Prph2 knock-in mice recapitulate human central areolar choroidal dystrophy retinal degeneration and exhibit aberrant synaptic remodeling and microglial activation.

Central areolar choroidal dystrophy is an inherited disorder characterized by progressive choriocapillaris atrophy and retinal degeneration and is usually associated with mutations in the PRPH2 gene. We aimed to generate and characterize a mouse model with the p.Arg195Leu mutation previously described in patients. Heterozygous (Prph2WT/KI) and homozygous (Prph2KI/KI) mice were generated using the CRISPR/Cas9 system to introduce the p.Arg195Leu mutation. Retinal function was assessed by electroretinography and optomotor tests at 1, 3, 6, 9, 12, and 20 months of age. The structural integrity of the retinas was evaluated at the same ages using optical coherence tomography. Immunofluorescence and transmission electron microscopy images of the retina were also analyzed. Genetic sequencing confirmed that both Prph2WT/KI and Prph2KI/KI mice presented the p.Arg195Leu mutation. A progressive loss of retinal function was found in both mutant groups, with significantly reduced visual acuity from 3 months of age in Prph2KI/KI mice and from 6 months of age in Prph2WT/KI mice. Decreased amplitudes in the electroretinography responses were observed from 1 month of age in Prph2KI/KI mice and from 6 months of age in Prph2WT/KI mice. Morphological analysis of the retinas correlated with functional findings, showing a progressive decrease in retinal thickness of mutant mice, with earlier and more severe changes in the homozygous mutant mice. We corroborated the alteration of the outer segment structure, and we found changes in the synaptic connectivity in the outer plexiform layer as well as gliosis and signs of microglial activation. The new Prph2WT/KI and Prph2KI/KI murine models show a pattern of retinal degeneration similar to that described in human patients with central areolar choroidal dystrophy and appear to be good models to study the mechanisms involved in the onset and progression of the disease, as well as to test the efficacy of new therapeutic strategies.

Canine Models of Inflammatory Skin Diseases and Their Application in Pharmacological Research.

The purpose of this article is to provide an overview of existing pharmacological models of canine dermatitis. Canine models of dermatitis have contributed significantly to our current understanding of the pathology of dermatitis and to the development of corresponding pharmacological interventions. Specifically, canine atopic dermatitis (AD) is reviewed here, as it is one of the most common inflammatory skin diseases in dogs. Canine AD also shares clinicopathological features with human AD, making the dog a natural and optimal model for human disease. Thus, pharmacological models of canine AD may be uniquely applicable to human pharmacological research. In this article, particular attention is dedicated to relevant in vivo, in vitro, and ex vivo models of canine AD, skin barrier defect models, pruritus models, and skin immunology models. Additionally, models of superficial pyoderma and food allergy are also discussed. With understanding of findings from canine models, researchers can select the most salient features for future pharmacological drug development. © 2023 Wiley Periodicals LLC.

Ischemia-Reperfusion Increases TRPM7 Expression in Mouse Retinas.

Ischemia is the main cause of cell death in retinal diseases such as vascular occlusions, diabetic retinopathy, glaucoma, or retinopathy of prematurity. Although excitotoxicity is considered the primary mechanism of cell death during an ischemic event, antagonists of glutamatergic receptors have been unsuccessful in clinical trials with patients suffering ischemia or stroke. Our main purpose was to analyze if the transient receptor potential channel 7 (TRPM7) could contribute to retinal dysfunction in retinal pathologies associated with ischemia. By using an experimental model of acute retinal ischemia, we analyzed the changes in retinal function by electroretinography and the changes in retinal morphology by optical coherence tomography (OCT) and OCT-angiography (OCTA). Immunohistochemistry was performed to assess the pattern of TRPM7 and its expression level in the retina. Our results show that ischemia elicited a decrease in retinal responsiveness to light stimuli along with reactive gliosis and a significant increase in the expression of TRPM7 in Müller cells. TRPM7 could emerge as a new drug target to be explored in retinal pathologies associated with ischemia.

Microglia activation and neuronal alterations in retinas from COVID-19 patients: correlation with clinical parameters.

BACKGROUND: Different ocular alterations have been described in patients with coronavirus disease 2019 (COVID-19). Our aim was to determine whether COVID-19 affected retinal cells and establish correlations with clinical parameters. METHODS: Retinal sections and flat-mount retinas from human donors with COVID-19 (n = 16) and controls (n = 15) were immunostained. The location of angiotensin-converting enzyme 2 (ACE2) and the morphology of microglial cells, Müller cells, astrocytes, and photoreceptors were analyzed by confocal microscopy. Microglial quantification and the area occupied by them were measured. Correlations among retinal and clinical parameters were calculated. RESULTS: ACE2 was mainly located in the Müller cells, outer segment of cones and retinal pigment epithelium. Cell bodies of Müller cells in COVID-19 group showed greater staining of ACE2 and cellular retinaldehyde-binding protein (CRALBP). The 81.3% of COVID-19 patients presented disorganization of honeycomb-like pattern formed by Müller cells. Gliosis was detected in 56.3% of COVID-19 patients compared to controls (40%) as well as epiretinal membranes (ERMs) or astrocytes protruding (50%). Activated or ameboid-shape microglia was the main sign in the COVID-19 group (93.8%). Microglial migration towards the vessels was greater in the COVID-19 retinas (P < 0.05) and the area occupied by microglia was also reduced (P < 0.01) compared to control group. Cone degeneration was more severe in the COVID-19 group. Duration of the disease, age and respiratory failure were the most relevant clinical data in relation with retinal degeneration. CONCLUSIONS: The retinas of patients with COVID-19 exhibit glial activation and neuronal alterations, mostly related to the inflammation, hypoxic conditions, and age.

Purinergic Receptors P2X7 and P2X4 as Markers of Disease Progression in the rd10 Mouse Model of Inherited Retinal Dystrophy.

The purinergic receptor P2X7 (P2X7R) is implicated in all neurodegenerative diseases of the central nervous system. It is also involved in the retinal degeneration associated with glaucoma, age-related macular degeneration, and diabetic retinopathy, and its overexpression in the retina is evident in these disorders. Retinitis pigmentosa is a progressive degenerative disease that ultimately leads to blindness. Here, we investigated the expression of P2X7R during disease progression in the rd10 mouse model of RP. As the purinergic receptor P2X4 is widely co-expressed with P2X7R, we also studied its expression in the retina of rd10 mice. The expression of P2X7R and P2X4R was examined by immunohistochemistry, flow cytometry, and western blotting. In addition, we analyzed retinal functionality by electroretinographic recordings of visual responses and optomotor tests and retinal morphology. We found that the expression of P2X7R and P2X4R increased in rd10 mice concomitant with disease progression, but with different cellular localization. Our findings suggest that P2X7R and P2X4R might play an important role in RP progression, which should be further analyzed for the pharmacological treatment of inherited retinal dystrophies.

Cellular and molecular alterations in neurons and glial cells in inherited retinal degeneration.

Multiple gene mutations have been associated with inherited retinal dystrophies (IRDs). Despite the spectrum of phenotypes caused by the distinct mutations, IRDs display common physiopathology features. Cell death is accompanied by inflammation and oxidative stress. The vertebrate retina has several attributes that make this tissue vulnerable to oxidative and nitrosative imbalance. The high energy demands and active metabolism in retinal cells, as well as their continuous exposure to high oxygen levels and light-induced stress, reveal the importance of tightly regulated homeostatic processes to maintain retinal function, which are compromised in pathological conditions. In addition, the subsequent microglial activation and gliosis, which triggers the secretion of pro-inflammatory cytokines, chemokines, trophic factors, and other molecules, further worsen the degenerative process. As the disease evolves, retinal cells change their morphology and function. In disease stages where photoreceptors are lost, the remaining neurons of the retina to preserve their function seek out for new synaptic partners, which leads to a cascade of morphological alterations in retinal cells that results in a complete remodeling of the tissue. In this review, we describe important molecular and morphological changes in retinal cells that occur in response to oxidative stress and the inflammatory processes underlying IRDs.

Less is more: Enterobactin concentration dependency in copper tolerance and toxicity.

The ability of siderophores to play roles beyond iron acquisition has been recently proven for many of them and evidence continues to grow. An earlier work showed that the siderophore enterobactin is able to increase copper toxicity by reducing Cu2+ to Cu+, a form of copper that is more toxic to cells. Copper toxicity is multifaceted. It involves the formation of reactive oxygen species (ROS), mismetallation of enzymes and possibly other mechanisms. Given that we previously reported on the capacity of enterobactin to alleviate oxidative stress caused by various stressors other than copper, we considered the possibility that the siderophore could play a dual role regarding copper toxicity. In this work, we show a bimodal effect of enterobactin on copper toxicity (protective and harmful) which depends on the siderophore concentration. We found that the absence of enterobactin rendered Escherichia coli cells more sensitive to copper, due to the reduced ability of those cells to cope with the metal-generated ROS. Consistently, addition of low concentrations of the siderophore had a protective effect by reducing ROS levels. We observed that in order to achieve this protection, enterobactin had to enter cells and be hydrolyzed in the cytoplasm. Further supporting the role of enterobactin in oxidative stress protection, we found that both oxygen and copper, induced the expression of the siderophore and also found that copper strongly counteracted the well-known downregulation effect of iron on enterobactin synthesis. Interestingly, when enterobactin was present in high concentrations, cells became particularly sensitive to copper most likely due to the Cu2+ to Cu+ reduction, which increased the metal toxicity leading to cell death.

Inherited Retinal Dystrophies: Role of Oxidative Stress and Inflammation in Their Physiopathology and Therapeutic Implications.

Inherited retinal dystrophies (IRDs) are a large group of genetically and clinically heterogeneous diseases characterized by the progressive degeneration of the retina, ultimately leading to loss of visual function. Oxidative stress and inflammation play fundamental roles in the physiopathology of these diseases. Photoreceptor cell death induces an inflammatory state in the retina. The activation of several molecular pathways triggers different cellular responses to injury, including the activation of microglia to eliminate debris and recruit inflammatory cells from circulation. Therapeutical options for IRDs are currently limited, although a small number of patients have been successfully treated by gene therapy. Many other therapeutic strategies are being pursued to mitigate the deleterious effects of IRDs associated with oxidative metabolism and/or inflammation, including inhibiting reactive oxygen species' accumulation and inflammatory responses, and blocking autophagy. Several compounds are being tested in clinical trials, generating great expectations for their implementation. The present review discusses the main death mechanisms that occur in IRDs and the latest therapies that are under investigation.

Analfabetismo da população brasileira nas análises de Giorgio Mortara sobre o censo de 1940 / Illiteracy of the Brazilian population in Giorgio Mortara's analyses of the 1940 census / Analfabetismo de la población brasileña en los análisis de Giorgio Mortara sobre el censo de 1940

Resumo Este artigo apresenta análises de Giorgio Mortara sobre as informações do recenseamento populacional brasileiro realizado em 1940 referentes especificamente ao analfabetismo no Distrito Federal (Rio de Janeiro) e no município de São Paulo. Mortara nasceu na Itália, onde se formou e se estabeleceu como reconhecido estatístico, e, em 1939, mudou-se para o Brasil, tendo colaborado decisivamente na constituição do IBGE (Instituto Brasileiro de Geografia e Estatística) e na produção demográfica brasileira. Vários de seus estudos dedicam-se à análise dos resultados dos levantamentos censitários brasileiros e são amplamente citados e conhecidos no país. No presente artigo, contudo, o foco são algumas análises elaboradas pelo autor sobre o analfabetismo, publicadas em 1945 na Revista Brasileira de Estudos Pedagógicos, que são pouco citadas na literatura sobre o tema. Nesses estudos, o autor identifica aspectos e tendências que ainda não compunham o repertório analítico no período. São os casos da observação do alfabetismo mais acentuado nas gerações mais jovens, da tendência de menor índice de analfabetismo entre as meninas e das diferenças de índice em relação à categoria cor.

Abstract This article presents analyses by Giorgio Mortara on the information from the Brazilian population census carried out in 1940 referring specifically to illiteracy in the Federal District (Rio de Janeiro) and in the municipality of São Paulo. Mortara was born in Italy, where he graduated and established himself as a recognized statistician, and in 1939 moved to Brazil, where he significantly contributed to the constitution of the IBGE (Brazilian Institute of Geography and Statistics) and to Brazilian demographic studies. Several of his studies are devoted to the analysis of results of the Brazilian census surveys and are widely cited and well known in the country. This article, however, focuses on some analyses elaborated by the author regarding illiteracy, which were published in the Revista Brasileira de Estudos Pedagógicos in 1945 and are rarely mentioned in the literature on the subject. In these studies, the author identifies aspects and trends that had not yet become part of the analytical repertoire in the period. This is the case of the observation of more pronounced literacy in younger generations, the lower illiteracy rate trend among girls and the index differences regarding the color category.

Resumen Este artículo presenta el análisis de Giorgio Mortara sobre las informaciones del censo poblacional brasileño de 1940 referentes específicamente al analfabetismo en el distrito federal de Rio de Janeiro y en el municipio de São Paulo. Mortara nació en Italia, donde se formó y se estableció como reconocido estadístico, y en 1939 se mudó a Brasil, para colaborar decisivamente en la constitución del Instituto Brasileño de Geografía e Estadística (IBGE) y en la producción demográfica brasileña. Varios de sus estudios se dedican al análisis de los resultados de los censos brasileños y son ampliamente citados y conocidos en el país. En el presente artículo, sin embargo, el foco se pone en algunos análisis del autor que se refieren al analfabetismo, que fueron publicados en la Revista Brasileira de Estudos Pedagógicos en 1945 y de los que se encuentra poca referencia en la literatura sobre el tema. En estos estudios, el autor identifica aspectos y tendencias que aún no componían el repertorio analítico en el período, como la observación del alfabetismo más acentuado en las generaciones más jóvenes, de la tendencia de menor índice de analfabetismo entre las niñas y de las diferencias de índice en relación a la categoría color.

Short-term high-fat feeding exacerbates degeneration in retinitis pigmentosa by promoting retinal oxidative stress and inflammation.

A high-fat diet (HFD) can induce hyperglycemia and metabolic syndromes that, in turn, can trigger visual impairment. To evaluate the acute effects of HFD feeding on retinal degeneration, we assessed retinal function and morphology, inflammatory state, oxidative stress, and gut microbiome in dystrophic retinal degeneration 10 (rd10) mice, a model of retinitis pigmentosa, fed an HFD for 2 to 3 wk. Short-term HFD feeding impaired retinal responsiveness and visual acuity and enhanced photoreceptor degeneration, microglial cell activation, and Müller cell gliosis. HFD consumption also triggered the expression of inflammatory and oxidative markers in rd10 retinas. Finally, an HFD caused gut microbiome dysbiosis, increasing the abundance of potentially proinflammatory bacteria. Thus, HFD feeding drives the pathological processes of retinal degeneration by promoting oxidative stress and activating inflammatory-related pathways. Our findings suggest that consumption of an HFD could accelerate the progression of the disease in patients with retinal degenerative disorders.

Phenotypic Differences in a PRPH2 Mutation in Members of the Same Family Assessed with OCT and OCTA.

Choroidal dystrophies comprise a group of chorioretinal degenerations. However, the different findings observed among these patients make it difficult to establish a correct clinical diagnosis. The objective of this study was to characterize new clinical findings by optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA) in these patients. Four family members with a PRPH2 gene mutation (p.Arg195Leu) were included. OCT was performed at the macula, and the thickness of the outer and inner retina, total retina, and choroid was measured. The features of the vascular network were analyzed by OCTA. Patients showed a decreased outer nuclear layer in the avascular area compared with the controls. Two patients presented greater foveal and parafoveal degeneration of the outer retina, whereas the most degenerated area in the rest was the perifovea. Disruption of the third outer band at the foveola is one of the first-altered outer bands. Slow blood flow areas or capillary dropout were main signs in the deep capillary plexus. Microaneurysms were frequently observed in less degenerated retinas. Vascular loops and intraretinal microvascular abnormalities (IRMAs) were present in the superficial plexus. Extensive degeneration of the choriocapillaris was detected. Phenotypic differences were found between patients: two showed central areolar choroidal dystrophy and the rest had extensive chorioretinal atrophy. These signs observed in OCT and OCTA can help to more appropriately define the clinical disease in patients with choroidal dystrophies.

Gradual Increase in Environmental Light Intensity Induces Oxidative Stress and Inflammation and Accelerates Retinal Neurodegeneration.

Purpose: Retinitis pigmentosa (RP) is a blinding neurodegenerative disease of the retina that can be affected by many factors. The present study aimed to analyze the effect of different environmental light intensities in rd10 mice retina. Methods: C57BL/6J and rd10 mice were bred and housed under three different environmental light intensities: scotopic (5 lux), mesopic (50 lux), and photopic (300 lux). Visual function was studied using electroretinography and optomotor testing. The structural and morphological integrity of the retinas was evaluated by optical coherence tomography imaging and immunohistochemistry. Additionally, inflammatory processes and oxidative stress markers were analyzed by flow cytometry and western blotting. Results: When the environmental light intensity was higher, retinal function decreased in rd10 mice and was accompanied by light-dependent photoreceptor loss, followed by morphological alterations, and synaptic connectivity loss. Moreover, light-dependent retinal degeneration was accompanied by an increased number of inflammatory cells, which became more activated and phagocytic, and by an exacerbated reactive gliosis. Furthermore, light-dependent increment in oxidative stress markers in rd10 mice retina pointed to a possible mechanism for light-induced photoreceptor degeneration. Conclusions: An increase in rd10 mice housing light intensity accelerates retinal degeneration, activating cell death, oxidative stress pathways, and inflammatory cells. Lighting intensity is a key factor in the progression of retinal degeneration, and standardized lighting conditions are advisable for proper analysis and interpretation of experimental results from RP animal models, and specifically from rd10 mice. Also, it can be hypothesized that light protection could be an option to slow down retinal degeneration in some cases of RP.

Ethanol-Induced Oxidative Stress Modifies Inflammation and Angiogenesis Biomarkers in Retinal Pigment Epithelial Cells (ARPE-19): Role of CYP2E1 and its Inhibition by Antioxidants.

The retinal pigment epithelium (RPE) plays a key role in retinal health, being essential for the protection against reactive oxygen species (ROS). Nevertheless, excessive oxidative stress can induce RPE dysfunction, promoting visual loss. Our aim is to clarify the possible implication of CYP2E1 in ethanol (EtOH)-induced oxidative stress in RPE alterations. Despite the increase in the levels of ROS, measured by fluorescence probes, the RPE cells exposed to the lowest EtOH concentrations were able to maintain cell survival, measured by the Cell Proliferation Kit II (XTT). However, EtOH-induced oxidative stress modified inflammation and angiogenesis biomarkers, analyzed by proteome array, ELISA, qPCR and Western blot. The highest EtOH concentration used stimulated a large increase in ROS levels, upregulating the cytochrome P450-2E1 (CYP2E1) and promoting cell death. The use of antioxidants such as N-acetylcysteine (NAC) and diallyl sulfide (DAS), which is also a CYP2E1 inhibitor, reverted cell death and oxidative stress, modulating also the upstream angiogenesis and inflammation regulators. Because oxidative stress plays a central role in most frequent ocular diseases, the results herein support the proposal that CYP2E1 upregulation could aggravate retinal degeneration, especially in those patients with high baseline oxidative stress levels due to their ocular pathology and should be considered as a risk factor.

New Nrf2-Inducer Compound ITH12674 Slows the Progression of Retinitis Pigmentosa in the Mouse Model rd10.

BACKGROUND/AIMS: It is well established that oxidative stress and inflammation are common pathogenic features of retinal degenerative diseases. ITH12674 is a novel compound that induces the transcription factor Nrf2; in so doing, the molecule exhibits anti-inflammatory, and antioxidant properties, and affords neuroprotection in rat cortical neurons subjected to oxidative stress. We here tested the hypothesis that ITH12674 could slow the retinal degeneration that causes blindness in rd10 mice, a model of retinitis pigmentosa. METHODS: Animals were intraperitoneally treated with 1 or 10 mg/Kg ITH12674 or placebo from P16 to P30. At P30, retinal functionality and visual acuity were analyzed by electroretinography and optomotor test. By immunohistochemistry we quantified the photoreceptor rows and analyzed their morphology and connectivity. Oxidative stress and inflammatory state was studied by Western blot, and microglia reactivity was monitored by flow cytometry. The blood-brain barrier permeation of ITH12674 was evaluated using a PAMPA-BBB assay. RESULTS: In rd10 mice treated with 10 mg/Kg of the compound, the following changes were observed (with respect to placebo): (i) a decrease of vision loss with higher scotopic a- and b-waves; (ii) increased visual acuity; (iii) preservation of cone photoreceptors morphology, as well as their synaptic connectivity; (iv) reduced expression of TNF-α and NF-κB; (v) increased expression of p38 MAPK and Atg12-Atg5 complex; and (vi) decreased CD11c, MHC class II and CD169 positive cell populations. CONCLUSION: These data support the view that a Nrf2 inducer compound may arise as a new therapeutic strategy to combat retinal neurodegeneration. At present, we are chemically optimising compound ITH12674 with the focus on improving its neuroprotective potential in retinal neurodegenerative diseases.

Interpretation of OCT and OCTA images from a histological approach: Clinical and experimental implications.

Optical coherence tomography (OCT) and OCT angiography (OCTA) have been a technological breakthrough in the diagnosis, treatment, and follow-up of many retinal diseases, thanks to its resolution and its ability to inform of the retinal state in seconds, which gives relevant information about retinal degeneration. In this review, we present an immunohistochemical description of the human and mice retina and we correlate it with the OCT bands in health and pathological conditions. Here, we propose an interpretation of the four outer hyperreflective OCT bands with a correspondence to retinal histology: the first and innermost band as the external limiting membrane (ELM), the second band as the cone ellipsoid zone (EZ), the third band as the outer segment tips phagocytosed by the pigment epithelium (PhaZ), and the fourth band as the mitochondria in the basal portion of the RPE (RPEmitZ). The integrity of these bands would reflect the health of photoreceptors and retinal pigment epithelium. Moreover, we describe how the vascular plexuses vary in different regions of the healthy human and mice retina, using OCTA and immunohistochemistry. In humans, four, three, two or one plexuses can be observed depending on the distance from the fovea. Also, specific structures such as vascular loops in the intermediate capillary plexus, or spider-like structures of interconnected capillaries in the deep capillary plexus are found. In mice, three vascular plexuses occupy the whole retina, except in the most peripheral retina where only two plexuses are found. These morphological issues should be considered when assessing a pathology, as some retinal diseases are associated with structural changes in blood vessels. Therefore, the analysis of OCT bands and OCTA vascular plexuses may be complementary for the diagnosis and prognosis of retinal degenerative processes, useful to assess therapeutic approaches, and it is usually correlated to visual acuity.

ARPE-19-derived VEGF-containing exosomes promote neovascularization in HUVEC: the role of the melanocortin receptor 5.

ARPE-19 retinal pigment epithelial cells cultured in a medium containing 35 mM D-glucose led to an augmented ROS formation and release of vascular endothelial factor (VEGF)-containing exosomes compared to ARPE-19 cells cultured in a medium containing 5 mM D-glucose (standard medium). Exposing these cells to the melanocortin 5 receptor agonist (MCR5) PG-901 (10-10M), for 9 d reduced ROS generation, the number of exosomes released and their VEGF content. In contrast, incubating the cells with the melanocortin receptor MCR1 agonist BMS-470539 (10-5 M) or with the mixed MCR3/4 agonist MTII (0.30 nmol) did not produce any significant decrease in ROS levels. ARPE-19-derived VEGF-containing exosomes promoted neovascularization in human umbilical vein endothelial cells (HUVEC), an effect that was markedly reduced by PG-901 (10-10M) but not by the MCR3/4 agonist MTII (0.30 nmol) or the MCR1 agonist BMS-470539 (10-5 M). The MCR5-related action in the ARPE-19 cells was accompanied by the increased expression of two coupled factors, cytochrome p4502E1 (CYP2E1) and nuclear factor kappa b (Nf-κB). These are both involved in high glucose signalling, in ROS generation and, interestingly, were reduced by the MCR5 agonist in the ARPE-19 cells. Altogether, these data suggest that MCR5 is a modulator of the responses stimulated by glucose in ARPE-19 cells, which might possibly be translated into a modulation of the retinal pigment epithelium response to diabetes in vivo.

Genome-wide overview of Trichosporon akiyoshidainum HP-2023, new insights into its mechanism of dye discoloration.

Trichosporon akiyoshidainum HP-2023 completely discolorised Reactive Black 5 (200 mg/l) in 24 h. Manganese peroxidase and phenoloxidase, but no laccase activities were detected throughout the incubation. Total aromatic amines in media with Reactive Black 5 decreased 83% after 24 h, supporting an oxidative mechanism of azo dye discoloration. To unravel the genetic basis of these activities, the genome of Trichosporon akiyoshidainum HP-2023 was sequenced, assembled and annotated de novo. T. akiyoshidainum HP-2023 genome comprises 30 MB with a G+C content of 60.75% and 9019 gene models. Thirty-three putative carbohydrate-active enzymes with auxiliary activities, probably involved in lignin degradation and dye discoloration, were identified in the annotated genome, including two laccases, four extracellular fungal heme-peroxidases, nineteen hydrogen peroxide-producing enzymes, and four benzoquinone oxidoreductases. This report will facilitate further studies of textile-dye discoloration with this and closely related strains and poses questions about the ligninolytic potential of Trichosporon akiyoshidainum HP-2023 and related species.

Tratamientos innovadores utilizados en el manejo de las heridas crónicas / Innovative treatments used in the handling of chronic wounds / Tratamentos inovadores utilizados no manejo das feridas crónicas

Introducción: Del tipo de tratamiento y la eficacia del mismo depende la evolución y la mejora en la calidad de vida del paciente con heridas crónicas; existen diversos tratamientos para las heridas crónicas de acuerdo con el tipo de lesión, la duración del tratamiento y los factores individuales del paciente. Los diversos tratamientos innovadores demuestran resultados favorables en cuanto a la reducción del tiempo y el tamaño de las heridas crónicas. Este artículo tiene como objetivo describir los tratamientos innovadores utilizados en el manejo de las heridas crónicas, de uso poco frecuente en las clínicas de heridas. Metodología: Revisión de la literatura estructurada en tres fases: recolección de artículos en bases de datos como Scopus, Pubmed, Dialnet, Ebscohots, y Elsevier; uso de palabras clave como pie diabético, herida crónica y úlcera por presión; revisión y clasificación de 50 artículos en idioma español, inglés y portugués. Resultados: Se registraron 12 tratamientos innovadores para el manejo de las heridas cónicas, cada uno con evidencia científica de su utilidad en los distintos tipos de heridas crónicas. Conclusión: Conocer nuevos tratamientos ayuda al enfermero a ampliar las opciones de intervención, presentar alternativas de tratamiento de menor costo, o más rápida dependiendo del tipo de herida y la condición del paciente.

Introduction: The type of treatment and its efficacy depends on the evolution and the improvement of the quality of life of the patient with chronic wounds; diverse treatments exist for chronic wounds according to the type of injury, duration of the treatment, and the individual factors of the patient. The diverse innovative treatments demonstrate favorable results in terms of reduction of time and size of chronic wounds. This article has as its objective to describe the innovative treatments used in the handling of chronic wounds, of infrequent use in wound care centers. Methodology: Review of the structured literature in three phases: recollection of articles in databases such as Scopus, Pubmed, Dialnet, Ebscohots, and Elsevier; use of keywords such as diabetic foot, chronic wound, and pressure ulcer; review and classification of 50 articles in Spanish, English, and Portuguese. Results: 12 innovative treatments were registered for the handling of chronic wounds, each one with scientific evidence of their utility in the different types of chronic wounds. Conclusion: Determine new treatments helps the nurse to extent the intervention options, and present treatment alternatives of lower cost or faster treatment depending on the type of wound and the condition of the patient.

Introdução: Do tipo de tratamento e da eficácia do mesmo depende a evolução e a melhora na qualidade de vida do paciente com feridas crónicas; existem diversos tratamentos para as feridas crónicas de acordo ao tipo de lesão, à duração do tratamento, e aos fatores individuais do paciente. Os diversos tratamentos inovadores demostram resultados favoráveis em quanto à redução do tempo e o tamanho das feridas crónicas. Este artigo tem como objetivo descrever os tratamentos inovadores utilizados no manejo das feridas crónicas, de uso pouco frequente nas clínicas de feridas. Metodologia: Revisão da literatura estruturada em três fases: recolecção de artigos em bases de dados como Scopus, Pubmed, Dialnet, Ebscohots e Elsevier; uso de palavras chave como pé diabético, ferida crónica e úlcera por pressão; revisão e classificação de 50 artigos em idioma Espanhol, Inglês e Português. Resultados: Registraram-se 12 tratamentos inovadores para o manejo das feridas cónicas, cada um com evidencia científica de sua utilidade nos diferentes tipos de feridas crónicas. Conclusão: O conhecimento de novos tratamentos ajuda ao enfermeiro a ampliar as opções de intervenção, apresentando alternativas de tratamento mais rápidas ou de menor custo, dependendo do tipo de ferida e da condição do paciente.

Isquemia masiva de colon secundaria a vólvulo de sigma / Massive colonic ischemia secondary to sigmoid volvulus

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Linitis plástica como presentación de un carcinoma lobulillar de mama / Linitis plastica as a presentation of lobular breast carcinoma

El estómago es un lugar infrecuente de metastatización del cáncer de mama. Presentamos un caso de linitis plástica metastásica de un carcinoma lobulillar de mama localmente avanzado. La distinción entre el origen primario gástrico del secundario es fundamental, y se basa en estudios inmunohistoquímicos de las biopsias (AU)

The stomach is an infrequent site of breast cancer metastasis. We report a case of metastatic linitis plastica from locally advanced lobular breast carcinoma. The distinction between primary and secondary gastric origin is essential and is based on immunohistochemical studies of biopsies (AU)