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101.
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Lesions that contain abundant benign myoepithelial cells, including pleomorphic adenomas of salivary gland origin, may present a diagnostic challenge in fine‐needle aspiration (FNA) specimens. Benign metastasizing pleomorphic adenoma is a rare neoplasm, in which the benign appearing pleomorphic adenoma, without any histological evidence of malignancy, metastasizes to distant sites including lung. In the absence of clinical history of a pre‐existing myoepithelial neoplasm, the presence of myoepithelial cells in the lung or any other organs besides salivary glands may create diagnostic difficulty. Here we present the cytologic findings of such a metastatic tumor found in the lung FNA and pleural fluid specimens from a 64‐year‐old woman, with a history of local recurrent salivary gland pleomorphic adenomas, who presented with multiple bilateral pulmonary nodules and pleural effusion. The diagnosis of benign metastasizing pleomorphic adenoma was made based on clinical information and cytomorphology, and confirmed by immunocytochemistry. Diagn. Cytopathol. 2009. © 2009 Wiley‐Liss, Inc.  相似文献   
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Corneal neovascularization is one of the leading causes of blindness. The aim of this study was to evaluate the pro-angiogenic role of corneal fibroblast-derived membrane type-1 matrix metalloproteinase (MT1-MMP) on basic fibroblast growth factor (bFGF)-induced corneal neovascularization in vivo and in vitro. Immunohistochemical studies demonstrated that MT1-MMP was expressed in keratocytes and immortalized corneal fibroblast cell lines. Vascular endothelial growth factor protein levels were increased after bFGF-stimulation of wild-type fibroblast cells compared with MT1-MMP knockout fibroblast cells. Corneal vascularization was significantly increased after a combination of bFGF pellet implantation and naked MT1-MMP DNA injection in wild-type mouse corneas compared with either bFGF pellet implantation or naked MT1-MMP DNA-injected corneas. Western blotting analysis of the phosphorylation levels of the key signaling molecules (p38, JNK, and ERK) demonstrated that phosphorylation levels of both p38 and JNK were diminished after bFGF stimulation of MT1-MMP knockout cells compared with wild-type and MT1-MMP knockin cells. These results suggest that MT1-MMP potentiates bFGF-induced corneal neovascularization, likely by modulating the bFGF signal transduction pathway.The cornea is typically avascular in its normal state. However, corneal neovascularization (NV) occurs in conjunction with several corneal diseases such as infection, injury, and autoimmune reactions and is one of the leading causes of blindness. Recent studies have identified several tyrosine kinases and their corresponding ligands that mediate NV, including basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF).1,2,3bFGF was first identified as a pro-angiogenic factor and is studied extensively in corneal NV models because it is thought to be a major factor in the induction of corneal NV.4,5,6 bFGF is secreted by corneal epithelial cells, stromal fibroblasts, and endothelial cells, and is localized to the corneal extracellular matrix.7 Low levels of bFGF are produced in unwounded corneas; however, enhanced bFGF production was detected in corneal epithelial cells after injury.8 VEGF was also shown to promote NV in corneal wounding models,9 and cross talk is thought to occur between bFGF and VEGF during corneal NV. For example, bFGF was shown to induce corneal NV by activating the VEGF/VEGFR system10,11 and the systemic administration of anti-VEGF-A neutralizing antibodies dramatically reduces this effect.12Membrane type-1 matrix metalloproteinase (MT1-MMP) is the first transmembrane-containing matrix metalloproteinase to be identified.13 Based on previous reports using corneal wound-healing models, MT1-MMP mRNA is mainly localized to the corneal stroma.14 During NV, quiescent endothelial cells are activated and migration is facilitated by degrading the extracellular matrix through the action of specific proteases, including MT1-MMP.15,16,17 The importance of the enzymatic function of MT1-MMP in corneal NV was shown using the corneal pocket assay in MT1-MMP-deficient mice.18 Interestingly, the expression of MT1-MMP is up-regulated by bFGF stimulation in prostate carcinoma cell lines,19 and it was also reported that MT1-MMP promotes VEGF secretion.20,21,22,23,24,25In this study, we developed anti-MT1-MMP antibody to localize and characterize MT1-MMP protein in the mouse cornea. To assess the relationship between MT1-MMP and bFGF during corneal NV, we performed experiments that combined the corneal pocket assay using a bFGF pellet with the injection of naked MT1-MMP DNA. We observed an enhanced phosphorylation of MAP kinases in wild-type and MT1-MMP knockin (KI) cell lines over that of MT1-MMP knockout (KO) cell lines, suggesting a role of MT1-MMP in modulating bFGF-mediated signal transduction pathways.  相似文献   
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Background: Treatment of anaemia in renal‐insufficient patients relies on the use of an erythropoiesis‐stimulating agent (ESA). This study aimed to compare the impact of two different strategies of ESA prescribing on variation in haemoglobin (Hb) concentration in end‐stage renal disease (ESRD) patients. Methods: Patients with ESRD, on haemodialysis, and who had received ESA for >3 months were recruited. Different parameters were analysed: demographics, Hb level the last day of the year before dialysis, the most recent weekly ESA dose, risk factors for resistance and cost. Each institution continued its local practice for achieving the desired Hb level: increasing the ESA dose to overcome resistance in one centre and defining an upper ESA‐dose limit in the other. Results: A total of 185 patients were recruited. No significant differences in the biological parameters were found between the two populations. In both centres, Hb levels were comparable and mean levels exceeded 11 g/dL, despite the higher ESA doses given in one centre to achieve this target. This finding also held true for the subgroups with greater than or equal to two resistance factors. These two strategies led to large between‐centre differences in treatment costs. Conclusion: The ESA‐use strategy difference probably indicates that erythropoietin‐resistance was not overcome with increased dosing. The Hb concentrations remained stable even when ESA doses were increased. On current evidence, the cheaper ESA‐dose limitation strategy is preferable but randomized controlled studies, including comparisons of alternative ESA formulations are necessary.  相似文献   
108.
Susan Azar  Amisha Ramjiani  Jay A Van Gerpen 《Movement disorders》2005,20(4):513-4; author reply 514
A reply to this letter has been published in Movement Disorders Mov Disord (2005) 20 (4) 514 .  相似文献   
109.
Rehabilitation after an injury or surgery to the elbow joint complex is common when treating the overhead throwingathlete. The unique anatomical configuration of the elbow joint complex provides a significant challenge to the sports medicine team in rehabilitating throwers after elbow surgery. The programs discussed in this report emphasize immediate controlled motion following surgery and the importance of establishing full elbow extension as expeditiously as possible. This to prevent a frequently encountered side effect of elbow surgery, a flexion contracture. A strengthening program is initiated immediately after surgery in the form of isometrics. The strengthening program is progressed from isometrics to isotonics, then to an advanced strengthening phase consisting of plyometrics, neuromuscular control drills, proprioceptive training, and high speed muscle training. The advanced strengthening phase is instituted to train the throwing athlete to control the potentially harmful stresses imparted onto the elbow joint during the throwing motion. A functional progression for the overhead thrower is discussed. In this report, we will discuss postoperative rehabilitation following elbow arthroscopy, ulnar collateral ligament reconstruction, arthroscopic arthroplasty, uInar nerve subcutaneous transposition, and arthroscopic arthrolysis.  相似文献   
110.
To define the role of nurse and pup strain (spontaneously hypertensive rats: SHR nurses and shr pups; Wistar-Kyoto rats: WKY nurses and wky pups) and dietary salt in nurses and pups (low salt and high salt) upon pup body weight and blood pressure, we cross-suckled shr and wky from birth. Nurses after delivery and pups after weaning received either low- or high-salt diets. Pup body weight indicated that WKY dams were better nurses than SHR and that high salt in the nurse and pup diet decreased body weight. At 7 days, WKY on a low-salt diet normalized shr blood pressure and SHR on a high-salt diet reduced shr blood pressure. At 100 days, pup strain strongly affected blood pressure. Salt sensitivity to pup dietary salt depended upon a low-salt diet in nurses. Salt resistance depended on a high-salt diet in WKY nurses. At 300 days, pup strain accounted for most of the blood pressure variability. However, pup diet, pup strain and nurse diet also affected blood pressure (P = 0.05); the blood pressure of shr on a high-salt diet was higher if the nurse was an SHR on a high-salt diet. Thus, nurse environment modulated shr hypertension throughout life.  相似文献   
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