Wireless power transfer to a small, remote control boat

Over the past few decades, researchers have explored and implemented methods of wireless power transmission to operate devices that traditionally have been powered using plug-in power supplies and batteries. It is with this objective in mind that we built a boat, which is powered wirelessly from a field of harvestable energy. This project sought to develop a wirelessly powered remote control boat to be a proof of concept for the idea of wireless power transfer. Our criteria for success is that the boat should receive sufficient power to run anywhere in a 2.5 meter squared area. Having defined the field in which power will be required by our boat, we will fill this field with microwave RF energy. Finally, using a rectifying antenna, or rectenna, the energy will be harvested and delivered to the boat’s motors. We first developed three different topologies for our motor boat. For each boat, we made the minimization of power consumption a priority, while still maintaining speed and control. Operating between 100 and 200 milliwatts, each of the three topologies has a unique advantages and disadvantages with respect to its power consumption, speed, and controllability, and each has the ability to be powered wirelessly. From here, we plan to combine the rectenna with the boat, and deliver the power to our system. We will then characterize the radiation pattern of our power-receiving monopole antenna, and quantify the efficiencies of our various rectifier topologies

A manufacturable smart dressing with oxygen delivery and sensing capability for chronic wound management

Chronic non-healing wounds, impact over 6.5 million Americans, costs in excess of $25 billion to treat on an annual basis and its incidence is predicted to rise due to the prevalence of obesity and type-2 diabetes. One of the primary complications often associated with chronic wounds is the improper functionality of the peripheral vasculature to deliver O2-rich blood to the tissue which leads to wound hypoxia. Although hyperbaric oxygen therapy are widely used and accepted as an effective approach to bolster tissue O2 levels in hypoxic chronic wounds, most of such treatments require bulky equipment and often expose large areas of the body to unnecessarily elevated oxygen concentrations that can damage healthy tissue. In this paper, we present a smart low-cost wound dressing with integrated oxygen sensor and delivery for locally generating and delivering oxygen to selected hypoxic regions on the wound. The dressing is fabricated on a biocompatible water resistant/hydrophobic paper-based substrate with printed optical oxygen sensors and patterned catalytic oxygen generating regions that are connected to a flexible microfluidic systems. Oxygen generation occurs by flowing H2O2 through the channels and chemical decomposition at the catalyst printed regions on the paper substrate. The hydrophobic paper provides structural stability and flexibility while simultaneously offering printability, selective gaseous filtering, and physical/chemical protection. The fabrication process take advantage of scalable manufacturing technologies including laser processing, inkjet printing, and lamination

Activation of Protein Kinase A and Exchange Protein Directly Activated by cAMP Promotes Adipocyte Differentiation of Human Mesenchymal Stem Cells

Human mesenchymal stem cells are primary multipotent cells capable of differentiating into several cell types including adipocytes when cultured under defined in vitro conditions. In the present study we investigated the role of cAMP signaling and its downstream effectors, protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac) in adipocyte conversion of human mesenchymal stem cells derived from adipose tissue (hMADS). We show that cAMP signaling involving the simultaneous activation of both PKA- and Epac-dependent signaling is critical for this process even in the presence of the strong adipogenic inducers insulin, dexamethasone, and rosiglitazone, thereby clearly distinguishing the hMADS cells from murine preadipocytes cell lines, where rosiglitazone together with dexamethasone and insulin strongly promotes adipocyte differentiation. We further show that prostaglandin I2 (PGI2) may fully substitute for the cAMP-elevating agent isobutylmethylxanthine (IBMX). Moreover, selective activation of Epac-dependent signaling promoted adipocyte differentiation when the Rho-associated kinase (ROCK) was inhibited. Unlike the case for murine preadipocytes cell lines, long-chain fatty acids, like arachidonic acid, did not promote adipocyte differentiation of hMADS cells in the absence of a PPARγ agonist. However, prolonged treatment with the synthetic PPARδ agonist L165041 promoted adipocyte differentiation of hMADS cells in the presence of IBMX. Taken together our results emphasize the need for cAMP signaling in concert with treatment with a PPARγ or PPARδ agonist to secure efficient adipocyte differentiation of human hMADS mesenchymal stem cells

Catabolic enzyme activities in relation to premigratory fattening and muscle hypertrophy in the gray catbird ( Dumetella carolinensis )

The flight muscles of the gray catbird ( Dumetella carolinensis ) were examined to determine if short term adjustments occur in the activity of key catabolic enzymes during preparation for long distance migration. The aerobic capacity of the pectoralis muscle as indicated by citrate synthase activity (CS) is among the highest reported for skeletal muscle (200 μmoles [min·g fresh mass] −1 at 25°C). The mass specific aerobic capacity as indicated by CS activity or cytochrome c concentration does not change during premigratory fattening (Fig. 2) or in relation to the muscle hypertrophy that occurs concomitantly. The maintenance of mass specific aerobic capacity indicates that the total aerobic capacity increases in proportion to the increase in muscle size. The augmented potential for total aerobic power output is considered an adaptation to meet the increased power requirements of flight due to the increased body mass. Additionally, the capacity to oxidize fatty acids, as indicated by β-hydroxyacyl-CoA dehydrogenase activity, approximately doubles during premigratory fattening (from 35 to 70 μmoles [min·g fresh mass] −1 at 25°C; Fig. 1A). This adaptation should favor fatty acid oxidation, thereby sparing carbohydrate and prolonging endurance. The activity of phosphofructokinase, a key glycolytic enzyme, does not change before migration.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47125/1/360_2004_Article_BF01101461.pd