Attention Allocation to Financial Information: The Role of Color and Impulsivity Personality Trait.

BACKGROUND: In order to raise the level of investor's protection, the European Commission has recently introduced the key investor information document (KIID), a standard, plainly worded, and consumer-friendly document which should provide individuals with essential information for their investment decisions. KIID layout has been delineated relying on results from focus groups, surveys and telephone interviews, ignoring the reliable, and unbiased insights offered by neuroscientific approaches. AIM: The current study aims to elucidate the patterns of eye movements in the early phases of information acquisition during the reading of financial disclosure documents, disentangling the independent role of color and impulsivity at modulating attention distribution toward the different sources of financial information. MATERIALS AND METHODS: Oculomotor behavior was monitored in eighty-one healthy adults through the eye tracking technology (SMI REDn Scientific 60 Hz). An ecological protocol exploiting KIIDs was developed to control for several individual variables, through delivering standard visual stimuli based on official financial documents. Participants performed a passive exploration task (with the only specific instruction of visually exploring the document), followed by an active task where they were asked to rate the financial attractiveness of the products, as low, medium or high. The Barratt impulsiveness scale (BIS-11) was administered to each participant, to score such personality trait. RESULTS: Attention distribution over the different information sources, included in the KIIDs, has been quantified and found to be independently modulated by both color and impulsivity, with a greater role of the former over the latter. The addition of either red or blue information to some KIID's sections increases attention allocation toward the whole document, compared to the usual black and white version. BIS-11 total scores were inversely related to the first and average fixation duration in the neutral, though not in the colored condition. DISCUSSION: Bottom-up, stimulus-related mechanisms of attention allocation influence information acquisition during the reading of financial prospectuses to the point that the increased attention induced by color compensates for individual impulsivity. Such evidence should be considered by regulators when devising the disclosure documents in order to increase investors' protection.

Improvement of cardiac performance and cardiovascular risk factors in children with GH deficiency after two years of GH replacement therapy: an observational, open, prospective, case-control study.

CONTEXT: GH deficiency (GHD) in adults is associated with a cluster of cardiovascular risk factors that may contribute to an increased mortality for cardiovascular disease. OBJECTIVE: The aim of this study was to evaluate the effect of GHD and GH replacement therapy on cardiac performance, lipid profile, and insulin resistance in children. DESIGN: This was a 2-yr case-control prospective study. PATIENTS: Thirty children with GHD aged 9.3 +/- 0.5 yr and 30 healthy matched controls were studied. INTERVENTION: Children were studied before and after 1 and 2 yr of GH replacement (GHD children) or no treatment (controls). MAIN OUTCOME MEASURES: Lipid profile, serum insulin levels, homeostasis model of assessment (HOMA) index, and left ventricular (LV) mass and function by echocardiography were the main outcome measures. RESULTS: At study entry, the LV mass index was significantly lower in GHD children (50.2 +/- 1.7) than in controls (60.3 +/- 2.5 g/m(2); P < 0.002), whereas LV systolic and diastolic function, lipid profile, insulin levels, and HOMA index were similar. In GHD children LV mass index significantly increased (66.3 +/- 2.4 g/m(2); P < 0.0001) after 1 yr of GH replacement and remained stable thereafter. LV systolic and diastolic function did not change during treatment. After 2 yr of GH replacement, total cholesterol (P < 0.007) and the atherogenic index (P < 0.0001) significantly decreased, whereas fasting insulin levels (P < 0.001) and HOMA index (P < 0.0001) significantly increased compared with both pretreatment and control values. CONCLUSIONS: GHD in children is associated with a reduced cardiac size but with a normal cardiac function, lipid profile, and insulin sensitivity. Two years of GH replacement normalizes cardiac morphology, improves lipid profile, and slightly impairs insulin sensitivity.

Noninvasive investigation of hepatopulmonary syndrome in children and adolescents with chronic cholestasis.

Early detection of hepatopulmonary syndrome (HPS) may be delayed because of invasiveness of the diagnostic procedures. In this pilot study, we prospectively investigated the usefulness of determining transcutaneous O(2) tension after 100% O(2) (TcPO(2)100) breathing using a transcutaneous hyperoxia test (THT) in 11 children with chronic cholestasis and without primary cardiopulmonary disease. These patients also underwent alveolar-arterial O(2) gradient testing (AaDO(2)) at an inspired oxygen fraction (FiO(2)) of 0.21, lung scintiscan, and contrast transthoracic echocardiography (TTE). Three of them had a liver transplantation because of the downhill course of their liver disease and respiratory status. THT transcutaneous O(2) tension at 21% FiO(2) (TcPO(2)21) was 75 +/- 13 mm Hg, and increased to 488 +/- 106 mmHg after 100% O(2) breathing (TcPO(2)100). Both mean values were not significantly different from those found in 8 age-matched controls (P = 0.9 and P = 0.5, respectively). However, one patient, in spite of her stable liver function, showed an abnormal TcPO(2)21 and TcPO(2)100 (45 mmHg and 210 mmHg, respectively). This same subject was also the only patient with abnormalities of AaDO(2) (54.2 mm Hg; normal value, < 20 mm Hg), lung scintiscan (brain/lung ratio of technetium-99 fixation (B/L SI) = 9, normal value < 1), and TTE, suggesting intrapulmonary vasodilatations and shunts. Given the clinical development of cyanosis and platypnea, all criteria for HPS were fulfilled, and timing of her liver transplantation was therefore accelerated. This resulted in HPS regression. In children with chronic cholestasis, repeated transcutaneous bedside measurements are a rapid and reliable noninvasive test for characterizing the severity of abnormal oxygenation, and may prove useful also in liver posttransplantation monitoring.

Subtle alterations of cardiac performance in children with growth hormone deficiency: results of a two-year prospective, case-control study.

BACKGROUND: GH-deficient (GHD) children have reduced left ventricular (LV) mass, but impairment of cardiac function has never been documented. AIM: The aim of the study was to evaluate effects of GHD and GH therapy on cardiac function using load-dependent and load-independent indices of myocardial contractility. PATIENTS AND METHODS: Echocardiography was performed in 24 GHD children at baseline and 1 and 2 yr after GH therapy and in 24 controls. RESULTS: Compared with controls, GHD children at baseline had lower LV mass (LV mass/BSA 50.6 +/- 1.8 vs. 60.5 +/- 2.4 g/m(2); P < 0.002, and LV mass/H(2.7) 28.7 +/- 1.2 vs. 33.6 +/- 1.3 g/m(2.7); P < 0.009). Global systolic function was normal, with only a trend toward slight impairment of the fractional shortening (34.9 +/- 1.5 vs. 37.6 +/- 1.1%). However, subtle LV dysfunction was revealed by load-dependent and load-independent indices of myocardial contractility. In fact, GHD patients compared with controls showed lower rate-corrected mean velocity of circumferential fiber shortening (1.0 +/- 0.03 vs. 1.18 +/- 0.03 circ/sec; P = 0.0001) and stress shortening index (0.10 +/- 0.02 vs. 0.18 +/- 0.02; P < 0.007) and higher end-systolic stress (49.2 +/- 1.4 vs. 45.7 +/- 1.0 g/cm(2); P < 0.05). One year of GH treatment was associated with a significant improvement of cardiac size (LV mass/BSA 67.8 +/- 2.9 g/m(2); LV mass/H(2.7) 38.2 +/- 2.0 g/m(2.7); P < 0.0001 and P = 0.0003, respectively) and myocardial contractility (mean velocity of circumferential fiber shortening 1.2 +/- 0.04 circ/sec; P < 0.0002; stress shortening index 0.19 +/- 0.02; P < 0.003) and reduced afterload (end-systolic stress 43.9 +/- 1.4 g/cm(2); P < 0.03). CONCLUSIONS: Our data indicate that GH deficiency is associated with abnormalities in morphology and function in not only adults but also children and further supports the beneficial effect of GH on the heart.

Left ventricular mass and function in children with GH deficiency before and during 12 months GH replacement therapy.

OBJECTIVE: This open, prospective study was designed to evaluate the effect of GH deficiency (GHD) on left ventricular (LV) mass (LVM) and performance, by echocardiography, and on lipid profile during childhood. SUBJECTS: Twelve prepubertal children with GHD (eight boys and four girls) aged 8.1 +/- 1.7 years were studied before and after 6 and 12 months of GH replacement therapy at a dose of GH of 30 micro g/kg/day. Twelve healthy children sex-, height-, weight- and body surface area-matched with the patients, served as controls. METHODS: Echocardiography was performed at study entry and after 12 months both in GHD children and in controls. Only in GHD children, echocardiography was repeated also after 6 months of GH replacement. In all subjects, we measured LV posterior wall thickness (LVPWT), LV end-diastolic diameter (LVEDD), LVM index (LVMi), LV systolic and diastolic function. RESULTS: At study entry, LVPWT (5.3 +/- 0.8 vs. 6.2 +/- 1.1 mm, P < 0.05), LVEDD (34.0 +/- 2.4 vs. 36.7 +/- 2.1 mm, P < 0.007) and LVMi (47.0 +/- 6.9 vs. 59.6 +/- 9.5 g/m2, P < 0.005) were significantly lower in GHD children than in controls. Lipid profile, heart rate, blood pressure, LV systolic function and indices of ventricular filling were similar in patients and controls. After 12 months of GH replacement therapy, LVPWT (6.1 +/- 0.7 mm, P < 0.0005), LVEDD (38.8 +/- 4.3 mm, P < 0.002) and LVMi (71.5 +/- 12.7 g/m2, P < 0.0005) significantly increased in GHD children compared to pretreatment values. In particular, after 12 months of therapy GHD children achieved a normal LVMi when compared to controls (60.7 +/- 8.6, P = ns). LVMi increase was significantly correlated with the increase in IGF-I level (r = 0.49; P < 0.004). LV systolic performance, diastolic filling and blood pressure did not change significantly during GH therapy. After 12 months of treatment, the atherogenic index, measured as total/high-density lipoprotein-cholesterol ratio (2.7 +/- 0.8) was significantly lower than both pretreatment (3.4 +/- 0.3, P < 0.03) and control values (3.8 +/- 1.1, P < 0.04). CONCLUSIONS: GH deficiency in children affects heart morphology, by inducing a significant decrease in cardiac size, but does not modify cardiac function and lipid profile. Twelve months of GH replacement treatment normalizes cardiac mass, and reduces the atherogenic index.