Background: Body (fat) mass has been shown to decrease following bright light treatment for overweight women, irrespective of their seasonal (light) dependence. It is not known if this is due to an (immediate) increase of metabolism.
Methods: Ten women with seasonal affective disorder (SAD) and 10 non-SAD women matched by age, body mass index, and menopausal status participated in a laboratory study in the morning, twice within 1-5 days.
Therapy-induced cellular senescence (TCS), characterized by prolonged cell cycle arrest, is an in vivo response of human cancers to chemotherapy and radiation. Unfortunately, TCS is reversible for a subset of senescent cells, leading to cellular reproliferation and ultimately tumor progression. This invariable consequence of TCS recapitulates the clinical treatment experience of patients with advanced cancer.
View Article and Find Full Text PDFTherapy-induced accelerated cellular senescence (ACS) is a reversible tumor response to chemotherapy that is likely detrimental to the overall therapeutic efficacy of cancer treatment. To further understand the mechanism by which cancer cells can escape the sustained cell cycle arrest in ACS, we established a tissue culture model, in which the p53-null NCI-H1299 cells can be induced into senescence by an abbreviated exposure to a chemotherapeutic agent. Previously, we have reported that senescent cells overexpress Cdc2/Cdk1 when they bypassed the prolonged arrest and their viability is dependent on Cdc2/Cdk1 kinase activity.
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