The concept of synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome has been well clarified, after Chamot et al. suggested this peculiar disorder in 1987. The most commonly affected site in SAPHO syndrome is the anterior chest, followed by the spine. However, the clinical course and taxonomic concept of SAPHO spinal lesions are poorly understood. This study was performed to analyze: (1) the detailed clinical course of spinal lesions in SAPHO syndrome, and (2) the relationship between SAPHO syndrome with spinal lesions and seronegative spondyloarthropathy. Thirteen patients with spondylitis in SAPHO syndrome were analyzed. The features of spinal lesions were a chronic onset with a slight inflammatory reaction, and slowly progressing non-marginal syndesmophytes at multi spinal levels, besides the coexistence of specific skin lesions. SAPHO syndrome, especially spinal lesions related to palmoplantar pustulosis, can be recognized as a subtype of seronegative spondyloarthropathy.

A multifunctional biomaterial with the capacity bond to hard tissues, such as bones and teeth, is a real need for medical and dental applications in tissue engineering and regenerative medicine. Recently, we created phosphorylated-pullulan (PPL), capable of binding to hydroxyapatite in bones and teeth. In the present study, we employed PPL as a novel biocompatible material for bone engineering. First, an in vitro evaluation of the mechanical properties of PPL demonstrated both PPL and PPL/β-TCP composites have higher shear bond strength than materials in current clinical use, including polymethylmethacrylate (PMMA) cement and α-tricalcium phosphate (TCP) cement, Biopex-R. Further, the compressive strength of PPL/β-TCP composite was significantly higher than Biopex-R. Next, in vivo osteoconductivity of PPL/β-TCP composite was investigated in a murine intramedular injection model. Bone formation was observed 5 weeks after injection of PPL/β-TCP composite, which was even more evident at 8 weeks; whereas, no bone formation was detected after injection of PPL alone. We then applied PPL/β-TCP composite to a rabbit ulnar bone defect model and observed bone formation comparable to that induced by Biopex-R. Implantation of PPL/β-TCP composite induced new bone formation at 4 weeks, which was remarkably evident at 8 weeks. In contrast, Biopex-R remained isolated from the surrounding bone at 8 weeks. In a pig vertebral bone defect model, defects treated with PPL/β-TCP composite were almost completely replaced by new bone; whereas, PPL alone failed to induce bone formation. Collectively, our results suggest PPL/β-TCP composite may be useful for bone engineering.

Purpose: To verify the effectiveness of detecting medial meniscus posterior root tears (MMPRTs) using weightbearing posterior-anterior (PA) radiographs. Materials and methods: Twenty-three patients were diagnosed with an MMPRT using magnetic resonance imaging (Group A), with 23 matched individuals forming the control group (Group B). The distance between medial tibial eminence and the lateral edge of the medial femoral condyle (MTE-MFC distance) and medial joint space (MJS) width were measured on weight-bearing PA radiographs, with the knee flexed at 45°(Rosenberg view). Absolute medial meniscus extrusion (MME) was measured on magnetic resonance images. Results: The MTE-MFC distance was greater and the MJS width was smaller in Group A than Group B (7.7 ± 1.7 mm versus 6.0 ± 1.24 mm and 3.2 ± 0.8 mm versus 4.5 ± 0.7 mm, respectively; P < 0.05). The MTE-MFC distance and MJS width correlated with MME (r = 0.603 and 0.579, respectively; P < 0.05), and the extent of MME was greater in Group A than Group B (4.1 ± 1.1 mm versus 1.8 ± 1.5 mm, respectively; P < 0.05). Conclusions: MMPRTs increase the MTE-MFC distance and decrease the MJS width, with these measurements correlating to the MME. Therefore, measurement of the MTE-MFC distance and MJS width on the Rosenberg view could be a useful preliminary method for the diagnosis of an MMPRT.

T cells play central roles in liver diseases, but the regulatory mechanism by cytokine signaling is not well understood. In the present study, we explored the role of SOCS3 in T cells in concanavalin A (ConA)-induced hepatitis. Mice with T-cell-specific overexpression of SOCS3 (SOCS3-cTg) showed reduced hepatic damage and improved mice survival relative to the control, an event that was associated with decreased apoptotic signals Fas and pStat1. Expression of Th1-cytokines/chemokines was decreased in SOCS3-cTg liver with reduced expression of T-bet, a Th1-transcription factor. Flow cytometric analysis of the liver lymphocytes demonstrated that activated CD4(+) T cells, cytotoxic T cells and natural killer T cells were significantly decreased in SOCS3-cTg liver with decreased expression of perforin and granzyme B, injurious molecules for hepatocyte damage. These results suggest that forced expression of SOCS3 in T cells prevents ConA-induced liver injury by inhibiting several phases of Th1 responses.

Time-SLIP permits observation of CSF motion over a long period of time and detects patterns of flow velocity and direction. Thus, this novel approach to CSF flow analysis can be used to gain a more extensive understanding of spinal disease pathology and to optimize surgical access in the treatment of spinal lesions. Additionally, Time-SLIP has broad applicability in the field of spinal research.

Continuous hemodiafiltration using a hemofilter made from a membrane with cytokine adsorption properties is thought to be effective to remove cytokines in septic patients. In order to enhance cytokine removal capacity by increasing adsorption area, we devised a double polymethyl methacrylate continuous hemodiafiltration method, which involves serial connection of two polymethyl methacrylate membrane hemofilters, and we report clinical efficacy with this method. Of 74 patients who underwent continuous hemodiafiltration and had interleukin-6 blood levels measured during their ICU stay between March 2010 and June 2012, 13 patients with hypercytokinemia (interleukin-6 blood level >900 pg/mL) underwent series double continuous hemodiafiltration to be treated for hypercytokinemia. Cytokine reduction rate and clinical efficacy were compared between those 13 patients and those with a similar pathological condition who underwent continuous hemodiafiltration using the single polymethyl methacrylate membrane hemofilter. Interleukin-6 blood levels 6 h after continuous hemodiafiltration initiation increased in the single continuous hemodiafiltration group from 17040 ± 33660 pg/mL to 26290 ± 66250 pg/mL; however, interleukin-6 blood level significantly decreased in the series double continuous hemodiafiltration group from 20220 ± 29120 pg/mL to 6790 ± 10820 pg/mL. Interleukin-6 reduction rate during the period between initiation and 6 h after initiation of continuous hemodiafiltration was significantly higher in the series double continuous hemodiafiltration group(63.5 ± 38.9%) compared to that of the single continuous hemodiafiltration group (-342 ± 1306%)(P = 0.039). Series double continuous hemodiafiltration using two polymethyl methacrylate hemofilters with cytokine adsorbing capacity is effective to remove cytokine in hypercytokinemic septic patients.

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The regulatory mechanism behind T cell-mediated liver injury is not fully elucidated. Here, we demonstrate that forced expression of SOCS3 in T cells protects mice from a T cell dependent concanavalin A (ConA)-induced hepatitis. Mice with a T cell specific overexpression of SOCS3 (SOCS3-cTg) were resistant to ConA-hepatitis, as evidenced by decreased serum ALT level, reduced hepatic damage and improved mice survival relative to the control. Hepatic expression of T-bet, a Th1-specific transcription factor, was decreased in SOCS3-cTg liver relative to the control with the reduced expressions of Th1 associated cytokines (TNFa, IL-12, IFNg) and chemokines (CXCL9/10). Flow cytometric analysis of isolated hepatic lymphocytes demonstrated that activated CD4+T cells, cytotoxic T (Tc) cells and natural killer T (NKT) cells were significantly decreased in SOCS3-cTg liver. Expression of perforin and granzyme B, injurious molecules produced from Tc and NKT cells, was reduced in SOCS3-cTg liver. These results indicate that forced expression of SOCS3 in T cells prevents ConA-induced liver injury by inhibiting Th1 responses. SOCS3 delivery in T cells may be therapeutic strategy in T cell-mediated liver injury. Financial support: Grants-in-Aid from The Ministry of Education, Science, Sports and Culture, and The Ministry of Health and Welfare, Japan,