Life Cycle Greenhouse Gas Emissions of Brazilian Sugar Cane Ethanol Evaluated with the GREET Model Using Data Submitted to RenovaBio.

Brazil is the second-largest ethanol producer in the world, primarily using sugar cane as feedstock. To foster biofuel production, the Brazilian government implemented a national biofuel policy, known as RenovaBio, in which greenhouse gas (GHG) emission reduction credits are provided to biofuel producers based on the carbon intensities (CI) of the fuels they produce. In this study, we configured the GREET model to evaluate life cycle GHG emissions of Brazilian sugar cane ethanol, using data from 67 individual sugar cane mills submitted to RenovaBio in 2019/2020. The average CI per megajoule of sugar cane ethanol produced in Brazil for use in the U.S. was estimated to be 35.2 g of CO2 equivalent, a 62% reduction from U.S. petroleum gasoline blendstock without considering the impacts of land use change. The three major GHG sources were on-field N2O emissions (24.3%), sugar cane farming energy use (24.2%), and sugar cane ethanol transport (19.3%). With the probability density functions for key input parameters derived from individual mill data, we performed stochastic simulations with the GREET model to estimate the variations in sugar cane ethanol CI and confirmed that despite the larger variations in sugar cane ethanol CI, the fuel provided a robust GHG reduction benefit compared to gasoline blendstock.

LncRNA-Regulated Autophagy and its Potential Role in Drug-Induced Liver Injury.

INTRODUCTION AND AIM: Autophagy and its regulated pathways participate in many important cellular physiology and pathological processes involving protein aggregates, damaged mitochondria, excessive peroxisomes, ribosomes, and invading pathogens. This study aimed to review recently published studies and further describe the long noncoding RNA (lncRNA)-regulated autophagy during drug-induced liver injury (DILI). MATERIAL AND METHODS: DILI, autophagy, autophagy-related genes (ATGs), and lncRNA were used as key words to search published studies from PubMed, Google Scholar, and Web of Science. All related studies were reviewed and analyzed. RESULTS: Many studies explicitly indicated that DILI and its progression to acute liver failure were causatively linked to endoplasmic reticulum stress and subsequently induced autophagy, which protect hepatocytes during DILI. LncRNA, as a noncoding RNA, influences the regulation of the expression of ATGs to manipulate autophagy. CONCLUSIONS: This review described the recent findings on autophagy and its possible lncRNA-miRNA-associated pathways, thereby providing new insights for further studies on the pathogenesis of DILI.