Real-time 400 Gbps/carrier WDM transmission over 2,000†km of field-installed G.654.E fiber.

We combine erbium-doped fiber amplifier (EDFA) and backward distributed Raman amplifier (DRA) to achieve the real-time wavelength division multiplexing (WDM) transmission of 400 Gbps/carrier polarization division multiplexing (PDM) 16 quadrature amplitude modulation (QAM) signals over 2,000 km of terrestrial field-deployed cut-off shifted fiber (CSF) compliant with ITU-T G.654.E. This paper compares the transmission performance of 400 Gbps/carrier signals achieved in CSF and standard single-mode fiber (SMF). This transmission distance, 2,019 km, is, to the best of our knowledge, the longest in 400 Gbps/carrier WDM transmission field experiments using digital signal processing (DSP) application specific integrated circuit (ASIC) integrated real-time optical transponders with the technologies to compensate device imperfections; the backward DRA used is fully compliant with laser power safety requirements.

Proposal and experimental demonstration of SDM node enabling path assignment to arbitrary wavelengths, cores, and directions.

We propose a novel simple space division multiplexing (SDM) node which is rearrangeble nonblocking, and effectively utilizes enhanced network resources through SDM. The proposed node can reduce a number of ports of wavelength selective switches (WSSs) and a number of WSS modules by modifying conventional multi-stage switches and employing integrated multiple arrayed WSSs. We experimentally actualized the newly proposed node, and demonstrate wavelength, core, and direction switching functions based on 127-Gbps Dual Polarization Quadrature Phase Shift Keying (DP-QPSK) signals. We also confirm the feasibility of the proposed SDM node through SDM transmission experiments using a 40-km multicore fiber and a multicore amplifier.

Tumor endothelial cell-specific drug delivery system using apelin-conjugated liposomes.

BACKGROUND: A drug delivery system specifically targeting endothelial cells (ECs) in tumors is required to prevent normal blood vessels from being damaged by angiogenesis inhibitors. The purpose of this study was to investigate whether apelin, a ligand for APJ expressed in ECs when angiogenesis is taking place, can be used for targeting drug delivery to ECs in tumors. METHODS AND RESULTS: Uptake of apelin via APJ stably expressed in NIH-3T3 cells was investigated using TAMRA (fluorescent probe)-conjugated apelin. Both long and short forms of apelin (apelin 36 and apelin 13) were taken up, the latter more effectively. To improve efficacy of apelin- liposome conjugates, we introduced cysteine, with its sulfhydryl group, to the C terminus of apelin 13, resulting in the generation of apelin 14. In turn, apelin 14 was conjugated to rhodamine-encapsulating liposomes and administered to tumor-bearing mice. In the tumor microenvironment, we confirmed that liposomes were incorporated into the cytoplasm of ECs. In contrast, apelin non-conjugated liposomes were rarely found in the cytoplasm of ECs. Moreover, non-specific uptake of apelin-conjugated liposomes was rarely detected in other normal organs. CONCLUSIONS: ECs in normal organs express little APJ; however, upon hypoxic stimulation, such as in tumors, ECs start to express APJ. The present study suggests that apelin could represent a suitable tool to effectively deliver drugs specifically to ECs within tumors.

Changes in blood vessel maturation in the fibrous cap of the tumor rim.

It is widely accepted that blood vessels in the tumor microenvironment are immature because mural cell (MC) adhesion to endothelial cells (ECs) is broadly lacking. Hyperpermeability of the tumor vasculature then results in interstitial hypertension that mitigates against penetration of anticancer drugs into the depths of the tumor. It has been suggested that treatment with angiogenesis inhibitors normalizes blood vessels, resulting in restoration of normal permeability and improved drug delivery. However, recent reports suggest that cancer cell invasion is induced from the edge of the tumor into peripheral areas after treatment with angiogenesis inhibitors. Therefore, it is important to assess the status of blood vessels in the fibrous cap at the tumor rim after antiangiogenesis therapy. In the present study, we found that mature blood vessels in which ECs are covered with MCs are present in the fibrous cap. After treatment with angiogenesis inhibitors, immature blood vessels were destroyed and vascular function was significantly improved, but maturing blood vessels in which ECs were covered with MCs remained visible. These maturing blood vessels showed a less dilated character after treatment with the angiogenesis inhibitors. It is widely accepted that well-matured blood vessels are sheathed in extracellular matrix (ECM) and that cancer cells migrate along tracks made of ECM collagen fibers. Therefore, our data indicate the importance of destroying maturing blood vessels outside the tumor parenchyma to prevent cancer cell invasion.