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We numerically and experimentally demonstrate efficient light couplers between topological slow light waveguides in valley photonic crystals (VPhCs) and wire waveguides. By numerical simulations, we obtained a high coupling efficiency of -0.84 dB/coupler on average in the slow light regime of a group index n g  = 10 - 30. Experimentally, we fabricated the couplers in a Si slab and measured the transmitted power of the devices. We realized a high coupling efficiency of approximately -1.2 dB/coupler in the slow light region of n g  = 10 - 30, which is close to the result from the numerical simulations. These demonstrations will lay the groundwork for low-loss photonic integrated circuits using topological slow light waveguides.

We experimentally demonstrate topological slow light waveguides in valley photonic crystals (VPhCs). We employed a bearded interface formed between two topologically-distinct VPhCs patterned in an air-bridged silicon slab. The interface supports both topological and non-topological slow light modes below the light line. By means of optical microscopy, we observed light propagation in the topological mode in the slow light regime with a group index n g over 30. Furthermore, we confirmed light transmission via the slow light mode even under the presence of sharp waveguide bends. In comparison between the topological and non-topological modes, we found that the topological mode exhibits much more efficient waveguiding than the trivial one, demonstrating topological protection in the slow light regime. This work paves the way for exploring topological slow-light devices compatible with existing photonics technologies.

Valley photonic crystals (VPhCs) are an attractive platform for the implementation of topologically protected optical waveguides in photonic integrated circuits (PICs). The realization of slow light modes in the topological waveguides may lead to further miniaturization and functionalization of the PICs. In this Letter, we report an approach to realize topological slow light waveguides in semiconductor-slab-based VPhCs. We show that a bearded interface of two topologically distinct VPhCs can support topological kink modes with large group indices over 100 within the topological bandgap. We numerically demonstrate robust light propagation in the topological slow light waveguide with large group indices of ∼60, even under the presence of sharp bends. Our work opens a novel route to implement topological slow light waveguides in a way compatible with current PIC technology.

Objectives: To confirm the relationship between sleep bruxism (SB) and autonomic nervous (AN) activities to elucidate SB physiology., Methods: Subjects included 11 healthy males (mean age, 24.7 ± 2.3 years). These data were recorded in the sleep laboratory using a system composed of a two-axis accelerometer, an infrared camera, electroencephalography, electromyography, and electrocardiography. Time lapse analysis confirmed correlations between AN activity and SB events during sleep in subjects. Relationships between SB strength and length and AN activity were evaluated., Results: Sympathetic nerve (SN) and parasympathetic nerve (PSN) activities occurred significantly in 93.3% of cases (p < 0.01), with similar predictable patterns during SB. Furthermore, SB length and SN activity in seven of the subjects (four subjects, p < 0.05; three subjects p < 0.01), and PSN and SB muscle activities (% maximum voluntary contraction) in five subjects (four subjects, p < 0.05; one subject, p < 0.01) were significantly correlated., Discussion: The authors believe that SB is closely related to SN as well as PSN activities and may control the AN system.

Cancer immunotherapies such as antibodies targeting T cell checkpoints, or adaptive tumor-infiltrating lymphocyte (TIL) transfer, have been developed to boost the endogenous immune response against human malignancies. However, activation of T cells by such antibodies can lead to the risk of autoimmune diseases. Also, the selection of tumor-reactive T cells for TIL relies on information regarding mutated antigens in tumors and does not reflect other factors involved in protein antigenicity. It is therefore essential to engineer therapeutic interventions by which T cell reactivity against tumor cells is selectively enhanced (i.e., "focused cancer immunotherapy") based on tumor antigens that are specifically expressed in the tumor of a certain cancer and in many patients with this cancer. Immune complexes (ICs) are the direct and stable products of immunological recognition by humoral immunity. Here, we searched for tumor-specific IC antigens in each of five cancers (lung (n = 28), colon (n = 20), bladder (n = 20), renal cell (n = 15) and malignant lymphoma (n = 9)), by using immune complexome analysis that comprehensively identifies and profiles the constituent antigens in ICs. This analysis indicated that gelsolin and inter-alpha-trypsin inhibitor heavy chains were specifically and frequently detected (at a frequency higher than 80%), and that phosphoproteins (VENTX, VCIP135) were also specifically present in the ICs of lung cancer patients. Immune complexome analysis successfully identified several tumor-specific IC antigens with high detection frequency in lung cancer patients. These specific antigens are required to validate the clinical benefit by further analysis using a large number of patients., (© 2016 UICC.)

Immune complexes (ICs) are the direct and real-time products of humoral immune responses. The identification of constituent foreign or autoantigens within ICs might bring new insights into the pathology of infectious diseases. We applied immune complexome analysis of plasma to the study of Chagas disease caused by Trypanosoma cruzi. Twenty seropositive plasma samples including cardiac and/or megacolon determinate patients (n = 11) and indeterminate (n = 9) were analysed along with 10 seronegative individuals to characterize the antigens bound to circulating ICs. We identified 39 T. cruzi antigens and 114 human autoantigens specific to patients with Chagas. Among those antigens, two T. cruzi antigens (surface protease GP63, glucose-6-isomerase) and six human autoantigens (CD180 antigen, ceruloplasmin, fibrinogen beta chain, fibrinogen beta chain isoform 2 preprotein, isoform gamma-A of fibrinogen γ-chain, serum paraoxonase) were detected in more than 50% of the patients tested. Human isoform short of complement factor H-related protein 2 and trans-sialidase of T. cruzi were more frequently found in the indeterminate (5/9 for both) compared with in the determinate Chagas (0/11, P = 0·046 for human, 1/11, P = 0·0498 for T. cruzi). The immune complexome could illustrate the difference of immune status between clinical forms of chronic Chagas disease., (© 2016 John Wiley & Sons Ltd.)

Drug resistance often critically limits the efficacy of molecular targeted drugs. Although pharmacological inhibition of phosphatidylinositol 3-kinase (PI3K) is an attractive therapeutic strategy for cancer therapy, molecular determinants for efficacy of PI3K inhibitors (PI3Kis) remain unclear. We previously identified that overexpression of insulin-like growth factor 1 receptor (IGF1R) contributed to the development of drug resistance after long-term exposure to PI3Kis. In this study, we examined the involvement of basal IGF1R expression in intrinsic resistance of drug-naïve cancer cells to PI3Kis and whether inhibition of IGF1R overcomes the resistance. We found that cancer cells highly expressing IGF1R showed resistance to dephosphorylation of Akt and subsequent antitumor effect by ZSTK474 treatment. Knockdown of IGF1R by siRNAs facilitated the dephosphorylation and enhanced the drug efficacy. These cells expressed tyrosine-phosphorylated insulin receptor substrate 1 at high levels, which was dependent on basal IGF1R expression. In these cells, the efficacy of ZSTK474 in vitro and in vivo was improved by its combination with the IGF1R inhibitor OSI-906. Finally, we found a significant correlation between the basal expression level of IGF1R and the inefficacy of ZSTK474 in an in vivo human cancer panel, as well as in vitro. These results suggest that basal IGF1R expression affects intrinsic resistance of cancer cells to ZSTK474, and IGF1R is a promising target to improve the therapeutic efficacy. The current results provide evidence of combination therapy of PI3Kis with IGF1R inhibitors for treating IGF1R-positive human cancers., (© 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.)