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Retinal vein occlusion (RVO) is a common retinal vascular disease. RVO may be complicated by pronounced ischemia that often leads to severe loss of visual function. The present work aimed at studying the retinal proteome of RVO complicated by ischemia. In six Danish Landrace pigs RVO was induced with argon laser in the right eye of each animal. As four retinal veins were occluded, the RVO best corresponded to a central retinal vein occlusion (CRVO). Left control eyes received a similar laser treatment without inducing occlusion. RVO and retinal ischemia were verified by angiography. The retinas were collected 15 days after RVO for proteomic analysis. RVO resulted in a downregulation of proteins involved in visual perception, including rhodopsin, transducin alpha chain, and peripherin-2. RVO also caused a downregulation of proteins involved in neurotransmitter transport, including glutamate decarboxylase 1 (GAD1), glutamate decarboxylase 2 (GAD2), and complexins 2–4. RVO lead to increased contents of proteins involved in inflammation, including interleukin-18 (IL-18), S100A12, and annexin A1 (ANXA1). Immunohistochemistry revealed a general retinal upregulation of IL-18 and ANXA1 while S100A12 was highly abundant in retinal ganglion cells in RVO. IL-18 and S100A12 are likely to be driving forces in the inflammatory response of RVO complicated by ischemia. Our findings also suggest that RVO results in compromised neurotransmission and a downregulation of proteins involved in visual perception.

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The present report is a detailed analysis of facial growth and oral function in a girl with juvenile rheumatoid arthritis of the temporomandibular joints. She was followed from 9 to 17 years of age prior to and after orthognathic surgery. Facial growth was assessed by facial photographs, dental casts, and roentgencephalometry, and oral function was assessed clinically by electromyography, kinesiography, and bite force. In addition, histological and histochemical analysis was performed on biopsy material from her masseter muscle obtained at the time of surgery. The study showed a clear relationship between facial growth and oral function. Dysplastic growth of the mandible led to an increasingly unstable occlusion with poor working conditions for the masticatory muscles. The muscles became weak, and even revealed marked structural histological and histochemical changes. Based on these observations it is suggested that the conventional treatment strategy with postponement of orthodontic or orthognathic surgical treatment until cessation of growth is abandoned and that early treatment should be undertaken to maintain occlusal stability throughout the growth period.