Robot versus human barista: Comparison of volatile compounds and consumers' acceptance, sensory profile, and emotional response of brewed coffee.

The increasing trend of integrating robots into the food industry has sparked debates regarding their potential influence on consumer attitudes toward food technology. This study investigated volatile compound profiles via gas chromatography-mass spectrometry (GC-MS), consumer acceptability, sensory profiling, and emotional responses of consumers toward coffee samples brewed by robot and human baristas. Moreover, the effect of the robot experience on food technology neophobia (FTN) was investigated. The principal component analysis of the volatile compound profiles revealed that the samples by the robot barista exhibited a higher degree of similarity compared to those prepared by the human barista. The range of relative standard deviations of volatile compounds from the robot barista brewed coffee was 1.4-83.1% and the variation was smaller than that of the human barista, which was 5.0-118.3%. Participants had a significant decrease in FTN scores after evaluating the robot-brewed coffee (p < 0.05), but there was no significant difference in FTN scores before and after evaluating the coffee brewed by the human barista (p > 0.05). Sensory evaluation studies revealed no significant differences in acceptability ratings and purchase intentions between the two groups (p > 0.05). However, emotional responses to the coffee samples significantly varied, with the robot-brewed coffee inducing more dynamic and positive emotions and the human-brewed coffee inducing more static and positive emotions (p < 0.05). Overall, this study provides valuable insights into consumer attitudes toward food robot service to humans and indicates that consumer's experience with food robots may significantly reduce FTN (p < 0.001).

Photobiomodulation (660 nm) therapy reduces oxidative stress and induces BDNF expression in the hippocampus.

Photobiomodulation therapy (PBMT) effects an important role in neural regeneration and function enhancement, such as expression of nerve growth factor and nerve regeneration, in neuronal tissues, and inhibition of cell death by amyloid beta in neurons is inhibited by PBMT. However, there no studies evaluated the effects of PBMT on oxidative stress in the hippocampus. The aim of this study is to evaluate the effects of PBMT on oxidative stress in the hippocampus. This study assessed the anti-oxidative effect, the expression of BDNF and antioxidant enzymes, as well as the activation of cAMP response element binding (CREB) and extracellular signal-regulated kinase (ERK) signal transduction pathways assess using a hippocampal cell line (HT-22) and mouse organotypic hippocampal tissues by PBMT (LED, 660 nm, 20 mW/cm2). PBMT inhibited HT-22 cell death by oxidative stress and increased BDNF expression via ERK and CREB signaling pathway activation. In addition, PBMT increased BDNF expression in hippocampal organotypic slices and the levels of phosphorylated ERK and CREB, which were reduced by oxidative stress, as well as the expression of the antioxidant enzyme superoxide dismutase. These data demonstrate that PBMT inhibits hippocampal damage induced by oxidative stress and increases the expression of BDNF, which can be used as an alternative to treat a variety of related disorders that lead to nerve damage. Activation and redox homeostasis in neuronal cells may be a notable mechanism of the 660-nm PBMT-mediated photobioreactivity.

Glucagon-like peptide-1 protects NSC-34 motor neurons against glucosamine through Epac-mediated glucose uptake enhancement.

Bioenergetic deficits are considered a common cause of neurodegenerative diseases. Although creatine supplementation has been shown to be effective in certain neurodegenerative disorders, it is less effective in amyotrophic lateral sclerosis, a disease that primarily affects motor neurons. These neurons are particularly vulnerable to a cellular energy deficit. Using the ATP-depleting drug glucosamine, we evaluated whether the incretin hormone glucagon-like peptide (GLP)-1 protects motor neurons against glucosamine-induced cytotoxicity. Undifferentiated NSC-34 cells were differentiated into glutamate-sensitive motor neurons by a modified serum deprivation technique. Glucosamine inhibited the viability of differentiated NSC-34 cells in a time- and dose-dependent manner. Glucosamine also acutely reduced cellular glucose uptake, glucokinase activity and intracellular ATP levels. As a result, the activity of AMP-activated protein kinase as well as endoplasmic reticulum stress increased. Pretreatment with GLP-1 significantly alleviated glucosamine-mediated neurotoxicity by restoring cellular glucose uptake, glucokinase activity and intracellular ATP levels. The protective effect of GLP-1 was replicated by Exendin-4 but not Exendin-9, and not blocked by inhibitors of phosphoinositide-3 kinase, protein kinase A, cSrc, or epidermal growth factor receptor, but it was blocked by an adenylate cyclase inhibitor. A selective activator for exchange proteins directly activated by cAMP (Epac), but not a selective activator for protein kinase A, mimicked the GLP-1 effect. Therefore GLP-1 may exert its effect mainly through cAMP-dependent, Epac-mediated restoration of glucose uptake that is typically impaired by glucosamine. These findings indicate that GLP-1 could be employed therapeutically to protect motor neurons that are susceptible to bioenergetic deficits.