Oxidative dispersion has been widely used in regeneration of sintered metal catalysts and fabrication of single atom catalysts, which is attributed to an oxidation-induced dispersion mechanism. However, the interplay of gas-metal-support interaction in the dispersion processes, especially the gas-metal interaction has not been well illustrated. Here, we show dynamic dispersion of silver nanostructures on silicon nitride surface under reducing/oxidizing conditions and during carbon monoxide oxidation reaction. Utilizing environmental scanning (transmission) electron microscopy and near-ambient pressure photoelectron spectroscopy/photoemission electron microscopy, we unravel a new adsorption-induced dispersion mechanism in such a typical oxidative dispersion process. The strong gas-metal interaction achieved by chemisorption of oxygen on nearly-metallic silver nanoclusters is the internal driving force for dispersion. In situ observations show that the dispersed nearly-metallic silver nanoclusters are oxidized upon cooling in oxygen atmosphere, which could mislead to the understanding of oxidation-induced dispersion. We further understand the oxidative dispersion mechanism from the view of dynamic equilibrium taking temperature and gas pressure into account, which should be applied to many other metals such as gold, copper, palladium, etc. and other reaction conditions.Sodium iodate (SI) is a widely used oxidant for generating retinal degeneration models by inducing the death of retinal pigment epithelium (RPE) cells. However, the mechanism of RPE cell death induced by SI remains unclear. In this study, we investigated the necrotic features of cultured human retinal pigment epithelium (ARPE-19) cells treated with SI and found that apoptosis or necroptosis was not the major death pathway. Instead, the death process was accompanied by significant elevation of intracellular labile iron level, ROS, and lipid peroxides which recapitulated the key features of ferroptosis. Ferroptosis inhibitors deferoxamine mesylate (DFO) and ferrostatin-1(Fer-1) partially prevented SI-induced cell death. Further studies revealed that SI treatment did not alter GPX4 (glutathione peroxidase 4) expression, but led to the depletion of reduced thiol groups, mainly intracellular GSH (reduced glutathione) and cysteine. The study on iron trafficking demonstrated that iron influx was not altered by SI treatment but iron efflux increased, indicating that the increase in labile iron was likely due to the release of sequestered iron. This hypothesis was verified by showing that SI directly promoted the release of labile iron from a cell-free lysate. We propose that SI depletes GSH, increases ROS, releases labile iron, and boosts lipid damage, which in turn results in ferroptosis in ARPE-19 cells.Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, which lacks effective treatment strategies. There is an urgent need for the development of new strategies for PDAC therapy. The genetic and phenotypic heterogeneity of PDAC cancer cell populations poses further challenges in the clinical management of PDAC. In this study, we performed single-cell RNA sequencing to characterize PDAC tumors from KPC mice. Functional studies and clinical analysis showed that PDAC cluster 2 cells with highly Hsp90 expression is much more aggressive than the other clusters. Genetic and pharmacologic inhibition of Hsp90 impaired tumor cell growth both in vitro and in vivo. Further mechanistic study revealed that HSP90 inhibition disrupted the interaction between HSP90 and OPA1, leading to a reduction in mitochondrial cristae amount and mitochondrial energy production. Collectively, our study reveals that HSP90 might be a potential therapeutic target for PDAC.Our ability to manipulate the behavior of complex networks depends on the design of efficient control algorithms and, critically, on the availability of an accurate and tractable model of the network dynamics. While the design of control algorithms for network systems has seen notable advances in the past few years, knowledge of the network dynamics is a ubiquitous assumption that is difficult to satisfy in practice. In this paper we overcome this limitation, and develop a data-driven framework to control a complex network optimally and without any knowledge of the network dynamics.  https://www.selleckchem.com/products/bay80-6946.html  Our optimal controls are constructed using a finite set of data, where the unknown network is stimulated with arbitrary and possibly random inputs. Although our controls are provably correct for networks with linear dynamics, we also characterize their performance against noisy data and in the presence of nonlinear dynamics, as they arise in power grid and brain networks.Nonalcoholic fatty liver disease (NAFLD) is prevalent clinically and can lead to more serious chronic liver disease. However, the pathological mechanism is still unclear, and thus, there are no approved drugs on the market. Transcriptional coactivator WW domain-binding protein 2 (WBP2) is a newly discovered oncogene that has an important relationship with the occurrence and development of breast cancer and mediates the interaction between Wnt and various other signaling pathways. The expression level of WBP2 was decreased in NAFLD. Overexpression of WBP2 with AAV in vivo alleviated liver fat deposition and insulin resistance induced by a high-fat diet (HFD). Knockdown of WBP2 with AAV aggravated HFD-induced fatty liver and insulin resistance. In vitro experiments showed that in the human normal hepatocyte cell line LO2 and primary hepatocytes isolated from mice, overexpression of WBP2 reduced fat deposition, and knocking out or knocking down WBP2 aggravated PA-induced fat deposition. Through mass spectrometry, we found that WBP2 can bind to AMPKβ1, and by mutating AMPKβ1, we found that WBP2 can induce phosphorylation of AMPKβ1 at S108 and then activate the AMPK pathway to affect lipid metabolism. The effect of WBP2 on NAFLD provides a possible new direction for future research on NAFLD.Multiple myeloma (MM), a treatable but incurable malignancy, is characterized by the growth of clonal plasma cells in protective niches in the bone marrow. MM cells depend on expression of BCL-2 family proteins, in particular MCL-1, for survival. The regulation of MCL-1 is complex and cell type-dependent. Unraveling the exact mechanism by which MCL-1 is overexpressed in MM may provide new therapeutic strategies for inhibition in malignant cells, preferably limiting side effects in healthy cells. In this study, we reveal that one cause of overexpression could be stabilization of the MCL-1 protein. We demonstrate this in a subset of MM and diffuse large B cell lymphoma (DLBCL) cell lines and MM patient samples. We applied a phosphatase siRNA screen to identify phosphatases responsible for MCL-1 stabilization in MM, and revealed PP2A as the MCL-1 stabilizing phosphatase. Using the PP2A inhibitor okadaic acid, we validated that PP2A dephosphorylates MCL-1 at Ser159 and/or Thr163, and thereby stabilizes MCL-1 in MM cells with long MCL-1 half-life, but not in DLBCL cells.