bluuebunny/crossref_metadata_2025_split huggingface dataset:
Separating the Wheat from the Chaff: Dating Charred Plant Remains Extracted from Daub (With Reference to the 14C Chronology of the Epi-Lengyel Culture in Upper Silesia)
Authors: Chmielewski Tomasz J , Sady Agata , Goslar Tomasz , Furmanek Mirosław , Juchelka Jiři 
Published: March 2017

AbstractDespite their great potential, charred particles of chaff-and-straw temper from daub architecture have very rarely been considered as material suitable for 14C dating. This short paper is intended to change this situation. With this aim in mind, we first present the rationale and objectives of the sampling procedure based on archaeobotanical exploration of prehistoric remains of daub architecture, and then report and discuss the results of a short chronometric exercise based on such samples. The empirical verification of the sampling procedure was based on finds related to the epi-Lengyel culture from Upper Silesia.
ὌΡΧΙΣ: TESTICLE, TESTICULATE AND GLANS PENIS
Authors: Cotter Joseph 
Published: March 2017

Goffredo Coppola, the Italian editor of this papyrus, supposed that τὸν ὄρχιν (the testicle) = τοὺς ὄρχεις; but he was puzzled when no likely erotic word seemed available to finish the line. He suggested φαλ[ῆς, from φαλός = λευκός (‘white’) to be followed by some metaphorical word for penis such as κέρκου. Romagnoli noted that it made no sense to have the testicle(s) dependent on the penis, and argued that Hipponax here intended ὄρχις to refer metaphorically to the glans penis; therefore, he emended to καί μοι τὸν ὄρχιν τῆς φαλ[ῆς ἐκλέψασα (= peeling back the penis’ foreskin); but his feminine form τῆς φαλ[ῆς is unlikely given the masculine form τοῦ φάλεω in Hipponax fr. 21 W. Medeiros suggested ὄρχις, sing. = ὄσχη ‘scrotum’; West actually exalted the role of the testicle by emending to τῆς φαλ[άκρης ἕλκουσα ‘pulling my testicle by the bald spot’; but it is not obvious why hitting the testicles merits such attention in a narrative fixed on the failure to attain an erection.
Venturing Abroad: The Internationalisation of Mexican Banks Prior to the 1982 Crisis
Authors: ALVAREZ SEBASTIAN 
Published: March 2017

AbstractThis article explores the international expansion of Mexican banks and its implications for the domestic banking system during the decade leading up to the 1982 debt crisis. In contrast to the prevalent focus in the literature on profitability and performance, I examine the asset and liability structure of the banking sector and show that there were clear signs of deterioration in its financial condition well before the onset of the crisis. Financial statement analysis reveals that the banks engaged in international lending and foreign funding were the ones with the greatest propensity to be adversely affected by this problem. The international expansion of Mexican banks emerged and developed as an exit option to domestic funding problems and increasing competition from foreign bank loans, in a context of growing needs for financing and foreign exchange in Mexico.
Groupoid Fell bundles for product systems over quasi-lattice ordered groups
Authors: RENNIE ADAM , ROBERTSON DAVID , SIMS AIDAN 
Published: March 2017

AbstractConsider a product system over the positive cone of a quasi-lattice ordered group. We construct a Fell bundle over an associated groupoid so that the cross-sectional algebra of the bundle is isomorphic to the Nica–Toeplitz algebra of the product system. Under the additional hypothesis that the left actions in the product system are implemented by injective homomorphisms, we show that the cross-sectional algebra of the restriction of the bundle to a natural boundary subgroupoid coincides with the Cuntz–Nica–Pimsner algebra of the product system. We apply these results to improve on existing sufficient conditions for nuclearity of the Nica–Toeplitz algebra and the Cuntz–Nica–Pimsner algebra, and for the Cuntz–Nica–Pimsner algebra to coincide with its co-universal quotient.
Geranylgeranyl diphosphate synthase inhibition induces apoptosis that is dependent upon GGPP depletion, ERK phosphorylation and caspase activation
Authors: Agabiti Sherry S , Li Jin , Wiemer Andrew J 
Published: March 2017

AbstractBisphosphonates are diphosphate analogs that inhibit the intermediate enzymes of the mevalonate pathway. Here, we compared the effects of a farnesyl diphosphate synthase inhibitor, zoledronate, and a geranylgeranyl diphosphate synthase (GGDPS) inhibitor, digeranyl bisphosphonate (DGBP), on lymphocytic leukemia cell proliferation and apoptosis. Both zoledronate and DGBP inhibited proliferation with DGBP doing so more potently. DGBP was markedly less toxic than zoledronate toward the viability of healthy human peripheral blood mononuclear cells. Addition of GGPP, but not farnesyl diphosphate (FPP), prevented the anti-proliferative effects of DGBP. Both GGPP and FPP partially rescued the effects of zoledronate. Co-treatment with DGBP and zoledronate was antagonistic. To further assess the effects of the bisphosphonates, we analyzed annexin V and propidium iodide staining via flow cytometry and found that DGBP induced apoptosis more potently than zoledronate. Western blots show that DGBP treatment altered expression and membrane affinity of some but not all geranylgeranylated small GTPases, activated caspases and increased ERK phosphorylation. Importantly, the anti-proliferative effects of DGBP were blocked by treatment with a caspase inhibitor and by treatment with a MEK inhibitor. Together, our findings indicate that DGBP is a more potent and selective compound than zoledronate in inducing apoptosis mediated through pathways that include caspases and MEK/ERK. These findings support the further development of GGDPS inhibitors as anticancer therapeutics.
Immunoproteomic identification and characterization of Ni2+-regulated proteins implicates Ni2+ in the induction of monocyte cell death
Authors: Jakob Annika , Mussotter Franz , Ohnesorge Stefanie , Dietz Lisa , Pardo Julian , Haidl Ian D , Thierse Hermann-Josef 
Published: March 2017

AbstractNickel allergy is the most common cause of allergic reactions worldwide, with cutaneous and systemic effects potentially affecting multiple organs. Monocytes are precursors of not only macrophages but also dendritic cells, the most potent activators of nickel hypersensitivity. Monocytes are themselves important antigen-presenting cells, capable of nickel-specific T-cell activationin vivoandin vitro, in addition to being important for immediate innate immune inflammation. To elucidate early Ni2+-dependent inflammatory molecular mechanisms in human monocytes, a Ni2+-specific proteomic approach was applied. Quantitative two-dimensional (2D) differential gel electrophoresis and Delta2D software analyses coupled with matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) revealed that Ni2+significantly regulated 56 protein species, of which 36 were analyzed by MALDI-MS. Bioinformatics analyses of all identified proteins resulted in Ni2+-associated functional annotation clusters, such as cell death, metal ion binding, and cytoskeletal remodeling. The involvement of Ni2+in the induction of monocyte cell death, but not T-cell death, was observed at Ni2+concentrations at or above 250 μM. Examination of caspase activity during Ni2+-mediated cell death revealed monocytic cell death independent of caspase-3 and -7 activity. However, confocal microscopy analysis demonstrated Ni2+-triggered cytoskeletal remodeling and nuclear condensation, characteristic of cellular apoptosis. Thus, Ni2+-specific peripheral blood mononuclear cell stimulation suggests monocytic cell death at Ni2+concentrations at or above 250 μM, and monocytic effects on immune regulation at lower Ni2+concentrations.
Induction of intestinal stemness and tumorigenicity by aberrant internalization of commensal non-pathogenic E. coli
Authors: Sahu Upasana , Choudhury Arnab , Parvez Suhel , Biswas Subhrajit , Kar Sudeshna 
Published: March 2017

AbstractCommensal Escherichia coli has been identified as a major protagonist of microbe-induced colorectal oncogenesis. Its tumour-promoting attribute is linked to the expression of DNA-damaging genotoxins. Using a constitutively invasive variant of non-pathogenic E. coli, we demonstrate that chronic presence of internalized E. coli leads to enhanced oncogenicity in colon cancer cells. Instead of genomic damage, the tumorigenic effect is mediated through an expansion of the cancer stem cell (CSC) population, likely through dedifferentiation of lineage-committed intestinal epithelial cells. Stemness-linked intestinal tumorigenicity is directly correlated to absence of microbial virulence factor expression and is specific for intestinal cells. The enriched CSC fraction remains stable in the absence of the instigating bacteria and can foster stemness traits in unexposed cells through secreted factors. Mechanistically, aberrant host invasion leads to realignment of multiple host signal transduction cascades, notably mutually re-enforcing NF-κB and β-catenin activation, through reciprocal modulation of microbe sensing pathways Nod1/Rip2 and TLR/MyD88. The expanded tumorigenic CSC population is marked by enhanced malignancy traits, long-term self-renewal capacity and robust tumorigenic ability, both in vitro and in vivo. Our study shows that microbe-induced oncogenicity is not a strict correlate of commensal virulence and can be invoked by even non-pathogenic E. coli by engendering tumorigenic stemness in host cells.
Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth
Authors: Li Juan , Liu Jie , Liang Zheyong , He Fang , Yang Lu , Li Pingping , Jiang Yina , Wang Bo , Zhou Can , Wang Yaochun , Ren Yu , Yang Jin , Zhang Jianmin , Luo Zhijun , Vaziri Cyrus , Liu Peijun 
Published: March 2017

AbstractLoss or dysfunction of tumor suppressor retinoblastoma (RB) is a common feature in various tumors, and contributes to cancer cell stemness and drug resistance to cancer therapy. However, the strategy to suppress or eliminate Rb-deficient tumor cells remains unclear. In the present study, we accidentally found that reduction of DNA replication licensing factor MCM7 induced more apoptosis in RB-deficient tumor cells than in control tumor cells. Moreover, after a drug screening and further studies, we demonstrated that statin drug Simvastatin and Atorvastatin were able to inhibit MCM7 and RB expressions. Further study showed that Simvastatin and Atorvastatin induced more chromosome breaks and gaps of Rb-deficient tumor cells than control tumor cells. In vivo results showed that Simvastatin and Atorvastatin significantly suppressed Rb-deficient tumor growth than control in xenograft mouse models. The present work demonstrates that ‘old’ lipid-lowering drugs statins are novel weapons against RB-deficient tumors due to their effects on suppressing MCM7 protein levels.
CD95 ligand induces senescence in mismatch repair-deficient human colon cancer via chronic caspase-mediated induction of DNA damage
Authors: Raats Danielle A , Frenkel Nicola , van Schelven Susanne J , Rinkes Inne HMBorel , Laoukili Jamila , Kranenburg Onno 
Published: March 2017

AbstractCD95 is best known for its ability to induce apoptosis via a well-characterized pathway involving caspase-mediated proteolytic events. However, in apoptosis-resistant cell lines of diverse cancer types stimulation of CD95 primarily has pro-tumorigenic effects that affect many of the hallmarks of cancer. For instance, in colon cancer cells with a mutant KRAS gene CD95 primarily promotes invasion and metastasis. In the current study, we further investigated the context dependency of the consequences of CD95 activation in colon cancer. We used a series of patient-derived three-dimensional colon cancer cultures and studied their response to stimulation with CD95 ligand (CD95L). CD95L had a strong inhibitory effect on the clone-forming capacity of five out of nine cultures. In line with previous work, these cultures all had a wild-type KRAS gene and expressed high levels of CD95. Furthermore, the most sensitive cultures were characterized by microsatellite instability (MSI) and deficient mismatch repair. The reduced clonogenic growth of MSI-type colonospheres resulting from chronic CD95 stimulation was only partly due to apoptosis as many tumor cells survived treatment, yet were unable to regenerate clones. CD95 stimulation caused an irreversible cell cycle arrest, which was associated with cytokine secretion, similar to the senescence-associated secretory phenotype (SASP), and expression of senescence-associated β-galactosidase. In human colon cancer cohorts, CD95 expression was strongly correlated with the recently identified consensus molecular subtype 1 (CMS1), which mainly consists of MSI-high tumors, and with two independent SASP signatures. Mechanistically, CD95-induced senescence was caused by chronic DNA damage via caspase-activated DNAse resulting in p53 activation and p21 expression, with a minor contribution of the SASP. We conclude that induction of senescence is a hitherto unrecognized consequence of high CD95 expression, which appears to be most relevant for CMS1.
Digoxin-induced retinal degeneration depends on rhodopsin
Authors: Landfried Britta , Samardzija Marijana , Barben Maya , Schori Christian , Klee Katrin , Storti Federica , Grimm Christian 
Published: March 2017

AbstractNa,K-ATPases are energy consuming ion pumps that are required for maintaining ion homeostasis in most cells. In the retina, Na,K-ATPases are especially important to sustain the dark current in photoreceptor cells needed for rapid hyperpolarization of rods and cones in light. Cardiac glycosides like digoxin inhibit the activity of Na,K-ATPases by targeting their catalytic alpha subunits. This leads to a disturbed ion balance, which can affect cellular function and survival. Here we show that the treatment of wild-type mice with digoxin leads to severe retinal degeneration and loss of vision. Digoxin induced cell death specifically in photoreceptor cells with no or only minor effects in other retinal cell types. Photoreceptor-specific cytotoxicity depended on the presence of bleachable rhodopsin. Photoreceptors of Rpe65 knockouts, which have no measurable rhodopsin and photoreceptors of Rpe65R91W mice that have <10% of the rhodopsin found in retinas of wild-type mice were not sensitive to digoxin treatment. Similarly, cones in the all-cone retina of Nrl knockout mice were also not affected. Digoxin induced expression of several genes involved in stress signaling and inflammation. It also activated proteins such as ERK1/2, AKT, STAT1, STAT3 and CASP1 during a period of up to 10 days after treatment. Activation of signaling genes and proteins, as well as the dependency on bleachable rhodopsin resembles mechanisms of light-induced photoreceptor degeneration. Digoxin-mediated photoreceptor cell death may thus be used as an inducible model system to study molecular mechanisms of retinal degeneration.
Enhancing CO2 electrolysis through synergistic control of non-stoichiometry and doping to tune cathode surface structures
Authors: Ye Lingting , Zhang Minyi , Huang Ping , Guo Guocong , Hong Maochun , Li Chunsen , Irvine John T. S. , Xie Kui 
Published: March 2017

AbstractSustainable future energy scenarios require significant efficiency improvements in both electricity generation and storage. High-temperature solid oxide cells, and in particular carbon dioxide electrolysers, afford chemical storage of available electricity that can both stabilize and extend the utilization of renewables. Here we present a double doping strategy to facilitate CO2 reduction at perovskite titanate cathode surfaces, promoting adsorption/activation by making use of redox active dopants such as Mn linked to oxygen vacancies and dopants such as Ni that afford metal nanoparticle exsolution. Combined experimental characterization and first-principle calculations reveal that the adsorbed and activated CO2 adopts an intermediate chemical state between a carbon dioxide molecule and a carbonate ion. The dual doping strategy provides optimal performance with no degradation being observed after 100 h of high-temperature operation and 10 redox cycles, suggesting a reliable cathode material for CO2 electrolysis.
Induction of apoptosis and ganoderic acid biosynthesis by cAMP signaling in Ganoderma lucidum
Authors: You Bang-Jau , Tien Ni , Lee Miin-Huey , Bao Bo-Ying , Wu Yih-Shyuan , Hu Tsung-Chi , Lee Hong-Zin 
Published: March 2017

AbstractApoptosis is an essential physiological process that controls many important biological functions. However, apoptosis signaling in relation to secondary metabolite biosynthesis in plants and fungi remains a mystery. The fungusGanoderma lucidumis a popular herbal medicine worldwide, but the biosynthetic regulation of its active ingredients (ganoderic acids, GAs) is poorly understood. We investigated the role of 3′,5′-cyclic adenosine monophosphate (cAMP) signaling in fungal apoptosis and GA biosynthesis inG. lucidum. Two phosphodiesterase inhibitors (caffeine and 3-isobutyl-1-methylxanthine, IBMX) and an adenylate cyclase activator (sodium fluoride, NaF) were used to increase intracellular cAMP levels. Fungal apoptosis was identified by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) assay and a condensed nuclear morphology. Our results showed that GA production and fungal apoptosis were induced when the mycelium was treated with NaF, caffeine, or cAMP/IBMX. Downregulation of squalene synthase and lanosterol synthase gene expression by cAMP was detected in the presence of these chemicals, which indicates that these two genes are not critical for GA induction. Transcriptome analysis indicated that mitochondria might play an important role in cAMP-induced apoptosis and GA biosynthesis. To the best of our knowledge, this is the first report to reveal that cAMP signaling induces apoptosis and secondary metabolite production in fungi.
Novel Microwave Torso Scanner for Thoracic Fluid Accumulation Diagnosis and Monitoring
Authors: Ahdi Rezaeieh S. , Zamani A. , Bialkowski K. S. , Abbosh A. M. 
Published: March 2017

AbstractThoracic fluid accumulation is one of the significant and early-stage manifestations of fatal diseases, such as lung-cancer, liver-failure and congestive heart-failure. Currently, computational-tomography (CT)-Scan is the most widely used tool for the detection of thoracic fluid. Yet, it is unable to detect small amounts of fluid, has ionizing radiation and lacks mobility. On the other hand, microwave imaging systems have emerged as an accurate and portable complementary diagnostic tool. However, there is a lack of a complete clinical platform that can fulfill the requirements of accurate and reliable imaging. Therefore, a microwave torso scanner that is designed to meet those requirements is presented. In this system, two elliptical-arrays of microwave antennas (sensors) transmit signals towards the torso and collect the back-scattered signals. The captured signals are then processed by a frequency-based imaging algorithm to form microwave images that display a possible accumulated fluid. The system successfully detects and localized small volumes (3 mL) of fluid injected at different places inside a torso-phantom. As preparations for future clinical trials, the system is tested on healthy subjects to define the threshold range of healthy scenario images.
Synchrony of plant cellular circadian clocks with heterogeneous properties under light/dark cycles
Authors: Okada Masaaki , Muranaka Tomoaki , Ito Shogo , Oyama Tokitaka 
Published: March 2017

AbstractIndividual cells in a plant can work independently as circadian clocks, and their properties are the basis of various circadian phenomena. The behaviour of individual cellular clocks in Lemna gibba was orderly under 24-h light/dark cycles despite their heterogeneous free-running periods (FRPs). Here, we reveal the entrainment habits of heterogeneous cellular clocks using non-24-h light/dark cycles (T-cycles). The cellular rhythms of AtCCA1::LUC under T = 16 h cycles showed heterogeneous entrainment that was associated with their heterogeneous FRPs. Under T = 12 h cycles, most cells showed rhythms having ~24-h periods. This suggested that the lower limit of entrainment to the light/dark cycles of heterogeneous cellular circadian clocks is set to a period longer than 12 h, which enables them to be synchronous under ~24-h daily cycles without being perturbed by short light/dark cycles. The entrainment habits of individual cellular clocks are likely to be the basis of the circadian behaviour of plant under the natural day–night cycle with noisy environmental fluctuations. We further suggest that modifications of EARLY FLOWERING3 (ELF3) in individual cells deviate the entrainability to shorter T-cycles possibly by altering both the FRPs and light responsiveness.
Damage-Induced Cell Regeneration in the Midgut of Aedes albopictus Mosquitoes
Authors: Janeh Maria , Osman Dani , Kambris Zakaria 
Published: March 2017

AbstractMosquito-transmitted diseases cause over one million deaths every year. A better characterization of the vector’s physiology and immunity should provide valuable knowledge for the elaboration of control strategies. Mosquitoes depend on their innate immunity to defend themselves against pathogens. These pathogens are acquired mainly through the oral route, which places the insects’ gut at the front line of the battle. Indeed, the epithelium of the mosquito gut plays important roles against invading pathogens acting as a physical barrier, activating local defenses and triggering the systemic immune response. Therefore, the gut is constantly confronted to stress and often suffers cellular damage. In this study, we show that dividing cells exist in the digestive tract of adult A. albopictus and that these cells proliferate in the midgut after bacterial or chemical damage. An increased transcription of signaling molecules that regulate the EGFR and JAK/STAT pathways was also observed, suggesting a possible involvement of these pathways in the regeneration of damaged guts. This work provides evidence for the presence of regenerative cells in the mosquito guts, and paves the way towards a molecular and cellular characterization of the processes required to maintain mosquito’s midgut homeostasis in both normal and infectious conditions.
High photon-to-heat conversion efficiency in the wavelength region of 250–1200 nm based on a thermoelectric Bi2Te3 film structure
Authors: Hu Er-Tao , Yao Yuan , Zang Kai-Yan , Liu Xin-Xing , Jiang An-Qing , Zheng Jia-Jin , Yu Ke-Han , Wei Wei , Zheng Yu-Xiang , Zhang Rong-Jun , Wang Song-You , Zhao Hai-Bin , Yoshie Osamu , Lee Young-Pak , Wang Cai-Zhuang , Lynch David W. , Guo Jun-Peng , Chen Liang-Yao 
Published: March 2017

AbstractIn this work, 4-layered SiO2/Bi2Te3/SiO2/Cu film structures were designed and fabricated and the optical properties investigated in the wavelength region of 250–1200 nm for their promising applications for direct solar-thermal-electric conversion. A typical 4-layered film sample with the structure SiO2 (66.6 nm)/Bi2Te3 (7.0 nm)/SiO2 (67.0 nm)/Cu (>100.0 nm) was deposited on a Si or K9-glass substrate by magnetron sputtering. The experimental results agree well with the simulated ones showing an average optical absorption of 96.5%, except in the shorter wavelength region, 250–500 nm, which demonstrates the superior absorption property of the 4-layered film due to the randomly rough surface of the Cu layer resulting from the higher deposition power. The high reflectance of the film structure in the long wavelength region of 2–20 μm will result in a low thermal emittance, 0.064 at 600 K. The simpler 4-layered structure with the thermoelectric Bi2Te3 used as the absorption layer may provide a straightforward way to obtain solar-thermal-electric conversion more efficiently through future study.