23 research outputs found
Intraocular involvement in multifocal fibrosclerosis11The authors have no financial interest in any product, drug, instrument, or piece of equipment mentioned in this article.
Glia–neuron interactions in the mammalian retina
AbstractThe mammalian retina provides an excellent opportunity to study glia–neuron interactions and the interactions of glia with blood vessels. Three main types of glial cells are found in the mammalian retina that serve to maintain retinal homeostasis: astrocytes, Müller cells and resident microglia. Müller cells, astrocytes and microglia not only provide structural support but they are also involved in metabolism, the phagocytosis of neuronal debris, the release of certain transmitters and trophic factors and K+ uptake. Astrocytes are mostly located in the nerve fibre layer and they accompany the blood vessels in the inner nuclear layer. Indeed, like Müller cells, astrocytic processes cover the blood vessels forming the retinal blood barrier and they fulfil a significant role in ion homeostasis. Among other activities, microglia can be stimulated to fulfil a macrophage function, as well as to interact with other glial cells and neurons by secreting growth factors. This review summarizes the main functional relationships between retinal glial cells and neurons, presenting a general picture of the retina recently modified based on experimental observations. The preferential involvement of the distinct glia cells in terms of the activity in the retina is discussed, for example, while Müller cells may serve as progenitors of retinal neurons, astrocytes and microglia are responsible for synaptic pruning. Since different types of glia participate together in certain activities in the retina, it is imperative to explore the order of redundancy and to explore the heterogeneity among these cells. Recent studies revealed the association of glia cell heterogeneity with specific functions. Finally, the neuroprotective effects of glia on photoreceptors and ganglion cells under normal and adverse conditions will also be explored
Time-dependent changes in gene expression in myocytes from the non-infarcted myocardium of rats with evolving heart failure
A simple method for noninvasive estimation of pulmonary vascular resistance
AbstractObjectivesWe sought to test whether the ratio of peak tricuspid regurgitant velocity (TRV, ms) to the right ventricular outflow tract time-velocity integral (TVIRVOT, cm) obtained by Doppler echocardiography (TRV/TVIRVOT) provides a clinically reliable method to determine pulmonary vascular resistance (PVR).BackgroundPulmonary vascular resistance is an important hemodynamic variable used in the management of patients with cardiovascular and pulmonary disease. Right-heart catheterization, with its associated disadvantages, is required to determine PVR. However, a reliable noninvasive method is unavailable.MethodsSimultaneous Doppler echocardiographic examination and right-heart catheterization were performed in 44 patients. The ratio of TRV/TVIRVOTwas then correlated with invasive PVR measurements using regression analysis. An equation was modeled to calculate PVR in Wood units (WU) using echocardiography, and the results were compared with invasive PVR measurements using the Bland-Altman analysis. Using receiver-operating characteristics curve analysis, a cutoff value for the Doppler equation was generated to determine PVR >2WU.ResultsAs calculated by Doppler echocardiography, TRV/TVIRVOTcorrelated well (r = 0.929, 95% confidence interval 0.87 to 0.96) with invasive PVR measurements. The Bland-Altman analysis between PVR obtained invasively and that by echocardiography, using the equation: PVR= TRV/TVIRVOT× 10 + 0.16 , showed satisfactory limits of agreement (mean 0 ± 0.41). A TRV/TVIRVOTcutoff value of 0.175 had a sensitivity of 77% and a specificity of 81% to determine PVR >2WU.ConclusionsDoppler echocardiography may provide a reliable, noninvasive method to determine PVR
