Sensitivity of Oncomelania hupensis to Niclosamide: A Nation-Wide Survey in China

Schistosomiasis japonica, transmitted by the intermediate host snail Oncomelania hupensis of the causative agent Schistosoma japonicum, remains a major public-health concern in China, and control of this snail is one of the major approaches used in attempts to interrupt the transmission of this neglected tropical disease. Niclosamide is currently the only commercial molluscicide available for the control of O. hupensis snails in China. The purpose of this study was to evaluate the current sensitivity of O. hupensis to niclosamide in China. O. hupensis snails derived from 17 sampling sites from eight schistosomiasis-endemic provinces of China were used for the molluscicidal tests. Active adult snails (10 for each drug concentration), were immersed in solutions of 1, 0.5, 0.25, 0.125, 0.063, 0.032, 0.016 and 0.008 mg/L of 50% wettable powder of niclosamide ethanolamine salt (WPN) for 24 and 48 h at 25°C, and then the snail mortality was estimated and LC50 values were calculated. All field-derived O. hupensis snails were dead following immersion in 0.5 and 1 mg/L WPN for 24 h, whereas no death was observed after immersion in 0.008 mg/L WPN for 24 h. Immersion in 0.5, 0.25, 0.125, 0.063, 0.032 and 0.016 mg/L WPN for 24 h resulted in 80%–100%, 63.33%–100%, 0%–85%, 0%–50%, 0%–15%, and 0%–5% snail mortalities, respectively. The 24 h WPN LC50 values for the O. hupensis snails derived from the 17 sampling sites in China ranged from 0.0743 to 0.2285 mg/L, and no significant difference was detected by the Kolmogorov-Smirnov test (p = 0.2). The results indicate that there is no regional variation in the current susceptibility to niclosamide in O. hupensis populations in China. It is suggested that the current sensitivity of niclosamide against O. hupensis remains high and has not changed after more than two decades of repeated, extensive application for snail control in the main endemic areas of China

Hydrovoltaic effect-enhanced photocatalysis by polyacrylic acid/cobaltous oxide–nitrogen doped carbon system for efficient photocatalytic water splitting

The construction of efficient photocatalyst system by utilizing hydrovoltaic technology bring promise but a challenge for photocatalytic water splitting. Here, the authors report a hydrovoltaic effect-enhanced photocatalytic system that shows high efficiency and quick kinetics of water splitting

Deep defect passivation and shallow vacancy repair via an ionic silicone polymer toward highly stable inverted perovskite solar cells

Additive engineering is an effective strategy for defect passivation and performance improvement of perovskite solar cells (PSCs). However, few additives have achieved outstanding stability with high efficiency by simultaneously passivating deep and shallow defects. Herein, we design a novel ionic silicone polymer (PECL) with multi-active sites as an additive to modify inverted PSCs. The C-O groups in the PECL polymer can chelate with undercoordinated Pb2+ and Pb clusters to passivate deep defects; and the ionic groups in the PECL polymer can generate electrostatic interaction with both positively and negatively charged vacancies, which help to repair shallow defects. Moreover, we quantitatively reveal the effect of deep and shallow defects on the efficiency and stability of PSCs separately, by establishing the correlation between additives with different functional groups and the performance of devices. Consequently, the power conversion efficiency of the PECL-modified inverted PSC increases from 20.02% to 23.11%. More importantly, the encapsulated PSCs maintain 95% of their initial steady-state power output after 1500 hours under AM 1.5 illumination at the maximum power point at 45 degrees C. Therefore, we provide a universal guideline of polymer structure design for defect healing in stabilizing PSCs with high efficiency

Lipophagy-mediated cholesterol synthesis inhibition is required for the survival of hepatocellular carcinoma under glutamine deprivation

Glutamine is critical for tumor progression, and restriction of its availability is emerging as a potential therapeutic strategy. The metabolic plasticity of tumor cells helps them adapting to glutamine restriction. However, the role of cholesterol metabolism in this process is relatively unexplored. Here, we reported that glutamine deprivation inhibited cholesterol synthesis in hepatocellular carcinoma (HCC). Reactivation of cholesterol synthesis enhanced glutamine-deprivation-induced cell death of HCC cells, which is partially duo to augmented NADPH depletion and lipid peroxidation. Mechanistically, glutamine deprivation induced lipophagy to transport cholesterol from lipid droplets (LDs) to endoplasmic reticulum (ER), leading to inhibit SREBF2 maturation and cholesterol synthesis, and maintain redox balance for survival. Glutamine deprivation decreased mTORC1 activity to induce lipophagy. Importantly, administration of U18666A, CQ, or shTSC2 viruses further augmented GPNA-induced inhibition of xenograft tumor growth. Clinical data supported that glutamine utilization positively correlated with cholesterol synthesis, which is associated with poor prognosis of HCC patients. Collectively, our study revealed that cholesterol synthesis inhibition is required for the survival of HCC under glutamine-restricted tumor microenvironment