The invariants of the Clifford groups

The automorphism group of the Barnes-Wall lattice L_m in dimension 2^m (m not 3) is a subgroup of index 2 in a certain ``Clifford group'' C_m (an extraspecial group of order 2^(1+2m) extended by an orthogonal group). This group and its complex analogue CC_m have arisen in recent years in connection with the construction of orthogonal spreads, Kerdock sets, packings in Grassmannian spaces, quantum codes, Siegel modular forms and spherical designs. In this paper we give a simpler proof of Runge's 1996 result that the space of invariants for C_m of degree 2k is spanned by the complete weight enumerators of the codes obtained by tensoring binary self-dual codes of length 2k with the field GF(2^m); these are a basis if m >= k-1. We also give new constructions for L_m and C_m: let M be the Z[sqrt(2)]-lattice with Gram matrix [2, sqrt(2); sqrt(2), 2]. Then L_m is the rational part of the mth tensor power of M, and C_m is the automorphism group of this tensor power. Also, if C is a binary self-dual code not generated by vectors of weight 2, then C_m is precisely the automorphism group of the complete weight enumerator of the tensor product of C and GF(2^m). There are analogues of all these results for the complex group CC_m, with ``doubly-even self-dual code'' instead of ``self-dual code''.Comment: Latex, 24 pages. Many small improvement

Qudit versions of the qubit "pi-over-eight" gate

When visualised as an operation on the Bloch sphere, the qubit "pi-over-eight" gate corresponds to one-eighth of a complete rotation about the vertical axis. This simple gate often plays an important role in quantum information theory, typically in situations for which Pauli and Clifford gates are insufficient. Most notably, when it supplements the set of Clifford gates then universal quantum computation can be achieved. The "pi-over-eight" gate is the simplest example of an operation from the third level of the Clifford hierarchy (i.e., it maps Pauli operations to Clifford operations under conjugation). Here we derive explicit expressions for all qudit (d-level, where d is prime) versions of this gate and analyze the resulting group structure that is generated by these diagonal gates. This group structure differs depending on whether the dimensionality of the qudit is two, three or greater than three. We then discuss the geometrical relationship of these gates (and associated states) with respect to Clifford gates and stabilizer states. We present evidence that these gates are maximally robust to depolarizing and phase damping noise, in complete analogy with the qubit case. Motivated by this and other similarities we conjecture that these gates could be useful for the task of qudit magic-state distillation and, by extension, fault-tolerant quantum computing. Very recent, independent work by Campbell, Anwar and Browne confirms the correctness of this intuition, and we build upon their work to characterize noise regimes for which noisy implementations of these gates can (or provably cannot) supplement Clifford gates to enable universal quantum computation.Comment: Version 2 changed to reflect improved distillation routines in arXiv:1205.3104v2. Minor typos fixed. 12 Pages,2 Figures,3 Table

From Skew-Cyclic Codes to Asymmetric Quantum Codes

We introduce an additive but not $\mathbb{F}_4$-linear map $S$ from $\mathbb{F}_4^{n}$ to $\mathbb{F}_4^{2n}$ and exhibit some of its interesting structural properties. If $C$ is a linear $[n,k,d]_4$-code, then $S(C)$ is an additive $(2n,2^{2k},2d)_4$-code. If $C$ is an additive cyclic code then $S(C)$ is an additive quasi-cyclic code of index $2$. Moreover, if $C$ is a module $\theta$-cyclic code, a recently introduced type of code which will be explained below, then $S(C)$ is equivalent to an additive cyclic code if $n$ is odd and to an additive quasi-cyclic code of index $2$ if $n$ is even. Given any $(n,M,d)_4$-code $C$, the code $S(C)$ is self-orthogonal under the trace Hermitian inner product. Since the mapping $S$ preserves nestedness, it can be used as a tool in constructing additive asymmetric quantum codes.Comment: 16 pages, 3 tables, submitted to Advances in Mathematics of Communication

How to obtain lattices from (f,σ,δ)-codes via a generalization of Construction A

We show how cyclic (f,σ,δ)-codes over finite rings canonically induce a Z-lattice in RN by using certain quotients of orders in nonassociative division algebras defined using the skew polynomial f. This construction generalizes the one using certain σ-constacyclic codes by Ducoat and Oggier, which used quotients of orders in non-commutative associative division algebras defined by f, and can be viewed as a generalization of the classical Construction A for lattices from linear codes. It has the potential to be applied to coset coding, in particular to wire-tap coding. Previous results by Ducoat and Oggier are obtained as special cases

Phenotypic Variation and Bistable Switching in Bacteria

Microbial research generally focuses on clonal populations. However, bacterial cells with identical genotypes frequently display different phenotypes under identical conditions. This microbial cell individuality is receiving increasing attention in the literature because of its impact on cellular differentiation, survival under selective conditions, and the interaction of pathogens with their hosts. It is becoming clear that stochasticity in gene expression in conjunction with the architecture of the gene network that underlies the cellular processes can generate phenotypic variation. An important regulatory mechanism is the so-called positive feedback, in which a system reinforces its own response, for instance by stimulating the production of an activator. Bistability is an interesting and relevant phenomenon, in which two distinct subpopulations of cells showing discrete levels of gene expression coexist in a single culture. In this chapter, we address techniques and approaches used to establish phenotypic variation, and relate three well-characterized examples of bistability to the molecular mechanisms that govern these processes, with a focus on positive feedback.

Actin polymerization stabilizes α4β1 integrin anchors that mediate monocyte adhesion

Leukocytes arrested on inflamed endothelium via integrins are subjected to force imparted by flowing blood. How leukocytes respond to this force and resist detachment is poorly understood. Live-cell imaging with Lifeact-transfected U937 cells revealed that force triggers actin polymerization at upstream α4β1 integrin adhesion sites and the adjacent cortical cytoskeleton. Scanning electron microscopy revealed that this culminates in the formation of structures that anchor monocyte adhesion. Inhibition of actin polymerization resulted in cell deformation, displacement, and detachment. Transfection of dominant-negative constructs and inhibition of function or expression revealed key signaling steps required for upstream actin polymerization and adhesion stabilization. These included activation of Rap1, phosphoinositide 3-kinase γ isoform, and Rac but not Cdc42. Thus, rapid signaling and structural adaptations enable leukocytes to stabilize adhesion and resist detachment forces

Phospholipid Scramblase 4 (PLSCR4) Regulates Adipocyte Differentiation via PIP3-Mediated AKT Activation

Phospholipid scramblase 4 (PLSCR4) is a member of a conserved enzyme family with high relevance for the remodeling of phospholipid distribution in the plasma membrane and the regulation of cellular signaling. While PLSCR1 and -3 are involved in the regulation of adipose-tissue expansion, the role of PLSCR4 is so far unknown. PLSCR4 is significantly downregulated in an adipose-progenitor-cell model of deficiency for phosphatase and tensin homolog (PTEN). PTEN acts as a tumor suppressor and antagonist of the growth and survival signaling phosphoinositide 3-kinase (PI3K)/AKT cascade by dephosphorylating phosphatidylinositol-3,4,5-trisphosphate (PIP3). Patients with PTEN germline deletion frequently develop lipomas. The underlying mechanism for this aberrant adipose-tissue growth is incompletely understood. PLSCR4 is most highly expressed in human adipose tissue, compared with other phospholipid scramblases, suggesting a specific role of PLSCR4 in adipose-tissue biology. In cell and mouse models of lipid accumulation, we found PLSCR4 to be downregulated. We observed increased adipogenesis in PLSCR4-knockdown adipose progenitor cells, while PLSCR4 overexpression attenuated lipid accumulation. PLSCR4 knockdown was associated with increased PIP3 levels and the activation of AKT. Our results indicated that PLSCR4 is a regulator of PI3K/AKT signaling and adipogenesis and may play a role in PTEN-associated adipose-tissue overgrowth and lipoma formation