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AIMS: Prescribing for athletes requires an up-to-date knowledge of the World Anti-Doping Agency's list of prohibited substances. As the London 2012 Olympic Games attract athletes from around the world, we review the current guidelines with respect to all medications licensed for ophthalmic use in the United Kingdom. We describe the process that an ophthalmologist can use to check for permissible medications and also highlight treatments that are contraindicated. METHODS: We systematically reviewed all 77 drugs listed in Section 11 of the British National Formulary (Issue 63) for use in the treatment of ophthalmic conditions, and referenced these against the 2012 Prohibited List published by the World Anti-Doping Agency. RESULTS: The majority of ophthalmic preparations are suitable for use in- and out-of-competition. Some preparations, such as glucocorticoids, are prohibited when administered systemically but permitted for topical administration. Beta-blockers are prohibited in-competition and oral carbonic anhydrase inhibitors are prohibited in- and out-of competition. CONCLUSION: The 2012 Prohibited List has important implications for the pharmacological treatment of ophthalmic conditions in athletes. Clinicians prescribing for athletes have a duty to familiarize themselves with the list in order to avoid causing significant damage to their patient's career and reputation.

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BACKGROUND: Inducible nitric oxide synthase (nitric oxide synthase 2, NOS 2) inhibition significantly suppresses chronically ischaemic skin flap survival, possibly because of reduced angiogenesis. OBJECTIVES: To investigate the effect of genetic NOS 2 inhibition on cutaneous wound angiogenesis in two in vivo murine models. The impact of NOS 2 manipulation on vascular endothelial growth factor (VEGF)-A stimulated and fibroblast growth factor (FGF)-2 stimulated angiogenesis was also investigated in the Matrigel(®) plug assay. METHODS: (i) Matrigel plugs/incisional wounds: two groups of NOS 2-/- mice and two groups of wild-type (WT) mice had bilateral Matrigel plugs containing 500 ng mL(-1) VEGF-A or 1000 ng mL(-1) FGF-2 injected subcutaneously in the abdomen. A 2·5 cm long dorsal incisional skin wound was created and sutured closed in the same animals. Wounds and plugs were explored at 7 or 12 days. (ii) Excisional wounds: dorsal 0·5 × 1·0 cm excisional skin wounds were created in four groups (two NOS 2-/- and two WT) and explored at 7 or 14 days. Wounds and Matrigel plugs were examined histologically and morphometrically for determination of percentage vascular volume (PVV). RESULTS: The PVV in NOS 2-/- incisional wounds and excisional wounds was significantly less than in WT wounds (P = 0·05 and P < 0·001, respectively). The PVV was significantly less in VEGF-A stimulated Matrigel plugs compared with FGF-2 stimulated plugs in NOS 2-/- mice (P < 0·01), but not in WT mice. CONCLUSIONS: NOS 2 is significantly involved in angiogenic signalling in healing skin wounds, particularly within the first 7 days. However, Matrigel plug vascularization suggests that the role of NOS 2 in angiogenesis is related to VEGF-A but not FGF-2 stimulated angiogenesis.

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OBJECTIVE: To investigate the potential of inflammation to induce new adipose tissue formation in the in vivo environment. METHODS AND RESULTS: Using an established model of in vivo adipogenesis, a silicone chamber containing a Matrigel and fibroblast growth factor 2 (1 microg/ml) matrix was implanted into each groin of an adult male C57Bl6 mouse and vascularized with the inferior epigastric vessels. Sterile inflammation was induced in one of the two chambers by suspending Zymosan-A (ZA) (200-0.02 microg/ml) in the matrix at implantation. Adipose tissue formation was assessed at 6, 8, 12 and 24 weeks. ZA induced significant adipogenesis in an inverse dose-dependent manner (P<0.001). At 6 weeks adipose tissue formation was greatest with the lowest concentrations of ZA and least with the highest. Adipogenesis occurred both locally in the chamber containing ZA and in the ZA-free chamber in the contralateral groin of the same animal. ZA induced a systemic inflammatory response characterized by elevated serum tumour necrosis factor-alpha levels at early time points. Aminoguanidine (40 microg/ml) inhibited the adipogenic response to ZA-induced inflammation. Adipose tissue formed in response to ZA remained stable for 24 weeks, even when exposed to the normal tissue environment. CONCLUSIONS: These results demonstrate that inflammation can drive neo-adipogenesis in vivo. This suggests the existence of a positive feedback mechanism in obesity, whereby the state of chronic, low-grade inflammation, characteristic of the condition, may promote further adipogenesis. The mobilization and recruitment of a circulating population of adipose precursor cells is likely to be implicated in this mechanism.

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