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Abstract: Mn-K edge EXAFS and XANES spectra of La0.87Na0.13MnO3 manganite films with different thicknesses (750, 250, 125 and 50Å), have been acquired at RT. In the 50Å film a shift of the Fermi level downward in energy is found if compared to the other films. In addition, the density of the empty minority spin states is decreased. This finding has been attributed to the presence of some Mn ions experiencing a different local chemical environment that results in the breaking of some DE paths, and in addition to an Anderson localisation of the charge carriers. This last conclusion can explain both the strongly insulating nature and the spin glass like behaviour of the magnetic response of the 50Å film, and has been corroborated by the results of the EXAFS analysis. [Copyright &y& Elsevier]

Introduction: The available studies on extraction wound repair in humans are affected by significant limitations and have failed to evaluate tissue alterations occurring in all compartments of the hard tissue defect. Aim: To monitor during a 6-month period the healing of human extraction sockets and include a semi-quantitative analysis of tissues and cell populations involved in various stages of the processes of modeling/remodeling. Material and Methods: Twenty-seven biopsies, representative of the early (2–4 weeks, n=10), intermediate (6–8 weeks, n=6), and late phase (12–24 weeks, n=11) of healing, were collected and analysed. Results: Granulation tissue that was present in comparatively large amounts in the early healing phase of socket healing, was in the interval between the early and intermediate observation phase replaced with provisional matrix and woven bone. The density of vascular structures and macrophages slowly decreased from 2 to 4 weeks over time. The presence of osteoblasts peaked at 6–8 weeks and remained almost stable thereafter; a small number of osteoclasts were present in a few specimens at each observation interval. Conclusions: The present findings demonstrated that great variability exists in man with respect to hard tissue formation within extraction sockets. Thus, whereas a provisional connective tissue consistently forms within the first weeks of healing, the interval during which mineralized bone is laid down is much less predictable. [ABSTRACT FROM AUTHOR]

We have recently reported that viral vector-mediated supplementation of fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF) in a lesioned, epileptogenic rat hippocampus limits neuronal damage, favors neurogenesis, and reduces spontaneous recurrent seizures. To test if this treatment can also prevent hippocampal circuit reorganization, we examined here its effect on mossy fiber sprouting, the best studied form of axonal plasticity in epilepsy. A herpes-based vector expressing FGF-2 and BDNF was injected into the rat hippocampus 3 days after an epileptogenic insult (pilocarpine-induced status epilepticus). Continuous video-electroencephalography (EEG) monitoring was initiated 7 days after status epilepticus, and animals were sacrificed at 28 days for analysis of cell loss (measured using NeuN immunofluorescence) and mossy fiber sprouting (measured using dynorphin A immunohistochemistry). The vector expressing FGF-2 and BDNF decreased both mossy fiber sprouting and the frequency and severity of spontaneous seizures. The effect on sprouting correlated strictly with the cell loss in the terminal fields of physiologic mossy fiber innervation (mossy cells in the dentate gyrus hilus and CA3 pyramidal neurons). These data suggest that the supplementation of FGF-2 and BDNF in an epileptogenic hippocampus may prevent epileptogenesis by decreasing neuronal loss and mossy fiber sprouting, that is, reducing some forms of circuit reorganization. [ABSTRACT FROM AUTHOR]

Under certain experimental conditions, neurotrophic factors may reduce epileptogenesis. We have previously reported that local, intrahippocampal supplementation of fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF) increases neurogenesis, reduces neuronal loss, and reduces the occurrence of spontaneous seizures in a model of damage-associated epilepsy. Here, we asked if these possibly anti-epileptogenic effects might involve anti-inflammatory mechanisms. Thus, we used a Herpes-based vector to supplement FGF-2 and BDNF in rat hippocampus after pilocarpine-induced status epilepticus that established an epileptogenic lesion. This model causes intense neuroinflammation, especially in the phase that precedes the occurrence of spontaneous seizures. The supplementation of FGF-2 and BDNF attenuated various parameters of inflammation, including astrocytosis, microcytosis and IL-1β expression. The effect appeared to be most prominent on IL-1β, whose expression was almost completely prevented. Further studies will be needed to elucidate the molecular mechanism(s) for these effects, and for that on IL-1β in particular. Nonetheless, the concept that neurotrophic factors affect neuroinflammation in vivo may be highly relevant for the understanding of the epileptogenic process. [ABSTRACT FROM AUTHOR]

A loss of neurons is observed in the hippocampus of many patients with epilepsies of temporal lobe origin. It has been hypothesized that damage limitation or repair, for example using neurotrophic factors (NTFs), may prevent the transformation of a normal tissue into epileptic (epileptogenesis). Here, we used viral vectors to locally supplement two NTFs, fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF), when epileptogenic damage was already in place. These vectors were first characterized in vitro, where they increased proliferation of neural progenitors and favored their differentiation into neurons, and they were then tested in a model of status epilepticus-induced neurodegeneration and epileptogenesis. When injected in a lesioned hippocampus, FGF-2/BDNF expressing vectors increased neuronogenesis, embanked neuronal damage, and reduced epileptogenesis. It is concluded that reduction of damage reduces epileptogenesis and that supplementing specific NTFs in lesion areas represents a new approach to the therapy of neuronal damage and of its consequences. [ABSTRACT FROM AUTHOR]

Fibroblast growth factor 2 (FGF-2) has multiple, pleiotropic effects on the nervous system that include neurogenesis, neuroprotection and neuroplasticity. Thus, alteration in FGF-2 expression patterns may have a profound impact in brain function, both in normal physiology and in pathology. Here, we used FGF-2 transgenic mice (TgFGF2) to study the effects of endogenous FGF-2 overexpression on susceptibility to seizures and to the pathological consequences of seizures. TgFGF2 mice display increased FGF-2 expression in hippocampal pyramidal neurons and dentate granule cells. Increased density of glutamatergic synaptic vesicles was observed in the hippocampus of TgFGF2 mice, and electrophysiological data (input/output curves and patch-clamp recordings in CA1) confirmed an increase in excitatory inputs in CA1, suggesting the presence of a latent hyperexcitability. Indeed, TgFGF2 mice displayed increased susceptibility to kainate-induced seizures compared with wild-type (WT) littermates, in that latency to generalized seizure onset was reduced, whereas behavioral seizure scores and lethality were increased. Finally, WT and TgFGF2 mice with similar seizure scores were used for examining seizure-induced cellular consequences. Neurogenesis and mossy fiber sprouting were not significantly different between the two groups. In contrast, cell damage (assessed with Fluoro-Jade B, silver impregnation and anti-caspase 3 immunohistochemistry) was significantly lower in TgFGF2 mice, especially in the areas of overexpression (CA1 and CA3), indicating reduction of seizure-induced necrosis and apoptosis. These data suggest that FGF-2maybe implicated in seizure susceptibility and in seizure-induced plasticity, exerting different, and apparently contrasting effects: favoring ictogenesis but reducing seizure-induced cell death. [ABSTRACT FROM AUTHOR]

The aim of this paper is to report our clinical experience of Sweet's syndrome, a severe dermatological disease which may be extremely important to recognize for the early diagnosis of a neoplastic disorder. Eleven patients affected by Sweet's syndrome, treated at the Department of Dermatology, University of Ferrara, Ferrara, Italy, during 1998 to 2004, were evaluated. A retrospective analysis was performed. Data on age, sex distribution, clinical data, histopathological and immunohistochemical findings and therapy were collected. We observed one patient with idiopathic form, 5 patients affected by the para-inflammatory variant and 5 para-neoplastic cases (with haemoproliferative diseases). The cases with the para-inflammatory form were affected by minor infectious manifestations. Prolonged follow-up is necessary to verify that a case of idiopathic variant is not really a paraneoplastic form. Based on immunohistochemical analysis, we cannot exclude that true histiocytes, immunoreactive for CD68/PGM, infiltrate the dermis in Sweet's syndrome lesions. [ABSTRACT FROM AUTHOR]

We have investigated the presence of non-classical soluble HLA-G molecules (sHLA-G) in cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients and the possible relationships between CSF levels of sHLA-G, classical soluble HLA-I (sHLA-I) molecules, IL-10 amounts and Magnetic Resonance Imaging (MRI) findings were evaluated.We studied by ELISA technique the sHLA-I, sHLA-G and IL-10 levels in CSF of 50 relapsing–remitting (RR) MS patients stratified according to clinical and MRI evidence of disease activity. Thirty-six patients with other inflammatory neurological disorders (OIND) and 41 with non-inflammatory neurological disorders (NIND) were used as controls. CSF mean levels were significantly higher in MS and OIND than in NIND for sHLA-I (p<0.001) and in MS than in controls for sHLA-G (p<0.001), with no differences among the various groups for IL-10 mean concentrations. An increase in CSF sHLA-I was found in MS patients with Gd-enhancing lesions (p<0.01), while sHLA-G and IL-10 were more represented in MS patients without lesional activity on MRI scans (p<0.02). In MRI-inactive MS, CSF IL-10 mean concentrations were significantly greater in patients with CSF-detectable levels of sHLA-G than in those without any evidence of CSF sHLA-G expression (p<0.05). Our findings suggest that CSF classical sHLA-I and non-classical sHLA-G levels may modulate MS activity as assessed by MRI acting in opposite directions. The association observed between sHLA-G and IL-10 when Gd-enhancing lesion resolved indicates a potential immunoregulatory role for IL-10 in the control of MS disease activity by shifting the sHLA-I/sHLA-G balance towards sHLA-G response. [Copyright &y& Elsevier]

The case of a 72-year-old woman with diffuse large B-cell lymphoma of the lacrimal sac is reported. The patient was evaluated for the first time in out department for tearing of the right eye. One month later, a slightly aching mass appeared over the right lacrimal sac. An acute infectious etiology was suspected and anibiotic therapy was given. When she finally presented with a rapidly growing lesion, she underwent echography and computed tomography followd by incisional biopsy. Results of histopathologic and immunohistochemical evaluation showed a primary, diffuse, large B-cell non-Hodgkin Lymphoma of the lacrimal sac. The case demonstrates how difficult the clinical diagnosis of tumors of the lacrimal sac may be in the early stages. The clinical signs, usually aspecific, may be misleading and the diagnosis delayed. [ABSTRACT FROM AUTHOR]

Erdheim-Chester disease is an idiopathic condition characterized by a xanthogranulomatous process infiltrating the bones, lungs, heart, retroperitoneum and other tissues. This condition is often fatal. Ocular findings are rare. The authors report a case of bilateral xanthelasmas and bilateral massive orbital infiltration in a 61-year-old man with severe retroperitoneal fibrosis, renal and cardiovascular problems. The ophthalmic manifestations and differential diagnosis of this peculiar pathologic condition are discussed. [ABSTRACT FROM AUTHOR]

The article presents a case study of a woman who was evaluated for a painless nodule that had developed slowly on her right forearm. The patient underwent treatment with 800 milligrams per day of oral ribavirin. The said treatment has a successful result that leads to an undetectable viral load and an improvement in the results of liver enzyme tests by the fourth week of therapy.