YouTube video by Litai

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ATE era lo spirito personificato ( daimona ) 05che conduceva gli uomini sulla via della rovina. Il suo potere era contrastato dalle Litai (Litae) (Preghiere) che la seguivano. FAMIGLIA DI ATE GENITORI  ERIS (Teogonia Esiodo 230)  ZEUS (Omero Iliade 19,85) PROLE PEITHO (Eschilo, Agamennone 385) Atê, secondo Esiodo ( Teogonia 230), figlia di Eris, e secondo Omero (Il. 19. 91) di Zeus, era un'antica divinità greca che induceva dèi e uomini ad azioni avventate e sconsiderate, causandone la sofferenza.

Ekonomikos ir inovacijų ministerija pradeda steigti dirbtinio intelekto (DI) gamyklą „LitAI“ – skelbiamas kvietimas teikti paraišką valstybės biudžeto lėšų dalies skyrimui.

YouTube video by Litai

YouTube video by Litai

Psoriasis is a chronic inflammatory dermatosis characterized by pathological keratinocyte hyperproliferation and dysregulated immune activation. While ubiquitin-specific peptidase 16 (USP16) has been implicated in modulating multiple cellular signaling pathways, its functional role in psoriatic pathogenesis remains poorly understood. Our investigation revealed pronounced upregulation of USP16 expression in psoriatic epidermis compared with normal controls. Keratinocyte-specific USP16 knockdown demonstrated remarkable therapeutic efficacy, significantly ameliorating characteristic psoriatic phenotypes including epidermal hyperplasia and inflammatory infiltration. RNA-seq analysis showed that USP16 has substantial effects on cell cycle transition and keratinocytes proliferation. Through KEGG analysis, it was found that USP16 primarily regulates the NLRP3 signaling pathway, leading to enhanced cell proliferation and inflammation. Mechanically, USP16 directly binds to the NLRP3 protein to eliminate K48 ubiquitination modification, enhancing the stability of the NLRP3 protein, activating inflammasome activity. Further studies showed that the therapeutic effects of reducing USP16 on psoriasis progression were counteracted by an NLRP3 activator and keratinocyte-specific NLRP3 overexpression adenovirus. Collectively, these results shed light on how USP16 promotes NLRP3 signaling in keratinocytes, exacerbating psoriasis development. This positive regulation highlights the potential of USP16 as a therapeutic target for psoriasis.