Suchergebnisse

O lazer como fenômeno social e experiência pessoal adquiriu, nos últimos anos, uma importância que não adquiria desde a antiguidade. Vivemos uma transformação relevante de atitudes em relação ao lazer, cuja consequência é o aumento da importância desta área da vivência social no bem-estar, na satisfação e na qualidade de vida em geral. Também tem induzido, entre pesquisadores e universidades, um aumento do interesse em explicar e conhecer esse fenômeno, que se acredita ser o elo que faltava para a compreensão do comportamento e da sociedade atual. Este artigo tem como objetivo explorar as pesquisas realizadas que relacionam o lazer e o tempo livre com a vida do estudante universitário. Essas investigações evidenciam a importância do lazer entendido como práticas que buscam relaxamento, descanso e desligamento das rotinas do dia-a-dia e, por outro lado, todas aquelas atividades que têm a ver com as práticas de convivência e / ou vivências. relacionadas aos cuidados físicos de cada indivíduo. Além disso, os estudos discutidos no artigo destacam os fatores inclusivos que ocorrem entre os estudantes universitários e aqueles relacionados ao bem-estar socioeducativo, o florescimento de valores que melhoram a convivência social e a melhoria da qualidade de vida: práticas culturais, formativas ou experiências relacionadas ao turismo.

PURPOSE: To explore the distribution of guanylyl cylase-activating proteins 1 and 2 (GCAP1 and GCAP2) in the mammalian retina. METHODS: Cryostat and vibratome vertical sections and wholemount retinas from mouse, rat, cat, bovine, monkey, and human eyes were prepared for immunocytochemistry and viewing by light and confocal microscopy. RESULTS: In all mammalian retinas investigated, intense GCAP1 immunoreactivity (GCAP1-IR) was seen in cone photoreceptor inner and outer segments, cell bodies, and synaptic regions. Intensity of the GCAP1-IR was strong in inner segments of rods in all species but weaker in outer segments-particularly so in primates and cats. GCAP2 immunoreactivity (GCAP2-IR) was weak in bovine, mouse, and rat cones but was intense in human and monkey cones. In all species except primates, GCAP2 staining was intense in rod inner and outer segments. In primates GCAP2-IR was intense in the rod inner segment but faint in the rod outer segment. A striking difference from the GCAP1 pattern of immunoreactivity was seen with GCAP2 antibodies as far as the inner retina was concerned. GCAP2-IR was evident in certain populations of bipolar, amacrine, and ganglion cells in all species. CONCLUSIONS: GCAP1 and GCAP2, which are involved in Ca2+-dependent stimulation and inhibition of photoreceptor guanylyl cyclase, can be detected in mammalian photoreceptor inner and outer segments, consistent with their physiological function. The occurrence of both GCAPs in the synaptic region of the photoreceptors indicates participation of these proteins in pathways other than regulation of phototransduction. The occurrence of GCAP2 in inner retinal neurons is indicative of second-messenger chemical transduction, possibly in metabotropic glutamate, gamma-aminobutyric acid (GABA) receptor, and nitric oxide-activated neural circuits. ; Supported by grant EYO3323 from the National Eye Institute, National Institutes of Health, Bethesda, Maryland; a grant to the Department of Ophthalmology, Moran Eye Center, Salt Lake City, Utah; and a grant from Research to Prevent Blindness, New York, New York. NC was supported in part by grant DGICYT PB 94-1501 from the government of Valencia, Spain. The confocal microscope in the Moran Eye Center is supported by donations from the Lions Clubs of Utah.

Retinal neurodegenerative diseases involve a scenario of inflammation and cell death that leads to morphological alterations and visual impairment. Non-ocular inflammatory processes could affect neurodegenerative retinal disorders and their progression, at least in part by activating microglial cells and releasing pro-inflammatory cytokines. Our purpose was to study the consequences of a systemic inflammatory process in the progression of retinal degeneration in P23H rats, a retinitis pigmentosa (RP) model. In order to induce a mild chronic systemic inflammation, we administered low doses of lipopolysaccharide (LPS) from age P20 to P60 to dystrophic P23H rats and healthy SD rats. Visual responsiveness was assessed by electroretinography (ERG). The morphological state of the retinas was analyzed by fluorescent immunohistochemistry (IHC), evaluating the number, morphology, and connectivity of different neuronal populations by means of cell type-specific markers. Microglia density, distribution, and degree of activation were evaluated by IHC and flow cytometry. The expression levels of inflammation- and apoptosis-related genes were analyzed by qRT-PCR arrays. Low-dose LPS administration did not induce significant functional or morphological changes in the retina of SD rats, although at the molecular level, we detected expression changes in genes related to apoptosis. Otherwise, systemic injection of LPS into P23H rats induced a further deterioration in the ERG response, with greater loss of photoreceptors and worsening of synaptic connectivity, accompanied by increasing numbers of microglial cells, which also showed a more intense activation state. Several inflammation- and apoptosis-related genes were upregulated. Our results indicate that chronic exacerbation of the inflammatory response in response to LPS accelerates neurodegeneration in dystrophic P23H rats, suggesting that in patients with ocular neurodegenerative diseases, peripheral damage, as a systemic infection or chronic inflammatory process, could accelerate disease progression, and should be taken into account in order to select an appropriate therapy to revert, block or slow-down the degenerative process. ; This research was supported by grants from the Spanish Ministry of Economy and Competitiveness (MINECO-FEDER BFU2015-67139-R), Instituto de Salud Carlos III (RETICS-FEDER RD16/0008/0016), Asociación Retina Asturias, and the Regional Government of Valencia (PROMETEO/2016/158).

Retinitis pigmentosa (RP) includes a group of genetic disorders that involve the loss of visual function due to mutations mainly in photoreceptors but also in other retinal cells. Apoptosis, retinal disorganization, and inflammation are common in the progression of the disease. Epigallocatechin gallate (EGCG) has been proved as beneficial in different eye diseases. Pigmented heterozygous P23H rat was used as an animal model of RP. Visual function was assessed by optomotor and electroretinogram (ERG) and circadian rhythms were evaluated by telemetry. Hepatic oxidative damage and antioxidant defenses were assessed using biochemical tests. The visual function of the EGCG P23H group was preserved, with a deterioration in the activity period and lower values in the interdaily stability parameter. Control rats treated with EGCG were less active than the sham group. EGCG increased antioxidant levels in P23H rats but reduced total hepatic antioxidant capacity by almost 42% in control rats compared to the sham group. We conclude that treatment with EGCG improves visual function and antioxidant status in P23H rats but diminishes antioxidant defenses in wild-type control animals, and slightly worsens activity circadian rhythms. Further studies are necessary to clarify the beneficial effects in disease conditions and in healthy organisms. ; This research was supported by the Spanish Ministry of Economy and Competitiveness (MINECO-FEDER BFU2015-67139-R), the Instituto de Salud Carlos III (project PI13/01124 and Ocular Pathology National Net RETICS-Oftared RETICS-FEDER RD16/0008/0016), FARPE-FUNDALUCE, ACIF/2016/055, FEDER IDIFEDER/2017/064, the Fondo Europeo de Desarrollo Regional (FEDER) funds: "Una manera de hacer Europa", and the Government of Aragon (Group B08_17R and Predoctoral Grant L. Perdices, C060/2014).

Multiple system atrophy (MSA) is a rare adult-onset rapidly progressive fatal neurodegenerative disorder characterized by the abnormal aggregation of misfolded α-synuclein primarily in oligodendrocytes. ; NIH (U54-NS065736-01), Multiple System Atrophy Coalition, Michael J. Fox Foundation, Dysautonomia Foundation, Regional Government of Valencia (Prometeo 2016/158), Spanish Health Research Institute Carlos III (ISCIII RETICS-FEDER RD12/0034/0010), Ministry of Economy of Spain (MINECO-FEDER-BFU2015-67139-R), and Ministry of Education of Spain (FPU14/03166).

Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by a progressive loss of visual function that primarily affect photoreceptors, resulting in the complete disorganization and remodeling of the retina. Progression of the disease is enhanced by increased oxidative stress in the retina, aqueous humor, plasma, and liver of RP animal models and patients. Melatonin has beneficial effects against age-related macular degeneration, glaucoma, and diabetic retinopathy, in which oxidative stress plays a key role. In the present study, we used the P23HxLE rat as an animal model of RP. Melatonin treatment (10 mg/kg b.w. daily in drinking water for 6 months) improved the parameters of visual function and decreased the rate of desynchronization of the circadian rhythm, both in P23HxLE and wild-type rats. Melatonin reduced oxidative stress and increased antioxidant defenses in P23HxLE animals. In wild-type animals, melatonin did not modify any of the oxidative stress markers analyzed and reduced the levels of total antioxidant defenses. Treatment with melatonin improved visual function, circadian synchronization, and hepatic oxidative stress in P23HxLE rats, an RP model, and had beneficial effects against age-related visual damage in wild-type rats. ; This research was funded by the Instituto de Salud Carlos III Ocular Pathology National Net RETICS-Oftared (RD16/0008) and project PI13/01124; the Government of Aragon (Group B08_17R and a predoctoral grant to L. Perdices, C060/2014); and Fondo Europeo de Desarrollo Regional (FEDER) funds: "Una manera de hacer Europa".

Retinitis pigmentosa (RP) is a group of inherited retinal disorders that lead to photoreceptor loss. RP has been reported to be related to oxidative stress, autophagy, and inflammation. (-)-Epigallocatechin gallate (EGCG), the most abundant catechin-based flavonoid in green tea leaves, has significant antioxidant, anti-carcinogenic, antimicrobial, and neuroprotective properties. EGCG, given its low molecular weight and hydrophilic properties, can cross the blood-retinal barrier and is able to reach different ocular tissues such as the lens, cornea, and retina. EGCG has been shown to provide retinal protection against ischemia; sodium nitroprusside-, N-methyl-D-aspartate-, lipopolysaccharide-, light-, sodium iodate-, or H2O2-induced damage and diabetic retinopathy. This suggests that systemic EGCG administration has the potential to protect against retinal degenerative or neurodegenerative diseases such as RP. The aim of this work was to investigate whether EGCG can protect against RP progression in the animal P23H line 1, the model of RP. Albino P23H rats were crossed with pigmented Long Evans rats to produce offspring exhibiting the clinical features of RP. Pigmented P23H rats were treated via intraperitoneal injection with saline or EGCG at a dose of 25 mg/kg every week from P100 to P160 and then compared to wild-type Long Evans rats. Rats treated with EGCG showed better visual and retinal electrical function with increased contrast sensitivity and b-wave values compared with those observed in P23H rats treated with vehicle. EGCG reduced lipid peroxidation and increased total antioxidant capacity and catalase and superoxide dismutase activities. No differences were observed in visual acuity, nitrate levels, nitrite levels or glutathione S-transferase activity. In conclusion, EGCG not only reduced the loss of visual function in P23H rats but also improved the levels of antioxidant enzymes and reduced oxidative damage. This study was approved by the Institutional Animal Care and Use Committee (CEICA) from the University of Zaragoza under project license PI12/14 on July 11, 2014. ; This study was supported by the Instituto de Salud Carlos III (project PI13/01124 and Ocular Pathology National Net RETICS-Oftared RD16/ 0008) the Fondo Europeo de Desarrollo Regional (FEDER) funds: "Una manera de hacer Europa"; and the Government of Aragon (Group B08_17R and Predoctoral Grant L. Perdices, C060/2014).

Aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) is a photoreceptor-specific chaperone that stabilizes the effector enzyme of phototransduction, cGMP phosphodiesterase 6 (PDE6). Mutations in the AIPL1 gene cause a severe inherited retinal dystrophy, Leber congenital amaurosis type 4 (LCA4), that manifests as the loss of vision during the first year of life. In this study, we generated three-dimensional (3D) retinal organoids (ROs) from human induced pluripotent stem cells (hiPSCs) derived from an LCA4 patient carrying a Cys89Arg mutation in AIPL1. This study aimed to (i) explore whether the patient hiPSC-derived ROs recapitulate LCA4 disease phenotype, and (ii) generate a clinically relevant resource to investigate the molecular mechanism of disease and safely test novel therapies for LCA4 in vitro. We demonstrate reduced levels of the mutant AIPL1 and PDE6 proteins in patient organoids, corroborating the findings in animal models; however, patient-derived organoids maintained retinal cell cytoarchitecture despite significantly reduced levels of AIPL1. ; This work was supported by Institute of Health Carlos III (ISCIII)/ ERDF (European Research Development Fund), Spain, ((PI16/00409 (DL); DL, AAC, and SE are members of PRB3 supported by a grant (PT17/0019/0024) of the PE I + D + i 2013–2016, funded by ISCIII and ERDF. The work was also supported by ISCIII-ERDF (PI16/00425), CIBERER 06/07/0036, IIS-FJD Biobank PT13/0010/0012, RAREGENOMICS funded by Regional Government of Madrid, (CAM, B2017/BMD3721) and ERDF, the University Chair UAM-IIS-FJD of Genomic Medicine, the Spanish National Organization of the Blind (ONCE), the Spanish Fighting Blindness Foundation (FUNDALUCE), and the Ramon Areces Foundation. MC is supported by the Miguel Servet Program (CPII17_00006) from ISCIII. DL is supported by Miguel Servet I Program (CP18/00033). VR is supported by National Institute of Health (R01 EY028035, R01 EY025536). Transcriptome profiling and analyses were supported by the Intramural Research Program of the National Eye Institute (ZIAEY000450, ZIAEY000474) and utilized the high-performance computational capabilities of the Biowulf Linux cluster at NIH (http://biowulf.nih.gov).