ABSTRACT
The aim of this research is to identify the digital technology impact and experience innovation of cultural heritages in the context of the epidemic. The authors created an analytical framework and used a qualitative exploratory multi-case study of three cultural heritages in Taiwan. The findings indicate that digital technology has facilitated further innovations in cultural heritages under the epidemic to be closer to consumers' daily life and more connected with the young generation. Compared to traditional cultural heritages, profit-making cultural heritages need sales of its products to sustain operations, while live streaming, which is interactive, is rising as a new way to promote sales. Using multiple digital platforms can maintain consumers' interest in the cultural heritages, encouraging follow-up visits and thus resulting in more traffic online and offline. This paper illustrates the advantages of digital technology in the context of the epidemic, highlighting the innovative technology of live streaming and social platforms introduced that are different from the traditional cultural heritages.
ABSTRACT
Metabolic associated fatty liver disease (MAFLD) is one of the most common causes of chronic liver disease worldwide. To date, there is no FDA-approved treatment, so there is an urgent need to determine its pathophysiology and underlying molecular mechanisms. Autophagy is a lysosomal degradation pathway that removes damaged organelles and misfolded proteins after cell injury through endoplasmic reticulum stress or starvation, which inhibits apoptosis and promotes cell survival. Recent studies have shown that autophagy plays an important role in removing lipid droplets from hepatocytes. Autophagy has also been reported to inhibit the production of pro-inflammatory cytokines and provide energy for the hepatic stellate cells activation during liver fibrosis. Thyroid hormone, irisin, melatonin, hydrogen sulfide, sulforaphane, DA-1241, vacuole membrane protein 1, nuclear factor erythroid 2-related factor 2, sodium-glucose co-transporter type-2 inhibitors, immunity-related GTPase M, and autophagy-related gene 7 have been reported to ameliorate MAFLD via autophagic induction. Lipid receptor CD36, SARS-CoV-2 Spike protein and leucine aminopeptidase 3 play a negative role in the autophagic function. This review summarizes recent advances in the role of autophagy in MAFLD. Autophagy modulates major pathological changes, including hepatic lipid metabolism, inflammation, and fibrosis, suggesting the potential of modulating autophagy for the treatment of MAFLD.