bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diagonal nematicity in the pseudogap phase of HgBa2CuO4+δ
Authors: Murayama H. , Sato Y. , Kurihara R. , Kasahara S. , Mizukami Y. , Kasahara Y. , Uchiyama H. , Yamamoto A. , Moon E.-G. , Cai J. , Freyermuth J. , Greven M. , Shibauchi T. , Matsuda Y. 
Published: July 2019

AbstractThe pseudogap phenomenon in the cuprates is arguably the most mysterious puzzle in the field of high-temperature superconductivity. The tetragonal cuprate HgBa2CuO4+δ, with only one CuO2 layer per primitive cell, is an ideal system to tackle this puzzle. Here, we measure the magnetic susceptibility anisotropy within the CuO2 plane with exceptionally high-precision magnetic torque experiments. Our key finding is that a distinct two-fold in-plane anisotropy sets in below the pseudogap temperature T*, which provides thermodynamic evidence for a nematic phase transition with broken four-fold symmetry. Surprisingly, the nematic director orients along the diagonal direction of the CuO2 square lattice, in sharp contrast to the bond nematicity along the Cu-O-Cu direction. Another remarkable feature is that the enhancement of the diagonal nematicity with decreasing temperature is suppressed around the temperature at which short-range charge-density-wave formation occurs. Our result suggests a competing relationship between diagonal nematic and charge-density-wave order in HgBa2CuO4+δ.
RIF1 promotes replication fork protection and efficient restart to maintain genome stability
Authors: Mukherjee Chirantani , Tripathi Vivek , Manolika Eleni Maria , Heijink Anne Margriet , Ricci Giulia , Merzouk Sarra , de Boer H. Rudolf , Demmers Jeroen , van Vugt Marcel A. T. M. , Ray Chaudhuri Arnab 
Published: July 2019

AbstractHomologous recombination (HR) and Fanconi Anemia (FA) pathway proteins in addition to their DNA repair functions, limit nuclease-mediated processing of stalled replication forks. However, the mechanism by which replication fork degradation results in genome instability is poorly understood. Here, we identify RIF1, a non-homologous end joining (NHEJ) factor, to be enriched at stalled replication forks. Rif1 knockout cells are proficient for recombination, but displayed degradation of reversed forks, which depends on DNA2 nuclease activity. Notably, RIF1-mediated protection of replication forks is independent of its function in NHEJ, but depends on its interaction with Protein Phosphatase 1. RIF1 deficiency delays fork restart and results in exposure of under-replicated DNA, which is the precursor of subsequent genomic instability. Our data implicate RIF1 to be an essential factor for replication fork protection, and uncover the mechanisms by which unprotected DNA replication forks can lead to genome instability in recombination-proficient conditions.
Nanoscale mapping of quasiparticle band alignment
Authors: Ulstrup Søren , Giusca Cristina E. , Miwa Jill A. , Sanders Charlotte E. , Browning Alex , Dudin Pavel , Cacho Cephise , Kazakova Olga , Gaskill D. Kurt , Myers-Ward Rachael L. , Zhang Tianyi , Terrones Mauricio , Hofmann Philip 
Published: July 2019

AbstractControl of atomic-scale interfaces between materials with distinct electronic structures is crucial for the design and fabrication of most electronic devices. In the case of two-dimensional materials, disparate electronic structures can be realized even within a single uniform sheet, merely by locally applying different vertical gate voltages. Here, we utilize the inherently nano-structured single layer and bilayer graphene on silicon carbide to investigate lateral electronic structure variations in an adjacent single layer of tungsten disulfide (WS2). The electronic band alignments are mapped in energy and momentum space using angle-resolved photoemission with a spatial resolution on the order of 500 nm (nanoARPES). We find that the WS2 band offsets track the work function of the underlying single layer and bilayer graphene, and we relate such changes to observed lateral patterns of exciton and trion luminescence from WS2.
Trace-free counterfactual communication with a nanophotonic processor
Authors: Alonso Calafell I. , Strömberg T. , Arvidsson-Shukur D. R. M. , Rozema L. A. , Saggio V. , Greganti C. , Harris N. C. , Prabhu M. , Carolan J. , Hochberg M. , Baehr-Jones T. , Englund D. , Barnes C. H. W. , Walther P. 
Published: July 2019

AbstractIn standard communication information is carried by particles or waves. Counterintuitively, in counterfactual communication particles and information can travel in opposite directions. The quantum Zeno effect allows Bob to transmit a message to Alice by encoding information in particles he never interacts with. A first remarkable protocol for counterfactual communication relied on thousands of ideal optical operations for high success rate performance. Experimental realizations of that protocol have thus employed post-selection to demonstrate counterfactuality. This post-selection, together with arguments concerning a so-called “weak trace” of the particles traveling from Bob to Alice, have led to a discussion regarding the counterfactual nature of the protocol. Here we circumvent these controversies, implementing a new, and fundamentally different, protocol in a programmable nanophotonic processor, based on reconfigurable silicon-on-insulator waveguides that operate at telecom wavelengths. This, together with our telecom single-photon source and highly efficient superconducting nanowire single-photon detectors, provides a versatile and stable platform for a high-fidelity implementation of counterfactual communication with single photons, allowing us to actively tune the number of steps in the Zeno measurement, and achieve a bit error probability below 1%, without post-selection and with a vanishing weak trace. Our demonstration shows how our programmable nanophotonic processor could be applied to more complex counterfactual tasks and quantum information protocols.
Comprehensive review on virtual reality for the treatment of violence: implications for youth with schizophrenia
Authors: Dellazizzo Laura , Potvin Stéphane , Bahig Sami , Dumais Alexandre 
Published: July 2019

AbstractYouth violence is a complex and multifactorial issue that has severe health and social consequences. While treatment options exist to treat/reduce violence in at-risk populations such as schizophrenia, there remains limitations in the efficacy of current interventions. Virtual reality (VR) appears to be a unique possibility to expose offenders and to train coping skills in virtual situations that are capable of eliciting aggression‐relevant behavior without threatening others. The focus of this paper is to provide a comprehensive review of studies using VR to manage violence across several at-risk populations, with a particular emphasis on youth with schizophrenia. Despite the encouraging success of VR applications for the treatment of different mental health problems, no studies have explored the usability of VR to specifically treat violence in patients with schizophrenia. A limited number of studies have focused on violence risk factors in other mental health problems (i.e., emotion regulation in individual suffering from post-traumatic disorders) that may be targeted in treatments to reduce the risk of violence. The preliminary studies using VR as a therapeutic element have shown reductions in anger, improvements in conflict-resolution skills as well as in empathy levels, and decreases in aggression. Possible applications of these interventions in youth with schizophrenia will be discussed.
Honeybee pupal length assessed by CT-scan technique: effects of Varroa infestation, developmental stage and spatial position within the brood comb
Authors: Facchini Elena , Nalon Laura , Andreis Maria Elena , Di Giancamillo Mauro , Rizzi Rita , Mortarino Michele 
Published: July 2019

AbstractHoneybee pupae morphology can be affected by a number of stressor, but in vivo investigation is difficult. A computed tomography (CT) technique was applied to visualize a comb’s inner structure without damaging the brood. The CT scan was performed on a brood comb containing pupae developed from eggs laid by the queen during a time window of 48 hours. From the CT images, the position of each pupa was determined by recording coordinates to a common reference point. Afterwards, every brood cell was inspected in order to assess the developmental stage of the pupa, the presence of Varroa destructor, the number and progeny of foundress mites. Using data on 651 pupae, the relationships between varroa infestation status, developmental stage and spatial position of the pupa within the brood comb, and its length were investigated. Pupae at 8 post-capping days were shorter than pupae at 7 post-capping days. Pupae in infected cells were significantly shorter than those in varroa-free cells and this effect was linked both to mite number and stage and to the position in the comb. Overall, the results suggest that the CT-scan may represent a suitable non-invasive tool to investigate the morphology and developing status of honeybee brood.
Coupled feedback regulation of nuclear factor of activated T-cells (NFAT) modulates activation-induced cell death of T cells
Authors: Shin Sung-Young , Kim Min-Wook , Cho Kwang-Hyun , Nguyen Lan K. 
Published: July 2019

AbstractA properly functioning immune system is vital for an organism’s wellbeing. Immune tolerance is a critical feature of the immune system that allows immune cells to mount effective responses against exogenous pathogens such as viruses and bacteria, while preventing attack to self-tissues. Activation-induced cell death (AICD) in T lymphocytes, in which repeated stimulations of the T-cell receptor (TCR) lead to activation and then apoptosis of T cells, is a major mechanism for T cell homeostasis and helps maintain peripheral immune tolerance. Defects in AICD can lead to development of autoimmune diseases. Despite its importance, the regulatory mechanisms that underlie AICD remain poorly understood, particularly at an integrative network level. Here, we develop a dynamic multi-pathway model of the integrated TCR signalling network and perform model-based analysis to characterize the network-level properties of AICD. Model simulation and analysis show that amplified activation of the transcriptional factor NFAT in response to repeated TCR stimulations, a phenomenon central to AICD, is tightly modulated by a coupled positive-negative feedback mechanism. NFAT amplification is predominantly enabled by a positive feedback self-regulated by NFAT, while opposed by a NFAT-induced negative feedback via Carabin. Furthermore, model analysis predicts an optimal therapeutic window for drugs that help minimize proliferation while maximize AICD of T cells. Overall, our study provides a comprehensive mathematical model of TCR signalling and model-based analysis offers new network-level insights into the regulation of activation-induced cell death in T cells.
The effects of valve leaflet mechanics on lymphatic pumping assessed using numerical simulations
Authors: Li Huabing , Mei Yumeng , Maimon Nir , Padera Timothy P. , Baish James W. , Munn Lance L. 
Published: July 2019

AbstractThe lymphatic system contains intraluminal leaflet valves that function to bias lymph flow back towards the heart. These valves are present in the collecting lymphatic vessels, which generally have lymphatic muscle cells and can spontaneously pump fluid. Recent studies have shown that the valves are open at rest, can allow some backflow, and are a source of nitric oxide (NO). To investigate how these valves function as a mechanical valve and source of vasoactive species to optimize throughput, we developed a mathematical model that explicitly includes Ca2+ -modulated contractions, NO production and valve structures. The 2D lattice Boltzmann model includes an initial lymphatic vessel and a collecting lymphangion embedded in a porous tissue. The lymphangion segment has mechanically-active vessel walls and is flanked by deformable valves. Vessel wall motion is passively affected by fluid pressure, while active contractions are driven by intracellular Ca2+ fluxes. The model reproduces NO and Ca2+ dynamics, valve motion and fluid drainage from tissue. We find that valve structural properties have dramatic effects on performance, and that valves with a stiffer base and flexible tips produce more stable cycling. In agreement with experimental observations, the valves are a major source of NO. Once initiated, the contractions are spontaneous and self-sustained, and the system exhibits interesting non-linear dynamics. For example, increased fluid pressure in the tissue or decreased lymph pressure at the outlet of the system produces high shear stress and high levels of NO, which inhibits contractions. On the other hand, a high outlet pressure opposes the flow, increasing the luminal pressure and the radius of the vessel, which results in strong contractions in response to mechanical stretch of the wall. We also find that the location of contraction initiation is affected by the extent of backflow through the valves.
A critical role of autophagy in regulating the mesenchymal transition of ductular cells in liver cirrhosis
Authors: Hung Tzu-Min , Huang Yu-Jen , Lin Yu-Chun , Chen Yu-Hsuan , Wu Yao-Ming , Lee Po-Huang 
Published: July 2019

AbstractOur previous studies have shown that autophagy mediates the link between ductular reaction (DR) and liver cirrhosis. Whether the subsequent fibrogenic response is regulated by increased autophagy in DR remains unclear. Here, using both human liver specimens and a rat model of liver cirrhosis induced by 2-acetylaminofluorene (AAF) and carbon tetrachloride (CCL4), we explored the involvement of autophagy in regulating mesenchymal transition of ductular cells. Ductular cells from AAF/CCL4 livers exhibited increased autophagy compared to those of normal livers. These cells showed morphological and functional characteristics of mesenchymal cells. Blocking autophagy using bafilomycin A1 or siRNA targeting ATG7 reduced the expression of mesenchymal markers in these ductular cells from AAF/CCL4 livers, indicating a role for autophagy in regulating the mesenchymal phenotype of ductular cells. Furthermore, we show that the mesenchymal transition in DR requires the activation of transforming growth factor-β (TGF-β) signaling in an autophagy-dependent manner. Importantly, in cirrhotic human livers, ductular cells that are positive for LC3B also showed increased expression of TGF-β and fibroblast-specific protein-1. Our data suggest activation of autophagy in ductular cells, and also demonstrate that it is required for the mesenchymal transition during the DR, processes that are critically involved in the pathogenesis of cirrhosis.
Energy-flux control of the steady-state, creep, and dynamic slip modes of faults
Authors: Reches Ze’ev , Zu Ximeng , Carpenter Brett M. 
Published: July 2019

AbstractFaults exhibit a gamut of slip styles from stable sliding and creep events to earthquakes. These slip styles are affected by the fault properties, e.g., weakening or strengthening, and the properties of the loading system. Here, we investigate the poorly understood effect of energy-flux to the fault that should equal or exceed the energy-dissipation-rate along the slipping fault. We explore the relationship between energy-flux and slip style in shear experiments along granite and diorite laboratory faults, during which the faults were subjected to controlled energy-flux, and responded spontaneously to it. The monitored evolution of slip-velocity, shear stress, and slip-distance revealed three slip styles that depend on the applied energy-flux: (1) steady-state slip; (2) spontaneous creep events of small displacement with negligible weakening; and (3) spontaneous, unstable events with slip-velocities up to 0.8 m/s, slip-distances up to 0.5 m, and stress-drops up to 1 MPa, which are comparable to observed values of moderate earthquakes. These slip styles are similar in character to those observed along natural faults. We further propose that the rate of energy flow from crustal blocks can control the slip velocity during earthquakes.
Manufacturing and preclinical validation of CAR T cells targeting ICAM-1 for advanced thyroid cancer therapy
Authors: Vedvyas Yogindra , McCloskey Jaclyn E. , Yang Yanping , Min Irene M. , Fahey Thomas J. , Zarnegar Rasa , Hsu Yen-Michael S. , Hsu Jing-Mei , Van Besien Koen , Gaudet Ian , Law Ping , Kim Nak Joon , Hofe Eric von , Jin Moonsoo M. 
Published: July 2019

AbstractWhile the majority of thyroid cancer patients are easily treatable, those with anaplastic or poorly differentiated recurrent thyroid carcinomas have a very poor prognosis with a median survival of less than a year. Previously, we have shown a significant correlation between ICAM-1 overexpression and malignancy in thyroid cancer, and have pioneered the use of ICAM-1 targeted CAR T cells as a novel treatment modality. For clinical translation of this novel modality, we designed CAR T cells possessing micromolar rather than nanomolar affinity to ICAM-1 to avoid cytotoxicity in normal cells with basal levels of ICAM-1 expression. Herein, we report the automated process of CAR T cell manufacturing with CliniMACS Prodigy (Miltenyi Biotec) using cryopreserved peripheral blood leukocytes from apheresis collections. Using Prodigy, thawed leukopak cells were enriched for CD4+and CD8+T cells, subjected to double transduction using lentiviral vector, and expanded in culture for a total of 10 days with a final yield of 2–4 × 109cells. The resulting CAR T cells were formulated for cryopreservation to be used directly for infusion into patients after thawing with no further processing. We examined cross-reactivity of CAR T cells toward both human and murine ICAM-1 and ICAM-1 expression in human and mouse tissues to demonstrate that both efficacy and on-target, off-tumor toxicity can be studied in our preclinical model. Selective anti-tumor activity in the absence of toxicity provides proof-of-concept that micromolar affinity tuned CAR T cells can be used to target tumors expressing high levels of antigen while avoiding normal tissues expressing basal levels of the same antigen. These studies support the initiation of a phase I study to evaluate the safety and potential efficacy of micromolar affinity tuned CAR T cells against newly diagnosed anaplastic and refractory or recurrent thyroid cancers.
MTP18 is a Novel Regulator of Mitochondrial Fission in CNS Neuron Development, Axonal Growth, and Injury Responses
Authors: Kreymerman Alexander , Buickians David N. , Nahmou Michael M. , Tran Tammy , Galvao Joana , Wang Yan , Sun Nicholas , Bazik Leah , Huynh Star K. , Cho In-Jae , Boczek Tomasz , Chang Kun-Che , Kunzevitzky Noelia J. , Goldberg Jeffrey L. 
Published: July 2019

AbstractThe process of mitochondrial fission-fusion has been implicated in diverse neuronal roles including neuronal survival, axon degeneration, and axon regeneration. However, whether increased fission or fusion is beneficial for neuronal health and/or axonal growth is not entirely clear, and is likely situational and cell type-dependent. In searching for mitochondrial fission-fusion regulating proteins for improving axonal growth within the visual system, we uncover that mitochondrial fission process 1,18 kDa (MTP18/MTFP1), a pro-fission protein within the CNS, is critical to maintaining mitochondrial size and volume under normal and injury conditions, in retinal ganglion cells (RGCs). We demonstrate that MTP18’s expression is regulated by transcription factors involved in axonal growth, Kruppel-like factor (KLF) transcription factors-7 and -9, and that knockdown of MTP18 promotes axon growth. This investigation exposes MTP18’s previously unexplored role in regulating mitochondrial fission, implicates MTP18 as a downstream component of axon regenerative signaling, and ultimately lays the groundwork for investigations on the therapeutic efficacy of MTP18 expression suppression during CNS axon degenerative events.
Achieving excellent microformability in aluminum by engineering a unique ultrafine-grained microstructure
Authors: Dhal A. , Panigrahi S. K. , Shunmugam M. S. 
Published: July 2019

AbstractDuring microforming of conventional materials, specimen and microstructural length-scales are close to each other. This leads to an abnormal deformation behavior of the material and reduces microformability. Engineering ultrafine-grained (UFG) microstructure in the material is a possible solution. However, micro-scale deformation behavior of UFG material is not fully understood. Present work attempts to comprehensively investigate the micro-scale deformation of four distinctly engineered microstructures: UFG with residual dislocations and elongated grains, UFG free of residual dislocation with equiaxed grains, bimodal-grained and coarse-grained. The deformation behavior is captured via micro-scale uniaxial tensile test and micro-deep drawing operation. Micro-cups generated from UFG material with equiaxed grains show excellent surface quality, form-accuracy and minimal process scatter. Postmortem microscopy of the formed micro-cups attributes this improved microformability to the activation of grain boundary-mediated plasticity in the material which results in synergetic grain migration and rotation. Presence of residual dislocations and elongated grains hinders the grain migration and rotation leading to strain localization and thinning. In case of bimodal and coarse-grained material, cross-slip based deformation mode progressively dominates over grain migration and rotation, which results in a reduction in microformability due to the influence of size-effect.
A collagen-based microwell migration assay to study NK-target cell interactions
Authors: Olofsson Per E. , Brandt Ludwig , Magnusson Klas E. G. , Frisk Thomas , Jaldén Joakim , Önfelt Björn 
Published: July 2019

AbstractNatural killer (NK) cell cytotoxicity in tissue is dependent on the ability of NK cells to migrate through the extracellular matrix (ECM) microenvironment. Traditional imaging studies of NK cell migration and cytotoxicity have utilized 2D surfaces, which do not properly reproduce the structural and mechanical cues that shape the migratory response of NK cells in vivo. Here, we have combined a microwell assay that allows long-term imaging and tracking of small, well-defined populations of NK cells with an interstitial ECM-like matrix. The assay allows for long-term imaging of NK–target cell interactions within a confined 3D volume. We found marked differences in motility between individual cells with a small fraction of the cells moving slowly and being confined to a small volume within the matrix, while other cells moved more freely. A majority of NK cells also exhibited transient variation in their motility, alternating between periods of migration arrest and movement. The assay could be used as a complement to in vivo imaging to study human NK cell heterogeneity in migration and cytotoxicity.