Specific Learning Disorders and Eating Disorders: an Italian retrospective study.

BACKGROUND: Although Anorexia Nervosa (AN) patients show dysfunctional behaviour in information processing, visual and verbal memory performance, and different cognitive fields, regardless of their BMI, the literature on the correlations between Eating Disorders (ED) and Neurodevelopmental Disorders (NDD) does not provide conclusive data. Rather than a consequence of the mental disorder, cognitive dysfunctions may be a risk factor for AN. METHODS: Our retrospective study investigates the prevalence of Specific Learning Disorder (SLD) among patients with ED. We considered 262 patients being treated at the Emilia Romagna Feeding and Eating Disorders Outpatient Service in Bologna, Italy. We compared the results with the Italian reference values, according to the most recent data provided by the Italian Ministry of Education. RESULTS: We found that 25 patients out of 262 (9.54%) presented a comorbid diagnosis of SLD. This SLD prevalence is higher than the Italian reference values (4.9% in the school year 2018/19, p < 0.001). Comorbidity with SLD was significantly more frequent in males. A diagnosis of SLD was not associated with a higher frequency of any specific ED diagnosis or with psychiatric comorbidity in general. Positive family history for SLD was not significantly associated with either a positive family history for ED or a diagnosis of SLD. CONCLUSIONS: This is the first Italian study to investigate the prevalence of SLD in ED patients during childhood and adolescence. Our data support previous research documenting that neuropsychological deficit could lead to the development of ED.

Multi-stage bioengineering of a layered oesophagus with in vitro expanded muscle and epithelial adult progenitors.

A tissue engineered oesophagus could overcome limitations associated with oesophageal substitution. Combining decellularized scaffolds with patient-derived cells shows promise for regeneration of tissue defects. In this proof-of-principle study, a two-stage approach for generation of a bio-artificial oesophageal graft addresses some major challenges in organ engineering, namely: (i) development of multi-strata tubular structures, (ii) appropriate re-population/maturation of constructs before transplantation, (iii) cryopreservation of bio-engineered organs and (iv) in vivo pre-vascularization. The graft comprises decellularized rat oesophagus homogeneously re-populated with mesoangioblasts and fibroblasts for the muscle layer. The oesophageal muscle reaches organised maturation after dynamic culture in a bioreactor and functional integration with neural crest stem cells. Grafts are pre-vascularised in vivo in the omentum prior to mucosa reconstitution with expanded epithelial progenitors. Overall, our optimised two-stage approach produces a fully re-populated, structurally organized and pre-vascularized oesophageal substitute, which could become an alternative to current oesophageal substitutes.

[From bench to bedside: new insights into the treatment of heart failure]. / Dalla ricerca di base alla pratica clinica: nuove prospettive terapeutiche nello scompenso cardiaco.

Despite significant advances in pharmacological and clinical treatment, heart failure remains a leading cause of morbidity and mortality worldwide. G-protein coupled receptors are a wide superfamily of plasma membrane receptors which represent an important target of heart failure drug therapy. Since heart failure is characterized by the overactivity of different neurohormones, such as catecholamines and angiotensin II, responsible for several detrimental effects on the cardiovascular system, over the last decade therapeutic strategies targeting beta-adrenergic and angiotensin receptors have been developed. Despite the introduction of successful drug classes, such as beta-adrenergic receptor blockers, angiotensin-converting enzyme inhibitors and sartans, heart failure still poses an enormous challenge, thus indicating the urgent need to develop innovative treatments that might counteract mechanisms involved in heart failure onset and progression. It is now established that a single receptor, activated by the same agonist, can elicit several different signaling pathways often resulting in opposite cellular responses, some beneficial and some detrimental. However, drugs currently used in heart failure target receptors on their extracellular domain by competing with the endogenous agonists. Thus, they can inhibit non-specifically all the receptor-related signaling pathways including those with beneficial activity whose blockade would not be desirable in heart failure. These observations stress the need for the generation of new therapeutic molecules able to target specific signaling pathways which might result in innovative therapies for cardiovascular disease.