Efficient Simulation of Leakage Errors in Quantum Error Correcting Codes Using Tensor Network Methods

Leakage errors, in which a qubit is excited to a level outside the qubit subspace, represent a significant obstacle in the development of robust quantum computers. We present a computationally efficient simulation methodology for studying leakage errors in quantum error correcting codes (QECCs) using tensor network methods, specifically Matrix Product States (MPS). Our approach enables the simulation of various leakage processes, including thermal noise and coherent errors, without approximations (such as the Pauli twirling approximation) that can lead to errors in the estimation of the logical error rate. We apply our method to two QECCs: the one-dimensional (1D) repetition code and a thin $3\times d$ surface code. By leveraging the small amount of entanglement generated during the error correction process, we are able to study large systems, up to a few hundred qudits, over many code cycles. We consider a realistic noise model of leakage relevant to superconducting qubits to evaluate code performance and a variety of leakage removal strategies. Our numerical results suggest that appropriate leakage removal is crucial, especially when the code distance is large.Comment: 14 pages, 12 figure

RUNNING ECONOMY AND GASTROCNEMIUS MUSCLE LENGTH DURING RUNNING FOR KENYAN AND JAPANESE ELITE DISTANCE RUNNERS

The purpose of this study was to compare running economy and gastrocnemius muscle length during running for Kenyan and Japanese elite distance runners. Running economy was measured on the treadmill at 340 m/min while running motion was captured on the inside straight track at their racing speed. Gastrocnemius muscle length was estimated by the equation of Grieve et al. (1978) during the support phase at race speed running on the track. Kenyan runners showed higher running economy and smaller shortening length change of gastrocnemius during support phase than Japanese. These results suggest that shortening gastrocnemius during support phase of the running relates to running economy

Phospholipid scrambling induced by an ion channel/metabolite transporter complex.

Cells establish the asymmetrical distribution of phospholipids and alter their distribution by phospholipid scrambling (PLS) to adapt to environmental changes. Here, we demonstrate that a protein complex, consisting of the ion channel Tmem63b and the thiamine transporter Slc19a2, induces PLS upon calcium (Ca2+) stimulation. Through revival screening using a CRISPR sgRNA library on high PLS cells, we identify Tmem63b as a PLS-inducing factor. Ca2+ stimulation-mediated PLS is suppressed by deletion of Tmem63b, while human disease-related Tmem63b mutants induce constitutive PLS. To search for a molecular link between Ca2+ stimulation and PLS, we perform revival screening on Tmem63b-overexpressing cells, and identify Slc19a2 and the Ca2+-activated K+ channel Kcnn4 as PLS-regulating factors. Deletion of either of these genes decreases PLS activity. Biochemical screening indicates that Tmem63b and Slc19a2 form a heterodimer. These results demonstrate that a Tmem63b/Slc19a2 heterodimer induces PLS upon Ca2+ stimulation, along with Kcnn4 activation

Collective fusion activity determines neurotropism of an en bloc transmitted enveloped virus

麻疹（はしか）ウイルスが「協力」して脳炎を引き起こす仕組みを解明 --新規治療薬の開発やウイルス共通の進化メカニズム解明に期待--. 京都大学プレスリリース. 2023-01-30.Measles virus (MeV), which is usually non-neurotropic, sometimes persists in the brain and causes subacute sclerosing panencephalitis (SSPE) several years after acute infection, serving as a model for persistent viral infections. The persisting MeVs have hyperfusogenic mutant fusion (F) proteins that likely enable cell-cell fusion at synapses and "en bloc transmission" between neurons. We here show that during persistence, F protein fusogenicity is generally enhanced by cumulative mutations, yet mutations paradoxically reducing the fusogenicity may be selected alongside the wild-type (non-neurotropic) MeV genome. A mutant F protein having SSPE-derived substitutions exhibits lower fusogenicity than the hyperfusogenic F protein containing some of those substitutions, but by the wild-type F protein coexpression, the fusogenicity of the former F protein is enhanced, while that of the latter is nearly abolished. These findings advance the understanding of the long-term process of MeV neuropathogenicity and provide critical insight into the genotype-phenotype relationships of en bloc transmitted viruses

Sevoflurane Stimulates MAP Kinase Signal transduction through the Activation of PKC α and βII in Fetal Rat Cerebral Cortex Cultured Neuron

Protein kinase C (PKC) is a key enzyme that participates in various neuronal functions. PKC has also been identified as a target molecule for general anesthetic actions. Raf, mitogen-activated protein kinase (MEK) and extracellular signal-regulated kinase (ERK1/2) have been thought to be target effectors of PKC. In the present study, we attempted to evaluate the effect of sevoflurane on PKC/MAPK cascade signaling in cultured fetal rat cerebral ­cortex neurons, prepared from embryonic day 18 fetuses. The effects of sevoflurane on the translocation of 7 PKC isoforms (α, βI, βII, γ, δ, ɛ and ζ) were observed by immunoblotting using isoform-selective antibodies to PKCs. The treatment of neurons with sevoflurane induced the translocation of PKC α and PKC βII species from the cytosol to the membrane fraction, which indicated the activation of these PKC isoforms. In contrast, there was no clear change in the distribution of other PKC isoforms. We next examined whether the specific activation of PKC α and βII by sevoflurane could stimulate the MAP kinase signaling pathway in cultured neurons. Raf phosphorylation was increased by the administration of 0.25 mM sevoflurane. The phosphorylation of Raf proteins reached a maximum at 5–10 min. Subsequently, the phosphorylation of MEK proteins was increased at 10–15 min after sevoflurane treatments. That of ERK proteins was induced at 15–60 min. Moreover, the phosphorylation of ERK induced by sevoflurane was significantly decreased by the treatment of PKC inhibitor (staurosporine) and MEK inhibitor (PD98059). On the other hand, the contents of total Raf, MEK and ERK proteins were relatively constant at all times examined. To examine the ­localization of phosphorylated-ERK protein, immunohistochemical staining of sevoflurane-treated cultured neurons was performed. The phosphorylated-ERK proteins were markedly accumulated in both the cytosol of the cell body and the neurites in the neuronal cells with time after 0.25 mM sevoflurane-treatment. These results demonstrated that sevoflurane induced the phosphorylation of the MAP kinase cascade through the activation of the PKC α and PKC βII species

The Effect of Deep Micro Vibrotactile Stimulation on Cognitive Function of Mild Cognitive Impairment and Mild Dementia

Background: The purpose of this study was to clarify the effect of Deep Micro Vibrotactile (DMV) stimulation on the cognitive functions in elderly people with mild cognitive impairment or mild dementia. Methods: A total of 35 participants with dementia from three nursing homes, who had completed treatment with DMV stimulation at 15–40 Hz (hereinafter, 15–40 Hz DMV stimulation) for a month were recruited for this study. The subjects had received continuous 15–40 Hz DMV stimulation for 24 h a day for 1 month. We assessed the effect of the treatment on the cognitive functions (by the word list memory (WM) test, trail making test-part A (TMT-A) and part B (TMT-B), and symbol digit substitution task (SDST)) and physical functions (grip strength (GS) and usual walking speed (UWS)), by comparing the results at the baseline and after the 1-month intervention (DMV stimulation). Results: The results revealed that the performances in the WM test (p < 0.05), TMT-B (p < 0.05), and SDST (p < 0.01) improved significantly after the intervention. Conclusion: Our findings suggest that 15–40 Hz DMV stimulation is might be effective for improving the cognitive functions in elderly people with dementia. Furthermore, our novel findings showed the different effectiveness of the treatment depending on the stage of cognitive impairments

Receptor interacting protein kinase mediates necrotic cone but not rod cell death in a mouse model of inherited degeneration

Retinitis pigmentosa comprises a group of inherited retinal photoreceptor degenerations that lead to progressive loss of vision. Although in most cases rods, but not cones, harbor the deleterious gene mutations, cones do die in this disease, usually after the main phase of rod cell loss. Rod photoreceptor death is characterized by apoptotic features. In contrast, the mechanisms and features of subsequent nonautonomous cone cell death remain largely unknown. In this study, we show that receptor-interacting protein (RIP) kinase mediates necrotic cone cell death in rd10 mice, a mouse model of retinitis pigmentosa caused by a mutation in a rod-specific gene. The expression of RIP3, a key regulator of programmed necrosis, was elevated in rd10 mouse retinas in the phase of cone but not rod degeneration. Although rd10 mice lacking Rip3 developed comparable rod degeneration to control rd10 mice, they displayed a significant preservation of cone cells. Ultrastructural analysis of rd10 mouse retinas revealed that a substantial fraction of dying cones exhibited necrotic morphology, which was rescued by Rip3 deficiency. Additionally, pharmacologic treatment with a RIP kinase inhibitor attenuated histological and functional deficits of cones in rd10 mice. Thus, necrotic mechanisms involving RIP kinase are crucial in cone cell death in inherited retinal degeneration, suggesting the RIP kinase pathway as a potential target to protect cone-mediated central and peripheral vision loss in patients with retinitis pigementosa

Pressure-Induced Antiferromagnetic Bulk Superconductor EuFe2_2As2_2

We present the magnetic and superconducting phase diagram of EuFe$_2$As$_2$ for $B \parallel c$ and $B \parallel ab$. The antiferromagnetic phase of the Eu$^{2+}$ moments is completely enclosed in the superconducting phase. The upper critical field vs. temperature curves exhibit strong concave curvatures, which can be explained by the Jaccarino-Peter compensation effect due to the antiferromagnetic exchange interaction between the Eu$^{2+}$ moments and conduction electrons.Comment: submitted to the proceedings of the M2S-IX Toky

The CRKL gene encoding an adaptor protein is amplified, overexpressed, and a possible therapeutic target in gastric cancer

<p>Abstract</p> <p>Background</p> <p>Genomic DNA amplification is a genetic factor involved in cancer, and some oncogenes, such as <it>ERBB2</it>, are highly amplified in gastric cancer. We searched for the possible amplification of other genes in gastric cancer.</p> <p>Methods and Results</p> <p>A genome-wide single nucleotide polymorphism microarray analysis was performed using three cell lines of differentiated gastric cancers, and 22 genes (including <it>ERBB2</it>) in five highly amplified chromosome regions (with a copy number of more than 6) were identified. Particular attention was paid to the <it>CRKL</it> gene, the product of which is an adaptor protein containing Src homology 2 and 3 (SH2/SH3) domains. An extremely high <it>CRKL</it> copy number was confirmed in the MKN74 gastric cancer cell line using fluorescence <it>in situ</it> hybridization (FISH), and a high level of CRKL expression was also observed in the cells. The RNA-interference-mediated knockdown of CRKL in MKN74 disclosed the ability of CRKL to upregulate gastric cell proliferation. An immunohistochemical analysis revealed that CRKL protein was overexpressed in 24.4% (88/360) of the primary gastric cancers that were analyzed. The <it>CRKL</it> copy number was also examined in 360 primary gastric cancers using a FISH analysis, and <it>CRKL</it> amplification was found to be associated with CRKL overexpression. Finally, we showed that MKN74 cells with <it>CRKL</it> amplification were responsive to the dual Src/BCR-ABL kinase inhibitor BMS354825, likely via the inhibition of CRKL phosphorylation, and that the proliferation of MKN74 cells was suppressed by treatment with a CRKL-targeting peptide.</p> <p>Conclusion</p> <p>These results suggested that CRKL protein is overexpressed in a subset of gastric cancers and is associated with <it>CRKL</it> amplification in gastric cancer. Furthermore, our results suggested that CRKL protein has the ability to regulate gastric cell proliferation and has the potential to serve as a molecular therapy target for gastric cancer.</p