bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Early Cretaceous Shangzhuang layered mafic intrusion and its bearing on decratonization of the North China Craton
Authors: TENG XUE-MING , SANTOSH M. , TANG LI 
Published: May 2017

AbstractThe North China Craton (NCC) is one of the classic examples of decratonization through extensive lithospheric destruction during Mesozoic time. Among the various pulses of magmatism associated with cratonic erosion are the rare mafic intrusions in the Yanshan Belt. Here we investigate the Shangzhuang layered intrusion belonging to this suite, which is characterized by compositional layering with troctolite, noritic gabbro and gabbro/gabbroic anorthosite/gabbrodiorite from the bottom to top. The different lithologies of this intrusion exhibit close field relationships, similar chemical patterns and overall identical Lu–Hf isotopes indicating a co-magmatic nature. The fine-grained gabbros occurring near the margin of the intrusion display U–Pb ages similar to those of the other rocks and are considered to represent the composition of the parent magma, characterized by Fe, Mg and Ti enrichment. The magma was sourced from low-degree partial melting of spinel lherzolite sub-continental lithospheric mantle, which had been enriched by crust–mantle interaction and metasomatic fluids derived from the Mongolian oceanic slab subduction beneath the NCC during Late Palaeozoic time. In addition, limited asthenospheric or deeper-mantle materials were also locally mixed with the enriched mantle as the final source component. Our zircon U–Pb data constrain the emplacement age of this intrusion asc. 128–123 Ma in Early Cretaceous time, and correlates with the regional extensional tectonics betweenc. 135 and 115 Ma in the eastern and central NCC. Mantle upwelling associated with this event resulted in the thermal and chemical erosion of the lithospheric mantle, and emplacement of the parent magma of this layered intrusion.
Update on the distribution of the co-invasiveSchyzocotyle acheilognathi(=Bothriocephalus acheilognathi), the Asian fish tapeworm, in freshwater fishes of Mexico
Authors: Pérez-Ponce de León G. , Lagunas-Calvo O. , García-Prieto L. , Briosio-Aguilar R. , Aguilar-Aguilar R. 
Published: May 2017

AbstractThe Asian fish tapeworm,Schyzocotyle acheilognathi(syn.Bothriocephalus acheilognathi) represents a threat to freshwater fish, mainly cyprinids, across the globe. This tapeworm possesses an extraordinary ability to adapt to different environmental conditions and, because of that, from its natural geographical origin in mainland Asia, it has colonized every continent except Antarctica. It is thought that this pathogenic tapeworm was first co-introduced into Mexico in 1965 from China, with the grass carpCtenopharyngodon idella, although the first formal record of its presence was published in 1981. Over the past 35 years, the Asian fish tapeworm has invaded about 22% of the freshwater fish in Mexico. Because fish communities in Mexico are characterized by high species richness and levels of endemism,S. acheilognathiis considered as a co-introduced and co-invasive species. In this review, we update the geographic distribution and host spectrum of the Asian fish tapeworm in Mexico. Up until December 2016, the tapeworm had been recorded in 110 freshwater fish species (96 native and 14 introduced), included in 51 genera, 11 families and 4 orders; it was also widely distributed in all types of aquatic environments, and has been found in 214 localities. We present novel data from a survey aimed at establishing the distribution pattern of the tapeworm in native freshwater fishes of two rivers in north-central Mexico, and the genetic variation among individuals of this co-invasive species collected from different host species and localities. We discuss briefly the factors that have determined the remarkable invasive success of this parasite in freshwater systems in Mexico.
Adjunctive memantine for schizophrenia: a meta-analysis of randomized, double-blind, placebo-controlled trials
Authors: Zheng W. , Li X-H. , Yang X-H. , Cai D-B. , Ungvari G. S. , Ng C. H. , Wang S-B. , Wang Y-Y. , Ning Y-P. , Xiang Y-T. 
Published: May 2017

BackgroundDysfunction of N-methyl-D-aspartate receptor (NMDAR) is involved in the pathophysiology of schizophrenia. A meta-analysis of randomized controlled trials (RCTs) was conducted to examine the efficacy and safety of memantine, a non-competitive NMDAR antagonist, in the treatment of schizophrenia.MethodsStandardized/weighted mean differences (SMDs/WMDs), risk ratio (RR), and their 95% confidence intervals (CIs) were calculated and analyzed.ResultsIncluded in the meta-analysis were eight RCTs (n = 452) of 11.5 ± 2.6 weeks duration, with 229 patients on memantine (20 mg/day) and 223 patients on placebo. Adjunctive memantine outperformed placebo in the measures of Positive and Negative Syndrome Scale and Brief Psychiatric Rating Scale negative symptoms [SMD: −0.63 (95% CI −1.10 to −0.16), p = 0.009, I2 = 77%], but not in the total, positive and general symptoms [SMD: −0.46 to −0.08 (95% CI −0.93 to 0.22), p = 0.06–0.60, I2 = 0–74%] or the Clinical Global Impression Severity Scale [WMD: 0.04 (95% CI −0.24 to 0.32), p = 0.78]. The negative symptoms remained significant after excluding one outlying RCT [SMD: −0.41 (95% CI −0.72 to −0.11), p = 0.008, I2 = 47%]. Compared with the placebo group, adjunctive memantine was associated with significant improvement in neurocognitive function using the Mini-Mental State Examination (MMSE) [WMD: 3.09, (95% CI 1.77–4.42), p < 0.00001, I2 = 22%]. There was no significant difference in the discontinuation rate [RR: 1.34 (95% CI 0.76–2.37), p = 0.31, I2 = 0%] and adverse drug reactions between the two groups.ConclusionsThis meta-analysis showed that adjunctive memantine appears to be an efficacious and safe treatment for improving negative symptoms and neurocognitive performance in schizophrenia. Higher quality RCTs with larger samples are warranted to confirm these findings.
White matter connectivity disruptions in early and chronic schizophrenia
Authors: Di Biase M. A. , Cropley V. L. , Baune B. T. , Olver J. , Amminger G. P. , Phassouliotis C. , Bousman C. , McGorry P. D. , Everall I. , Pantelis C. , Zalesky A. 
Published: May 2017

BackgroundWhite matter disruptions in schizophrenia have been widely reported, but it remains unclear whether these abnormalities differ between illness stages. We mapped the connectome in patients with recently diagnosed and chronic schizophrenia and investigated the extent and overlap of white matter connectivity disruptions between these illness stages.MethodsDiffusion-weighted magnetic resonance images were acquired in recent-onset (n = 19) and chronic patients (n = 45) with schizophrenia, as well as age-matched controls (n = 87). Whole-brain fiber tracking was performed to quantify the strength of white matter connections. Connections were tested for significant streamline count reductions in recent-onset and chronic groups, relative to separate age-matched controls. Permutation tests were used to assess whether disrupted connections significantly overlapped between chronic and recent-onset patients. Linear regression was performed to test whether connectivity was strongest in controls, weakest in chronic patients, and midway between these extremities in recent-onset patients (controls > recent-onset > chronic).ResultsCompared with controls, chronic patients displayed a widespread network of connectivity disruptions (p < 0.01). In contrast, connectivity reductions were circumscribed to the anterior fibers of the corpus callosum in recent-onset patients (p < 0.01). A significant proportion of disrupted connections in recent-onset patients (86%) coincided with disrupted connections in chronic patients (p < 0.01). Linear regression revealed that chronic patients displayed reduced connectivity relative to controls, while recent-onset patients showed an intermediate reduction compared with chronic patients (p < 0.01).ConclusionsConnectome pathology in recent-onset patients with schizophrenia is confined to select tracts within a more extensive network of white matter connectivity disruptions found in chronic illness. These findings may suggest a trajectory of progressive deterioration of connectivity in schizophrenia.
Face and Object Perception in Body Dysmorphic Disorder versus Obsessive-Compulsive Disorder: The Mooney Faces Task
Authors: Toh Wei Lin , Castle David J. , Rossell Susan L. 
Published: May 2017

AbstractObjectives: Body dysmorphic disorder (BDD) is characterized by repetitive behaviors and/or mental acts occurring in response to preoccupations with perceived defects or flaws in physical appearance. There are some similarities, but also important differences, between BDD and obsessive-compulsive disorder (OCD), not just in terms of core clinical symptoms, but possibly in the domain of perception. This study compared the nature and extent of perceptual anomalies in BDD versus OCD and health controls (HC), using a modified Mooney task. Methods: We included 21 BDD, 19 OCD, and 21 HC participants, who were age-, sex-, and IQ-matched. A set of 40 Mooney faces and 40 Mooney objects arranged in three configurations (i.e., upright, inverted, or scrambled) were presented under brief (i.e., 500 ms) free-viewing conditions. Participants were asked to decide whether each image represented a human face, an object, or neither in a forced-choice paradigm. Results: The BDD group showed significantly reduced face and object inversion effects relative to the other two groups. This was accounted for by BDD participants being significantly more accurate in identifying inverted Mooney faces and objects than the other participants. Conclusions: These data were interpreted as reflecting an overreliance on independent components at the expense of holistic (configural) processing in BDD. (JINS, 2017, 23, 471–480)
Agronomic and physiological aspects of nitrogen use efficiency in conventional and organic cereal-based production systems
Authors: Kubota Hiroshi , Iqbal Muhammad , Quideau Sylvie , Dyck Miles , Spaner Dean 
Published: May 2017

AbstractBetter management of synthetic nitrogen (N) fertilizers in conventional agricultural systems laid the foundation for feeding the increasing world's population since the Green Revolution. However, excessive reliance on inorganic fertilizer has resulted in environmental degradation issues. Difficulties in soil nutrition management in organic cropping systems often results in lower and variable yields, also raising questions of sustainability. Improving nitrogen use efficiency (NUE) is thus of key importance to overcome environmental concerns in conventional systems and production limitations in organic systems. The differences in the two farming systems have impacts on crop traits and N cycles, making it difficult to enhance NUE with a single strategy. Different approaches need to be adopted to improve NUE in each system. Extensive efforts have been made to better understand mechanisms to potentially improve NUE in cereal crops under both systems. This review suggests that NUE may be improved through a combination of management practices and breeding strategies specific to the management system. Diversified crop rotations with legumes are effective practices to optimize the N cycle in both conventional and organic systems. Best Management Practices coupled with nitrification inhibitors, controlled release products and split-application practices can reduce N loss in conventional systems. In organic systems, we need to take advantage of available N sources and adapt practices such as no-tillage, cover crops, and catch crops. Utilization of beneficial soil microorganisms is fundamental to optimizing availability of soil N. Estimation of soil organic matter mineralization using prediction models may be useful to enhance NUE if models are calibrated for target environments. Cereal crops are often bred under optimum N conditions and may not perform well under low N conditions. Thus, breeders can integrate genetic and phenotypic information to develop cultivars adapted to specific environments and cultivation practices. The proper choice and integration of strategies can synchronize N demand and supply within a system, resulting in reduced risk of N loss while improving NUE in both conventional and organic systems.
Effects of concomitant inactivation of p53 and pRb on response to doxorubicin treatment in breast cancer cell lines
Authors: Huun Johanna , Lønning Per Eystein , Knappskog Stian 
Published: May 2017

AbstractLoss of TP53 and RB1 function have both been linked to poor response to DNA damaging drugs in breast cancer patients. We inactivated TP53 and/or RB1 by siRNA mediated knockdown in breast cancer cell lines varying with respect to ER/PgR and Her-2 status as well as TP53 and RB1 mutation status (MCF-7, T47D, HTB-122 and CRL2324) and determined effects on cell cycle arrest, apoptosis and senescence with or without concomitant treatment with doxorubicin. In T47D cells, we found the cell cycle phase distribution to be altered when inactivating TP53 (P=0.0003) or TP53 and RB1 concomitantly (P≤0.001). No similar changes were observed in MCF-7, HTB-122 or CRL2324 cells. While no significant change was observed for the CRL2324 cells upon doxorubicin treatment, MCF-7, T47D as well as HTB-122 cells responded to knockdown of TP53 and RB1 in concert, with a decrease in the fraction of cells in G1/G0-phase (P=0.042, 0.021 and 0.027, respectively). Inactivation of TP53 and/or RB1 caused no change in induction of apoptosis. Upon doxorubicin treatment, inactivation of TP53 or RB1 separately caused no induction of apoptosis in MCF-7 and HTB-122 cells; however, concomitant inactivation leads to a slightly reduced activation of apoptosis. Interestingly, upon doxorubicin treatment, concomitant inactivation of TP53 and RB1 caused a decrease in senescence in MCF-7 cells (P=0.027). Comparing the effects of concomitant knockdown on apoptosis and senescence, we observed a strong interaction (P=0.001). We found concomitant inactivation of TP53 and RB1 to affect various routes of response to doxorubicin treatment in breast cancer cells.
Thermogenetic neurostimulation with single-cell resolution
Authors: Ermakova Yulia G. , Lanin Aleksandr A. , Fedotov Ilya V. , Roshchin Matvey , Kelmanson Ilya V. , Kulik Dmitry , Bogdanova Yulia A. , Shokhina Arina G. , Bilan Dmitry S. , Staroverov Dmitry B. , Balaban Pavel M. , Fedotov Andrei B. , Sidorov-Biryukov Dmitry A. , Nikitin Evgeny S. , Zheltikov Aleksei M. , Belousov Vsevolod V. 
Published: May 2017

AbstractThermogenetics is a promising innovative neurostimulation technique, which enables robust activation of neurons using thermosensitive transient receptor potential (TRP) cation channels. Broader application of this approach in neuroscience is, however, hindered by a limited variety of suitable ion channels, and by low spatial and temporal resolution of neuronal activation when TRP channels are activated by ambient temperature variations or chemical agonists. Here, we demonstrate rapid, robust and reproducible repeated activation of snake TRPA1 channels heterologously expressed in non-neuronal cells, mouse neurons and zebrafish neurons in vivo by infrared (IR) laser radiation. A fibre-optic probe that integrates a nitrogen−vacancy (NV) diamond quantum sensor with optical and microwave waveguide delivery enables thermometry with single-cell resolution, allowing neurons to be activated by exceptionally mild heating, thus preventing the damaging effects of excessive heat. The neuronal responses to the activation by IR laser radiation are fully characterized using Ca2+ imaging and electrophysiology, providing, for the first time, a complete framework for a thermogenetic manipulation of individual neurons using IR light.
Constraining climate sensitivity and continental versus seafloor weathering using an inverse geological carbon cycle model
Authors: Krissansen-Totton Joshua , Catling David C. 
Published: May 2017

AbstractThe relative influences of tectonics, continental weathering and seafloor weathering in controlling the geological carbon cycle are unknown. Here we develop a new carbon cycle model that explicitly captures the kinetics of seafloor weathering to investigate carbon fluxes and the evolution of atmospheric CO2 and ocean pH since 100 Myr ago. We compare model outputs to proxy data, and rigorously constrain model parameters using Bayesian inverse methods. Assuming our forward model is an accurate representation of the carbon cycle, to fit proxies the temperature dependence of continental weathering must be weaker than commonly assumed. We find that 15–31 °C (1σ) surface warming is required to double the continental weathering flux, versus 3–10 °C in previous work. In addition, continental weatherability has increased 1.7–3.3 times since 100 Myr ago, demanding explanation by uplift and sea-level changes. The average Earth system climate sensitivity is "Equation missing" K (1σ) per CO2 doubling, which is notably higher than fast-feedback estimates. These conclusions are robust to assumptions about outgassing, modern fluxes and seafloor weathering kinetics.
Upregulation of CYP17A1 by Sp1-mediated DNA demethylation confers temozolomide resistance through DHEA-mediated protection in glioma
Authors: Chuang J-Y , Lo W-L , Ko C-Y , Chou S-Y , Chen R-M , Chang K-Y , Hung J-J , Su W-C , Chang W-C , Hsu T-I 
Published: May 2017

AbstractSteroidogenesis-mediated production of neurosteroids is important for brain homeostasis. Cytochrome P450 17A1 (CYP17A1), which converts pregnenolone to dehydroepiandrosterone (DHEA) in endocrine organs and the brain, is required for prostate cancer progression and acquired chemotherapeutic resistance. However, whether CYP17A1-mediated DHEA synthesis is involved in brain tumor malignancy, especially in glioma, the most prevalent brain tumor, is unknown. To investigate the role of CYP17A1 in glioma, we determined that CYP17A1 expression is significantly increased in gliomas, which secrete more DHEA than normal astrocytes. We found that as gliomas became more malignant, both CYP17A1 and DHEA were significantly upregulated in temozolomide (TMZ)-resistant cells and highly invasive cells. In particular, the increase of CYP17A1 was caused by Sp1-mediated DNA demethylation, whereby Sp1 competed with DNMT3a for binding to the CYP17A1 promoter in TMZ-resistant glioma cells. CYP17A1 was required for the development of glioma cell invasiveness and resistance to TMZ-induced cytotoxicity. In addition, DHEA markedly attenuated TMZ-induced DNA damage and apoptosis. Together, our results suggest that components of the Sp1–CYP17A1–DHEA axis, which promotes the development of TMZ resistance, may serve as potential biomarkers and therapeutic targets in recurrent glioma.
Genome sequencing as a platform for pharmacogenetic genotyping: a pediatric cohort study
Authors: Cohn Iris , Paton Tara A. , Marshall Christian R. , Basran Raveen , Stavropoulos Dimitri J. , Ray Peter N. , Monfared Nasim , Hayeems Robin Z. , Meyn M. Stephen , Bowdin Sarah , Scherer Stephen W. , Cohn Ronald D. , Ito Shinya 
Published: May 2017

AbstractWhole-genome sequencing and whole-exome sequencing have proven valuable for diagnosing inherited diseases, particularly in children. However, usage of sequencing data as a pharmacogenetic screening tool to ensure medication safety and effectiveness remains to be explored. Sixty-seven variants in 19 genes with known effects on drug response were compared between genome sequencing and targeted genotyping data for coverage and concordance in 98 pediatric patients. We used targeted genotyping data as a benchmark to assess accuracy of variant calling, and to identify copy number variations of the CYP2D6 gene. We then predicted clinical impact of these variants on drug therapy. We find genotype concordance across those panels to be > 97%. Concordance of CYP2D6 predicted phenotype between estimates of whole-genome sequencing and targeted genotyping panel were 90%; a result from a lower coverage depth or variant calling difficulties in our whole-genome sequencing data when copy number variation and/or the CYP2D6*4 haplotype were present. Importantly, 95 children had at least one clinically actionable pharmacogenetic variant. Diagnostic genomic sequencing data can be used for pre-emptive pharmacogenetic screening. However, concordance between genome-wide sequencing and target genotyping needs to be characterized for each of the pharmacologically important genes.
A multifactorial study on nutritional status, binge eating and physical activity as main factors directly influencing body weight in Parkinson’s disease
Authors: Bril Andrea , Perez-Lloret Santiago , Rossi Malco , Fariña Sofía , Morisset Pierre , Sorrentino Laura , Iglesias Micaela , Medina Escobar Alex , Millar Vernetti Patricio , Cerquetti Daniel , Merello Marcelo 
Published: May 2017

AbstractWeight lossisa multifactorial disorder commonly affecting Parkinson’s disease patients. The aim of this study was to investigate the relationship between body weight, nutritional status, physical activity, and Parkinson’s disease-related factors. A total of 114 consecutive Parkinson’s disease patients without dietary restrictions were evaluated prospectively with respect to: nutritional status (Mini Nutritional Assessment), physical activity level (Yale Physical Activity Survey), MDS-UPDRS score, olfactory function, depression, cognitive functionand impulse-control disorders, among other variables. Structural equation modeling was used to build multivariate models and to calculate standardized regression weights (srw) for pairs of variables, which are homologous to correlation coefficients, taking into account the effects of all other variables in the model. Sixty (53%) patients were males. Mean age was 66.1 ± 9.8 years and mean disease duration was 8.3 ± 5.6 years. Longer disease duration was negatively related to nutritional status (srw = −0.25; p = 0.01). UPDRS II + III score was associated with reduced cognitive function (srw = −0.39; p = 0.01), which was positivelyrelated to nutritional status (srw = 0.23; p = 0.01). Finally, nutritional status was positively related to body weight (srw = 0.22, p < 0.01). Binge eating and physical activity were also directly and positively related to body weight (srw = 0.32; p = 0.001 and srw = 0.23; p = 0.001). Nutritional status, binge eating and physical activity were directly and independently related to body weight in our sample of Parkinson’s disease patients. Therefore, physicians should actively explore nutritional status and binge eating in Parkinson’s disease patients to avoid alterations in body weight regulation. Effects of physical activity should be further explored.