An intronic RNA element modulates Factor VIII exon-16 splicing.

Pathogenic variants in the human Factor VIII (F8) gene cause Hemophilia A (HA). Here, we investigated the impact of 97 HA-causing single-nucleotide variants on the splicing of 11 exons from F8. For the majority of F8 exons, splicing was insensitive to the presence of HA-causing variants. However, splicing of several exons, including exon-16, was impacted by variants predicted to alter exonic splicing regulatory sequences. Using exon-16 as a model, we investigated the structure-function relationship of HA-causing variants on splicing. Intriguingly, RNA chemical probing analyses revealed a three-way junction structure at the 3'-end of intron-15 (TWJ-3-15) capable of sequestering the polypyrimidine tract. We discovered antisense oligonucleotides (ASOs) targeting TWJ-3-15 partially rescue splicing-deficient exon-16 variants by increasing accessibility of the polypyrimidine tract. The apical stem loop region of TWJ-3-15 also contains two hnRNPA1-dependent intronic splicing silencers (ISSs). ASOs blocking these ISSs also partially rescued splicing. When used in combination, ASOs targeting both the ISSs and the region sequestering the polypyrimidine tract, fully rescue pre-mRNA splicing of multiple HA-linked variants of exon-16. Together, our data reveal a putative RNA structure that sensitizes F8 exon-16 to aberrant splicing.

Rescue of blood coagulation Factor VIII exon-16 mis-splicing by antisense oligonucleotides.

The human Factor VIII ( F8 ) protein is essential for the blood coagulation cascade and specific F8 mutations cause the rare bleeding disorder Hemophilia A (HA). Here, we investigated the impact of HA-causing single-nucleotide mutations on F8 pre-mRNA splicing. We found that 14/97 (∼14.4%) coding sequence mutations tested in our study induced exon skipping. Splicing patterns of 4/11 (∼36.4%) F8 exons tested were especially sensitive to the presence of common disease-causing mutations. RNA-chemical probing analyses revealed a three-way junction structure at the 3' end of intron 15 (TWJ-3-15). TWJ-3-15 sequesters the polypyrimidine tract, a key determinant of 3' splice site strength. Using exon-16 of the F8 gene as a model, we designed specific antisense oligonucleotides (ASOs) that target TWJ-3-15 and identified three that promote the splicing of F8 exon-16. Interaction of TWJ-3-15 with ASOs increases accessibility of the polypyrimidine tract and inhibits the binding of hnRNPA1-dependent splicing silencing factors. Moreover, ASOs targeting TWJ-3-15 rescue diverse splicing-sensitive HA-causing mutations, most of which are distal to the 3' splice site being impacted. The TWJ-3-15 structure and its effect on mRNA splicing provide a model for HA etiology in patients harboring specific F8 mutations and provide a framework for precision RNA-based HA therapies.

Consumption of oil macerated with garlic produces renovascular protective effects in adult apolipoprotein E-deficient mice.

Oxidative stress and chronic inflammatory conditions contribute as key determinants in the development of vascular and renal diseases. Organosulfur compounds (OSCs) of oil macerated with garlic (OMG) are promising phytochemicals which could protect us from hyper-inflammation and oxidative stress-induced organ damage. The present work evaluated the effect of OMG intake in apolipoprotein E-knockout (ApoE-KO) mice. Adult female ApoE-KO mice were randomly divided into three groups and fed with control chow, oil-supplemented diet and OMG-supplemented diet. After 8 weeks, the animals were euthanized and blood, aorta, kidneys, liver and abdominal adipose tissues were obtained for further analysis. Biochemical parameters were measured in plasma, lipid peroxidation as malondialdehyde (MDA) levels was determined in the adipose tissue, oil red O was used to stain atherosclerotic lesions, and histological and ultrastructural analyses of the kidneys were performed. Renal expression levels of Tumor Necrosis Factor α (TNF-α), Interleukin-6 (IL-6) and Wilms' Tumor Protein (WT-1) were determined by western blotting and the co-immunoprecipitation assay (p53/WT-1). Also, transmission electron microscopy for studying the expression of mitofusin 2 (Mfn-2) was used to assess mitochondrial damage. The results showed that long-term moderate intake of OMG improved serum triglyceride levels, diminished the atheroma plaque area, and reduced lipid peroxidation. Furthermore, we found a decrease in oxidative and inflammatory markers, less apoptosis and reduced WT-1 expression in the kidneys. Also, OMG increased p53/WT-1 protein interactions and reduced mitochondrial damage. Our findings suggest that OMG intake would produce anti-atherosclerotic, antifibrotic, anti-inflammatory and antiapoptotic effects in adult ApoE-KO mice, conferring significant renovascular protective actions in a mechanism mediated, at least in part, by WT-1.

Antioxidant and Anti-atherogenic Properties of Prosopis strombulifera and Tessaria absinthioides Aqueous Extracts: Modulation of NADPH Oxidase-Derived Reactive Oxygen Species.

Despite popular usage of medicinal plants, their effects as cardiovascular protective agents have not been totally elucidated. We hypothesized that treatment with aqueous extract from Prosopis strombulifera (AEPs) and Tessaria absinthioides (AETa), Argentinian native plants, produces antioxidant effects on vascular smooth muscle cells (VSMCs) and attenuates atherogenesis on apolipoprotein E-knockout (ApoE-KO) mice. In VSMCs, both extracts (5-40 µg/ml) inhibited 10% fetal calf serum-induced cell proliferation, arrested cell in G2/M phase, reduced angiotensin II-induced reactive oxygen species (ROS) generation, and decreased NADPH oxidase subunit expression. In ApoE-KO mice, extracts significantly reduced triglycerides and lipid peroxidation [plasma thiobarbituric acid reactive substances (TBARS)], increased plasma total antioxidant status (TAS), and improved glutathione peroxidase activity in the liver. Under high-fat diet (HFD), both extracts were able to inhibit O2 - generation in the aortic tissue and caused a significant regression of atheroma plaques (21.4 ± 1.6% HFD group vs. 10.2 ± 1.2%∗ AEPs group and 14.3 ± 1.0%∗ AETa group; ∗ p < 0.01). Consumption of AEPs and AETa produces antioxidant/antimitogenic/anti-atherosclerotic effects, and their use may be beneficial as a complementary strategy regarding cardiovascular disease therapies.

2-Vinyl-4H-1,3-Dithiin, a Bioavailable Compound from Garlic, Inhibits Vascular Smooth Muscle Cells Proliferation and Migration by Reducing Oxidative Stress.

Organosulfur compounds (OSCs) of garlic have various health benefits including anti-hypertensive effect. It has been described that volatile OSCs uptake occurs into a moderate extent. Among the bioavailable OSCs present in garlic, 2-vinyl-4H-1,3-dithiin (2VD) is a main component in garlic macerated oil and stir-fried garlic but has been poorly investigated compared with others OSCs, such allyl mercaptan (AM) and S-allyl cysteine (SAC). The aim of this study was to evaluate the effects of 2VD on vascular smooth muscle cells (VSMCs) isolated from spontaneous hypertensive rats (SHR) and compare them with those produced by AM and SAC. Cell viability and proliferation were measured using tetrazolium dye MTT assay and flow cytometry. Cell migration was evaluated by scrape-wound migration assay. OSCs anti-oxidative capacity was determined by measuring reactive oxygen species (ROS) generation, and total antioxidant status (TAS). Non-toxic plasmatic concentrations (10 µg L-1) of 2VD and AM inhibited VSMCs proliferation stimulated with 5% fetal bovine serum and impaired cell migration. In further flow cytometry analysis 2VD treatment resulted in a partial cell cycle arrest at G2 phase. The OSCs tested were able to prevent ROS increase after angiotensin II stimulation and surprisingly 2VD induced higher total antioxidant status compared with AM and SAC. Our results showed that 2VD produces equivalent or superior beneficial effects on VSMCs to those reported for other bioavailable compounds of garlic. This preliminary evidence suggests that 2VD intake could also exert important protective effects against arterial remodeling in hypertension.

Effect of Garlic's Active Constituents in Inflammation, Obesity and Cardiovascular Disease.

PURPOSE OF REVIEW: Several studies have attributed garlic's beneficial properties to its high content of organosulfur compounds (OSCs). Here, we summarized recent studies published and some own findings regarding OSCs and its effects on cardiovascular disease, inflammation, and obesity. RECENT FINDING: The analysis of the multiple actions produced by OSCs suggests that many of its bioactivities interfere against inflammation, oxidative stress, obesogenic effects, and mitochondrial dysfunction. Accumulating evidence from in vitro, animal, and human studies reinforce the notion that OSCs modify signaling pathways that trigger chronic diseases, and to highlight, actions over these pathways are related to the treatment of disorders addressed in this review. Garlic's bioactive OSCs behave like a nutraceutical panacea because they cover a broad spectrum of applications with promising impact for the prevention and treatment of prevalent chronic pathologies associated with low-grade inflammation.

Modulación de marcadores de inflamación y estrés oxidativo en pacientes con diabetes tipo 1 y sobrepeso que participan en un programa de cambio de estilo de vida / Modulation of Inflammatory and oxidative stress markers in overweight type 1 Diabetes patients participating in a lifestyle change program

Introduction: Reduction in the expression of inflammatory markers and oxidative stress associated with exercise will protect against cardiovascular complications in Diabetes Mellitus (DM). Aim: The aim of this study was evaluated cardiovascular fitness (VO2 Max), interleukin-6 (IL-6), monocyte chemo-attractant protein 1 (MCP-1) and serum lipid peroxidation (TBARS) in overweight patients with Type-1 diabetes (T1DM) participating in a lifestyle-change program. Results: 20 T1DM overweight patients (43.3 ± 13.8 years), with BMI= 29.6 ± 3.5 kg/m2 , initial HbA1c 7.9 ± 0.91% and treated with multiple insulin injections, were included in this work. The lifestyle-change program consisted of: a) walking 10,000 steps/day, b) sequence of exercises of 24 minutes, 3-5 times/week, c) ¨healthy-plate¨ (and counting carbohydrates, and d) prandial insulin as blood-glucose levels. VO2 max, HbA1c, TBARS, IL6, MCP-1 were determined before starting the lifestyle-change program. Six months of adherence later, participants showed an average number of steps of 8242 ± 1834, a significant increase in VO2 max, (33.4 ±1.3 vs 36.2 ±1.5 ml.Kg-1.min-1 p= 0.008), a significant decrease in serum MCP-1 (314 ±42 vs 235 ±43 MFI p= 0.02), and less TBARS (3.01 ±0.44 vs 2.12 ±0.22 µmol/mL p= 0.015). IL-6 and HbA1c showed no significant decrease. Conclusion: Our results showed that a 6-month systemized and simple exercise plan improves cardiorespiratory fitness (VO2 max), and reduces both circulating oxidative stress and inflammation markers in overweight patients with T1DM.

Introducción: La reducción en la expresión de marcadores inflamatorios y de estrés oxidativo asociado con el ejercicio podría proteger contra las complicaciones cardiovasculares de la diabetes mellitus (DM). Objetivo: El objetivo de este estudio fue evaluar en pacientes con DM tipo1 (DMT1) y sobrepeso, la capacidad cardiorespiratoria (VO2 Max), la expresión sérica de marcadores inflamatorios (IL-6 y MCP-1) y la peroxidación lipídica sérica (TBARS), luego de participar por 6 meses de un programa de cambios de estilo de vida. Resultados: Veinte pacientes adultos (43.3 ± 13.8 años), de ambos sexos, con un Índice de Masa Corporal de 29.6 ± 3.5 kg/m2 , HbA1c inicial de 7,9% ± 0,91, en tratamiento con inyecciones múltiples de insulina participaron del estudio. Se indicó: 1) caminar 10.000 pasos/día, 2) realizar en domicilio una secuencia de ejercicios de 20 minutos, 3-5 veces/semana, 3) plato saludable (consumo de 1 fruta antes de las 3 comidas principales), 4) Insulina prandial según glucemia y conteo de carbohidratos. Se registraron parámetros antropométricos, presión arterial, se determinó VO2 max, y se midieron los niveles séricos de HbA1c, IL6, MCP-1 y TBARs. Luego de seis meses, los participantes alcanzaron un número promedio de pasos de 8242 ± 1834 y mostraron un aumento significativo en VO2 max, (33.4 ±1.3 vs 36.2 ±1.5 ml.Kg-1.min-1 p= 0.008). Además, se encontró una disminución significativa de MCP-1 (314 ±42 vs 235 ±43 MFI p=0.02) y TBARs (3.01 ±0.44 vs 2.12 ±0.22 µmol/mL p= 0.015) en comparación con el día 0. No se observaron modificaciones en los niveles de IL-6 y HbA1c. Conclusión: Nuestros resultados demuestran que el ejercicio, implementado como un plan accesible y acompañado, es adecuado para reducir los riesgos de inflamación y estado pro-oxidativo en pacientes con DM tipo1.

Vascular dysfunction elicited by a cross talk between periaortic adipose tissue and the vascular wall is reversed by pioglitazone.

AIM: Perivascular adipose tissue (PVAT) is in intimate contact with the vessel wall and extravascular PVAT-derived inflammatory mediators may adversely influence atherosclerotic plaque formation and stability through outside-to-inside signaling. We sought to investigate the role of PVAT on the atheroma development in an experimental animal model of metabolic syndrome (MS) associated with oxidative stress and low-grade inflammatory state. We also studied the effect of pioglitazone an insulin sensitizer, on the aortic wall and its surrounding PVAT, considering a bi-directional communication between both layers. METHODS: Apolipoprotein E-deficient mice (ApoE-/- ) were fed with standard diet (CD, control diet) or fructose overload (10% w/v) (FD, fructose diet) for 8 weeks and treated with or without pioglitazone the latest 4 weeks. RESULTS: Biochemical variables show that glycemia and lipid peroxidation determined by thiobarbituric acid reactive species (TBARS) significantly increased in FD-fed ApoE-/- mice. FD significantly increased aortic PVAT expression of oxidative stress associated genes: p22phox , Nox1, Nox2, Nox4 and p47phox , and proinflammatory genes: Visfatin, MCP-1, and MMP-9. Pioglitazone diminished PVAT-oxidative damage elicited by fructose treatment and markedly down-regulated proinflammatory markers. Even pioglitazone did not prevent the development of the aortic atheroma plaques stimulated by FD, significantly diminished VCAM-1 expression, MMP-9 expression and activity in aortic media wall and significantly reduced the accumulation of lipids and macrophages in atheroma plaques. CONCLUSION: Our results support the fact that PVAT contributes to the development and progression of cardiovascular disease by underlying mechanisms elicited by "outside-in" signaling. Treatment with pioglitazone may offer a new effect on the whole vessel wall, promoting the stability of advanced atherosclerotic plaques.

Zinc ionophore activity of quercetin and epigallocatechin-gallate: from Hepa 1-6 cells to a liposome model.

Labile zinc, a tiny fraction of total intracellular zinc that is loosely bound to proteins and easily interchangeable, modulates the activity of numerous signaling and metabolic pathways. Dietary plant polyphenols such as the flavonoids quercetin (QCT) and epigallocatechin-gallate act as antioxidants and as signaling molecules. Remarkably, the activities of numerous enzymes that are targeted by polyphenols are dependent on zinc. We have previously shown that these polyphenols chelate zinc cations and hypothesized that these flavonoids might be also acting as zinc ionophores, transporting zinc cations through the plasma membrane. To prove this hypothesis, herein, we have demonstrated the capacity of QCT and epigallocatechin-gallate to rapidly increase labile zinc in mouse hepatocarcinoma Hepa 1-6 cells as well as, for the first time, in liposomes. In order to confirm that the polyphenols transport zinc cations across the plasma membrane independently of plasma membrane zinc transporters, QCT, epigallocatechin-gallate, or clioquinol (CQ), alone and combined with zinc, were added to unilamellar dipalmitoylphosphocholine/cholesterol liposomes loaded with membrane-impermeant FluoZin-3. Only the combinations of the chelators with zinc triggered a rapid increase of FluoZin-3 fluorescence within the liposomes, thus demonstrating the ionophore action of QCT, epigallocatechin-gallate, and CQ on lipid membrane systems. The ionophore activity of dietary polyphenols may underlay the raising of labile zinc levels triggered in cells by polyphenols and thus many of their biological actions.

Adipocytokine levels in women with anorexia nervosa. Relationship with weight restoration and disease duration.

OBJECTIVE: Starvation-induced depletion of fat stores in anorexia nervosa (AN) is known to be accompanied by alterations in some circulating adipocytokines. We analyzed a panel of circulating adipocytokines in women with AN compared with normal-weight controls and their relation with the disease duration and weight restoration. METHOD: We analyzed circulating adipocytokine levels in 28 patients with AN and in 33 normal-weight controls who were eating healthily. We determined by enzyme-linked immunosorbent assay the circulating levels of total and high molecular weight (HMW) adiponectin, lipocalin-2 (LCN2), leptin, tumor necrosis factor receptor-II (TNFRII), interleukin-6 (IL6), adipocyte fatty acid binding protein-4 (FABP4), ghrelin, and resistin. RESULTS: The two circulating forms of adiponectin are higher in AN women compared with controls. Both total and HMW adiponectin related negatively to the duration of the disease (r = -0.372, p = 0.033; r = -0.450, p = 0.038, respectively). Furthermore, the lipid binding-proteins LCN2 and FABP4 are lower in AN compared to the control group. Finally, leptin levels are lower in AN against controls and correlated positively with disease duration (r = 0.537, p = 0.007). Resistin, ghrelin, TNFRII, and IL6 have similar values in both groups, although TNFRII and ghrelin related negatively to body mass index variation at the end of treatment (r = -0.456, p = 0.039; r = -0.536, p = 0.015, respectively). DISCUSSION: These results suggest there is a need to investigate if changes in adipocytokine levels could serve as weight restoration biomarkers. Further studies are warranted to elucidate the specific role of these molecules in the timing of weight restoration.

Retinol binding protein-4 circulating levels were higher in nonalcoholic fatty liver disease vs. histologically normal liver from morbidly obese women.

OBJECTIVE: We aimed to analyze the retinol binding protein-4 (RBP4) messenger RNA (mRNA) expression profiles in adipose tissues and liver of morbidly obese (MO) women with or without nonalcoholic fatty liver disease (NAFLD), and to study the relationships with other pro- and anti-inflammatory adipokines in vivo and in vitro. DESIGN AND METHODS: We performed a cross-sectional analysis of subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT) and liver samples from four lean and 45 MO women with or without NAFLD by enzyme-linked immunosorbent assay and real-time reverse transcription-PCR. We also studied RBP4 expression in HepG2 hepatocytes under various inflammatory stimuli. RESULTS: Circulating RBP4 levels were higher in MO women, and specifically, in MO subjects with NAFLD compared with normal liver controls (lean and MO). RBP4 liver expression was higher in nonalcoholic steatohepatitis (NASH)-moderate/severe than in NASHmild. Overall RBP4 gene expression was higher in liver than in adipose tissues. Among them, the higher expression corresponded to SAT. VAT expression was lower in the MO cohort. In HepG2, RBP4 mRNA expression was reduced by tumor necrosis factor (TNF)-α and increased by adiponectin treatment. CONCLUSIONS: The results obtained in MO women with NAFLD, brings up the use of RBP4 and other adipokines as a panel of noninvasive molecular biomarkers when NAFLD is suspected. Further studies are needed with other obesity groups.

Increased levels and adipose tissue expression of visfatin in morbidly obese women: the relationship with pro-inflammatory cytokines.

OBJECTIVE: The controversial results on the physiopathological role of visfatin led us to examine both circulating visfatin levels and gene expression in visceral (VAT) and subcutaneous fat (SAT) in a homogeneous group of morbidly obese women. DESIGN, PATIENTS AND MEASUREMENTS: We analysed circulating levels of several adipo/cytokines in 133 Spanish women: 40 lean (C) [body mass index (BMI) < 25 kg/m(2) ] and 93 morbidly obese (MO) (BMI > 40 kg/m(2) ). In the MO group, we found 31 diabetic and 62 nondiabetic subjects. We obtained follow-up blood samples at 6 and 12 months after bariatric surgery from 30 MO patients. We determined the circulating levels of visfatin, adiponectin, interleukin-6 (IL6), C-reactive protein (CRP), resistin and tumour necrosis factor-α (TNFα) by ELISA, and visfatin, adiponectin, IL6, resistin and TNFα gene expression in SAT and VAT by real-time RT-PCR. RESULTS: Circulating visfatin levels were higher in MO women compared with lean controls (C = 1·43 ± 0·14 µg/l, MO = 3·60 ± 0·29 µg/l, P < 0·001). After bariatric surgery-induced weight loss, visfatin levels were reduced significantly over 12 months. Visfatin expression in SAT and VAT was similar, but significantly higher in MO compared to C and independent of the presence of diabetes mellitus. Circulating visfatin levels were positively related to IL6 and CRP levels. Visfatin gene expression in VAT and SAT was strongly related to IL6 and TNFα expression. CONCLUSION: In a homogeneous cohort of morbidly obese women, our findings show that visfatin has a strong relationship with pro-inflammatory factors in severe obesity.

Dietary catechins and procyanidins modulate zinc homeostasis in human HepG2 cells.

Catechins and their polymers procyanidins are health-promoting flavonoids found in edible vegetables and fruits. They act as antioxidants by scavenging reactive oxygen species and by chelating the redox-active metals iron and copper. They also behave as signaling molecules, modulating multiple cell signalling pathways and gene expression, including that of antioxidant enzymes. This study aimed at determining whether catechins and procyanidins interact with the redox-inactive metal zinc and at assessing their effect on cellular zinc homeostasis. We found that a grape-seed procyanidin extract (GSPE) and the green tea flavonoid (-)-epigallocatechin-3-gallate (EGCG) bind zinc cations in solution with higher affinity than the zinc-specific chelator Zinquin, and dose-dependently prevent zinc-induced toxicity in the human hepatocarcinoma cell line HepG2, evaluated by the lactate dehydrogenase test. GSPE and EGCG hinder intracellular accumulation of total zinc, measured by atomic flame absorption spectrometry, concomitantly increasing the level of cytoplasmic labile zinc detectable by Zinquin fluorescence. Concurrently, GSPE and EGCG inhibit the expression, evaluated at the mRNA level by quantitative reverse transcriptase-polymerase chain reaction, of zinc-binding metallothioneins and of plasma membrane zinc exporter ZnT1 (SLC30A1), while enhancing the expression of cellular zinc importers ZIP1 (SLC39A1) and ZIP4 (SLC39A4). GSPE and EGCG also produce all these effects when HepG2 cells are stimulated to import zinc by treatment with supplemental zinc or the proinflammatory cytokine interleukin-6. We suggest that extracellular complexation of zinc cations and the elevation of cytoplasmic labile zinc may be relevant mechanisms underlying the modulation of diverse cell signaling and metabolic pathways by catechins and procyanidins.

Grape seed procyanidins inhibit the expression of metallothione in genes in human HepG2 cells.

Procyanidins are the most abundant polyphenols in red wine and are also found in cereals, fruits, chocolate and tea. They exert many beneficial health effects, especially on the cardiovascular system (Bagchi et al. in Mutat Res 523-524:87-97, 2003; Williams et al. in Free Radic Biol Med 36:838-849, 2004; Dell'Agli et al. in Cardiovasc Res 63(4):593-602, 2004; Del Bas et al. FASEB J 19:479-480, 2005). Here, we show that oral administration of a grape seed procyanidins extract (GSPE) to healthy rats results, 5 h after treatment, in a 70% inhibition of metallothionein (MT) gene expression in the liver, as determined by oligonucleotide microarray hybridization. Similarly, in cultured human hepatocytes HepG2, GSPE downregulate the expression of MT genes at the mRNA level, as evaluated by quantitative RTPCR. Thus, mRNA levels of six functional MT genes, MT1A, 1E, 1F, 1G, 1X and MT2A, are diminished between 50 and 80% when HepG2 cells are treated during 12 h with GSPE. Only the expression of two human MT genes, MT1G and MT1E, is transiently increased during the first 2 h of treatment. GSPE-induced inhibition of MT genes expression is dose dependent, at concentrations that are not toxic for the cells. Our findings demonstrate that metallothionein genes are direct targets of procyanidins action, both in vivo and in vitro, in hepatic cells. Thus, this study will help to elucidate the mechanisms by which procyanidin exert their beneficial actions.

Estudio de los tratamientos tópicos y los cuidados de enfermería en el paciente dermatológico / Study of topical treatments and nursing care in the dermatologic patient

Se presenta un estudio del uso de distintas medicaciones externas dermatológicas en pacientes ingresados en dermatología y se describen las formas de aplicación de estos medicamentos. Se confecciona una guía de los cuidados de enfermería en los pacientes dermatológicos

Estudio de los tratamientos tópicos y los cuidados de enfermería en el paciente dermatológico / Study of topical treatents and nursing care in the dermatologic patient

Se presenta un estudio del uso de distintas medicaciones externas dermatológicas en pacientes ingresados en dermatología y se describen las formas de aplicación de estos medicamentos. Se confecciona una guía de los cuidados de enfermería en los pacientes dermatológicos