Parylene stiction

This paper presents a preliminary study into stiction between parylene C and substrate surfaces for biocompatible check-valve applications. During fabrication, parylene C is used as the structural material for the check-valve. The substrate surfaces studied include Au, Al, Si, parylene C, XeF_2 treated Si, and silicon dioxide. Stiction between different surfaces is created after sacrificial photoresist etching. Then, the stiction is measured using blister tests, and stiction mechanisms for different materials are investigated. The devices are released with different recipes to examine their effects. Finally, the results of the study reveal methods to control the cracking pressure of parylene check-valves

Stiction of parylene C to silicon surface measured using blister tests

Micro-fabricated biocompatible check valves are integral parts of many implantable micro-fluidic devices. The cracking pressure of check valves is usually controlled by stiction between polymeric films and the underlying substrate. The following paper presents the first comprehensive study of stiction between parylene and silicon surfaces. The valves are fabricated using surface micromachining with parylene C as the structural material. Deep Reactive Ion Etching (DRIE) is used to create through holes in the wafer for the passage of fluids. Blister test is employed to calculate stiction. From experimental results, stiction between parylene C and silicon surfaces is found to be 2.59 J/m2, which is comparable to the stiction between silicon and other polymeric thin films

Minimally Invasive Parylene Dual-Valved Flow Drainage Shunt for Glaucoma Implant

A parylene-enabled microvalved shunt implant for glaucoma drainage is presented in this paper. Enabled by the dual-checkvalve operation, this device can physically drain the extra intraocular fluid and regulate the intraocular pressure (IOP) within the normal range (15-20 mmHg). Improved surgical features, in addition to the functional/microfluidic components, such as parylene-tube carrier and anchors, are also incorporated in such device to realize minimally invasive suture-less implantation, suitable for practical in vivo use. With the optimized micromachining and post-fabrication process procedures, the developed implant is the first checkvalved glaucoma drainage device (GDD), which is passive, consumes no additional power, and functions without any circuit involved to pursue its medical application

Efficient Prodrug Activator Gene Therapy by Retroviral Replicating Vectors Prolongs Survival in an Immune-Competent Intracerebral Glioma Model.

Prodrug activator gene therapy mediated by murine leukemia virus (MLV)-based retroviral replicating vectors (RRV) was previously shown to be highly effective in killing glioma cells both in culture and in vivo. To avoid receptor interference and enable dual vector co-infection with MLV-RRV, we have developed another RRV based on gibbon ape leukemia virus (GALV) that also shows robust replicative spread in a wide variety of tumor cells. We evaluated the potential of GALV-based RRV as a cancer therapeutic agent by incorporating yeast cytosine deaminase (CD) and E. coli nitroreductase (NTR) prodrug activator genes into the vector. The expression of CD and NTR genes from GALV-RRV achieved highly efficient delivery of these prodrug activator genes to RG-2 glioma cells, resulting in enhanced cytotoxicity after administering their respective prodrugs 5-fluorocytosine and CB1954 in vitro. In an immune-competent intracerebral RG-2 glioma model, GALV-mediated CD and NTR gene therapy both significantly suppressed tumor growth with CB1954 administration after a single injection of vector supernatant. However, NTR showed greater potency than CD, with control animals receiving GALV-NTR vector alone (i.e., without CB1954 prodrug) showing extensive tumor growth with a median survival time of 17.5 days, while animals receiving GALV-NTR and CB1954 showed significantly prolonged survival with a median survival time of 30 days. In conclusion, GALV-RRV enabled high-efficiency gene transfer and persistent expression of NTR, resulting in efficient cell killing, suppression of tumor growth, and prolonged survival upon CB1954 administration. This validates the use of therapeutic strategies employing this prodrug activator gene to arm GALV-RRV, and opens the door to the possibility of future combination gene therapy with CD-armed MLV-RRV, as the latter vector is currently being evaluated in clinical trials

Mass flowmeter using a multi-sensor chip

We report here a novel mass flowmeter using a multisensor chip that includes a 1-D array of pressure, temperature and shear stress sensors. This shear stress sensor based flowmeter is capable of high sensitivity and wide measurement range. Our study also shows that the mass flowmeter using shear-stress sensors produces better resolution than that from pressure sensors in the laminar flow regime. Extensive tests have been carried out to evaluate the effects of overheat ratio, channel height and gas properties. We also find the V^2 ∝ τ^(1/3) law for conventional hot film sensors does not hold for our micromachined shear stress sensor

Fucosyltransferase 1 and 2 play pivotal roles in breast cancer cells.

FUT1 and FUT2 encode alpha 1, 2-fucosyltransferases which catalyze the addition of alpha 1, 2-linked fucose to glycans. Glycan products of FUT1 and FUT2, such as Globo H and Lewis Y, are highly expressed on malignant tissues, including breast cancer. Herein, we investigated the roles of FUT1 and FUT2 in breast cancer. Silencing of FUT1 or FUT2 by shRNAs inhibited cell proliferation in vitro and tumorigenicity in mice. This was associated with diminished properties of cancer stem cell (CSC), including mammosphere formation and CSC marker both in vitro and in xenografts. Silencing of FUT2, but not FUT1, significantly changed the cuboidal morphology to dense clusters of small and round cells with reduced adhesion to polystyrene and extracellular matrix, including laminin, fibronectin and collagen. Silencing of FUT1 or FUT2 suppressed cell migration in wound healing assay, whereas FUT1 and FUT2 overexpression increased cell migration and invasion in vitro and metastasis of breast cancer in vivo. A decrease in mesenchymal like markers such as fibronectin, vimentin, and twist, along with increased epithelial like marker, E-cadherin, was observed upon FUT1/2 knockdown, while the opposite was noted by overexpression of FUT1 or FUT2. As expected, FUT1 or FUT2 knockdown reduced Globo H, whereas FUT1 or FUT2 overexpression showed contrary effects. Exogenous addition of Globo H-ceramide reversed the suppression of cell migration by FUT1 knockdown but not the inhibition of cell adhesion by FUT2 silencing, suggesting that at least part of the effects of FUT1/2 knockdown were mediated by Globo H. Our results imply that FUT1 and FUT2 play important roles in regulating growth, adhesion, migration and CSC properties of breast cancer, and may serve as therapeutic targets for breast cancer