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Статті в журналах з теми "378.147:796.012.656 (043.3)"

1

Ritchlin, C. T., P. Rahman, P. Helliwell, W. H. Boehncke, I. Mcinnes, A. B. Gottlieb, S. Kafka, et al. "AB0538 POOLED SAFETY RESULTS FROM TWO PHASE-3 TRIALS OF GUSELKUMAB IN PATIENTS WITH PSORIATIC ARTHRITIS THROUGH 1 YEAR." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1300–1301. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1334.

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Background:DISCOVER 1 & 2, two double-blind, phase-3, psoriatic arthritis (PsA) trials of guselkumab (GUS, an IL-23 inhibitor), demonstrated significant improvement with GUS vs placebo (PBO) in signs and symptoms of PsA, with good tolerability, at week (w) 24 during the PBO-controlled period.1,2 Beyond w24, all patients (pts) switched to GUS. Continued treatment maintained efficacy through w52.3,4Objectives:To describe pooled safety results from the DISCOVER 1 & 2 trials through 1-year of GUS treatment.Methods:Adults with active PsA (DISCOVER 1: ≥3 tender/swollen joints and C-Reactive protein [CRP] ≥0.3 mg/dL; DISCOVER 2: ≥5 tender/swollen joints and CRP ≥0.6 mg/dL) were randomized to subcutaneous GUS 100 mg at w0, w4, then every 8 w (q8w); GUS 100 mg q4w; or PBO. At w24, PBO pts switched to GUS 100 mg q4w. Pts were biologic naive except ~30% pts in DISCOVER 1. Safety was reported through w60 in DISCOVER 1 and through w52 in DISCOVER 2.Results:Baseline characteristics were similar between treatment groups in the pooled studies. Through w24 and 1 year, numbers of pts per 100 patient years with ≥1 event were similar among treatment groups for adverse events (AEs), serious AEs, infections, serious infections, and discontinuations due to AE (Table 1). At 1 year, there were no cases of active tuberculosis, opportunistic infections (including candida), or inflammatory bowel disease in GUS-treated pts; 2 deaths in PBO pts; and low incidences that were similar across treatment groups for malignancy, major adverse cardiac events, and injection-site reactions. Incidence of anti-GUS antibodies was 4.5%, and most were not neutralizing. Mild elevations in serum hepatic transaminases and decreases in neutrophil counts were consistent at 1 year with the results at w24 (Table 1).Conclusion:GUS regimens of q8w and q4w were well tolerated in PsA pts through 1 year of treatment in the phase-3 DISCOVER trials, consistent with the w24 results. No meaningful differences between incidences of AEs were reported in the q8w and q4w groups. The safety profile of GUS in PsA pts is generally comparable with the previously established safety profile of GUS.References:[1]Deodhar A et al. Lancet. 2020;395:1115[2]Mease P et al. Lancet. 2020;395:1126[3]Ritchlin C et al. EULAR 2020 # SAT0397[4]McInnes I et al. EULAR 2020 # SAT0402Table 1.Number of Patients with AEs per 100 PY and Incidence of AEs of InterestTime Period24 Weeks1 Year*Treatment GroupPBOGUS SC 100 mgPBO to GUS‡GUS SC 100 mgDosing ScheduleMatchingq8wq4wGUSCombined†q4wq8wq4wGUSCombined‡ N3723753737483523753731100Total PY Follow-Up173173172346204384385589Patients with AEs per 100 PY, n (95% CI)≥1 AE143 (123, 166)148 (127, 171)154 (132, 178)151 (136, 167)92 (77, 108)114 (100, 130)115 (101, 131)109 (100, 117)≥1 Serious AE7.1 (3.7, 12)4.1 (1.6, 8.4)4.7 (2.0, 9.3)4.4 (2.5, 7.3)7.0 (3.8, 11.8)4.8 (2.9, 7.6)4.0 (2.2, 6.6)4.9 (3.6, 6.6)≥1 Infection50 (39, 62)47 (37, 59)52 (42, 65)49 (42, 58)39 (31, 49)41 (34, 48)38 (31, 45)39 (35, 44)≥1 Serious Infection1.7 (0.4, 5.1)0.6 (0.0, 3.2)1.8 (0.4, 5.1)1.2 (0.3, 3.0)2.5 (0.8, 5.8)1.3 (0.4, 3.1)0.8 (0.2, 2.3)1.3 (0.7, 2.3)Discontinued due to AE4.1 (1.6, 8.4)2.9 (1.0, 6.8)4.7 (2.0, 9.3)3.8 (2.0, 6.5)3.5 (1.4, 7.1)2.1 (0.9, 4.1)2.6 (1.3, 4.8)2.6 (1.7, 3.8)AEs of Interest§, n (%)Death2 (0.5)0000000Malignancy1 (0.3)2 (0.5)02 (0.3)1 (0.3)2 (0.5)03 (0.3)Major Adverse Cardiac Events1 (0.3)01 (0.3)1 (0.1)001 (0.3)1 (0.1)Opportunistic Infections00000000Tuberculosis00000000Inflammatory Bowel Disease1 (0.3)0000000Injection-Site Reaction1 (0.3)5 (1.3)4 (1.1)9 (1.2)4 (1.1)6 (1.6)9 (2.4)19 (1.7)Anti-GUS Antibody+-6/373 (1.6)9/371 (2.4)15/744 (2.0)14/350 (4.0)18/373 (4.8)17/371 (4.6)49/1094 (4.5)*Through w60 for DISCOVER 1 and w52 for DISCOVER 2; †Combined GUS q8w and q4w; ‡For patients who switched from PBO to GUS, only data on and after first GUS administration were included in this group; §PBO N=370.AE, adverse event; CI, confidence interval; GUS, guselkumab; PBO, placebo; PY, patient year; q4w, every 4 weeks; q8w, every 8 weeks; SC, subcutaneous; w, weekDisclosure of Interests:Christopher T. Ritchlin Grant/research support from: Received grant/research support from UCB Pharma, AbbVie, Amgen, consultation fees from UCB Pharma, Amgen, AbbVie, Lilly, Pfizer, Novartis, Gilead, Janssen, Proton Rahman Speakers bureau: Received speakers fees from Abbott, AbbVie, Amgen, BMS, Celgene, Lilly, Janssen, Novartis, Pfizer, Grant/research support from: Received grant/research support from Janssen and Novartis, consultation fees from Abbott, AbbVie, Amgen, BMS, Celgene, Lilly, Janssen, Novartis, and Pfizer., Philip Helliwell Consultant of: Consultation fees paid to charity (AbbVie, Amgen, Pfizer, UCB) or himself (Celgene, Galapagos), Grant/research support from: Received grants/research support paid to charity (AbbVie, Janssen, Novartis), Wolf-Henning Boehncke Consultant of: Received consultation fees from Janssen, Grant/research support from: Received grant/research support from Janssen Research & Development, LLC, Iain McInnes Consultant of: Received consultation fees from AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Gilead, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: Received grant/research support from Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Janssen, and UCB, Alice B Gottlieb Speakers bureau: Received speakers fees from Pfizer, AbbVie, BMS, Lilly, MSD, Novartis, Roche, Sanofi, Sandoz, Nordic, Celltrion and UCB, Consultant of: Received consultation fees from Pfizer, AbbVie, BMS, Lilly, MSD, Novartis, Roche, Sanofi, Sandoz, Nordic, Celltrion and UCB, Grant/research support from: Received grant/research support from Pfizer, AbbVie, BMS, Lilly, MSD, Novartis, Roche, Sanofi, Sandoz, Nordic, Celltrion and UCB, Shelly Kafka Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Alexa Kollmeier Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Elizabeth C Hsia Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Xie L Xu Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, May Shawi Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Shihong Sheng Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Prasheen Agarwal Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Bei Zhou Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Paraneedharan Ramachandran Shareholder of: Shareholder of Johnson & Johnson, Employee of: Employee of Janssen Research & Development, LLC, Philip J Mease Speakers bureau: Received speakers fees from Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau, Consultant of: Received consultation fees from Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB, Grant/research support from: Received grant/research support from Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB.
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2

Diklic, Aleksandar, Vladan Zivaljevic, Ivan Paunovic, Nevena Kalezic, and Svetislav Tatic. "Surgical procedures in patients with thyroid autoimmune disease." Srpski arhiv za celokupno lekarstvo 133, Suppl. 1 (2005): 77–83. http://dx.doi.org/10.2298/sarh05s1077d.

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Анотація:
Autoimmune thyroid disease is a serious medical problem in which various operative procedures are performed. The objective of the study is to explore the type of applied surgical procedures in autoimmune thyroid disease, advantages and disadvantages of various procedures, and criteria they have to meet. This is retrospective clinical study on 1478 patients, operated for Graves? toxic goiter (117 males and 795 females mean age 37.7) and Hashimoto thyroiditis (27 males and 539 females mean age 50.6) from 1995 to April 2005. Cancer in Graves? disease was found in 61 patients (6.7%), papillary in 60 (occult in 53 or 6.6%) and metastatic in 1, Hashimoto thyroiditis and thyroid cancer was found in 141 patients (24.9%), papillary in 116 or 20.5% (occult in 55 or 9.7%), follicular in 2 (0.3%), Hurthle in 11 (1.9%), medullary in 8 (1.4%), anaplastic in 2 (0.3%) and lymphoma in 3 (0.5%). We performed subtotal bilateral lobectomy in 344 (312 in Graves and 32 in Hashimoto), total lobectomy on one side with subtotal on the oposite in 307 (228 in Graves and 79 in Hashimoto); out of them, in 59 patients, the remnant was left in the region of the upper pole which we called atypic lobectomy. The most common procedure, total or near by total thyroidectomy, performed in 719 (371 in Graves and 349 in Hashimoto). One side lobectomy was performed in 103 patients with Hashimoto thyroiditis. Lymph node dissection was performed in 21 ( 1 in Graves and 20 in Hashimoto), in all central, in 10 lateral functional and in 6 mediastinal, in 15 patients with cancer and in 6 patients with benign disease. There was no operative mortality. In Graves? disease, there was postoperative bleeding in 4 (0.4%), wound infection in 2 (0.2%) recurrent pulsy in 18 (2%) and permanent hypoparathyroidism in 13 (1.4%). In Hashimoto thyroiditis, there was postoperative bleeding in 2 (0.4%), recurrent nerve pulsy in 11 (1.9%) and permanent hypoparathyroidism in 6 (1.1%). The most common surgical procedure in autoimmune thyroid disease is total thyroidectomy which is followed by low complication rate in specialised centers. Cancer is more frequent in Hashimoto than in Graves? disease.
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3

Graham, George G., William C. MacLean, Kenneth H. Brown, Enrique Morales, Jorge Lembcke, and Arturo Gastañaduy. "Protein Requirements of Infants and Children: Growth During Recovery From Malnutrition." Pediatrics 97, no. 4 (April 1, 1996): 499–505. http://dx.doi.org/10.1542/peds.97.4.499.

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Objective. To evaluate the adequacy of protein intakes now recommended as safe for infants and toddlers. Methods. Subjects were recovering malnourished infants, age 5.3 to 17.9 months, length age (LA) 2.5 to 6.4 months, weight age (WA) 1.5 to 5.2 months, weight/length (W/L) 78% to 100% of National Center for Health Statistics data; and toddlers age 11.4 to 31.6 months, LA 6.1 to 17.9 months, WA 3.9 to 12.0 months, W/L 79% to 99%. Infants were assigned at random to formulas with 5.5%, 6.7%, or 8.0% energy as 60:40 whey:casein protein. The 5.5% was based on FAO-WHO-UNU safe protein and average energy for ages 2.5 to 6.0 months. Toddlers received 4.7% (recommended for 6 to 18 months), 6.4%, or 8.0%. Identical concentrations (weight/kcal) of other nutrients were maintained; intakes were adjusted weekly to reach, in 90 days, the 50th percentile of weight for a LA 3 months greater than the initial one. Results. Infants consumed 125 ± 11 (SD), 116 ± 10, and 126 ± 14 kcal and 1.7 ± 0.1, 1.9 ± 0.2, and 2.5 ± 0.3 g protein Kg-1· d-1; gained 2.4 ± 0.7, 2.9 ± 0.7, and 2.6 ± 0.5 months in LA, and reached a W/L of 105 ± 5, 103 ± 6, and 105 ± 5% of reference. Sum of four fat-folds (Σ FF) grew 13.1 ± 6.9, 10.4 ± 4.8, and 11.7 ± 5.3 mm to 32.5 ± 5.2, 31.7 ± 4.7, and 30.5 ± 5.5 mm; arm muscle areas (AMA) 57%, 51%, 70% to 1004 ± 109, 1017 ± 110, and 1004 ± 116 mm2, still low; arm fat areas (AFA) 93%, 66%, and 93% to higher-than-normal 598 ± 105, 610 ± 101, and 541 ± 116 mm2. Regression of intake on weight gain estimated energy for maintenance + activity to be 81.0 ± 7.5 (SEM) kcal · kg-1· d-1, and cost of gain (storage + metabolic cost) as 7.6 ± 1.7 kcal/g, with no significant effect of % protein. Toddlers consumed 107 ± 9, 103 ± 12, and 105 ± 10 kcal and 1.3 ±0.1, 1.6 ± 0.2, and 2.1 ± 0.2 g protein kg-1 · d-1; gained 3.3 ± 0.7, 2.9 ± 0.6, and 3.3 ± 0.7 months in LA; to a W/L of 102 ± 1, 102 ± 3, and 101 ± 4%. Σ FF grew 9.2 ± 4.0, 7.4 ± 4.3, and 6.0 ± 3.8 to 28.9 ± 5.2, 30.5 ± 3.7, and 27.0 ± 2.7 mm; AMA 31%, 33%, and 34% to 1121 ± 115, 1124 ± 110, and 1117 ± 120 mm2; AFA 53%, 44%, and 45% to higher-than-normal 578 ± 106, 636 ± 99, and 569 ± 68 mm2. Cost of maintenance + activity was 70.8 ± 3.8 (SEM) kcal · kg-1 · d-1, that of weight gain 9.7 ± 1.35 kcal/g, with no effect of % protein. Conclusions. Within age groups, there were no significant protein-related differences in growth. In both infants and toddlers, high-energy intakes resulted in mild obesity, with lean body mass still deficient. Protein intakes two SD below the means in the lowest protein/energy cells, 1.5 g · kg-1 · d-1 for infants and 1.1 g · Kg-1 · d-1 for toddlers, should still be safe for nearly all children of comparable biological ages.
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4

Bardan, I., K. M. Fagerli, J. Sexton, G. Bakland, P. Mielnik, L. M. Paucar Loli, T. K. Kvien, E. Kristianslund, and A. B. Aga. "POS1305 TREATMENT RESPONSE TO TUMOR NECROSIS FACTOR INHIBITORS IN ADULTS WITH JUVENILE IDIOPATHIC ARTHRITIS: DATA FROM THE NOR-DMARD STUDY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 934.2–935. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1708.

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Background:Juvenile idiopathic arthritis (JIA) can cause considerable pain and disability in childhood and adulthood. Studies exploring the efficacy of medications in adult JIA patients are limited, although tumor necrosis factor inhibitors (TNFi) have been increasingly used in this patient group.Objectives:To explore the efficacy of TNFi ± comedication on disease activity in adult JIA patients, compared to a weighted rheumatoid arthritis (RA) cohort.Methods:Data from NOR-DMARD, a longitudinal observational study including patients > 18 years starting or switching DMARD treatment, was used [1]. Patients with a clinical JIA diagnosis, or patients with other inflammatory joint diseases diagnosed before 16 years were identified from the study population. RA patients were included for comparative purposes.Disease activity measurements and remission rates among patients starting treatment with TNFi ± comedication were collected at baseline, 3 and 6 months. Changes in disease activity and absolute remission rates after 3 and 6 months were calculated. Remission rates and change in disease activity from baseline were compared between JIA patients and a weighted RA cohort with weights based on age and gender, using linear and logistic regression for continuous and categorical variables, respectively.Results:281 JIA patients (68.9% female, mean (SD) age 32.1 (11.1) years, mean (SD) diagnosis duration 23.5 (12.2) years) and 1374 RA patients (71.6% female, mean (SD) age 52.7 (14.5) years, mean (SD) diagnosis duration 9.5 (10.0) years) were included in the analyses. Age, gender distribution and disease duration differed significantly between cohorts.Both groups had a significant improvement across all disease activity measures after 3 months (Table 1), which was maintained after 6 months across all measures except MHAQ. The RA group had a significantly greater 3- and 6-month improvement in SJC28. Both groups had an overall 6-month increase in absolute remission rates. The JIA group had a significantly higher 3-month DAS28 remission rate (Figure 1). This difference was not significant after 6 months, as remission rates from 3 to 6 months in the JIA group declined across all measures.Table 1.BaselineChange to 3 monthsChange to 6 monthsJIA*RA*Diff.§JIA*RA*Diff.§JIA*RA*Diff.§ESR, mm/h18.7 (18.9)25.5 (22.0)1.3 (-2.3 to 4.9)-7.4 (15.8)-7.6 (16.6)-0.3 (-4.4 to 3.8)-7.4 (16.8)-8.5 (18.2)0.0 (-5.7 to 5.7)SJC282.5 (3.6)5.5 (5.4)1.6 (1.3 to 2.0)-1.4 (3.4)-3.1 (4.7)-1.0 (-1.7 to -0.3)-1.6 (3.2)-3.5 (5.1)-1.0 (-1.9 to -0.1)TJC 284.0 (5.6)6.6 (6.4)1.3 (0.4 to 2.3)-1.8 (3.9)-3.1 (5.9)-0.6 (-1.4 to 0.2)-1.8 (3.9)-3.9 (6.2)-1.0 (-2.0 to 0.1)DAS283.6 (1.4)4.5 (1.6)0.3 (0.1 to 0.6)-1.2 (1.3)-1.2 (1.4)-0.0 (-0.3 to 0.3)-1.2 (1.3)-1.5 (1.4)-0.2 (-0.6 to 0.2)SDAI16.8 (10.6)23.1 (14.3)2.4 (0.3 to 4.5)-7.7 (9.9)-10.9 (12.7)-2.0 (-4.2 to 0.2)-7.9 (8.6)-13.2 (13.6)-2.8 (-5.8 to 0.2)PGA51.4 (26.3)49.9 (25.5)-4.0 (-8.5 to 0.5)-20.6 (26.7)-17.0 (26.7)2.7 (-2.2 to 7.6)-21.6 (25.3)-19.1 (28.7)3.4 (-3.0 to 9.8)MHAQ0.6 (0.5)0.7 (0.5)0.0 (-0.1 to 0.1)-0.24 (0.42)-0.22 (0.42)0.0(-0.1 to 0.1)-0.23 (0.40)-0.25 (0.45)0.0 (-0.1 to 0.1)*Mean (SD)§ Weighted group difference, RA coefficient (95 % confidence interval)Figure 1.Mean 3- and 6-month remission rates with error bars (SE)Conclusion:TNFi was equally effective in reducing disease activity in the JIA and RA cohort after 3 and 6 months, and in inducing remission after 6 months. Absolute remission rates in the JIA group declined from 3 to 6 months across all measures, and studies with longer duration are needed to explore the long-term efficacy of TNFi in the patient groups.References:[1]Kvien, T.K., et al., A Norwegian DMARD register: prescriptions of DMARDs and biological agents to patients with inflammatory rheumatic diseases. Clin Exp Rheumatol, 2005. 23(5 Suppl 39): p. S188-94.Disclosure of Interests:Imane Bardan: None declared, Karen Minde Fagerli: None declared, Joe Sexton: None declared, Gunnstein Bakland Speakers bureau: Abbvie, Consultant of: UCB, Pfizer, Novartis, Pawel Mielnik: None declared, Liz Marina Paucar Loli: None declared, Tore K. Kvien Speakers bureau: Fees for speaking: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofi, Consultant of: Fees for consulting: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gliead, Mylan, Novartis, Pfizer, Sandoz, Sanofi, Grant/research support from: Received research funding to Diakonhjemmet Hospital from Abbvie, Amgen, BMS, MSD, Pfizer and UCB, Eirik kristianslund: None declared, Anna-Birgitte Aga Grant/research support from: Dr. Aga reports personal fees from Abbvie, Eli Lilly, Novartis and Pfizer, outside the submitted work
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5

Bai, Xue, Alexander Noor Shoushtari, Allison Betof Warner, Henry Quach, Christopher G. Cann, Michael Zhang, Lalit Pallan, et al. "Discrepancies in response and immune-related adverse events (irAE) of anti-PD-1 monotherapy between races and primary sites in patients (pts) with advanced nonacral cutaneous melanoma (NACM)." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 9530. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.9530.

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9530 Background: Ultraviolet (UV)-induced high tumor mutation burden (TMB) of NACM is associated with response to anti-PD-1 monotherapy (aPD-1). Anatomic location of the primary lesion (reflecting UV exposure) and race (reflecting eumelanin level) may serve as surrogates for TMB and be associated with varying response and irAE patterns. Methods: Pts with advanced NACM receiving aPD-1 between 2009-2019 were retrospectively analyzed from 5 institutions in the US, Australia and China. Best response, survival (PFS and OS), and organ/system-specific irAEs were compared by race (Caucasian [C] vs non-Caucasian [NC]) and primary anatomic site. Results: Among 697 patients, 616 were C, 81 were NC. Complete response rate (CRR) was 24.8% (95%CI, 21.4-28.4) and 2.6% (95%CI, 0.3-9.1) and ORR was 54.9% (95%CI, 50.9-58.9) and 15.6% (95%CI, 8.3-25.6) in C and NC, respectively (both P<.001). Median PFS was 16.5 (95%CI, 12.0-23.1) and 5.2 (95%CI, 3.6-7.6) months, median OS was 60.5 (95%CI, 49.9-not reached [NR]) and 29.2 (95%CI, 17.9-NR) months, in C and NC, respectively (P<.001 and =.04). In multivariate analyses, C had significantly higher CRR (OR 13.4, 95%CI 3.1-57.4), ORR (OR 10.6, 95%CI 4.6-24.5), and longer PFS (HR 0.5, 95%CI 0.4-0.7) than NC. Compared to a head primary site, NACM from less UV-exposed regions had significantly lower CRR (upper trunk, OR 0.6, 95%CI 0.4-0.96; lower limb, OR 0.5, 95%CI 0.2-0.9), ORR (lower limb, OR 0.6, 95%CI 0.3-0.9) and poorer PFS (perineum/buttock, HR 2.1, 95%CI 1.2-3.5; lower limb, HR 1.6, 95%CI 1.2-2.2) and OS (perineum/buttock, HR 3.8, 95%CI 2.2-6.8; lower limb, HR 1.7, 95%CI 1.2-2.4). Overall irAE incidence was similar between C and NC but irAE subtypes varied. C had significantly higher incidence of GI (12.2%, 95%CI 9.5-15.3% vs 1.2%, 95%CI, 0.03-6.7%, P=.001), respiratory (10.3%, 95%CI 7.8-13.2% vs 0, P<.001) and grade 3/4 (15.4%, 95%CI 12.4-18.8% vs 6.2%, 95%CI 2.0-13.8%, P=.03) irAEs; and lower incidence of endocrine (13.8%, 95%CI 10.9-17.0% vs 32.1%, 95%CI 22.2-43.4%, P<.001) and liver (4.8%, 95%CI 3.2-7.1% vs 13.6%, 95%CI, 7.0-23.0%, P=.005) irAEs. IrAEs did not vary by primary NACM site. Conclusions: Race and primary site are independently correlated with distinct response and survival outcomes in pts with advanced NACM receiving aPD-1. IrAE subtypes vary by race although overall irAE incidence does not.
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6

Квітіньйо Макарена Мартінез, Соріано Федеріко Ґонзало, Яйченко Вірджинія, Стіб Бренда, and Барейро Хуан Пабло. "Predictors of Picture Naming and Picture Categorization in Spanish." East European Journal of Psycholinguistics 6, no. 1 (June 30, 2019): 6–18. http://dx.doi.org/10.29038/eejpl.2019.6.1.cui.

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Анотація:
The aim of this paper was to identify which psycholinguistic variables are better predictors of performance for healthy participants in a picture naming task and in a picture categorization task. A correlation analysis and a Path analysis were carried out. The correlation analysis showed that naming accuracy and naming latency are significant and positively correlated with lexical frequency and conceptual familiarity variables, whereas they are negatively correlated with H index. Reaction times in the categorization task were negatively correlated with lexical frequency and conceptual familiarity variables and positively correlated with visual complexity variable. The Path analysis showed that subjective lexical frequency and H index are the better predictors for picture naming task. In picture categorization task, for reaction times, the better predictor variables were subjective lexical frequency, conceptual familiarity and visual complexity. 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