4,158 research outputs found
Structural and electronic transformation in low-angle twisted bilayer graphene
Experiments on bilayer graphene unveiled a fascinating realization of
stacking disorder where triangular domains with well-defined Bernal stacking
are delimited by a hexagonal network of strain solitons. Here we show by means
of numerical simulations that this is a consequence of a structural
transformation of the moir\'{e} pattern inherent of twisted bilayer graphene
taking place at twist angles below a crossover angle
. The transformation is governed by the interplay
between the interlayer van der Waals interaction and the in-plane strain field,
and is revealed by a change in the functional form of the twist energy density.
This transformation unveils an electronic regime characteristic of vanishing
twist angles in which the charge density converges, though not uniformly, to
that of ideal bilayer graphene with Bernal stacking. On the other hand, the
stacking domain boundaries form a distinct charge density pattern that provides
the STM signature of the hexagonal solitonic network.Comment: published version with supplementary materia
Topological Aspects of Charge-Carrier Transmission across Grain Boundaries in Graphene
We systematically investigate the transmission of charge carriers across the
grain-boundary defects in polycrystalline graphene by means of the
Landauer-B\"uttiker formalism within the tight-binding approximation.
Calculations reveal a strong suppression of transmission at low energies upon
decreasing the density of dislocations with the smallest Burger's vector
. The observed transport anomaly is explained from the point
of view of back-scattering due to localized states of topological origin. These
states are related to the gauge field associated with all dislocations
characterized by with ().
Our work identifies an important source of charge-carrier scattering caused by
topological defects present in large-area graphene samples produced by chemical
vapor deposition.Comment: 5 pages, 4 figure
Density distribution of particles upon jamming after an avalanche in a 2D silo
We present a complete analysis of the density distribution of particles in a
two dimensional silo after discharge. Simulations through a pseudo-dynamic
algorithm are performed for filling and subsequent discharge of a plane silo.
Particles are monosized hard disks deposited in the container and subjected to
a tapping process for compaction. Then, a hole of a given size is open at the
bottom of the silo and the discharge is triggered. After a clogging at the
opening is produced, and equilibrium is restored, the final distribution of the
remaining particles at the silo is analyzed by dividing the space into cells
with different geometrical arrangements to visualize the way in which the
density depression near the opening is propagated throughout the system. The
different behavior as a function of the compaction degree is discussed.Comment: 11 pages, 10 figure
Electronic transport within a quasi two-dimensional model for rubrene single-crystal field effect transistors
Spectral and transport properties of the quasi two-dimensional adiabatic
Su-Schrieffer-Heeger model are studied adjusting the parameters in order to
model rubrene single-crystal field effect transistors with small but finite
density of injected charge carriers. We show that, with increasing temperature
, the chemical potential moves into the tail of the density of states
corresponding to localized states, but this is not enough to drive the system
into an insulating state. The mobility along different crystallographic
directions is calculated including vertex corrections which give rise to a
transport lifetime one order of magnitude smaller than spectral lifetime of the
states involved in the transport mechanism. With increasing temperature, the
transport properties reach the Ioffe-Regel limit which is ascribed to less and
less appreciable contribution of itinerant states to the conduction process.
The model provides features of the mobility in close agreement with
experiments: right order of magnitude, scaling as a power law ,
with close or larger than two, and correct anisotropy ratio between
different in-plane directions. Due to a realistic high dimensional model, the
results are not biased by uncontrolled approximations.Comment: 10 pages, 9 figures, Submitte
Letter to the Editor: "COVID-19 and the endocrine system: exploring the unexplored". Focus on acromegaly
Disorder engineering and conductivity dome in ReS2 with electrolyte gating
Atomically thin rhenium disulphide (ReS2) is a member of the transition metal
dichalcogenide (TMDC) family of materials characterized by weak interlayer
coupling and a distorted 1T structure. Here, we report on the electrical
transport study of mono- and multilayer ReS2 with polymer electrolyte gating.
We find that the conductivity of monolayer ReS2 is completely suppressed at
high carrier densities, an unusual feature unique to monolayers, making ReS2
the first example of such a material. While thicker flakes of ReS2 also exhibit
a conductivity dome and an insulator-metal-insulator sequence, they do not show
a complete conductivity suppression at high doping densities. Using dual-gated
devices, we can distinguish the gate-induced doping from the electrostatic
disorder induced by the polymer electrolyte itself. Theoretical calculations
and a transport model indicate that the observed conductivity suppression can
be explained by a combination of a narrow conduction band and Anderson
localization due to electrolyte-induced disorder.Comment: Submitted versio
Apoptotic cell death in canine hair follicle
Apoptotic cell death is an essential homeostatic mechanism involved in the control of cellular turnover in a variety of adult tissues. Cytoplasmic and nuclear condensation morphologically define this process whose biochemical hallmark is extensive DNA fragmentation into discrete oligonucleosomic units. Hair follicle growth and regression has been shown to be correlated with apoptosis in humans, mice, rats and guinea pigs. The present study was carried out to evaluate its implication in canine hair biology in order to define the spatio-temporal relationship between apoptosis and the hair cycle in dogs. As assessed by terminal deoxy-nucleotidyl transferase-mediated d-UTP nick-end-labelling (TUNEL) and by basic histological and ultrastructural assays, apoptotic cells appeared both in the growing and in the regressing follicle epithelium showing the well characterized morphological features described in the previous relevant literature
Comparative expression profiling of wild type Drosophila Malpighian tubules and von Hippel-Lindau haploinsufficient mutant
The von-Hippel Lindau (VHL) disease is a hereditary genetic disorder that predisposes to the onset of several highly vascularized benign and malignant tumors, developing with elevate frequency in the central nervous system and kidneys. The most-aggressive VHL tumor is ccRCC, the clear-cell renal cell carcinoma, affecting the kidney. VHL disease etiology can be attributed to the inheritance of a VHL loss-of-function allele, typically a deletion (Gnarra et al., 1994; Herman et al., 1994); this facilitates the somatic inactivation of the other allele (through amorphic mutations or gene silencing through promoter methylation), leading to the onset of the tumorous phenotype (Latif et al., 1993). This reveals the haploinsufficient behavior of the VHL gene.
The high vascularization of VHL tumors can be explained considering that human VHL protein is the substrate-binding subunit of an E3 ubiquitin ligase (Lonergan et al., 1998; Iwai et al., 1999; Kamura et al., 1999) involved in the poly-ubiquitination of HIF-1α transcription factor. This post-translational modification leads HIF-1α to proteosomal degradation (Maxwell et al., 1999). Loss of VHL function causes the stabilization of HIF-1α, triggering cellular response and adaptation to hypoxic conditions (expression of genes involved in glycolysis, angiogenesis and erythropoiesis) (Bader and Hsu, 2012). While this represents the canonical function of VHL, other HIF-1α-independent function of VHL have been identified, thanks to the contribution of model organisms (Hsu, 2012). Indeed, VHL gene function is conserved and also Drosophila has a VHL homolog, the dVHL gene (Adryan et al., 2000; Aso et al., 2000). dVHL is involved in the development of Drosophila vascular system (Adryan et al., 2000; Hsouna et al., 2010) and in morphogenesis of follicular epithelium of the egg chamber (Duchi et al., 2010). Interestingly, some VHL functions are mediated by Awd, an endocytic mediator whose human orthologs are NME1/2 metastasis suppressors (Rosengard et al., 1989). Awd is broadly required during Drosophila development since it is involved in epithelial morphogenesis (Nallamothu et al., 2008; Woolworth et al., 2009; Ignesti et al., 2014) and required for maintaining genomic stability (Romani et al., 2017). Moreover, Awd is also present into the extracellular fluids of Drosophila larvae (Romani et al., 2016, 2018).
In Drosophila, two pairs of monolayered epithelial Malpighian tubules, each composed of 100-150 cells, absolve to osmoregulation and excretion functions (Denholm and Skaer, 2009). Transcriptomic analysis of Malpighian tubules revealed that among genes that are here enriched there are homologs of human genes implicated into renal pathologies (Wang et al., 2004). This justifies the use of Drosophila Malpighian tubules as model system to gain insights into pathophysiology of human kidneys (Dow and Romero, 2010; Miller et al., 2013).
The dVHL1.1 allele is a loss of function mutation of the dVHL locus (Duchi et al., 2010; Hsouna et al., 2010). dVHL1.1/+ flies mimic the genetic condition of VHL patients. We carried out a genome-wide gene expression profiling of whole Malpighian tubules dissected from Drosophila females both heterozygous for the dVHL1.1 mutation and with two wild type copies of the dVHL gene. The comparison of differentially expressed genes in the two genetic backgrounds potentially allows to identify genes that are sensible to dVHL functional copy number. Quality control assessments of the data were performed and results obtained from the differential expression analysis were confirmed by qRT-PCR. With this approach we aimed to provide a well-controlled dataset for a better understanding of the VHL disease. Indeed, even if further molecular and functional characterization are needed, human homologs of the differentially expressed genes, if existing, could have a role in the somatic inactivation of the wild type copy of VHL and/or into the very first phase of cancer onset
Vps28 is involved in the intracellular trafficking of AWD, the Drosophila homolog of NMe1/2
The Awd (abnormal wing discs) gene is the Drosophila homolog of human NME1 and NME2 metastasis suppressor genes. These genes play a key role in tumor progression. Extensive studies revealed that intracellular NME1/2 protein levels could be related to either favorable or poor prognosis depending on tissue context. More recently, extracellular activities of NME1/2 proteins have also been reported, including a tumor- promoting function. We used Drosophila as a genetic model to investigate the mechanism controlling intra- and extracellular levels of NME1/2. We examined the role of several components of the ESCRT (endosomal sorting complex required for transport) complex in controlling Awd trafficking. We show that the Vps28 component of the ESCRT 12I complex is required for maintenance of normal intracellular level of Awd in larval adipocytes. We already showed that blocking of Shibire (Shi)/Dynamin function strongly- lowers Awd intracellular level. To further investigate this down regulative effect, we analyzed the distribution of endosomal markers in wild type and Shi-defective adipocytes. Our results suggest that Awd does not enter CD63-positive endosomes. Interestingly, we found that in fat body cells, Awd partly- colocalizes with the ESCRT accessory component ALiX, the ALG-2 (apoptosis-linked gene 2)-interacting protein X. Moreover, we show that the intracellular levels of both proteins are downregulated by blocking the function of the Dynamin encoded by the shibire gene
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