11 research outputs found

    Control of adult neurogenesis by programmed cell death in the mammalian brain

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    Quasi-stable temperature of the steady state of microwave heated hematite

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    Microwave heated materials often reach a quasi-stable temperature resulting in thermal runaway. To control steady state in microwave processing, it is important to predict the quasi-stable temperature of the steady state. We demonstrated that the microwave heating behavior of hematite varies significantly with its initial temperature. In microwave heating, hematite samples could not be heated from room temperature, whereas hematite samples preheated to 410 °C or higher was heated to a temperature of 1020 °C. The microwave heating behavior can be accurately predicted by considering the steady-state energy balance

    Foxj1 expressing ependymal cells do not contribute new cells to sites of injury or stroke in the mouse forebrain

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    Abstract The stem cell source of neural and glial progenitors in the periventricular regions of the adult forebrain has remained uncertain and controversial. Using a cell specific genetic approach we rule out Foxj1+ ependymal cells as stem cells participating in neurogenesis and gliogenesis in response to acute injury or stroke in the mouse forebrain. Non stem- and progenitor-like responses of Foxj1+ ependymal cells to injury and stroke remain to be defined and investigated

    Ependymal cell contribution to scar formation after spinal cord injury is minimal, local and dependent on direct ependymal injury

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    Ependyma have been proposed as adult neural stem cells that provide the majority of newly proliferated scar-forming astrocytes that protect tissue and function after spinal cord injury (SCI). This proposal was based on small, midline stab SCI. Here, we tested the generality of this proposal by using a genetic knock-in cell fate mapping strategy in different murine SCI models. After large crush injuries across the entire spinal cord, ependyma-derived progeny remained local, did not migrate and contributed few cells of any kind and less than 2%, if any, of the total newly proliferated and molecularly confirmed scar-forming astrocytes. Stab injuries that were near to but did not directly damage ependyma, contained no ependyma-derived cells. Our findings show that ependymal contribution of progeny after SCI is minimal, local and dependent on direct ependymal injury, indicating that ependyma are not a major source of endogenous neural stem cells or neuroprotective astrocytes after SCI
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