278 research outputs found
Trades in complex Hadamard matrices
A trade in a complex Hadamard matrix is a set of entries which can be changed
to obtain a different complex Hadamard matrix. We show that in a real Hadamard
matrix of order all trades contain at least entries. We call a trade
rectangular if it consists of a submatrix that can be multiplied by some scalar
to obtain another complex Hadamard matrix. We give a
characterisation of rectangular trades in complex Hadamard matrices of order
and show that they all contain at least entries. We conjecture that all
trades in complex Hadamard matrices contain at least entries.Comment: 9 pages, no figure
Pathogenic Variants in Fucokinase Cause a Congenital Disorder of Glycosylation
FUK encodes fucokinase, the only enzyme capable of converting L-fucose to fucose-1-phosphate, which will ultimately be used for synthesizing GDP-fucose, the donor substrate for all fucosyltransferases. Although it is essential for fucose salvage, this pathway is thought to make only a minor contribution to the total amount of GDP-fucose. A second pathway, the major de novo pathway, involves conversion of GDP-mannose to GDP-fucose. Here we describe two unrelated individuals who have pathogenic variants in FUK and who presented with severe developmental delays, encephalopathy, intractable seizures, and hypotonia. The first individual was compound heterozygous for c.667T>C (p.Ser223Pro) and c.2047C>T (p.Arg683Cys), and the second individual was homozygous for c.2980A>C (p.Lys994Gln). Skin fibroblasts from the first individual confirmed the variants as loss of function and showed significant decreases in total GDP-[3H] fucose and [3H] fucose-1-phosphate. There was also a decrease in the incorporation of [5,6-3H]-fucose into fucosylated glycoproteins. Lys994 has previously been shown to be an important site for ubiquitin conjugation. Here, we show that loss-of-function variants in FUK cause a congenital glycosylation disorder characterized by a defective fucose-salvage pathway
Preassociative aggregation functions
The classical property of associativity is very often considered in
aggregation function theory and fuzzy logic. In this paper we provide
axiomatizations of various classes of preassociative functions, where
preassociativity is a generalization of associativity recently introduced by
the authors. These axiomatizations are based on existing characterizations of
some noteworthy classes of associative operations, such as the class of
Acz\'elian semigroups and the class of t-norms.Comment: arXiv admin note: text overlap with arXiv:1309.730
All Teleportation and Dense Coding Schemes
We establish a one-to-one correspondence between (1) quantum teleportation
schemes, (2) dense coding schemes, (3) orthonormal bases of maximally entangled
vectors, (4) orthonormal bases of unitary operators with respect to the
Hilbert-Schmidt scalar product, and (5) depolarizing operations, whose Kraus
operators can be chosen to be unitary. The teleportation and dense coding
schemes are assumed to be ``tight'' in the sense that all Hilbert spaces
involved have the same finite dimension d, and the classical channel involved
distinguishes d^2 signals. A general construction procedure for orthonormal
bases of unitaries, involving Latin Squares and complex Hadamard Matrices is
also presented.Comment: 21 pages, LaTe
Exotic complex Hadamard matrices, and their equivalence
In this paper we use a design theoretical approach to construct new,
previously unknown complex Hadamard matrices. Our methods generalize and extend
the earlier results of de la Harpe--Jones and Munemasa--Watatani and offer a
theoretical explanation for the existence of some sporadic examples of complex
Hadamard matrices in the existing literature. As it is increasingly difficult
to distinguish inequivalent matrices from each other, we propose a new
invariant, the fingerprint of complex Hadamard matrices. As a side result, we
refute a conjecture of Koukouvinos et al. on (n-8)x(n-8) minors of real
Hadamard matrices.Comment: 10 pages. To appear in Cryptography and Communications: Discrete
Structures, Boolean Functions and Sequence
On quaternary complex Hadamard matrices of small orders
One of the main goals of design theory is to classify, characterize and count
various combinatorial objects with some prescribed properties. In most cases,
however, one quickly encounters a combinatorial explosion and even if the
complete enumeration of the objects is possible, there is no apparent way how
to study them in details, store them efficiently, or generate a particular one
rapidly. In this paper we propose a novel method to deal with these
difficulties, and illustrate it by presenting the classification of quaternary
complex Hadamard matrices up to order 8. The obtained matrices are members of
only a handful of parametric families, and each inequivalent matrix, up to
transposition, can be identified through its fingerprint.Comment: 7 page
TSPO interacts with VDAC1 and triggers a ROS-mediated inhibition of mitochondrial quality control
The 18-kDa TSPO (translocator protein) localizes on the outer mitochondrial membrane (OMM) and participates in cholesterol transport. Here, we report that TSPO inhibits mitochondrial autophagy downstream of the PINK1-PARK2 pathway, preventing essential ubiquitination of proteins. TSPO abolishes mitochondrial relocation of SQSTM1/p62 (sequestosome 1), and consequently that of the autophagic marker LC3 (microtubule-associated protein 1 light chain 3), thus leading to an accumulation of dysfunctional mitochondria, altering the appearance of the network. Independent of cholesterol regulation, the modulation of mitophagy by TSPO is instead dependent on VDAC1 (voltage-dependent anion channel 1), to which TSPO binds, reducing mitochondrial coupling and promoting an overproduction of reactive oxygen species (ROS) that counteracts PARK2-mediated ubiquitination of proteins. These data identify TSPO as a novel element in the regulation of mitochondrial quality control by autophagy, and demonstrate the importance for cell homeostasis of its expression ratio with VDAC1
Voltage-dependent Anion Channel-1 (VDAC-1) Contributes to ATP Release and Cell Volume Regulation in Murine Cells
Extracellular ATP regulates several elements of the mucus clearance process important for pulmonary host defense. However, the mechanisms mediating ATP release onto airway surfaces remain unknown. Mitochondrial voltage-dependent anion channels (mt-VDACs) translocate a variety of metabolites, including ATP and ADP, across the mitochondrial outer membrane, and a plasmalemmal splice variant (pl-VDAC-1) has been proposed to mediate ATP translocation across the plasma membrane. We tested the involvement of VDAC-1 in ATP release in a series of studies in murine cells. First, the full-length coding sequence was cloned from a mouse airway epithelial cell line (MTE7b−) and transfected into NIH 3T3 cells, and pl-VDAC-1-transfected cells exhibited higher rates of ATP release in response to medium change compared with mock-transfected cells. Second, ATP release was compared in cells isolated from VDAC-1 knockout [VDAC-1 (−/−)] and wild-type (WT) mice. Fibroblasts from VDAC-1 (−/−) mice released less ATP than WT mice in response to a medium change. Well-differentiated cultures from nasal and tracheal epithelia of VDAC-1 (−/−) mice exhibited less ATP release in response to luminal hypotonic challenge than WT mice. Confocal microscopy studies revealed that cell volume acutely increased in airway epithelia from both VDAC-1 (−/−) and WT mice after luminal hypotonic challenge, but VDAC-1 (−/−) cells exhibited a slower regulatory volume decrease (RVD) than WT cells. Addition of ATP or apyrase to the luminal surface of VDAC-1 (−/−) or WT cultures with hypotonic challenge produced similar initial cell height responses and RVD kinetics in both cell types, suggesting that involvement of VDAC-1 in RVD is through ATP release. Taken together, these studies suggest that VDAC-1, directly or indirectly, contributes to ATP release from murine cells. However, the observation that VDAC-1 knockout cells released a significant amount of ATP suggests that other molecules also play a role in this function
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