AimsLung ultrasound (LUS) is a useful tool with which to assess subclinical pulmonary congestion and to stratify the prognosis of patients with heart failure (HF). The aim of this study was to evaluate whether an LUS‐guided follow‐up protocol improves the outcomes of patients with HF.Methods and resultsIn this single‐blind clinical trial, 123 patients admitted for HF were randomized to either a standard follow‐up (n = 62, control group) or a LUS‐guided follow‐up (n = 61, LUS group). The primary endpoint was a composite of urgent visit, hospitalization for worsening HF and death during follow‐up. Visits were scheduled at 14, 30, 90 and 180 days after discharge. Treating physicians were encouraged to modify diuretic therapy in accordance with the number of B‐lines recorded by LUS. The mean ± standard deviation (SD) age of the patients was 69 ± 12 years and 72% were male. The mean ± SD left ventricular ejection fraction was 39 ± 14%. The hazard ratio for the primary outcome in the LUS group was 0.518 [95% confidence interval (CI) 0.268–0.998; P = 0.049], mainly resulting from a decrease in the number of urgent visits for worsening HF. The number of patients needed to treat to avoid an event was 5 (95% CI 3–62). Other secondary endpoints such as N‐terminal pro‐B‐type natriuretic peptide reduction were not achieved. The safety parameters were similar in the two groups. Patients in the LUS group received more loop diuretics [51 (91%) vs. 42 (75%); P = 0.02] and showed an improvement in the distance achieved in the 6‐min walking test [60 m (interquartile range: 29–125 m) vs. 37 m (interquartile range: 5–70 m); P = 0.023].ConclusionsTailored LUS‐guided diuretic treatment of pulmonary congestion in this proof‐of‐concept study reduced the number of decompensations and improved walking capacity in patients with HF. LUS is a non‐invasive, safe and easy‐to‐use technique with potential clinical applicability to guide pulmonary congestion treatment in patients with HF.

Despite the evidence regarding the influence of certain polyphenol food sources on the metabolic profile in feces, the association between the different phenolics provided by the diet and the fecal phenolic profile has not been elucidated. In this study, the composition of phenolic metabolites in fecal solutions was analyzed by UPLC-ESI-MS/MS in 74 volunteers. This fecal phenolic profile showed a high interindividual variation of the different compounds analyzed, phenylacetic and phenylpropionic acids being the major classes of phenolic metabolites excreted in feces. Subjects with higher adherence to a Mediterranean dietary pattern presented greater fecal concentrations of benzoic and 3-hydroxyphenylacetic acids, positively correlated with the intake of the principal classes and subclasses of polyphenols and fibers, and higher levels of Clostridium cluster XVIa and Faecalibacterium prausnitzii. These results provide a link among the Mediterranean dietary pattern, the bioactive compounds of the diet, and the fecal metabolic phenolic profile.

Tumor cell plasticity is a major obstacle for the cure of malignancies as it makes tumor cells highly adaptable to microenvironmental changes, enables their phenotype switching among different forms, and favors the generation of prometastatic tumor cell subsets. Phenotype switching toward more aggressive forms involves different functional, phenotypic, and morphologic changes, which are often related to the process known as epithelial-mesenchymal transition (EMT). In this study, we report natural killer (NK) cells may increase the malignancy of melanoma cells by inducing changes relevant to EMT and, more broadly, to phenotype switching from proliferative to invasive forms. In coculture, NK cells induced effects on tumor cells similar to those induced by EMT-promoting cytokines, including upregulation of stemness and EMT markers, morphologic transition, inhibition of proliferation, and increased capacity for Matrigel invasion. Most changes were dependent on the engagement of NKp30 or NKG2D and the release of cytokines including IFNγ and TNFα. Moreover, EMT induction also favored escape from NK-cell attack. Melanoma cells undergoing EMT either increased NK-protective HLA-I expression on their surface or downregulated several tumor-recognizing activating receptors on NK cells. Mass spectrometry-based proteomic analysis revealed in two different melanoma cell lines a partial overlap between proteomic profiles induced by NK cells or by EMT cytokines, indicating that various processes or pathways related to tumor progression are induced by exposure to NK cells. NK cells can induce prometastatic properties on melanoma cells that escape from killing, providing important clues to improve the efficacy of NK cells in innovative antitumor therapies. .