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Tampone floccato e metodo per il prelievo ed il trasferimento di campioni di materiale biologico. USA en. Polyester yarn of high strength possessing an unusually stable internal structure. EPA1 fr. Process to enclose flock tow in a permeable sleeve for dyeing or textile treatment before cutting into a flock. JPHA en. EPA2 fr. JPHA ja. USB1 en. Arrangement for mounting a parallel-guiding device in a force measuring apparatus.

USA1 en. Fibre composite du type mer-ile utilisee pour le tricotage sur metier chaine et procede de preparation de cette fibre. Fibre composite du type mer-ilot pour tissu a maille jetee molletonne et son procede de preparation. Multifilament conjugue de type sea island comportant un composant de teinture dans la masse, et son procede de preparation.

JPA ja. Systeme pour coloration de cheveux et dispositif de test pouvant s'utiliser dans ce systeme.


WOA2 fr. Appareil et procedes d'echantillonnage de surface microbien a haut rendement. Method and apparatus for simultaneously collecting exocervical and endocervical samples. Sea-island typed conjugate multi filament comprising dope dyeing component and a process of preparing for the same. Sanitary swab collection system, microfluidic assay device, and methods for diagnostic assays.

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Abu-Diab et al. Biggs et al " Evaluation. Body et al. Certified English translation of JP Apr. Chan et al :Comparison of nasopharyngeal flocked swabs and aspirates for rapid diagnosis of respiratory viruses in children" Journal of Clinical Virology " Article in Press doi EP A1 Gueret Nov. European Search Report dated Jul. Fedorova, N. GB A Mislowitzer, abstract published Mar. It has also been recently demonstrated that the IFNa-inducible IFI16 protein—normally localized in the nucleus—translocates in the cytoplasm of affected skin cells from lupus patients and in UV irradiated keratinocytes—leading to generation of antibodies against the IFNa-inducible IFI16 recently detected in sera of lupus patients [90].

Neuropsychiatric systemic lupus erythematosus NPSLE — among the most severe manifestations of SLE—includes a variety of manifestations involving central, peripheral, and autonomic nervous system as well as psychiatric disorders after other underlying causes have been carefully excluded. These cytokines have been shown to induce peripheral depletion of tryptophan—previously implicated in the pathogenesis of depression—through stimulation of the enzyme indoleamine 2,3-dioxygenase [92].

Induction of SLE-like syndromes and neuropsychiatric manifestations have been reported after therapeutic use of IFNa approximately in one-third of patients mainly with hepatitis C or certain malignancies giving potential insights of type I IFN implication in lupus-related clinical syndromes []. While depression seems to be among the most common IFNa-related neuropsychiatric side effects and a main contraindication for IFNa administration, psychotic features, confusion, bipolar disorders, and seizures can also occur [92]. IFNa production by astrocytes in transgenic mouse models revealed structural and functional abnormalities ranging from seizures and severe behavioral.

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Notably, calcium and phosphorus deposition in the brain in this experimental model resembled the mineral deposition observed in basal ganglia from patients with the Aicardi-Goutieres syndrome, an early-onset encephalopathy with elevated CSF IFNa levels. The Aicardi-Goutieres syndrome is an autosomal recessive disease related to mutations in 5 genes, including among others the 3-repair DNA exonuclease 1 TREX1 , recently associated with lupus [98]. Both of these patients suffered from psychosis and were characterized by the presence of CSF oligoclonal IgG [99].

In accord with the above findings, elevated IFNa levels have been subsequently detected in CSFs of five out of 6 lupus patients with psychosis but with no other NP manifestations. In the brain autopsy of one of the study participants who died from generalized seizures, the presence of IFNa in neurons and microglia has been demonstrated by immunochemistry []. While no significant differences have been observed in serum levels of interferogenic activity— measured by bioassay—between SLE patients with and without neuropsychiatric involvement, CSF interferogenic activity has been found to be elevated in NPSLE patients compared to controls with other autoimmune disorders and CNS features.

This was partially attributed to an inhibitory effect of serum IgG, providing a potential explanation for the success of intravenous immunoglobulin IVIG treatment in some cases of NPSLE [] and other neurological diseases [, ]. The CSF interferogenic activity seems to result from pDC stimulation by CSF-containing immunocomplexes formed by autoantibodies and antigens released by neurocytotoxic Abs or other injured brain cells [93].

Such an association was not, however, observed in a larger cohort of 77 SLE patients by Kirou et al. Table 1. Moreover, in. Prospective studies with larger number of patients and careful collection of clinical, serological, and imaging data are required to further understand its contribution in pathogenesis ofNSPLE. A population-based case-control analysis, using general practice database data, found a relative CV disease risk of 2 for women with SLE [, ].

Strikingly, a fifty-fold increased risk of myocardial infarction was reported. While several traditional risk factors for atherosclerosis are more prevalent among SLE patients, they cannot fully explain their increased CV burden []. Additionally, the effect on CV risk of SLE is more pronounced comparing to the impact of other inflammatory diseases like rheumatoid arthritis [].

These observations support the hypothesis that accelerated atherosclerosis and premature CV disease are significantly enhanced by factors inherent to the pathogenesis of SLE. It is widely believed that atherosclerosis results from chronic endothelial injury paired with a defective vascular repair mechanism leading to invasion of inflammatory cells, lipid deposition, vascular smooth muscle proliferation, and neointima formation. Several studies suggest that circulating myeloid-derived endothelial progenitor cells EPCs and myelomonocytic circulating angiogenic cells CACs are the key players in the vascular repair mechanism [, ].

Moreover, heightened type I IFN. In accord with the human studies, in a lupus-prone murine model, elevated levels oftype I IFN led to reduced number and EPCs dysfunction []. Moreover, the presence of IFNa inhibited EPCs from nonlupus-prone mice to differentiate into mature endothelial cells. Thacker et al. In vivo confirmation of this antiangiogenic pathway of IFNa interfering with IL1 pathways was established by examining renal biopsies of patients with lupus nephritis [].

A recently studied subset of proinflammatory neutrophils, termed low-density granulocytes LDG , was identified in the blood of SLE patients. Interestingly a recent study investigating the immuno-modulatory effects of statins in SLE demonstrated that simvastatin and pitavastatin significantly inhibit type I IFN production both from pDCs isolated from lupus patients and from healthy pDCs treated with sera from SLE patients. These findings imply that statins exert a beneficial effect in the atherosclerotic process not only due to its lipid-lowering properties but also through inhibition of the type I IFN production.

It also provides a rationale for a potential therapeutic use of statins in IFN-mediated autoimmune diseases such as SLE []. In a recent study, Lood et al. Given that the same platelet phenotype has been observed in patients with a history of vascular disease, they hypothesized that type I IFN-induced platelet activation. Further supporting evidence for the role of type I IFN in atherosclerosis and especially in the formation of foam cells came from a study by Li et al.

Foam cells derive from infiltrating monocytes in the subintima where they differentiate into macrophages. Upon exposure to oxidized-LDL ox-LDL , macrophages expressing scavenger receptors SR internalize cholesteryl ester from ox-LDL and are transformed into foam cells which represent the primary components of the early atherosclerotic lesion. In this study, IFNa priming induced upregulation of SR in the macrophages and increased foam-cell formation. Finally, a recent Swedish study showed that SLE patients with the risk allele rs G in the STAT4 gene had a significantly increased risk of ischemic cerebrovascular disease ICVD , comparable in magnitude to that of hypertension.

These data indicate that premature atherosclerosis in SLE patients can at least partially be attributed to increased activation of the type I IFN system. Current attempts to block the type I IFN activity in SLE patients may provide therapeutic approaches that achieve successful overall disease activity control and reduce the fatal vascular events that afflict these patients. Over the past years, the role of type I interferon system in generation of distinct lupus-related clinical phenotypes arising from skin, renal, and CNS involvement has been increasingly appreciated.

NEJM: At the Heart of Discovery

Moreover, growing evidence suggests the implication of type I IFN pathway in the patho-genesis of atherosclerosis, a frequent comorbidity in these patients, often not fully explained by the presence of coexisting traditional CV risk factors. The authors would like to thank Profs M. Crow, MD, and H.

Moutsopoulos, MD, for their inspiration, guidance and fruitful suggestions. They are also grateful to Dr. Ioakeimidis, MD, for providing valuable clinical data and continuous support. Borchers, S. Naguwa, Y. Shoenfeld, and M. Gershwin, "The geoepidemiology of systemic lupus erythematosus," Autoimmunity Reviews, vol. AA, Hooks, H. Moutsopoulos, and S.

Geis, "Immune interferon in the circulation of patients with autoimmune disease," The New England Journal of Medicine, vol. Ronnblom, G.

References | E. coli Food Poisoning

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Kirou, C. Lee, S. George, K. Louca, M. Peterson, and M. Crow, "Activation of the interferon- a pathway identifies a subgroup of systemic lupus erythematosus patients with distinct serologic features and active disease," Arthritis and Rheumatism, vol. Feng, H.

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Grossman et al. Weckerle et al. Bagavant and S. Fu, "Pathogenesis of kidney disease in systemic lupus erythematosus," Current Opinion in Rheumatology, vol. Rich, "Human lupus inclusions and interferon," Science, vol. Peterson, J. Huang, J. Zhu et al. Papadimitraki, M. Tzardi, G. Bertsias, E. Sotsiou, and D. Boumpas, "Glomerular expression of Toll-like receptor-9 in lupus nephritis but not in normal kidneys: implications for the amplification of the inflammatory response," Lupus, vol. Moser, J. Kelly, C. Lessard, and J. Harley, "Recent insights into the genetic basis of systemic lupus erythematosus," Genes and Immunity, vol.

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Moore, K. Kirou, M. Crow, T. Utset, and T. Niewold, "Age- and gender-specific modulation of serum osteopontin and interferon- a by osteopontin genotype in systemic lupus erythematosus," Genes and Immunity, vol. Kariuki, M. Crow, and T. Niewold, "The PTPN22 CT polymorphism is associated with skewing of cytokine profiles toward high interferon- a activity and low tumor necrosis factor a levels in patients with lupus," Arthritis and Rheumatism, vol. Sigurdsson, G. Nordmark, S. Garnier et al. Remmers, R. Plenge, A. Lee et al.

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    Cao et al. In press. Braun, P. Geraldes, and J. Demengeot, "Type I Interferon controls the onset and severity of autoimmune manifestations in lpr mice," Journal of Autoimmunity, vol. Jorgensen, J. Thurman, S. Izui et al. Triantafyllopoulou, C. Potential role of antiepileptic drugs". CNS Drugs. Nature Reviews. Citizens United for Research in Epilepsy. Retrieved 18 March Categories : Epilepsy Medical terminology. Hidden categories: CS1: long volume value CS1 errors: chapter ignored Articles with short description.