Dynamics of Davydov Ansatze

Following the Dirac-Frenkel time-dependent variational principle, dynamics of a one-dimensional Holstein polaron is probed by employing the Davydov D2 Ansatz with two sets of variational parameters, one for each constituting particle in the exciton-phonon system, and a simplified variant of the Davydov D1 Ansatz, also known as the $\tilde{D}$ Ansatz, with an additional set of phonon displacement parameters. A close examination of variational outputs from the two trial states reveals fine details of the polaron structure and intricacies of dynamic exciton-phonon interactions. Superradiance coherence sizes, speeds of exciton-induced phonon wave packets, linear optical absorption, and polaron energy compositions are also included in the study.Comment: 14 pages and 11 figue

The Mediator Complex: A Regulatory Hub for Transcriptional Activity of Nuclear Receptors

The Mediator complex plays a key role in gene transcription. In particular, the interaction of the Mediator complex with nuclear receptors, the known transcription factors, regulates multiple nuclear receptor-mediated gene transcription pathways and associated cellular functions. Dysregulation of the interaction of the Mediator complex with nuclear receptors results in many pathological processes, such as cancer, metabolic and neuronal diseases. Thus, understanding of the mechanism by which the Mediator complex regulates the nuclear receptor-mediated transcriptional activity and biological function is crucial for therapy of both the Mediator complex- and nuclear receptor-associated diseases. In this review article, we attempt to summarize current research progress in the interaction of the Mediator complex with nuclear receptors and the associated nuclear receptor transcriptional signaling pathways, explore the clinical potential of the Mediator complex as a therapeutic target, and provide new perspectives for the treatment of diseases associated with the Mediator complex and nuclear receptors

Pathogenesis and Therapy of Hermansky–Pudlak Syndrome (HPS)-Associated Pulmonary Fibrosis

Hermansky–Pudlak syndrome (HPS)-associated pulmonary fibrosis (HPS-PF) is a progressive lung disease that is a major cause of morbidity and mortality in HPS patients. Previous studies have demonstrated that the HPS proteins play an essential role in the biogenesis and function of lysosome-related organelles (LROs) in alveolar epithelial type II (AT2) cells and found that HPS-PF is associated with dysfunction of AT2 cells and abnormal immune reactions. Despite recent advances in research on HPS and the pathology of HPS-PF, the pathological mechanisms underlying HPS-PF remain poorly understood, and no effective treatment has been established. Therefore, it is necessary to refresh the progress in the pathogenesis of HPS-PF to increase our understanding of the pathogenic mechanism of HPS-PF and develop targeted therapeutic strategies. This review summarizes the recent progress in the pathogenesis of HPS-PF provides information about the current treatment strategies for HPS-PF, and hopefully increases our understanding of the pathogenesis of HPS-PF and offers thoughts for new therapeutic interventions

Molecular Mechanisms Underlying Initiation and Activation of Autophagy

Autophagy is an important catabolic process to maintain cellular homeostasis and antagonize cellular stresses. The initiation and activation are two of the most important aspects of the autophagic process. This review focuses on mechanisms underlying autophagy initiation and activation and signaling pathways regulating the activation of autophagy found in recent years. These findings include autophagy initiation by liquid–liquid phase separation (LLPS), autophagy initiation in the endoplasmic reticulum (ER) and Golgi apparatus, and the signaling pathways mediated by the ULK1 complex, the mTOR complex, the AMPK complex, and the PI3KC3 complex. Through the review, we attempt to present current research progress in autophagy regulation and forward our understanding of the regulatory mechanisms and signaling pathways of autophagy initiation and activation