Examination of the dielectrophoretic spectra of MCF7 breast cancer cells and leukocytes

The detection of circulating tumor cells (CTCs) in blood is crucial to assess metastatic progression and to guide therapy. Dielectrophoresis (DEP) is a powerful cell surface marker-free method that allows intrinsic dielectric properties of suspended cells to be exploited for CTC enrichment/isolation from blood. Design of a successful DEP-based CTC enrichment/isolation system requires that the DEP response of the targeted particles should accurately be known. This paper presents a DEP spectrum method to investigate the DEP spectra of cells without directly analyzing their membrane and cytoplasmic properties in contrast to the methods in literature, which employ theoretical assumptions and complex modeling. Integrating electric field simulations based on DEP theory with the experimental data enables determination of the DEP spectra of leukocyte subpopulations, polymorphonuclear and mononuclear leukocytes, and MCF7 breast cancer cells as a model of CTC due to their metastatic origin over the frequency range 100 kHz-50 MHz at 10 V-pp. In agreement with earlier findings, differential DEP responses were detected for mononuclear and polymorphonuclear leukocytes due to the richness of the cell surface features and morphologies of the different leukocyte types. The data reveal that the strength of the DEP force exerted on MCF7 cells was particularly high between 850 kHz and 20 MHz. These results illustrate that the proposed technique has the potential to provide a generic platform to identify DEP responses of different biological particles

Post-Burn Skin Deformities of the Face and Neck Region in Pediatric Patients: Single-Stage Treatment Using Collagen Elastin Matrix

Objective: Treating severe post-burn deformities of the face and neck region in pediatric populations is challenging because of technical difficulties (e.g., limited full thickness skin graft donor site, limited flap options, unavailability for expander placement) and increased donor site morbidity (e.g., related to flap and graft donor sites). In this study, we present the single-stage treatment of severe post-burn skin deformities of the face and neck region in pediatric patients using collagen-elastin matrix (Matriderm®) combined with partial thickness skin grafts. Material and Methods: The total number of cases was eight (four females, four males), and the ages were between two and 11 years. All cases were operated on for only one region. Following the release of contractures and/or excision of wide excessive/ unfavorable dermal scars, defects were reconstructed using collagen- elastin matrix (Matriderm®) combined with partial-thickness skin grafts. The final functional and aesthetic results were evaluated using photography and examination. Results: The deformities were in the form of contractures and/ or excessive dermal scarring. The involved regions were the face (n=3) and neck (n=5). The grafts yielded favorable plication and texture, and no recurrence of excessive dermal scarring was observed. All contractures healed unproblematically. Two patients were re-operated on for regrafting caused by minor graft loss (5% and 12% of the total area, respectively). Conclusion: In this study, we observed that collagen elastin matrix combined with partial-thickness skin grafts provides a favorable option for the treatment of pediatric late post-burn complications in the face and neck region with limited surgical options

Phosphodiesterase 10A deactivation induces long-term neurological recovery, peri-infarct remodeling and pyramidal tract plasticity after transient focal cerebral ischemia in mice

The phosphodiesterase (PDE) superfamily comprises enzymes responsible for the cAMP and cGMP degradation to AMP and GMP. PDEs are abundant in the brain, where they are involved in several neuronal functions. High PDE10A abundance was previously observed in the striatum; however its consequences for stroke recovery were unknown. Herein, we evaluated the effects of PDE10A deactivation by TAK-063 (0.3 or 3 mg/kg, initiated 72 h post-stroke) in mice exposed to intraluminal middle cerebral artery occlusion. We found that PDE10A deactivation over up to eight weeks dose-dependently increased long-term neuronal survival, angiogenesis, and neurogenesis in the peri-infarct striatum, which represents the core of the middle cerebral artery territory, and reduced astroglial scar formation, whole brain atrophy and, more specifically, striatal atrophy. Functional motor-coordination recovery and the long-distance plasticity of pyramidal tract axons, which originate from the contralesional motor cortex and descend through the contralesional striatum to innervate the ipsilesional facial nucleus, were enhanced by PDE10A deactivation. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) revealed a set of dopamine receptor-related and neuronal plasticity-related PDE10A targets, which were elevated (e.g., protein phosphatase-1 regulatory subunit 1B) or reduced (e.g., serine/threonine protein phosphatase 1α, β-synuclein, proteasome subunit α2) by PDE10A deactivation. Our results identify PDE10A as a therapeutic target that critically controls post-ischemic brain tissue remodeling and plasticity