Coffee is one of the most consumed beverages in the world, and its popularity has prompted the necessity to constantly increase the variety and improve the characteristics of coffee as a general commodity. The popularity of coffee as a staple drink has also brought undesired side effects, since coffee production, processing and consumption are all accompanied by impressive quantities of coffee-related wastes which can be a threat to the environment. In this review, we integrated the main studies on fermentative yeasts used in coffee-related industries with emphasis on two different directions: (1) the role of yeast strains in the postharvest processing of coffee, the possibilities to use them as starting cultures for controlled fermentation and their impact on the sensorial quality of processed coffee, and (2) the potential to use yeasts to capitalize on coffee wastes—especially spent coffee grounds—in the form of eco-friendly biomass, biofuel or fine chemical production.

Cerebrovascular accidents are currently the second major cause of death and the third leading cause of disability in the world, according to the World Health Organization (WHO), which has provided protocols for stroke prevention. Although there is a multitude of studies on the health benefits associated with anthocyanin (ACN) consumption, there is no a rigorous systematization of the data linking dietary ACN with stroke prevention. This review is intended to present data from epidemiological, in vitro, in vivo, and clinical studies dealing with the stroke related to ACN-rich diets or ACN supplements, along with possible mechanisms of action revealed by pharmacokinetic studies, including ACN passage through the blood-brain barrier (BBB).

The Ca²⁺‐dependent response to oxidative stress caused by H₂O₂ or tert‐butylhydroperoxide (tBOOH) was investigated in Saccharomyces cerevisiae cells expressing transgenic cytosolic aequorin, a Ca²⁺‐dependent photoprotein. Both H₂O₂ and tBOOH induced an immediate and short‐duration cytosolic Ca²⁺ increase that depended on the concentration of the stressors. Sublethal doses of H₂O₂ induced Ca²⁺ entry into the cytosol from both extracellular and vacuolar sources, whereas lethal H₂O₂ shock mobilized predominantly the vacuolar Ca²⁺. Sublethal and lethal tBOOH shocks induced mainly the influx of external Ca²⁺, accompanied by a more modest vacuolar contribution. Ca²⁺ transport across the plasma membrane did not necessarily involve the activity of the Cch1p/Mid1p channel, whereas the release of vacuolar Ca²⁺ into the cytosol required the vacuolar channel Yvc1p. In mutants lacking the Ca²⁺ transporters, H₂O₂ or tBOOH sensitivity correlated with cytosolic Ca²⁺ overload. Thus, it appears that under H₂O₂‐induced or tBOOH‐induced oxidative stress, Ca²⁺ mediates the cytotoxic effect of the stressors and not the adaptation process.