The demand for infrared transmitting materials has grown steadily for several decades as markets realize new applications for longer wavelength sensing and imaging. With this growth has come the demand for new and challenging material requirements that cannot be satisfied with crystalline products alone. Chalcogenide materials, with their unique physical, thermal, and optical properties, have found acceptance by designers and fabricators to meet these demands. No material is perfect in every regard, and chalcogenides are no exception. A cause for concern has been the relatively low fracture toughness and the propensity of the bulk material to fracture. This condition is amplified when traditional subtractive manufacturing processes are employed. This form of processing leaves behind micro fractures and sub surface damage, which act as propagation points for both local and catastrophic failure of the material. Precision lens molding is not a subtractive process, and as a result, micro fractures and sub surface damage are not created. This results in a stronger component than one produced by traditional methods. New processing methods have also been identified that result in an even stronger surface that is more resistant to breakage, without the need for post processing techniques that may compromise surface integrity. This paper will discuss results achieved in the process of lens molding development at Edmund Optics that result in measurably stronger chalcogenide components. Various metrics will be examined and data will be presented that quantifies component strength for different manufacturing processes.Acute limb ischemia is one of the most common peripheral arterial disease, while surgical restoration of blood flow often results in ischemia/reperfusion (I/R) injury. Our previous study revealed the inflammation intensity in arterial tissue, characterized by expression of high mobility group box protein 1 (HMGB1), was contrary to the fluctuation of hemodynamics in reperfusion limbs in a rat model. This study meant to clarify the role of HMGB1 during this process. Laser Doppler perfusion imaging evaluated limb hemodynamics in mean and max perfusion unit (PU). Femoral arterial tissue was collected for molecular biology examination. The results revealed that HMGB1 promoted vascular structure remodeling and vasomotor dysfunction during acute I/R, characterized by degradation of collagenous fibers, disruption of elastic lamellae, intensive inflammation and phenotype transfer of smooth muscle cells. Blockade of HMGB1 preserved vascular homeostasis and improved PUs (P-meanPU < 0.001, P-maxPU < 0.001). The elevated expression of TNF-alpha, IL-6, ICAM, VCAM, MMP-2, MMP-9, alpha-SM actin correlated with HMGB1 positively. In conclusion, HMGB1 promoted vascular remodeling and dysfunction via initiating an inflammation cascade during I/R. Blockade of HMGB1 would preserve vascular homeostasis and facilitate the blood perfusion of ischemic limb. (C) 2017 Elsevier Inc. All rights reserved.