Activating ZnO nanorods photoanodes in visible light by CdS surface sensitiser

Thin films of c-axis aligned uniform ZnO nanorods (NRs) were fabricated on to fluorine-doped tin oxide-coated soda lime glass substrate by a two-step chemical route. Thereafter ZnO NRs/CdS core shell structures were successfully synthesised by depositing CdS layer on top of vertically aligned ZnO NRs using less hazardous nanocrystal layer deposition technique. The presence of CdS in ZnO NRs/CdS core shell structures was confirmed by energy dispersive X-ray analysis. Examination of structure and morphology of the fabricated films by X-ray diffraction (XRD) and field emission scanning electron microscopy (FESEM) revealed that both films have one-dimensional hexagonal wurtzite structure. Optical properties evaluated from ultraviolet-visible and photoluminescence spectra demonstrated better photo response of ZnO NRs/CdS core shell structure with respect to bare ZnO NR structure. Optical to chemical conversion efficiency of ZnO NRs/CdS photoanode was found to be similar to 1.75 times higher than bare ZnO NRs photoanode in photo electrochemical water splitting under visible light

Activating ZnO nanorods photoanodes in visible light by CdS surface sensitiser

Thin films of c-axis aligned uniform ZnO nanorods (NRs) were fabricated on to fluorine-doped tin oxide-coated soda lime glass substrate by a two-step chemical route. Thereafter ZnO NRs/CdS core shell structures were successfully synthesised by depositing CdS layer on top of vertically aligned ZnO NRs using less hazardous nanocrystal layer deposition technique. The presence of CdS in ZnO NRs/CdS core shell structures was confirmed by energy dispersive X-ray analysis. Examination of structure and morphology of the fabricated films by X-ray diffraction (XRD) and field emission scanning electron microscopy (FESEM) revealed that both films have one-dimensional hexagonal wurtzite structure. Optical properties evaluated from ultraviolet–visible and photoluminescence spectra demonstrated better photo response of ZnO NRs/CdS core shell structure with respect to bare ZnO NR structure. Optical to chemical conversion efficiency of ZnO NRs/CdS photoanode was found to be ∼1.75 times higher than bare ZnO NRs photoanode in photo electrochemical water splitting under visible light

Lung adenocarcinoma promotion by air pollutants

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for  PM2.5 air pollutants  and provide impetus for public health policy initiatives to address air pollution to reduce disease burden

Lung adenocarcinoma promotion by air pollutants

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden