Benign Neural Sheath Tumours of Major Nerves: Characteristics in119 Surgical Cases

Peripheral benign nerve sheath tumours are infrequent tumours and affect major nerve trunks. Some authors have indicated a high and prohibitive incidence of neurological injury in resection of these lesions. The authors describe their findings in a retrospective study comprising 119 patients with spontaneous benign nerve sheath tumours of the peripheral nervous system. Seventy-three patients had a schwannoma, 41 had neurofibroma and 5 had plexiform neurofibroma; 25 of the 119 patients suffered from neurofibromatosis. All schwannomas were excised completely and the outcome of patients was 41.0% improved, 6.8% worsened, 52.0% unchanged. Twenty-eight neurofibromas were excised completely and 13 subtotally; the outcome for patients was 19.5% improved, 19.5% worsened and 61% unchanged. All plexiform neurofibromas were removed subtotally and the outcome for patients was 20% improved and 80% unchanged. The best surgical results at average follow-up of 6 years were observed in the patients with schwannoma, the worst in those with plexiform neurofibroma. Our results demonstrated that it is often possible to remove schwannomas as well as neurofibromas with an acceptable risk of injury to the nerve

Growth factors, Cytokines and VEGF in human neoplastic and inflammatory pathologies:Immunohistochemical basis for nuclear medicine studies

Despite the success of antiangiogenic therapy, a large percentage of patients does not benefit from this targeted therapy. Currently, it is impossible to predict which patient will benefit from antiangiogenic therapy. Reasons for treatment failure may be that the target for the drug is not present or that the drug may not reach the target. Tumor cells produce VEGF, which can lead to paracrine effects in the microenvironment. VEGF121 is freely soluble, whereas VEGF165 is secreted, though a significant fraction remains localized to the extracellular matrix, such as VEGF189 and VEGF206. This will most likely lead to locally high VEGF levels. It is currently impossible to evaluate these local VEGF levels . Noninvasive measurement of VEGF in the tumor (IHC, PCR, Western blotting) might give insight to the available target for VEGF-dependent antiangiogenic therapy and thus assist in tumor response prediction. Moreover, growth factors and cytokines expression in normal and pathological tissues substantially changes in different clinical and physiological conditions. These variations (whose different tissue expressions may be effectively studied by immunohistochemistry) are important and constitute the biological basis for a correct tissue analysis. The last one may represent a previous modality screening and a precious therapeutical support in order to ameliorate the knowledge of nuclear medicine targets in oncological patients

Adverse events associated with intraocular injection of anti-VEGF(bevacizumab) in retinal vein ccclusion: a case report

Introduction: Antiangiogenic agents are often administered for treatment of Branch Retinal Vein Occlusion (BRVO). Among them, Bevacizumab has noticeable antiangiogenic and antiedemigenic properties and possesses great capacity to penetrate the retinal tissue, particularly in pathological circumstances characterized by altered external or internal blood-retinal barrier.Bevacizumab has an optimal bio-efficacy based on inhibition of the activity of Vascular Endothelial Growth Factor (VEGF). Nonetheless, despite its efficacy, here we describe the adverse effects associated with intraocular injection of bevacizumab in a patient affected by retinal vein occlusion. Case presentation: We present a case report of an 11-year old Caucasian malesubject affected by BRVO in his left eye. The patient underwent an intra-vitreal (i.v.) injection of bevacizumab 100 (1.25 mg/0.05ml). After that, the patient was monitored over time through a series of analyses including Ocular Coherence Tomography, Fluorangiography, Bulbar Ultrasound, Angio MRI BCVA scores and Intra Ocular Pressure. Results: Immediately after the i.v. injection, the patient experienced a strong and relentless pain radiating from the left ocular orbit, caused by a serious and unexpected malignant glaucoma and phthisis bulbi. Furthermore, the patient did not show any sign of improvement in visual function in the follow-up and at last required an ophthalmic prosthesisas a result of a subatrophic and hypotonic eyeball. Conclusion: This case report suggests that i.v. injections of anti-VEGFs should be considered wit

Bifid median nerve: report of two cases

The median nerve divides into its terminal branches at or proximal to the distal edge of the flexor retinaculum. An anatomy of the median nerve within the carpal tunnel is reported in two separate cases. Emphasis has been given to the value of direct vision when incising the flexor retinaculum in order to avoid injure of the median nerve

Occlusion of retinal capillaries caused by glial cell proliferation in chronic ocular inflammation

The inner blood-retinal barrier is a gliovascular unit in which glial cells surround capillary endothelial cells and regulate retinal capillaries by paracrine interactions. During chronic ocular inflammation, microvascular complications can give rise to vascular proliferative lesions, which compromise visual acuity. This pathologic remodelling caused by proliferating Müller cells determines occlusion of retinal capillaries. The aim of the present study was to identify qualitative and quantitative alterations in the retinal capillaries in patients with post-traumatic chronic ocular inflammation or post-thrombotic vascular glaucoma. Moreover, we investigated the potential role of vascular endothelial growth factor (VEGF) and pro-inflammatory cytokines in retinal inflammation. Our electron microscopy findings demonstrated that during chronic ocular inflammation, thickening of the basement membrane, loss of pericytes and endothelial cells and proliferation of Müller cells occur with irreversible occlusion of retinal capillaries. Angiogenesis takes place as part of a regenerative reaction that results in fibrosis. We believe that VEGF and pro-inflammatory cytokines may be potential therapeutic targets in the treatment of this disease although further studies are required to confirm these findings

Lithium limits trimethyltin-induced cytotoxicity and proinflammatory response in microglia without affecting the concurrent autophagy impairment

Trimethyltin (TMT) is a highly toxic molecule present as an environmental contaminant causing neurodegeneration particularly of the limbic system both in humans and in rodents. We recently described the occurrence of impairment in the late stages of autophagy in TMT-intoxicated astrocytes. Here we show that similarly to astrocytes also in microglia, TMT induces the precocious block of autophagy indicated by the accumulation of the autophagosome marker, microtubule associated protein light chain 3. Consistent with autophagy impairment we observe in TMT-treated microglia the accumulation of p62/SQSTM1, a protein specifically degraded through this pathway. Lithium has been proved effective in limiting neurodegenerations and, in particular, in ameliorating symptoms of TMT intoxication in rodents. In our in vitro model, lithium displays a pro-survival and anti-inflammatory action reducing both cell death and the proinflammatory response of TMT-treated microglia. In particular, lithium exerts these activities without reducing TMT-induced accumulation of light chain 3 protein. In fact, the autophagic block imposed by TMT is unaffected by lithium administration. These results are of interest as defects in the execution of autophagy are frequently observed in neurodegenerative diseases and lithium is considered a promising therapeutic agent for these pathologies. Thus, it is relevant that this cation can still maintain its pro-survival and anti-inflammatory role in conditions of autophagy bloc