Publications by authors named "Michael A Zieger"

Chronic wounds affect over 6.5 million Americans and are notoriously difficult to treat. Suboptimal oxygenation of the wound bed is one of the most critical and treatable wound management factors, but existing oxygenation systems do not enable concurrent measurement and delivery of oxygen in a convenient wearable platform.

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A novel and flexible oxygen sensing patch was successfully developed for wearable, industrial, food packaging, pharmaceutical and biomedical applications using a cost-efficient and rapid prototypable additive inkjet print manufacturing process. An oxygen sensitive ink was formulated by dissolving ruthenium dye and ethyl cellulose polymer in ethanol in a 1 : 1 : 98 (w/w/w) ratio. The patch was fabricated by depositing the oxygen sensitive ink on a flexible parchment paper substrate using an inkjet printing process.

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Due to their small size, high metabolic rate, and large surface to volume ratio, mice are a challenge to work with surgically and pre-operatively. Working with mice that are more susceptible to anesthetic agents, aged, or obese (e.g.

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We hypothesized that the addition of silver nanoparticles (AgNP) to a dermal substrate would impart antibacterial properties without inhibiting the proliferation of contained cells. Our in vitro model was based on the commercial substrate, Integra. The substrate was prepared by simple immersion into 0 to 1% suspension of AgNP (75 or 200 nm diameter) followed by rinsing for 20 minutes and sterilization under an ultraviolet C lamp.

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Unlabelled: Adipose-derived stem cells (ASC) have received considerable attention in oncology because of the known direct link between obesity and cancer as well as the use of ASCs in reconstructive surgery after tumor ablation. Previous studies have documented how cancer cells commandeer ASCs to support their survival by altering extracellular matrix composition and stiffness, migration, and metastasis. This study focused on delineating the effects of ASCs and adipocytes on the self-renewal of stem/progenitor cells and hierarchy of breast epithelial cells.

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Background: Understanding how human cells in tissue culture adapt to hypothermia may aid in developing new clinical procedures for improved ischemic and hypothermic protection. Human coronary artery endothelial cells grown to confluence at 37°C and then transferred to 25°C become resistant over time to oxidative stress and injury induced by 0°C storage and rewarming. This protection correlates with an increase in intracellular glutathione at 25°C.

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Hypothermia for myocardial protection or storage of vascular grafts may damage the endothelium and impair vascular function upon reperfusion/rewarming. Catalytic iron pools and oxidative stress are important mediators of cold-induced endothelial injury. Because endothelial cells are highly adaptive, we hypothesized that hypothermic preconditioning (HPC) protects cells at 0 degrees C by a heme oxygenase-1 (HO-1) and ferritin-dependent mechanism.

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There is growing evidence that oxidative stress plays an important role in mediating the injury induced by hypothermia during the preservation of cells and tissues for clinical or research use. In cardiovascular allografts, endothelial cell loss or injury may lead to impaired control of vascular permeability and tone, thrombosis, and inflammation. We hypothesized that hypothermia-induced damage to the endothelium is linked to increases in intracellular catalytic iron pools and oxidative stress.

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Ultraprofound hypothermia (< 5 degrees C) induces changes to cell membranes such as liquid-to-gel lipid transitions and oxidative stress that have a negative effect on membrane function and cell survival. We hypothesized that fatty acid substitution of endothelial cell lipids and alterations in their unsaturation would modify cell survival at 0 degrees C, a temperature commonly used during storage and transportation of isolated cells or tissues and organs used in transplantation. Confluent bovine aortic endothelial cells were treated with 18-carbon fatty acids (C18:0, C18:1n-9, C18:2n-6, or C18:3n-3), C20:5n-3 or C22:6n-3 (DHA), and then stored at 0 degrees C without fatty acid supplements.

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