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Shinichi Usui,1,2 Yasushi Ikuno,2 Sato Uematsu,1 Yuko Morimoto,1 Yoshiaki Yasuno,3 Yasumasa Otori11National Hospital Organization, Osaka National Hospital, Osaka, Japan; 2Department of Ophthalmology, Osaka University Graduate School of Medicine, Suita, Japan; 3Computational Optics Group, University of Tsukuba, Tsukuba, JapanPurpose: To evaluate changes in axial length and choroidal thickness after trabeculectomy.Patients and methods: Fourteen patients under 80 years of age with glaucoma, were enrolled. The choroid was imaged using prototypical high-penetration optic coherence tomography (OCT) and the thickness was measured. Axial length, choroidal thickness, and intraocular pressure (IOP) were measured bilaterally at 3 pm 1 day before and 6 days after trabeculectomy. The choroidal thickness was measured at the fovea and four other locations (2 mm superior, temporal, inferior, and nasal to the center of the optic nerve head).Results: The IOP and axial length significantly decreased in eyes that underwent trabeculectomy (P < 0.0001 for the IOP; P < 0.001 for axial length comparisons). The mean choroidal thicknesses significantly increased in eyes that underwent trabeculectomy compared to preoperatively (P < 0.0001 for the fovea; P < 0.01 for four locations around the optic disc). The mean magnitude of change in IOP was correlated positively with the mean magnitude of change in axial length, but not correlated with the mean magnitude of change in choroidal thickness at the fovea that underwent trabeculectomy. The sum of the axial length and subfoveal choroidal thickness in eyes decreased significantly postoperatively (P

Author(s): K S Lang; M Recher; T Junt; A A Navarini; N L Harris; S Freigang; B Odermatt; C Conrad; L M Ittner; S Bauer; S A Luther; S Uematsu; [...]

Toll-like receptor 5 (TLR5) has been widely studied in an inflammatory context, but the effect of TLR5 on the adaptive response to bacterial flagellin has received considerably less attention. Here, we demonstrate that TLR5 expression by dendritic cells (DCs) allows a 1,000-fold enhancement of T-cell sensitivity to flagellin, and this enhancement did not require the expression of NLRC4 or Myd88. The effect of TLR5 on CD4 T-cell sensitivity was independent of the adjuvant effect of flagellin and TLR5 ligation did not alter the sensitivity of ovalbumin (OVA)-specific T cells to OVA. In the spleen, the exquisite T-cell sensitivity to flagellin was regulated by CD4−CD8α− DCs and was blocked by a monoclonal antibody to TLR5. In the mesenteric lymph nodes, flagellin-specific T-cell activation was regulated by a population of CD103−CD11b+ DCs. Thus, TLR5 expression by mucosal and systemic DC subsets controls the sensitivity of the adaptive immune response to flagellated pathogens. [ABSTRACT FROM AUTHOR]

Toll-like receptors (TLRs) recognize distinct microbial components and induce innate immune responses. TLR5 has been shown to recognize bacterial flagellin. Unlike other TLRs, TLR5 is not expressed on conventional dendritic cells or macrophages. By contrast, TLR5 is mainly expressed on intestinal CD11c(+) lamina propria cells (LPCs), which do not express TLR4. These cells detect pathogenic bacteria and secreted proinflammatory cytokines, mainly in a TLR5-dependent manner. Notably, transport of pathogenic Salmonella typhimurium from the intestinal tract to mesenteric lymph nodes was impaired in Tlr5 (-/-) mice, suggesting that CD11c(+) LPCs expressing TLR5 are used by S. typhimurium for systemic infection. CD11c(+) LPCs consist of four subsets distinguished by differential expression patterns of CD11c and CD11b. CD11c(hi)CD11b(hi) LPDCs have been identified as TLR5-expressing cells. In response to flagellin, these LPDCs induce the differentiation of naive B cells into IgA(+) plasma cells via a mechanism independent of gut-associated lymphoid tissue (GALT), and trigger the differentiation of antigen-specific Th17 and Th1 cells. These LPDCs have unique properties in that they can induce acquired immunity as well as innate immunity via TLR5 in the intestine. [ABSTRACT FROM AUTHOR]

Structured Abstract Authors – Usui T, Uematsu S, Kanegae H, Morimoto T, Kurihara S Objective – To clarify the correlation between variations in maximum occlusal force and the maxillofacial skeletal pattern in subjects with malocclusion using a compact device. Design – Three hundred and fifty patients (150 males 200 females) with malocclusion were included. The male and female subjects were divided into five groups each based on chronological age. The maximum occlusal force was measured with a simplified occlusal force meter. The maxillofacial skeletal pattern was analyzed with lateral cephalograms. On the basis of these data, we studied the correlation between the maximum occlusal force and the maxillofacial skeletal pattern in each age group. Results – The maximum occlusal force tended to increase with age, with a tendency to be greater in male than in female subjects. In the male subjects, up to their 20s, the maximum occlusal force continued to increase, while in the female subjects its increase almost terminated in the later teens. In some of the age groups, the maximum occlusal force showed a negative correlation with the mandibular plane angle. Conclusions – Maximum occlusal force tended to increase with age. There was a gender difference in the maximum occlusal force at all age groups, values being larger in the males. In the males, the maximum occlusal force continued to increase until their 20s, while in the females, this increase almost terminated at the age of 17. [ABSTRACT FROM AUTHOR]

A paste comprising fine alumina particles was applied on surfaces of steel plate specimens and a welded joint specimen, and the effects of the paste on restraint and visual detection of fatigue crack growth were experimentally investigated by performing fatigue tests with in situ observations by a harge oupled evice (CCD) microscope and through various kinds of fractographic observations and elemental analyses using an scanning electron microscope (SEM) and an electron probe microanalyser (EPMA). As a result, the crack growth rate in the plate specimen was drastically retarded by the wedge effect of the alumina particles, and a 311% increase in failure life was produced on an average. The restraint of crack opening displacement (COD) value by the wedge materials was estimated by elastic finite element (FE) analyses, and the results were compared with the experimental data. Similar crack growth restraint effects were also observed on the welded joint specimen, producing a 117% increase in failure life. In the fatigue tests of the specimens on which the alumina paste was applied, a remarkable black colour developed in the white alumina paste along the paths of crack propagation, facilitating the visual detection of the cracks. An analysis using an X-ray diffractometer showed that the black matter in the paste consists of fine debris derived from the base metal. [ABSTRACT FROM AUTHOR]

Inorganic polyphosphates [Poly(P)] are often distributed in osteoblasts. We undertook the present study to verify the hypothesis that Poly(P) stimulates osteoblasts and facilitates bone formation. The osteoblast-like cell line MC 3T3-E1 was cultured with Poly(P), and gene expression and potential mineralization were evaluated by reverse-transcription polymerase chain-reaction. Alkaline phosphatase activity, von Kossa staining, and resorption pit formation analyses were also determined. The potential role of Poly(P) in bone formation was assessed in a rat alveolar bone regeneration model. Poly(P) induced osteopontin, osteocalcin, collagen 1α, and osteoprotegerin expression and increased alkaline phosphatase activity in MC 3T3-E1 cells. Dentin slice pit formation decreased with mouse osteoblast and bone marrow macrophage co-cultivation in the presence of Poly(P). Promotion of alveolar bone regeneration was observed locally in Poly(P)-treated rats. These findings suggest that Poly(P) plays a role in osteoblastic differentiation, activation, and bone mineralization. Thus, local poly(P) delivery may have a therapeutic benefit in periodontal disease. [ABSTRACT FROM AUTHOR]

Membrane cofactor protein (MCP, CD46) is one of the complement regulatory proteins, and is widely distributed in human organs and protects cells from complement-mediated cytotoxicity. We analysed the distribution and the intensities of MCP in liver diseases and evaluated the role of MCP during hepatocarcinogenesis. Western blot analysis revealed that relative densities (density of the sample/density of the standard sample) of MCP in 27 HCC, 18 liver cirrhosis, nine chronic hepatitis and 12 normal liver were 0.63 ± 0.23, 0.21 ± 0.07, 0.25 ± 0.10 and 0.11 ± 0.03 (mean ± s.d.) respectively. MCP expression in hepatocellular carcinoma (HCC) was significantly higher than that in both liver cirrhosis and chronic hepatitis (P < 0.01). The difference in the tumour sizes, the grades of differentiation and viral marker status did not affect the expression. Immunohistological analysis revealed that MCP was distributed mainly in the basolateral membrane of the hepatic cord in non-cancerous liver, along with endothelial cells and bile duct cells. In HCC, the protein was observed on the membrane in a non-polarized fashion. These data suggest that HCC cells acquire the increased MCP expression in a development of HCC and may escape from tumour-specific complement-mediated cytotoxicity. [ABSTRACT FROM AUTHOR]