We demonstrate robust soliton crystals generation with a fixed frequency pump laser through a thermoelectric-cooler-based thermal-tuning approach in a butterfly-packaged complementary-metal-oxide-semiconductor-compatible microresonator. Varieties of soliton crystal states, exhibiting "palm-like" optical spectra that result from the strong interactions between the dense soliton ensembles and reflect their temporal distribution directly, are experimentally observed by sweeping one cavity resonance across the pump frequency from the blue-detuned side by reducing the operating temperature of the resonator. Benefitting from the tiny intra-cavity energy change, repeatable interconversion between the chaotic modulation instability and stable soliton crystal states can be successfully achieved via simple tuning of the temperature or pump power, showing the easy accessibility and excellent stability of such soliton crystals. This work could facilitate microresonator-based optical frequency combs towards a portable, adjustable, and low-cost system while avoiding the requirements of delicate frequency-sweeping pump techniques.

We report a method to monitor and control laser frequencies with an optical cavity and a digital feedback system. A frequency-stabilized He-Ne laser provides the reference that is transferred to several other lasers using a scanning Fabry-Pérot cavity. A personal computer-based multifunction data acquisition system generates the scan wave form, and reads the detector outputs synchronously with the cavity scan. The computer determines the positions of all of the peaks in the scan, and generates output signals to control the laser frequencies. It also provides a visual display of cavity spectra. We have successfully used the setup to achieve a long-term lock of the lasers for magneto-optical trapping of radioactive francium atoms.

SPHK1 (sphingosine kinase 1), a regulator of sphingolipid metabolites, plays a causal role in the development of hepatocellular carcinoma (HCC) through augmenting HCC invasion and metastasis. However, the mechanism by which SPHK1 signaling promotes invasion and metastasis in HCC remains to be clarified. Here, we reported that SPHK1 induced the epithelial-mesenchymal transition (EMT) by accelerating CDH1/E-cadherin lysosomal degradation and facilitating the invasion and metastasis of HepG2 cells. Initially, we found that SPHK1 promoted cell migration and invasion and induced the EMT process through decreasing the expression of CDH1, which is an epithelial marker. Furthermore, SPHK1 accelerated the lysosomal degradation of CDH1 to induce EMT, which depended on TRAF2 (TNF receptor associated factor 2)-mediated macroautophagy/autophagy activation. In addition, the inhibition of autophagy recovered CDH1 expression and reduced cell migration and invasion through delaying the degradation of CDH1 in SPHK1-overexpressing cells. Moreover, the overexpression of SPHK1 produced intracellular sphingosine-1-phosphate (S1P). In response to S1P stimulation, TRAF2 bound to BECN1/Beclin 1 and catalyzed the lysine 63-linked ubiquitination of BECN1 for triggering autophagy. The deletion of the RING domain of TRAF2 inhibited autophagy and the interaction of BECN1 and TRAF2. Our findings define a novel mechanism responsible for the regulation of the EMT via SPHK1-TRAF2-BECN1-CDH1 signal cascades in HCC cells. Our work indicates that the blockage of SPHK1 activity to attenuate autophagy may be a promising strategy for the prevention and treatment of HCC.

We report on a long-cavity passively mode-locked fiber laser in the anomalous dispersion regime. The nonlinear polarization rotation technique is employed to achieve mode locking. The output pulse from the fiber laser has a rectangular shape and a corresponding gaussian-shape spectral profile. Stable mode-locked pulses at a repetition rate of 278 kHz with single pulse energy as high as 715 nJ are obtained under equal bidirectional pumping power of 500 mW in cavity. The experimental results demonstrate that the passively mode-locked fiber laser operating in the anomalous regime can also realize a high-energy pulse, which is different from the conventional low-energy soliton pulse.

Background: EpCAM or CD133 has been used as the tumor initiating cells (TICs) marker in hepatocellular carcinoma (HCC). We investigated whether cells expressing with both EpCAM and CD133 surface marker were more representative for TICs in hepatocellular carcinoma Huh7 cells.Methods: Four different phenotypes of CD133+EpCAM+, CD133+EpCAM-, CD133-EpCAM+ and CD133-EpCAM- in Huh7 cells were sorted by flow cytometry. Then cell differentiation, self-renewal, drug-resistance, spheroid formation and the levels of stem cell-related genes were detected to compare the characteristics of TICs. The ability of tumorigenicity was measured in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice to verify TICs.Results: CD133+EpCAM+ cells have many characteristics of TICs in Huh7 cells compared with CD133+EpCAM-, CD133-EpCAM+, CD133-EpCAM- cells, including enrichment in side population cells, higher differentiation capacity, increased colony-formation ability, preferential expression of stem cell-related genes, appearance of drug-resistant to some chemotherapeutics, more spheroid formation of culture cells and stronger tumorigenicity in NOD/SCID mice.Conclusion: CD133+EpCAM+ phenotype is precisely represented TICs in Huh7 cells. It might be useful for studying biology mechanism of TICs in hepatocellular carcinoma and screening new targets for cancer therapy.

Ras-GTPase-activating protein SH3 domain-binding proteins (G3BP) are overexpressed in various human tumors and participate in several signaling pathways involved in growth, differentiation and apoptosis. G3BP interact with RasGAP (Ras-GTPase activating protein) only in growing cells and depend on Ras activation, and participate in the Ras signal pathway. Therefore, the blockage and downregulation of G3BP may be a new strategy for cancer therapy. In this report, we demonstrate that a novel peptide GAP161 blocked the functions of G3BP and markedly suppressed HCT116 cell growth through the induction of apoptosis. The peptide bound with G3BP, which interfered with the interaction of G3BP1 with RasGAP and further suppressed Ras signaling pathways. GAP161 downregulated G3BP1 and G3BP2 proteins. Similarly, the knockdown of G3BP substantially decreased the proliferation of HCT116 cells and inhibited Ras signal pathways. Furthermore, the downregulation of G3BP could enhance cisplatin-induced apoptosis and growth inhibition of HCT116 cells. We also found that GAP161 suppressed the growth of BALB/c mice bearing colon CT26 tumors and nude mice bearing HCT116 xenografts. These results suggest that downregulation of G3BP might be useful in cancer therapy and that GAP161 is a promising new therapeutic agent for cancers. (Cancer Sci 2012; 103: 1848-1856 T he G3BP protein family contains G3BP1 and G3BP2, with similar molecular structures. Both proteins are dramatically overexpressed in human cancers, especially in breast, head and neck, colon and lung.(1-3) G3BP are involved in a variety of growth-related signaling pathways that are involved in carcinogenesis and metastasis, (4,5) including NF-jB, Ras signaling and the ubiquitin proteasome system.(1,6-8) The expression level of G3BP1 changes reciprocally to the level of phosphatase and tensin homolog deleted on chromosome ten (PTEN). The negative effect of PTEN expression on the protein level of G3BP1 is recapitulated by direct inhibition of PI3K.(9) G3BP1 and G3BP2 also interact with p53 and MDM2 to modulate their expression and localization.(10) In addition, G3BP1 is an important marker of stress granules (SG). The NTF2-like domain of G3BP1 mediates its recruitment to SG influenced by Ras. (11) Stresses like hypoxia, heat shock and chemotherapy could induce SG formation, and SG could inhibit apoptosis by suppressing stress-responsive MAPK pathways.(12) Taken together, several lines of evidence suggest that the overexpressed G3BP in a wide range of cancers could be a target for anticancer therapy.It is believed that RasGAP, a regulator of Ras and Rho GTPbinding proteins, (13,14) have dual functions: the negative effect of GTPase pathways and downstream signaling transduction using effectors such as Raf-1, PI3K and MAPK.(15) The SH3 domain of RasGAP is contributed to binding of G3BP and is essential for Ras downstream signaling. Two independent groups found that p120-RasGAP was cleaved by caspases, which induced both anti-apoptotic and pro-apoptotic signals, depending on the ex...

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We have theoretically and experimentally investigated the dual-peak feature of tilted fiber gratings with excessively tilted structure (named as Ex-TFGs). We have explained the dual-peak feature by solving eigenvalue equations for TM_0m and TE_0m of a circular waveguide, in which the TE (transverse electric) and TM (transverse magnetic) core modes are coupled into TE and TM cladding modes, respectively. Meanwhile, in the experiment, we have verified that one of the dual peaks at the shorter wavelength is due to the TM mode coupling whereas the other one at the longer wavelength arises from TE mode coupling when a linearly polarized light launched into the Ex-TFG. We have also investigated the peak separation of TE and TM cladding mode for different surrounding medium refractive indexes (SRI), revealed that the dual peaks separation is decreasing as increasing of SRI, which agrees very well with the theoretical analysis results.