In adult brain, new neurons are generated throughout adulthood in the subventricular zone and the dentate gyrus; this process is commonly known as adult neurogenesis. The regulation or modulation of adult neurogenesis includes various intrinsic pathways (signal transduction pathway and epigenetic or genetic modulation pathways) or extrinsic pathways (metabolic growth factor modulation, vascular, and immune system pathways). Altered neurogenesis has been identified in Alzheimer’s disease (AD), in both human AD brains and AD rodent models. The exact mechanism of the dysregulation of adult neurogenesis in AD has not been completely elucidated. However, neuroinflammation has been demonstrated to alter adult neurogenesis. The presence of various inflammatory components, such as immune cells, cytokines, or chemokines, plays a role in regulating the survival, proliferation, and maturation of neural stem cells. Neuroinflammation has also been considered as a hallmark neuropathological feature of AD. In this review, we summarize current, state-of-the art perspectives on adult neurogenesis, neuroinflammation, and the relationship between these two phenomena in AD. Furthermore, we discuss the potential therapeutic approaches, focusing on the anti-inflammatory and proneurogenic interventions that have been reported in this field.
Hutchinson-Gilford progeria syndrome is a progeroid disorder of children caused by de novo mutations in LMNA that lead to the synthesis of an internally truncated form of prelamin A (commonly called progerin). The production of progerin causes multiple disease phenotypes, including an unusual vascular phenotype characterized by the loss of smooth muscle cells in the arterial media and fibrosis of the adventitia. In this report, we show that progerin expression, combined with mechanical stress, promotes smooth muscle cell death. Disrupting the LInker of Nucleoskeleton and Cytoskeleton (LINC) complex in smooth muscle cells ameliorates the toxic effects of progerin on smooth muscle cells and limits the accompanying adventitial fibrosis.
We are indebted to Robert I. Webb (the editor) and an anonymous referee for valuable comments and suggestions. We are responsible for any remaining errors.This study extends the long-term temperature model proposed by Alaton et al. (2002) by taking into account ARCH/GARCH effects to reflect the clustering of volatility in temperature. The fixed variance model and the ARCH model are estimated using Taiwan weather data from 1974 through 2003. The results show that for HDD/CDD the call price is higher under ARCH-effects variance than under fixed variance, while the put price is lower. Although different pricing methods are employed in pricing weather options, the effects of mean and standard deviation on option prices are mathematically proved to be the same as those in pricing traditional financial derivatives using the Black-Scholes formula.
Adaptive optics is a technology that improves the performance of optical systems by
reducing wavefront distortion. Currently, it is playing a more important role in astronomy,
laser physics, nonlinear optics, medicine, vision and the defense industry. In this paper, we
demonstrate a microelectromechanical system (MEMS) deformable mirror that is made of a
2.15 µm
thick polyimide film and is actuated by electrostatic force. We made a large-stroke
MEMS deformable mirror with a 20 mm diameter circular opening and 67
hexagonal actuation electrodes. We also used modeling software, ANSYS,
to simulate the deformation behavior of the membrane and discussed the
device parameter tuning for versatile applications. The maximum stroke was
39 µm
as 195 V was applied. Because of the large stroke of the device, the resonant frequency was
approximately 40 Hz. The resonant frequency can be increased by thickening the polyimide
membrane. The polymer deformable mirror is a strong candidate for active wavefront
control, based on our experimental results.
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