54 research outputs found

    Central defect type partial ACL injury model on goat knees: the effect of infrapatellar fat pad excision

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    BACKGROUND: The mid-substance central defect injury has been used to investigate the primary healing capacity of the anterior cruciate ligament (ACL) in a goat model. The sagittal plane stability on this model has not been confirmed, and possible effects of fat pad excision on healing have not been evaluated. We hypothesize that excising the fat pad tissue results in poorer ligament healing as assessed histologically and decreased tensile strength of the healing ligament. We further hypothesize that the creation of a central defect does not affect sagittal plane knee stability. METHODS: A mid-substance central defect was created with a 4-mm arthroscopic punch in the ACLs of right knees of all the subjects through a medial mini-arthrotomy. Goats were assigned to groups based on whether the fat pad was preserved (group 1, n = 5) or excised completely (group 2, n = 5). The left knees served as controls in each goat. Histopathology of the defect area along with measurement of type I collagen in one goat from each group were performed at 10th week postoperatively. The remaining knees were evaluated biomechanically at the 12th week, by measuring anterior tibial translation (ATT) of the knee joints at 90° of flexion and testing tensile properties (ultimate tensile load (UTL), ultimate elongation (UE), stiffness (S), failure mode (FM)) of the femur-ACL-tibia complex. RESULTS AND DISCUSSION: Histopathology analysis revealed that the central defect area was fully filled macroscopically and microscopically. However, myxoid degeneration and fibrosis were observed in group 2 and increased collagen type I content was noted in group 2. There were no significant differences within and between groups in terms of ATT values (p = 0.715 and p = 0.149, respectively). There were no significance between or within groups in terms of ultimate tensile load and ultimate elongation; however, group 2 demonstrated greater stiffness than group 1 that was correlated with the fibrotic changes detected microscopically (p = 0.043). CONCLUSIONS: The central defect type injury model was confirmed to be biomechanically stable in a goat model. Resection of the fat pad was noted to negatively affect defect healing and increase ligament stiffness in the central defect injury model

    Digitally reinforced hematoxylin-eosin polarization technique in diagnosis of rectal amyloidosis

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    Perianal fibroadenoma, case report

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    WOS: 000252515600019PubMed ID: 18212553Extramammary fibroadenomas, occurring in the anogenital region, are rare lesions thought to be arising from "mammary-like anogenital sweet glands" described by van der Putte. We present a 42-year-old woman with a slow-growing, 4-cm, well-circumscribed but nonencapsulated mass in perianal region. The cut surface of the lesion was bulging, gray-white, and slightly lobulated. Microscopically, it was identical to mammary fibroadenoma and composed of concurrent glandular and stromal elements. Low columnar or cuboidal cells with focal, apical cytoplasmic snouts lined the glands, whereas the underlying layer had myoepithelial cell features, expressing smooth muscle actin and S-100. Epithelial component was immunoreactive for human milk fat globulin I. Progesterone receptor positivity was 80%, whereas the estrogen receptor expression was 60%. Gross cystic disease fluid protein and human milk fat globulin 11 were negative. The case is presented to increase the awareness on mammary-like glands of anogenital region, which may give rise to not only fibroadenomas but also fibrocystic disease, phyllodes tumor, carcinoma in situ, invasive carcinoma and lactating adenoma, hidrocystoma, hidradenoma papilliferum, intraductal papilloma, and sclerosing adenosis, although very rare

    Histopathological Findings in Gastrointestinal Tractus in Patients with Common Variable Immunodeficiency (CVID)

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    105th Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology -- MAR 12-18, 2016 -- Seattle, WAWOS: 000370302501250US & Canadian Acad Patho
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