Dynamic correlations in the conserved Manna sandpile

We study dynamic correlations for current and mass, as well as the associated power spectra, in the one-dimensional conserved Manna sandpile. We show that, in the thermodynamic limit, the variance of cumulative bond current up to time $T$ grows subdiffusively as $T^{1/2-\mu}$ with the exponent $\mu \ge 0$ depending on the density regimes considered and, likewise, the power spectra of current and mass at low frequency $f$ varies as $f^{1/2+\mu}$ and $f^{-3/2+\mu}$, respectively; our theory predicts that, far from criticality, $\mu = 0$ and, near criticality, $\mu = (\beta+1)/2 \nu_{\perp} z > 0$ with $\beta$, $\nu_{\perp}$ and $z$ being the order-parameter, correlation-length and dynamic exponents, respectively. The anomalous suppression of fluctuations near criticality signifies a ``dynamic hyperuniformity'', characterized by a set of fluctuation relations, in which current, mass and tagged-particle displacement fluctuations are shown to have a precise quantitative relationship with the density-dependent activity (or, it's derivative). In particular, the relation, ${\mathcal{D}}_s(\bar{\rho}) = a(\bar{\rho}) / \bar{\rho}$, between the self-diffusion coefficient ${\mathcal{D}}_s(\bar{\rho})$, activity $a(\bar{\rho})$ and density $\bar{\rho}$ explains a previous simulation observation [Eur. Phys. J. B \textbf{72}, 441 (2009)] that, near criticality, the self-diffusion coefficient in the Manna sandpile has the same scaling behavior as the activity.Comment: 28 pages, 7 figure

Dynamic fluctuations of current and mass in nonequilibrium mass transport processes

We study steady-state dynamic fluctuations of current and mass, as well as the corresponding power spectra, in conserved-mass transport processes on a ring of $L$ sites; these processes violate detailed balance, have nontrivial spatial structures, and their steady states are not described by the Boltzmann-Gibbs distribution. We exactly calculate, for all times $T$, the fluctuations $\langle \mathcal{Q}_i^2(T) \rangle$ and $\langle \mathcal{Q}_{sub}^2(l, T) \rangle$ of the cumulative currents upto time $T$ across $i$th bond and across a subsystem of size $l$ (summed over bonds in the subsystem), respectively; we also calculate the (two-point) dynamic correlation function for subsystem mass. In particular, we show that, for large $L \gg 1$, the bond-current fluctuation grows linearly for $T \sim {\cal O}(1)$, subdiffusively for $T \ll L^2$ and then again linearly for $T \gg L^2$. The scaled subsystem current fluctuation $\lim_{l \rightarrow \infty, T \rightarrow \infty} \langle \mathcal{Q}^2_{sub}(l, T) \rangle/2lT$ converges to the density-dependent particle mobility $\chi$ when the large subsystem size limit is taken first, followed by the large time limit. Remarkably, the scaled current fluctuation $D \langle \mathcal{Q}_i^2(T)\rangle/2 \chi L \equiv {\cal W}(y)$ as a function of scaled time $y=DT/L^2$ is expressed in terms of a universal scaling function ${\cal W}(y)$, where $D$ is the bulk-diffusion coefficient. Similarly, the power spectra for current and mass time series are characterized by the respective universal scaling functions, which are calculated exactly. We provide a microscopic derivation of equilibrium-like Green-Kubo and Einstein relations, that connect the steady-state current fluctuations to the response to an external force and to mass fluctuation, respectively.Comment: 24 pages, 13 figures, submitted for review in PR

A Self-organising Model of Market with Single Commodity

We have studied here the self-organising features of the dynamics of a model market, where the agents `trade' for a single commodity with their money. The model market consists of fixed numbers of economic agents, money supply and commodity. We demonstrate that the model, apart from showing a self-organising behaviour, indicates a crucial role for the money supply in the market and also its self-organising behaviour is seen to be significantly affected when the money supply becomes less than the optimum. We also observed that this optimal money supply level of the market depends on the amount of `frustration' or scarcity in the commodity market.Comment: 8 pages, 3 figures (encapsulated postscript

Microglial activation induces neuronal death in Chandipura virus infection

Neurotropic viruses induce neurodegeneration either directly by activating host death domains or indirectly through host immune response pathways. Chandipura Virus (CHPV) belonging to family Rhabdoviridae is ranked among the emerging pathogens of the Indian subcontinent. Previously we have reported that CHPV induces neurodegeneration albeit the root cause of this degeneration is still an open question. In this study we explored the role of microglia following CHPV infection. Phenotypic analysis of microglia through lectin and Iba-1 staining indicated cells were in an activated state post CHPV infection in cortical region of the infected mouse brain. Cytokine Bead Array (CBA) analysis revealed comparatively higher cytokine and chemokine levels in the same region. Increased level of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), Nitric Oxide (NO) and Reactive Oxygen species (ROS) in CHPV infected mouse brain indicated a strong inflammatory response to CHPV infection. Hence it was hypothesized through our analyses that this inflammatory response may stimulate the neuronal death following CHPV infection. In order to validate our hypothesis supernatant from CHPV infected microglial culture was used to infect neuronal cell line and primary neurons. This study confirmed the bystander killing of neurons due to activation of microglia post CHPV infection

Crinipellis cupreostipes (Marasmiaceae, Agaricales, Basidiomycota): a new distributional record from India

The present study reports Crinipellis cupreostipes (first described from Thailand) as a new record for Indian mycobiota. A phylogenetic analysis based on nrDNA ITS shows that C. cupreostipes can be readily distinguished from other morphologically similar species such as Crinipellis nigricaulis var. macrospora. A detailed taxonomic description with illustrations and an artificial key to Crinipellis species previously reported from India and its neighboring countries are provided

On the group theoretic structure of a class of quantum dialogue protocols

Intrinsic symmetry of the existing protocols of quantum dialogue are explored. It is shown that if we have a set of mutually orthogonal $n$-qubit states {\normalsize $\{|\phi_{0}>,|\phi_{1}>,....,|\phi_{i}\}$ and a set of $m-qubit$ ($m\leq n$) unitary operators $\{U_{0},U_{2},...,U_{2^{n}-1}\}:U_{i}|\phi_{0}>=|\phi_{i}>$ and $\{U_{0},U_{2},...,U_{2^{n}-1}\}$ forms a group under multiplication then it would be sufficient to construct a quantum dialogue protocol using this set of quantum states and this group of unitary operators}. The sufficiency condition is used to provide a generalized protocol of quantum dialogue. Further the basic concepts of group theory and quantum mechanics are used here to systematically generate several examples of possible groups of unitary operators that may be used for implementation of quantum dialogue. A large number of examples of quantum states that may be used to implement the generalized quantum dialogue protocol using these groups of unitary operators are also obtained. For example, it is shown that GHZ state, GHZ-like state, W state, 4 and 5 qubit Cluster states, Omega state, Brown state, $Q_{4}$ state and $Q_{5}$ state can be used for implementation of quantum dialogue protocol. The security and efficiency of the proposed protocol is appropriately analyzed. It is also shown that if a group of unitary operators and a set of mutually orthogonal states are found to be suitable for quantum dialogue then they can be used to provide solutions of socialist millionaire problem.Comment: 15 page

Advanced row-column designs for animal feed experiments

Not AvailableInappropriate statistical designs may misinterpret results of animal feed experiments. Thus complete statistical designs can make animal feed research more appropriate and cost effective. Usually factorial row-column designs are used when the heterogeneity in the experimental material is in two directions and the experimenter is interested in studying the effect of two or more factors simultaneously. Attempts have been to develop the method of construction of balanced nested row column design under factorial setup. Factorial experiments are used in designs when two or more factors have same levels or different levels. The designs that are balanced symmetric factorials nested in blocks are called block designs with nested row-column balanced symmetric factorial experiments. These designs were constructed by using confounding through equation methods.Construction of confounded asymmetrical factorial experiments in row-column settings and efficiency factor of confounded effects was worked out. The design can be used in animal feed experiment with fewer resources by not compromising the test accuracy.Not Availabl

Paradoxical Role of AT-rich Interactive Domain 1A in Restraining Pancreatic Carcinogenesis

Background & Aims: ARID1A is postulated to be a tumor suppressor gene owing to loss-of-function mutations in human pancreatic ductal adenocarcinomas (PDAC). However, its role in pancreatic pathogenesis is not clear despite recent studies using genetically engineered mouse (GEM) models. We aimed at further understanding of its direct functional role in PDAC, using a combination of GEM model and PDAC cell lines. Methods: Pancreas-specific mutant Arid1a-driven GEM model (Ptf1a-Cre; KrasG12D; Arid1af/f or “KAC”) was generated by crossing Ptf1a-Cre; KrasG12D (“KC”) mice with Arid1af/f mice and characterized histologically with timed necropsies. Arid1a was also deleted using CRISPR-Cas9 system in established human and murine PDAC cell lines to study the immediate effects of Arid1a loss in isogenic models. Cell lines with or without Arid1a expression were developed from respective autochthonous PDAC GEM models, compared functionally using various culture assays, and subjected to RNA-sequencing for comparative gene expression analysis. DNA damage repair was analyzed in cultured cells using immunofluorescence and COMET assay. Results: Retention of Arid1a is critical for early progression of mutant Kras-driven pre-malignant lesions into PDAC, as evident by lower Ki-67 and higher apoptosis staining in “KAC” as compared to “KC” mice. Enforced deletion of Arid1a in established PDAC cell lines caused suppression of cellular growth and migration, accompanied by compromised DNA damage repair. Despite early development of relatively indolent cystic precursor lesions called intraductal papillary mucinous neoplasms (IPMNs), a subset of “KAC” mice developed aggressive PDAC in later ages. PDAC cells obtained from older autochthonous “KAC” mice revealed various compensatory (“escaper”) mechanisms to overcome the growth suppressive effects of Arid1a loss. Conclusions: Arid1a is an essential survival gene whose loss impairs cellular growth, and thus, its expression is critical during early stages of pancreatic tumorigenesis in mouse models. In tumors that arise in the setting of ARID1A loss, a multitude of “escaper” mechanisms drive progression

Lactate-Mediated Epigenetic Reprogramming Regulates Formation of Human Pancreatic Cancer-Associated Fibroblasts

Even though pancreatic ductal adenocarcinoma (PDAC) is associated with fibrotic stroma, the molecular pathways regulating the formation of cancer associated fibroblasts (CAFs) are not well elucidated. An epigenomic analysis of patient-derived and de-novo generated CAFs demonstrated widespread loss of cytosine methylation that was associated with overexpression of various inflammatory transcripts including CXCR4. Co-culture of neoplastic cells with CAFs led to increased invasiveness that was abrogated by inhibition of CXCR4. Metabolite tracing revealed that lactate produced by neoplastic cells leads to increased production of alpha-ketoglutarate (aKG) within mesenchymal stem cells (MSCs). In turn, aKG mediated activation of the demethylase TET enzyme led to decreased cytosine methylation and increased hydroxymethylation during de novo differentiation of MSCs to CAF. Co-injection of neoplastic cells with TET-deficient MSCs inhibited tumor growth in vivo. Thus, in PDAC, a tumor-mediated lactate flux is associated with widespread epigenomic reprogramming that is seen during CAF formation