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      Multiphysics microfluidics for cell manipulation and separation: a review

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          Abstract

          We reviewed the state-of-the-art field of multiphysics microfluidics, in which multiple functional physical processes are combined in a microfluidic platform, examining the different formats of cascaded connections and physical coupling.

          Abstract

          Multiphysics microfluidics, which combines multiple functional physical processes in a microfluidics platform, is an emerging research area that has attracted increasing interest for diverse biomedical applications. Multiphysics microfluidics is expected to overcome the limitations of individual physical phenomena through combining their advantages. Furthermore, multiphysics microfluidics is superior for cell manipulation due to its high precision, better sensitivity, real-time tunability, and multi-target sorting capabilities. These exciting features motivate us to review this state-of-the-art field and reassess the feasibility of coupling multiple physical processes. To confine the scope of this paper, we mainly focus on five common forces in microfluidics: inertial lift, elastic, dielectrophoresis (DEP), magnetophoresis (MP), and acoustic forces. This review first explains the working mechanisms of single physical phenomena. Next, we classify multiphysics techniques in terms of cascaded connections and physical coupling, and we elaborate on combinations of designs and working mechanisms in systems reported in the literature to date. Finally, we discuss the possibility of combining multiple physical processes and associated design schemes and propose several promising future directions.

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          Ror2 signaling regulates Golgi structure and transport through IFT20 for tumor invasiveness

          Signaling through the Ror2 receptor tyrosine kinase promotes invadopodia formation for tumor invasion. Here, we identify intraflagellar transport 20 (IFT20) as a new target of this signaling in tumors that lack primary cilia, and find that IFT20 mediates the ability of Ror2 signaling to induce the invasiveness of these tumors. We also find that IFT20 regulates the nucleation of Golgi-derived microtubules by affecting the GM130-AKAP450 complex, which promotes Golgi ribbon formation in achieving polarized secretion for cell migration and invasion. Furthermore, IFT20 promotes the efficiency of transport through the Golgi complex. These findings shed new insights into how Ror2 signaling promotes tumor invasiveness, and also advance the understanding of how Golgi structure and transport can be regulated.
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            Re-epithelialization and immune cell behaviour in an ex vivo human skin model

            A large body of literature is available on wound healing in humans. Nonetheless, a standardized ex vivo wound model without disruption of the dermal compartment has not been put forward with compelling justification. Here, we present a novel wound model based on application of negative pressure and its effects for epidermal regeneration and immune cell behaviour. Importantly, the basement membrane remained intact after blister roof removal and keratinocytes were absent in the wounded area. Upon six days of culture, the wound was covered with one to three-cell thick K14+Ki67+ keratinocyte layers, indicating that proliferation and migration were involved in wound closure. After eight to twelve days, a multi-layered epidermis was formed expressing epidermal differentiation markers (K10, filaggrin, DSG-1, CDSN). Investigations about immune cell-specific manners revealed more T cells in the blister roof epidermis compared to normal epidermis. We identified several cell populations in blister roof epidermis and suction blister fluid that are absent in normal epidermis which correlated with their decrease in the dermis, indicating a dermal efflux upon negative pressure. Together, our model recapitulates the main features of epithelial wound regeneration, and can be applied for testing wound healing therapies and investigating underlying mechanisms.
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              Ultrastructural Characterization of the Lower Motor System in a Mouse Model of Krabbe Disease

              Krabbe disease (KD) is a neurodegenerative disorder caused by the lack of β- galactosylceramidase enzymatic activity and by widespread accumulation of the cytotoxic galactosyl-sphingosine in neuronal, myelinating and endothelial cells. Despite the wide use of Twitcher mice as experimental model for KD, the ultrastructure of this model is partial and mainly addressing peripheral nerves. More details are requested to elucidate the basis of the motor defects, which are the first to appear during KD onset. Here we use transmission electron microscopy (TEM) to focus on the alterations produced by KD in the lower motor system at postnatal day 15 (P15), a nearly asymptomatic stage, and in the juvenile P30 mouse. We find mild effects on motorneuron soma, severe ones on sciatic nerves and very severe effects on nerve terminals and neuromuscular junctions at P30, with peripheral damage being already detectable at P15. Finally, we find that the gastrocnemius muscle undergoes atrophy and structural changes that are independent of denervation at P15. Our data further characterize the ultrastructural analysis of the KD mouse model, and support recent theories of a dying-back mechanism for neuronal degeneration, which is independent of demyelination.
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                Author and article information

                Contributors
                Journal
                LCAHAM
                Lab on a Chip
                Lab Chip
                Royal Society of Chemistry (RSC)
                1473-0197
                1473-0189
                February 01 2022
                2022
                : 22
                : 3
                : 423-444
                Affiliations
                [1 ]Queensland Micro- and Nanotechnology Centre, Griffith University, Nathan, Queensland 4111, Australia
                [2 ]Centre for Regional and Rural Futures, Deakin University, Geelong, Victoria 3216, Australia
                Article
                10.1039/D1LC00869B
                35048916
                31ecbcba-f622-479e-adb6-c7db255db1ad
                © 2022

                http://rsc.li/journals-terms-of-use

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                Self URI (article page): http://xlink.rsc.org/?DOI=D1LC00869B

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