70 research outputs found

    A giant plexiform schwannoma of the brachial plexus: case report

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    We report the case of a patient who noticed muscle weakness in his left arm 5 years earlier. On examination, a biloculate mass was observed in the left supraclavicular area, and Tinel's sign caused paresthesia in his left arm. Magnetic resonance imaging showed a continuous, multinodular, plexiform tumor from the left C5 to C7 nerve root along the course of the brachial plexus to the left brachia. Tumor excision was attempted. The median and musculocutaneous nerves were extremely enlarged by the tumor, which was approximately 40 cm in length, and showed no response to electric stimulation. We resected a part of the musculocutaneous nerve for biopsy and performed latissimus dorsi muscle transposition in order to repair elbow flexion. Morphologically, the tumor consisted of typical Antoni A areas, and immunohistochemistry revealed a Schwann cell origin of the tumor cells moreover, there was no sign of axon differentiation in the tumor. Therefore, the final diagnosis of plexiform Schwannoma was confirmed

    Enhanced wound healing associated with Sharpey’s fiber-like tissue formation around FGF-2-apatite composite layers on percutaneous titanium screws in rabbits

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    BACKGROUND:Pin-tract infections are the most common complications of external fixation. To solve the problem, we developed a fibroblast growth factor-2 (FGF-2)-apatite composite layer for coating titanium screws. The purpose of this study was to elucidate the mechanism of the improvement in infection resistance associated with FGF-2-apatite composite layers.METHOD:We analyzed FGF-2 release from the FGF-2-apatite composite layer and the mitogenic activity of the FGF-2-apatite composite layer. We evaluated time-dependent development of macroscopic pin-tract infection around uncoated titanium control screws (n = 10). Screws coated with the apatite layer (n = 16) and FGF-2-apatite composite layer (n = 16) were percutaneously implanted for 4 weeks in the medial proximal tibia in rabbits.RESULTS:A FGF-2-apatite composite layer coated on the screws led to the retention of the mitogenic activity of FGF-2. FGF-2 was released from the FGF-2-apatite composite layer in vitro for at least 4 days, which corresponds to a period when 30% of pin-tract infections develop macroscopically in the percutaneous implantation of uncoated titanium control screws. The macroscopic infection rate increased with time, reaching a plateau of 80-90% within 12 days. This value remained unchanged until 4 weeks after implantation. The screws coated with an FGF-2-apatite composite layer showed a significantly higher wound healing rate than those coated with an apatite layer (31.25 vs. 6.25%, p < 0.05). The interfacial soft tissue that bonded to the FGF-2-apatite composite layer is a Sharpey\u27s fiber-like tissue, where collagen fibers are inclined at angles from 30 to 40° to the screw surface. The Sharpey\u27s Wber-like tissue is rich in blood vessels and directly bonds to the FGF-2-apatite composite layer via a thin cell monolayer (0.8-1.7 μm thick).CONCLUSION:It is suggested that the enhanced wound healing associated with the formation of Sharpey\u27s fiber-like tissue triggered by FGF-2 released from the FGF-2-apatite composite layer leads to the reduction in the pin-tract inflammation rate

    Cell death and cell proliferation in cartilage layers in human anterior cruciate ligament tibial insertions after rupture

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    The purpose of this study is to investigate cellular responses and histological changes of cartilaginous layers in human anterior cruciate ligament (ACL) tibial insertions after rupture compared with those in normal insertions. Fully 16 tibial insertions of ruptured ACLs were obtained during primary ACL reconstructions. We also obtained 16 normal ACL tibial insertions from cadavers. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) to detect apoptosis, proliferating cell nuclear antigen (PCNA) staining, and histological examination were performed. The percentage of TUNEL-positive chondrocytes in ruptured ACL insertions (30.2 ± 15.6%) was higher than that in normal insertions (9.6 ± 5.8%). The percentage of PCNA-positive chondrocytes was significantly different between ruptured ACL insertions (19.9 ± 15.0%) and normal insertions (12.3 ± 7.3%). The average thickness of the cartilage layer, the glycosaminoglycan-stained area, and the number of chondrocytes per millimeter in ruptured ACL insertions was smaller than those in normal insertions. The decrease in the number of chondrocytes owing to an imbalance between cell death and cell proliferation in the ACL insertions after rupture, as compared with normal insertions, may lead to histological changes of the cartilage layer in the insertions. An in-depth understanding of injured ACL insertion may help elucidate the etiology of histological changes and the function and significance of the existence of the cartilage layer of insertion. This understanding may help in developing optimal treatment protocols for ACL injuries if apoptosis and cell proliferation are controlled

    Correlation of histopathology with magnetic resonance imaging in Kienböck disease.

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    PURPOSE:Diagnosis and treatment remain controversial for Kienböck disease. A few reports have correlated magnetic resonance imaging (MRI), which is essential for early diagnosis, and histopathology of Kienböck biopsy specimens, but histopathological correlations of whole lunate bones or histological slices compared with MRI images are lacking. The purpose of this study was to compare presurgical MRI scans with corresponding histological slices of Kienböck-diseased lunates.METHODS:We excised whole lunates at the time of surgery from 6 patients with Kienböck disease (stage IIIB) undergoing tendon-ball replacement or a Graner procedure. We stained paraffin-embedded, coronally sectioned specimens with hematoxylin-eosin and compared them with presurgical coronal scans using MRI with a 47-mm microscopy surface coil.RESULTS:Toward the center of the lunates, the signal intensity in the proton density-weighted images was reduced, whereas the dorsal and palmar sides of the lunates exhibited no changes in intensity. In correlation, histopathological findings revealed strongly disrupted trabeculae toward the center of the lunates and intact trabeculae in the dorsal side of the lunates. Likewise, the necrotic and vitalized bone exhibited low and high signal intensities, respectively, in the proton density-weighted images; however, in the fast-field echo images, there were no correlations with histopathological observations.CONCLUSIONS:Proton density-weighted MRIs but not fast-field echo images using a 47-mm microscopy coil reflected the extent and localization of the necrotic area in Kienböck-diseased lunates, as evidenced by comparison with histological analyses of the lunate specimens.CLINICAL RELEVANCE:Proton density-weighted MRIs accurately reflect the vascular status of the lunate and may help plan treatment on a case-by-case basis
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