High-confidence and high-throughput quantification of synapse engulfment by oligodendrocyte precursor cells.

Oligodendrocyte precursor cells (OPCs) sculpt neural circuits through the phagocytic engulfment of synapses during development and adulthood. However, existing techniques for analyzing synapse engulfment by OPCs have limited accuracy. Here we describe the quantification of synapse engulfment by OPCs via a two-pronged cell biological approach that combines high-confidence and high-throughput methodologies.

Exercise activates AMPK in mouse and human pancreatic islets to decrease senescence.

Beta (β)-cell senescence contributes to type 2 diabetes mellitus (T2DM). While exercise is vital for T2DM management and significantly affects cellular ageing markers, its effect on β-cell senescence remains unexplored. Here, we show that short-term endurance exercise training (treadmill running, 1 h per day for 10 days) in two male and female mouse models of insulin resistance decreases β-cell senescence.

Integrated high-confidence and high-throughput approaches for quantifying synapse engulfment by oligodendrocyte precursor cells.

Oligodendrocyte precursor cells (OPCs) sculpt neural circuits through the phagocytic engulfment of synapses during development and in adulthood. However, precise techniques for analyzing synapse engulfment by OPCs are limited. Here, we describe a two-pronged cell biological approach for quantifying synapse engulfment by OPCs which merges low- and high-throughput methodologies.

Decreased IGF1R attenuates senescence and improves function in pancreatic β-cells.

Introduction: The enhanced β-cell senescence that accompanies insulin resistance and aging contributes to cellular dysfunction and loss of transcriptional identity leading to type 2 diabetes (T2D). While senescence is among the 12 recognized hallmarks of aging, its relation to other hallmarks including altered nutrient sensing (insulin/IGF1 pathway) in β-cells is not fully understood. We previously reported that an increased expression of IGF1R in mouse and human β-cells is a marker of older β-cells; however, its contribution to age-related dysfunction and cellular senescence remains to be determined.

Clinicogenetic characteristics and the effect of radiation on the neural stem cell niche in subventricular zone-contacting glioblastoma.

Background And Purpose: Neural stem cells (NSCs) in the subventricular zone (SVZ) are recognized as the cellular origin of glioblastoma (GBM) and a potential therapeutic target. However, the characteristics of SVZ contacting GBM (SVZ + GBM) and radiotherapeutic strategies for NSCs are still controversial. Here, we investigated the clinicogenetic features of SVZ + GBM and evaluated the dose effect of NSC irradiation depending on SVZ involvement.