Publications by authors named "Gaolei Hu"

The hybrid integration of two-dimensional (2D) materials on various photonic integration platforms has attracted widespread research interest because of the new functionalities enabled by the 2D materials for applications in photodetection, optical modulation and nonlinear optical signal processing. Tellurium is known to have high mobility, and quasi-2D tellurium is stable in air and has a small bandgap that may make it suitable for platform-independent scalable integration of high-performance photodetectors in the infrared band. In this work, we propose and implement a new structure for integrating tellurium with silicon nitride (SiN) waveguides, adding photodetector capability to an otherwise passive waveguide platform.

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Energy-time (E-T) entanglement is widely employed in long-distance quantum entanglement distribution due to its strong robustness against transmission fluctuations. In this Letter, we report what we believe to be the first silicon monolithically integrated E-T entanglement system, which integrates the photon sources, wavelength demultiplexers, and Franson interferometers on a single chip. Also, by utilizing low-loss multimode waveguides in Franson interferometers, we measured an on-chip quantum interference visibility of 99.

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Integrated spectrometers offer the advantages of small sizes and high portability, enabling new applications in industrial development and scientific research. Integrated Fourier-transform spectrometers (FTS) have the potential to realize a high signal-to-noise ratio but typically have a trade-off between the resolution and bandwidth. Here, we propose and demonstrate the concept of the two-dimensional FTS (2D-FTS) to circumvent the trade-off and improve scalability.

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Atherosclerosis (AS) is a serious cardiovascular disease. One of its hallmarks is hyperlipidemia. Inhibiting the formation of macrophage foam cells is critical for alleviating AS.

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We propose and validate a new, to the best of our knowledge, approach to designing a polarization-independent waveguide grating coupler, using an optimized polysilicon overlay on a silicon grating structure. Simulations predicted coupling efficiencies of about -3.6 dB and -3.

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The chip-scale integration of optical spectrometers may offer new opportunities for in situ bio-chemical analysis, remote sensing, and intelligent health care. The miniaturization of integrated spectrometers faces the challenge of an inherent trade-off between spectral resolutions and working bandwidths. Typically, a high resolution requires long optical paths, which in turn reduces the free-spectral range (FSR).

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In this Letter, we propose and demonstrate an integrated mode-size converter (MSC) with a compact footprint, low losses, and a broad bandwidth. By exploiting a parabolic mirror, the divergent light from a narrow waveguide (450 nm) is collimated to match the mode size of a wide waveguide (10 µm). The measured insertion loss (IL) is ≈ 0.

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Our previous studies show that the mitotic phosphorylation of SUMO-specific protease 3 (SENP3) can inhibit its de-SUMOylation activity in G2/M phase of the cell cycle. Inhibition of SENP3 plays a critical role in the correct separation of sister chromatids in mitosis. The mutation of mitotic SENP3 phosphorylation causes chromosome instability and promotes tumorigenesis.

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The metabolic program is altered during macrophage activation and influences macrophage polarization. Glutaminolysis promotes accumulation of α-ketoglutarate (αKG), leading to Jumonji domain-containing protein D3 (Jmjd3)-dependent demethylation at H3K27me3 during M2 polarization of macrophages. However, it remains unclear how αKG accumulation is regulated during M2 polarization of macrophages.

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Metabolic programming and mitochondrial dynamics along with T cell differentiation affect T cell fate and memory development; however, how to control metabolic reprogramming and mitochondrial dynamics in T cell memory development is unclear. Here, we provide evidence that the SUMO protease SENP1 promotes T cell memory development via Sirt3 deSUMOylation. SENP1-Sirt3 signalling augments the deacetylase activity of Sirt3, promoting both OXPHOS and mitochondrial fusion.

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In cancers, apoptosis evasion through dysregulation of pro-apoptotic and anti-apoptotic intracellular signals is a recurring event. Accordingly, selective inhibition of specific proteins represents an exciting therapeutic opportunity. Myeloid cell leukemia 1 (MCL1) is an anti-apoptotic protein of the BCL-2 family, which is overexpressed in many cancers.

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In response to DNA damage, p53-mediated signaling is regulated by protein phosphorylation and ubiquitination to precisely control G2 checkpoint. Here we demonstrated that protein SUMOylation also engaged in regulation of p53-mediated G2 checkpoint. We found that G2 DNA damage suppressed SENP3 phosphorylation at G2/M phases in p53-dependent manner.

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Background: EHBP1 rs721048(A) was first identified as a prostate cancer (PCa) risk in Caucasians by genome-wide association study, but subsequent replication studies involving Caucasian and other ethnicities did not produce consistent results. The aim of this study was to obtain a more definite association between rs721048(A) and PCa risk.

Methods: We comprehensively searched several databases updated to September 2014, including PubMed, Web of Science, EBSCO, and Google Scholar.

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We attempted to systematically elucidate the association between monocyte chemoattractant protein-1 (MCP-1) -2518A>G polymorphism and risk of coronary artery disease (CAD). Eligible studies were identified through PubMed, EBSCO, and Web of Science Databases. The magnitude of MCP-1 polymorphism effect and its possible mode of action on CAD were estimated.

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Estrogen receptors (ERs) are critical regulators of breast cancer development. Identification of molecules that regulate the function of ERs may facilitate the development of more effective breast cancer treatment strategies. In this study, we showed that the forkhead transcription factor FOXK2 interacted with ERα, and inhibited ERα-regulated transcriptional activities by enhancing the ubiquitin-mediated degradation of ERα.

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