study of two alternative cooling systems of a mold insert used in die casting process of light alloy components

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FRI0191 CRANIAL-LIMITED AND LARGE-VESSEL GIANT CELL ARTERITIS: PRESENTING FEATURES AND OUTCOME

Background:Giant cell arteritis (GCA) comprises two main phenotypes: cranial (C) and large-vessel (LV) disease1. A full baseline steroid-free vascular imaging evaluation is required to properly diagnose LV involvement2Objectives:To compare presenting and prognostic features of LV-GCA and C-GCA patients after an adequate vascular imaging evaluation at baselineMethods:Data from GCA patients followed-up at our Institution were retrospectively collected. Only patients who underwent large-vessel imaging (PET, CTA, MRA) at disease onset or within 1 week after steroid introduction were included. Patients with evidence of LV involvement were classified as LV-GCA. Differences between LV-GCA and C-GCA patients regarding presenting features, treatment, prognosis were evaluated. Non-parametric tests were usedResults:In our cohort, we identified 161/280 patients who underwent LV-imaging study at baseline. Of these, 100 (62.1%) had signs of LV inflammation. Table 1 compares demographic features, diagnostic delay, pre-existing comorbidities and complementary treatment between the 2 groups. Table 2 compares disease features at diagnosis. Mean follow-up was similar between LV- and C-GCA patients (31.8±31.8 vs 27.8±29.1 months; 70% vs 73.8% followed-up ≥12 months). Corrected cumulative prednisone dose (CCPD, grams/months) was equivalent (LV, 0.67±0.57; C, 0.87±1.37; p=0.871). A DMARD was added in 73% of LV- and in 55.7% of C-GCA patients (p=0.027), but, notably, it was introduced at baseline in 52% of LV- vs 23.5% of C-GCA patients (p=0.006). CCPD was equivalent even considering only patients who did not receive DMARDs (LV, 0.92±0.81; C, 0.94±1.18; p=0.522). Frequency of relapses was not significantly different (LV, 51%; C, 57.3%, p=0.515), even when considering only DMARD-receiving patients (LV, 36.1%; C, 38.2%, p=0.833). Aortic aneurysms incidence at 5 years was similar (LV, 17.3%; C, 15.7%; p=0.826). Rate of metabolic and infective complications was similar, in terms of arterial hypertension (LV, 3%; C, 0%, p=0.286), diabetes (2% vs 0%, p=0.524), osteoporotic fractures (7% vs 5%, p=0.742), severe infections (3% vs 3.3%, p=1)Table 1.Demographic features, diagnostic delay, pre-existing comorbidities, and complementary treatment at baseline in LV and C-GCA patientsLV imaging +n=100 (%)LV imaging-n=61 (%)p-valueAge (years)73.2 ± 8.976 ± 8.80.018Sex (female)65 (65)40 (65)1Diagnostic delay (months)3.5 ± 4.62.3 ± 4.90.001Pre-existing comorbidities- CAD3 (3)7 (11.5)0.043- Diabetes4 (4)6 (9.8)0.181- Dyslipidemia17 (17)17 (27.9)0.114- Hypertension42 (42)34 (55.7)0.105- Stroke3 (3)3 (5)0.674- Cancer20 (20)6 (9.8)0.122Ongoing complementary treatment- Antiplatelet18 (18)15 (25)0.322- Anticoagulant1 (1)6 (9.8)0.012- Statin14 (14)14 (23)0.198Table 2.Diseases features at onset in LV and C-GCA patientsLV imaging +n=100 (%)LV imaging-n=61 (%)p-valueTemporal biopsy positive17/31 (55)9(43)0.573Symptoms- Headache65 (65)52 (85)0.006- Jaw claudication22 (22)20 (32.8)0.142- Scalp tenderness31 (31)26 (42.6)0.174- Ocular symptoms14 (14)20 (32.8)0.006- Ischemic optic neuropathy7 (7)17 (27.9)<0.001- Stroke3 (3)0 (0)0.290- Polymyalgia rheumatica42 (42)31 (50.8)0.328- Fever44 (44)12 (19.7)0.002- Fatigue72 (72)21 (34.4)<0.001- Weight loss37 (37)7 (11.5)<0.001- Cough10 (10)1 (1.6)0.053Laboratory findings, mean- C-reactive protein, mg/L80.8 ± 60.865.7 ± 58.20.057- Erythrocyte sedimentation rate76.8 ± 3071.5 ± 270.360- Hemoglobin, g/dL11.4 ± 1.512 ± 1.60.007- Platelet count389.4 ± 116.6366.8 ± 125.20.758Conclusion:LV-GCA patients are younger and suffer of a greater diagnostic delay. Although a greater systemic inflammation seems to be a feature of LV-GCA patients, the vascular prognosis is similar to C-GCA patients, who, conversely, have a greater incidence of ocular complicationsReferences:[1]Dejaco C, et al. Nat Rev Rheumatol (2017)[2]Kermani T, et al. Rheumatology (2019)Disclosure of Interests:Alessandro Tomelleri: None declared, Corrado Campochiaro Speakers bureau: Novartis, Pfizer, Roche, GSK, SOBI, Silvia Sartorelli: None declared, Nicola Farina: None declared, Elena Baldissera Speakers bureau: Novartis, Pfizer, Roche, Alpha Sigma, Sanofi, Lorenzo Dagna Grant/research support from: Abbvie, BMS, Celgene, Janssen, MSD, Mundipharma Pharmaceuticals, Novartis, Pfizer, Roche, SG, SOBI, Consultant of: Abbvie, Amgen, Biogen, BMS, Celltrion, Novartis, Pfizer, Roche, SG, and SOB

FRI0506 EFFICACY AND SAFETY OF CANAKINUMAB IN ADULT-ONSET STILL'S DISEASE: A SINGLE-CENTER REAL-LIFE EXPERIENCE

Background:The pro-inflammatory cytokine interleukin (IL)-1 has a central role in the pathogenesis of adult-onset Still's disease (AOSD), a rare auto-inflammatory condition. Anakinra, has been for years the cornerstone of IL-1-blocking therapy in AOSD. More recently, the monoclonal antibody canakinumab, a new agent blocking IL-1, has become availableObjectives:To describe our real-life experience with CNK in a cohort of AOSD patients from a single Italian CenterMethods:AOSD patients diagnosed according to Yamaguchi's criteria followed-up at our Autoinflammatory Unit and treated with CNK for at least 3 months were included. Demographic features, disease characteristics, reasons for CNK introduction, concomitant therapies, variation in systemic steroids dose, adverse events, and response to treatment were retrospectively evaluated. Non-parametric tests were used for statistical comparisonResults:13 patients (5 women; median age 49 years, range 21-74), treated with subcutaneous CNK 4 mg/kg 4-weekly, were identified. Median disease duration before CNK introduction was 12 (6-240) months. After CNK introduction, 2 patients were followed-up for 18 months, 3 for 12 months, 6 for 6 months, 2 for 3 months. CNK was introduced as first-line biologic DMARD in 6 patients. The other 7 patients had been already treated with at least one other bDMARD, for a total of 15 treatment courses (7, anakinra, ANK; 4, tocilizumab; 4, TNF-inhibitors), with a median bDMARD therapy duration of 8 (4-178) months. Previous bDMARDs had been interrupted because of inefficacy (8 cases) or adverse events (AE, 7 cases); of the 7 ANK-treated patients, therapy interruption was due to inefficacy in 3 cases. At CNK introduction, 11 patients were on systemic steroid therapy, prednisone (PDN) equivalent dose 15 (5-80) mg, and 10 were concomitantly receiving a conventional DMARD (7, methotrexate; 2, colchicine; 1, cyclosporine-A).Graphic 1summarizes main clinical features at CNK introduction. After CNK start, a striking and rapid clinical response was observed, as demonstrated by a substantial decrease of modified Pouchot score and a normalization of acute phase reactants after only 3 months (see Table 1 for details). CNK showed also a significant steroid-sparing effect: median PDN dose was reduced to 7.5 (2.5-12.5) mg at month 3 and 5 (0-7.5) mg at month 6; PDN was stopped in 3 patients (1 at month 3, 1 at month 6, 1 at month 12) due to optimal disease control. CNK was temporarily held-off in 3 patients (zoster reactivation, 1; prostatitis, 1; mild leukopenia, 1). We observed no case of primary inefficacyTable 1.Disease activity and blood tests at canakinumab introduction and during follow-upDaily prednisone dosemgBaseline(n=13)3 months(n=13)6 months(n=11)12 months(n=5)18 months(n=2)Pouchot score15 (5-80)7.5 (2.5-12.5)5 (0-7.5)5 (0-7.5)2.5VAS pain3 (2-5)1 (0-2)0 (0-1)00Erythrocyte sedimentation ratemm/h7 (2-10)3 (1-8)2 (1-4)1 (1-2)1C-reactive proteinmg/L42 (8-120)21 (2-69)13 (2-55)14 (2-41)11Ferritinng/mL20.8 (3-180)3.1 (0.5-22.5)1.6 (0.5-8.4)1 (0.3-6.3)0.5Hemoglobing/dL379.5 (161-914)282 (82-552)215 (34-464)177 (77-401)19913.1 (9.4-15.7)13.2 (10.7-15.3)13.8 (11.5-15.5)13.9 (11.3-14.3)13.5Figure 1.Graphic 1 Main clinical features at canakinumab introductionConclusion:Our real-life data confirm that CNK is highly effective and safe in AOSD treatment and has significant steroid-sparing effects. CNK showed its efficacy both as first-line therapy and after other bDMARDs failure, also in patients who have previously failed IL-1 inhibition through ANKReferences:[1] Cavalli G, et al. Treating rheumatological diseases and co-morbidities with interleukin-1 blocking therapies. Rheumatology (2015)[2] Cavalli G, et al. Efficacy of Canakinumab as First-Line Biologic Agent in Adult-Onset Still's Disease. Arthritis Res Ther (2019)Disclosure of Interests:Alessandro Tomelleri: None declared, Corrado Campochiaro Speakers bureau: Novartis, Pfizer, Roche, GSK, SOBI, Giacomo De Luca Speakers bureau: SOBI, Novartis, Celgene, Pfizer, MSD, Nicola Farina: None declared, Elena Baldissera Speakers bureau: Novartis, Pfizer, Roche, Alpha Sigma, Sanofi, Giulio Cavalli Speakers bureau: SOBI, Novartis, Pfizer, Lorenzo Dagna Grant/research support from: Abbvie, BMS, Celgene, Janssen, MSD, Mundipharma Pharmaceuticals, Novartis, Pfizer, Roche, SG, SOBI, Consultant of: Abbvie, Amgen, Biogen, BMS, Celltrion, Novartis, Pfizer, Roche, SG, and SOB

Herbário das pastagens naturais: 41 anos de história.

Resumo

Fibra em Gramíneas Forrageiras Tropicais.

bitstream/item/28965/1/ClicNews-2010-12.pd

Using Conducting Polymers as Active Agents for Marine Antifouling Paints

Antifouling coatings were prepared with paints containing polyaniline (PAni) and derivatives as active pigment, and evaluated by antifouling performance on metallic or polyvinyl chloride substrates. The paints, PAni and its derivatives were characterized by FT-IR spectrophotometry, thermogravimetric analysis, electrical conductivity and scanning electron microscopy. Coatings were also characterized by salt spray, leaching and erosion tests. Antifouling coatings’ performance was evaluated by immersion tests in a marine environment or in fresh water. Paints containing PAni-ES, PAni/DBSA and SPAN, and a co-biocide PyZn, showed antifouling performance similar to a commercial antifouling paint