Droplet microactuator system

The present invention relates to a droplet microactuator system. According to one embodiment, the droplet microactuator system includes: (a) a droplet microactuator configured to conduct droplet operations; (b) a magnetic field source arranged to immobilize magnetically responsive beads in a droplet during droplet operations; (c) a sensor configured in a sensing relationship with the droplet microactuator, such that the sensor is capable of sensing a signal from and/or a property of one or more droplets on the droplet microactuator; and (d) one or more processors electronically coupled to the droplet microactuator and programmed to control electrowetting-mediated droplet operations on the droplet actuator and process electronic signals from the sensor

Systems, methods, and products for graphically illustrating and controlling a droplet actuator

Systems for controlling a droplet microactuator are provided. According to one embodiment, a system is provided and includes a controller, a droplet microactuator electronically coupled to the controller, and a display device displaying a user interface electronically coupled to the controller, wherein the system is programmed and configured to permit a user to effect a droplet manipulation by interacting with the user interface. According to another embodiment, a system is provided and includes a processor, a display device electronically coupled to the processor, and software loaded and/or stored in a storage device electronically coupled to the controller, a memory device electronically coupled to the controller, and/or the controller and programmed to display an interactive map of a droplet microactuator. According to yet another embodiment, a system is provided and includes a controller, a droplet microactuator electronically coupled to the controller, a display device displaying a user interface electronically coupled to the controller, and software for executing a protocol loaded and/or stored in a storage device electronically coupled to the controller, a memory device electronically coupled to the controller, and/or the controller

Expression of hMLH1 is inactivated in the gastric adenomas with enhanced microsatellite instability

Microsatellite instability (MSI) and frameshift mutations in the genes containing coding nucleotide repeats have been reported in a subset of gastric adenomas, however the inactivation profiles of DNA mismatch repair genes in MSI-positive gastric adenomas have not been characterized. To address the origin of MSI in gastric adenomas, expressions of hMLH1 and hMSH2 were explored in 86 gastric adenomas. Gastric carcinomas, of which 16 were MSI-positive and 22 MSI-negative, were used as controls. MSI was found in 15 (17%) of gastric adenomas. Absent or decreased hMLH1 expression by immunohistochemistry was noted in most of the MSI-positive adenomas (13/15, 87%) and carcinomas (14/16, 88%), and all of these tumours showed methylation of the hMLH1 gene promoter. In contrast, rare inactivation of hMLH1 expression was found in MSI-negative adenomas (3/71, 4%) and carcinomas (2/22, 9%). Intense expression of hMSH2 gene product was observed in most of the gastric adenomas and carcinomas regardless of MSI status. These findings indicate that the inactivation of hMLH1 gene expression by promoter methylation is an early event and might be the origin of MSI-positive gastric adenomas. © 2001 Cancer Research Campaign  http://www.bjcancer.co

Digital Microfluidics Sample Analyzer

Three innovations address the needs of the medical world with regard to microfluidic manipulation and testing of physiological samples in ways that can benefit point-of-care needs for patients such as premature infants, for which drawing of blood for continuous tests can be life-threatening in their own right, and for expedited results. A chip with sample injection elements, reservoirs (and waste), droplet formation structures, fluidic pathways, mixing areas, and optical detection sites, was fabricated to test the various components of the microfluidic platform, both individually and in integrated fashion. The droplet control system permits a user to control droplet microactuator system functions, such as droplet operations and detector operations. Also, the programming system allows a user to develop software routines for controlling droplet microactuator system functions, such as droplet operations and detector operations. A chip is incorporated into the system with a controller, a detector, input and output devices, and software. A novel filler fluid formulation is used for the transport of droplets with high protein concentrations. Novel assemblies for detection of photons from an on-chip droplet are present, as well as novel systems for conducting various assays, such as immunoassays and PCR (polymerase chain reaction). The lab-on-a-chip (a.k.a., lab-on-a-printed-circuit board) processes physiological samples and comprises a system for automated, multi-analyte measurements using sub-microliter samples of human serum. The invention also relates to a diagnostic chip and system including the chip that performs many of the routine operations of a central labbased chemistry analyzer, integrating, for example, colorimetric assays (e.g., for proteins), chemiluminescence/fluorescence assays (e.g., for enzymes, electrolytes, and gases), and/or conductometric assays (e.g., for hematocrit on plasma and whole blood) on a single chip platform

Polarization rotation via a monoclinic phase in the piezoelectric 92%PbZn1/3Nb2/3O3-8%PbTiO3

The origin of ultrahigh piezoelectricity in the relaxor ferroelectric PbZn1/3Nb2/3O3-PbTiO3 was studied with an electric field applied along the [001] direction. The zero-field rhombohedral R phase starts to follow the direct polarization path to tetragonal symmetry via an intermediate monoclinic M phase, but then jumps irreversibly to an alternate path involving a different type of monoclinic distortion. Details of the structure and domain configuration of this novel phase are described. This result suggests that there is a nearby R-M phase boundary as found in the Pb(Ti,Zr)O3 system.Comment: REVTeX file. 4 pages. New version after referees' comment

Oxide two-dimensional electron gas with high mobility at room-temperature

The prospect of 2‐dimensional electron gases (2DEGs) possessing high mobility at room temperature in wide‐bandgap perovskite stannates is enticing for oxide electronics, particularly to realize transparent and high‐electron mobility transistors. Nonetheless only a small number of studies to date report 2DEGs in BaSnO(3)‐based heterostructures. Here, 2DEG formation at the LaScO(3)/BaSnO(3) (LSO/BSO) interface with a room‐temperature mobility of 60 cm(2) V(−1) s(−1) at a carrier concentration of 1.7 × 10(13) cm(–2) is reported. This is an order of magnitude higher mobility at room temperature than achieved in SrTiO(3)‐based 2DEGs. This is achieved by combining a thick BSO buffer layer with an ex situ high‐temperature treatment, which not only reduces the dislocation density but also produces a SnO(2)‐terminated atomically flat surface, followed by the growth of an overlying BSO/LSO interface. Using weak beam dark‐field transmission electron microscopy imaging and in‐line electron holography technique, a reduction of the threading dislocation density is revealed, and direct evidence for the spatial confinement of a 2DEG at the BSO/LSO interface is provided. This work opens a new pathway to explore the exciting physics of stannate‐based 2DEGs at application‐relevant temperatures for oxide nanoelectronics

Droplet actuator analyzer with cartridge

A droplet actuator with cartridge is provided. According to one embodiment, a sample analyzer is provided and includes an analyzer unit comprising electronic or optical receiving means, a cartridge comprising self-contained droplet handling capabilities, and a wherein the cartridge is coupled to the analyzer unit by a means which aligns electronic and/or optical outputs from the cartridge with electronic or optical receiving means on the analyzer unit. According to another embodiment, a sample analyzer is provided and includes a sample analyzer comprising a cartridge coupled thereto and a means of electrical interface and/or optical interface between the cartridge and the analyzer, whereby electrical signals and/or optical signals may be transmitted from the cartridge to the analyzer

β-catenin activation down-regulates cell-cell junction-related genes and induces epithelial-to-mesenchymal transition in colorectal cancers

WNT signaling activation in colorectal cancers (CRCs) occurs through APC inactivation or β-catenin mutations. Both processes promote β-catenin nuclear accumulation, which up-regulates epithelial-to-mesenchymal transition (EMT). We investigated β-catenin localization, transcriptome, and phenotypic differences of HCT116 cells containing a wild-type (HCT116-WT) or mutant β-catenin allele (HCT116-MT), or parental cells with both WT and mutant alleles (HCT116-P). We then analyzed β-catenin expression and associated phenotypes in CRC tissues. Wild-type β-catenin showed membranous localization, whereas mutant showed nuclear localization; both nuclear and non-nuclear localization were observed in HCT116-P. Microarray analysis revealed down-regulation of Claudin-7 and E-cadherin in HCT116-MT vs. HCT116-WT. Claudin-7 was also down-regulated in HCT116-P vs. HCT116-WT without E-cadherin dysregulation. We found that ZEB1 is a critical EMT factor for mutant β-catenin-mediated loss of E-cadherin and Claudin-7 in HCT116-P and HCT116-MT cells. We also demonstrated that E-cadherin binds to both WT and mutant β-catenin, and loss of E-cadherin releases β-catenin from the cell membrane and leads to its degradation. Alteration of Claudin-7, as well as both Claudin-7 and E-cadherin respectively caused tight junction (TJ) impairment in HCT116-P, and dual loss of TJs and adherens junctions (AJs) in HCT116-MT. TJ loss increased cell motility, and subsequent AJ loss further up-regulated that. Immunohistochemistry analysis of 101 CRCs revealed high (14.9%), low (52.5%), and undetectable (32.6%) β-catenin nuclear expression, and high β-catenin nuclear expression was significantly correlated with overall survival of CRC patients (P = 0.009). Our findings suggest that β-catenin activation induces EMT progression by modifying cell-cell junctions, and thereby contributes to CRC aggressiveness