128 research outputs found
From Skew-Cyclic Codes to Asymmetric Quantum Codes
We introduce an additive but not -linear map from
to and exhibit some of its interesting
structural properties. If is a linear -code, then is an
additive -code. If is an additive cyclic code then
is an additive quasi-cyclic code of index . Moreover, if is a module
-cyclic code, a recently introduced type of code which will be
explained below, then is equivalent to an additive cyclic code if is
odd and to an additive quasi-cyclic code of index if is even. Given any
-code , the code is self-orthogonal under the trace
Hermitian inner product. Since the mapping 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
Magic state distillation in all prime dimensions using quantum Reed-Muller codes
We propose families of protocols for magic state distillation -- important
components of fault tolerance schemes --- for systems of odd prime dimension.
Our protocols utilize quantum Reed-Muller codes with transversal non-Clifford
gates. We find that, in higher dimensions, small and effective codes can be
used that have no direct analogue in qubit (two-dimensional) systems. We
present several concrete protocols, including schemes for three-dimensional
(qutrit) and five-dimensional (ququint) systems. The five-dimensional protocol
is, by many measures, the best magic state distillation scheme yet discovered.
It excels both in terms of error threshold with respect to depolarising noise
(36.3%) and the efficiency measure know as "yield", where, for a large region
of parameters, it outperforms its qubit counterpart by many orders of
magnitude.Comment: Updated from V1 to include results on the remarkable d=5 cas
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
Small integral membrane protein 10 like 1 downregulation enhances differentiation of adipose progenitor cells
Small integral membrane protein 10 like 1 (SMIM10L1) was identified by RNA sequencing as the most significantly downregulated gene in Phosphatase and Tensin Homologue (PTEN) knockdown adipose progenitor cells (APCs). PTEN is a tumor suppressor that antagonizes the growth promoting Phosphoinositide 3-kinase (PI3K)/AKT/mechanistic Target of Rapamycin (mTOR) cascade. Diseases caused by germline pathogenic variants in PTEN are summarized as PTEN Hamartoma Tumor Syndrome (PHTS). This overgrowth syndrome is associated with lipoma formation, especially in pediatric patients. The mechanisms underlying this adipose tissue dysfunction remain elusive. We observed that SMIM10L1 downregulation in APCs led to an enhanced adipocyte differentiation in two- and three-dimensional cell culture and increased expression of adipogenesis markers. Furthermore, SMIM10L1 knockdown cells showed a decreased expression of PTEN, pointing to a mutual crosstalk between PTEN and SMIM10L1. In line with these observations, SMIM10L1 knockdown cells showed increased activation of PI3K/AKT/mTOR signaling and concomitantly increased expression of the adipogenic transcription factor SREBP1. We computationally predicted an α-helical structure and membrane association of SMIM10L1. These results support a specific role for SMIM10L1 in regulating adipogenesis, potentially by increasing PI3K/AKT/mTOR signaling, which might be conducive to lipoma formation in pediatric patients with PHTS
Three-qubit entangled embeddings of CPT and Dirac groups within E8 Weyl group
In quantum information context, the groups generated by Pauli spin matrices,
and Dirac gamma matrices, are known as the single qubit Pauli group P, and
two-qubit Pauli group P2, respectively. It has been found [M. Socolovsky, Int.
J. Theor. Phys. 43, 1941 (2004)] that the CPT group of the Dirac equation is
isomorphic to P. One introduces a two-qubit entangling orthogonal matrix S
basically related to the CPT symmetry. With the aid of the two-qubit swap gate,
the S matrix allows the generation of the three-qubit real Clifford group and,
with the aid of the Toffoli gate, the Weyl group W(E8) is generated (M. Planat,
Preprint 0904.3691). In this paper, one derives three-qubit entangling groups ?
P and ? P2, isomorphic to the CPT group P and to the Dirac group P2, that are
embedded into W(E8). One discovers a new class of pure theequbit quantum states
with no-vanishing concurrence and three-tangle that we name CPT states. States
of the GHZ and CPT families, and also chain-type states, encode the new
representation of the Dirac group and its CPT subgroup.Comment: 12 page
Immune function biomarkers in children exposed to lead and organochlorine compounds: a cross-sectional study
BACKGROUND: Different organochlorines and lead (Pb) have been shown to have immunomodulating properties. Children are at greater risk for exposure to these environmental toxicants, but very little data exist on simultaneous exposures to these substances. METHODS: We investigated whether the organochlorine compounds (OC) dichlorodiphenylethylene (DDE), hexachlorobenzene (HCB), hexachlorocyclohexane (Îł-HCH), the sum of polychlorinated biphenyls (ÎŁPCBs) and Pb were associated with immune markers such as immunoglobulin (Ig) levels, white blood cell (WBC), counts of lymphocytes; eosinophils and their eosinophilic granula as well as IgE count on basophils. The investigation was part of a cross-sectional environmental study in Hesse, Germany. In 1995, exposure to OC and Pb were determined, questionnaire data collected and immune markers quantified in 331 children. For the analyses, exposure (OC and Pb) concentrations were grouped in quartiles (Îł-HCH into tertiles). Using linear regression, controlling for age, gender, passive smoking, serum lipids, and infections in the previous 12 months, we assessed the association between exposures and immune markers. Adjusted geometric means are provided for the different exposure levels. RESULTS: Geometric means were: DDE 0.32 ÎĽg/L, ÎŁPCBs 0.50 ÎĽg/L, HCB 0.22 ÎĽg/L, Îł-HCH 0.02 ÎĽg/L and Pb 26.8 ÎĽg/L. The ÎŁPCBs was significantly associated with increased IgM levels, whereas HCB was inversely related to IgM. There was a higher number of NK cells (CD56+) with increased Îł-HCH concentrations. At higher lead concentrations we saw increased IgE levels. DDE showed the most associations with significant increases in WBC count, in IgE count on basophils, IgE, IgG, and IgA levels. DDE was also found to significantly decrease eosinophilic granula content. CONCLUSION: Low-level exposures to OC and lead (Pb) in children may have immunomodulating effects. The increased IgE levels, IgE count on basophils, and the reduction of eosinophilic granula at higher DDE concentrations showed a most consistent pattern, which could be of clinical importance in the etiology of allergic diseases
A meta-analysis of genome-wide association studies identifies multiple longevity genes
Human longevity is heritable, but genome-wide association (GWA) studies have had limited success. Here, we perform two meta-analyses of GWA studies of a rigorous longevity phenotype definition including 11,262/3484 cases surviving at or beyond the age corresponding to the 90th/99th survival percentile, respectively, and 25,483 controls whose age at death or at last contact was at or below the age corresponding to the 60th survival percentile. Consistent with previous reports, rs429358 (apolipoprotein E (ApoE) epsilon 4) is associated with lower odds of surviving to the 90th and 99th percentile age, while rs7412 (ApoE epsilon 2) shows the opposite. Moreover, rs7676745, located near GPR78, associates with lower odds of surviving to the 90th percentile age. Gene-level association analysis reveals a role for tissue-specific expression of multiple genes in longevity. Finally, genetic correlation of the longevity GWA results with that of several disease-related phenotypes points to a shared genetic architecture between health and longevity
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