ABSTRACT
@#AIM: To explore the characteristics and application value of ultra-wide-field auto-fluorescence in Stargardt disease. <p>METHODS: A retrospective study of clinical characteristics and genetically confirmed Stargardt disease patients, using Optos P200Tx for ultra-wide-field auto-fluorescence imaging, and comparing the imaging features of traditional fundus color photographs, fundus 55° auto-fluorescence, and optical coherence tomography, to evaluate the ultra-wide-field auto-fluorescence in Stargardt disease image characteristics and advantages of clinical application. <p>RESULTS:All 76 eyes(100%)had high posterior auto-fluorescence, while only 42 eyes(55%)of traditional 55° auto-fluorescence showed obvious posterior high auto-fluorescence. Sixty-six eyes(87%)of the 76 eyes showed different numbers of spots, which were distributed from the posterior pole to the peripheral retina. UWAF can show clearer and more number of retinal spots than fundus color photographs, and more completely shows the number and distribution of spots area. All 76 eyes(100%)of the patients showed the oval low auto-fluorescence area induced by retinal pigment epithelium(RPE)atrophy in the center of the macula. As the disease progressed, the atrophy area expanded and the low fluorescence area expanded accordingly. Ultra-wide-field auto-fluorescence can completely display the atrophy range and area, but it cannot display in dystrophy depth. In 48 eyes(63%)ultra-wide-field auto-fluorescence, strong background auto-fluorescence was seen extending from the macula to the nasal and inferior temporal of the optic disc, forming a clear approximately vertical dividing line below the optic disc.<p>CONCLUSION: Ultra-wide-field auto-fluorescence changes in Stargardt are not limited to the posterior pole and may extend more peripherally. Ultra-wide-field imaging is a useful tool for the assessment of patients with Stargardt macular dystrophy.
ABSTRACT
Objective To investigate the effects of retinal ganglion cell-conditioned medium on the differentiation of retinal stem cells.Methods Rettial stem cells and retinal ganglion cells were isolated from rats,and immunofluorescence staining was applied to identify rat retinal stem cells and retinal ganglion cells with Nestin and Thy-1 antibody,respectively.Retinal stem cells were cultured in presence or absence of retinal ganglion cell-conditioned medium for 72 h,followed by detection of Nestin,PAX6,Thy-1 and Bin-3 gene expression in retinal stem cells by qPCR.Results isolated retinal stem cells were Nestin positive,and retinal ganglion cells were Thy-1 positive,indicating the success of isolation.Compared to retinal stem cells cultured without ganglion cellconditioned medium,ones cultured with ganglion-conditioned medium had significantly downregulated expression of Nestin and PAX6 (both P ＜ 0.000 1),and markedly upregulated expression of Thy-1 and Brn-3 (both P ＜ 0.05).Conclusion Retinal ganglion cell-conditioned medium can induce the differentiation of retinal progenitor cells into retinal ganglion-like cells.
ABSTRACT
In order to investigate the effects of different terms of inhaled nitric oxide (NO) preconditioning with low concentration on the activations of Toll-like receptor 2 and 4 (TLR2/4) in the lung ischemia-reperfusion (IR) injury in mice, we divided the male C57BL mice into five groups: sham (S) group, IR group, NO 1-min preconditioning group (15 ppm NO inhalation for 1 min before ischemia, NO 1-min), NO 10-min preconditioning group (15 ppm NO inhalation for 10 min before ischemia, NO 10-min), NO 60-min preconditioning group (15 ppm NO inhalation for 60 min before ischemia, NO 60-min). The changes of partial pressure of oxygen in artery (PaO2), left lung wet-to-dry weight ratio (W/D), and myeloperoxidase (MPO) in the injured lung were measured in every group at 6th h of reperfusion after 60 min of left lung ischemia. The changes of TLR2/4 activations and plasma TNF-α were measured in this procedure in additional mice. As compared with IR group, PaO2 increased, MPO and W/D decreased evidently after reperfusion in NO 10-min group. The changes in NO 60-min group were similar to those in NO 10-min group. There was no difference between NO 1-min and IR group. In NO inhalation group, the expressions levels of TLR2/4 mRNA and proteins were diminished, TNF-α concentrations were decreased, and the lung injuries were ameliorated effectively. We concluded that short term inhalation of NO protected lung IR injury. But the protective effect of NO was not increased with extension of inhaled NO. Inhaled NO could inhibit the activations of TLR2/4 in the lung after IR injury. TLR signal pathway might contribute to the effect of protection with NO in this model.
ABSTRACT
In order to investigate the effects of different terms of inhaled nitric oxide (NO) preconditioning with low concentration on the activations of Toll-like receptor 2 and 4 (TLR2/4) in the lung ischemia-reperfusion (IR) injury in mice, we divided the male C57BL mice into five groups: sham (S) group, IR group, NO 1-min preconditioning group (15 ppm NO inhalation for 1 min before ischemia, NO 1-min), NO 10-min preconditioning group (15 ppm NO inhalation for 10 min before ischemia, NO 10-min), NO 60-min preconditioning group (15 ppm NO inhalation for 60 min before ischemia, NO 60-min). The changes of partial pressure of oxygen in artery (PaO2), left lung wet-to-dry weight ratio (W/D), and myeloperoxidase (MPO) in the injured lung were measured in every group at 6th h of reperfusion after 60 min of left lung ischemia. The changes of TLR2/4 activations and plasma TNF-α were measured in this procedure in additional mice. As compared with IR group, PaO2 increased, MPO and W/D decreased evidently after reperfusion in NO 10-min group. The changes in NO 60-min group were similar to those in NO 10-min group. There was no difference between NO 1-min and IR group. In NO inhalation group, the expressions levels of TLR2/4 mRNA and proteins were diminished, TNF-α concentrations were decreased, and the lung injuries were ameliorated effectively. We concluded that short term inhalation of NO protected lung IR injury. But the protective effect of NO was not increased with extension of inhaled NO. Inhaled NO could inhibit the activations of TLR2/4 in the lung after IR injury. TLR signal pathway might contribute to the effect of protection with NO in this model.