Effect of root perforation repair with mineral aggregate-based cements on the retention of customized fiberglass posts

Odontology - The purpose of this study was to investigate whether the root perforation repair with mineral aggregate-based cements affects the retention of customized fiberglass posts to bovine...     

Insights into the pathogenesis of ATP1A1‐related CMT disease using patient‐specific iPSCs

The development of patient‐specific induced pluripotent stem cells (iPSCs) offered interesting insights in modeling the pathogenesis of Charcot‐Marie‐Tooth (CMT) disease and thus we decided to explore the phenotypes of iPSCs derived from a single CMT patient carrying a mutant ATP1A1 allele (p.Pro600Ala). iPSCs clones generated from CMT and control fibroblasts, were induced to differentiate into neural precursors and then into post‐mitotic neurons. Control iPSCs differentiated into neuronal precursors and then into post‐mitotic neurons within 6‐8 days. On the contrary, the differentiation of CMT iPSCs was clearly defective. Electrophysiological properties confirmed that post‐mitotic neurons were less mature compared to the normal counterpart. The impairment of in vitro differentiation of CMT iPSCs only concerned with the neuronal pathway, because they were able to differentiate into mesendodermal cells and other ectodermal derivatives. ATP1A1 was undetectable in the few neuronal cells derived from CMT iPSCs. ATP1A1 gene mutation (p.Pro600Ala), responsible for a form of axonal CMT disease, is associated in vitro with a dramatic alteration of the differentiation of patient‐derived iPSCs into post‐mitotic neurons. Thus, the defect in neuronal cell development might lead in vivo to a decreased number of mature neurons in ATP1A1‐CMT disease.     

Perioperative Bevacizumab-based Triplet Chemotherapy in Patients With Potentially Resectable Colorectal Cancer Liver Metastases

Background

In colorectal cancer liver metastases (CRCLM), bevacizumab-based neoadjuvant strategies provide increased pathologic response. We aimed at assessing the activity of perioperative capecitabine, oxaliplatin, irinotecan, and bevacizumab (COI-B regimen) in patients with potentially resectable CRCLM, and investigating biomarkers for early prediction of pathologic response.

Nutritional Surveillance for the Best Start in Life,Promoting Health for Neonates,Infants and Children

This Special Issue aims to examine the crucial role of nutritional status starting from pregnancy in modulating fetal, neonatal and infant growth and metabolic pathways, with potential long-term impacts on adult health. Poor maternal nutritional conditions in the earliest stages of life during fetal development and early life may induce both short-term and longer lasting effects; in particular, an increased risk of noncommunicable diseases (NCDs) and other chronic diseases such as obesity, which itself is a major risk factor for NCDs, is observed over the lifespan. Poor maternal nutrition affects the fetal developmental schedule, leading to irreversible changes and slowdown in growth. The fetus limits its size to conserve the little energy available for cardiac functions and neuronal development. The organism will retain memory of the early insult, and the adaptive response will result in pathology later on. Epigenetics may contribute to disease manifestation affecting developmental programming. After birth, even though there is a limited evidence base suggesting a relationship between breastfeeding, timing and type of foods used in weaning with disease later in life, nutritional surveillance is also mandatory in infants in the first year of life. We will explore the latest findings on nutrition in early life and term and preterm babies, as well as the role of malnutrition in the short- and long-term impact over the lifespan. Focusing on nutritional interventions represents part of an integrated life-cycle approach to prevent communicable and non-communicable diseases.