bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of inflammasome proteins and inflammasome activation occurs in human, but not in murine keratinocytes
Authors: Sand Jennifer , Haertel Eric , Biedermann Thomas , Contassot Emmanuel , Reichmann Ernst , French Lars E. , Werner Sabine , Beer Hans-Dietmar 
Published: January 2018

AbstractInflammasomes are multimeric protein complexes that assemble upon sensing of a variety of stress factors. Their formation results in caspase-1-mediated activation and secretion of the pro-inflammatory cytokines pro-interleukin(IL)-1β and -18, which induce an inflammatory response. Inflammation is supported by a lytic form of cell death, termed pyroptosis. Innate immune cells, such as macrophages or dendritic cells, express and activate inflammasomes. However, it has also been demonstrated that human primary keratinocytes activate different types of inflammasomes in vitro, for example, upon UVB irradiation or viral infection. Keratinocytes are the main cell type of the epidermis, the outermost layer of the body, and form a protective barrier consisting of a stratified multi-layered epithelium. In human, gain-of-function mutations of theNLRP1gene cause syndromes mediated by inflammasome activation in keratinocytes that are characterised by skin inflammation and skin cancer susceptibility. Here we demonstrate that murine keratinocytes do not activate inflammasomes in response to stimuli, which induce IL-1β and -18 secretion by human keratinocytes. Whereas murine keratinocytes produced caspase-1 and proIL-18, expression of the inflammasome proteins Nlrp1, Nlrp3, Aim2, Asc, and proIL-1β was, compared to human keratinocytes or murine dendritic cells, very low or even undetectable. Priming of murine keratinocytes with cytokines commonly used for induction of proIL-1β and inflammasome protein expression did not rescue inflammasome activation. Nevertheless, UVB-induced inflammation and neutrophil recruitment in murine skin was dependent on IL-1β and caspase-1. However, also under these conditions, we did not detect expression of proIL-1β by keratinocytes in murine skin, but by immune cells. These results demonstrate a higher immunological competence of human compared to murine keratinocytes, which is reflected by stress-induced IL-1β secretion that is mediated by inflammasomes. Therefore, keratinocytes in human skin can exert immune functions, which are carried out by professional immune cells in murine skin.
Dual suppression of inner and outer mitochondrial membrane functions augments apoptotic responses to oncogenic MAPK inhibition
Authors: Serasinghe Madhavika N. , Gelles Jesse D. , Li Kent , Zhao Lauren , Abbate Franco , Syku Marie , Mohammed Jarvier N. , Badal Brateil , Rangel Cuahutlehuanitzin A. , Hoehn Kyle L. , Celebi Julide Tok , Chipuk Jerry Edward 
Published: January 2018

AbstractMitogen-activated protein kinase (MAPK) pathway inhibitors show promise in treating melanoma, but are unsuccessful in achieving long-term remission. Concordant with clinical data, BRAFV600E melanoma cells eliminate glycolysis upon inhibition of BRAFV600E or MEK with the targeted therapies Vemurafenib or Trametinib, respectively. Consequently, exposure to these therapies reprograms cellular metabolism to increase mitochondrial respiration and restrain cell death commitment. As the inner mitochondrial membrane (IMM) is sub-organellar site of oxidative phosphorylation (OXPHOS), and the outer mitochondrial membrane (OMM) is the major site of anti-apoptotic BCL-2 protein function, we hypothesized that suppressing these critical mitochondrial membrane functions would be a rational approach to maximize the pro-apoptotic effect of MAPK inhibition. Here, we demonstrate that disruption of OXPHOS with the mitochondria-specific protonophore BAM15 promotes the mitochondrial pathway of apoptosis only when oncogenic MAPK signaling is inhibited. Based on RNA-sequencing analyses of nevi and primary melanoma samples, increased pro-apoptotic BCL-2 family expression positively correlates with high-risk disease suggesting a highly active anti-apoptotic BCL-2 protein repertoire likely contributes to worse outcome. Indeed, combined inhibition of the anti-apoptotic BCL-2 repertoire with BH3-mimetics, OXPHOS, and oncogenic MAPK signaling induces fulminant apoptosis and eliminates clonogenic survival. Altogether, these data suggest that dual suppression of IMM and OMM functions may unleash the normally inadequate pro-apoptotic effects of oncogenic MAPK inhibition to eradicate cancer cells, thus preventing the development of resistant disease, and ultimately, supporting long-term remission.
Ultrasensitive reversible chromophore reaction of BODIPY functions as high ratio double turn on probe
Authors: Hu Dehui , Zhang Tao , Li Shayu , Yu Tianjun , Zhang Xiaohui , Hu Rui , Feng Jiao , Wang Shuangqing , Liang Tongling , Chen Jianming , Sobenina Lyubov N. , Trofimov Boris A. , Li Yi , Ma Jinshi , Yang Guoqiang 
Published: January 2018

AbstractChromophore reactions with changes to conjugation degree, especially those between the conjugated and unconjugated state, will bring a large spectral variation. To realize such a process, a meso-naked BODIPY (MNBOD) with two electron-withdrawing groups around the core is designed and synthesized. The resulting system is extremely sensitive to bases. The red, highly fluorescent solution readily becomes colorless and non-fluorescent after base addition; however, the color and fluorescence can be totally and instantly restored by addition of acid or formaldehyde. Analyses show that two identical MNBODs are connected by a C–C single bond (sp3) at the meso-position through a radical reaction that results in an unconjugated, colorless dimer complexed with bases. When the bases are consumed, the dimer immediately dissociates into the red, highly fluorescent, conjugated MNBOD monomer. With 260 nm spectral change and over 120,000 turn-on ratio, this chromophore-reaction can be utilized as a sensitive reaction-based dual-signal probe.
Single-cell variability in multicellular organisms
Authors: Smith Stephen , Grima Ramon 
Published: January 2018

AbstractNoisy gene expression is of fundamental importance to single cells, and is therefore widely studied in single-celled organisms. Extending these studies to multicellular organisms is challenging since their cells are generally not isolated, but individuals in a tissue. Cell–cell coupling via signalling, active transport or pure diffusion, ensures that tissue-bound cells are neither fully independent of each other, nor an entirely homogeneous population. In this article, we show that increasing the strength of coupling between cells can either increase or decrease the single-cell variability (and, therefore, the heterogeneity of the tissue), depending on the statistical properties of the underlying genetic network. We confirm these predictions using spatial stochastic simulations of simple genetic networks, and experimental data from animal and plant tissues. The results suggest that cell–cell coupling may be one of several noise-control strategies employed by multicellular organisms, and highlight the need for a deeper understanding of multicellular behaviour.
Controllable population dynamics in Landau-quantized graphene
Authors: Ding Chunling , Yu Rong , Hao Xiangying , Zhang Duo 
Published: January 2018

AbstractIn this paper, we carry out a theoretical investigation on the population dynamics of graphene system under continuous-wave (cw) laser and chirped pulse excitation. Results of our numerical simulations reveal that complete population transfer from an initially occupied ground state to the initially unoccupied excited states can be achieved by choosing appropriate values of the chirp rate, the laser field intensity and frequency, as well as other system parameters. Also, we observe coherent Rabi-like population oscillations between the initial ground state and the excited final state. It is induced by the combined effect of cw and chirped-pulse laser fields. These results will contribute to the understanding of carrier-carrier and carrier-phonon interactions in graphene system, and may find applications in graphene-based high-speed electronic and optoelectronic devices.
A stand-alone fiber-coupled single-photon source
Authors: Schlehahn Alexander , Fischbach Sarah , Schmidt Ronny , Kaganskiy Arsenty , Strittmatter André , Rodt Sven , Heindel Tobias , Reitzenstein Stephan 
Published: January 2018

AbstractIn this work, we present a stand-alone and fiber-coupled quantum-light source. The plug-and-play device is based on an optically driven quantum dot delivering single photons via an optical fiber. The quantum dot is deterministically integrated in a monolithic microlens which is precisely coupled to the core of an optical fiber via active optical alignment and epoxide adhesive bonding. The rigidly coupled fiber-emitter assembly is integrated in a compact Stirling cryocooler with a base temperature of 35 K. We benchmark our practical quantum device via photon auto-correlation measurements revealing g(2)(0) = 0.07 ± 0.05 under continuous-wave excitation and we demonstrate triggered non-classical light at a repetition rate of 80 MHz. The long-term stability of our quantum light source is evaluated by endurance tests showing that the fiber-coupled quantum dot emission is stable within 4% over several successive cool-down/warm-up cycles. Additionally, we demonstrate non-classical photon emission for a user-intervention-free 100-hour test run and stable single-photon count rates up to 11.7 kHz with a standard deviation of 4%.
Proteomic evidences for microcystin-RR-induced toxicological alterations in mice liver
Authors: Rai Ashutosh Kumar , Chaturvedi Rupesh , Kumar Ashok 
Published: January 2018

AbstractThis study deals with the isolation and purification of an important variant of microcystins namely microcystin-RR (MCYST-RR) fromMicrocystis aeruginosaand reports its effects on mice liver protein profile and cellular functions. Protein profiling by 2-dimensional gel electrophoresis revealed changes in the number and accumulation of protein spots in liver of mice treated with different concentrations of MCYST-RR. Untreated (control) mice liver showed 368 protein spots while the number was 355, 348 and 332 in liver of mice treated with 200, 300 and 400 µg kg body wt−1of MCYST-RR respectively. Altogether 102, 97, and 92 spots were differentially up-accumulated and 93, 91, and 87 spots were down- accumulated respectively with the treatment of 200, 300, 400 µg kg body wt−1. Eighteen differentially accumulated proteins present in all the four conditions were identified by MALDI-TOF MS. Of these eighteen proteins, 12 appeared to be involved in apoptosis/toxicological manifestations. Pathway analysis by Reactome and PANTHER database also mapped the identified proteins to programmed cell death/apoptosis clade. That MCYST-RR induces apoptosis in liver tissues was also confirmed by DNA fragmentation assay. Results of this study elucidate the proteomic basis for the hepatotoxicity of MCYST-RR which is otherwise poorly understood till date.
IL-36/LXR axis modulates cholesterol metabolism and immune defense to Mycobacterium tuberculosis
Authors: Ahsan Fadhil , Maertzdorf Jeroen , Guhlich-Bornhof Ute , Kaufmann Stefan H. E. , Moura-Alves Pedro 
Published: January 2018

AbstractMycobacterium tuberculosis(Mtb) is a life-threatening pathogen in humans. Bacterial infection of macrophages usually triggers strong innate immune mechanisms, including IL-1 cytokine secretion. The newer member of the IL-1 family, IL-36, was recently shown to be involved in cellular defense againstMtb. To unveil the underlying mechanism of IL-36 induced antibacterial activity, we analyzed its role in the regulation of cholesterol metabolism, together with the involvement of Liver X Receptor (LXR) in this process. We report that, inMtb-infected macrophages, IL-36 signaling modulates cholesterol biosynthesis and efflux via LXR. Moreover, IL-36 induces the expression of cholesterol-converting enzymes and the accumulation of LXR ligands, such as oxysterols. Ultimately, both IL-36 and LXR signaling play a role in the regulation of antimicrobial peptides expression and inMtbgrowth restriction. These data provide novel evidence for the importance of IL-36 and cholesterol metabolism mediated by LXR in cellular host defense againstMtb.
Population genetic structure of Diaphorina citri Kuwayama (Hemiptera: Liviidae): host-driven genetic differentiation in China
Authors: Meng Lixue , Wang Yongmo , Wei Wen-Hua , Zhang Hongyu 
Published: January 2018

AbstractThe Asian citrus psyllid Diaphorina citri Kuwayama is a major pest in citrus production, transmitting Candidatus Liberibacter asiaticus. It has spread widely across eastern and southern China. Unfortunately, little is known about the genetic diversity and population structure of D. citri, making pest control difficult. In this study, nine specifically developed SSR markers and three known mitochondrial DNA were used for population genetics study of D. citri using 225 samples collected from all 7 distribution regions in China. Based on the SSR data, D. citri was found highly diverse with a mean observed heterozygosity of 0.50, and three subgroups were structured by host plant: (i) Shatangju, NF mandarin and Ponkan; (ii) Murraya paniculata and Lemon; (iii) Citrus unshiu, Bingtangcheng, Summer orange and Navel. No significant genetic differences were found with mtDNA data. We suggested the host-associated divergence is likely to have occurred very recently. A unimodal distribution of paired differences, the negative and significant Tajima’s D and Fu’s F
S
parameters among mtDNA suggested a recent demographic expansion. The extensive citrus cultivation and increased suitable living habitat was recommended as a key for this expansion event.
Interaction between hippocampal-prefrontal plasticity and thalamic-prefrontal activity
Authors: Bueno-Junior Lezio S. , Peixoto-Santos José E. , Ruggiero Rafael N. , Ávila Milton A. V. , Marques Danilo B. , Lopes-Aguiar Cleiton , Leite João P. 
Published: January 2018

AbstractThe prefrontal cortex integrates a variety of cognition-related inputs, either unidirectional, e.g., from the hippocampal formation, or bidirectional, e.g., with the limbic thalamus. While the former is usually implicated in synaptic plasticity, the latter is better known for regulating ongoing activity. Interactions between these processes via prefrontal neurons are possibly important for linking mnemonic and executive functions. Our work further elucidates such dynamics usingin vivoelectrophysiology in rats. First, we report that electrical pulses into CA1/subiculum trigger late-onset (>400 ms) firing responses in the medial prefrontal cortex, which are increased after induction of long-term potentiation. Then, we show these responses to be attenuated by optogenetic control of the paraventricular/mediodorsal thalamic area. This suggests that recruitment and plasticity of the hippocampal-prefrontal pathway is partially related to the thalamic-prefrontal loop. When dysfunctional, this interaction may contribute to cognitive deficits, psychotic symptoms, and seizure generalization, which should motivate future studies combining behavioural paradigms and long-range circuit assessment.
GGA2 interacts with EGFR cytoplasmic domain to stabilize the receptor expression and promote cell growth
Authors: Uemura Takefumi , Kametaka Satoshi , Waguri Satoshi 
Published: January 2018

AbstractEpidermal growth factor receptor (EGFR) signaling and its downregulation upon ligand binding have been extensively documented. However, the mechanisms by which cells maintain steady-state EGFR expression remain poorly understood. Here, we report a novel role of Golgi-localized, γ-adaptin ear-containing, ADP ribosylation factor-binding protein 2 (GGA2) in the control of EGFR turnover. Whereas GGA1- or GGA3-depletion increased EGFR expression, GGA2-depletion by RNAi greatly reduced steady-state expression of EGFR, reflecting enhanced lysosomal degradation of EGFR. Subsequent pull-down assays showed interactions of VHS-GAT domains from three GGAs with the cytoplasmic juxtamembrane region (jxt) of EGFR, which was dependent on N108 in the VHS domain. Proximity ligation assay also revealed the steady-state interaction between GGA2 and EGFR in situ. Moreover, reduced expression of EGFR in GGA2-depleted cells was reversed by additional depletion of GGA1 or GGA3, suggesting that GGA1 and GGA3 promote EGFR degradation. In addition, GGA2-depleted cells had reduced EGF signaling and cell proliferation in cell culture and xenograft experiments. Finally, GGA2 was upregulated in 30.8% of human hepatocellular carcinomas and 23.3% of colorectal cancers. Together, these results indicate that GGA2 supports cell growth by interacting with EGFR for sustaining the receptor expression.
Distinct domain switching in Nd0.05Ce0.95CoIn5 at low and high fields
Authors: Mazzone D. G. , Yadav R. , Bartkowiak M. , Gavilano J. L. , Raymond S. , Ressouche E. , Lapertot G. , Kenzelmann M. 
Published: January 2018

AbstractNd0.05Ce0.95CoIn5 features a magnetic field-driven quantum phase transition that separates two antiferromagnetic phases with an identical magnetic structure inside the superconducting condensate. Using neutron diffraction we demonstrate that the population of the two magnetic domains in the two phases is affected differently by the rotation of the magnetic field in the tetragonal basal plane. In the low-field SDW-phase the domain population is only weakly affected while in the high-field Q-phase they undergo a sharp switch for fields around the a-axis. Our results provide evidence that the anisotropic spin susceptibility in both phases arises ultimately from spin-orbit interactions but are qualitatively different in the two phases. This provides evidence that the electronic structure is changed at the quantum phase transition, which yields a modified coupling between magnetism and superconductivity in the Q-phase.
Unanticipated functional diversity among the TatA-type components of the Tat protein translocase
Authors: Eimer Ekaterina , Kao Wei-Chun , Fröbel Julia , Blümmel Anne-Sophie , Hunte Carola , Müller Matthias 
Published: January 2018

AbstractTwin-arginine translocation (Tat) systems transport folded proteins that harbor a conserved arginine pair in their signal peptides. They assemble from hexahelical TatC-type and single-spanning TatA-type proteins. Many Tat systems comprise two functionally diverse, TatA-type proteins, denominated TatA and TatB. Some bacteria in addition express TatE, which thus far has been characterized as a functional surrogate of TatA. For the Tat system of Escherichia coli we demonstrate here that different from TatA but rather like TatB, TatE contacts a Tat signal peptide independently of the proton-motive force and restricts the premature processing of a Tat signal peptide. Furthermore, TatE embarks at the transmembrane helix five of TatC where it becomes so closely spaced to TatB that both proteins can be covalently linked by a zero-space cross-linker. Our results suggest that in addition to TatB and TatC, TatE is a further component of the Tat substrate receptor complex. Consistent with TatE being an autonomous TatAB-type protein, a bioinformatics analysis revealed a relatively broad distribution of the tatE gene in bacterial phyla and highlighted unique protein sequence features of TatE orthologs.
Defining the Akt1 interactome and its role in regulating the cell cycle
Authors: Duggal Shweta , Jailkhani Noor , Midha Mukul Kumar , Agrawal Namita , Rao Kanury V. S. , Kumar Ajay 
Published: January 2018

AbstractCell growth and proliferation are two diverse processes yet always linked. Akt1, a serine/threonine kinase, is a multi-functional protein implicated in regulation of cell growth, survival and proliferation. Though it has a role in G1/S progression, the manner by which Akt1 controls cell cycle and blends cell growth with proliferation is not well explored. In this study, we characterize the Akt1 interactome as the cell cycle progresses from G0 to G1/S and G2 phase. For this, Akt1-overexpressing HEK293 cells were subjected to AP-MS. To distinguish between individual cell cycle stages, cells were cultured in the light, medium and heavy labelled SILAC media. We obtained 213 interacting partners of Akt1 from these studies. GO classification revealed that a significant number of proteins fall into functional classes related to cell growth or cell cycle processes. Of these, 32 proteins showed varying association with Akt1 in different cell cycle stages. Further analyses uncovered a subset of proteins showing counteracting effects so as to tune stage-specific progression through the cycle. Thus, our study provides some novel perspectives on Akt1-mediated regulation of the cell cycle and offers the framework for a detailed resolution of the downstream cellular mechanisms that are mediated by this kinase.
Validation and Comparison of a Model of the Effect of Sea-Level Rise on Coastal Wetlands
Authors: Mogensen Laura A. , Rogers Kerrylee 
Published: January 2018

AbstractModels are used to project coastal wetland distribution under future sea-level rise scenarios to assist decision-making. Model validation and comparison was used to investigate error and uncertainty in the Sea Level Affecting Marshes Model, a readily available model with minimal validation, particularly for wetlands beyond North America. Accurate parameterisation is required to improve the performance of the model, and indeed any spatial model. Consideration of tidal attenuation further enhances model performance, particularly for coastal wetlands located within estuaries along wave-dominated coastlines. The model does not simulate vegetation changes that are known to occur, particularly when sedimentation exceeds rates of sea-level rise resulting in shoreline progradation. Model performance was reasonable over decadal timescales, decreasing as the time-scale of retrospection increased due to compounding of errors. Comparison with other deterministic models showed reasonable agreement by 2100. However, given the uncertainty of the future and the unpredictable nature of coastal wetlands, it is difficult to ascertain which model could be realistic enough to meet its intended purpose. Model validation and comparison are useful for assessing model efficacy and parameterisation, and should be applied before application of any spatially explicit model of coastal wetland response to sea-level rise.
Understanding the effect of wet etching on damage resistance of surface scratches
Authors: Da Costa Fernandes Benoit , Pfiffer Mathilde , Cormont Philippe , Dussauze Marc , Bousquet Bruno , Fargin Evelyne , Neauport Jerome 
Published: January 2018

AbstractFused silica optics often exhibit surface scratches after polishing that radically reduce their damage resistance at the wavelength of 351 nm in the nanosecond regime. Consequently, chemical treatments after polishing are often used to increase the damage threshold and ensure a safe operation of these optics in large fusion-scale laser facilities. Here, we investigate the reasons for such an improvement. We study the effect of an HF-based wet etching on scratch morphology and propose a simple analytic model to reflect scratch widening during etching. We also use a finite element model to evaluate the effect of the morphological modification induced by etching on the electric field distribution in the vicinity of the scratch. We evidence that this improvement of the scratch damage resistance is due to a reduction of the electric field enhancement. This conclusion is supported by secondary electron microscopy (SEM) imaging of damage sites initiated on scratches after chemical treatment.