The utility of apparent diffusion coefficients for predicting treatment response to uterine arterial embolization for uterine leiomyomas: a systematic review and meta-analysis.

PURPOSE: Apparent diffusion coefficient (ADC) values, which are derived from diffusion-weighted imaging, have a potential role for predicting treatment response. A systematic review was conducted to examine the value of baseline ADC values for predicting leiomyoma size reduction after uterine arterial embolization (UAE). METHODS: Study selection, quality appraisal and data extraction were conducted independently by two authors. Statistical analyses included the calculation of weighted means and summary correlation coefficients (under the random effects model). RESULTS: Eleven studies consisting of a total of 258 patients (age, weighted mean±standard deviation [SD], 43.1±10.1 years) were included. The weighted mean±SD ADC value was 1.2±1.5 ×10-3 s/mm2 at baseline (ten studies) and 1.3±2.8 ×10-3 s/mm2 at approximately 6 months after embolization (six studies). The weighted mean percentage leiomyoma volume reduction (VR) at 6 months was 47.1%±35.6% (seven studies). Based on four studies, the weighted summary correlation coefficient for the correlation between baseline ADC and leiomyoma VR at approximately 6 months was not significant (r=0.40; 95% CI, -0.07 to 0.72; I2=69.7%). No associations were found in three of the four studies that examined changes in ADC values as a predictor. CONCLUSION: Due to high heterogeneity, it is unclear whether ADC may be useful for predicting treatment responses to UAE.

AMPK activation of muscle autophagy prevents fasting-induced hypoglycemia and myopathy during aging.

The AMP-activated protein kinase (AMPK) activates autophagy, but its role in aging and fasting-induced muscle function has not been defined. Here we report that fasting mice lacking skeletal muscle AMPK (AMPK-MKO) results in hypoglycemia and hyperketosis. This is not due to defective fatty acid oxidation, but instead is related to a block in muscle proteolysis that leads to reduced circulating levels of alanine, an essential amino acid required for gluconeogenesis. Markers of muscle autophagy including phosphorylation of Ulk1 Ser555 and Ser757 and aggregation of RFP-LC3 puncta are impaired. Consistent with impaired autophagy, aged AMPK-MKO mice possess a significant myopathy characterized by reduced muscle function, mitochondrial disease, and accumulation of the autophagy/mitophagy proteins p62 and Parkin. These findings establish an essential requirement for skeletal muscle AMPK-mediated autophagy in preserving blood glucose levels during prolonged fasting as well as maintaining muscle integrity and mitochondrial function during aging.