Classification of simple linearly compact n-Lie superalgebras

We classify simple linearly compact n-Lie superalgebras with n>2 over a field F of characteristic 0. The classification is based on a bijective correspondence between non-abelian n-Lie superalgebras and transitive Z-graded Lie superalgebras of the form L=\oplus_{j=-1}^{n-1} L_j, such that L_{-1}=g, where dim L_{n-1}=1, L_{-1} and L_{n-1} generate L, and [L_j, L_{n-j-1}] =0 for all j, thereby reducing it to the known classification of simple linearly compact Lie superalgebras and their Z-gradings. The list consists of four examples, one of them being the n+1-dimensional vector product n-Lie algebra, and the remaining three infinite-dimensional n-Lie algebras.Comment: Final version to appear in Communications in Mathematical Physic

First Report of Circulating MicroRNAs in Tumour Necrosis Factor Receptor-Associated Periodic Syndrome (TRAPS)

Tumor necrosis factor-receptor associated periodic syndrome (TRAPS) is a rare autosomal dominant autoinflammatory disorder characterized by recurrent episodes of long-lasting fever and inflammation in different regions of the body, such as the musculo-skeletal system, skin, gastrointestinal tract, serosal membranes and eye. Our aims were to evaluate circulating microRNAs (miRNAs) levels in patients with TRAPS, in comparison to controls without inflammatory diseases, and to correlate their levels with parameters of disease activity and/or disease severity. Expression levels of circulating miRNAs were measured by Agilent microarrays in 29 serum samples from 15 TRAPS patients carrying mutations known to be associated with high disease penetrance and from 8 controls without inflammatory diseases. Differentially expressed and clinically relevant miRNAs were detected using GeneSpring GX software. We identified a 6 miRNAs signature able to discriminate TRAPS from controls. Moreover, 4 miRNAs were differentially expressed between patients treated with the interleukin (IL)-1 receptor antagonist, anakinra, and untreated patients. Of these, miR-92a-3p and miR-150-3p expression was found to be significantly reduced in untreated patients, while their expression levels were similar to controls in samples obtained during anakinra treatment. MiR-92b levels were inversely correlated with the number of fever attacks/year during the 1st year from the index attack of TRAPS, while miR-377-5p levels were positively correlated with serum amyloid A (SAA) circulating levels. Our data suggest that serum miRNA levels show a baseline pattern in TRAPS, and may serve as potential markers of response to therapeutic intervention

Np95 Is Implicated in Pericentromeric Heterochromatin Replication and in Major Satellite Silencing

Heterochromatin plays an important role in transcriptional repression, for the correct segregation of chromosomes and in the maintenance of genome stability. Pericentric heterochromatin (PH) replication and formation have been proposed to occur in the pericentric heterochromatin duplication body (pHDB). A central question is how the underacetylated state of heterochromatic histone H4 tail is established and controlled, because it is a key event during PH replication and is essential to maintain the compacted and silenced state of these regions. Np95 is a cell cycle regulated and is a nuclear histone-binding protein that also recruits HDAC-1 to target promoters. It is essential for S phase and for embryonic formation and is implicated in chromosome stability. Here we show that Np95 is part of the pHDB, and its functional ablation causes a strong reduction in PH replication. Depletion of Np95 also causes a hyperacetylation of lysines 8, 12, and 16 of heterochromatin histone H4 and an increase of pericentromeric major satellite transcription, whose RNAs are key players for heterochromatin formation. We propose that Np95 is a new relevant protein involved in heterochromatin replication and formation

Acute idiopathic pericarditis: current immunological theories

Alida LP Caforio,1 Renzo Marcolongo,2 Antonio Brucato,3 Luca Cantarini,4 Massimo Imazio,5 Sabino Iliceto11Division of Cardiology, Department of Cardiology, Thoracic and Vascular Sciences, University of Padua, Padua; 2Haematology and Clinical Immunology, Department of Medicine, University of Padua, Padua, 3Internal Medicine, Ospedali Riuniti, Bergamo, 4Rheumatology Unit, Policlinico Le Scotte, University of Siena, Siena, 5Department of Cardiology, Maria Vittoria Hospital, Torino, ItalyAbstract: Idiopathic recurrent acute pericarditis (IRAP) is a rare disease of suspected immune-mediated pathogenesis. It represents a diagnosis of exclusion. It is necessary to rule out infectious and noninfectious causes of pericardial inflammation, including systemic autoimmune and immune-related disorders, eg, Sjögren's disease, systemic lupus erythematosus. Since pericarditis may precede diagnosis of these disorders, IRAP diagnosis is often made after a long follow-up. According to the two main pathogenetic theories IRAP may represent an organ-specific autoimmune disease or an autoinflammatory disease (AInfD). The main evidence for autoimmunity in IRAP is provided by the detection of serum antiheart and antiintercalated-disk autoantibodies, and the response to anti-inflammatory or immunosuppressive therapy. The findings of familial forms and of proinflammatory cytokines in the pericardial fluid in IRAP would be in keeping with both organ-specific autoimmune disease and AInfD. In fact, AInfD are genetic disorders characterized by primary dysfunction of the innate immune system, due to mutations of genes involved in the regulation of the inflammatory response, in the absence of antigen specific T cells or autoantibodies. In AInfD there are active disease phases with raised non-cardiac specific inflammatory markers, such as C-reactive protein, as well as symptom-free intervals with possible C-reactive protein normalization. A minority of IRAP patients (6%) carry a mutation in the TNFRSF1A gene, encoding the receptor for tumor necrosis factor-alfa. This suggests that some IRAP patients may have an atypical or subclinical form of AInfD. Thus, IRAP may represent a syndrome with distinct pathogenetic mechanisms in different patients' subsets.Keywords: pericarditis, autoimmunity, autoantibodies, heart disease, immune factor

The common NOD2/CARD15 variant P268S in patients with non-infectious uveitis: A cohort study

Background: The etiology of Autoimmune chronic uveitis (ACU) is still unknown; NOD2/CARD15 gene mutations are responsible for the Blau Syndrome and can induce uveitis in animal models. Presentation of the hypothesis: Aim of our study was to assess if NOD2/CARD15 variants have a role in the etiology or in the clinical course of patients with ACU, either idiopathic or associated with other inflammatory diseases. Testing the hypothesis: We consecutively enrolled 25 patients (19 pediatric and 6 adults) affected with ACU. For each patient medical history was reviewed and clinical data were recorded. Allelic and genotypic frequencies of NOD2/CARD15 variations were calculated in patients and matched with those of 25 healthy controls. The statistical analysis was performed. Fifteen patients showed the polymorphism P268S/SNP5 (SNP rs2066842) as heterozygous carriers while two patients were homozygous for the same polymorphism; one patient carried also the variant c647 18-16 TCT on intron 3, not previously reported in the literature. Statistical analysis for NOD2/CARD15 genotyping showed significant differences between patients and controls for allelic frequencies (p=0.04, OR: 4.03, 95 %; CI=1.2-13.5) but not for genotypic frequencies. We could not identify a significant phenotype-genotype correlation. Implications of the hypothesis: In our cohort of Italian patients, the NOD2/CARD15 common variant P268S/SNP5 could potentially be significantly associated with ACU

Neridronate for transient osteoporosis of the hip in a child

Transient osteoporosis of the hip (TOH) is usually reported in middle-aged men or during pregnancy as a benign self-limiting condition. Nevertheless, its impact on quality of life in terms of pain and disability is considerable. Also, it can lead to insufficiency fractures or, more rarely, evolve into osteonecrosis. This condition is anecdotally described in the pediatric age and very little is known about how it may affect the growing bone. We herein describe a case of TOH in a 10-year-old child treated at our pediatric rheumatology service and summarize the pediatric cases of TOH previously reported in literature. There are two points of interest in our case report, the first one being the unusual complication of TOH with a femoral physis fracture and the second the complete recovery after the off-label therapy with bisphosphonates. We suggest that interventional medical treatment could be considered in selected cases of juvenile TOH, to prevent any possible irreversible damage on the femoral physis. As far as we know, this is the first report of neridronate employment in children affected by TOH

Paget's disease

n/