Differential proteomics profile of microcapillary networks in response to sound pattern-driven local cell density enhancement.

Spatial cell organization and biofabrication of microcapillary networks in vitro has a great potential in tissue engineering and regenerative medicine. This study explores the impact of local cell density enhancement achieved through an innovative sound-based patterning on microcapillary networks formation and their proteomic profile. Human umbilical vein endothelial cells (HUVEC) and human pericytes from placenta (hPC-PL) were mixed in a fibrin suspension. The mild effect of sound-induced hydrodynamic forces condensed cells into architected geometries showing good fidelity to the numerical simulation of the physical process. Local cell density increased significantly within the patterned areas and the capillary-like structures formed following the cell density gradient. Over five days, these patterns were well-maintained, resulting in concentric circles and honeycomb-like structures. Proteomic analysis of the pre-condensed cells cultured for 5 days, revealed over 900 differentially expressed proteins when cells were preassembled through mild-hydrodynamic forces. Gene ontology (GO) enrichment analysis identified cellular components, molecular functions, and biological processes that were up- and down-regulated, providing insights regarding molecular processes influenced by the local density enhancement. Furthermore, we employed Ingenuity Pathway Analysis (IPA) to identify altered pathways and predict upstream regulators. Notably, VEGF-A emerged as one of the most prominent upstream regulators. Accordingly, this study initiates the unraveling of the changes in microcapillary networks at both molecular and proteins level induced by cell condensation obtained through sound patterning. The findings provide valuable insights for further investigation into sound patterning as a biofabrication technique for creating more complex microcapillary networks and advancing in vitro models.

Arterial spin labelling qualitative assessment in paediatric patients with MRI-negative epilepsy.

AIM: To evaluate the usefulness of arterial spin labelling (ASL) qualitative analysis for the localisation of seizure-related perfusion abnormalities in paediatric patients with negative brain magnetic resonance imaging (MRI) epilepsy. MATERIALS AND METHODS: Forty-two patients with a diagnosis of MRI-negative focal or generalised epilepsy, who underwent electroencephalogram (EEG) and MRI with ASL in the interictal phase were included. Perfusion abnormalities were evaluated through a qualitative assessment and then compared to EEG seizure focus. RESULTS: Among the 42 patients, 26 had focal epilepsy and 16 had generalised epilepsy. Thirty-three patients (79%) showed a perfusion abnormality, mainly hypoperfusion (74.5% of all ASL alterations), whereas hyperperfused alterations were more represented in patients who experienced the last seizure either less than 48 hours prior to ASL acquisition or in the time interval from 1 week to 1 month prior to ASL acquisition (p=0.034). Concordance of ASL abnormality and EEG focus was found in 33 patients (78.5%), as complete in 17 (40.5%) and as partial in 16 (38%). A trend of higher concordance was found in focal epilepsies compared to generalised epilepsies (p=0.059). The concordance between ASL and EEG major alterations was higher for hyperperfused anomalies than for hypoperfused ones (p=0.009). Variables such as age, sedation, and time from last seizure were not significant contributors for concordance. CONCLUSIONS: The combined use of qualitative ASL and brain MRI and scalp EEG could be a potential tool in daily clinical practice.

A case of work-related donkey milk allergy

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Atypical Manifestations in Glut1 Deficiency Syndrome.

Glucose transporter type 1 deficiency syndrome is a genetically determined, treatable, neurologic disorder that is caused by an insufficient transport of glucose into the brain. It is caused by a mutation in the SCL2A1 gene, which is so far the only known to be associated with this condition. Glucose transporter type 1 deficiency syndrome consists of a wide clinical spectrum that usually presents with cognitive impairment, epilepsy, paroxysmal exercise-induced dyskinesia, acquired microcephaly, hemolytic anemia, gait disturbance, and dyspraxia in different combinations. However, there are other clinical manifestations that we consider equally peculiar but that have so far been poorly described in literature. In this review, supported by a video contribution, we will accurately describe this type of clinical manifestation such as oculogyric crises, weakness, paroxysmal kinesigenic and nonkinesigenic dyskinesia in order to provide an additional instrument for a correct, rapid diagnosis.