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Resumen Introduccion y objetivos La utilidad de la ecografia pulmonar (EP) en la insuficiencia cardiaca (IC) aguda esta bien definida, pero no asi en la IC cronica. Este estudio investigo el valor pronostico de la EP en pacientes estables con IC cronica. Metodos Se incluyo a pacientes ambulatorios consecutivos con visita programada en una unidad de IC. La EP se realizo in situ, con los datos clinicos enmascarados, y evaluo 8 areas toracicas. La suma de lineas B en todas las areas pulmonares y los cuartiles de dicha adicion se utilizaron para los analisis de regresion lineal y de Cox. Los objetivos principales fueron el compuesto de muerte por cualquier causa u hospitalizacion por IC y mortalidad por cualquier causa. Resultados Se incluyo a 577 individuos (edad, 69 ± 12 anos; el 72% varones). La media de lineas B fue de 5 ± 6. Durante un seguimiento de 31 ± 7 meses, en 157 pacientes se produjo el resultado compuesto y 111 fallecieron. Tener ≥ 8 lineas B (Q4) doblo el riesgo de padecer el evento compuesto (p Conclusiones La EP identifico a pacientes con IC cronica estable y alto riesgo de muerte u hospitalizacion por IC.

Summary Background & aims Nutritional status is an important prognostic factor in patients with heart failure (HF). In a pilot study we previously observed that the Mini Nutritional Assessment Short Form tool (MNA-SF) was the best approach for the screening of nutritional status in HF outpatients over other screening tools. The current study aimed to determine whether the MNA-SF has prognostic value in outpatients with HF and whether the impact of malnutrition differs depending on left ventricular ejection fraction (LVEF). Methods Prospective study performed in outpatients attending a HF clinic at a university hospital. All subjects completed the MNA-SF at study entry. The primary endpoint was all-cause mortality. Secondary end-points were the number of recurrent HF-related hospitalizations and the composite end-point of all-cause death or HF-related hospitalizations. Patients with malnutrition and at risk of malnutrition were merged and considered as having abnormal nutritional status for statistical analysis. Results From October 2016 to November 2017, 555 patients were included (age 69 ± 11.5 years, 71% male, LVEF 44.6 ± 13.2). Abnormal nutritional status was identified in 103 (18.6%) subjects. HF patients with preserved LVEF had a higher proportion of abnormal nutritional status (23%) than patients with HF and mid-range LVEF (HFmrEF) (16.4%) or those with HF with reduced LVEF (HFrEF) (15.9%.). During a mean follow-up of 23.8 ± 6.6 months, 99 patients died (17.8%), 74 were hospitalized due to HF (13.3%) and the composite end-point was observed in 181 (32.6%). In the univariate analysis, abnormal nutritional status was significantly associated with all-cause mortality (p = 0.02) and the composite end-point (p = 0.02) in the total cohort. However, in the multivariate analysis including age, sex, NYHA functional class, BMI, ischemic aetiology, diabetes, hypertension and HF duration, abnormal nutritional status remained significantly associated with all-cause mortality (HR 3.32 [95%CI 1.47–7.52], p = 0.004), and the composite end-point (HR 2.53 [95%CI 1.30–4.94], p = 0.006) only in HFmrEF patients. Patients with abnormal nutritional status suffered double the crude number of recurrent HF-related hospitalizations (16.4 vs. 8.4 per 100 patients-years, p Conclusions The implementation of MNA-SF as a routine screening tool allowed the detection of abnormal nutritional status in almost one out of five ambulatory HF patients. Nutritional status assessed by the MNA-SF was an independent predictor of all-cause death and the composite end-point of all-cause death or HF-related hospitalization in outpatients with HFmrEF. Furthermore, abnormal nutritional status was significantly related to recurrent hospitalizations across the HF spectrum.

The function of the tumour suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is tightly controlled by post-translational modifications (PTMs) including ubiquitin or Small Ubiquitin-related MOdifiers (SUMO). It is known that SUMOylation by SUMO-1, SUMO-2/-3, mono- or polyubiquitylation have a distinct impact on PTEN activity, localisation and/or stability, however the molecular mechanisms governing these processes are still unclear. Studying PTM regulated events has always been a difficult task due to their labile nature. Here, we propose an update on the role of these PTMs on PTEN function, as well as a methodological overview on the use of molecular traps named SUMO Binding Entities (SUBEs) or Tandem Ubiquitin Binding Entities (TUBEs) to capture SUMOylated or Ubiquitylated forms of PTEN respectively. When combined with in vitro SUMOylation or Ubiquitylation assays, the use of molecular traps facilitate the detection of modified forms of PTEN. SUMO and ubiquitin-traps are also suitable to capture endogenously modified forms of PTEN after expression of E3 ligases or treatment with chemical inhibitors. This versatile approach represents an interesting alternative to explore PTEN regulation by SUMO and ubiquitin under physiological or pathological conditions.

Background Use of the transradial approach (TRA) in percutaneous coronary intervention (PCI) has increased in recent years. TRA has a lower mortality rate than the transfemoral approach (TFA) in patients with acute coronary syndrome. Comparative studies have systematically excluded patients with cardiogenic shock (CS). Methods We performed a prospective, observational registry study of consecutive patients undergoing emergent revascularization between February 2007 and January 2012. An analysis of the clinical evolution of patients with CS during hospitalization was performed. Results Of 1,400 emergency procedures, 122 had CS, of which 80 underwent PCI by TRA (65.6%) and 42 underwent PCI by TFA (34.3%). The main reason for choosing TFA was the absence of radial pulse (54.9%). Mortality (64.3% vs 32.5%, P = .001), serious access site complications (11.9% vs 2.5%, P = .03), access site complications requiring blood transfusion (7.1% vs 0%, P = .04), and major adverse cardiac events (death, infarction, stroke, serious bleeding, and postanoxic encephalopathy) (73.8% vs 43.8%, P = .001) were greater in patients treated by TFA. In the multivariate analysis, TRA was a predictor of mortality (odds ratio [OR] 0.39 [0.15-0.97]); other predictive factors were age ≥75 years (3.47 [1.35-8.92]), previous treatment with diuretics (3.67 [1.21-11.12]), and success of the procedure (0.07 [0.02-0.24]). Conclusions Transradial approach for PCI is possible and safe in up to two-thirds of patients with CS. Absence of radial pulse was the main factor preventing use of TRA. In multivariate analysis, TRA was associated with a lower risk of mortality.

p73 shares structural and functional homology to p53. p73 generates different proteins using alternative promoters and splicing which have different biological characteristics. We investigated the pattern (monoallelic or biallelic) of expression of TAp73 and DeltaNp73 in normal lymphocytes and lymphomas using two p73 polymorphisms. We found monoallelic expression of TAp73 in normal lymphocytes and tumors, and a selective expression of AT allele in all cases. Moreover, the quantitative expression analysis revealed DeltaNp73 over-expression in both B- and T-cell lymphomas comparing with normal lymphoid cells, suggesting a role in tumorigenesis. Finally, we have confirmed that although DeltaNp73 over-expression could be an alternative mechanism of p53 inactivation, both alterations may appear together.

The potential efficacy of prodrug activation of a transduced suicide gene in a cancer cell may be impaired or enhanced by oncoproteins produced by that cell. In the context of a gene therapy protocol for chronic myeloid leukemia (CML) we examined whether the Bcr-Abl fusion protein would have either of these effects. Thus, the mechanism of cell killing by transfer of herpes simplex virus thymidine kinase (HSV -tk ) and subsequent ganciclovir (GCV) treatment was examined in pre-B (TonB210.1) cells and myeloid cells (32D) and in their BCR-ABL -expressing counterparts. HSV- tk -transduced cell lines, either in the presence or in the absence of BCR-ABL expression, became susceptible to GCV at concentrations which were nontoxic to the nontransduced cells. This susceptibility was represented by apoptotic cell death in all cases. Apoptosis was observed after 24 h of treatment with GCV in the tk -transduced parental cells and in the BCR-ABL -expressing TonB210.1 cells but only after a delay of more than 24 h in the 32Dp210 cells compared to 32D. Cell death in the BCR-ABL -expressing clones was preceded by S- and G2/M-phase cell cycle arrest. Activation of FAS/APO-1 and caspase-8 was observed in all the tk -transduced cell lines after GCV treatment. However, the caspase-8 inhibitor Z-IETD-FMK only partially abrogated tk /GCV-induced apoptosis. A possible role for inhibition of Bcl-2 or Bcl-x L expression in the apoptosis induced by GCV was observed in the tk -transduced TonB210.1 cells but not in the 32D or 32Dp210 cells. The data demonstrate that expression of the Bcr-Abl oncoprotein does not block the apoptosis induced by the HSV- tk /GCV system, suggesting that this suicide gene therapy strategy could be considered for the treatment of CML in blast crisis.

Introduccion: Los diagnosticos de enfermeria como motor del plan de cuidados resultan imprescindibles en el desempeno cotidiano del trabajo enfermero. Los diagnosticos neonatales surgidos de una valoracion a fondo del neonato dirigen el plan de actuacion de la enfermeria neonatal. Material, metodos y resultados: En el presente estudio se extrajeron de las historias clinicas los diagnosticos mas frecuentes y se elaboro un manual que recoge objetivos y actividades que serviran de guia en la practica clinica. Tambien estandarizamos un plan de cuidados al neonato pretermino que incluye todos aquellos diagnosticos, objetivos y actividades que dirigiran la actuacion de enfermeria ante cualquier neonato de menos de 37 semanas de edad gestacional. Discusion: Hemos constatado la deteccion de muchos problemas de riesgo, lo que significa que las enfermeras planifican sus cuidados para evitar que dichos problemas de riesgo se conviertan en reales y, si lo hacen, que sus consecuencias sean lo mas leves posible. Por el contrario, los diagnosticos referidos a la esfera psicosocial no aparecen con la importancia que sin duda tienen, lo que se explica por el enfasis que desde siempre le hemos dado al plano fisico. Se pretende para el futuro, con el apoyo informatico, solventar estos y otros inconvenientes que se han detectado.

The ultrastructural aspects of the replication cycle of the turbot aquareovirus (TRV) were studied using CHSE-214 cells. Although this virus in general followed the typical pattern of reovirus replication and morphogenesis, it presented some important differences. Internalisation of virions into the host cell occurred by direct penetration through the plasma membrane (even at temperatures below 4°C), and this step was independent of trypsin treatment. Two size classes of viral particles were detected in the cytoplasm of infected cells: (i) particles of 30 nm diameter, probably corresponding to cores, located inside cytoplasmic viroplasms, and (ii) 45 nm diameter particles, located in vesicles of the endoplasmic reticulum, probably corresponding to single-shelled virions. Double-shelled complete viral particles (75–80 nm diameter) were only detected at the exterior of the cell. Cores formed inside the viroplasms were transformed into 45 nm immature virions by budding from viroplasms to cytoplasmic vesicles. The vesicles carried those subviral particles towards the periphery of the cell. Final maturation occurred by budding of the immature virions through the plasma membrane. During this process, incomplete virions acquired an external protein layer, to form the 75 nm double-shelled complete virions released to the exterior. Thus, release of TRV viral progeny was not necessarily associated with cell lysis. Replication of TRV was cytoplasmic, and some of the ultrastructural changes caused by the viral replication included development of many dense fibrillar bodies, and cell cytoskeleton alterations.

A new family of complexes containing bulky pyrazoles substituted in the 3 or the 3 and 5 positions, [RhCl(L2)(HpzR′,R″)] (L2  NBD, 2CO; R′  But, Ph, p-CH3OC6H4 (An), R″  H; R′  But, Ph, R″  CH3; R′  R″  H, CH3), has been obtained. A dynamic behaviour has been observed only in complexes with the less demanding pyrazole ligands, relating with a metallotropic equilibrium when R′  R″  H, Me, or a diolefin reorientation when R′  But, Ph, An, R″  H. The X-ray crystal structure of [RhCl(CO)2(HpzAn)] has been solved, showing a molecular stacking with a RhRh separation of 3.398(3) A along the one-dimensional chain.

In this study 51 aquatic birnaviruses were isolated from environmental samples (molluscs, wild fish and sediments) during routine surveys around fish farms located in Galicia (NW of Spain). These viruses were identified as IPN-like viruses based on their physical and chemical characteristics. Furthermore, these isolates were molecular and serologically compared to the reference strains VR-299, Sp and Ab. Although they caused no mortalities in oysters and showed varying degrees of virulence in trout, all isolates were recovered from the inoculated animals, indicating that oysters can become carriers. The results obtained in this study indicate the role of the molluscs, sediments or fish feed as important agents to consider in the epidemiology of birnaviruses.

Antigenic relationships between a Spanish rotavirus isolate from turbot and four North American isolates from smelt, striped bass and Atlantic salmon (two isolates) indicated that the American strains are closely related and are different from the Spanish rotavirus. These results agree with previous studies on molecular characterization of the viruses.

The reaction of [Rh(μ-Cl)(NBD)] 2 (NBD = 2,5-norbornadiene) and [TpBu t ] − (TpBu t = hydrotris(3- tert -butylpyrazol-1-yl)borate, HB[3-Bu t pz] 3 0 yields [Rh(3-Bu t pz) (NDB)(3-Bu t pzH)] (pz = C 3 N 2 H 2 ) instead of the expected complex [Rh(TpBu t )(NBD)]. The crystal structure of the title compound shows the presence of an asymmetric H bond between the two pyrazole rings. The formation of the pyrazole/pyrazolate complex implies a degradation reaction of the ligand.