Implementation of three-qubit Toffoli gate in a single step

Single-step implementations of multi-qubit gates are generally believed to provide a simpler design, a faster operation, and a lower decoherence. For coupled three qubits interacting with a photon field, a realizable scheme for a single-step Toffoli gate is investigated. We find that the three qubit system can be described by four effective modified Jaynes-Cummings models in the states of two control qubits. Within the rotating wave approximation, the modified Jaynes-Cummings models are shown to be reduced to the conventional Jaynes-Cummings models with renormalized couplings between qubits and photon fields. A single-step Toffoli gate is shown to be realizable with tuning the four characteristic oscillation periods that satisfy a commensurate condition. Possible values of system parameters are estimated for single-step Toffli gate. From numerical calculation, further, our single-step Toffoli gate operation errors are discussed due to imperfections in system parameters, which shows that a Toffoli gate with high fidelity can be obtained by adjusting pairs of the photon-qubit and the qubit-qubit coupling strengthes. In addition, a decoherence effect on the Toffoli gate operation is discussed due to a thermal reservoir.Comment: 8 pages, 4 figures, to appear in PR

Imunosni odgovor BALB/c miševa oralno imuniziranih rekombinantnim cjepivom od serovara Salmonella Typhimurium s ugrađenim antigenima enterotoksigenog soja Escherichia coli

Salmonella Typhimurium ghost vaccines containing antigens of enterotoxigenic Escherichia coli (ETEC) were obtained by a strain harboring pMMP184, which carries a ghost cassette. The immune responses of BALB/c mice orally vaccinated with these ghost vaccines were determined in this study. Total IgG against S. Typhimurium were highly detected by the oral immunization route in BALB/c mice. IgGs against ETEC antigens in the ghost cells carrying F41 and intimin were detected at 4 weeks after vaccination. However, FedF elicited a delayed induction of IgGs, whereas FedA immune response failed to or barely induced IgGs after vaccination. Proliferations of CD3e/CD4-T cells were observed in splenocytes of BALB/c mice immunized with S. Typhimurium ghost cells carrying FedF. However, CD45R-B220/CD23-B cells were proliferated by ghost cells carrying FedA, F41, and intimin. The immunized BALB/c mice showed 25~50% protection against challenge with wild type S. Typhimurium, when compared to control mice. Therefore, it is assumed that oral vaccination of S. Typhimurium ghost cells has the potential to protect mice against pathogenic E. coli.Salmonella Typhimurium rekombinantna cjepiva što sadrže antigene enterotoksigenih sojeva Escherichia coli (ETEC) proizvedena su od soja koji posjeduje pMMP184 i nosi rekombinantnu kasetu. Istražen je imunosni odgovor BALB/c miševa oralno cijepljenih tim rekombinantnim cjepivima. Ustanovljena je visoka razina ukupnih IgG za S. Typhimurium nakon oralne imunizacije miševa BALB/c. Imunoglobulini IgG za antigene ETEC u rekombinantnom cjepivu koje sadrži F41 i intimin bili su dokazani četiri tjedna nakon cijepljenja. Ipak, FedF je potaknuo kasnu tvorbu imunoglobulina IgG, dok FedA nije potaknuo ili je potaknuo slab imunosni odgovor nakon cijepljenja. Proliferacija CD3e/CD4-T stanica bila je dokazana u splenocitima miševa BALB/c imuniziranih rekombinantnim cjepivom S. Typhimurium s ugrađenim FedF. Međutim, stanice CD45R-B220/CD23-B proliferirale su nakon cijepljenja rekombinantom FedA, F41 i intimin. Imunizirani miševi BALB/c pokazivali su 25~50% zaštitu nakon izazivačke infekcije serovarom S. Typhimurium u usporedbi s necijepljenim kontrolnim miševima. Stoga se pretpostavlja da oralno cijepljenje s rekombinantnim stanicama serovara S. Typhimurium ima potencijal da zaštiti miševe od infekcije patogenim sojevima E. coli

12-h clock regulation of genetic information flow by XBP1s

© The Author(s), 2020. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Pan, Y., Ballance, H., Meng, H., Gonzalez, N., Kim, S., Abdurehman, L., York, B., Chen, X., Schnytzer, Y., Levy, O., Dacso, C. C., McClung, C. A., O'Malley, B. W., Liu, S., & Zhu, B. 12-h clock regulation of genetic information flow by XBP1s. Plos Biology, 18(1), (2020): e3000580, doi:10.1371/journal.pbio.3000580.Our group recently characterized a cell-autonomous mammalian 12-h clock independent from the circadian clock, but its function and mechanism of regulation remain poorly understood. Here, we show that in mouse liver, transcriptional regulation significantly contributes to the establishment of 12-h rhythms of mRNA expression in a manner dependent on Spliced Form of X-box Binding Protein 1 (XBP1s). Mechanistically, the motif stringency of XBP1s promoter binding sites dictates XBP1s’s ability to drive 12-h rhythms of nascent mRNA transcription at dawn and dusk, which are enriched for basal transcription regulation, mRNA processing and export, ribosome biogenesis, translation initiation, and protein processing/sorting in the Endoplasmic Reticulum (ER)-Golgi in a temporal order consistent with the progressive molecular processing sequence described by the central dogma information flow (CEDIF). We further identified GA-binding proteins (GABPs) as putative novel transcriptional regulators driving 12-h rhythms of gene expression with more diverse phases. These 12-h rhythms of gene expression are cell autonomous and evolutionarily conserved in marine animals possessing a circatidal clock. Our results demonstrate an evolutionarily conserved, intricate network of transcriptional control of the mammalian 12-h clock that mediates diverse biological pathways. We speculate that the 12-h clock is coopted to accommodate elevated gene expression and processing in mammals at the two rush hours, with the particular genes processed at each rush hour regulated by the circadian and/or tissue-specific pathways.This study was supported by the American Diabetes Association junior faculty development award 1-18-JDF-025 to B.Z., by funding from National Institute of Health HD07879 and 1P01DK113954 to B.W.O, by funding from National Science Foundation award 1703170 to C.C.D. and B.Z., and by funding from Brockman Foundation to C.C.D and B.W.O. This work was further supported by the UPMC Genome Center with funding from UPMC’s Immunotherapy and Transplant Center. This research was supported in part by the University of Pittsburgh Center for Research Computing through the resources provided. Research reported in this publication was further supported by the National Institute of Diabetes And Digestive And Kidney Diseases of the National Institutes of Health under award number P30DK120531 to Pittsburgh Liver Research Center, in which both S.L. and B.Z. are members. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Proteomic Detection of Non-Annotated Protein-Coding Genes in Pseudomonas fluorescens Pf0-1

Genome sequences are annotated by computational prediction of coding sequences, followed by similarity searches such as BLAST, which provide a layer of possible functional information. While the existence of processes such as alternative splicing complicates matters for eukaryote genomes, the view of bacterial genomes as a linear series of closely spaced genes leads to the assumption that computational annotations that predict such arrangements completely describe the coding capacity of bacterial genomes. We undertook a proteomic study to identify proteins expressed by Pseudomonas fluorescens Pf0-1 from genes that were not predicted during the genome annotation. Mapping peptides to the Pf0-1 genome sequence identified sixteen non-annotated protein-coding regions, of which nine were antisense to predicted genes, six were intergenic, and one read in the same direction as an annotated gene but in a different frame. The expression of all but one of the newly discovered genes was verified by RT-PCR. Few clues as to the function of the new genes were gleaned from informatic analyses, but potential orthologs in other Pseudomonas genomes were identified for eight of the new genes. The 16 newly identified genes improve the quality of the Pf0-1 genome annotation, and the detection of antisense protein-coding genes indicates the under-appreciated complexity of bacterial genome organization

Role of Rho-kinase in regulation of insulin action and glucose homeostasis

SummaryAccumulating evidence indicates an important role for serine phosphorylation of IRS-1 in the regulation of insulin action. Recent studies suggest that Rho-kinase (ROK) is a mediator of insulin signaling, via interaction with IRS-1. Here we show that insulin stimulation of glucose transport is impaired when ROK is chemically or biologically inhibited in cultured adipocytes and myotubes and in isolated soleus muscle ex vivo. Inactivation of ROK also reduces insulin-stimulated IRS-1 tyrosine phosphorylation and PI3K activity. Moreover, inhibition of ROK activity in mice causes insulin resistance by reducing insulin-stimulated glucose uptake in skeletal muscle in vivo. Mass spectrometry analysis identifies IRS-1 Ser632/635 as substrates of ROK in vitro, and mutation of these sites inhibits insulin signaling. These results strongly suggest that ROK regulates insulin-stimulated glucose transport in vitro and in vivo. Thus, ROK is an important regulator of insulin signaling and glucose metabolism

Identification of ROCK1 kinase as a critical regulator of Beclin1 mediated autophagy during metabolic stress

The Ser/Thr Rho kinase 1 (ROCK1) is known to play major roles in a wide range of cellular activities, including those involved in tumor metastasis and apoptosis. Here we identify an indispensable function of ROCK1 in metabolic stress-induced autophagy. Applying a proteomics approach, we characterize Beclin1, a proximal component of the PI(3)kinase class III lipid-kinase complex that induces autophagy, as an interacting partner of ROCK1. Upon nutrient deprivation, activated ROCK1 promotes autophagy by binding and phosphorylating Beclin1 at Thr119. This results in the specific dissociation of the Beclin1-Bcl-2 complex, without affecting the Beclin1-UVRAG interaction. Conversely, inhibition of ROCK1 activity increases Beclin1-Bcl-2 association, thus reducing nutritional stress-mediated autophagy. Genetic knockout of ROCK1 function in mice also leads to impaired autophagy as evidenced by reduced autophagosome formation. These results show that ROCK1 acts as a prominent upstream regulator of Beclin1-mediated autophagy and maintains a homeostatic balance between apoptosis and autophagy

High-throughput measurement of fibroblast rhythms reveals genetic heritability of circadian phenotypes in diversity outbred mice and their founder strains.

Circadian variability is driven by genetics and Diversity Outbred (DO) mice is a powerful tool for examining the genetics of complex traits because their high genetic and phenotypic diversity compared to conventional mouse crosses. The DO population combines the genetic diversity of eight founder strains including five common inbred and three wild-derived strains. In DO mice and their founders, we established a high-throughput system to measure cellular rhythms using in vitro preparations of skin fibroblasts. Among the founders, we observed strong heritability for rhythm period, robustness, phase and amplitude. We also found significant sex and strain differences for these rhythms. Extreme differences in period for molecular and behavioral rhythms were found between the inbred A/J strain and the wild-derived CAST/EiJ strain, where A/J had the longest period and CAST/EiJ had the shortest. In addition, we measured cellular rhythms in 329 DO mice, which displayed far greater phenotypic variability than the founders-80% of founders compared to only 25% of DO mice had periods of ~ 24 h. Collectively, our findings demonstrate that genetic diversity contributes to phenotypic variability in circadian rhythms, and high-throughput characterization of fibroblast rhythms in DO mice is a tractable system for examining the genetics of circadian traits

Measurement of E2 Transitions in the Coulomb Dissociation of 8B

In an effort to understand the implications of Coulomb dissociation experiments for the determination of the 7Be(p,gamma)8B reaction rate, longitudinal momentum distributions of 7Be fragments produced in the Coulomb dissociation of 44 and 81 MeV/nucleon 8B beams on a Pb target were measured. These distributions are characterized by asymmetries interpreted as the result of interference between E1 and E2 transition amplitudes in the Coulomb breakup. At the lower beam energy, both the asymmetries and the measured cross sections are well reproduced by perturbation theory calculations, allowing a determination of the E2 strength.Comment: 8 pages, 3 figure