Microbial ecology and functional coffee fermentation dynamics with Pichia kudriavzevii.

Specialty coffee can be developed by the application of explicit microorganisms or starters to obtain desired fermentation. In the present study, natural fermentation (NF) of Arabica coffee was carried out spontaneously, the other set was inoculated with Pichia kudriavzevii (Y) starter culture (isolated, identified and mass cultured). The effect of microbial fermentation, metagenomics, production of functional metabolites, volatiles and their sensorial aspects were studied. The bioprocess illustrated cohesive interface of coffee nutrients and microbial communities like Mycobacterium, Acinetobacter, Gordonia, etc., in NF, Lactobacillus and Leuconostoc were prevailing in Y. The Pichia and Rhodotorula dominated in both the groups. The bioactivity of bacteria and fungi induced complex changes in physicochemical features like pH (4.2-5.2), Brix° (9.5-3.0), and metabolic transition in sugar (3.0-0.7%), alcohol (1.4-2.7%), organic acids modulating flavour precursors and organoleptics in the final brew. In the roasted bean, Y exhibited higher sugar (42%), protein (25%), polyphenol (3.5%), CGA (2.5%), caffeine (17.2%), and trigonelline (2.8%) than NF. The volatile profile exhibited increased flavour molecules like furans, ketones, and pyrazines in Y, besides lactone complexes. The organoleptics in Y were highlighted with honey, malt and berry notes. P. kudriavzevii coffee fermentation could be beneficial in specialty coffee production and enhancement of distinct characteristic flavours.

In silico and In vivo Evaluation of Oxidative Stress Inhibitors Against Parkinson's Disease using the C. elegans Model.

BACKGROUND: Parkinson's disease ranks second, after Alzheimer's as the major neurodegenerative disorder, for which no cure or disease-modifying therapies exist. Ample evidence indicate that PD manifests as a result of impaired anti-oxidative machinery leading to neuronal death wherein Cullin-3 has ascended as a potential therapeutic target for diseases involving damaged anti-oxidative machinery. OBJECTIVE: The design of target specific inhibitors for the Cullin-3 protein might be a promising strategy to increase the Nrf2 levels and to decrease the possibility of "off-target" toxic properties. METHODS: In the present study, an integrated computational and wet lab approach was adopted to identify small molecule inhibitors for Cullin-3. The rational drug designing process comprised homology modeling and derivation of the pharmacophore for Cullin-3, virtual screening of Zinc natural compound database, molecular docking and Molecular dynamics based screening of ligand molecules. In vivo validations of an identified lead compound were conducted in the PD model of C. elegans. RESULTS AND DISCUSSION: Our strategy yielded a potential inhibitor; (Glide score = -12.31), which was evaluated for its neuroprotective efficacy in the PD model of C. elegans. The inhibitor was able to efficiently defend against neuronal death in PD model of C. elegans and the neuroprotective effects were attributed to its anti-oxidant activities, supported by the increase in superoxide dismutase, catalase and the diminution of acetylcholinesterase and reactive oxygen species levels. In addition, the Cullin-3 inhibitor significantly restored the behavioral deficits in the transgenic C. elegans. CONCLUSION: Taken together, these findings highlight the potential utility of Cullin-3 inhibition to block the persistent neuronal death in PD. Further studies focusing on Cullin-3 and its mechanism of action would be interesting.