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Following intensive research and development, Suntech Power has successfully commercialised its Pluto technology with 0.5 GW annual production capacity, delivering up to 10% performance advantage over conventional screen-printed cells. The next generation of Pluto involves the development of improved rear surface design based on the design features of passivated emitter and rear locally diffused cells. Cells with an average efficiency over 20% were fabricated on 155 cm 2 commercial-grade p-type wafers using mass-manufacturing processes and equipment, with the highest single-cell efficiency independently confirmed at 20.3%. This is believed to be a record efficiency for this wafer type. Further optimisation work on contact pattern and rear surface passivation suggests the potential for further efficiency increase approaching 23%.

Cancer stem cells (CSCs) are a small subset of malignant cells, possessing stemness, with strong tumorigenic capability, conferring resistance to therapy and leading to the relapse of nasopharyngeal carcinoma (NPC). Our previous study suggested that cyclooxygenase-2 (COX-2) would be a novel target for the CSCs-like side population (SP) cells in NPC. In the present study, we further found that COX-2 maintained the stemness of NPC by enhancing the activity of mitochondrial dynamin-related protein 1 (Drp1), a mitochondrial fission mediator, by studying both sorted SP cells from NPC cell lines and gene expression analyses in NPC tissues. Using both overexpression and knockdown of COX-2, we demonstrated that the localization of COX-2 at mitochondria promotes the stemness of NPC by recruiting the mitochondrial translocation of p53, increasing the activity of Drp1 and inducing mitochondrial fisson. Inhibition of the expression or the activity of Drp1 by siRNA or Mdivi-1 downregulates the stemness of NPC. The present study also found that inhibition of mitochondrial COX-2 with resveratrol (RSV), a natural phytochemical, increased the sensitivity of NPC to 5-fluorouracil (5-FU), a classical chemotherapy drug for NPC. The underlying mechanism is that RSV suppresses mitochondrial COX-2, thereby reducing NPC stemness by inhibiting Drp1 activity as demonstrated in both the in vitro and the in vivo studies. Taken together, the results of this study suggest that mitochondrial COX-2 is a potential theranostic target for the CSCs in NPC. Inhibition of mitochondrial COX-2 could be an attractive therapeutic option for the effective clinical treatment of therapy-resistant NPC.

In this work, we investigate the possibility of replacing the 2 loss with perceptually derived loss functions (SSIM, MS-SSIM, etc.) in training an end-to-end dehazing neural network. Objective experimental results suggest that by merely changing the loss function we can obtain significantly higher PSNR and SSIM scores on the SOTS set in the RESIDE dataset, compared with a state-of-the-art endto-end dehazing neural network (AOD-Net) that uses the 2 loss. The best PSNR we obtained was 23.50 (4.2% relative improvement), and the best SSIM we obtained was 0.8747 (2.3% relative improvement.)

Hepatitis B virus X (HBx) protein contributes to the progression of hepatitis B virus (HBV)-related hepatic injury and diseases, but the exact mechanism remains unclear. Protein phosphatase 2 A (PP2A) is a major serine/threonine phosphatase involved in regulating many cellular phosphorylation signals that are important for regulation of cell cycle and apoptosis. Does HBx target to PP2A-B56γ and therefore affect HBx-induced hepatotoxicity? In the present study, the expression of B56γ positively correlated with the level of HBx in HBV-infected primary human hepatocytes in human-liver-chimeric mice, HBx-transgenic mice, HBV-infected cells, and HBx-expressing hepatic cells. B56γ promoted p53/p21-dependent cell cycle arrest and apoptosis. Mechanistically, B56γ was transactivated by AP-1, which was under the regulation of endoplasmic reticulum (ER) stress induced CREBH signaling in HBx-expressing hepatic cells. B56γ dephosphorylated p-Thr55-p53 to trigger p53/p21 pathway-dependent cell cycle G1 phase arrest, resulting in apoptosis of hepatic cells. In conclusion, this study provides a novel insight into a mechanism of B56γ mediating cell cycle arrest and apoptosis of HBx-expressing hepatic cells and a basis for B56γ being a potential therapeutic target for HBV-infected hepatic cells.

Purpose: Androgen receptor-independent prostate cancers do not respond to androgen blockage therapies and suffer from high recurrence rate. We aim to contribute to the establishment of novel therapeutic approaches against such malignancies. Materials and Methods: We examined whether and how cold atmospheric plasma delivers selectivity against AR-independent prostate cancers via cell viability, transwell assay, wound healing, cell apoptosis assay, flow cytometry, intracellular hydrogen peroxide determination assay, RONS scavenger assay and western blot using human normal epithelial prostatic cells PNT1A and AR-negative DU145 prostate cancer cells. Results: We show that cold atmospheric plasma could selectively halt cell proliferation and migration in androgen receptor-independent cells as a result of induced cell apoptosis and G0/G1 stage cell cycle arrest, and such outcomes were achieved through modulations on the MAPK and NF-kB pathways in response to physical plasma induced intracellular redox level. Conclusion: Our study reports cold atmospheric plasma induced reduction on the proliferation and migration of androgen receptor-independent prostate cancer cells that offers novel therapeutic insights on the treatment of such cancers, and provides the first evidence on physical plasma induced cell cycle G0/G1 stage arrest that warrants the exploration on the synergistic use of cold atmospheric plasma and drugs such as chemotherapies in eradicating such cancer cells.

Hepatitis B virus (HBV) infection and aflatoxin B1 (AFB1) exposure have been recognized as independent risk factors for the occurrence and exacerbation of hepatic steatosis but their combined impacts and the potential mechanisms remain to be further elucidated. Here, we showed that exposure to AFB1 impaired mitochondrial dynamics and increased intracellular lipid droplets (LDs) in the liver of HBV‐transgenic mice in vivo and the hepatitis B virus X protein (HBx)‐expressing human hepatocytes both ex vivo and in vitro. HBx combined with AFB1 exposure also up‐regulated receptor interaction protein 1 (RIP1), receptor interaction protein 3 (RIP3) and activated mixed lineage kinase domain like protein (MLKL), providing evidence of necrosome formation in the hepatocytes. The shift of the mitochondrial dynamics towards imbalance of fission and fusion was rescued when MLKL was inhibited in the HBx and AFB1 co‐treated hepatocytes. Most importantly, based on siRNA or CRISPR/Cas9 system, we found that the combination of HBx and AFB1 exposure increased cyclooxygenase‐2 (COX‐2) to mediate up‐regulation of RIP3 and dynamin‐related protein 1 (Drp1), which in turn promoted location of RIP3‐MLKL necrosome on mitochondria, subsequently exacerbated steatosis in hepatocytes. Taken together, these findings advance the understanding of mechanism associated with HBx and AFB1‐induced hepatic necrosome formation, mitochondrial dysfunction and steatosis and make COX‐2 a good candidate for treatment.

Objective: To explore the efficacy of functional electrical stimulation (FES)-assisted rehabilitation cycling on the functional recovery of lower limbs in patients with hemiplegic stroke and the assessment value of surface electromyography (sEMG). Methods: A total of 66 patients with stroke accompanied by hemiplegia of the lower limbs were enrolled in the present prospective study and randomly divided into the experimental group and control group, with 33 patients in each group. FES-assisted rehabilitation cycling was applied in the experimental group, while only rehabilitation cycling was performed without setting the stimulation parameters in the control group. sEMG and the Fugl–Meyer assessment (FMA) were carried out, and the modified Barthel index (MBI) of the lower limbs was assessed before treatment and after 4 weeks and 8 weeks of treatment. Results: There were no significant differences in the evaluation results of sEMG, FMA, and MBI of the lower limbs between the two groups of patients before the treatment (p > 0.05). After 4 weeks of treatment, compared with the control group, there were significant differences in the results of sEMG, FMA, and MBI of the lower limbs in the experimental group (p < 0.05). In the experimental group, the difference in sEMG was statistically significant (p < 0.05). After 8 weeks of treatment, compared with the control group, there were significant differences in the results of sEMG, FMA, and MBI of the lower limbs in the experimental group (p < 0.05). In the experimental group, the differences in the results of sEMG, FMA, and MBI of the lower limbs were statistically significant (p < 0.05). The inter-group comparison of the results of sEMG, FMA and MBI of the lower limbs was statistically significant (p < 0.05) in the control group. Conclusion: FES-assisted rehabilitation cycling might promote the recovery of the motor function of the lower limbs in patients with stroke and improve the sEMG signal of the lower limbs.