Quantum circuit mapping for universal and scalable computing in MZI-based integrated photonics.

Linear optical quantum computing (LOQC) offers a quantum computation paradigm based on well-established and robust technology and flexible environmental conditions following DiVincenzo's criteria. Within this framework, integrated photonics can be utilized to achieve gate-based quantum computing, defining qubits by path-encoding, quantum gates through the use of Mach-Zehnder interferometers (MZIs), and measurements through single-photon detectors. In particular, universal two-qubit gates can be achieved by suitable structures of MZIs together with post-selection or heralding. The most resource-efficient choice is given by the post-selected Controlled-Z (CZ) gate. However, this implementation is characterized by a design which has a non-regular structure and cannot be cascaded. This limits the implementation of large-scale LOQC. Starting from these issues, we suggest an approach to move toward a universal and scalable LOQC on the integrated photonic platform. First of all, choosing the post-selected CZ as a universal two-qubit gate, we extend the path-encoded dual-rail qubit to a triplet of waveguides, composed of an auxiliary waveguide and the pair of waveguides corresponding to the qubit basis states. Additionally, we introduce a swap photonic network that maps the regularly-labeled structure of the new path-encoded qubits to the structure needed for the post-selected CZ. We also discuss the optical swap gate that allows the connection of non-nearest neighbor path-encoded qubits. In this way, we can deterministically exchange the locations of the qubits and execute controlled quantum gates between any path-encoded qubits. Next, by truncating the auxiliary waveguides after any post-selected CZ, we find that it is possible to cascade this optical gate when it acts on different pairs that share only one qubit. Finally, we show the Bell state and the Greenberger-Horne-Zeilinger (GHZ) state generation circuits implementing the regular structure, the cascading procedure of post-selected CZ and the optical swap.

Obtusifolin isolated from the seeds of Cassia obtusifolia regulates the gene expression and production of MUC5AC mucin in airway epithelial cells via affecting NF-κB pathway.

We investigated whether obtusin, obtusifolin, and cassiaside isolated from the seeds of Cassia obtusifolia inhibit the gene expression and production of airway mucin 5AC (MUC5AC). Confluent NCI-H292 cells were pretreated with obtusin, obtusifolin, or cassiaside for 30 min and then stimulated with epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA), or tumor necrosis factor-α (TNF-α) for 24 hr. The MUC5AC mucin gene expression was measured by reverse transcription-polymerase chain reaction. Production of MUC5AC mucin protein was measured by enzyme-linked immunosorbent assay. To elucidate the action mechanism of obtusifolin, effect of obtusifolin on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway was investigated by western blot analysis. Obtusin, obtusifolin, or cassiaside inhibited the expression of MUC5AC mucin gene and the production of MUC5AC mucin protein, induced by EGF, PMA, or TNF-α. Obtusifolin inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase, and thus phosphorylation and degradation of inhibitory kappa B alpha. Obtusifolin inhibited PMA-induced nuclear translocation of NF-κB p65. These results suggest that obtusifolin can regulate the production and gene expression of mucin by acting on airway epithelial cells through regulation of NF-κB signaling pathway.

Tussilagone suppressed the production and gene expression of MUC5AC mucin via regulating nuclear factor-kappa B signaling pathway in airway epithelial cells.

In the present study, we investigated whether tussilagone, a natural product derived from Tussilago farfara, significantly affects the production and gene expression of airway MUC5AC mucin. Confluent NCI-H292 cells were pretreated with tussilagone for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. To elucidate the action mechanism of tussilagone, effect of tussilagone on PMA-induced NF-κB signaling pathway was investigated by western blot analysis. Tussilagone significantly inhibited the production of MUC5AC mucin protein and down-regulated the expression of MUC5AC mucin gene, induced by EGF or PMA. Tussilagone inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Ba (IκBα). Tussilagone inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) p65. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. These results suggest that tussilagone can regulate the production and gene expression of mucin by acting on airway epithelial cells through regulation of NF-κB signaling pathway.

Sirt3 controls chromosome alignment by regulating spindle dynamics during mitosis.

Sirt3, one of mammalian sirtuins is a prominent mitochondrial deacetylase that controls mitochondrial oxidative pathways and the rate of reactive oxygen species. Sirt3 also regulates energy metabolism by deacetylating enzymes involved in the metabolic pathway related with lifespan. We report here a novel function of Sirt3 which was found to be involved in mitosis. Depletion of the Sirt3 protein generated unaligned chromosomes in metaphase which caused mitotic arrest by activating spindle assembly checkpoint (SAC). Furthermore, the shape and the amount of the spindles in Sirt3 depleted cells were abnormal. Microtubule (MT) polymerization also increased in Sirt3 depleted cells, suggesting that Sirt3 is involved in spindle dynamics. However, the level of acetylated tubulin was not increased significantly in Sirt3 depleted cells. The findings collectively suggest that Sirt3 is not a tubulin deacetylase but regulates the attachment of spindle MTs to the kinetochore and the subsequent chromosome alignment by increasing spindle dynamics.

Rspo 1 promotes osteoblast differentiation via Wnt signaling pathway.

R-spondin (Rspo)s proteins are a new group of Wnt/beta-catenin signaling agonists. These signaling molecules are known to be involved in the developmental stages of skeletal system. Recent studies in various murine osteoblast models have proposed that Rspo 1 may interact with Wnt signaling pathway to induce differentiation in osteoblasts. Though findings in murine osteoblasts implicate a synergestic role of Rspo 1 with Wnt signaling, still no study has addressed the similar role in more clinically applicable osteoblast models i.e., human cell lines or primary cells. Therefore, in the present study, we investigated the possible role of Rspo 1 during differentiation process of human in vitro osteoblast cell models like primary osteoblasts or human osteoprogenitor cell line hFOB 1.19 along with murine preosteoblast cell line MC3T3 E-1. Our results showed increase in Rspo 1 at transcript level during differentiating phase of human primary osteoblasts and human FOB 1.19 cells. We also found that Rspo 1 (100 ng/mL) acts additively with Wnt3a to activate Wnt signaling, as confirmed by luciferase activity after transfection of TOPFLASH construct to hFOB 1.19 cells. Similar additive role of Rspo 1 and Wnt3a was apparent in alkaline phosphatase (ALP) activity analysis of human primary cells. Moreover, a reduction in ALP activity was observed with knock-down of Rspo 1 by transfected shRNA in hFOB 1.19 cells. These results suggested the possibility of autocrine regulation by Rspo 1 on the osteogenic activities in human in vitro osteoblast models. Furthermore, these results were corroborated in MC3T3-E1, murine osteoblast cell model. Osteoblastic differentiation was induced by transfection of Rspo 1 which was confirmed by increased ALP staining and qRT-PCR analysis of osteogenic markers, such as Runx2 and osteocalcin. In conclusion, present study highlights the role of Rspo 1 in bone remodeling where it activates Wnt signaling to induce differentiation, as shown in human as well murine in vitro osteoblast cell models.

Evaluation of Renal Function in Obstructed Ureter Model Using 99mTc-DMSA.

BACKGROUND/AIM: Urinary obstruction is a condition of impaired urinary drainage, which may result in progressive renal deterioration. This study applied 99mTc-labeled dimercaptosuccinic acid (99mTc-DMSA) renal scintigraphy to a rabbit model of right ureter obstruction and evaluated its utility in studying obstructive renal diseases. MATERIALS AND METHODS: Complete unilateral ureter obstruction in rabbits was generated by complete ligation of the right ureter. Renal function was investigated during a 4-week post-obstruction period by obtaining planar images of 99mTc-DMSA activity following ear vein injection. Renal blood perfusion was evaluated by non-invasive scintigraphy in conjunction with parallel histological and hematological examinations. RESULTS: Renal perfusion was remarkably and rapidly reduced in the ureter-obstructed kidneys. During the experimental period, the size of left kidney appeared normal in the scintigraphic images, but the ureter-obstructed right kidney progressively became larger. Histopathological examination showed flattening and atrophy of tubules, enlargement of interstitial areas, accumulation of extracellular martices and infiltration of inflammatory cells in the obstreucted kidney. CONCLUSION: 99mTc-DMSA scintigraphy is a sensitive, non-invasive method to assess renal function in unilateral kidney diseases.

Efficient decomposition methods for controlled-R n using a single ancillary qubit.

We consider decomposition for a controlled-R n gate with a standard set of universal gates. For this problem, a method exists that uses a single ancillary qubit to reduce the number of gates. In this work, we extend this method to three ends. First, we find a method that can decompose into fewer gates than the best known results in decomposition of controlled-R n . We also confirm that the proposed method reduces the total number of gates of the quantum Fourier transform. Second, we propose another efficient decomposition that can be mapped to a nearest-neighbor architecture with only local CNOT gates. Finally, we find a method that can minimize the depth to 5 gate steps in a nearest-neighbor architecture with only local CNOT gates.

The effect of TNFα secreted from macrophages activated by titanium particles on osteogenic activity regulated by WNT/BMP signaling in osteoprogenitor cells.

Wear particles are the major cause of osteolysis associated with failure of implant following total joint replacement. During this pathologic process, activated macrophages mediate inflammatory responses to increase osteoclastogenesis, leading to enhanced bone resorption. In osteolysis caused by wear particles, osteoprogenitors present along with macrophages at the implant interface may play significant roles in bone regeneration and implant osteointegration. Although the direct effects of wear particles on osteoblasts have been addressed recently, the role of activated macrophages in regulation of osteogenic activity of osteoblasts has scarcely been studied. In the present study, we examined the molecular communication between macrophages and osteoprogenitor cells that may explain the effect of wear particles on impaired bone forming activity in inflammatory bone diseases. It has been demonstrated that conditioned medium of macrophages challenged with titanium particles (Ti CM) suppresses early and late differentiation markers of osteoprogenitors, including alkaline phosphatase (ALP) activity, collagen synthesis, matrix mineralization and expression of osteocalcin and Runx2. Moreover, bone forming signals such as WNT and BMP signaling pathways were inhibited by Ti CM. Interestingly, TNFα was identified as a predominant factor in Ti CM to suppress osteogenic activity as well as WNT and BMP signaling activity. Furthermore, Ti CM or TNFα induces the expression of sclerostin (SOST) which is able to inhibit WNT and BMP signaling pathways. It was determined that over-expression of SOST suppressed ALP activity, whereas the inhibition of SOST by siRNA partially restored the effect of Ti CM on ALP activity. This study highlights the role of activated macrophages in regulation of impaired osteogenic activity seen in inflammatory conditions and provides a potential mechanism for autocrine regulation of WNT and BMP signaling mediated by TNFα via induction of SOST in osteprogenitor cells.

A winged-helix transcription factor foxg1 induces expression of mss4 gene in rat hippocampal progenitor cells.

Foxg1 (previously named BF1) is a winged-helix transcription factor with restricted expression pattern in the telencephalic neuroepithelium of the neural tube and in the anterior half of the developing optic vesicle. Previous studies have shown that the targeted disruption of the Foxg1 gene leads to hypoplasia of the cerebral hemispheres with severe defect in the structures of the ventral telencephalon. To further investigate the molecular mechanisms by which Foxg1 plays essential roles during brain development, we have adopted a strategy to isolate genes whose expression changes immediately after introduction of Foxg1 in cultured neural precursor cell line, HiB5. Here, we report that seventeen genes were isolated by ordered differential displays that are up-regulated by over-expression of Foxg1, in cultured neuronal precursor cells. By nucleotide sequence comparison to known genes in the GeneBank database, we find that nine of these clones represent novel genes whose DNA sequences have not been reported. The results suggest that these genes are closely related to developmental regulation of Foxg1.