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Justificación: Paciente infantil con estancia hospitalaria prolongada y hábitos alimenticios diferentes. Presenta déficit nutricional, relacionado en principio con su patología neurológica y posteriormente con la prolongación de su estancia, que le lleva a aborrecer la comida, se intenta solucionar con dieta especial. Con esta dieta se detectaron déficit nutricional, agravándose en este caso, por sus costumbres alimenticias, rechaza algunos alimentos. Se presenta en sesión clínica, surge un plan de mejora en el que familia y paciente tienen mayor protagonismo en su alimentación, aumentando conocimientos y motivación. Objetivos: Conseguir un estado nutricional adecuado en el niño. Aumentar conocimientos familiares. Implicar a los padres en cuidados alimentarios. Eliminar déficit nutricional de dietas especiales. Aumentar peso. Metodología: Estudio de caso único. Se ha valorado según el modelo Virginia Henderson elaborándose un Plan de Cuidado individualizado, dándole seguimiento y evaluando los objetivos. Sesión clínica: Plan de mejora: Consenso enfermera-familia en los menús y Enseñar necesidades nutricionales y componentes de los alimentos para que sepan adaptarlo a sus hábitos. Resultados: Mejora la ingesta Peso: Aumento del peso de 21 kg a 26,400 kg en tres semanas. Participación de familia-paciente en elaboración de menús y registro. Conclusiones: La participación familiar es posible y necesaria, tanto para conocer las preferencias alimenticias y ajustarlas a la dieta, como en registro y motivación del niño. La familia adquiere los conocimientos para seguir tomando los nutrientes necesarios en su dieta habitual al alta (energéticos, ricos en potasio…etc). Implicación multidisciplinar. [ABSTRACT FROM AUTHOR]

Negative pressure wound therapy (NPWT) has been widely used in the adult patient, contrary to what happens in children, with just a few long series papers. NPWT avoids long and expensive hospital admissions, reducing the hospital costs; it also decreases the family dynamics and allows for an early return to everyday activities. In this article, we present three clinical cases consisting of a toddler, a child and a teenager with complex wounds treated with NPWT in the pediatric surgery department of the Virgen de las Nieves University Hospital in Granada. The results were excellent, with a good adherence to treatment in all cases, achieving a complete closure in two cases; the third case needed a deferred surgical closure after surgical site preparation, and showed a decrease of the wound size after the NPWT. Moreover, successful pain management was achieved during the wound cleansing, which was done under an ambulatory regime. No general anesthesia was needed. From our experience, we propose the NPWT as an alternative therapy to the classic surgical approach for this type of complex lesions in children, which offers the same advantages and results than in adults., (Copyright © 2016 Elsevier España, S.L.U. All rights reserved.)

AG490 is a tyrphostin originally described as a Janus Activated Kinase (JAK) 2 inhibitor. AG490 also inhibits epidermal growth factor receptor (EGFR) and guanylyl cyclases (GC). More recently, AG490 was associated with oxidative stress protection in experimental acute kidney injury models. We now show that AG490 is also a strong activator of the Hypoxia Inducible Factor (HIF)-1. Under normoxic conditions HIF-1α is degraded through hydroxylation, von Hippel Lindau protein (VHL)-mediated ubiquitin tagging and proteasomal degradation. AG490 increased HIF-1α protein, but not HIF-1α mRNA levels, dose- and time-dependently in cultured endothelial, vascular smooth muscle and kidney proximal tubular epithelial cells. AG490 increased HIF-1α protein half-life, suggesting that HIF-1α protein accumulation resulted from a decreased degradation. In this regard, AG490 prevented HIF-1α hydroxylation and increased HIF-1α protein levels in human renal carcinoma cells expressing VHL, but did not further increase HIF-1α in VHL negative cells. AG490 did not prevent the proteasomal degradation of other proteins. HIF-1α was not upregulated by dominant negative JAK2constructs, tyrphostin AG9, the EGFR inhibitors erbstatin and genistein, the GC inhibitor Ly83583 or cGMP analogues. Finally, AG490 also increased HIF-1α transcriptional activity evidenced by the increased HIF-1α-dependent VEGF expression. In conclusion, AG490 is a novel HIF-1α activator that increases HIF-1α half-life and protein levels through interference with HIF-1α hydroxylation and VHL-mediated degradation. This action may contribute to the cell and tissue protective effects of AG490.

Transcriptional regulation of vascular endothelial growth factor (VEGF) is critically dependent on hypoxia-inducible factor 1 (HIF-1). However, not only hypoxia, but selected growth factors can induce HIF-1. High levels of both VEGF and HIF-1 coexist in certain conditions, e.g. tumors. Nonetheless, the possibility that the stimulatory relationship between HIF-1 and VEGF may be bi-directional has not been addressed up to date. The present study in endothelial cells analyzed whether HIF-1 is regulated by a product of its own transcriptionally activated genes, namely, VEGF. As a main finding, VEGF-A(165) induced the increase of HIF-1alpha mRNA and HIF-1alpha protein and nuclear translocation. Autologous endothelial cell VEGF mRNA and protein were also increased upon exposure to exogenous VEGF. The signaling implication of reactive oxygen species was examined by comparison with H(2)O(2) and hypoxanthine/xanthine oxidase and by the superoxide dismutase mimetic, MnTMPyP, the Rac1-NAD(P)H oxidase complex inhibitor, apocynin, transfection of a dominant negative Rac1 mutant, and transfection of a p67phox antisense oligonucleotide. Superoxide anion, largely dependent on Rac1-NAD(P)H oxidase complex activity, was the critical signaling element. The transductional functionality of the pathway was confirmed by means of a reporter gene flanked by a transcription site-related VEGF sequence and by quantitative PCR. In summary, the present results reveal a previously undescribed action of VEGF on the expression of its own transcription factor, HIF-1, and on VEGF itself. This effect is principally mediated by superoxide anion, therefore identifying a new, potentially relevant role of reactive oxygen species in VEGF signaling.

Inhibition of the JAK2/STAT pathway has been implicated recently in cytoprotective mechanisms in both vascular smooth muscle cells and astrocytes. The advent of JAK2-specific inhibitors provides a practical tool for the study of this pathway in different cellular types. An interest in finding methods to improve endothelial cell (EC) resistance to injury led us to examine the effect of JAK2/STAT inhibition on EC protection. Furthermore, the signaling pathways involved in JAK2/STAT inhibition-related actions were examined. Our results reveal, for the first time, that blockade of JAK2 with the tyrosine kinase inhibitor AG490 strongly protects cultured EC against cell detachment-dependent death and serum deprivation and increases reseeding efficiency. Confirmation of the specificity of the effects of JAK2 inhibition was attained by finding protective effects on transfection with a dominant negative JAK2. Furthermore, AG490 blocked serum deprivation-induced phosphorylation of JAK2. In terms of mechanism, treatment with AG490 induces several relevant responses, both in monolayer and detached cells. These mechanisms include the following: 1) Increase and nuclear translocation of the active, dephosphorylated form of beta-catenin. In functional terms, this translocation is transcriptionally active, and its protective effect is further supported by the stimulation of EC cytoprotection by transfectionally induced excess of beta-catenin. 2) Increase of platelet endothelial cell adhesion molecule (PECAM)/CD31 levels. 3) Increase in total and phosphorylated AKT. 4) Increase in phosphorylated glycogen synthase kinase (GSK)3alpha/beta. The present findings imply potential practical applications of JAK2 inhibition on EC. These applications affect not only EC in the monolayer but also circulating detached cells and involve mechanistic interactions not previously described.

F12511(S)-2',3',5'-trimethyl-4'-hydroxy-alpha-dodecylthio-alpha-phenylacetanilide (F12511) is a new Acyl-CoA cholesterol acyltransferase (ACAT) inhibitor that not only reduces the plasma cholesterol levels but also has anti-atherosclerotic actions in animals models. The study's aim was to analyze if F12511 may directly modify the ability of tumor necrosis factor--alpha (TNF-alpha)-incubated bovine aortic endothelial cells (BAEC) to express endothelial nitric oxide synthase (eNOS) protein and inflammatory-related proteins such as platelet endothelial cell adhesion molecule (PECAM) and CD40 ligand (CD40L). The addition of increasing concentrations of F12511 (10 to 10 mol/L) failed to modify the level of eNOS protein expressed in control BAEC. TNF-alpha (10 ng/mL) reduced the expression of eNOS protein. In TNF-alpha--incubated BAEC, F12511 protected eNOS expression in a concentration-dependent manner. TNF-alpha stimulated the expression of both CD40L and PECAM in cultured BAEC. F12511 (10 mol/L) failed to modify the expression of CD40L and PECAM in control and TNF-alpha-incubated BAEC. Reverse transcriptase polymerase chain reaction showed a marked expression of the ACAT-2 isoform and absent of expression of the ACAT-1 isoform in BAEC. The presence of ACAT-2 isoform in BAEC was further confirmed by Western blot. F12511 failed to modify the expression of the proinflammatory associated proteins PECAM and CD40L in the endothelium but protected eNOS expression in the endothelial cells exposed to inflammatory conditions.

Inflammation and platelet activation are critical phenomena in the setting of acute coronary syndromes. Platelets may contribute to increase ischemic injury by enhancing the inflammatory response of leukocytes and endothelial myocardial cells. Pharmacological inhibition of platelet activation prevents ischemic complications in patients with coronary diseases. Agents directed against the integrin glycoprotein IIb/IIIa (GP IIb/IIIa) receptor not only inhibit platelet aggregation but also have been demonstrated to limit the inflammatory response in acute coronary syndromes. The question then raised is if the inhibition of platelet activation by other mechanisms than the blockade of GP IIb/IIIa may also exert anti-inflammatory effects. The aim of the present study was to analyze if clopidogrel may exert anti-inflammatory effects during the acute phase of myocardial infarction. A ligature was placed around the left anterior descending coronary artery of New Zealand White rabbits. After 15 min of ischemia, the myocardium was reperfused and the ischemic coronary artery was isolated 24 h after the ischemia. A group of ischemic rabbits was given a single oral dose of clopidogrel (20 mg kg(-1)) just after the arterial occlusion and the animal was recovered. Sham-operated animals served as control. P-selectin expression was significantly increased in infarcted rabbits with respect to control rabbits. Clopidogrel administration reduced P-selectin expression with respect to untreated infarcted rabbits. CD40 ligand and tissue factor expression was increased in the ischemic coronary artery and reduced after clopidogrel administration. Clopidogrel also protected endothelial nitric oxide synthase protein expression in the ischemic coronary artery, a protein that has been found downregulated under inflammatory conditions. In conclusion, inhibition of platelet activation by clopidogrel exerted anti-inflammatory effects on the ischemic coronary artery.

Objective: To analyze the factors which cause stress at work among hospital nursing staff according to their socio-demographic and professional characteristics and their affects on psychological welfare., Methods: A cross study carried out on a randomly chosen group of 201 nursing professionals composed of nurses and nurses aides from a general public hospital in the city of Valencia. The data was gathered by means of a self-administered questionnaire. To measure the variable response, psychological welfare, The Goldberg General Health 28 item version questionnaire, GHQ-28, was used. Work stress factors were evaluated by means of a scale valid for our cultural environment, Spain,: the Nursing Stress Scale, NSS, which consists of 34 items having a range from 0 to 102. In addition, information about diverse socio-demographic and professional variables were gathered. The authors carried out a simple analysis on all the data obtained., Results: The scores registered on the work stress factors scale were lower for nursing professionals older than 55 and for those who have more than 20 years experience in their service, with a medium of 23.28 (IC 95% = 9.87-54.84) and 25.29 (IC 95% = 11.80-54.22) respectively. On the other hand, the medium was higher for nurses with a medium of 34.16 (IC: 15.29-76.29) in comparison to the score for nurses aides. The total score on the work stress factors scale was higher in the "probable situations" of psychological stress with a medium of 42.40 (IC 95% = 21.35-84.21)., Conclusions: The results of this study demonstrate that a higher level exposure to work stress factors lowers the psychological welfare among nursing staff.