Natural recovery from disease and damage in the adult mammalian central nervous system (CNS) is limited compared with that in lower vertebrate species, including fish and salamanders. Species-specific differences in the plasticity of the CNS reflect these differences in regenerative capacity. Despite numerous extensive studies in the field of CNS regeneration, our understanding of the molecular mechanisms determining the regenerative capacity of the CNS is still relatively poor. The discovery of adult neural stem cells (aNSCs) in mammals, including humans, in the early 1990s has opened up new possibilities for the treatment of CNS disorders via self-regeneration through the mobilization of these cells. However, we now know that aNSCs in mammals are not plastic enough to induce significant regeneration. In contrast, aNSCs in some regenerative species have been found to be as highly plastic as early embryonic neural stem cells (NSCs). We must expand our knowledge of NSCs and of regenerative processes in lower vertebrates in an effort to develop effective regenerative treatments for damaged CNS in humans.
Radiation recall is an acute inflammatory reaction that can be triggered when systemic agents are administered long time after radiotherapy. Because radiotherapy is now indicated for many types of cancer, care should be taken regarding possible toxic events relating to radiotherapy in combination with radio-sensitizing agents. Gemcitabine, one such anti-cancer agent, is widely used, especially for urologic cancers. We report an intriguing case of possible radiation recall in the rectum caused by gemcitabine administration 37 years after radiation therapy. From a review of the literature, it appears that there have been no reported cases of radiation recall in the rectum with such a long interval between radiation therapy and chemotherapy. Here, we describe the case and provide a literature review.
Rapid growing cells like tumor cells need a vast amount of energy to match their high metabolic demand. Guanine triphosphate (GTP) is one of major cellular metabolites and served as a building block for RNA and DNA as well as an energy source to drive cellular activities such as intracellular trafficking, the cell migration and translation. However, how cancer cells regulate GTP energy levels to adapt for their high demand remain largely unknown yet. In addition, how cells detect GTP levels remains unknown. In this seminar, I will introduce our recent findings that uncover dramatic change of GTP metabolism in cancer cells and a GTP sensing kinase that regulate metabolism for tumorigenesis.(Presented at the 1918th Meeting, March 3, 2016)
Cognitive deficits are the major manifestation of Alzheimer’s disease (AD); however, weight loss can precede the mental decline and correlates with disease severity. Thus, brain circuits controlling body weight may be altered early in AD and could be intrinsic to AD pathobiology. In mouse models, we found that amyloid-beta, a major pathogenic factor in AD, could inhibit hypothalamic neurons in the leptin pathway, which was associated with early body weight/metabolic deficits. Ongoing research seeks to elucidate the mechanisms underlying the body weight/metabolic deficits and hypothalamic dysfunction in AD using both mouse models and clinically relevant human studies.(Presented at the 1919th Meeting, March 2, 2016)
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