[Management of heart failure in cardiology and primary care (MICCAP) program: Improving the management of patients with heart failure]. / Programa MICCAP (Manejo de la Insuficiencia Cardiaca en Cardiología y en Atención Primaria): mejorando el manejo del paciente con insuficiencia cardiaca.

Despite current treatments, morbidity and mortality of patients with heart failure remain high. The late diagnosis of heart failure, the insufficient heart failure treatment (i.e. not using the appropriate drugs, prescribing lower doses of drugs than recommended, etc.), and a poor coordination between different health care levels, may explain, at least in part, these figures. The Management of Heart Failure in Cardiology and Primary Care (MICCAP) program has been developed with the aim of optimising the integrated management of patients with heart failure between Primary Care and Cardiology, through the improvement of coordination between both health care levels. This includes continuous medical education to reinforce the diagnostic and therapeutic skills of general practitioners in the field of heart failure. The rationale and objectives of the MICCAP program are summarised in this article.

De los ensayos clínicos a la práctica clínica. Evidencias con rivaroxaban en el tratamiento anticoagulante del paciente con fibrilación auricular no valvular / From clinical trials to clinical practice. Experience with rivaroxaban in the anticoagulant treatment of patients with non-valvular atrial fibrillation

A pesar de que la información proporcionada por los ensayos clínicos es importante, existen diferencias relevantes entre los pacientes incluidos en los ensayos clínicos y los pacientes de la consulta diaria. En consecuencia, en algunos casos los resultados de los ensayos clínicos no se podrían trasladar directamente a los pacientes en la práctica clínica. En este contexto, la realización de registros en «la vida real» es fundamental. En ROCKET-AF, rivaroxaban, un anticoagulante oral de acción directa de toma única diaria, fue al menos tan eficaz como warfarina en la prevención del ictus o embolismo sistémico, con tasas similares de sangrados mayores, pero con un menor riesgo de hemorragias intracraneales, críticas y mortales. En los últimos años, diferentes registros han confirmado que rivaroxaban es eficaz e incluso más seguro en los pacientes de la vida real que en ROCKET-AF. El objetivo de esta revisión es actualizar la evidencia actual sobre la eficacia, la efectividad y la seguridad de rivaroxaban en pacientes de la vida real (AU)

Despite the information provided by clinical trials is important, there are relevant clinical differences between those patients included in clinical trials and data of daily outpatient clinics. As a result, in some cases, the results of randomized clinical trials could not be directly applied to clinical practice. In this context, to perform «real-life» registries is mandatory. In the ROCKET-AF study, rivaroxaban, a once-daily direct oral anticoagulant, was at least as effective as warfarin for preventing stroke or systemic embolism, with similar rates of major bleeding, but with a lesser risk of intracranial, critical and fatal bleedings. In the last years, different large registries have confirmed that rivaroxaban is effective and even safer in real-life patients than in ROCKET-AF. The aim of this review is to update the current evidence about the efficacy, effectiveness and safety of rivaroxaban in real-life patients (AU)

[From clinical trials to clinical practice. Experience with rivaroxaban in the anticoagulant treatment of patients with non-valvular atrial fibrillation]. / De los ensayos clínicos a la práctica clínica. Evidencias con rivaroxaban en el tratamiento anticoagulante del paciente con fibrilación auricular no valvular.

Despite the information provided by clinical trials is important, there are relevant clinical differences between those patients included in clinical trials and data of daily outpatient clinics. As a result, in some cases, the results of randomized clinical trials could not be directly applied to clinical practice. In this context, to perform «real-life¼ registries is mandatory. In the ROCKET-AF study, rivaroxaban, a once-daily direct oral anticoagulant, was at least as effective as warfarin for preventing stroke or systemic embolism, with similar rates of major bleeding, but with a lesser risk of intracranial, critical and fatal bleedings. In the last years, different large registries have confirmed that rivaroxaban is effective and even safer in real-life patients than in ROCKET-AF. The aim of this review is to update the current evidence about the efficacy, effectiveness and safety of rivaroxaban in real-life patients.

Performance of innovative PU-foam and natural fiber-based composites for the biofiltration of a mixture of volatile organic compounds by a fungal biofilm.

The performance of perlite and two innovative carriers that consist of polyurethane (PU) chemically modified with starch; and polypropylene reinforced with agave fibers was evaluated in the biofiltration of a mixture of VOCs composed of hexane, toluene and methyl-ethyl-ketone. At a total organic loading rate of 145 gCm(-3)h(-1) the elimination capacities (ECs) obtained were 145, 24 and 96 gCm(-3)h(-1) for the biofilters packed with the PU, the reinforced polypropylene, and perlite, respectively. Specific maximum biodegradation rates of the mixture, in the biofilters, were 416 mgCg(protein)(-1) h(-1) for the PU and 63 mgCg(protein)(-1) h(-1) for perlite, which confirms the highest performance of the PU-composite. 18S rDNA analysis from the PU-biofilter revealed the presence of Fusarium solani in its sexual and asexual states, respectively. The modified PU carrier significantly reduced the start-up period of the biofilter and enhanced the EC of the VOCs. Thus, this study gives new alternatives in the field of packing materials synthesis, promoting the addition of easily biodegradable sources to enhance the performance of biofilters.

Mecanismos reguladores del metabolismo energético / No disponible

El balance entre el ingreso y gasto energético está regulado a través de un complejo sistema de señales aferentes y eferentes que conectan bidireccionalmente al sistema nervioso central con el resto del organismo. La convergencia e integración de estas señales, así como la puesta en marcha de respuestas fisiológicas está coordinada por el hipotálamo. Las señales periféricas que informan sobre el ingreso de nuevos aportes calóricos, así como sobre el estado de disponibilidad y reserva energética proceden, fundamentalmente, de dos fuentes, el aparato digestivo y el tejido adiposo. Además, todas las células disponen de sus propios sensores energéticos, que interactúan con el resto de señales centrales y periféricas. En esta revisión actualizaremos el conocimiento actual del complejo engranaje de control neuroendocrinológico de la homeostasis energética (AU)

Body energy balance is regulated through a complex network of afferent and efferent signals connecting the central nervous system and the entire body bidirectionally. The hypothalamus is the key point where these signals converge and are integrated, generating coordinated physiological responses. Peripheral signals informing about caloric intake and energy availability and stores are generated preferently from two sources, the gastrointestinal system and adipose tissue. Moreover, every cell has its own energy sensors, interacting with central and peripheral signals. This review is an update of the current knowledge about complex neuroendocrinological control of energy homeostasis (AU)

The natriuretic effect of nifedipine gastrointestinal therapeutic system remains despite the presence of mild-to-moderate renal failure.

BACKGROUND: Calcium channel blockers facilitate the renal excretion of sodium and this effect is maintained during chronic administration of these drugs. However, it is unknown whether this natriuretic effect remains despite the presence of a decreased renal function. OBJECTIVE: To compare the natriuretic capacity of nifedipine gastrointestinal therapeutic system (GITS) and lisinopril in patients with mild-to-moderate chronic renal failure. METHODS: An open-label, randomized, comparative study was conducted to compare the natriuretic capacity of nifedipine GITS and lisinopril in the presence of mild-to-moderate renal failure (creatinine clearance 30-80 ml/min). After a wash-out period of 4 weeks an intravenous saline infusion (30 ml/kg of body weight of isotonic saline in 4 h) was performed and repeated after 4 weeks of active therapy. Two sex- and age-matched groups of hypertensive patients (n = 25) were included in the study. Renal failure was diagnosed as secondary to nephrosclerosis in all the patients. RESULTS: A significant increase in the renal capacity to excrete the sodium load was observed in patients receiving nifedipine GITS (n = 11) but not in those taking lisinopril (n = 13). Both drugs controlled blood pressure to a similar extent. No changes were observed in body weight, glomerular filtration rate and renal plasma flow (measured as inulin and paraaminohippurate clearances). A significant drop was observed in urinary albumin excretion after lisinopril, but not after nifedipine. Heart rate was higher in nifedipine group. CONCLUSION: The natriuretic capacity of nifedipine GITS remains despite the presence of mild-to-moderate chronic renal failure. Such an effect takes place in the absence of changes in renal hemodynamics, suggesting that it is caused by a direct tubular effect.

Response of rat cerebral somatostatinergic system to a high ammonia diet.

It has been reported that ingestion of an ammonium-containing diet produces hyperammonemia without encephalopathy, thus permitting the study of the specific effects of ammonia toxicity. The present study investigated the rat cerebral somatostatinergic system using this experimental model of hyperammonemia. Wistar rats were fed a high ammonia diet prepared by mixing a standard diet with ammonium acetate (20% w/w); in addition, 5 mM of ammonium acetate was added to their water supply. Control rats were fed with a standard diet. The animals were sacrificed at 3, 7 and 15 days of ammonia ingestion. Ammonia levels in blood had increased approximately 3-fold at 7 days of ammonia ingestion. These changes were associated with a significant decrease in the specific binding of somatostatin (SS) to putative receptors sites in the frontoparietal cortex and hippocampus at 7 and 15 days after starting the high ammonia diet. Scatchard analysis shows that the decrease in SS binding resulted from a decrease in the number of available SS receptors rather than a change in receptor affinity. No changes in the somatostatin-like immunoreactivity content (SSLI) were detected in either brain area at the three study times. These results suggest that hyperammonemia alone can affect the rat brain somatostatinergic system. However, the animal model of hyperammonemia used here is insufficient to produce encephalopathy despite the significant increase in serum ammonia.

Acute nicotine administration increases somatostatin content and binding in the rat hypothalamus.

Within 4 minutes a single, intravenous injection of nicotine (0.3 mg/Kg) induced increases in somatostatin-like immunoreactivity concentrations in the rat hypothalamus but not in the striatum. These changes were associated with a significant increase in the specific binding of somatostatin to putative receptor sites in hypothalamic membranes, while no significant changes were found in striatum. The enhancement of somatostatin binding resulted from a rapid increase in the number of available receptors rather than a change in receptor affinity. This effect appears to be mediated by nicotinic cholinergic receptors, because pretreatment with a centrally active nicotinic receptor antagonist, mecamylamine (5.0 mg/Kg i.v.), prevented the nicotine-induced changes in somatostatin content and binding in the hypothalamus. Mecamylamine alone had no observable effect on the hypothalamic somatostatinergic system. These results suggest that the rat hypothalamic somatostatinergic system can be regulated by nicotine-like acetylcholine receptors.