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BackgroundMedical simulations have emerged as a valuable tool in anatomical-medical training, allowing healthcare professionals to gain hands-on experience in a controlled and safe environment. One such simulation platform is SimLife®, which uses the Pulse for Practice (P4P) system to enable realistic restoration of airflow (“re-ventilation”) and blood flow (“revascularization”) in bodies donated to science.ObjectiveThis study aimed to evaluate the feasibility of introducing SimLife® technology in Italy. Additionally, it assessed the impact of this technology across various medical specialties, utilizing a minimal number of donated bodies.MethodsThe study utilized the existing body donation program and dissection rooms at the Anatomy Center of the University of Bologna. 62 participants from 13 medical specialties performed simulations using the SimLife® P4P platform. Post-simulation, structured interviews were used to collect data on the interventions performed, participant perceptions of the technology’s usefulness, enjoyment, and willingness to repeat the experience, as well as critical issues encountered.ResultsKey findings include that 86% of participants rated SimLife® technology as extremely useful for post-lauream training, while 84% found it highly beneficial for team-building activities. A total of 31 interventions were successfully performed across various anatomical regions, with participants reporting high satisfaction and a strong willingness to repeat the simulation experience.ConclusionThe findings support the effectiveness of SimLife® technology for body donor re-ventilation and revascularization, reinforcing its value for medical training across various specialties.

Lamin B1 is an essential protein of the nuclear lamina that plays a crucial role in nuclear function and organization. It has been demonstrated that lamin B1 is essential for organogenesis and particularly brain development. The important role of lamin B1 in physiological brain development and aging has only recently been at the epicenter of attention and is yet to be fully elucidated. Regarding the development of brain, glial cells that have long been considered as supporting cells to neurons have overturned this representation and current findings have displayed their active roles in neurogenesis and cerebral development. Although lamin B1 has increased levels during the differentiation of the brain cells, during aging these levels drop leading to senescent phenotypes and inciting neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease. On the other hand, overexpression of lamin B1 leads to the adult-onset neurodegenerative disease known as Autosomal Dominant Leukodystrophy. This review aims at highlighting the importance of balancing lamin B1 levels in glial cells and neurons from brain development to aging.

Polyphosphoinositides (PPIns) and their modulating enzymes are involved in regulating many important cellular functions including proliferation, differentiation or gene expression, and their deregulation is involved in human diseases such as metabolic syndromes, neurodegenerative disorders and cancer, including Acute Myeloid Leukemia (AML). Given that PPIns regulating enzymes are highly druggable targets, several studies have recently highlighted the potential of targeting them in AML. For instance many inhibitors targeting the PI3K pathway are in various stages of clinical development and more recently other novel enzymes such as PIP4K2A have been implicated as AML targets. PPIns have distinct subcellular organelle profiles, in part driven by the specific localisation of enzymes that metabolise them. In particular, in the nucleus, PPIns are regulated in response to various extracellular and intracellular pathways and interact with specific nuclear proteins to control epigenetic cell state. While AML does not normally manifest with as many mutations as other cancers, it does appear in large part to be a disease of dysregulation of epigenetic signalling and many novel therapeutics are aimed at reprogramming AML cells toward a differentiated cell state or to one that is responsive to alternative successful but limited AML therapies such as ATRA. Here, we propose that by combining bioinformatic analysis with inhibition of PPIns pathways, especially within the nucleus, we might discover new combination therapies aimed at reprogramming transcriptional output to attenuate uncontrolled AML cell growth. Furthermore, we outline how different part of a PPIns signalling unit might be targeted to control selective outputs that might engender more specific and therefore less toxic inhibitory outcomes.