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Eye globe enucleation due to other than amalignant tumor is very rare today. Solitary intraocular neurofibroma without other signs of neurofibromatosis is arare benign tumor and few cases have been reported to date.
In 10 year interval from Jan 1 2007 to Dec 31 2016 we analyzed non-malignant eye globe enucleations.
Of the 49 enucleated blind eyes, each patient had visual acuity with no light perception, 34 (69.4%) were indicated for enucleation due to complications following previous postoperative surgery after trauma, 14 patients (28.6%) were due to secondary glaucoma and other complications following previous intraocular surgery, and in one patient (2%) the primary isolated intraocular neurofibroma was verified after enucleation.
Apatient with isolated intrabulbar neurofibroma has been monitored since childhood for intraocular lesion and histologically verified at adult age. At the time of enucleation, he was 25 years old, squint since childhood and was observed for hamartoma in his right eye since he was 13 years old. Due to the progression of intrabulbar lesion, loss of visual acuity (functional state - no light perception) and secondary glaucoma, the right eye globe was enucleated at adult age and histopathological examination confirmed intraocular neurofibroma in the absence of neurofibromatosis.
Every enucleated eye globe should be subjected to athorough histopathological examination. Isolated intraocular neurofibromas can occur as isolated orbital or intrabulbar masses without systemic features.
Every enucleated eye globe should be subjected to a thorough histopathological examination. Isolated intraocular neurofibromas can occur as isolated orbital or intrabulbar masses without systemic features.Uveal melanoma (UM) is a deadly cancer that leads to metastatic disease in more than 50 % of the patients. Despite the improvement in the treatment of primary disease, there is still no effective therapy to prevent the development of metastases. Therefore, the disease requires intensive research to identify new treatment strategies. In preclinical UM models, epigenetic drugs have been shown to increase the sensitivity of resistant tumour cells to treatment. The successful use of histone deacetylase inhibitors, which induced cell cycle arrest, reprogramming consistent with melanocyte differentiation and inhibition of tumour growth in preclinical models, demonstrates the role of epigenetic regulation in UM metastasis. Identification of epigenetic changes associated with UM development an progression could contribute to the discovery of more effective drugs that, in combination with traditional approaches, may yield better therapeutic results for high-risk patients.In this work, we report on the stability of oxygen-rich plasma-polymerized (pp) films in an aqueous environment. The pp films were deposited via atmospheric-pressure plasma jet treatment of polymerizable organic liquids. The monomers used for the plasma-assisted polymerization were tetrahydrofurfuryl methacrylate, 1,2,4-trivinylcyclohexane, and mixtures thereof. The pp films were deposited at different plasma input powers ranging from 3 to 7 W. The stability of the obtained pp films was studied upon long-time storage in pure water and in buffer solutions of pHs 4, 7, and 10. After 24 h of storage of the pp films in de-ionized water, all of the studied pp films experienced thickness losses along with the formation of various ringlike structures at their surface, whereas Fourier transformed infrared (FT-IR) analysis showed no changes in their chemical composition. The pp films stored in pH 10 were completely delaminated from the substrate surface, while the pp films stored for 24 h in pH 4 showed swelling behavior, partial delamination, and the formation of wrinkles at the coatings' surface. The pp films stored for 24 h in pH 7 experienced minor thickness losses and formation of wrinkles at their surface. FT-IR analysis of the pp films stored in buffer solutions of pH 4 and pH 7 showed a decrease of C=O and an increase of O-H stretching signals in all of the cases. The observed chemical changes corresponded to the hydrolysis of esters presented in the pp films' structure.Therapeutic options to treat multidrug resistant bacteria, especially when present in biofilms, are limited due to their high levels of antibiotic resistance. Here, we report the anti-biofilm and immunomodulatory activities of the host defense peptide (HDP)-mimicking β-peptide polymer (2080 BuDM) and investigated its activity in vivo. The polymer outperformed antibiotics in the removal and reduction of the viability of established biofilms, achieving a maximum activity of around 80% reduction in viability. Interestingly the polymer also exhibited HDP-like immunomodulation in inducing chemokines and anti-inflammatory cytokines and suppressing lipopolysaccharide-induced proinflammatory cytokines. When tested in a murine, high-density skin infection model using P. selleckchem aeruginosa LESB58, the polymer was effective in diminishing abscess size and reducing bacterial load. This study demonstrates the dual functionality of HDP-mimicking β-peptide polymers in inhibiting biofilms and modulating innate immunity, as well as reducing tissue dermonecrosis.We present a version of the coarse-grained Cooke lipid model, modified to simulate asymmetric lipid membranes. It is inspired by a method employed by Wang et al. [ Commun. Comput. Phys. 2013, 13, 1093-1106] for artificially penalizing lipid flip-flop but copes more robustly with differential stress, at the cost of one additional bead per lipid and the concomitant increase in computational overhead. Bilayer asymmetry ultimately breaks down beyond a system size dependent critical differential stress, which can be predicted from a simple analytical model. We remeasure many important material parameters for the new model and find it to be consistent with typical fluid lipid membranes. Maintaining a stable stress asymmetry has many applications, and we give two examples (i) connecting monolayer stress to lipid number asymmetry in order to directly measure the monolayer area modulus and (ii) finding its strain-dependent higher-order correction by monitoring the equilibrium bilayer area.
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