University of Modena and Reggio Emilia

About: University of Modena and Reggio Emilia is a education organization based out in Modena, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 8179 authors who have published 22418 publications receiving 671337 citations. The organization is also known as: Università degli Studi di Modena e Reggio Emilia & Universita degli Studi di Modena e Reggio Emilia.

Bisphosphonate-associated jawbone osteonecrosis: a correlation between imaging techniques and histopathology

Abstract: Objectives Recently, jawbone osteonecrosis has been reported as a potential adverse effect of bisphosphonates administration. This paper considers and highlights histopathologic and radiologic features of this condition. Study design Eleven patients, owing to unresponsiveness to conservative treatment and uncontrollable pain, underwent surgical resection of diseased jawbone after extensive hyperbaric oxygen therapy. A thorough clinical, laboratory, and imaging study was performed. Surgical specimens underwent histopathologic and immunohistochemical evaluation. Results Computerized tomography (CT) scans showed increased bone density, periosteal reaction, and bone sequestration in advanced stages. With magnetic resonance imaging (MRI), exposed areas showed a low signal in T1- and T2-weighted and inversion recovery images, which suggests low water content and is histopathologically correlated with paucity in cells and vessels (osteonecrotic pattern). Unexposed diseased bone was characterized by T1 hypointensity and T2 and IR hyperintensity, which suggests high water content and inflammation, associated with hypercellularity, osteogenesis, and hypervascularity (osteomyelitic pattern). Conclusions Diseased bone extends beyond the limits of the bone exposed in the oral cavity. Histopathologic examination correlated well with CT and MRI, which are the choice for the evaluation of bisphosphonate-associated jawbone osteonecrosis.

C/EBPδ regulates cell cycle and self-renewal of human limbal stem cells

Abstract: Human limbal stem cells produce transit amplifying progenitors that migrate centripetally to regenerate the corneal epithelium. Coexpression of CCAAT enhancer binding protein δ (C/EBPδ), Bmi1, and ΔNp63α identifies mitotically quiescent limbal stem cells, which generate holoclones in culture. Upon corneal injury, a fraction of these cells switches off C/EBPδ and Bmi1, proliferates, and differentiates into mature corneal cells. Forced expression of C/EBPδ inhibits the growth of limbal colonies and increases the cell cycle length of primary limbal cells through the activity of p27Kip1 and p57Kip2. These effects are reversible; do not alter the limbal cell proliferative capacity; and are not due to apoptosis, senescence, or differentiation. C/EBPδ, but not ΔNp63α, indefinitely promotes holoclone self-renewal and prevents clonal evolution, suggesting that self-renewal and proliferation are distinct, albeit related, processes in limbal stem cells. C/EBPδ is recruited to the chromatin of positively (p27Kip1 and p57Kip2) and negatively (p16INK4A and involucrin) regulated gene loci, suggesting a direct role of this transcription factor in determining limbal stem cell identity.

Detection of human herpesvirus-6 in mesial temporal lobe epilepsy surgical brain resections.

Abstract: The human herpesvirus-6 (HHV-6) is a ubiquitous β-herpesvirus,1,2 which infects a wide spectrum of cell types including glial cells.3–5 The virus is acquired early in childhood and is the causative agent of roseola infantum (exanthem subitum), a benign and otherwise self-limiting disease.6 Primary infection may result in seizures and severe neurologic complications such as meningitis or meningoenceph-alitis.7 As with all herpesviruses, HHV-6 can establish lifelong latent infection,8 and reactivation can occur in immunosuppressed patients such as bone marrow transplant recipients.9 Two HHV-6 variants have been characterized with respect to their antigenic and genomic composition.10 HHV-6B is primarily associated with most symptomatic infections during infancy,11 whereas HHV-6A has been suggested to be more neurotropic and is associated with viral persistence and reactivation in the CNS.12 HHV-6 variant A has also been detected more frequently in multiple sclerosis patient samples compared with variant B.13 However, HHV-6B has also been shown to have neurotropic potential4,14 and has recently been associated with limbic encephalitis.15 Although the role of HHV-6 in human CNS disease remains to be fully defined, a number of studies have suggested that the CNS can be a site for persistent HHV-6 infection.16,17 Autopsy material from a wide variety of normal18 and diseased19,20 brains has documented HHV-6 infection in the CNS, although its role as a causative agent is unclear. Cell types reported to be infected include oligodendrocytes, astrocytes, and possibly neurons.21,22 In limbic encephalitis, HHV-6 DNA was detected in the CSF, and astrocytes were shown to be the most represented cell type harboring HHV-6B in the hippocampus.15 This localization is consistent with the report of HHV-6 hippocampal encephalitis after bone marrow transplantation23 and of hippocampal injury in patients with prolonged focal febrile seizures,24,25 a frequent complication of a primary HHV-6 infection. In an attempt to characterize further the extent and distribution of HHV-6 in human glial cells, brain tissues from surgical specimens were processed to establish cultures of primary astrocytes and oligodendrocytes to be used for in vitro virologic examinations. Brain resections are a therapy for pharmacologically untreatable seizures,26 and specimens from patients with mesial temporal lobe epilepsy (MTLE) and neocortical epilepsy (NE) were collected for analysis.