ABSTRACT
The teleconsultation model of the National Telemedicine and Connected Health Center is cited as an example, to study the pricing formulation of video teleconsultation. This refers to the pricing composed of such four parties as the inviter′s hospital, invitee′s hospital, technical support, and business operation. Based on such pricing standard, teleconsultation charges can be collected. From 2015 to 2017, the annual applications of teleconsultation is on the rise year by year. Such pricing has been accepted by patients at large, as it embodies the value of each party, and ensures the long-term running of telemedicine system. Therefore, this pricing formulation could be a referable model for the localities to formulate their teleconsultation pricing.
ABSTRACT
Objective To investigate radiological imaging tele-consultation in clinical application. Methods All cases of the tele-consultation analyzed retrospectively came from the Hospital′s telemedicine center from January to December of 2015. The statistical analysis covered the level of applying hospital, modality type of imaging,inspection area,as well as the timing and purpose of the consultation.Results A total of 179 medical institutions required image consultation in 2015,most of which secondary hospitals,up to 58.66%. A total of 2 454 cases were consulted,including X-ray of 278 cases (11.33%),CT of 1 353 cases (55.13%), and MRI of 823 cases (33.54%). Purposes of tele-consultation vary from differential diagnosis of 1 602 cases(65.28%),definitive diagnosis of 766 cases(31.21%),and confirmative review of 86 cases (3.51%). 90.59% of the consultation cases were finished within 24 hours. Conclusions Radiological imaging tele-consultation could offer local hospitals with diagnosis efficiently effectively. On one hand,this service saves patients'costs and gains time for treatment. On the other,it makes primary hospitals more efficient in radiological imaging diagnosis.
ABSTRACT
Background Our previous study demonstrated that microglial activation is closely associated with photoreceptor apoptosis in rd mice.Recent studies on central nervous system (CNS) showed that activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a key role in the microglia activation and neural cell death.However,the mechanism of NADPH oxidase during the retinal degeneration and the effect of NADPH oxidase inhibitor on photoreceptor apoptosis are concerned.Objective The aim of this study was to further explore the production of reactive oxygen species (ROS) by NADPH oxidase in the retinal degenerative process of rd mice and protection of NADPH oxidase inhibitor on photoreceptors.Methods Sixty rd mice at postnatal day 9 (P9) were randomized into the experimental group and the control group by throwing coins method.Apocynin,a NADPH oxidase inhibitor,was intraperitoneally injected in the dose of 10 mg/kg (0.01 ml/kg) once daily for 5 days (P13) in the experimental group,and the equal amount of PBS was used in the same way in the control group,and 10 C57BL/6N mice without injection of any drugs served as the wild type mice group.All the mice were sacrificed in P14 for the preparation of retinal sections.The expression of ROS in the retina was detected by dihydroethidium (DHE) fluorescence staining.Expression level of rhodopsin mRNA in the photoreceptor of the mice was determined by real-time PCR,and the thickness of retinal outer nuclear layer (ONL) in the mice of the experimental group and the control group was measured using hematoxylin & eosin staining.The use and care of the animals complied with the Statement of Association for Research in Vision and Ophthalmology.Results DHE staining showed that the ROS presented with the red fluorescence in the mouse retinas.In the rd mice of the experimental group,the ROS fluorescence intensity was dramatically enhanced in comparison with C57BL/6N mice,but weakened in comparison with the rd mice of the control group.Real-time PCR revealed that the relative expressing level of rhodopsin mRNA in the photoreceptor was (4.21±0.33) in the experimental group and (0.93±0.24) in the control group,showing a significant difference between them (t =2.360,P =0.000).The thickness value of retinal ONL was (35.95±1.63)μm in the mice of the experimental group,which was significantly higher than that in the mice of the control group ([23.17±1.38] μm) (t=3.850,P=0.016).Conclusions In the retinal degeneration of rd mice,activation of NADPH oxidase increases the ROS production.Apocynin can slow the apoptosis procedure of photoreceptor cells of rd mice.
ABSTRACT
Background Studies showed that activation of microglia-derived nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a key role in the neurodegenerative diseases and neural cell death in central nervous system.The effect of NADPH on cone degeneration have been determined in rd rats,its role in rod degeneration is relatively less studied.Objective This study was to study the expression of NADPH oxidase in the retinal degenerative process in rd mice and further explore its role in the photoreceptor degeneration.Methods rd Mice at postnatal day 8 (P8),P10,P12,P14,P16 and P18 were collected.The mice were sacrificed,and retinal sections,RNAs and proteins were prepared in above-mentioned time points.The expressions of the gp91 phox,a major subunit of NADPH oxidase,in transcript level and protein level in the retinas were semi-quantitatively detected by real-time PCR and Western blot respectively.Expression of gp91phox was localized in the rd retinas as ageing by immunohistochemstry,and the co-expression of gp91phox with CD11b,a specific marker of microglial cells,was assayed by immunofluorescent double labeling.The C57BL/6N mice were served as controls.The use and care of the animals complied with the Guideline of ARVO.Results Real-time PCR showed that gp91phox mRNA was not expressed in the retinas of C57BL/6N mice.Gp91phox mRNA was found to have less expressed in retinas of P8 rd mice.With aging,the expression level of gp91phox mRNA (gp91phox mRNA/β-actin) in rd mouse retinas was gradually increased with the highest level in P14 mice(1.136±0.370).A significant difference was seen in the gp91 phox mRNA expression among various groups of mice (F=17.81,P =0.00),and gp91phox mRNA expression was significantly elevated in P10,P12,P14,P16 and P18 rd mice compared with P8 rd mice(all at P＜0.05).The expression level of gp91phox protein (A value) in the retinas presented with a similar trend in the rd mice,with a significant difference among the various ages of rd mice and C57BL/6N mice (F =354.00,P＜0.01).The expression level of gp91 phox protein was increased in the rd mice in comparison with the C57BL/6N mice (all at P＜0.05).Immunochemistry revealed that the positive response cells for gp91phox increased in the inner layers of retinas in P10 rd mice and peaked in P14 mice.Immunofluorescent double labeling exhibited that gp91phox were seen to present a co-expression with CD11b,showing an orange fluorescence.Conclusions Expression of NADPH oxidase in the rctinas in the rd mice up-regulates and is parallels to the microglial activation and photoreceptor degeneration,suggesting that NADPH oxidase plays a role in the retinal dystrophy associated with microglial activation.
ABSTRACT
Objective To investigate the effects of different temperature seawater immersion on the hemodynamic of traumato-hemorrhagic shock rats. Methods 40 male traumato-hemorrhagic shock rats were utilized in this experiment. The hemodynamic parameters were determined in rats at preshock, shock, 10min, 30min, 1h, 3h, 5h after immersion in 15℃, 21℃ and 31℃ seawater respectively. Results The hemodynamic parameters of rats immersed in 21℃ seawater were markedly decreased compared with those of land control group. The hemodynamic parameters of rats immersed in 15℃ seawater rapidly decreased as compared with other groups. After 1 hour immersed in 15℃ seawater, the MAP, HR, ?dpdtmax of traumato-hemorrhagic shock rats were significantly decreased (P