Two-stage orchiopexy for intra-abdominal testis with short spermatic vessels wrapped in anti-adhesion conduit. 25 years of experience.

Background: Treatment of high cryptorchidism can be challenging, often with frustrating results. We report 25 years of experience in the treatment of the cryptorchidism with very short spermatic vessels using an original two-stage orchiopexy that preserves the spermatic vessels.

Methods: We reviewed the clinical charts of children affected by cryptorchidism with very short spermatic vessels treated through our original surgical approach in tree Institutes of Pediatric Surgery.

Unveiling the signaling network of FLT3-ITD AML improves drug sensitivity prediction.

Currently, the identification of patient-specific therapies in cancer is mainly informed by personalized genomic analysis. In the setting of acute myeloid leukemia (AML), patient-drug treatment matching fails in a subset of patients harboring atypical internal tandem duplications (ITDs) in the tyrosine kinase domain of the FLT3 gene. To address this unmet medical need, here we develop a systems-based strategy that integrates multiparametric analysis of crucial signaling pathways, and patient-specific genomic and transcriptomic data with a prior knowledge signaling network using a Boolean-based formalism.

Curation of causal interactions mediated by genes associated with autism accelerates the understanding of gene-phenotype relationships underlying neurodevelopmental disorders.

Autism spectrum disorder (ASD) comprises a large group of neurodevelopmental conditions featuring, over a wide range of severity and combinations, a core set of manifestations (restricted sociality, stereotyped behavior and language impairment) alongside various comorbidities. Common and rare variants in several hundreds of genes and regulatory regions have been implicated in the molecular pathogenesis of ASD along a range of causation evidence strength. Despite significant progress in elucidating the impact of few paradigmatic individual loci, such sheer complexity in the genetic architecture underlying ASD as a whole has hampered the identification of convergent actionable hubs hypothesized to relay between the vastness of risk alleles and the core phenotypes.

SIGNOR 3.0, the SIGnaling network open resource 3.0: 2022 update.

The SIGnaling Network Open Resource (SIGNOR 3.0, https://signor.uniroma2.