics (AgomiR-425) treatment attenuated necroptosis activation and dopaminergic neuron loss, and improved locomotor behaviors. In conclusion, our study suggests that miR-425 deficiency triggers necroptosis of dopaminergic neurons, and targeting miR-425 in MPTP-treated mice restored dysfunctional dopaminergic neurodegeneration and ameliorated behavioral deficits. These findings identify brain delivery of miR-425 as a potential therapeutic approach for the treatment of PD.
O-cyclic phytosphingosine-1-phosphate stimulates HIF1α-dependent glycolytic reprogramming to enhance the therapeutic potential of mesenchymal stem cells
Authors: Lee Hyun Jik , Jung Young Hyun , Choi Gee Euhn , Kim Jun Sung , Chae Chang Woo , Lim Jae Ryong , Kim Seo Yihl , Lee Joo Eun , Park Min Chul , Yoon Jee Hyeon , Choi Myeong Jun , Kim Kye-Seong , Han Ho Jae 
Published: August 2019

AbstractO-cyclic phytosphingosine-1-phosphate (cP1P) is a novel chemically synthesized sphingosine metabolite derived from phytosphingosine-1-phosphate. Although structurally similar to sphingosine-1-phosphate (S1P), its biological properties in stem cells remain to be reported. We investigated the effect of cP1P on the therapeutic potential of mesenchymal stem cells (MSCs) and their regulatory mechanism. We found that, under hypoxia, cP1P suppressed MSC mitochondrial dysfunction and apoptosis. Metabolic data revealed that cP1P stimulated glycolysis via the upregulation of glycolysis-related genes. cP1P-induced hypoxia-inducible factor 1 alpha (HIF1α) plays a key role for MSC glycolytic reprogramming and transplantation efficacy. The intracellular calcium-dependent PKCα/mammalian target of the rapamycin (mTOR) signaling pathway triggered by cP1P regulated HIF1α translation via S6K1, which is critical for HIF1 activation. Furthermore, the cP1P-activated mTOR pathway induced bicaudal D homolog 1 expression, leading to HIF1α nuclear translocation. In conclusion, cP1P enhances the therapeutic potential of MSC through mTOR-dependent HIF1α translation and nuclear translocation.
Cigarette smoke activates the parthanatos pathway of cell death in human bronchial epithelial cells
Authors: Künzi Lisa , Holt Gregory E. 
Published: August 2019

AbstractTobacco smoke negatively affects human bronchial epithelial (HBE) cells and is directly implicated in the etiology of smoking related respiratory diseases. Smoke exposure causes double-stranded DNA breaks and DNA damage activates PARP-1, the key mediator of the parthanatos pathway of cell death. We hypothesize that smoke exposure activates the parthanatos pathway in HBE cells and represents a cell death mechanism that contributes to smoking related lung diseases. We exposed fully differentiated, primary HBE cells grown at the air liquid interface to cigarette smoke and evaluated them for parthanatos pathway activation. Smoke exposure induced mitochondrial to nuclear translocation of Apoptosis-Inducing Factor (AIF) and Endonuclease G (EndoG) within the first three hours characteristic of the parthanatos pathway. Exposing cells to an increasing number of cigarettes revealed that significant activation of the parthanatos pathway occurs after exposure to higher levels of smoke. Use of the specific PARP-1 inhibitor, BMN673, abrogated the effect of smoke induced activation of the parthanatos pathway. Smoke-mediated activation of the parthanatos pathway is increased in HBE cells originating from habitual smokers compared to non-smokers. This suggests that chronic smoke exposure leads to an increase in smoke-mediated activation of the parthanatos pathway and implicates its contribution in the pathogenesis of smoke-related lung diseases.
Autoantibodies as diagnostic biomarkers for lung cancer: A systematic review
Authors: Yang Bin , Li Xiaoyan , Ren Tianyi , Yin Yiyu 
Published: August 2019

AbstractLung cancer (LC) accounts for the largest number of tumor-related deaths worldwide. As the overall 5-year survival rate of LC is associated with its stages at detection, development of a cost-effective and noninvasive cancer screening method is necessary. We conducted a systematic review to evaluate the diagnostic values of single and panel tumor-associated autoantibodies (TAAbs) in patients with LC. This review included 52 articles with 64 single TAAbs and 19 with 20 panels of TAAbs. Enzyme-linked immunosorbent assays (ELISA) were the most common detection method. The sensitivities of single TAAbs for all stages of LC ranged from 3.1% to 92.9% (mean: 45.2%, median: 37.1%), specificities from 60.6% to 100% (mean: 88.1%, median: 94.9%), and AUCs from 0.416 to 0.990 (mean: 0.764, median: 0.785). The single TAAb with the most significant diagnostic value was the autoantibody against human epididymis secretory protein (HE4) with the maximum sensitivity 91% for NSCLC. The sensitivities of the panel of TAAbs ranged from 30% to 94.8% (mean: 76.7%, median: 82%), specificities from 73% to 100% (mean: 86.8%, median: 89.0%), and AUCs from 0.630 to 0.982 (mean: 0.821, median: 0.820), and the most significant AUC value in a panel (M13 Phage 908, 3148, 1011, 3052, 1000) was 0.982. The single TAAb with the most significant diagnostic calue for early stage LC, was the autoantibody against Wilms tumor protein 1 (WT1) with the maximum sensitivity of 90.3% for NSCLC and its sensitivity and specificity in a panel (T7 Phage 72, 91, 96, 252, 286, 290) were both above 90.0%. Single or TAAbs panels may be useful biomarkers for detecting LC patients at all stages or an early-stage in high-risk populations or health people, but the TAAbs panels showed higher detection performance than single TAAbs. The diagnostic value of the panel of six TAAbs, which is higher than the panel of seven TAAbs, may be used as potential biomarkers for the early detection of LC and can probably be used in combination with low-dose CT in the clinic.
Maintenance of cell type-specific connectivity and circuit function requires Tao kinase
Authors: Tenedini Federico Marcello , Sáez González Maria , Hu Chun , Pedersen Lisa Hedegaard , Petruzzi Mabel Matamala , Spitzweck Bettina , Wang Denan , Richter Melanie , Petersen Meike , Szpotowicz Emanuela , Schweizer Michaela , Sigrist Stephan J. , Calderon de Anda Froylan , Soba Peter 
Published: August 2019

AbstractSensory circuits are typically established during early development, yet how circuit specificity and function are maintained during organismal growth has not been elucidated. To gain insight we quantitatively investigated synaptic growth and connectivity in the Drosophila nociceptive network during larval development. We show that connectivity between primary nociceptors and their downstream neurons scales with animal size. We further identified the conserved Ste20-like kinase Tao as a negative regulator of synaptic growth required for maintenance of circuit specificity and connectivity. Loss of Tao kinase resulted in exuberant postsynaptic specializations and aberrant connectivity during larval growth. Using functional imaging and behavioral analysis we show that loss of Tao-induced ectopic synapses with inappropriate partner neurons are functional and alter behavioral responses in a connection-specific manner. Our data show that fine-tuning of synaptic growth by Tao kinase is required for maintaining specificity and behavioral output of the neuronal network during animal growth.
Broadband THz to NIR up-converter for photon-type THz imaging
Authors: Bai Peng , Zhang Yueheng , Wang Tianmeng , Fu Zhanglong , Shao Dixiang , Li Ziping , Wan Wenjian , Li Hua , Cao Juncheng , Guo Xuguang , Shen Wenzhong 
Published: August 2019

AbstractHigh performance terahertz imaging devices have drawn wide attention due to their significant application in healthcare, security of food and medicine, and nondestructive inspection, as well as national security applications. Here we demonstrate a broadband terahertz photon-type up-conversion imaging device, operating around the liquid helium temperature, based on the gallium arsenide homojunction interfacial workfunction internal photoemission (HIWIP)-detector-LED up-converter and silicon CCD. Such an imaging device achieves broadband response in 4.2–20 THz and can absorb the normal incident light. The peak responsivity is 0.5 AW−1. The light emitting diode leads to a 72.5% external quantum efficiency improvement compared with the one widely used in conventional up-conversion devices. A peak up-conversion efficiency of 1.14 × 10−2 is realized and the optimal noise equivalent power is 29.1 pWHz−1/2. The up-conversion imaging for a 1000 K blackbody pin-hole is demonstrated. This work provides a different imaging scheme in the terahertz band.