12 research outputs found
A Transect Through the Pre-Silurian Rocks of Central Vermont; The Lincoln Massic and Its Immediate Cover; The Pre-Silurian Hinterland Along the Valleys of the White and Mad Rivers, Central Vermont; Metamorphism of Pre-Silurian Rocks, Central Vermont; Regional Geochemical Variations in Greenstones from the Central Vermont Appalachians
Guidebook for field trips in Vermont: New England Intercollegiate Geological Conference, 79th annual meeting, October 16, 17 and 18, 1987: Trips B-8; C-
Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy
mTor, acting mainly via mTORC1, controls dystrophin transcription in a raptor- and rictor-independent mechanism
Recommended from our members
Autophagy and Hematopoietic Stem Cell Potential During Aging
Aging of the hematopoietic system promotes various immune and systemic disorders and is driven in-part by dysfunction of life-long self-renewing hematopoietic stem cells (HSC). Autophagy is required for the benefit associated with activation of conserved longevity signaling programs and is essential for HSC function in response to various stressors. With age, some HSCs basally increase autophagy flux and maintain inert metabolic activity. This autophagy-activated subset is responsible for the residual regenerative capacity of old stem cells, but the mechanisms promoting autophagy activation in HSC aging remain unknown. Here, we demonstrate that autophagy is a response to chronic inflammation in the aging HSC niche.
Chronic inflammation impairs glucose metabolism in young and old HSCs (oHSC) by impeding AKT-FOXO intracellular signaling networks. We find that autophagy enables metabolic adaptation of oHSCs to non-glucose energy substrates for functional maintenance. Notably, water-only fasting transiently further activates autophagy in oHSCs, and upon refeeding normalizes glucose uptake and glycolytic flux as well as regenerative output. Our results demonstrate that inflammation-driven glucose hypometabolism impairs oHSC regenerative capacity, that autophagy activation metabolically adapts oHSCs to an inflamed niche, and that autophagy is a modulable node to restore glycolytic and regenerative capacity during stem cell aging
Effective repetitive dystrophin gene transfer into skeletal muscle of adultmdx mice using a helper-dependent adenovirus vector expressing the coxsackievirus and adenovirus receptor (CAR) and dystrophin
Functional correction of adult mdx mouse muscle using gutted adenoviral vectors expressing full-length dystrophin
Distinct claudin expression characterizes BRCA1-related breast cancer
AimsMembers of the claudin family are involved in cancer progression and are differentially expressed in subtypes of breast cancer. Breast cancers in BRCA1 germ line mutation carriers have distinct clinicopathological characteristics. Biomarkers that discriminate between BRCA1-related and sporadic breast cancer cases are needed to improve early identification of mutation carriers. In this study we evaluated protein expression of five major claudins in BRCA1-related breast cancers in comparison with sporadic controls. Methods and resultsForty breast cancers in BRCA1 mutation carriers and 40 age-matched sporadic breast cancers were immunohistochemically stained for claudins 1, 3, 4, 6 and 7. Total intratumoural expression levels were compared to those in the surrounding normal tissue. In addition, subcellular claudin expression was scored. Higher overexpression rates were observed for all five claudins in BRCA1-related breast cancers when compared to sporadic controls. In multivariate analysis, overexpression of claudin 3, 4, and 7 was mainly dependent on ER-status, whereas overexpression of claudin 6 and high membranous expression of claudin 1 were independent of other characteristics. ConclusionsBRCA1-related breast cancers are characterized by frequent overexpression of claudins. Especially claudin 1 and 6 expression may help to discriminate mutation carriers from sporadic breast cancer cases