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Introduction: This report details a case of a preseptal fat necrosis in a 55-year old female, following a revision endoscopic dacryocystorhinostomy (DCR)., Case Description: Upon initial examination, significant right eyelid swelling, tenderness, and pain in the peritrochlear area, was observed. An overlying skin edema was noted in the supero-medial portion of the right upper eyelid. This edema was palpable, firm, and tender. Orbital computed tomography revealed heterogeneous infiltration including an ill-defined margin in the preseptal regions of the clinically evident location. Marked, soft tissue edema and thickening in the inner preseptal area were demonstrated through magnetic resonance images (MRI). An excision biopsy was required as the lesion did not respond to medical treatment. A necrosis of adipose tissue surrounded by abundant foamy macrophages and inflammatory infiltrates, was exposed., Conclusion: This is an exceptionally rare case of orbital fat necrosis following a DCR. Four possible mechanisms for the development of fat necrosis are discussed.

Focal eosinophilic myositis (FEM) is a rare disease that is even more uncommon in affecting the periocular area. The authors are reporting the first case of FEM occurring in the lower eyelid of a 45-year-old Caucasian female who presented with localized painful area of glossy induration and peau d'orange skin lesion. Magnetic resonance image shows significant hyperintense thickening of the pre-septal orbicularis muscle region on T2-weighted images. Incisional biopsy of the induration revealed marked fibrinoid degeneration of the orbicularis muscle and adjacent fascia, mixed cellular infiltration of lymphocytes and eosinophils and a predominant CD8+ lymphocytic infiltrates in the immunohistochemical study. The final diagnosis was FEM. Oral prednisolone improved symptoms and the lesions disappeared, with no recrudescence in a one year follow-up.

Nitric oxide (NO) plays a relevant role during cell death regulation in tumor cells. The overexpression of nitric oxide synthase type III (NOS-3) induces oxidative and nitrosative stress, p53 and cell death receptor expression and apoptosis in hepatoblastoma cells. S-nitrosylation of cell death receptor modulates apoptosis. Sorafenib is the unique recommended molecular-targeted drug for the treatment of patients with advanced hepatocellular carcinoma. The present study was addressed to elucidate the potential role of NO during Sorafenib-induced cell death in HepG2 cells. We determined the intra- and extracellular NO concentration, cell death receptor expression and their S-nitrosylation modifications, and apoptotic signaling in Sorafenib-treated HepG2 cells. The effect of NO donors on above parameters has also been determined. Sorafenib induced apoptosis in HepG2 cells. However, low concentration of the drug (10nM) increased cell death receptor expression, as well as caspase-8 and -9 activation, but without activation of downstream apoptotic markers. In contrast, Sorafenib (10 µM) reduced upstream apoptotic parameters but increased caspase-3 activation and DNA fragmentation in HepG2 cells. The shift of cell death signaling pathway was associated with a reduction of S-nitrosylation of cell death receptors in Sorafenib-treated cells. The administration of NO donors increased S-nitrosylation of cell death receptors and overall induction of cell death markers in control and Sorafenib-treated cells. In conclusion, Sorafenib induced alteration of cell death receptor S-nitrosylation status which may have a relevant repercussion on cell death signaling in hepatoblastoma cells., (Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.)

Trousseau's syndrome includes a wide range of coagulation disorders, migratory thrombotic phenomena being the main associated entities. Treatment is difficult and venous gangrene constitutes a rare but deadly final stage that is particularly painful for the patient. The outlook after treatment is poor.

This prospective experimental study aimed to assess the regenerative capability of demineralised bone autografts resected and replaced orthotopically, compared with traditional fresh and deep frozen mandibular autografts in rats. In 60 adult Wistar rats, a bone defect 4 x 4 mm was created at the left ascending mandibular ramus and the removed bone was used as a fresh (n = 20), deep frozen (n = 20), or demineralised (n = 20) graft which was implanted orthotopically 2 weeks later. Ten rats in each group were killed at 2 and 6 weeks later. Outcome was measured by cellular proliferation on histological examination. The number of mesenchymal cells was significantly greater (P < 0.05) at both 2 and 6 weeks in the demineralised grafts than in the other two groups. There were no differences between the 2- and 6-week examinations of deep frozen bone, nor between the medullary and peripheral aspects. It was concluded that demineralised bony autografts cause greater osteoinduction both in the short (2 weeks) and the medium (6 weeks) term.

Two cases of multiple idiopathic ulcers of the small intestine are reported, which were found in two aged patients with a significant history of vascular pathology. Despite this, the pathological examination of the surgical specimens could not demonstrate a vascular origin of such lesions.