66 research outputs found

    Low Temperature Glass Sintering Based on Silico Sodium Resins

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    By using silicate inorganic binders and glass waste it is possible to mould technical and artistic elements which later can be compacted by means of low temperature, and subsequently apply the sintering through high-temperature processing, which is generally lower than current melting glass processes, close to 1250 °C. The experimental phase established thermal ranges from 600°C to 750°C, a fact that allows for an effective sintering temperature (of around 650°C/18 hours). The mixtures and proportions for this experiment were fixed including ethyl silicate as a fluidizer in mixtures,as well as the size of glass grains.The results indicate good compaction of the samples after the initial phase (80°C/24h), allowing proper handling without alterations in samples edges.During heating treatment, mechanical resistance increases gradually (600-750°C), although the volume of porosity was inversely proportional. According to the matrix vs grain size relationship, the partial fusion of both materials is evident in the rounding of the glass grains as well as the resin bonds joined between them. The resins appeared in a homogenous fashion, covering and gluing the grains, a development which improves the joining of sintered samples. Samples with a mixture of sodium silicate and ethyl silicate resins experienced less melting between grains due to a lower volume of fluxing elements, which means a lower percentage volume of sodium (Na). This study concludes that a sintering process for new vitreous composites could be carried out between 650°C and 700°C, offering the opportunity for a substantial reduction in the amount of energy required to produce industrial glass. Keywords: Water-glass, glass recycling, low temperatur

    Cost analysis of chronic obstructive pulmonary disease (COPD): a systematic review

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    Background Chronic Obstructive Pulmonary Disease (COPD) is a treatable disease with a high prevalence, and high morbidity associated with significant socioeconomic costs. Objective To carry out a systematic review of the literature to analyze the main cost studies associated with COPD, in order to determine the main factors that influence the costs of the disease. Methods Searches were conducted in PubMed, SCOPUS and Web of Science databases for cost studies on COPD published in English, between the years 2015 and 2020. The search terms were ?COPD? OR ?pulmonary disease, chronic obstructive?, ?cost*? OR ?cost of illness?, ?economic impact? AND ?burden of disease?. The inclusion criteria included the identification of reported cost of the disease, economic burden, medical care expenses or use resources for COPD, the methodology used, data sources, and variables studied. Results 18 publications were analyzed: 17 included direct health costs, 6 included direct non-medical costs, 12 analyzed indirect costs and two reported intangible costs. Most of the studies reported data for developed and European countries, with direct costs being the most studied. Trends were observed in multiple studies of direct and healthcare costs for European countries measured by patient and year, where the higher costs were associated with more severe COPD and a frequent history of exacerbations. The highest costs reported corresponded to hospitalizations and the associated pharmacological treatment. The importance of the loss of productivity and premature retirement within the profile of the COPD patient was also highlighted as the main generator of indirect costs of the disease. Conclusion COPD generates substantial costs for the health system, mainly related to moderate to severe stages and the exacerbations and complications entailed. It is important to strengthen health systems with monitoring, evaluation and health education models that allow these patients to remain stable to avoid decompensation and subsequent hospitalizations

    Estudio de materiales de construcción vernáculos empleados en el patrimonio cultural: guía para la restauración arquitectónica del Colegio Máximo de Cartuja. Granada-España (siglo XIX)

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    This work was supported by Research Project MAT2016-75889-R, 2017-2019 (Spanish Ministry of Economy and Competitiveness); Research Groups HUM 629 and RNM 0179 of the Junta de Andalucia; TOP-Heritage Programme (Madrid Regional Government, ref. P2018/NMT-4372); REMINE Programme for Research and Innovation Horizon 2020 Marie Sklodowska-Curie Actions, and WARMEST Research and Innovation Staff Exchange (RISE) H2020-MSCA-RISE-2017; Scientific Unit of excellence "Ciencia en la Alhambra", ref. UCE-PP2018-01, University of Granada. The professional support of the Spanish Network TechnoHeritage (Red de Ciencia y Tecnologia para la Conservacion del Patrimonio) is also acknowledged.Colegio Maximo de Cartuja in Granada (Spain) was built by the Jesuits in 19th century. Using an archaeometric study of the building materials: bricks, glazed tiles, stained glass windows and lime-gypsum mortars (mortar masonry and concrete masonry), the vernacular concept of this construction was established within the geological framework of the “Alhambra formation”, and raw materials and techniques first used by the Nasrids in the 13th century have been identified. The results of XRD, XRF and DTA analyzes indicate the use of local clays in the manufacture of bricks and tiles fired at temperatures of ≤750 ºC. The clays contained NaCl additives, which improved the ceramic sintering, and traditional Nasrid colours (Cu, Fe, Sn) were used in the glazes and stained glass windows. Local raw materials were also used for air binders. These results have been combined to create a good-practice guide for the sustainable restoration of cultural heritage buildings.El Colegio Máximo de Cartuja en Granada fue construido por los jesuitas en el siglo XIX. El estudio arqueométrico de sus materiales: ladrillos, azulejos, vidrieras y morteros, define el concepto vernáculo de esta construcción, referenciada en el marco geológico de la “formación Alhambra”, junto a la identificación de materias primas y técnicas utilizadas por los nazaríes desde el siglo XIII. Los resultados de XRD, XRF y DTA confirman el uso de arcillas locales para fabricación de ladrillos y losetas que se hornearon a temperaturas de ≤750 ºC. Las arcillas debieron contener aditivos de NaCl que beneficiaron la sinterización cerámica, y se comprobó el uso de colores de tradición nazarí (Cu, Fe, Sn) en los esmaltes y vidrieras. Las materias primas locales también se usaron para producir aglomerantes aéreos. Estos resultados se han combinado para crear una guía de buenas prácticas para la restauración sostenible de los edificios del patrimonio cultural.Spanish Ministry of Economy and Competitiveness MAT2016-75889-RJunta de Andalucia HUM 629 RNM 0179TOP-Heritage Programme (Madrid Regional Government) P2018/NMT-4372REMINE Programme for Research and Innovation Horizon 2020 Marie Sklodowska-Curie ActionsWARMEST Research and Innovation Staff Exchange (RISE) H2020-MSCA-RISE-2017Scientific Unit of excellence "Ciencia en la Alhambra", University of Granada UCE-PP2018-0

    Multimodal Imaging, OCT en Face, and OCT Angiography of an Anomalous Retinal Artery: Case Report and Review of the Literature

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    The purpose is to study for the first time the vascular plexuses and the retinal nerve fiber layer and raphe of a patient with a very uncommon anatomical variation: an anomalous retinal artery supplying the whole macula. We used multimodal imaging, en face spectral-domain optic coherence tomography, and spectral-domain optic coherence tomography angiography. One patient presented in his left eye a very unusual anatomical variation of macular vascularization. A retinal artery deriving from the inferior temporal retinal artery irrigated the whole macula. The formation of the papillomacular bundle and the temporal raphe nerve fiber layer has been attributed to the earlier development of the central retina and to the existence of 2 distinct watershed zones. However, there are very uncommon anatomical variations of the retinal vasculature in which large retinal vessels cross the raphe and could influence the morphology and structure of the nerve fiber layer of the posterior pole. We review the literature on the subject and document for the first time an anomalous artery that irrigates the whole macula, normal thickness and morphology of the nerve fiber layer, and the temporal raphe

    Early Events in Retinal Degeneration Caused by Rhodopsin Mutation or Pigment Epithelium Malfunction: Differences and Similarities

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    To study the course of photoreceptor cell death and macro and microglial reactivity in two rat models of retinal degeneration with different etiologies. Retinas from P23H-1 (rhodopsin mutation) and Royal College of Surgeon (RCS, pigment epithelium malfunction) rats and age-matched control animals (Sprague-Dawley and Pievald Viro Glaxo, respectively) were cross-sectioned at different postnatal ages (from P10 to P60) and rhodopsin, L/M- and S-opsin, ionized calcium-binding adapter molecule 1 (Iba1), glial fibrillary acid protein (GFAP), and proliferating cell nuclear antigen (PCNA) proteins were immunodetected. Photoreceptor nuclei rows and microglial cells in the different retinal layers were quantified. Photoreceptor degeneration starts earlier and progresses quicker in P23H-1 than in RCS rats. In both models, microglial cell activation occurs simultaneously with the initiation of photoreceptor death while GFAP over-expression starts later. As degeneration progresses, the numbers of microglial cells increase in the retina, but decreasing in the inner retina and increasing in the outer retina, more markedly in RCS rats. Interestingly, and in contrast with healthy animals, microglial cells reach the outer nuclei and outer segment layers. The higher number of microglial cells in dystrophic retinas cannot be fully accounted by intraretinal migration and PCNA immunodetection revealed microglial proliferation in both models but more importantly in RCS rats. The etiology of retinal degeneration determines the initiation and pattern of photoreceptor cell death and simultaneously there is microglial activation and migration, while the macroglial response is delayed. The actions of microglial cells in the degeneration cannot be explained only in the basis of photoreceptor death because they participate more actively in the RCS model. Thus, the retinal degeneration caused by pigment epithelium malfunction is more inflammatory and would probably respond better to interventions by inhibiting microglial cells.Fundación Séneca, Agencia de Ciencia y Tecnología Región de Murcia (19881/GERM/15) and the Spanish Ministry of Economy and Competitiveness, Instituto de Salud Carlos III, Fondo Europeo de Desarrollo Regional “Una Manera de Hacer Europa” ISCIII-FEDER PI16/00380, PI16/00031, RD16/0008/0026, RD16/0008/0016, SAF2015-67643

    Different Ipsi-and Contralateral Glial Responses to Anti- VEGF and Triamcinolone Intravitreal Injections in Rats

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    Citation: Di Pierdomenico J, García-Ayuso D, Jiménez-López M, AgudoBarriuso M, Vidal-Sanz M, VillegasPérez MP. Different ipsi-and contralateral glial responses to anti-VEGF and triamcinolone intravitreal injections in rats. Invest Ophthalmol Vis Sci. 2016;57:3533-3544. DOI:10.1167/iovs.16-19618 PURPOSE. To investigate the glial response of the rat retina to single or repeated intravitreal injections (IVI). METHODS. Albino Sprague-Dawley rats received one or three (one every 7 days) IVI of anti-rat VEGF (5 lL; 0.015 lg/lL), triamcinolone (2.5 or 5 lL; 40 lg/lL; Trigón Depot), bevacizumab (5 lL; 25 lg/lL; Avastin), or their vehicles (PBS and balanced salt solution) and were processed 7 days after the last injection. Retinas were dissected as whole mounts and incubated with antibodies against: Iba1 (Ionized Calcium-Binding Adapter Molecule 1) to label retinal microglia, GFAP (Glial Fibrillary Acidic Protein) to label macroglial cells, and vimentin to label Müller cells. The retinas were examined with fluorescence and confocal microscopy, and the numbers of microglial cells in the inner retinal layers were quantified using a semiautomatic method. RESULTS. All the injected substances caused an important micro-and macroglial response locally at the injection site and all throughout the injected retina that was exacerbated by repeated injections. The microglial response was also observed but was milder in the contralateral noninjected eyes. The IVI of the humanized antibody bevacizumab caused a very strong microglial reaction in the ipsilateral retina. Two types of macroglial response were observed: astrocyte hypertrophy and Müller end-foot hypertrophy. While astrocyte hypertrophy was widespread throughout the injected retina, Müller end-foot hypertrophy was localized and more extensive with triamcinolone use or after repeated injections. CONCLUSIONS. Intravitreal injections cause micro-and macroglial responses that vary depending on the injected agent but increase with repeated injections. This inflammatory glial response may influence the effects of the injected substances on the retina

    Role of microglial cells in photoreceptor degeneration

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    Inherited photoreceptor degeneration in humans constitutes a major cause of irreversible blindness in the world. They comprise various diseases, but retinitis pigmentosa is the most frequently observed. Retinitis pigmentosa is commonly limited to the eye, where there is progressive photoreceptor degeneration, rods and secondarily cones. The mechanisms of cone and rod degeneration continue to be investigated, since most of the mutations causing retinitis pigmentosa affect rods and thus, the secondary death of cones is an intriguing question but, ultimately, the cause of blindness. Understanding the mechanisms of rod and cone degeneration could help us to develop therapies to stop or, at least, slow down the degeneration process. Secondary cone degeneration has been attributed to the trophic dependence between rods and cones, but microglial cell activation could also have a role. In this review, based on previous work carried out in our laboratory in early stages of photoreceptor degeneration in two animal models of retinitis pigmentosa, we show that microglial cell activation is observed prior to the the initiation of photoreceptor death. We also show that there is an increase of the retinal microglial cell densities and invasion of the outer retinal layers by microglial cells. The inhibition of the microglial cells improves photoreceptor survival and morphology, documenting a role for microglial cells in photoreceptor degeneration. Furthermore, these results indicate that the modulation of microglial cell reactivity can be used to prevent or diminish photoreceptor death in inherited photoreceptor degenerations

    Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush.

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    Purpose To study the effect of topical administration of bromfenac, a nonsteroidal anti-inflammatory drug (NSAID), on retinal gliosis and levels of prostaglandin E2 (PGE2) after complete optic nerve crush (ONC). Methods Adult albino rats were divided into the following groups (n = 8 retinas/group): (1) intact, (2) intact and bromfenac treatment (twice a day during 7 days), (3) ONC (7 days), and (4) ONC (7 days) + bromfenac treatment (twice a day during 7 days). Animals from groups 3 and 4 were imaged in vivo with spectral-domain optical coherence tomography (SD-OCT) before the procedure and 15 minutes, 3, 5, or 7 days later. Retinas from all groups were analyzed by immunodetection, Western blotting, or enzyme-linked immunoabsorbent assay (ELISA). Results Quantification of Brn3a (brain-specific homeobox/POU domain protein 3A) +RGCs (retinal ganglion cells) in cross sections showed that bromfenac treatment does not accelerate ONC-induced degeneration. Cellular retinaldehyde binding protein 1 regulation indicated that bromfenac improves retinal homeostasis in injured retinas. Spectral-domain OCT showed that the thickness of the retina and the retinal nerve fiber layer at 7 days post ONC was significantly reduced in bromfenac-treated animals when compared to untreated animals. In agreement with these data, hypertrophy of astrocytes and Muller cells and expression of glial fibrillary acidic protein and vimentin were greatly diminished by bromfenac treatment. While no changes in cyclooxygenase (COX) enzyme COX1 and COX2 expression were observed, there was a significant increase of PGE2 after ONC that was controlled by bromfenac treatment. Conclusions Topical administration of bromfenac is an efficient and noninvasive treatment to control the retinal gliosis and release of proinflammatory mediators that follow a massive insult to the RGC population

    Tracing the retina to analyze the integrity and phagocytic capacity of the retinal pigment epithelium

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    We have developed a new technique to study the integrity, morphology and functionality of the retinal neurons and the retinal pigment epithelium (RPE). Young and old control albino (Sprague-Dawley) and pigmented (Piebald Virol Glaxo) rats, and dystrophic albino (P23H-1) and pigmented (Royal College of Surgeons) rats received a single intravitreal injection of 3% Fluorogold (FG) and their retinas were analyzed from 5 minutes to 30 days later. Retinas were imaged in vivo with SD-OCT and ex vivo in flat-mounts and in cross-sections. Fifteen minutes and 24 hours after intravitreal administration of FG retinal neurons and the RPE, but no glial cells, were labeled with FG-filled vesicles. The tracer reached the RPE 15 minutes after FG administration, and this labeling remained up to 30 days. Tracing for 15 minutes or 24 hours did not cause oxidative stress. Intraretinal tracing delineated the pathological retinal remodelling occurring in the dystrophic strains. The RPE of the P23H-1 strain was highly altered in aged animals, while the RPE of the RCS strain, which is unable to phagocytose, did not accumulate the tracer even at young ages when the retinal neural circuit is still preserved. In both dystrophic strains, the RPE cells were pleomorphic and polymegathic.This study was supported by the Spanish Ministry of Economy and Competitiveness, Instituto de Salud Carlos III, Fondo Europeo de Desarrollo Regional “Una manera de hacer Europa” (PI16/00031, PI16/00380, PI19/00071, PI19/00203, SAF2015-67643-P, RD16/0008, RD16/0008/0026 and RD16/0008/0016) and by the Fundación Séneca, Agencia de Ciencia y Tecnología Región de Murcia (19881/GERM/15)
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