bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chemometric analysis reveals links in the formation of fragrant bio-molecules during agarwood (Aquilaria malaccensis) and fungal interactions
Authors: Sen Supriyo , Dehingia Madhusmita , Talukdar Narayan Chandra , Khan Mojibur 
Published: March 2017

AbstractFragrant agarwood, arguably the costliest wood in the world, is formed by plant-fungal interactions in Aquilaria spp. However, very little is known about this fragrant outcome of interaction. Therefore, mimicking the ancient traditions of agarwood production in Assam (Northeast India), a chemometric assessment of the agarwood-fungus interaction was made by chemical profiling (GC-MS) coupled with statistical analysis (principal component, correlation network analysis) across three platforms, viz. callus, juvenile plants and resinous wood-chips with an associated Fusarium. In the study of callus-fungus interaction, increased accumulation of key aroma compounds such as pentatriacontane {fold change (log2FC) = 3.47)}, 17-pentatriacontene (log2FC = 2.95), tetradecane, 2-methyl- (log2FC = 1.10) over callus and activation of pathways related to defense and secondary metabolism indicated links to aroma production. Study on fungal interactions in juvenile plants and resinous wood-chips indicated formation of terpenoid precursors (e.g. farnesol, geranylgeraniol acetate) and agarwood sesquiterpenes (e.g. agarospirol, γ-eudesmol). Correlation network analysis revealed the possible regulation of sesquiterpene biosynthesis involving squalene. Also a direct role of fungus in aroma (e.g. dodecane, 4-methyl-, tetracosane) was highlighted. Appearance of fragrant molecules unknown to agarwood during interaction featured as a new possibility for future research.
Electrospun Nb-doped TiO2 nanofiber support for Pt nanoparticles with high electrocatalytic activity and durability
Authors: Kim MinJoong , Kwon ChoRong , Eom KwangSup , Kim JiHyun , Cho EunAe 
Published: March 2017

AbstractThis study explores a facile method to prepare an efficient and durable support for Pt catalyst of polymer electrolyte membrane fuel cell (PEMFC). As a candidate, Nb-doped TiO2 (Nb-TiO2) nanofibers are simply fabricated using an electrospinning technique, followed by a heat treatment. Doping Nb into the TiO2 nanofibers leads to a drastic increase in electrical conductivity with doping level of up to 25 at. % (Nb0.25Ti0.75O2). Pt nanoparticles are synthesized on the prepared 25 at. % Nb-doped TiO2-nanofibers (Pt/Nb-TiO2) as well as on a commercial powdered carbon black (Pt/C). The Pt/Nb-TiO2 nanofiber catalyst exhibits similar oxygen reaction reduction (ORR) activity to that of the Pt/C catalyst. However, during an accelerated stress test (AST), the Pt/Nb-TiO2 nanofiber catalyst retained more than 60% of the initial ORR activity while the Pt/C catalyst lost 65% of the initial activity. The excellent durability of the Pt/Nb-TiO2 nanofiber catalyst can be attributed to high corrosion resistance of TiO2 and strong interaction between Pt and TiO2.
Antagonizing effects of membrane-acting androgens on the eicosanoid receptor OXER1 in prostate cancer
Authors: Kalyvianaki Konstantina , Gebhart Veronika , Peroulis Nikolaos , Panagiotopoulou Christina , Kiagiadaki Fotini , Pediaditakis Iosif , Aivaliotis Michalis , Moustou Eleni , Tzardi Maria , Notas George , Castanas Elias , Kampa Marilena 
Published: March 2017

AbstractAccumulating evidence during the last decades revealed that androgen can exert membrane initiated actions that involve signaling via specific kinases and the modulation of significant cellular processes, important for prostate cancer cell growth and metastasis. Results of the present work clearly show that androgens can specifically act at the membrane level via the GPCR oxoeicosanoid receptor 1 (OXER1) in prostate cancer cells. In fact, OXER1 expression parallels that of membrane androgen binding in prostate cancer cell lines and tumor specimens, while in silico docking simulation of OXER1 showed that testosterone could bind to OXER1 within the same grove as 5-OxoETE, the natural ligand of OXER1. Interestingly, testosterone antagonizes the effects of 5-oxoETE on specific signaling pathways and rapid effects such as actin cytoskeleton reorganization that ultimately can modulate cell migration and metastasis. These findings verify that membrane-acting androgens exert specific effects through an antagonistic interaction with OXER1. Additionally, this interaction between androgen and OXER1, which is an arachidonic acid metabolite receptor expressed in prostate cancer, provides a novel link between steroid and lipid actions and renders OXER1 as new player in the disease. These findings should be taken into account in the design of novel therapeutic approaches in prostate cancer.
Identifying Life-Threatening Admissions for Drug Dependence or Abuse (ILIADDA): Derivation and Validation of a Model.
Authors: Nguyen Tri-Long , Boudemaghe Thierry , Leguelinel-Blache Géraldine , Eiden Céline , Kinowski Jean-Marie , Le Manach Yannick , Peyrière Hélène , Landais Paul 
Published: March 2017

AbstractGiven that drug abuse and dependence are common reasons for hospitalization, we aimed to derive and validate a model allowing early identification of life-threatening hospital admissions for drug dependence or abuse. Using the French National Hospital Discharge Data Base, we extracted 66,101 acute inpatient stays for substance abuse, dependence, mental disorders or poisoning associated with medicines or illicit drugs intake, recorded between January 1st, 2009 and December 31st, 2014. We split our study cohort at the center level to create a derivation cohort and a validation cohort. We developed a multivariate logistic model including patient’s age, sex, entrance mode and diagnosis as predictors of a composite primary outcome of in-hospital death or ICU admission. A total of 2,747 (4.2%) patients died or were admitted to ICU. The risk of death or ICU admission was mainly associated with the consumption of opioids, followed by cocaine and other narcotics. Particularly, methadone poisoning was associated with a substantial risk (OR: 35.70, 95% CI [26.94–47.32], P < 0.001). In the validation cohort, our model achieved good predictive properties in terms of calibration and discrimination (c-statistic: 0.847). This allows an accurate identification of life-threatening admissions in drug users to support an early and appropriate management.
Ndrg3 gene regulates DSB repair during meiosis through modulation the ERK signal pathway in the male germ cells
Authors: Pan Hongjie , Zhang Xuan , Jiang Hanwei , Jiang Xiaohua , Wang Liu , Qi Qi , Bi Yuan , Wang Jian , Shi Qinghua , Li Runsheng 
Published: March 2017

AbstractThe N-myc downstream regulated gene (NDRG) family consists of 4 members, NDRG-1, -2, -3, -4. Physiologically, we found Ndrg3, a critical gene which led to homologous lethality in the early embryo development, regulated the male meiosis in mouse. The expression of Ndrg3 was enhanced specifically in germ cells, and reached its peak level in the pachytene stage spermatocyte. Haplo-insufficiency of Ndrg3 gene led to sub-infertility during the male early maturation. In the Ndrg3+/− germ cells, some meiosis events such as DSB repair and synaptonemal complex formation were impaired. Disturbances on meiotic prophase progression and spermatogenesis were observed. In mechanism, the attenuation of pERK1/2 signaling was detected in the heterozygous testis. With our primary spermatocyte culture system, we found that lactate promoted DSB repair via ERK1/2 signaling in the male mouse germ cells in vitro. Deficiency of Ndrg3 gene attenuated the activation of ERK which further led to the aberrancy of DSB repair in the male germ cells in mouse. Taken together, we reported that Ndrg3 gene modulated the lactate induced ERK pathway to facilitate DSB repair in male germ cells, which further regulated meiosis and subsequently fertility in male mouse.
Experimental contextuality in classical light
Authors: Li Tao , Zeng Qiang , Song Xinbing , Zhang Xiangdong 
Published: March 2017

AbstractThe Klyachko, Can, Binicioglu, and Shumovsky (KCBS) inequality is an important contextuality inequality in three-level system, which has been demonstrated experimentally by using quantum states. Using the path and polarization degrees of freedom of classical optics fields, we have constructed the classical trit (cetrit), tested the KCBS inequality and its geometrical form (Wright’s inequality) in this work. The projection measurement has been implemented, the clear violations of the KCBS inequality and its geometrical form have been observed. This means that the contextuality inequality, which is commonly used in test of the conflict between quantum theory and noncontextual realism, may be used as a quantitative tool in classical optical coherence to describe correlation characteristics of the classical fields.
Porewater methane transport within the gas vesicles of diurnally migrating Chaoborus spp.: An energetic advantage
Authors: McGinnis Daniel F. , Flury Sabine , Tang Kam W. , Grossart Hans-Peter 
Published: March 2017

AbstractDiurnally-migrating Chaoborus spp. reach populations of up to 130,000 individuals m−2 in lakes up to 70 meters deep on all continents except Antarctica. Linked to eutrophication, migrating Chaoborus spp. dwell in the anoxic sediment during daytime and feed in the oxic surface layer at night. Our experiments show that by burrowing into the sediment, Chaoborus spp. utilize the high dissolved gas partial pressure of sediment methane to inflate their tracheal sacs. This mechanism provides a significant energetic advantage that allows the larvae to migrate via passive buoyancy rather than more energy-costly swimming. The Chaoborus spp. larvae, in addition to potentially releasing sediment methane bubbles twice a day by entering and leaving the sediment, also transport porewater methane within their gas vesicles into the water column, resulting in a flux of 0.01–2 mol m−2 yr−1 depending on population density and water depth. Chaoborus spp. emerging annually as flies also result in 0.1–6 mol m−2 yr−1 of carbon export from the system. Finding the tipping point in lake eutrophication enabling this methane-powered migration mechanism is crucial for ultimately reconstructing the geographical expansion of Chaoborus spp., and the corresponding shifts in the lake’s biogeochemistry, carbon cycling and food web structure.
Microbial communities of aquatic environments on Heard Island characterized by pyrotag sequencing and environmental data
Authors: Allen Michelle A. , Cavicchioli Ricardo 
Published: March 2017

AbstractHeard Island in the Southern Ocean is a biological hotspot that is suffering the effects of climate change. Significant glacier retreat has generated proglacial lagoons, some of which are open to the ocean. We used pyrotag sequencing of SSU rRNA genes and environmental data to characterize microorganisms from two pools adjacent to animal breeding areas, two glacial lagoons and Atlas Cove (marine site). The more abundant taxa included Actinobacteria, Bacteroidetes and Proteobacteria, ciliates and picoflagellates (e.g. Micromonas), and relatively few Archaea. Seal Pool, which is rich in organic matter, was characterized by a heterotrophic degradative community, while the less eutrophic Atlas Pool had more eucaryotic primary producers. Brown Lagoon, with the lowest nutrient levels, had Eucarya and Bacteria predicted to be oligotrophs, possess small cell sizes, and have the ability to metabolize organic matter. The marine influence on Winston Lagoon was evident by its salinity and the abundance of marine-like Gammaproteobacteria, while also lacking typical marine eucaryotes indicating the system was still functioning as a distinct niche. This is the first microbiology study of Heard Island and revealed that communities are distinct at each location and heavily influenced by local environmental factors.
Epithelial LTβR signaling controls the population size of the progenitors of medullary thymic epithelial cells in neonatal mice
Authors: Wu Weiwei , Shi Yaoyao , Xia Huan , Chai Qian , Jin Caiwei , Ren Boyang , Zhu Mingzhao 
Published: March 2017

AbstractThe establishment of T cell central tolerance critically relies on the development and maintenance of the medullary thymic epithelial cells (mTECs). Disrupted signaling of lymphotoxin beta receptor (LTβR) results in dramatically reduced mTEC population. However, whether LTβR directly or indirectly control mTECs remains undetermined; how LTβR controls this process also remain unclear. In this study, by utilizing K14-Cre × Ltbrfl/flconditional knockout (cKO) mice, we show that epithelial intrinsic LTβR was essential for the mTEC development postnatally. Mechanistically, LTβR did not directly impact the proliferation or survival of mTECs; the maturation of mTECs from MHC-IIloto MHC-IIhistage was also unaltered in the absence of LTβR; interestingly, the number of mTEC progenitors (Cld3,4hiSSEA-1+) was found significantly reduced in LTβR cKO mice at the neonatal stage, but not at E18.5. Consequently, epithelial deficiency of LTβR resulted in significant defect of thymic negative selection as demonstrated using OT-I and RIP-OVA transgenic mouse system. In summary, our study clarifies the epithelial intrinsic role of LTβR on mTEC development and function; more importantly, it reveals a previously unrecognized function of LTβR on the control of the size of mTEC progenitor population.
ICOSL expression in human bone marrow-derived mesenchymal stem cells promotes induction of regulatory T cells
Authors: Lee Hyun-Joo , Kim Si-Na , Jeon Myung-Shin , Yi TacGhee , Song Sun U. 
Published: March 2017

AbstractMesenchymal stem cells (MSCs) can modulate lymphocyte proliferation and function. One of the immunomodulatory functions of MSCs involves CD4+CD25+FoxP3+ regulatory T cells (Tregs), which negatively regulate inflammatory responses. MSC-mediated Treg induction is supposed to be regulated by mechanisms requiring both soluble and cell contact-dependent factors. Although the involvement of soluble factors has been revealed, the contact-dependent mechanisms in MSC-mediated Treg induction remain unclear. We attempted to identify molecule(s) other than secreted factors that are responsible for MSC-mediated Treg induction and to uncover the underlying mechanisms. Under in vitro Treg-inducing conditions, ICOSL expression in MSCs coincided with Treg induction in co-cultures of MSCs with CD4+ T cells. When cultured in a transwell plate, MSCs failed to induce Tregs. Neutralization or knockdown of ICOSL significantly reduced Tregs and their IL-10 release. ICOSL overexpression in MSCs promoted induction of functional Tregs. ICOSL-ICOS signaling promoted Treg differentiation from CD4+ T cells through activation of the phosphoinositide 3-kinase-Akt pathway. MSCs primed with Interleukin-1β significantly induced Tregs through ICOSL upregulation. We demonstrated that the Treg-inducing activity of MSCs is proportionate to their basal ICOSL expression. This study provides evidence that ICOSL expression in human MSCs plays an important role in contact-dependent regulation of MSC-mediated Treg induction.
Historical changes of the Mediterranean Sea ecosystem: modelling the role and impact of primary productivity and fisheries changes over time
Authors: Piroddi Chiara , Coll Marta , Liquete Camino , Macias Diego , Greer Krista , Buszowski Joe , Steenbeek Jeroen , Danovaro Roberto , Christensen Villy 
Published: March 2017

AbstractThe Mediterranean Sea has been defined “under siege” because of intense pressures from multiple human activities; yet there is still insufficient information on the cumulative impact of these stressors on the ecosystem and its resources. We evaluate how the historical (1950–2011) trends of various ecosystems groups/species have been impacted by changes in primary productivity (PP) combined with fishing pressure. We investigate the whole Mediterranean Sea using a food web modelling approach. Results indicate that both changes in PP and fishing pressure played an important role in driving species dynamics. Yet, PP was the strongest driver upon the Mediterranean Sea ecosystem. This highlights the importance of bottom-up processes in controlling the biological characteristics of the region. We observe a reduction in abundance of important fish species (~34%, including commercial and non-commercial) and top predators (~41%), and increases of the organisms at the bottom of the food web (~23%). Ecological indicators, such as community biomass, trophic levels, catch and diversity indicators, reflect such changes and show overall ecosystem degradation over time. Since climate change and fishing pressure are expected to intensify in the Mediterranean Sea, this study constitutes a baseline reference for stepping forward in assessing the future management of the basin.
Bidirectional Shifting Effects of the Sound Intensity on the Best Frequency in the Rat Auditory Cortex
Authors: Tao Can , Zhang Guangwei , Zhou Chang , Wang Lijuan , Yan Sumei , Zhou Yi , Xiong Ying 
Published: March 2017

AbstractFrequency and intensity are two independent attributes of sound stimuli. Psychoacoustic studies have found that the sound intensity can affect the perception of frequency; however, the underlying neuronal mechanism remains largely unknown. To investigate if and how the sound level affects the frequency coding for auditory cortical neurons, we recorded the activities of neuronal ensembles and single neurons, as well as the synaptic input evoked by pure tones of different frequency and intensity combinations, in layer 4 of the rat primary auditory cortex. We found that the best frequency (BF) shifted bidirectionally with the increases in intensity. Specifically, the BF of neurons with a low characteristic frequency (CF) shifted lower, whereas the BF of neurons with a higher CF shifted higher. Meanwhile, we found that these shifts in the BF can lead to the expansion of high- and low-frequency areas in the tonotopic map, increasing the evenness of the BF distribution at high intensities. Our results revealed that the frequency tuning can bidirectionally shift with an increase in the sound intensity at both the cellular and population level. This finding is consistent with the perceptual illusions observed in humans and could provide a potential mechanism for this psychoacoustic effect.
Liver-specific deletion of the Plpp3 gene alters plasma lipid composition and worsens atherosclerosis in apoE−/− mice
Authors: Busnelli Marco , Manzini Stefano , Hilvo Mika , Parolini Cinzia , Ganzetti Giulia S. , Dellera Federica , Ekroos Kim , Jänis Minna , Escalante-Alcalde Diana , Sirtori Cesare R. , Laaksonen Reijo , Chiesa Giulia 
Published: March 2017

AbstractThe PLPP3 gene encodes for a ubiquitous enzyme that dephosphorylates several lipid substrates. Genome-wide association studies identified PLPP3 as a gene that plays a role in coronary artery disease susceptibility. The aim of the study was to investigate the effect of Plpp3 deletion on atherosclerosis development in mice. Because the constitutive deletion of Plpp3 in mice is lethal, conditional Plpp3 hepatocyte-specific null mice were generated by crossing floxed Plpp3 mice with animals expressing Cre recombinase under control of the albumin promoter. The mice were crossed onto the athero-prone apoE−/− background to obtain Plpp3f/fapoE−/−Alb-Cre+ and Plpp3f/fapoE−/−Alb-Cre− offspring, the latter of which were used as controls. The mice were fed chow or a Western diet for 32 or 12 weeks, respectively. On the Western diet, Alb-Cre+ mice developed more atherosclerosis than Alb-Cre− mice, both at the aortic sinus and aorta. Lipidomic analysis showed that hepatic Plpp3 deletion significantly modified the levels of several plasma lipids involved in atherosclerosis, including lactosylceramides, lysophosphatidic acids, and lysophosphatidylinositols. In conclusion, Plpp3 ablation in mice worsened atherosclerosis development. Lipidomic analysis suggested that the hepatic Plpp3 deletion may promote atherosclerosis by increasing plasma levels of several low-abundant pro-atherogenic lipids, thus providing a molecular basis for the observed results.
Site-to-site interdomain communication may mediate different loss-of-function mechanisms in a cancer-associated NQO1 polymorphism
Authors: Medina-Carmona Encarnación , Neira Jose L. , Salido Eduardo , Fuchs Julian E. , Palomino-Morales Rogelio , Timson David J. , Pey Angel L. 
Published: March 2017

AbstractDisease associated genetic variations often cause intracellular enzyme inactivation, dysregulation and instability. However, allosteric communication of mutational effects to distant functional sites leading to loss-of-function remains poorly understood. We characterize here interdomain site-to-site communication by which a common cancer-associated single nucleotide polymorphism (c.C609T/p.P187S) reduces the activity and stability in vivo of NAD(P)H:quinone oxidoreductase 1 (NQO1). NQO1 is a FAD-dependent, two-domain multifunctional stress protein acting as a Phase II enzyme, activating cancer pro-drugs and stabilizing p53 and p73α oncosuppressors. We show that p.P187S causes structural and dynamic changes communicated to functional sites far from the mutated site, affecting the FAD binding site located at the N-terminal domain (NTD) and accelerating proteasomal degradation through dynamic effects on the C-terminal domain (CTD). Structural protein:protein interaction studies reveal that the cancer-associated polymorphism does not abolish the interaction with p73α, indicating that oncosuppressor destabilization largely mirrors the low intracellular stability of p.P187S. In conclusion, we show how a single disease associated amino acid change may allosterically perturb several functional sites in an oligomeric and multidomain protein. These results have important implications for the understanding of loss-of-function genetic diseases and the identification of novel structural hot spots as targets for pharmacological intervention.
Mecp2-mediated Epigenetic Silencing of miR-137 Contributes to Colorectal Adenoma-Carcinoma Sequence and Tumor Progression via Relieving the Suppression of c-Met
Authors: Chen Tao , Cai Shi-Lun , Li Jian , Qi Zhi-Peng , Li Xu-Quan , Ye Le-Chi , Xie Xiao-Feng , Hou Ying-Yong , Yao Li-Qing , Xu Mei-Dong , Zhou Ping-Hong , Xu Jian-Min , Zhong Yun-Shi 
Published: March 2017

AbstractThe molecular mechanisms underlying colorectal cancer (CRC) development remain elusive. In this study, we examined the miRNA and mRNA expressions in the adenoma-carcinoma sequence (ACS), a critical neoplastic progression in CRC development. We found that miR-137 was down-regulated in all adenoma and carcinoma tissues. Low miR-137 levels were correlated negatively with tumor progression and metastasis. Then we identified the inhibition effect of the miR-137 in CRC development, both in CRC cell lines and mouse models. MiR-137 was shown to control CRC cell proliferation, colony formation, migration and invasion and to control tumor growth and metastasis. We further confirmed the negative association between miR-137 and c-Met expression and thus validated this important oncogene as the target of miR-137 in CRC. In addition, we found a DNA methyl-CpG-binding protein, Mecp2, was up-regulated in ACS tissues via mRNA sequencing. Further experiment showed that miR-137 expression in CRC was subjected to epigenetic regulation mediated by Mecp2. We also confirmed c-Met expression can be up-regulated by silencing of miR-137 and suppressed by coexpression of Mecp2 and miR-137. These findings highlight the critical role of miR-137-c-Met nexus in CRC development and reveal Mecp2-regulated epigenetic silence causes the downregulation of miR-137 in colorectal adenoma and carcinoma.