Background Lung ultrasound (LU) has been widely used to diagnose and monitor acute lung diseases in neonates, but its role in chronic diseases has not been elucidated. Objective We aim to describe the evolution of a lung ultrasound score (LU score) in very low birth weight infants (VLBWI) with and without bronchopulmonary dysplasia (BPD). Methods We prospectively included 59 VLBWI and performed LU in the first 24 and 72 hours of life, and then weekly until 36 weeks´ postmenstrual age (PMA). We calculated the LU score as a semiquantitative score representing the aeration (0‐3) in three different areas of each lung. Results The non‐BPD group (n = 38) had lower LU score at 1, 2, 3, 4, and 36 weeks' PMA than the BPD group: median score of 1 (0‐4) vs 7 (3‐10), P < .001; 0 (0‐1) vs 7 (4‐9), P < .001; 0 (0‐1) vs 8 (7‐11), P < .001; 0 (0‐2) vs 9 (4‐12), P < .001; 0 (0‐0) vs 3 (0‐6), P < .001. A LU score of 5 or above at 1 week of life predicted BPD with a sensitivity (Se) of 71%, specificity (Sp) 80%, area under the ROC curve (AUC) 0.8, and at 2 weeks of life with Se 74%, Sp 100%, and AUC 0.93. An LU score of 4 or above at 4 weeks predicted moderate‐severe BPD (Se 100%, Sp 80%, and AUC 0.89). Conclusion In VLBWI without BPD, LU score increases during the first week of life and decreases thereafter, whereas among subjects with BPD, the LU score remains high until 36 weeks´ PMA. LU score can predict the diagnosis of BPD at 1 week and 2 weeks of life, and may predict moderate‐severe BPD at 4 weeks of life.

Background: Both Alzheimer's disease (AD) and type 2 diabetes (T2D) share common pathological features including inflammation, insulin signaling alterations, or vascular damage. AD has no successful treatment, and the close relationship between both diseases supports the study of antidiabetic drugs to limit or slow down brain pathology in AD. Empagliflozin (EMP) is a sodium-glucose co-transporter 2 inhibitor, the newest class of antidiabetic agents. EMP controls hyperglycemia and reduces cardiovascular comorbidities and deaths associated to T2D. Therefore, we have analyzed the role of EMP at the central level in a complex mouse model of AD-T2D. Methods: We have treated AD-T2D mice (APP/PS1xdb/db mice) with EMP 10 mg/kg for 22 weeks. Glucose, insulin, and body weight were monthly assessed. We analyzed learning and memory in the Morris water maze and the new object discrimination test. Postmortem brain assessment was conducted to measure brain atrophy, senile plaques, and amyloid-β levels. Tau phosphorylation, hemorrhage burden, and microglia were also measured in the brain after EMP treatment. Results: EMP treatment helped to maintain insulin levels in diabetic mice. At the central level, EMP limited cortical thinning and reduced neuronal loss in treated mice. Hemorrhage and microglia burdens were also reduced in EMPtreated mice. Senile plaque burden was lower, and these effects were accompanied by an amelioration of cognitive deficits in APP/PS1xdb/db mice. Conclusions: Altogether, our data support a feasible role for EMP to reduce brain complications associated to AD and T2D, including classical pathological features and vascular disease, and supporting further assessment of EMP at the central level.