Background: Treatment of osteonecrosis of the talus is challenging. Total talar replacement has the potential to restore the function of the ankle joint without an associated leg-length discrepancy. The purpose of the present study was to investigate postoperative function and pain after total talar replacement in patients with osteonecrosis of the talus.Methods: Fifty-five ankles in fifty-one consecutive patients with osteonecrosis of the talus who were treated with a total talar replacement from 2005 to 2012 were included in the investigation. Scores according to the Japanese Society for Surgery of the Foot (JSSF) ankle-hindfoot scale and the Ankle Osteoarthritis Scale (AOS) were assessed before surgery and at the final follow-up evaluation.Results: According to the JSSF ankle-hindfoot scale, the score for pain improved from a mean (and standard deviation) of 15 ± 9.4 points (range, 0 to 20 points) to 34 ± 5.6 points (range, 20 to 40 points); the score for function, from 21.2 ± 9.7 points (range, 4 to 38 points) to 45.1 ± 4.0 points (range, 37 to 50 points); the score for alignment, from 6.0 ± 2.8 points (range, 5 to 10 points) to 9.8 ± 0.9 points (range, 5 to 10 points); and the total score, from 43.1 ± 17.0 points (range, 11 to 68 points) to 89.4 ± 8.4 points (range, 76 to 100 points). According to the AOS scale, the score for "pain at its worst" improved from a mean of 6.1 ± 3.3 points (range, 0 to 9.9 points) to 2.0 ± 1.7 points (range, 0 to 6.3 points).Conclusions: Prosthetic talar replacement is a useful procedure for patients with osteonecrosis of the talus as it maintains ankle function.
We originally cloned and identified murine Zizimin2 (Ziz2, Dock11) as a guanine nucleotide exchange factor (GEF) for Cdc42 and demonstrated that it activated the formation of filopodia. Since its expression pattern is restricted in immune tissues and Rho GTPases such as Cdc42 function in B cell development and immune responses, we expected Ziz2 to also be associated with B cell development and immune responses. However, the function of Ziz2 has not yet been fully examined in vivo. We also recently discovered that Ziz2 expression levels in immune tissues were reduced with aging in the mouse, suggesting that its expression is also associated with the mechanisms of immuno-senescence.To gain insights into the mechanisms underlying immuno-senescence, we generated Ziz2 knock out (KO) mice and examined the functions of Ziz2 in B cell development and immune responses. We also obtained Zizimin3 (Ziz3; Dock10) KO mice and examined the functions of Ziz3.The results revealed that Ziz2 KO mice had a higher percentage of early bone marrow B cells (Fraction A), but a reduced fraction of marginal zone (MZ) B cells. In addition, an examination of B cell-specific Ziz2 KO mice revealed that Ziz2 was intrinsically required for MZ B cell development, but not for mature follicular B cells. However, immune responses against NP-CGG (T cell-dependent), TNP-LPS (T cell-independent, TI, type I), and TNP-Ficoll (TI, type II) were not altered in KO mice. We finally demonstrated that CD1d-positive MZ B cell region outside CD169-positive marginal metallophilic macrophages (MMM) was narrowed in Ziz2 KO mice. Furthermore, MMM morphology appeared to be altered in Ziz2 KO mice.In conclusion, we herein showed that Ziz2 was associated with early bone marrow B cell development, MZ B cell formation, MZ B number/localization around MZ, and MMM morphology which may explain in part the mechanism underlying immuno-senescence.Electronic supplementary materialThe online version of this article (doi:10.1186/s12979-015-0028-x) contains supplementary material, which is available to authorized users.
IntroductionEndothelial progenitor cells (EPCs) play a critical role in restoration of ischemic diseases. However, the actual status of EPC development and the mechanisms of EPC dysfunctions in patients with various ischemic diseases remain unknown.MethodsTo investigate the detailed function of EPCs in experimental murine models, we have established an EPC colony forming assay (EPC-CFA) in murine EPCs. The abilities of murine EPCs in differentiation, adhesive capacity, proliferative potency, and transplantation in vitro and in vivo were then examined.ResultsPeripheral blood mononuclear cells (PB-MNCs), bone marrow mononuclear cells (BM-MNCs) or bone marrow c-Kit+/Sca-1+ lineage negative (BM-KSL) cells differentiated into two types of EPC colony forming units (EPC-CFUs), large sized EPC (large-EPC)-CFUs and small sized EPC (small-EPC)-CFUs. Gene expression analysis demonstrated that both EPC-CFU-derived cells expressed eNOS, Flk-1 and VE-cadherin, markers of endothelial cells (ECs), although the small-EPCs derived from small-EPC-CFU were higher in number and showed more immature features (higher population of KSL cells). Functionally, the large-EPCs derived from large-EPC-CFU had higher adhesive capacity but lower proliferative potency than small-EPCs, showing improved tubular forming capacity and incorporation potency into primary EC-derived tube formation. Importantly, hindlimb ischemia increased the frequencies of large-EPC-CFUs differentiated from PB-MNCs and bone marrow. Actually, transplantation of large-EPCs into ischemic hindlimb enhanced neovascularization in hindlimb ischemia model, although small-EPCs or murine ECs did not, suggesting that large-EPC-CFUs might play an important role in restoration of ischemic diseases.ConclusionsWe demonstrated, using a murine ischemia model, that the EPC-CFA could be a useful way to investigate the differentiation levels of murine EPCs, further providing a crucial clue that large-EPC-CFU status may be more functional or effective EPCs to promote neovascularization.
The 3-layered cell-sheet improved cardiac function associated with angiogenic and anti-fibrotic effects. Thus, CSC is a promising cell-source to use with the cell-sheet method for the treatment of cardiac failure, as long as a sufficient number of cells are delivered.
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