bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vertical and horizontal distribution of phytoplankton around an oceanic archipelago of the Equatorial Atlantic
Authors: De Queiroz Andressa Ribeiro , Flores Montes Manuel , de Castro Melo Pedro Augusto Mendes , da Silva Rodolfo Araújo , Koening Maria Luise 
Published: October 2015

The surrounding area of the St. Peter and St. Paul Archipelago (SPSPA) (0°55′10″N 29°20′33″W) was investigated in order to verify the physical and chemical influences in species composition and abundance, and the patterns of distribution of phytoplankton in the water column, especially in the thermocline depths. The expedition was held on board the Cruzeiro do Sul Hydro-oceanographic ship, from 21 to 23 July 2010 in two perpendicular and opposite transects. A cylinder-conical net and Niskin bottles were used. Two water masses were identified (Tropical Water and South Atlantic Central Water), and the thermocline depths varied from 40 to 110 m. A total of 128 species of phytoplanktonic organisms were identified, belonging to four phyla. The most conspicuous species was the cyanobacteriaTrichodesmium thiebautii; nevertheless, 22 species were considered new registers for the region. The total phytoplanktonic density (1 × 103to 183 × 103 cells l−1) was low and typical of oligotrophic regions, decreasing slightly with depth. Among the 35 species identified in the vertical distribution, 22 were present in the thermocline depth. The total density ofTrichodesmium thiebautii, Oxytoxum longicepsandProtoperidinium minimumhad significant correlations with the physical and chemical parameters. These data indicate that SPSPA can be associated to an island mass effect in the local oceanic circulation that mainly affects the physical and chemical characteristics of the surrounding waters. Consequently, these interactions influence the phytoplanktonic community, mainly those located at the end of the photic zone and those that are under the influence of thermocline oscillation.
An in vitro evaluation of resonant frequency analysis to measure fixed bridge stability
Authors: Omer Khaled , Fox Kathryn , Palermo Deniel , Boyle Liam , Youngson Callum 
Published: October 2015

Abstract
Objectives/Aims:
To determine whether a clinically available resonance frequency analysis (RFA) device (Osstell Mentor), designed to assess implant integration, could identify a single uncemented retainer on fixed–fixed bridges, in vitro.

Materials and Methods:
All-metal fixed–fixed bridges were cemented to acrylic tooth analogue abutments with simulated periodontal ligaments. Dental stone bases provided 100 or 50% ‘bone support’ groups (n = 50 in each). Control groups had both retainers cemented, whereas the test groups had the ‘premolar’ uncemented, mimicking clinical failure. A RFA device was used to measure bridge stability, expressed as a modified Implant Stability Quotient (Bridge Stability Quotient—BSQ) from a Smartpeg temporarily affixed to the bridge via composite.

Results:
The BSQ recorded at the premolar site in both 100 and 50% support models demonstrated highly statistically significant differences (P <0.003) between the control and test groups. Sensitivity and specificity, area under the curve (receiver operating characteristic), analyses showed moderate test accuracy (0.735) for the 100% support group and good accuracy (0.96) for the 50% support group.

Conclusion:
The investigation suggests that RFA measurements were able to identify, reliably and non-destructively, in vitro, fixed–fixed bridges where the anterior retainer was uncemented. Further clinical research is required to determine whether this technique may allow early diagnosis of failing bridgework.
Early effects of the antineoplastic agent salinomycin on mitochondrial function
Authors: Managò A , Leanza L , Carraretto L , Sassi N , Grancara S , Quintana-Cabrera R , Trimarco V , Toninello A , Scorrano L , Trentin L , Semenzato G , Gulbins E , Zoratti M , Szabò I 
Published: October 2015

AbstractSalinomycin, isolated from Streptomyces albus, displays antimicrobial activity. Recently, a large-scale screening approach identified salinomycin and nigericin as selective apoptosis inducers of cancer stem cells. Growing evidence suggests that salinomycin is able to kill different types of non-stem tumor cells that usually display resistance to common therapeutic approaches, but the mechanism of action of this molecule is still poorly understood. Since salinomycin has been suggested to act as a K+ ionophore, we explored its impact on mitochondrial bioenergetic performance at an early time point following drug application. In contrast to the K+ ionophore valinomycin, salinomycin induced a rapid hyperpolarization. In addition, mitochondrial matrix acidification and a significant decrease of respiration were observed in intact mouse embryonic fibroblasts (MEFs) and in cancer stem cell-like HMLE cells within tens of minutes, while increased production of reactive oxygen species was not detected. By comparing the chemical structures and cellular effects of this drug with those of valinomycin (K+ ionophore) and nigericin (K+/H+ exchanger), we conclude that salinomycin mediates K+/H+ exchange across the inner mitochondrial membrane. Compatible with its direct modulation of mitochondrial function, salinomycin was able to induce cell death also in Bax/Bak-less double-knockout MEF cells. Since at the concentration range used in most studies (around 10 μM) salinomycin exerts its effect at the level of mitochondria and alters bioenergetic performance, the specificity of its action on pathologic B cells isolated from patients with chronic lymphocytic leukemia (CLL) versus B cells from healthy subjects was investigated. Mesenchymal stromal cells (MSCs), proposed to mimic the tumor environment, attenuated the apoptotic effect of salinomycin on B-CLL cells. Apoptosis occurred to a significant extent in healthy B cells as well as in MSCs and human primary fibroblasts. The results indicate that salinomycin, when used above μM concentrations, exerts direct, mitochondrial effects, thus compromising cell survival.
Pur-alpha functionally interacts with FUS carrying ALS-associated mutations
Authors: Di Salvio M , Piccinni V , Gerbino V , Mantoni F , Camerini S , Lenzi J , Rosa A , Chellini L , Loreni F , Carrì M T , Bozzoni I , Cozzolino M , Cestra G 
Published: October 2015

AbstractAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder due to motor neuron loss. Fused in sarcoma (FUS) protein carrying ALS-associated mutations localizes to stress granules and causes their coalescence into larger aggregates. Here we show that Pur-alpha physically interacts with mutated FUS in an RNA-dependent manner. Pur-alpha colocalizes with FUS carrying mutations in stress granules of motoneuronal cells differentiated from induced pluripotent stem cells and that are derived from ALS patients. We observe that both Pur-alpha and mutated FUS upregulate phosphorylation of the translation initiation factor eukaryotic translation initiation factor 2 alpha and consistently inhibit global protein synthesis. In vivo expression of Pur-alpha in different Drosophila tissues significatively exacerbates the neurodegeneration caused by mutated FUS. Conversely, the downregulation of Pur-alpha in neurons expressing mutated FUS significatively improves fly climbing activity. All these findings suggest that Pur-alpha, through the control of mRNA translation, might be involved in the pathogenesis of ALS associated with the mutation of FUS, and that an alteration of protein synthesis may be directly implicated in the disease. Finally, in vivo RNAi-mediated ablation of Pur-alpha produced locomotion defects in Drosophila, indicating a pivotal role for this protein in the motoneuronal function.
Impact of the combined loss of BOK, BAX and BAK on the hematopoietic system is slightly more severe than compound loss of BAX and BAK
Authors: Ke F , Grabow S , Kelly G L , Lin A , O’Reilly L A , Strasser A 
Published: October 2015

AbstractIt is well established that BAX and BAK play crucial, overlapping roles in the intrinsic pathway of apoptosis. Gene targeted mice lacking both BAX and BAK have previously been generated, but the majority of these animals died perinatally. BOK is a poorly studied relative of BAX and BAK that shares extensive amino acid sequence homology to both proteins, but its function remains largely unclear to date. To determine whether BOK plays an overlapping role with BAX and BAK, we utilized a hematopoietic reconstitution model where lethally irradiated wild type mice were transplanted withBok−/−Bax−/−Bak−/−triple knockout (TKO) fetal liver cells, and compared alongside mice reconstituted with aBax−/−Bak−/−double knockout (DKO) hematopoietic compartment. We report here that mice with a TKO and DKO hematopoietic system died at a similar rate and much earlier than control animals, mostly due to severe autoimmune pathology. Both TKO and DKO reconstituted mice also had altered frequencies of various leukocyte subsets in the thymus, bone marrow and spleen, displayed leukocyte infiltrates and autoimmune pathology in multiple tissues, as well as elevated levels of anti-nuclear autoantibodies. Interestingly, the additional deletion of BOK (on top of BAX and BAK loss) led to a further increase in peripheral blood lymphocytes, as well as enhanced lymphoid infiltration in some organs. These findings suggest that BOK may have some functions that are redundant with BAX and BAK in the hematopoietic system.
Dynamic control of light emission faster than the lifetime limit using VO2 phase-change
Authors: Cueff Sébastien , Li Dongfang , Zhou You , Wong Franklin J. , Kurvits Jonathan A. , Ramanathan Shriram , Zia Rashid 
Published: October 2015

AbstractModulation is a cornerstone of optical communication, and as such, governs the overall speed of data transmission. Currently, the two main strategies for modulating light are direct modulation of the excited emitter population (for example, using semiconductor lasers) and external optical modulation (for example, using Mach–Zehnder interferometers or ring resonators). However, recent advances in nanophotonics offer an alternative approach to control spontaneous emission through modifications to the local density of optical states. Here, by leveraging the phase-change of a vanadium dioxide nanolayer, we demonstrate broadband all-optical direct modulation of 1.5 μm emission from trivalent erbium ions more than three orders of magnitude faster than their excited state lifetime. This proof-of-concept demonstration shows how integration with phase-change materials can transform widespread phosphorescent materials into high-speed optical sources that can be integrated in monolithic nanoscale devices for both free-space and on-chip communication.
Largest known Mesozoic multituberculate from Eurasia and implications for multituberculate evolution and biology
Authors: Xu Li , Zhang Xingliao , Pu Hanyong , Jia Songhai , Zhang Jiming , Lü Junchang , Meng Jin 
Published: October 2015

AbstractA new multituberculate, Yubaartar zhongyuanensis gen. and sp. nov., is reported from the Upper Cretaceous of Luanchuan County, Henan Province, China. The holotype of the new taxon is a partial skeleton with nearly complete cranium and associated lower jaws with in situ dentitions. The new species is the southern-most record of a Late Cretaceous multituberculate from outside of the Mongolian Plateau in Asia and represents the largest known Mesozoic multituberculate from Eurasia. The new specimen displays some intriguing features previously unknown in multituberculates, such as the first evidence of replacement of the ultimate upper premolar and a unique paleopathological case in Mesozoic mammals in which the animal with a severely broken right tibia could heal and survive in natural condition. The phylogenetic analysis based on craniodental characters places Yubaartar as the immediate outgroup of Taeniolabidoidea, a group consisting of a North American clade and an Asian clade. This relationship indicates at least a faunal interchange of multituberculates before the K-Pg transition. The new evidence further supports the hypothesis that disparity in dental complexity, which relates to animal diets, increased with generic richness and disparity in body size and that an adaptive shift towards increased herbivory across the K-Pg transitional interval.
Aberrant Autophagic Response in The Muscle of A Knock-in Mouse Model of Spinal and Bulbar Muscular Atrophy
Authors: Rusmini Paola , Polanco Maria Josefa , Cristofani Riccardo , Cicardi Maria Elena , Meroni Marco , Galbiati Mariarita , Piccolella Margherita , Messi Elio , Giorgetti Elisa , Lieberman Andrew P. , Milioto Carmelo , Rocchi Anna , Aggarwal Tanya , Pennuto Maria , Crippa Valeria , Poletti Angelo 
Published: October 2015

AbstractSpinal and bulbar muscular atrophy (SBMA) is characterized by loss of motoneurons and sensory neurons, accompanied by atrophy of muscle cells. SBMA is due to an androgen receptor containing a polyglutamine tract (ARpolyQ) that misfolds and aggregates, thereby perturbing the protein quality control (PQC) system. Using SBMA AR113Q mice we analyzed proteotoxic stress-induced alterations of HSPB8-mediated PQC machinery promoting clearance of misfolded proteins by autophagy. In muscle of symptomatic AR113Q male mice, we found expression upregulation of Pax-7, myogenin, E2-ubiquitin ligase UBE2Q1 and acetylcholine receptor (AchR), but not of MyoD and of two E3-ligases (MuRF-1 and Cullin3). TGFβ1 and PGC-1α were also robustly upregulated. We also found a dramatic perturbation of the autophagic response, with upregulation of most autophagic markers (Beclin-1, ATG10, p62/SQSTM1, LC3) and of the HSPB8-mediated PQC response. Both HSPB8 and its co-chaperone BAG3 were robustly upregulated together with other specific HSPB8 interactors (HSPB2 and HSPB3). Notably, the BAG3:BAG1 ratio increased in muscle suggesting preferential misfolded proteins routing to autophagy rather than to proteasome. Thus, mutant ARpolyQ induces a potent autophagic response in muscle cells. Alteration in HSPB8-based PQC machinery may represent muscle-specific biomarkers useful to assess SBMA progression in mice and patients in response to pharmacological treatments.
TORC2: a novel target for treating age-associated memory impairment
Authors: Johnson Jennifer L. , Huang Wei , Roman Gregg , Costa-Mattioli Mauro 
Published: October 2015

AbstractMemory decline is one of the greatest health threats of the twenty-first century. Because of the widespread increase in life expectancy, 20 percent of the global population will be over 60 in 2050 and the problems caused by age-related memory loss will be dramatically aggravated. However, the molecular mechanisms underlying this inevitable process are not well understood. Here we show that the activity of the recently discovered mechanistic target of rapamycin (mTOR) complex 2 (mTORC2) declines with age in the brain of both fruit flies and rodents and that the loss of mTORC2-mediated actin polymerization contributes to age-associated memory loss. Intriguingly, treatment with a small molecule that activates mTORC2 (A-443654) reverses long-term memory (LTM) deficits in both aged mice and flies. In addition, we found that pharmacologically boosting either mTORC2 or actin polymerization enhances LTM. In contrast to the current approaches to enhance memory that have primarily targeted the regulation of gene expression (epigenetic, transcriptional and translational), our data points to a novel, evolutionarily conserved mechanism for restoring memory that is dependent on structural plasticity. These insights into the molecular basis of age-related memory loss may hold promise for new treatments for cognitive disorders.
Defective mitochondrial fission augments NLRP3 inflammasome activation
Authors: Park Sangjun , Won Ji-Hee , Hwang Inhwa , Hong Sujeong , Lee Heung Kyu , Yu Je-Wook 
Published: October 2015

AbstractDespite the fact that deregulated NLRP3 inflammasome activation contributes to the pathogenesis of chronic inflammatory or metabolic disorders, the underlying mechanism by which NLRP3 inflammasome signaling is initiated or potentiated remains poorly understood. Much attention is being paid to mitochondria as a regulator of NLRP3 inflammasome activation, but little is known about the role of mitochondrial dynamics for the inflammasome pathway. Here, we present evidence that aberrant mitochondrial elongation caused by the knockdown of dynamin-related protein 1 (Drp1) lead to a marked increase in NLRP3-dependent caspase-1 activation and interleukin-1-beta secretion in mouse bone marrow-derived macrophages. Conversely, carbonyl cyanide m-chlorophenyl hydrazone, a chemical inducer of mitochondrial fission, clearly attenuated NLRP3 inflammasome assembly and activation. Augmented activation of NLRP3 inflammasome by mitochondrial elongation is not resulted from the increased mitochondrial damages of Drp1-knockdown cells. Notably, enhanced extracellular signal-regulated kinase (ERK) signaling in Drp1-knockdown macrophages is implicated in the potentiation of NLRP3 inflammasome activation, possibly via mediating mitochondrial localization of NLRP3 to facilitate the assembly of NLRP3 inflammasome. Taken together, our results provide a molecular insight into the importance of mitochondrial dynamics in potentiating NLRP3 inflammasome activation, leading to aberrant inflammation.
Personality and morphological traits affect pigeon survival from raptor attacks
Authors: Santos Carlos D. , Cramer Julia F. , Pârâu Liviu G. , Miranda Ana C. , Wikelski Martin , Dechmann Dina K. N. 
Published: October 2015

AbstractPersonality traits have recently been shown to impact fitness in different animal species, potentially making them similarly relevant drivers as morphological and life history traits along the evolutionary pathways of organisms. Predation is a major force of natural selection through its deterministic effects on individual survival, but how predation pressure has helped to shape personality trait selection, especially in free-ranging animals, remains poorly understood. We used high-precision GPS tracking to follow whole flocks of homing pigeons (Columba livia) with known personalities and morphology during homing flights where they were severely predated by raptors. This allowed us to determine how the personality and morphology traits of pigeons may affect their risk of being predated by raptors. Our survival model showed that individual pigeons, which were more tolerant to human approach, slower to escape from a confined environment, more resistant to human handling, with larger tarsi and with lighter plumage, were more likely to be predated by raptors. We provide rare empirical evidence that the personality of prey influences their risk of being predated under free-ranging circumstances.
Comprehensive microRNA profiling in acetaminophen toxicity identifies novel circulating biomarkers for human liver and kidney injury
Authors: Vliegenthart A. D. B. , Shaffer J. M. , Clarke J. I. , Peeters L. E. J. , Caporali A. , Bateman D. N. , Wood D. M. , Dargan P. I. , Craig D. G. , Moore J. K. , Thompson A. I. , Henderson N. C. , Webb D. J. , Sharkey J. , Antoine D. J. , Park B. K. , Bailey M. A. , Lader E. , Simpson K. J. , Dear J. W. 
Published: October 2015

AbstractOur objective was to identify microRNA (miRNA) biomarkers of drug-induced liver and kidney injury by profiling the circulating miRNome in patients with acetaminophen overdose. Plasma miRNAs were quantified in age- and sex-matched overdose patients with (N = 27) and without (N = 27) organ injury (APAP-TOX and APAP-no TOX, respectively). Classifier miRNAs were tested in a separate cohort (N = 81). miRNA specificity was determined in non-acetaminophen liver injury and murine models. Sensitivity was tested by stratification of patients at hospital presentation (N = 67). From 1809 miRNAs, 75 were 3-fold or more increased and 46 were 3-fold or more decreased with APAP-TOX. A 16 miRNA classifier model accurately diagnosed APAP-TOX in the test cohort. In humans, the miRNAs with the largest increase (miR-122-5p, miR-885-5p, miR-151a-3p) and the highest rank in the classifier model (miR-382-5p) accurately reported non-acetaminophen liver injury and were unaffected by kidney injury. miR-122-5p was more sensitive than ALT for reporting liver injury at hospital presentation, especially combined with miR-483-3p. A miRNA panel was associated with human kidney dysfunction. In mice, miR-122-5p, miR-151a-3p and miR-382-5p specifically reported APAP toxicity - being unaffected by drug-induced kidney injury. Profiling of acetaminophen toxicity identified multiple miRNAs that report acute liver injury and potential biomarkers of drug-induced kidney injury.
Metabolomics reveals metabolic changes in male reproductive cells exposed to thirdhand smoke
Authors: Xu Bo , Chen Minjian , Yao Mengmeng , Ji Xiaoli , Mao Zhilei , Tang Wei , Qiao Shanlei , Schick Suzaynn F. , Mao Jian-Hua , Hang Bo , Xia Yankai 
Published: October 2015

AbstractThirdhand smoke (THS) is a new term for the toxins in cigarette smoke that linger in the environment long after the cigarettes are extinguished. The effects of THS exposure on male reproduction have not yet been studied. In this study, metabolic changes in male germ cell lines (GC-2 and TM-4) were analyzed after THS treatment for 24 h. THS-loaded chromatography paper samples were generated in a laboratory chamber system and extracted in DMEM. At a paper: DMEM ratio of 50 μg/ml, cell viability in both cell lines was normal, as measured by the MTT assay and markers of cytotoxicity, cell cycle, apoptosis and ROS production were normal as measured by quantitative immunofluorescence. Metabolomic analysis was performed on methanol extracts of GC-2 and TM-4 cells. Glutathione metabolism in GC-2 cells and nucleic acid and ammonia metabolism in TM-4 cells, was changed significantly by THS treatment. RT-PCR analyses of mRNA for enzyme genes Gss and Ggt in GC-2 cells and TK, SMS and Glna in TM-4 cells reinforced these findings, showing changes in the levels of enzymes involved in the relevant pathways. In conclusion, exposure to THS at very low concentrations caused distinct metabolic changes in two different types of male reproductive cell lines.
Graft revascularization is essential for non-invasive monitoring of transplanted islets with radiolabeled exendin
Authors: Eter Wael A. , Bos Desirée , Frielink Cathelijne , Boerman Otto C. , Brom Maarten , Gotthardt Martin 
Published: October 2015

AbstractIslet transplantation is a novel promising strategy to cure type 1 diabetes. However, the long-term outcome is still poor, because both function and survival of the transplant decline over-time. Non-invasive imaging methods have the potential to enable monitoring of islet survival after transplantation and the effects of immunosuppressive drugs on transplantation outcome. 111In-labeled exendin-3 is a promising tracer to visualize native and transplanted islets by SPECT (Single Photon Emission Computed Tomography). In the present study, we hypothesized that islet microvasculature plays an important role determining the uptake of exendin-3 in islets when monitoring transplant survival. We observed 111In-exendin-3 accumulation in the transplant as early as three days after transplantation and an increase in the uptake up to three weeks post-transplantation. Islet-revascularization correlated with the increase in 111In-exendin-3 uptake, whereas fully re-established islet vasculature coincided with a stabilized uptake of the radiotracer in the transplant. Here, we demonstrate the importance of islet vasculature for in vivo delivery of radiotracers to transplanted islets and we demonstrate that optimal and stable uptake of exendin four weeks after transplantation opens the possibility for long-term monitoring of islet survival by SPECT imaging.