Unique Human and Mouse β-Cell Senescence-Associated Secretory Phenotype (SASP) Reveal Conserved Signaling Pathways and Heterogeneous Factors.

The aging of pancreatic -cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging -cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to -cell failure. In this study, we defined the -cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from mouse and human senescent -cells and a chemically induced mouse model of DNA damage capable of inducing SASP.

Acceleration of β Cell Aging Determines Diabetes and Senolysis Improves Disease Outcomes.

Type 2 diabetes (T2D) is an age-related disease. Although changes in function and proliferation of aged β cells resemble those preceding the development of diabetes, the contribution of β cell aging and senescence remains unclear. We generated a β cell senescence signature and found that insulin resistance accelerates β cell senescence leading to loss of function and cellular identity and worsening metabolic profile.

Stripping analyses of mercury using gold electrodes: irreversible adsorption of mercury.

The electrochemical deposition and stripping of mercury on gold surfaces was investigated to assess whether gold electrodes would return to mercury-free states after stripping analyses. X-ray photoelectron spectroscopy studies demonstrate the presence of mercury on gold foil electrodes that have undergone controlled-potential deposition procedures in Hg(2+) solutions (10 nM-0.1 mM) followed by stripping and cleaning in mercury-free electrolyte.