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The basic principle for the operation of a thermally stimulated shape memory polymer (SMP) is a drastic change in elastic modulus above the glass transition temperature (T g ). This change from glassy modulus to rubbery modulus allows the material to be deformed above the T g and retain the deformed shape when cooled below the T g . The material will recover its original shape when heated above the T g again. However, thermal activation is not the only possibility for a polymer to exhibit this shape memory effect or change of modulus. This paper discusses results of an alternative approach to SMP activation.It is well known that the T g of a thermosetting polymer is proportional to its crosslinking density. It is possible for the crosslinking density of a room temperature elastomer to be modified through photo-crosslinking special photo-reactive monomer groups incorporated into the material system in order to increase its T g . Correspondingly, the modulus will be increased from the rubbery state to the glassy state. As a result, the material is transformed from an elastomer to a rigid glassy photoset, depending on the crosslinking density achieved during exposure to the proper wavelength of light. This crosslinking process is reversible by irradiation with a different wavelength, thus making it possible to produce light-activated SMP materials that could be deformed at room temperature, held in deformed shape by photo-irradiation using one wavelength, and recovered to the original shape by irradiation with a different wavelength.In this work, monomers which contain photo-crosslinkable groups in addition to the primary polymerizable groups were synthesized. These monomers were formulated and cured with other monomers to form photo-responsive polymers. The mechanical properties of these materials, the kinetics, and the reversibility of the photo-activated shape memory effect were studied to demonstrate the effectiveness of using photo-irradiation to effect change in modulus (and thus shape memory effect).

Clinical and laboratory studies have shown that environmental exposure to cadmium produces damage to several organs, including bones, lungs, and kidneys. The involvement of cadmium in central nervous system (CNS) disorders has also been widely reported, but the precise pathophysiological mechanism is not yet fully understood. Children who were exposed to cadmium during pregnancy are known to suffer from developmental delays, learning difficulties, attention deficit hyperactivity disorder (ADHD), and other cognitive and neurobehavioral deficits. Results from numerous studies suggest that dysfunction of the blood-brain barrier (BBB) structures is an important step in the neurotoxicity of cadmium. A rat-specific BBB marker protein, the endothelial barrier antigen (EBA), has been previously isolated and classified by Sternberger and others. The mouse IgG1 clone, anti-endothelial barrier antigen (anti-EBA), detects a protein triplet (23.5kDa, 25 kDa, and 30kDa) localized to the luminal surface of central and peripheral nervous system (CNS and PNS) vascular endothelial cells with selective permeability barrier functions. This marker has been widely used for characterizing BBB alterations under demyelinating, inflammatory, and other CNS pathologies. Many studies have been published using the rat model system for studying the neurotoxic effect of acute and chronic exposure to cadmium.We applied the indirect immunofluorescent techniques using the anti-EBA antibody in conjunction with the Olympus cellSens computerized image analysis to detect and quantify the surface areas of BBB-competent microvessel profiles in paraformaldehyde-fixed, paraffin-embedded brains of term-delivered young rats after intraperitoneal injection of a single dose of cadmium chloride. We detected a statistically significant reduction in EBA-positive microvessel surface areas in the forebrain (t = 5.86, df = 1789, p-value < 0.001) and cerebellum (t=73.40, df=1337, p < 0.001) of cadmium-treated rats compared to the normal controls. Thus, this study supports the hypothesis that the EBA is a sensitive and measurable indicator for quantitative assessment of the impact of cadmium exposure in the developing rat brain.

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Pulmonary arterial hypertension (PAH), a disease of the small pulmonary arteries, is characterized by pulmonary vasoconstriction, vascular cell proliferation, and vascular remodeling leading to right ventricular hypertrophy and failure. The remodeled vessels exhibit signs of endothelial layer damage and smooth muscle cell proliferation. It is also well‐established that mutations in the bone morphogenetic protein receptor 2 (BMPR2) predispose individuals to development of PAH. Recent studies in PAH mouse models and in cultured human pulmonary artery endothelial cells (where BMPR2 has been experimentally knocked down) suggest that endothelial cells involved in the vascular remodeling of PAH undergo transdifferentiation. Here, we show that pulmonary artery endothelial cells (PAECs) isolated from the rat Sugen (SU516)/hypoxia model of pulmonary arterial hypertension exhibit phenotypic changes characteristic of endothelial‐to‐mesenchymal transition (EndMT). Preliminary data also suggest decreased BMPR2 expression in the PAH model PAECs. Cells were obtained from the University of South Alabama Center for Lung Biology (CLB). Briefly, Fisher 344 rats were injected with SU5416 (20mg/kg) or vehicle control and exposed to hypoxia (10% O2 or normoxia for control animals) for three weeks and returned to normoxia for at least two weeks. PAECs were harvested using established CLB protocol. PAECs from the PAH animals (SURAT) exhibited a significant increase in alpha smooth muscle actin (αSMA) expression as compared to the control PAECs, as evidenced by immunocytochemistry and real time PCR. These cells retained expression of endothelial cell markers von Willebrand Factor (vWF) and platelet endothelial cell adhesion molecule (PECAM‐1). However, expression of both PECAM‐1 and vWF was decreased in the SURAT cells compared to control PAECs. Expression of tight junctional protein‐1, vascular adhesion molecule‐1 (VCAM‐1), intracellular adhesion molecule‐1 (ICAM‐1), claudin‐1, and selectin was also decreased in the SURAT PAECs as compared to control cells. These data suggest that PAECS exhibit signs of cellular reprogramming in Sugen/hypoxia‐treated animals, and also provide insight into a cellular model that directly correlates with a well‐established animal model of PAH.Support or Funding InformationSupported by NIH1R15HL137135‐01A1This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.