Seroepidemiological, clinical and virological studies were carried out in an HTLV‐I endemic area to find out if HTLV‐I caused an intraocular inflammatory disorder, uveitis. The seroprevalence in patients with uveitis without defined etiologies (62/175, 35.4%) was significantly higher than that in patients with non‐uveitic ocular diseases (42/261, 16.1%) or in patients with uveitis with defined etiologies (8/78, 10.3%). Moreover, the seroprevalence in young adults (20–49 years) with uveitis without defined etiologies was 30/67 (44.8%), whereas it was only 10/107 (9.3%) in the other two groups. The uveitis in HTLV‐I carriers was characterized clinically by a moderate inflammation of the vitreous body accompanied by a mild iritis and retinal vasculitis. The proviral DNA of HTLV‐I was detected by polymerase chain reaction from the inflammatory cells in the anterior chamber in 9 out of 9 seropositive patients with the uveitis, but not in any of the tested patients with other types of uveitis. These data, thus, indicate that HTLV‐I causes a specific type of intraocular inflammation, uveitis.

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Fibrosis is an important wound-healing process in injured tissues, but excessive fibrosis is often observed in patients with chronic inflammation. Although oncostatin M (OSM) has been reported to play crucial roles for recovery from acute liver injury by inducing tissue inhibitor of metalloproteinase 1 (Timp1) expression, the role of OSM in chronic liver injury (CLI) is yet to be elucidated. Here, we show that OSM exerts powerful fibrogenic activity by regulating macrophage activation during CLI. Genetic ablation of the OSM gene alleviated fibrosis in a mouse model of chronic hepatitis. Conversely, continuous expression of OSM in a normal mouse liver by hydrodynamic tail vein injection (HTVi) induced severe fibrosis without necrotic damage of hepatocytes, indicating that OSM is involved in the fundamental process of liver fibrosis (LF) after hepatitis. In a primary coculture of hepatic stellate cells (HSCs) and hepatic macrophages (HMs), OSM up-regulated the expression of fibrogenic factors, such as transforming growth factor-b and platelet-derived growth factor in HMs, while inducing Timp1 expression in HSCs, suggesting the synergistic roles of OSM for collagen deposition in the liver. Fluorescence-activated cell sorting analyses using OSM-HTVi and OSM knockout mice have revealed that bone-marrow-derived monocyte/macrophage are responsive to OSM for profibrotic activation. Furthermore, depletion or blocking of HMs by administration of clodronate liposome or chemokine inhibitor prevented OSM-induced fibrosis. Conclusion: OSM plays a crucial role in LF by coordinating the phenotypic change of HMs and HSCs. Our data suggest that OSM is a promising therapeutic target for LF. (HEPATOLOGY 2018;67:296-312). P atients with advanced liver fibrosis (LF) have poor prognosis because of impaired liver functions, adverse symptoms such as gastroesophageal varices and ascites, and hepatocellular carcinoma (HCC).(1,2) In the injured liver, activated hepatic stellate cells (HSCs) are the main producer of extracellular matrix (ECM), including type1 collagen, whereas the ECM can be degraded by various proteinases such as matrix metalloproteinases (MMPs). The balance between ECM production and degradation is

This paper presents a new method for constructing an example-based deformable human hand model from medical images. Realistic animation of human hands requires good estimates of the joint structure and properly weighted skeleton-driven surface deformation. For this purpose, we propose a method based on medical images of hands in several poses. Our method consists of the following 3 steps: First, using the measured bone shapes, we estimate the link structure (joint rotation centers) and the joint angles of each scan. Second, we construct a mutually consistent polygonal mesh of all the scans. For this purpose, a polygonal mesh of one pose, the base mesh, is deformed using skeletal subspace deformation, and then fitted interactively to the measured meshes from the other scans. Finally, the hand is deformed using a weighted pose space deformation. We demonstrate results of deformable hand models consisting of 100,000 triangle meshes derived from CT scans.

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