Background: The incidence and mortality of hepatocellular cancer (HCC) complicating alcoholic and non-alcoholic fatty liver diseases (ALD and NAFLD) is rising in western societies. Despite knowing the at risk populations for HCC development, the lack of sensitive and specific means of surveillance hampers disease detection at curable stages. The most widely used serum HCC marker is alpha-fetoprotein (AFP), while PIVKA-II, glypican-3 (GP3) and Squamous Cell Carcinoma Antigen -1 (SCCA-1) have been proposed as new biomarkers. Assessment of these HCC biomarkers has largely been performed in patients with viral hepatitis. We conducted a cross sectional study assessing the value of these serum proteins, as well a novel candidate biomarker -follistatin – in patients with HCC arising on a background of ALD or NAFLD. Methods: Pre-treatment serum samples from 50 patients with HCC arising on a background of ALD (n = 31) or NAFLD (n = 19) were assessed by specific ELISA assay for PIVKAII, Glypican-3, SCCA-1 and Follistatin. Results were compared and contrasted with a control patient group with biopsy proven steatohepatitis-related cirrhosis (n = 41). The diagnostic accuracy of each of the candidate biomarkers was evaluated using receiver operating characteristic (ROC) curve analysis, reporting the area under the curve (AUC) and its 95% confidence interval (CI). Performance was compared to that of the established biomarker, AFP. Results: Serum levels of all proteins were assessed by specific ELISA assays. GP3, SCCA-1 and follistatin had no HCC surveillance benefit in these patients. AFP and PIVKAII were superior to the other markers, particularly in combination. Conclusion: We conclude that while novel means of surveillance are urgently required, the combination of AFP and PIVKAII for HCC is an improvement on AFP alone in ALD/NAFLD patients. Furthermore, our data in this homogenous subset of patients- particularly that confirming no role for SCCA-1 – suggests that the choice of optimal biomarkers for HCC surveillance may be determined by the aetiology of underlying chronic liver disease.

Rationale: The open lung strategy aims at reopening (recruitment) of nonaerated lung areas in patients with acute respiratory distress syndrome, avoiding tidal alveolar hyperinflation in the limited area of normally aerated tissue (baby lung). Objectives: We tested the hypothesis that recruited lung areas do not resume elastic properties of adjacent baby lung. Methods: Twenty-five anesthetized, mechanically ventilated pigs were studied. Four lung-healthy pigs served as controls and the remaining 21 were divided into three groups (n = 7 each) in which lung injury was produced by surfactant lavage, lipopolysaccharide infusion, or hydrochloride inhalation. Computed tomography scans, respiratory mechanics, and gas exchange parameters were recorded under three conditions: at baseline, during lung recruitment maneuver, and at end-expiration and end-inspiration when ventilating after an open lung protocol. Measurements and Main Results: During recruitment maneuver and open lung protocol, the gas volume entering the insufficiently aerated compartment was 96% (75–117%) and 48% (41–63%) (median [interquartile range]) of the functional residual capacity measured before and at zero end-expiratory pressure, respectively. Nonetheless, the volume of hyperinflated lung increased during both recruitment maneuver (by 1–28% of total lung volume; P < 0.01) and open lung protocol ventilation at end-inspiration (by 1–15% of total lung volume; P < 0.01). Regional elastance of recruited lung tissue was consistently higher than that of the baby lung regardless of the ARDS model (P < 0.01). Conclusions: Alveolar recruitment is not protective against hyperinflation of the baby lung because lung parenchyma is inhomogeneous during ventilation with the open lung strategy.

Since Hans Asperger’s first description (Arch Psych Nervenkrankh 117:76–136, 1944), through Lorna Wing’s translation and definition (Psychol Med 11:115–129, 1981), to its introduction in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM, 1994), Asperger Syndrome has always aroused huge interest and debate, until vanishing in the DSM fifth edition (2013). The debate regarded its diagnostic validity and its differentiation from high functioning autism (HFA). The present study aimed to examine whether AS differed from HFA in clinical profiles and to analyze the impact of DSM-5’s innovation. Differences in cognitive, language, school functioning and comorbidities, were revealed when 80 AS and 70 HFA patients (3–18 years) were compared. Results suggested that an AS empirical distinction within autism spectrum disorder should be clinically useful.

Fenoldopam mesylate is a selective dopamine-1 agonist, with no effect on dopamine-2 and alpha1 receptors, producing a selective renal vasodilation. This may favor the kidney oxygen supply/demand ratio and prevent acute renal failure. The aim of the study was to investigate if fenoldopam can provide greater benefit than low-dose dopamine in early renal dysfunction of critically ill patients. Prospective, multiple-center, randomized, controlled trial. University and city hospital intensive care units. One hundred adult critically ill patients with early renal dysfunction (intensive care unit stayor=1.5 mg/dL and10% of the baseline value at the end of infusion, compared with only 46% in dopamine group (chi-square=4.06, p=.04). Total urinary output during drug infusion was not significantly different between groups. After 1 day, urinary output was lower in group F compared with group D (p<.05). In critically ill patients, a continuous infusion of fenoldopam at 0.1 microg/kg/min does not cause any clinically significant hemodynamic impairment and improves renal function compared with renal dose dopamine. In the setting of acute early renal dysfunction, before severe renal failure has occurred, the attempt to reverse renal hypoperfusion with fenoldopam is more effective than with low-dose dopamine.