Purpose:To implement a magnetic resonance (MR) imaging protocol to measure intracranial atherosclerotic disease (ICAD) in a population-based multicenter study and report examination and reader reliability of these MR imaging measurements and descriptive statistics representative of the general population. Materials and Methods:This prospective study was approved by the institutional review boards and compliant with HIPAA. Conclusion:Vessel wall MR imaging is a reliable tool for identifying and measuring ICAD and provided insight into ICAD distribution across a U.S. community-based population.q RSNA, 2016

Surface plasmon resonance (SPR), a promising technology, is beneficial for various applications, such as photothermal conversion, solar cells, photocatalysts, and sensing. However, the SPR performance may be restricted by the 1D-or 2D-distributed hotspots. The bicontinuous interconnected gyroidstructured materials have emerged in light energy conversion due to a high density of 3D-distributed hotspots, ultrahigh light− matter interactions and large scattering cross-section. Here, a series of bioinspired Au−CuS gyroid-structured materials are fabricated by precisely controlling the deposition time of CuS nanoparticles (NPs) and then adopted for solar steam generation. Specifically, Au−CuS/GMs-80 present the highest evaporation efficiency of 88.8% under normal 1 sun, with a suitable filling rate (57%) and a large inner surface area (∼2.72 × 10 5 nm 2 per unit cell), which simultaneously achieves a dynamic balance between water absorption and evaporation as well as efficient heat conduction with water in nanochannels. Compared with other state-of-the-art devices, Au−CuS/GMs-80 steam generator requires a much lower photothermal component loading (<1 mg cm −2 ) and still guarantees outstanding evaporation performance. This superior evaporation performance is attributed to broadband light absorption, continuous water supply, excellent heat generation and thermal insulation, and good light−heat−water interaction. The combination of 3D interconnected nanostructures with controllable metal− semiconductor deposition could provide a new method for the future design of high-performance plasmonic devices.

Cancer progression requires a permissive microenvironment that shields cancer from the host immunosurveillance. The presence of myeloid-derived suppressor cells (MDSC) is a key feature of a tumor-permissive microenvironment. Cullin 4B (CUL4B), a scaffold protein in the Cullin 4B-RING E3 ligase complex (CRL4B), represses tumor suppressors through diverse epigenetic mechanisms and is overexpressed in many malignancies. We report here that CUL4B unexpectedly functions as a negative regulator of MDSC functions in multiple tumor settings. Conditional ablation of CUL4B in the hematopoietic system, driven by Tek-Cre, resulted in significantly enhanced accumulation and activity of MDSCs. Mechanistically, we demonstrate that the aberrant abundance of MDSCs in the absence of CUL4B was mediated by the downregulation of the AKT/b-catenin pathway. Moreover, CUL4B repressed the phosphatases PP2A and PHLPP1/2 that dephosphorylate and inactivate AKT to sustain pathway activation. Importantly, the CUL4B/AKT/b-catenin axis was downregulated in MDSCs of healthy individuals and was further suppressed in tumor-bearing mice and cancer patients. Thus, our findings point to a proand antitumorigenic role for CUL4B in malignancy, in which its ability to impede the formation of a tumor-supportive microenvironment may be context-specific. Cancer Res; 75(23); 5070-83.Ó2015 AACR.

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ObjectivesAutophagy plays various roles in non-small-cell lung cancer (NSCLC). MCOLN1, a reactive oxygen species sensor, can regulate autophagy via lysosomal Ca(2+); however, the role of MCOLN1 in NSCLC is largely unknown. This study aimed to explore the effects of MCOLN1 on proliferation, invasion and migration in NSCLC and the underling mechanisms.Materials and methodsThe tissues of NSCLC patients were collected, then MCOLN1 expression in tumor and adjacent tissues was measured and its relationship with pathological staging was analyzed. The Cell Counting Kit-8 (CCK-8) assay, wound healing assay and transwell migration assay were used to evaluate the proliferation, migration and invasion ability, respectively. Live-cell imaging and transmission electron microscopy (TEM) were used to observe autophagic flux and autolysosomes.ResultsIt was found that MCOLN1 expression was significantly decreased in human NSCLC tissues compared with normal lung tissues while more MCOLN1 in stage III–IV was shown than stage I–II, indicating that MCOLN1 increased along with the progression of NSCLC. Furthermore, CCK-8 assay, wound healing assay and transwell migration assay confirmed that the inhibition of MCOLN1 suppressed NSCLC cells proliferation migration and invasion. Overexpression of MCOLN1 promoted autophagy in A549 and H1299 cells with increased LC3-II/I, lamp1 expression and autolysosomes as well as autophagic flux shown by live-cell imaging and TEM.ConclusionOur study shows that downregulated MCOLN1 reduced lysosome-autophagy activity contributing to inhibited tumor progression, which reveals a novel role of MCOLN1 in NSCLC, and targeting MCOLN1 may be a therapeutic potential for NSCLC.