The pumping of fluids in microfluidic discs by centrifugal forces has several advantages, however, centrifugal pumping only permits unidirectional fluid flow, restricting the number of processing steps that can be integrated before fluids reach the edge of the disc. As a solution to this critical limitation, we present a novel pumping technique for the centrifugal microfluidic disc platform, termed the thermo-pneumatic pump (TPP), that enables fluids to be transferred the center of a rotating disc by the thermal expansion of air. The TPP is easy to fabricate as it is a structural feature with no moving components and thermal energy is delivered to the pump via peripheral infrared (IR) equipment, enabling pumping while the disc is in rotation. In this report, an analytical model for the operation of the TPP is presented and experimentally validated. We demonstrate that the experimental behavior of the pump agrees well with theory and that flow rates can be controlled by changing how well the pump absorbs IR energy. Overall, the TPP enables for fluids to be stored near the edge of the disc and transferred to the center on demand, offering significant advantages to the microfluidic disc platform in terms of the handling and storage of liquids.

The field of centrifugal microfluidics has experienced tremendous growth during the past 15 years, especially in applications such as lab-on-a-disc (LoD) diagnostics. The strength of LoD systems lies in its potential for development into fully integrated sample-to-answer analysis systems. This review highlights the technologies necessary to develop the next generation of these systems. In addition to outlining valving and other fluid-handling operations, we discuss the recent advances and future outlook in four categories of LoD processes: reagent storage, sample preparation, nucleic acid amplification, and analyte detection strategies.

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This study characterizes a model of motor neuron (MN) loss on the molecular, cellular, and behavioral levels. Injection of the toxic lectin Ricinus communis agglutinin I (RCA I or ricin) caused cellular deficit and loss of function by damaging the sciatic nerve. Since the sciatic nerve supplies movement to most of the lower limb, damaging this motor system models lower limb paralysis and the deficits that occur in diseases like amyotrophic lateral sclerosis (ALS) and infantile progressive spinal muscular atrophy (SMA). We used motor-, sensorimotor-, locomotor-, and reflex-based tests to demonstrate loss of function after ricin injection. Loss of function was also demonstrated by decreased retrograde transport, and supported by measurements of muscle wasting. Histochemical and molecular methods were used to characterize sciatic nerve damage in axons and cell bodies, including apoptotic cell death in MNs. This battery of tests documents the extent of the ricin-induced damage and provides a baseline that can be used to judge the efficacy of MN treatment strategies in preclinical studies.