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Conducting detailed cellular analysis of complex biological samples poses challenges in cell sorting and recovery for downstream analysis. Label-free microfluidics provide a promising solution for these complex applications. In this work, we investigate particle manipulation on two label-free microdevice designs using cDEP to enrich E. coli from whole human blood to mimic infection workflows. E. coli is still a growing source of bacteremia, sepsis, and other infections in modern countries, affecting millions of patients globally. The two microfluidic designs were evaluated for throughput, scaling, precision targeting, and high-viability recovery. While CytoChip D had the potential for higher throughput, given its continuous method of DEP-based sorting to accommodate larger clinical samples like a 10 mL blood draw, it could not effectively recover the bacteria. CytoChip B achieved a high-purity recovery of over 98% of bacteria from whole human blood, even in concentrations on the order of <100 CFU/mL, demonstrating the feasibility of processing and recovering ultra-low concentrations of bacteria for downstream analysis, culture, and drug testing. Future work will aim to scale CytoChip B for larger volume throughput while still achieving high bacteria recovery. 

Undifferentiated neural stem and progenitor cells (NSPCs) encounter extracellular signals that bind plasma membrane proteins and influence differentiation. Membrane proteins are regulated by N-linked glycosylation, making it possible that glycosylation plays a critical role in cell differentiation. We assessed enzymes that control N-glycosylation in NSPCs and found that loss of the enzyme responsible for generating β1,6-branched N-glycans, N-acetylglucosaminyltransferase V (MGAT5), led to specific changes in NSPC differentiation in vitro and in vivo. Mgat5 homozygous null NSPCs in culture formed more neurons and fewer astrocytes compared with wild-type controls. In the brain cerebral cortex, loss of MGAT5 caused accelerated neuronal differentiation. Rapid neuronal differentiation led to depletion of cells in the NSPC niche, resulting in a shift in cortical neuron layers in Mgat5 null mice. Glycosylation enzyme MGAT5 plays a critical and previously unrecognized role in cell differentiation and early brain development.