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[Display omitted] To meet the requirements in air quality monitors for the public and industrial safety, sensors are required that can selectively detect the concentration of gaseous pollutants down to the parts per million (ppm) and ppb (parts per billion) levels. Herein, we report a remarkable NH 3 sensor using Ni-doped CeO 2 octahedral nanostructure which efficiently detects NH 3 as low as 45 ppb at room temperature. The Ni-doped CeO 2 sensor exhibits the maximum response of 42 towards 225 ppm NH 3 , which is ten-fold higher than pure CeO 2. The improved sensing performance is caused by the enhancement of oxygen vacancy, bandgap narrowing, and redox property of CeO 2 caused by Ni doping. Density functional theory confirms that O vacancy with Ni at Ce site (V O Ni Ce) augments the sensing capabilities. The Bader charge analysis predicts the amount of charge transfer (0.04 e) between the Ni-CeO 2 surface and the NH 3 molecule. As well, the high negative adsorption energy (≈750 meV) and lowest distance (1.40 Å) of the NH 3 molecule from the sensor surface lowers the detection limit. The present work enlightens the fabrication of sensing elements through defect engineering for ultra-trace detection of NH 3 to be useful further in the field of sensor applications. [ABSTRACT FROM AUTHOR]

The increasing prevalence of non-alcoholic fatty liver disease (NAFLD) is a growing concern for the high incidence rate of hepatocellular carcinoma (HCC) globally. The progression of NAFLD to HCC is heterogeneous and non-linear, involving intermediate stages of non-alcoholic steatohepatitis (NASH), liver fibrosis, and cirrhosis. There is a high unmet clinical need for appropriate diagnostic, prognostic, and therapeutic options to tackle this emerging epidemic. Unfortunately, at present, there is no validated marker to identify the risk of developing HCC in patients suffering from NAFLD or NASH. Additionally, the current treatment protocols for HCC don't differentiate between viral infection or NAFLD-specific etiology of the HCC and have a limited success rate. The mammalian target of rapamycin complex 1 (mTORc1) is an important protein involved in many vital cellular processes like lipid metabolism, glucose homeostasis, and inflammation. These cellular processes are highly implicated in NAFLD and its progression to severe liver manifestations. Additionally, hyperactivation of mTORc1 is known to promote cell proliferation, which can contribute to the genesis and progression of tumors. Many mTORc1 inhibitors are being evaluated for different types of cancers under various phases of clinical trials. This paper deliberates on the strong pathological implication of the mTORc1 signaling pathway in NAFLD and its progression to NASH and HCC and advocates for a systematic investigation of known mTORc1 inhibitors in suitable pre-clinical models of HCC having NAFLD/NASH-specific etiology. [Display omitted] [ABSTRACT FROM AUTHOR]