943 resultados para Glial Wedge
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This paper introduces a stabilization problem for an elementary impact control system in the plane. The rich dynamical properties of the wedge billiard, combined to the relevance of the associated stabilization problem for feedback control issues in legged robotics make it a valuable benchmark for energy-based stabilization of impact control systems.
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This paper studies the effects of magnetic wedges on the equivalent circuit parameters of the Brushless Doubly-Fed Machine (BDFM). Magnetic wedges are used in slot openings of large electrical machines to reduce magnetizing currents, but the study of their effects on the BDFM performance is not straightforward due to the complex magnetic fields in the BDFM. Equivalent circuit and FE models have been developed for a 250 kW BDFM taking into account the effects of wedges and verified experimentally.
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A new type of interferometer, the moving-optical-wedge interferometer, is presented, and its principle and properties are studied. The novel interferometer consists of one beam splitter, two flat fixed mirrors, two fixed compensating plates, one fixed optical wedge, and one moving optical wedge. The optical path difference (OPD) as a function of the displacement of the moving optical wedge from the zero path difference position is accomplished by the straight reciprocating motion of the moving optical wedge. A large physical shift of the moving optical wedge corresponds to a very short OPD value of the new interferometer if the values of the wedge angle and the refractive index of the two optical wedges are given properly. The new interferometer is not so sensitive to the velocity variation of the moving optical wedge and the mechanical disturbances compared with the Michelson interferometer, and it is very applicable to low-spectral-resolution application for any wavenumber region from the far infrared down to the ultraviolet. (C) 2008 Optical Society of America.
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Two well-defined deltaic sequences in the Bohai Sea and in the South Yellow Sea represent post-glacial accumulation of Yellow River-derived sediments. Another prominent depocenter on this epicontinental shelf, a pronounced clinoform in the North Yellow Sea, wraps around the northeastern and southeastern end of the Shandong Peninsula, extending into the South Yellow Sea. This Shandong mud wedge is 20 to 40 m thick and contains an estimated 300 km(3) of sediment. Radiocarbon dating, shallow seismic profiles, and regional sea-level history suggest that the mud wedge formed when the rate of post-glacial sea-level rise slackened and the summer monsoon intensified, at about 11 ka. Geomorphic configuration and mineralogical data indicate that present-day sediment deposited on the Shandong mud wedge comes not only from the Yellow River but also from coastal erosion and local rivers. Basin-wide circulation in the North Yellow Sea may transport and redistribute fine sediments into and out of the mud wedge.
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Aims/hypothesis: The impact of AGEs and advanced lipoxidation end-products (ALEs) on neuronal and Müller glial dysfunction in the diabetic retina is not well understood. We therefore sought to identify dysfunction of the retinal Müller glia during diabetes and to determine whether inhibition of AGEs/ALEs can prevent it.
Methods: Sprague-Dawley rats were divided into three groups: (1) non-diabetic; (2) untreated streptozotocin-induced diabetic; and (3) diabetic treated with the AGE/ALE inhibitor pyridoxamine for the duration of diabetes. Rats were killed and their retinas were evaluated for neuroglial pathology. Results: AGEs and ALEs accumulated at higher levels in diabetic retinas than in controls (p<0.001). AGE/ALE immunoreactivity was significantly diminished by pyridoxamine treatment of diabetic rats. Diabetes was also associated with the up-regulation of the oxidative stress marker haemoxygenase-1 and the induction of glial fibrillary acidic protein production in Müller glia (p<0.001). Pyridoxamine treatment of diabetic rats had a significant beneficial effect on both variables (p<0.001). Diabetes also significantly altered the normal localisation of the potassium inwardly rectifying channel Kir4.1 and the water channel aquaporin 4 to the Müller glia end-feet interacting with retinal capillaries. These abnormalities were prevented by pyridoxamine treatment.
Conclusions/interpretation: While it is established that AGE/ALE formation in the retina during diabetes is linked to microvascular dysfunction, this study suggests that these pathogenic adducts also play a role in Müller glial dysfunction.
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A downstream target of the Wnt pathway, neurone glial-related cell adhesion molecule (Nr-CAM) has recently been implicated in human cancer development. However, its role in colorectal cancer (CRC) pathobiology and clinical relevance remains unknown. In this study, we examined the clinical significance of Nr-CAM protein expression in a retrospective series of 428 CRCs using immunohistochemistry and tissue microarrays. Cox proportional hazards regression was used to calculate hazard ratios (HR) of mortality according to various clinicopathological features and molecular markers. All CRC samples were immunoreactive for Nr-CAM protein expression, compared to 10 / 245 (4%) matched normal tissue (P <0.0001). Of 428 CRC samples, 97 (23%) showed Nr-CAM overexpression, which was significantly associated with nodal (P = 0.012) and distant (P = 0.039) metastasis, but not with extent of local invasion or tumor size. Additionally, Nr-CAM overexpression was associated with vascular invasion (P = 0.0029), p53 expression (P = 0.036), and peritoneal metastasis at diagnosis (P = 0.013). In a multivariate model adjusted for other clinicopathological predictors of survival, Nr-CAM overexpression correlated with a significant increase in disease-specific (HR 1.66; 95% confidence interval 1.11-2.47; P = 0.014) and overall mortality (HR 1.57; 95% confidence interval 1.07-2.30; P = 0.023) in advanced but not early stage disease. Notably, 5-fluorouracil-based chemotherapy conferred significant survival benefit to patients with tumors negative for Nr-CAM overexpression but not to those with Nr-CAM overexpressed tumors. In conclusion, Nr-CAM protein expression is upregulated in CRC tissues. Nr-CAM overexpression is an independent marker of poor prognosis among advanced CRC patients, and is a possible predictive marker for non-beneficence to 5-fluorouracil- based chemotherapy.
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Neuronal dysfunction has been noted very soon after the induction of diabetes by streptozotocin injection in rats. It is not clear from anatomical evidence whether glial cell dysfunction accompanies the well-documented neuronal deficit. Here, we isolate the Müller cell driven slow-P3 component of the full-field electroretinogram and show that it is attenuated at 4 weeks following the onset of streptozotocin-hyperglycaemia. We also found a concurrent reduction in the sensitivity of the phototransduction cascade, as well as in the components of the electroretinogram known to indicate retinal ganglion cell and amacrine cell integrity. Our data support the idea that neuronal and Müller cell dysfunction occurs at the same time in streptozotocin-induced hyperglycaemia.
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The wedge shell, Donax trunculus, inhabits high energy environment of exposed sandy beaches from the Atlantic coast of France to Senegal. Like all Donacidae, it is relative small, flat-shaped with elongated solid shells. It is a highly demanded and valuable species mainly in Algarve, with the dredge fleet increasing the pressure on species stocks. In 1986 the Portuguese Institute for the Ocean and Atmosphere (IPMA) initiated a bivalve survey program to evaluate the stock status of species with economical valuable but always on the adult population. Since then, several managing measures were implemented to guarantee bivalves’ sustainable exploitation. Despite the available information on the abundance and distribution of the wedge shell along the Algarve coast, no information on the larval planktonic phase is available. To fill in this gap, the present study aimed at obtaining, for the first time information on the broodstock condition and on the pelagic phase of the wedge shell in the Algarve coast.
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Serum-free aggregating cell cultures of fetal rat telencephalon were examined by a combined biochemical and double-labeling immunocytochemical study for the developmental expression of glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS). It was found that these two astroglial markers are co-expressed at different developmental stages in vitro. During the phase of cellular maturation (i.e. between days 14 and 34), GFAP levels and GS activity increase rapidly and in parallel. At the same time, the number of immunoreactive cells increase while the long and thick processes staining in early cultures gradually disappear. The present results demonstrate that in this particular cell culture system only one type of astrocytes develops which expresses both GFAP and GS and which attains a relatively high degree of maturation.
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Management of chronic pain is a real challenge, and current treatments focusing on blocking neurotransmission in the pain pathway have only resulted in limited success. Activation of glia cells has been widely implicated in neuroinflammation in the central nervous system, leading to neruodegeneration in many disease conditions such as Alzheimer's and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-α and interleukin-1β can not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as BDNF and bFGF that are produced by glia to protect neurons. Thus, glia cells can powerfully control pain when they are activated to produce various pain mediators. We will review accumulating evidence supporting an important role of microglia cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We will also discuss possible signaling mechanisms in particular MAP kinase pathways that are critical for glia control of pain. Investigating signaling mechanisms in microglia may lead to more effective management of devastating chronic pain.
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