Depth Restoration in Under-Display Time-of-Flight Imaging

Under-display imaging has recently received considerable attention in both academia and industry. As a variation of this technique, under-display ToF (UD-ToF) cameras enable depth sensing for full-screen devices. However, it also brings problems of image blurring, signal-to-noise ratio and ranging accuracy reduction. To address these issues, we propose a cascaded deep network to improve the quality of UD-ToF depth maps. The network comprises two subnets, with the first using a complex-valued network in raw domain to perform denoising, deblurring and raw measurements enhancement jointly, while the second refining depth maps in depth domain based on the proposed multi-scale depth enhancement block (MSDEB). To enable training, we establish a data acquisition device and construct a real UD-ToF dataset by collecting real paired ToF raw data. Besides, we also build a large-scale synthetic UD-ToF dataset through noise analysis. The quantitative and qualitative evaluation results on public datasets and ours demonstrate that the presented network outperforms state-of-the-art algorithms and can further promote full-screen devices in practical applications

An overview of dealloyed nanoporous gold in bioelectrochemistry

peer-reviewedNanoporous gold (NPG) obtained via dealloying of Au alloys has potential applications in a range of fields, and in particular in bioelectrochemistry. NPG possesses a three dimensional bicontinuous network of interconnected pores with typical pore diameters of ca. 30-40 nm, features that are useful for the immobilisation of enzymes. This review describes the common routes of fabrication and characterization of NPG, the use of NPG as a support for oxidoreductases for applications in biosensors and biofuel cells together with recent progress in the use of NPG electrodes for applications in bioelectrochemistry

Cost-effectiveness analysis of aspirin for primary prevention of cardiovascular events among patients with type 2 diabetes in China.

The use of aspirin for primary prevention of cardiovascular disease (CVD) in patients with diabetes mellitus (DM) is associated with lower rates of cardiovascular events but increased risks of bleeding complications. We aimed to examine the cost-effectiveness of aspirin therapy for primary prevention of CVD in Chinese DM patients. A life-long Markov model was developed to compare aspirin therapy (100mg daily) versus no use of aspirin in DM patients with no history of CVD. Model validation was conducted by comparing the simulated event rates with data reported in a clinical trial. Direct medical costs and quality-adjusted life-years gained (QALYs) were the primary outcomes from the perspective of healthcare system in China. Sensitivity analyses were performed to examine the uncertainty of model inputs. Base-case analysis showed aspirin therapy was more costly (USD1,086 versus USD819) with higher QALYs gained (11.94 versus 11.86 QALYs) compared to no use of aspirin. The base-case results were sensitive to the odds ratio of all-cause death in aspirin therapy versus no use of aspirin. Probabilistic sensitivity analysis found that aspirin therapy gained an additional 0.066 QALYs (95% CI: -0.167 QALYs-0.286 QALYs) at higher cost by USD352 (95% CI: USD130-644)). Using 30,000 USD/QALY as willingness-to-pay threshold, aspirin therapy and no use of aspirin were the preferred option in 68.71% and 31.29% of 10,000 Monte Carlo simulations, respectively. In conclusion, aspirin therapy appears to be cost-effective compared with no use of aspirin in primary prevention of CVD in Chinese DM patients

CD317 maintains proteostasis and cell survival in response to proteasome inhibitors by targeting calnexin for RACK1-mediated autophagic degradation

Abstract Unbalanced protein homeostasis (proteostasis) networks are frequently linked to tumorigenesis, making cancer cells more susceptible to treatments that target proteostasis regulators. Proteasome inhibition is the first licensed proteostasis-targeting therapeutic strategy, and has been proven effective in hematological malignancy patients. However, drug resistance almost inevitably develops, pressing for a better understanding of the mechanisms that preserve proteostasis in tumor cells. Here we report that CD317, a tumor-targeting antigen with a unique topology, was upregulated in hematological malignancies and preserved proteostasis and cell viability in response to proteasome inhibitors (PIs). Knocking down CD317 lowered Ca2+ levels in the endoplasmic reticulum (ER), promoting PIs-induced proteostasis failure and cell death. Mechanistically, CD317 interacted with calnexin (CNX), an ER chaperone protein that limits calcium refilling via the Ca2+ pump SERCA, thereby subjecting CNX to RACK1-mediated autophagic degradation. As a result, CD317 decreased the level of CNX protein, coordinating Ca2+ uptake and thus favoring protein folding and quality control in the ER lumen. Our findings reveal a previously unrecognized role of CD317 in proteostasis control and imply that CD317 could be a promising target for resolving PIs resistance in the clinic

CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a

Background/Aims: CircRNAs regulate gene expression in different malignancies. However, the role of Cdr1as in the tumourigenesis of bladder cancer and its potential mechanisms remain unknown. Methods: qRT-PCR was used to detect Cdr1as and target miRNA expression in bladder cancer tissues and cell lines. Biological functional experiments were performed to detect the effects of Cdr1as on the biological behaviour of bladder cancer cells in vivo and in vitro. Bioinformatic analysis was utilised to predict potential miRNA target sites on Cdr1as. Ago2 RNA binding protein immunoprecipitation assay, RNA antisense purification assay, biotin pull down assay and RNA FISH were performed to detect the interaction between Cdr1as and target miRNAs. Western blot was used to determine the expression level of p21 in bladder cancer cells. Results: Cdr1as was significantly down-regulated in bladder cancer tissues compared with adjacent normal tissues. Overexpression of Cdr1as inhibited the proliferation, invasion and migration of bladder cancer cells in vitro and slowed down tumour growth in vivo. Cdr1as sponged multiple miRNAs in bladder cancer. Moreover, Cdr1as directly bound to miR-135a and inhibited its activity in bladder cancer. Conclusion: Cdr1as is down-regulated and sponges multiple miRNAs in bladder cancer. It exerts anti-oncogenic functions by sponging microRNA-135a

MicroRNA-218 Increases the Sensitivity of Bladder Cancer to Cisplatin by Targeting Glut1

Background/Aims: MicroRNA-218 (miR-218) is down-regulated in many malignancies that have been implicated in the regulation of diverse processes in cancer cells. However, the involvement of miR-218 in chemo-sensitivity to cisplatin and the precise mechanism of this action remained unknown in bladder cancer. Methods: qRT-PCR was used to detect miR-218 and its target Glut1 expression in bladder cancer cell lines T24 and EJ. CCK-8 method was utilized to measure the cell viability. IC 50 was calculated via a probit regression model. Glut1 was detected by western blotting for analysis of potential mechanism. Luciferase reporter assay was utilized to validate Glut1 as a direct target gene of miR-218. The intracellular level of GSH and ROS were determined using a commercial colorimetric assay kit and 2’, 7’-dichlorodihydro-fluorescein diacetate, respectively. Results: Over-expression of miR-218 significantly reduced the rate of glucose uptake and total level of GSH and enhanced the chemo-sensitivity of bladder cancer to cisplatin. Mechanistically, Glut1 was found to be a direct and functional target of miR-218. Up-regulation of Glut1 could restore chemo-resistance in T24 and EJ cells. On the contrary, knockdown of Glut1 could generate a similar effect as up-regulating the expression of miR-218. Conclusions: MiR-218 increases the sensitivity of bladder cancer to cisplatin by targeting Glut1. Restoration of miR-218 and repression of glut1 may provide a potential strategy to restore chemo-sensitivity in bladder cancer

Additional file 2: Table S2. of Rapid and high-efficiency generation of mature functional hepatocyte-like cells from adipose-derived stem cells by a three-step protocol

Showing hepatic pathways enriched in rHeps and iHeps cells, related to Fig. 3. (PDF 98 kb

Additional file 4: Figure S2. of Rapid and high-efficiency generation of mature functional hepatocyte-like cells from adipose-derived stem cells by a three-step protocol

Showing transplantation of iHeps into BALB/c nude mice, related to Fig. 4. HepG2 (1 × 106) or iHeps (1 × 106) cells were subcutaneously transplanted into the bank areas of nude mice. iHeps cells did not form tumors 8 weeks after transplantation. (PDF 118 kb