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Primary graft failure (PGF) is the leading cause of early mortality after heart transplantation (HT). Our aim is to propose a working definition of PGF and to develop a predictive risk score.PGF was defined by four criteria reflecting significant myocardial dysfunction, severe hemodynamic impairment, early onset after HT, and absence of secondary causes of graft dysfunction. We identified independent risk factors for PGF in a derivation series of 621 HTs and constructed a predictive model. After proving its internal consistency we tested the model in a prospective validation series.The incidence and lethality of PGF in our series were 9% and 80%, respectively. We identified 6 multivariate risk factors for PGF (Right atrial pressure ≥ 10 mm Hg, recipient Age ≥ 60 years, Diabetes mellitus, Inotrope dependence, donor Age ≥ 30 years, Length of ischemic time ≥ 240 minutes--i.e., RADIAL). Analysis of isolated right ventricular failure showed similar predictors. The RADIAL score was obtained by adding 1 point for each of these factors present in a given HT. PGF incidence increased significantly as the RADIAL score increased (p0.001 for trend). Rates of actual and predicted PGF incidence for RADIAL subgroups showed a good correlation (C-statistic = 0.74). In a prospective validation cohort, RADIAL score kept its predictive ability.PGF as defined by these criteria showed a high impact on early post-HT mortality in our series. The RADIAL score showed good ability to predict the development of PGF, and could be useful in the prevention and early treatment of this complication.

La amiloidosis cardiaca causa una miocardiopatia restrictiva de mal pronostico debida al deposito intersticial de proteina anomala en el miocardio. Esta proteina puede tener diversos origenes y dar lugar a subtipos de amiloidosis con diferente pronostico y manejo terapeutico. Los farmacos utilizados habitualmente en la insuficiencia cardiaca son poco eficaces en la amiloidosis, y la indicacion de trasplante cardiaco es controvertida porque la enfermedad afecta a multiples organos y por la probabilidad de recidiva en el organo trasplantado. La utilizacion de nuevas tecnicas para la identificacion del tipo de amiloidosis, la aparicion de procedimientos capaces de impedir o disminuir la produccion de amiloide, la posibilidad de monitorizar la respuesta al tratamiento y, sobre todo, la formacion de equipos multidisciplinarios capaces de realizar tratamientos combinados, que incluyen el trasplante multiorganico, han contribuido a mejorar sustancialmente el pronostico de la enfermedad.

Cardiac amyloidosis is associated with the interstitial deposition of abnormal protein in the myocardium, which can lead to a form of restrictive cardiomyopathy with a poor prognosis. This protein can have a number of different origins, which give rise to various subtypes of amyloidosis that have different prognoses and that require different therapeutic approaches. Drugs commonly used in heart failure have little effect in amyloidosis and the use of heart transplantation is controversial because amyloidosis is a multi-organ disease and because there is a possibility of disease recurrence in the graft. The use of new techniques to identify the specific amyloidosis subtype, the emergence of novel ways of preventing or decreasing amyloid production, the ability to monitor responses to therapy and, above all, the introduction of multidisciplinary teams that can implement a combination of therapies, including multiple organ transplantation, have contributed to a substantial improvement in the prognosis of this disease.

This paper proposes a Cooperative ARQ protocol to be used in delay-tolerant vehicular networks. The proposed scheme has been implemented and evaluated through an experimental testbed, showing that packet losses in transmissions from an access point to cars can be reduced to the half without any cost as long as cooperation takes place on areas where connectivity with access points is not present. In these areas, cars in a platoon recover from other cars packets that they have failed to receive from the access point.

Myotonic dystrophy (DM) is caused by an expansion of a CTG repeat sequence in the 3′ noncoding region of a protein kinase gene (DMPK) at 19q13.3. We used in situ hybridization to analyse the replication timing of the genomic region containing DMPK in fibroblasts and myoblasts from controls and myotonic dystrophy patients. In this method the relative proportion of singlet to doublet hybridization signals is used to infer the relative time of replication of specific loci or regions. Our results show that in cells from normal individuals approximately 65% of signals appear as doublets, indicating early replication. In DM patients with a number of CTG repeats ranging from about 600–1800 we observed a significant increase of singlet-doublets compared to the background level. These results suggest the existence of replication alternations and/or structural differences between the normal and mutant alleles induced by the presence of the DM mutation.