Kernel mapping for mitigating nonlinear impairments in optical short-reach communications

Nonlinear impairments induced by the opto-electronic components are one of the fundamental performance-limiting factors in high-speed optical short-reach communications, significantly hindering capacity improvement. This paper proposes to employ a kernel mapping function to map the signals in a Hilbert space to its inner product in a reproducing kernel Hilbert space, which has been successfully demonstrated to mitigate nonlinear impairments in optical short-reach communication systems. The operation principle is derived. An intensity modulation/direct detection system with 1.5-mu m vertical cavity surface emitting laser and 10-km 7-core fiber achieving 540.68-Gbps (net-rate 505.31-Gbps) has been carried out. The experimental results reveal that the kernel mapping based schemes are able to realize comparable transmission performance as the Volterra filtering scheme even with a high order. (C) 2019 Optical Society of America under the terms of the OSA Open Access Publishing Agreemen

Chemokine receptor CXCR3 is important for lung tissue damage and airway remodeling induced by short-term exposure to cigarette smoking in mice

Aim: To investigate the role of chemokine receptor CXCR3 in cigarette smoking (CS)-induced pulmonary damage. Methods: CXCR3 knockout (CXCR3-/-) mice were used. Differences in airspace enlargement, mRNA expression of matrix metalloproteinases (MMPs), transforming growth factor (TGF) β1, CXCL10 in lung homogenates, and CXCL10 content in bronchoalveolar lavage (BAL) fluids and homogenates were compared between CXCR3-/- mice and wild-type (WT) mice three days after three-day CS exposures. Results: The linear intercept was significantly less in CXCR3-/- mice than in WT mice (30.1±0.9 μm vs 40.3±2.4 μm, P<0.01). Morphologically, collagen was deposited less around airways and vessels in CXCR3-/- mice. The lung hydroxyproline content was significantly lower in CXCR3-/- mice than in WT mice (6.0±1.0 μg/mL vs 12.0±1.6 μg/mL, P<0.05). Profoundly lower mRNA expression of MMP2, MMP12, TGFβ1, and CXCL10 was seen in lung homogenates from CXCR3-/- mice. CXCL10 concentrations in BAL fluid and lung homogenates were significantly lower in CXCR3-/- mice than in WT mice (BAL fluid: 19.3±1.4 pg/mL vs 24.8±1.6 pg/mL, P<0.05; lung homogenates: 76.6±7.0 pg/mL vs 119.5±15.9 pg/mL, P<0.05). Conclusion: CXCR3 is important in mediating lung tissue damage and airway remodeling following a short-term CS insult, possibly through up-regulation of CXCL10 and inducement of mRNA expression of MMPs. Targeting CXCR3 may be helpful for prevention of CS-induced pulmonary pathology

Splice variant of growth hormone-releasing hormone receptor drives esophageal squamous cell carcinoma conferring a therapeutic target

The extrahypothalamic growth hormone-releasing hormone (GHRH) and its cognate receptors (GHRH-Rs) and splice variants are expressed in a variety of cancers. It has been shown that the pituitary type of GHRH-R (pGHRH-R) mediates the inhibition of tumor growth induced by GHRH-R antagonists. However, GHRH-R antagonists can also suppress some cancers that do not express pGHRH-R, yet the underlying mechanisms have not been determined. Here, using human esophageal squamous cell carcinoma (ESCC) as a model, we were able to reveal that SV1, a known splice variant of GHRH-R, is responsible for the inhibition induced by GHRH-R antagonist MIA-602. We demonstrated that GHRH-R splice variant 1 (SV1) is a hypoxia-driven promoter of tumor progression. Hypoxia-elevated SV1 activates a key glycolytic enzyme, muscle-type phosphofructokinase (PFKM), through the nuclear factor kappa B (NF-κB) pathway, which enhances glycolytic metabolism and promotes progression of ESCC. The malignant actions induced by the SV1-NF-κB-PFKM pathway could be reversed by MIA-602. Altogether, our studies demonstrate a mechanism by which GHRH-R antagonists target SV1. Our findings suggest that SV1 is a hypoxia-induced oncogenic promoter which can be an alternative target of GHRH-R antagonists

Experimental Demonstration of 503.61-Gbit/s DMT over 10-km 7-Core Fiber with 1.5-\mu m SM-VCSEL for Optical Interconnects

We experimentally demonstrate a net-rate 503.61-Gbit/s discrete multitone (DMT) transmission over 10-km 7-core fiber with 1.5-\mu m single mode VCSEL, where low-complexity kernelrecursive-least-squares algorithm is employed for nonlinear channel equalization.Comment: 3 pages, 44th European Conference on Optical Communication (ECOC 2018), Rome, Italy, 201