60 research outputs found

    Hemi-Castaing ligamentoplasty for the treatment of chronic lateral ankle instability: a retrospective assessment of outcome

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    Purpose: In the treatment of chronic ankle instability, most non-anatomical reconstructions use the peroneus brevis tendon. This, however, sacrifices the natural ankle stabilising properties of the peroneus brevis muscle. The aim of this study was to evaluate the functional outcome of patients treated with a hemi-Castaing procedure, which uses only half the peroneus brevis tendon. Methods: We performed a retrospective cohort study of patients who underwent hemi-Castaing ligamentoplasty for chronic lateral ankle instability between 1993 and 2010, with a minimum of one year follow-up. Patients were sent a postal questionnaire comprising five validated outcome measures: Olerud-Molander Ankle Score (OMAS), Karlsson Ankle Functional Score (KAFS), Tegner Activity Level Score (pre-injury, prior to surgery, at follow-up), visual analog scale on pain (VAS) and the Short Form 36 (SF-36). Results: Twenty patients completed the questionnaire on functional outcome. The OMAS showed good to excellent outcome in 80% and the KAFS in 65%, the Tegner Score improved from surgery but did not reach pre-injury levels, the VAS on pain was 1 of 10 and the SF-36 returned to normal compared with the average population. Conclusions: Even though most patients were satisfied with the results, outcome at long-term follow-up was less favourable compared with the literature on anatomical reconstructions. In accordance with the literature, we therefore conclude that the initial surgical treatment of chronic lateral ankle instability should be an anatomical repair with augmentation (i.e. the Broström-Gould technique) and the non-anatomical repair should be reserved for unsuccessful cases after anatomical repair or in cases where no adequate ligament remnants are available for reconstruction

    Shiga Toxin 1 Induces on Lipopolysaccharide-Treated Astrocytes the Release of Tumor Necrosis Factor-alpha that Alter Brain-Like Endothelium Integrity

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    The hemolytic uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia and renal dysfunction. The typical form of HUS is generally associated with infections by Gram-negative Shiga toxin (Stx)-producing Escherichia coli (STEC). Endothelial dysfunction induced by Stx is central, but bacterial lipopolysaccharide (LPS) and neutrophils (PMN) contribute to the pathophysiology. Although renal failure is characteristic of this syndrome, neurological complications occur in severe cases and is usually associated with death. Impaired blood-brain barrier (BBB) is associated with damage to cerebral endothelial cells (ECs) that comprise the BBB. Astrocytes (ASTs) are inflammatory cells in the brain and determine the BBB function. ASTs are in close proximity to ECs, hence the study of the effects of Stx1 and LPS on ASTs, and the influence of their response on ECs is essential. We have previously demonstrated that Stx1 and LPS induced activation of rat ASTs and the release of inflammatory factors such as TNF-α, nitric oxide and chemokines. Here, we demonstrate that rat ASTs-derived factors alter permeability of ECs with brain properties (HUVECd); suggesting that functional properties of BBB could also be affected. Additionally, these factors activate HUVECd and render them into a proagregant state promoting PMN and platelets adhesion. Moreover, these effects were dependent on ASTs secreted-TNF-α. Stx1 and LPS-induced ASTs response could influence brain ECs integrity and BBB function once Stx and factors associated to the STEC infection reach the brain parenchyma and therefore contribute to the development of the neuropathology observed in HUS

    Paramagnetic and fluorescent liposomes for target-specific imaging and therapy of tumor angiogenesis

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    Angiogenesis is essential for tumor growth and metastatic potential and for that reason considered an important target for tumor treatment. Noninvasive imaging technologies, capable of visualizing tumor angiogenesis and evaluating the efficacy of angiostatic therapies, are therefore becoming increasingly important. Among the various imaging modalities, magnetic resonance imaging (MRI) is characterized by a superb spatial resolution and anatomical soft-tissue contrast. Revolutionary advances in contrast agent chemistry have delivered versatile angiogenesis-specific molecular MRI contrast agents. In this paper, we review recent advances in the preclinical application of paramagnetic and fluorescent liposomes for noninvasive visualization of the molecular processes involved in tumor angiogenesis. This liposomal contrast agent platform can be prepared with a high payload of contrast generating material, thereby facilitating its detection, and is equipped with one or more types of targeting ligands for binding to specific molecules expressed at the angiogenic site. Multimodal liposomes endowed with contrast material for complementary imaging technologies, e.g., MRI and optical, can be exploited to gain important preclinical insights into the mechanisms of binding and accumulation at angiogenic vascular endothelium and to corroborate the in vivo findings. Interestingly, liposomes can be designed to contain angiostatic therapeutics, allowing for image-supervised drug delivery and subsequent monitoring of therapeutic efficacy

    Successful and unsuccessful approaches to imaging carcinoids: Comparison of a radiolabelled tryptophan hydroxylase inhibitor with a tracer of biogenic amine uptake and storage, and a somatostatin analogue

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    A mouse mastocytoma model was used to determine the biodistribution and tumour uptake of four radiopharmaceuticals developed to target the serotonin synthetic pathway in carcinoid tumours. Three of the compounds were competitive inhibitors of the rate-limiting enzyme of serotonin synthesis, tryptophan hydroxylase. Radiolabelled iodo- dl -phenylalanine (iodine-131 PIPA) was found to have the highest uptake and tumourto-liver ratio. Four patients with known carcinoid tumours were then injected with 0.5 mCi 131 I-PIPA and imaged at 1, 4, 24 and 48 h post-injection. The radiopharmaceutical, however, failed to localize in the known tumour sites. This result was in contrast to the authors' experience of 131 I- and 123 I-MIBG imaging of carcinoid tumours. Seven patients with known metastatic carcinoid tumours, two patients with symptoms of recurrence following tumour resection, one patient with completely resected disease, and two patients with a flushing syndrome of uncertain aetiology were studied with 131 I-MIBG. Three of the seven patients with known metastatic disease had positive 131 I-MIBG scans. Both patients with clinical evidence of recurrent disease had negative scans, as did the patient who was considered to have had complete resection of her primary tumour. The two patients with idiopathic flushing syndrome also had negative scans. Among seven patients imaged with 123 I-MIBG there were four true-negative scans and one falsenegative, the latter in a patient with biochemical and CT evidence of recurrence. In a seventh patient with distant metastases there was variable uptake in some of the lesions. Four patients were studied with indium-111 penetetreodide. Two patients with metastatic carcinoid disease had positive scans, although hepatic metastases were not seen in one. Another two with idiopathic flushing syndrome had normal studies. The literature suggests that up 50% of carcinoid tumour cases are detected with 131 I-MIBG, compared to a sensitivity of 87% reported with somatostatin receptor imaging using 111 In-pentetreotide. The experience with 123 I-MIBG is much less extensive. The mechanisms of carcinoid tumour localization for each of the three classes of radiotracers are discussed and contrasted to their varying sensitivities. The relative success of 131 I-MIBG and 111 In-pentetreotide relative to 131 I-PIPA may be related to the fact that 131 I-MIBG is actively taken up and stored by the enterochromaffin cells of the tumours and 111 In-pentetreotide binds to cell surface receptors, whereas 131 I-PIPA binds to tryptophan hydroxylase, which may be present in quantities too small to permit tumours to be imaged.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46840/1/259_2005_Article_BF01731835.pd
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