Aerobic exercise reverses aging-induced depth-dependent decline in cerebral microcirculation.

Aging is a major risk factor for cognitive impairment. Aerobic exercise benefits brain function and may promote cognitive health in older adults. However, underlying biological mechanisms across cerebral gray and white matter are poorly understood. Selective vulnerability of the white matter to small vessel disease and a link between white matter health and cognitive function suggests a potential role for responses in deep cerebral microcirculation. Here, we tested whether aerobic exercise modulates cerebral microcirculatory changes induced by aging. To this end, we carried out a comprehensive quantitative examination of changes in cerebral microvascular physiology in cortical gray and subcortical white matter in mice (3-6 vs. 19-21 months old), and asked whether and how exercise may rescue age-induced deficits. In the sedentary group, aging caused a more severe decline in cerebral microvascular perfusion and oxygenation in deep (infragranular) cortical layers and subcortical white matter compared with superficial (supragranular) cortical layers. Five months of voluntary aerobic exercise partly renormalized microvascular perfusion and oxygenation in aged mice in a depth-dependent manner, and brought these spatial distributions closer to those of young adult sedentary mice. These microcirculatory effects were accompanied by an improvement in cognitive function. Our work demonstrates the selective vulnerability of the deep cortex and subcortical white matter to aging-induced decline in microcirculation, as well as the responsiveness of these regions to aerobic exercise.

The microsatellite instability and loss of heterozygosity in head and neck squamous cell carcinomas / 中国病理生理杂志

AIM: To examine the microsatellite instability (MSI) and loss of heterozygosity (LOH) in head and neck squamous cell carcinomas (HNSCC). METHODS: 36 cases of HNSCC were analyzed with 15 microsatellite markers from chromosome 3,5,6,8,9,13,17 and 18. RESULTS: Among the 36 cases of HNSCC, 27.8%(10/36)of samples showed MSI in one to eight microsatellite markers. High frequent MSI occurred at D17S520(22.9%), D6S105(16 7%)and D8S264(13 9%). LOH was detected on the site of 9p21-p22 and 3p14. No correlations were found between allelic instability and grade or stage of the tumor. CONCLUSION: Our data suggest that MSI is a common genetic change in HNSCC. Tumor suppressor genes related to HNSCC may harbor at chromosome 9p21-p22 and 3p14 regions. [