bluuebunny/crossref_metadata_2025_split huggingface dataset:
Measuring the Research Productivity of Political Science Departments Using Google Scholar
Authors: Peress Michael 
Published: November 2018

ABSTRACTThis article develops a number of measures of the research productivity of political science departments using data collected from Google Scholar. Departments are ranked in terms of citations to articles published by faculty, citations to articles recently published by faculty, impact factors of journals in which faculty published, and number of top publications in which faculty published. Results are presented in aggregate terms and on a per-faculty basis.
Selbstregulationsstrategien bei Früh- und Reifgeborenen im Alter von zwei Jahren
Authors: Stern Maren , Gärtner Kim A. , Vetter Verena C. , Hertel Silke , Reuner Gitta 
Published: November 2018

Zusammenfassung. Frühgeburtlichkeit stellt einen Risikofaktor für die kognitive Entwicklung und die selbstregulatorischen Fähigkeiten dar. Bisher ist jedoch nicht bekannt, welche Strategien frühgeborene Kinder zur Regulation nutzen. Die aktuelle Studie untersuchte daher erfolgreiche Selbstregulationsstrategien von 30 früh- (Gestationsalter < 37 Wochen) und 30 reifgeborenen Kindern (Gestationsalter ≥ 37 Wochen) im (korrigierten) Alter von 2 Jahren. Die Kinder wurden während einer Aufgabe zum Bedürfnisaufschub videographiert und spezifische Verhaltensweisen (Blick, Sprache, Bewegungen der Hände, des Kopfes und des Körpers) kodiert. Mikroanalysen ergaben, dass Fokussierungs- als auch Ablenkungsstrategien, sowie motorische Kontrollstrategien für einen erfolgreichen Bedürfnisaufschub angewendet wurden. Die Gruppen unterschieden sich nicht signifikant im Gebrauch der Strategien; lediglich am Ende des letzten Durchgangs wurden bei Frühgeborenen vermehrt Ablenkungsstrategien beobachtet. Frühgeburtlichkeit scheint somit keinen direkten Einfluss auf die Anwendung der Strategien zu haben. Das Ausmaß der Frühgeburtlichkeit und das Alter der Kinder sollten in zukünftiger Forschung differenzierter betrachtet werden.
Downregulation of ASPP2 promotes gallbladder cancer metastasis and macrophage recruitment via aPKC-ι/GLI1 pathway
Authors: Tian Li , Deng Zhengdong , Xu Lei , Yang Tao , Yao Wei , Ji Lei , Lu Yun , Zhang Jian , Liu Yan , Wang Jianming 
Published: November 2018

AbstractGallbladder cancer (GBC) is a highly malignant bile duct cancer with poor prognosis due to early invasion and metastasis. However, the molecular mechanisms through which GBC cells interact with the tumor microenvironment (TME) remain poorly understood. Here, we examined the role of the tumor suppressor apoptosis-stimulating of p53 protein 2 (ASPP2) in regulating GBC invasion and metastasis and macrophage recruitment. The clinicopathological significance of ASPP2 expression was measured by immunohistochemical analysis in 72 patients with GBC. Lentivirus-mediated knockdown or overexpression of ASPP2 was used to investigate the biological functions and molecular mechanisms of ASPP2 in GBC cells. Our data showed that downregulation of ASPP2 in patients with GBC was linked to poor prognosis. Knockdown of ASPP2 induced epithelial–mesenchymal transition (EMT) in GBC cells and influenced the TME. Mechanistically, we further confirmed that ASPP2 affected the expression and protein binding between atypical protein kinase C (aPKC)-ι and glioma-associated oncogene homolog 1 (GLI1). ASPP2 also induced C−C motif chemokine ligand (CCL) 2, CCL5, and tumor necrosis factor-α secretion by cancer cells, thereby promoting macrophage recruitment. The latter also induced EMT-like changes in GBC. Furthermore, ASPP2 deficiency regulated GLI1 transcriptional activity via the noncanonical Hedgehog (Hh) pathway and aPKC-ι/GLI1 signaling loop and promoted GLI1 nuclear localization and binding to the promoters of target genes. Our findings revealed that downregulation of ASPP2 promoted GBC invasion and metastasis through the aPKC-ι/GLI1 pathway and enhanced macrophage recruitment. Thus, ASPP2/aPKC-ι/GLI1 pathway may be a potential therapeutic target for the treatment of GBC.
Tubeimoside I induces accumulation of impaired autophagolysosome against cervical cancer cells by both initiating autophagy and inhibiting lysosomal function
Authors: Feng Xuping , Zhou Jing , Li Jingyi , Hou Xueyan , Li Longhao , Chen Yongmin , Fu Shuyue , Zhou Li , Li Changlong , Lei Yunlong 
Published: November 2018

AbstractCervical cancer is one of the most aggressive human cancers with poor prognosis due to constant chemoresistance and repeated relapse. Tubeimoside I (TBM) has been identified as a potent antitumor agent that inhibits cancer cell proliferation by triggering apoptosis and inducing cell cycle arrest. Nevertheless, the detailed mechanism remains unclear and needs to be further elucidated, especially in cervical cancer. In this study, we found that TBM could induce proliferation inhibition and cell death in cervical cancer cells both in vitro and in vivo. Further results demonstrated that treatment with TBM could induce autophagosome accumulation, which was important to TBM against cervical cancer cells. Mechanism studies showed that TBM increased autophagosome by two pathways: First, TBM could initiate autophagy by activating AMPK that would lead to stabilization of the Beclin1-Vps34 complex via dissociating Bcl-2 from Beclin1; Second, TBM could impair lysosomal cathepsin activity and block autophagic flux, leading to accumulation of impaired autophagolysosomes. In line with this, inhibition of autophagy initiation attenuated TBM-induced cell death, whereas autophagic flux inhibition could exacerbated the cytotoxic activity of TBM in cervical cancer cells. Strikingly, as a novel lethal impaired autophagolysosome inducer, TBM might enhance the therapeutic effects of chemotherapeutic drugs towards cervical cancer, such as cisplatin and paclitaxel. Together, our study provides new insights into the molecular mechanisms of TBM in the antitumor therapy, and establishes potential applications of TBM for cervical cancer treatment in clinic.
Phosphatidylserine is a marker for axonal debris engulfment but its exposure can be decoupled from degeneration
Authors: Shacham-Silverberg Vered , Sar Shalom Hadas , Goldner Ron , Golan-Vaishenker Yarden , Gurwicz Neta , Gokhman Irena , Yaron Avraham 
Published: November 2018

AbstractApoptotic cells expose Phosphatidylserine (PS), that serves as an “eat me” signal for engulfing cells. Previous studies have shown that PS also marks degenerating axonsduring developmental pruning or in response to insults (Wallerian degeneration), but the pathways that control PS exposure on degenerating axons are largely unknown. Here, we used a series of in vitro assays to systematically explore the regulation of PS exposure during axonal degeneration. Our results show that PS exposure is regulated by the upstream activators of axonal pruning and Wallerian degeneration. However, our investigation of signaling further downstream revealed divergence between axon degeneration and PS exposure. Importantly, elevation of the axonal energetic status hindered PS exposure, while inhibition of mitochondrial activity caused PS exposure, without degeneration. Overall, our results suggest that the levels of PS on the outer axonal membrane can be dissociated from the degeneration process and that the axonal energetic status plays a key role in the regulation of PS exposure.
Manipulating azobenzene photoisomerization through strong light–molecule coupling
Authors: Fregoni J. , Granucci G. , Coccia E. , Persico M. , Corni S. 
Published: November 2018

AbstractThe formation of hybrid light–molecule states (polaritons) offers a new strategy to manipulate the photochemistry of molecules. To fully exploit its potential, one needs to build a toolbox of polaritonic phenomenologies that supplement those of standard photochemistry. By means of a state-of-the-art computational photochemistry approach extended to the strong-coupling regime, here we disclose various mechanisms peculiar of polaritonic chemistry: coherent population oscillations between polaritons, quenching by trapping in dead-end polaritonic states and the alteration of the photochemical reaction pathway and quantum yields. We focus on azobenzene photoisomerization, that encompasses the essential features of complex photochemical reactions such as the presence of conical intersections and reaction coordinates involving multiple internal modes. In the strong coupling regime, a polaritonic conical intersection arises and we characterize its role in the photochemical process. Our chemically detailed simulations provide a framework to rationalize how the strong coupling impacts the photochemistry of realistic molecules.
Three-dimensional localization spectroscopy of individual nuclear spins with sub-Angstrom resolution
Authors: Zopes J. , Cujia K. S. , Sasaki K. , Boss J. M. , Itoh K. M. , Degen C. L. 
Published: November 2018

AbstractNuclear magnetic resonance (NMR) spectroscopy is a powerful method for analyzing the chemical composition and molecular structure of materials. At the nanometer scale, NMR has the prospect of mapping the atomic-scale structure of individual molecules, provided a method that can sensitively detect single nuclei and measure inter-atomic distances. Here, we report on precise localization spectroscopy experiments of individual13C nuclear spins near the central electronic sensor spin of a nitrogen-vacancy (NV) center in a diamond chip. By detecting the nuclear free precession signals in rapidly switchable external magnetic fields, we retrieve the three-dimensional spatial coordinates of the nuclear spins with sub-Angstrom resolution and for distances beyond 10 Å. We further show that the Fermi contact contribution can be constrained by measuring the nuclearg-factor enhancement. The presented method will be useful for mapping atomic positions in single molecules, an ambitious yet important goal of nanoscale nuclear magnetic resonance spectroscopy.
TAp73-induced phosphofructokinase-1 transcription promotes the Warburg effect and enhances cell proliferation
Authors: Li Le , Li Lijia , Li Wei , Chen Taiqi , Bin Zou  , Zhao Lina , Wang Huili , Wang Xueying , Xu Lina , Liu Xiaohui , Wang Dong , Li Bo , Mak Tak W. , Du Wenjing , Yang Xiaolu , Jiang Peng 
Published: November 2018

AbstractThe Warburg effect is a prominent metabolic feature associated with neoplastic diseases; however, the underlying mechanism remains incompletely understood. TAp73, a structural homolog of the tumor suppressor p53, is frequently overexpressed in human tumors, indicating a proliferative advantage that it can confer to tumor cells. Here we show that TAp73 stimulates the expression of phosphofructokinase-1, liver type (PFKL), which catalyzes the committed step in glycolysis. Through this regulation, TAp73 enhances glucose consumption and lactate excretion, promoting the Warburg effect. By activating PFKL, TAp73 also increases ATP production and bolsters anti-oxidant defense. TAp73 deficiency results in a pronounced reduction in tumorigenic potential, which can be rescued by forced PFKL expression. These findings establish TAp73 as a critical regulator of glycolysis and reveal a mechanism by which tumor cells achieve the Warburg effect to enable oncogenic growth.
Electrochemically-mediated selective capture of heavy metal chromium and arsenic oxyanions from water
Authors: Su Xiao , Kushima Akihiro , Halliday Cameron , Zhou Jian , Li Ju , Hatton T. Alan 
Published: November 2018

AbstractThe removal of highly toxic, ultra-dilute contaminants of concern has been a primary challenge for clean water technologies. Chromium and arsenic are among the most prevalent heavy metal pollutants in urban and agricultural waters, with current separation processes having severe limitations due to lack of molecular selectivity. Here, we report redox-active metallopolymer electrodes for the selective electrochemical removal of chromium and arsenic. An uptake greater than 100 mg Cr/g adsorbent can be achieved electrochemically, with a 99% reversible working capacity, with the bound chromium ions released in the less harmful trivalent form. Furthermore, we study the metallopolymer response during electrochemical modulation by in situ transmission electron microscopy. The underlying mechanisms for molecular selectivity are investigated through electronic structure calculations, indicating a strong charge transfer to the heavy metal oxyanions. Finally, chromium and arsenic are remediated efficiently at concentrations as low as 100 ppb, in the presence of over 200-fold excess competing salts.
Plasma Tie2 is a tumor vascular response biomarker for VEGF inhibitors in metastatic colorectal cancer
Authors: Jayson Gordon C. , Zhou Cong , Backen Alison , Horsley Laura , Marti-Marti Kalena , Shaw Danielle , Mescallado Nerissa , Clamp Andrew , Saunders Mark P. , Valle Juan W. , Mullamitha Saifee , Braun Mike , Hasan Jurjees , McEntee Delyth , Simpson Kathryn , Little Ross A. , Watson Yvonne , Cheung Susan , Roberts Caleb , Ashcroft Linda , Manoharan Prakash , Scherer Stefan J. , del Puerto Olivia , Jackson Alan , O’Connor James P. B. , Parker Geoff J. M. , Dive Caroline 
Published: November 2018

AbstractOncological use of anti-angiogenic VEGF inhibitors has been limited by the lack of informative biomarkers. Previously we reported circulating Tie2 as a vascular response biomarker for bevacizumab-treated ovarian cancer patients. Using advanced MRI and circulating biomarkers we have extended these findings in metastatic colorectal cancer (n = 70). Bevacizumab (10 mg/kg) was administered to elicit a biomarker response, followed by FOLFOX6-bevacizumab until disease progression. Bevacizumab induced a correlation between Tie2 and the tumor vascular imaging biomarker,Ktrans(R:−0.21 to 0.47) implying that Tie2 originated from the tumor vasculature. Tie2 trajectories were independently associated with pre-treatment tumor vascular characteristics, tumor response, progression free survival (HR for progression = 3.01,p = 0.00014; median PFS 248 vs. 348 daysp = 0.0008) and the modeling of progressive disease (p < 0.0001), suggesting that Tie2 should be monitored clinically to optimize VEGF inhibitor use. A vascular response is defined as a 30% reduction in Tie2; vascular progression as a 40% increase in Tie2 above the nadir. Tie2 is the first, validated, tumor vascular response biomarker for VEGFi.
Combined effusive-explosive silicic volcanism straddles the multiphase viscous-to-brittle transition
Authors: Wadsworth Fabian B. , Witcher Taylor , Vossen Caron E. J. , Hess Kai-Uwe , Unwin Holly E. , Scheu Bettina , Castro Jonathan M. , Dingwell Donald B. 
Published: November 2018

AbstractMagma is a viscoelastic fluid that can support fracture propagation when local shear stresses are high, or relax and flow when shear stresses are low. Here we present experiments to confirm this using synthetic and natural magmatic liquids across eruptive conditions and use Maxwell’s linear viscoelasticity to parameterize our results and predict the maximum stresses that can be supported during flow. This model proves universal across a large range of liquid compositions, temperatures, crystallinity and rates of strain relevant to shallow crustal magma ascent. Our results predict that the 2008 Volcán Chaitén eruption resided in the viscous field at the onset of magma ascent, but transitioned to a mixed viscous-brittle regime during degassing, coincident with the observed combined effusive-explosive behaviour during dome extrusion. Taking a realistic maximum effusive ascent rate, we propose that silicic eruptions on Earth may straddle the viscous-to-brittle transition by the time they reach the surface.
CA1 Nampt knockdown recapitulates hippocampal cognitive phenotypes in old mice which nicotinamide mononucleotide improves
Authors: Johnson Sean , Wozniak David F. , Imai S. 
Published: November 2018

AbstractCognitive dysfunction is one of the most concerning outcomes in global population aging. However, the mechanisms by which cognitive functions are impaired during aging remain elusive. It has been established that NAD+ levels are reduced in multiple tissues and organs, including the brain. We found that NAD+ levels declined in the hippocampus of mice during the course of aging, and whereas we observed minimal age-related effects on spatial learning/memory capabilities in old mice, we discovered that they developed cognitive hypersensitivity in response to aversive stimulation during contextual fear conditioning tests. This cognitive hypersensitivity appears to be associated with alterations in emotionality (fear/anxiety) and sensory processing (shock sensitivity), rather than reflect genuine conditioning/retention effects, during aging. Supplementation of nicotinamide mononucleotide (NMN) improved the sensory processing aspect of the hypersensitivity and possibly other related behaviors. Specific knockdown of nicotinamide phosphoribosyltransferase (Nampt) in the CA1 region, but not in the dentate gyrus, recapitulates this cognitive hypersensitivity observed in old mice. We identified calcium/calmodulin-dependent serine protein kinase (Cask) as a potential downstream effector in response to age-associated NAD+ reduction in the hippocampus. Cask expression is responsive to NAD+ changes and also reduced in the hippocampus during aging. Short-term NMN supplementation can enhance Cask expression in the hippocampus of old mice. Its promoter activity is regulated in a Sirt1-dependent manner. Taken together, NAD+ reduction in the CA1 region contributes to development of age-associated cognitive dysfunction, aspects of which may be prevented or treated by enhancing NAD+ availability through supplementation of NAD+ intermediates, such as NMN.
Voxel-Based Morphometry Correlates of an Agitated-Aggressive Syndrome in the At-Risk Mental State for Psychosis and First Episode Psychosis
Authors: Huber Christian G. , Widmayer Sonja , Smieskova Renata , Egloff Laura , Riecher-Rössler Anita , Stieglitz Rolf-Dieter , Borgwardt Stefan 
Published: November 2018

AbstractThere are mixed reports on structural neuroimaging correlates of aggression in schizophrenia with weak evidence due to cohort overlaps and lack of replications. To our knowledge, no study examined volumetric neuroimaging correlates of aggression in early stages of psychosis. An agitated-aggressive syndrome is present in at-risk mental state (ARMS) and in first-episode psychosis (FEP) – it is unclear whether this syndrome is associated with structural brain abnormalities in early stages of psychosis. Using three-dimensional magnetic resonance imaging and a whole brain voxel-based morphometry approach, we examined 56 ARMS patients, 55 FEP patients and 25 healthy controls. We operationalized aggression using the Excited Component of the Brief Psychiatric Rating Scale (BPRS-EC) and dichotomized our patient group by median split into “BPRS-EC high” (n = 49) and “BPRS-EC low” groups (n = 62). The “BPRS-EC high” group had significantly smaller left lingual gyrus volume than HC. This finding was not present in the “BPRS-EC low” group. In addition, grey matter volume in the left lingual gyrus showed a negative linear correlation with BPRS-EC over all subjects (ρ = −0.318; p = 0.0001) and in the patient group (ρ = −0.202; p = 0.033). These findings provide first hints on structural brain abnormalities associated with an agitated-aggressive syndrome in ARMS and FEP patients.
The ALS-inducing factors, TDP43A315T and SOD1G93A, directly affect and sensitize sensory neurons to stress
Authors: Vaughan Sydney K. , Sutherland Natalia M. , Zhang Sihui , Hatzipetros Theo , Vieira Fernando , Valdez Gregorio 
Published: November 2018

AbstractThere is increased recognition that sensory neurons located in dorsal root ganglia (DRG) are affected in amyotrophic lateral sclerosis (ALS). However, it remains unknown whether ALS-inducing factors, other than mutant superoxide dismutase 1 (SOD1G93A), directly affect sensory neurons. Here, we examined the effect of mutant TAR DNA-binding protein 1 (TDP43A315T) on sensory neurons in culture and in vivo. In parallel, we reevaluated sensory neurons expressing SOD1G93A. We found that cultured sensory neurons harboring either TDP43A315T or SOD1G93A grow neurites at a slower rate and elaborate fewer neuritic branches compared to control neurons. The presence of either ALS-causing mutant gene also sensitizes sensory neurons to vincristine, a microtubule inhibitor that causes axonal degeneration. Interestingly, these experiments revealed that cultured sensory neurons harboring TDP43A315T elaborate shorter and less complex neurites, and are more sensitive to vincristine compared to controls and to SOD1G93A expressing sensory neurons. Additionally, levels of two molecules involved in stress responses, ATF3 and PERK are significantly different between sensory neurons harboring TDP43A315T to those with SOD1G93Ain vitro and in vivo. These findings demonstrate that sensory neurons are directly affected by two ALS-inducing factors, suggesting important roles for this neuronal subpopulation in ALS-related pathogenesis.
Bleomycin-induced genome structural variations in normal, non-tumor cells
Authors: Quispe-Tintaya Wilber , Lee Moonsook , Dong Xiao , Weiser Daniel A. , Vijg Jan , Maslov Alexander Y. 
Published: November 2018

AbstractMany anticancer drugs are genotoxic agents inducing DNA breaks in actively proliferating cancer cells. However, these same drugs also induce mutations, mostly genome structural variations (GSVs). The detection of GSVs in normal cells and tissues is a major challenge due to the very low abundance of these mutations, which are essentially only detectable in clonal outgrowths, such as tumors. Previously we developed Structural Variant Search (SVS) – an NGS-based assay for the quantitative detection of somatic GSVs in normal cells. Using an improved version of SVS we now demonstrate that the same dose of the anti-cancer drug bleomycin induces about 5 times more somatic GSVs in quiescent primary human fibroblasts than in proliferating cells. GVS induction in non-dividing, normal cells was subsequently confirmed in vivo by demonstrating that a single dose of bleomycin leads to a significant increase of GSV frequency in mouse liver and heart, two postmitotic tissues. Our findings suggest that normal non-cycling differentiated cells may serve as a reservoir of iatrogenically induced mutations. These results provide more insight into the possible molecular mechanisms that underlie late-life morbidities in cancer survivors exposed to chemotherapy.