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

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

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

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

Erratum to "Effect of hyaluronic acid (MW 500–730 kDa) on proteoglycan and nitric oxide production in human osteoarthritic chondrocyte cultures exposed to hydrostatic pressure" [Osteoarthritis Cartilage 13 (2005) 688–696]

n/

Technological and Enzymatic Characterization of Autochthonous Lactic Acid Bacteria Isolated from Viili Natural Starters

Viili, a Finnish ropy fermented milk, is traditionally manufactured through spontaneous fermentation, by mesophilic lactic acid bacteria and yeast-like fungi, or back-slopping. This study evaluated four natural viili starters as sources of lactic acid bacteria for dairy production. Back-slopping activation of the studied viili samples was monitored through pH and titratable acidity measurements and enumeration of mesophilic lactic acid bacteria. Sixty lactic acid bacteria isolates were collected, molecularly identified, and assayed for acidification performance, enzymatic activities, production of exopolysaccharides (EPSs), presence of the histidine decarboxylase (hdcA) gene of Gram-positive bacteria, and production of bacteriocins. A neat predominance of Lactococcus lactis emerged among the isolates, followed by Enterococcus faecalis, Enterococcus faecium, Enterococcus durans, Enterococcus lactis, and Lactococcus cremoris. Most isolates exhibited proteolytic activity, whereas only a few enterococci showed lipase activity. Five isolates identified as L. cremoris, L. lactis, and E. faecalis showed a good acidification performance. Most of the isolates tested positive for leucine arylamidase, whereas only one E. durans and two L. lactis isolates were positive for valine arylamidase. A few isolates also showed a positive reaction for beta-galactosidase and alpha- and beta-glucosidase. None of the isolates produced EPSs or bacteriocins. The hdcA gene was detected in five isolates identified as L. lactis and E. faecium. A few L. cremoris and L. lactis isolates for potential use as starter or adjunct cultures for dairy processing were finally identified

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

Biologic therapies and small molecules for the management of non-infectious scleritis: a narrative review

Scleritis refers to a wide spectrum of ocular conditions ranging from mild to sight-threatening scleral inflammation that may compromise visual function and threaten the anatomical integrity of the ocular globe. Most aggressive forms like necrotizing or posterior scleritis are often difficult-to-treat cases, refractory to conventional treatment. The association with systemic diseases, namely rheumatoid arthritis, Sjögren syndrome, granulomatosis with polyangiitis, and relapsing polychondritis, may have prognostic implications as well. A better understanding of the pathogenesis of ocular inflammatory diseases have paved the way to more effective and targeted treatment approaches. In this regard, a growing body of evidence supports the potential role of biologic agents in the management of non-infectious scleral inflammation, either idiopathic or in a background of immune-mediated systemic disorders. Biologic agents such as anti-tumor necrosis factor agents, interleukin-1 and interleukin-6 inhibitors as well as CD20 blockade have displayed promising results. More specifically, several studies have reported their ability to control scleral inflammation, reduce the overall scleritis relapses, and allow a glucocorticoid-sparing effect while being generally well tolerated. Anecdotal reports have also been described with other biologic agents including abatacept, ustekinumab, daclizumab, and alemtuzumab as well as targeted small molecules such as tofacitinib. Further studies are warranted to fully elucidate the role of biologic agents in non-infectious scleritis and investigate specific areas with the aim to administer treatments in the context of personalized medicine. This review summarizes the available data regarding clinical trials, small pilot studies, and real-life experience of the last two decades reporting the use of biologic agents in the management of non-infectious scleritis