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Two articles in this issue investigate the proliferation of neurons in the adult brain post-injury (stroke or irradiation). X-irradiation similar to that used in cranial radiation therapy inhibits neurogenesis in the adult rat. On page 955, Monje et al. show that hippocampal neural precursors from irradiated rats can, in culture, produce immature neurons, suggesting a disrupted brain microenvironment. On page 963, Arvidsson et al. show that following experimental stroke, neurons of the adult rat brain proliferate and migrate into damaged areas. The cover depicts a confocal image of cells cultured from an irradiated (10Gy) hippocampus, including type-IIIß tubulin-positive neurons (green), glial fibrillary acidic protein-positive oligodendrocytes (blue); x40 objective.
After more than 20 years working as a senior scientist at Toronto's Hospital for Sick Children, medical geneticist Lap-Chee Tsui is returning to his homeland this month to become vice chancellor at the University of Hong Kong. He shared his thoughts about the move with Nature Medicine.
The diversity in growth and morphological characteristics among endothelial cells in different normal tissues and tumors has been long recognized. Yet there has been no clear molecular explanation for such diversity at the level of vascular endothelial growth factor A (VEGF-A) and other established regulators of angiogenesis that are expressed widely and show little tissue selectivity in their angiogenic properties. Endocrine gland–derived VEGF represents the first example of a tissue-specific angiogenic factor, likely to be followed by others.
Pharmacological agents directed against the integrins αvβ3 and αvβ5 have been reported to inhibit angiogenesis. However, genetic ablations of the genes encoding these integrins fail to block angiogenesis and in some cases even enhance it. This apparent paradox suggests the hypotheses that these integrins are negative regulators of angiogenesis and that the drugs targeting them may be acting as agonists rather than antagonists.
The 1997 flu in Hong Kong infected only 18 patients, but killed 6 of them. Now, reverse genetics experiments have pinpointed the NS1 gene as a primary culprit.
Stroke and irradiation can cause severe brain damage, with consequences for neuronal replacement. The results of two new studies may help us understand the barriers to effective therapies to restore injured brain tissue (pages 955–962 and 963–970).
Asthma can originate via diverse causal and mechanistic pathways. A small bioactive lipid takes on this heterogeneity and offers the possibility of a broad-based treatment (pages 1018–1023).
Abnormal vessel growth in the eyes is a major cause of blindness. In mice, injection of stem cells from the bone marrow can alter vessel growth (pages 1004–1010).
A new study shows that TERT, a component of telomerase, shuttles between nuclear compartments during the cell cycle. TERT localization is disrupted in cancer and following ionizing radiation, perhaps affecting genome stability.
Accumulation of Aβ peptide in the brains of individuals with Alzheimer disease leads to an inflammatory response. New data suggest that this response may not always be harmful.
The most invasive types of brain tumors can release neurotoxic quantities of glutamate. A new study shows that changing the properties of glutamate receptors can shrink brain tumors in rats (pages 971–978).