In vivo in the present study. However, we failed to detect changes in the distinct regions or non-fractured sites. Irradiation affects bone tissues by both cellular and physicochemical processes, including bone metabolism and fracture healing. The altered compositions of bone tissues lead to differential response to irradiation. Different local environments and components were noted in the fracture or nonfractured sites. In other words, irradiation had different effects on distinct regions of bone. Given the lack of investigations focused on non-fractured bones, the generalization of our conclusion should be interpreted with caution. In addition, low-dose irradiation appeared to accelerate age-related changes in skeletal microarchitecture. In this study, limited passages of osteoblasts and adult animals were employed for in vitro and in vivo studies. However, it remains unclear whether the stimulatory effects of low-dose irradiation on osteoblasts and fracture healing represent an age-related phenomenon. The goal of uveitis treatment is to suppress inflammation and achieve regression when it occurs. However inflammation can recur with various complications, such as cataract and permanent cumulative damages. Administrations of corticosteroid are standard therapeutic strategy, but they have many potential side effects such as intraocular pressure increase, cataract formation and increase in infection susceptibility. Therefore, alternative TH-302 treatments which are safer and more long lasting are needed. The rat model of endotoxin-induced uveitis has been widely used for evaluating potential ocular anti-inflammatory compounds since it was reported in 1980. EIU can be induced by systemic injection of lipopolysaccharide, which generates inflammatory responses largely in the anterior uvea and mild responses in the posterior segments of the eye, mimicking the pathological conditions in human acute uveitis. It has been reported that LPS was recognized by membrane-bound cluster of differentiation 14 and Toll-like receptors on the surface of macrophages. Receptors activation in these immune surveillance cells resulted in phosphorylation of nuclear factor-kappa B and caused release of pro-inflammatory factors, such as tumor necrosis factor-a, interlukin-6 and monocyte chemoattractant protein-1. As a crucial proximal mediator, TNF-a stimulates acute phase reaction of inflammation by influencing leukocyte activation and infiltration, and inducing production of other mediators such as IL-6, a major cytokine regulator of acute phase response.