Higher-point conformal blocks and entanglement entropy in heavy states

We consider conformal blocks of two heavy operators and an arbitrary number of light operators in a (1+1)-d CFT with large central charge. Using the monodromy method, these higher-point conformal blocks are shown to factorize into products of 4-point conformal blocks in the heavy-light limit for a class of OPE channels. This result is reproduced by considering suitable worldline configurations in the bulk conical defect geometry. We apply the CFT results to calculate the entanglement entropy of an arbitrary number of disjoint intervals for heavy states. The corresponding holographic entanglement entropy calculated via the minimal area prescription precisely matches these results from CFT. Along the way, we briefly illustrate the relation of these conformal blocks to Riemann surfaces and their associated moduli space.Comment: 41 pages, 10 figures. (Published version; typos corrected and references added.

Radio frequency spectroscopy of the attractive Hubbard model in a trap

Attractive interaction between fermions can lead to pairing and superfluidity in an optical lattice. In contrast to the `continuum', on a lattice the trap induced density variation can generate a non monotonic profile of the pairing amplitude, and completely modify the spectral signatures of any possible pseudogap phase. Using a tool that fully captures the inhomogeneity and strong thermal fluctuations, we demonstrate how the crucial radio frequency signatures of pairing are `inverted' in a trapped attractive fermion lattice compared to the traditional continuum case. These features would be central in interpreting any spectroscopic hint of fermion pairing and superfluidity.Comment: this article supersedes arXiv:1104.491

AIM2 activates the inflammasome and cell death in response to cytoplasmic DNA.

Host- and pathogen-associated cytoplasmic double-stranded DNA triggers the activation of a NALP3 (also known as cryopyrin and NLRP3)-independent inflammasome, which activates caspase-1 leading to maturation of pro-interleukin-1beta and inflammation. The nature of the cytoplasmic-DNA-sensing inflammasome is currently unknown. Here we show that AIM2 (absent in melanoma 2), an interferon-inducible HIN-200 family member that contains an amino-terminal pyrin domain and a carboxy-terminal oligonucleotide/oligosaccharide-binding domain, senses cytoplasmic DNA by means of its oligonucleotide/oligosaccharide-binding domain and interacts with ASC (apoptosis-associated speck-like protein containing a CARD) through its pyrin domain to activate caspase-1. The interaction of AIM2 with ASC also leads to the formation of the ASC pyroptosome, which induces pyroptotic cell death in cells containing caspase-1. Knockdown of AIM2 by short interfering RNA reduced inflammasome/pyroptosome activation by cytoplasmic DNA in human and mouse macrophages, whereas stable expression of AIM2 in the non-responsive human embryonic kidney 293T cell line conferred responsiveness to cytoplasmic DNA. Our results show that cytoplasmic DNA triggers formation of the AIM2 inflammasome by inducing AIM2 oligomerization. This study identifies AIM2 as an important inflammasome component that senses potentially dangerous cytoplasmic DNA, leading to activation of the ASC pyroptosome and caspase-1

The AIM2 inflammasome is critical for innate immunity to Francisella tularensis.

Francisella tularensis, the causative agent of tularemia, infects host macrophages, which triggers production of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18. We elucidate here how host macrophages recognize F. tularensis and elicit this proinflammatory response. Using mice deficient in the DNA-sensing inflammasome component AIM2, we demonstrate here that AIM2 is required for sensing F. tularensis. AIM2-deficient mice were extremely susceptible to F. tularensis infection, with greater mortality and bacterial burden than that of wild-type mice. Caspase-1 activation, IL-1beta secretion and cell death were absent in Aim2(-/-) macrophages in response to F. tularensis infection or the presence of cytoplasmic DNA. Our study identifies AIM2 as a crucial sensor of F. tularensis infection and provides genetic proof of its critical role in host innate immunity to intracellular pathogens

Developing Tailor-Made Microbial Consortium for Effluent Remediation

The work describes a biofilm-based soluble sulphate reduction system, which can treat up to 1600 ppm of soluble sulphate within 3.5 hours of incubation to discharge level under ambient condition using a well-characterized sulphate-reducing bacterial (SRB) consortium. This system ensures the treatment of 1509 litres of sulphate solution in 24 hours using a 220-litre bioreactor. Performance of the system during series operation was compromised, indicating the presence of inhibitor in solution at a toxic level. A single unit bioreactor would be the ideal configuration for this consortium. Modified designs of bioreactors were tested for optimization of the process using response surface methodology (RSM), where the system could function optimally at an initial sulphate concentration of 1250 ppm with a flow rate of 1.8 litre/hour. The time course of sulphate reduction yielded a parabolic profile (with coefficient of determination r 2 = 0.99 and p value < 0.05). The rate of sulphate reduction was found to be independent of seasonal variation as well as the specific design characteristic

The C-terminal tail of presenilin regulates Omi/HtrA2 protease activity

Presenilin mutations are responsible for most cases of autosomal dominant inherited forms of early onset Alzheimer disease. Presenilins play an important role in amyloid beta-precursor processing, NOTCH receptor signaling, and apoptosis. However, the molecular mechanisms by which presenilins regulate apoptosis are not fully understood. Here, we report that presenilin-1 (PS1) regulates the proteolytic activity of the serine protease Omi/HtrA2 through direct interaction with its regulatory PDZ domain. We show that a peptide corresponding to the cytoplasmic C-terminal tail of PS1 dramatically increases the proteolytic activity of Omi/HtrA2 toward the inhibitor of apoptosis proteins and beta-casein and induces cell death in an Omi/HtrA2-dependent manner. Consistent with these results, ectopic expression of full-length PS1, but not PS1 lacking the C-terminal PDZ binding motif, potentiated Omi/HtrA2-induced cell death. Our results suggest that the C terminus of PS1 is an activation peptide ligand for the PDZ domain of Omi/HtrA2 and may regulate the protease activity of Omi/HtrA2 after its release from the mitochondria during apoptosis. This mechanism of Omi/HtrA2 activation is similar to the mechanism of activation of the related bacterial DegS protease by the outer-membrane porins

A numerical solution to enzyme emulsion liquid membrane reactor model for sequential bienzymatic reaction

307-313Dynamic mathematical models of liquid membrane-immobilized multienzyme reaction systems involve a large number of algebraic, ordinary and nonlinear partial differential equations with different types of boundary conditions. Solutions of such model equations are often difficult and stand in the way of realistic modeling efforts in this field. In the present study, attempt has been made to numerically solve such model equations for a liquid membrane-immobilized sequential bienzymatic reaction system through development of a software (MEMBSOL). In the solution process, partial differential equations have been converted into ordinary differential equations by using a finite difference technique in which the spatial derivatives have been discretized while leaving the temporal derivatives unconverted. Through mathematical manipulations, use of fictitious points at the boundaries has been eliminated thereby making the solution-approach a general-purpose one. To integrate the differential equations, Runge-Kutta-Fehlberg method has been applied. An automatic step-size adjustment mechanism has been incorporated in the integration process to produce results with a reasonably desired level of accuracy. In the present computations, numerical solutions with 0.1 percent relative error have been obtained

Studies on extraction of chromium(VI) from acidic solution by emulsion liquid membrane

713-718High molecular weight amines, quaternary salts etc. have the potential of removing heavy metal ions including the toxic ones at low concentrations. In the present work an attempt has been made to extract Cr(VI) through emulsion liquid surfactant membrane (or, emulsion liquid membrane-ELM) from it’s acidic solution using alamine-336 and caustic soda as extractant and striping reagents respectively. Around 97% extraction of Cr(VI) from aqueous solutions of potassium dichromate through batch experimentations have been achieved. Being crucial to the overall success of the ELM processes, experiments on emulsion stability have also been performed to arrive at a reasonably stable emulsion composition. Effect of various process parameters such as initial solute concentration, concentration of internal phase etc. as also that of pH on extraction of chromium have been investigated.</i