Статті в журналах з теми "628.161; 546.726"

AbstractMonoclonal antibodies targeting cytotoxic T-lymphocyte antigen-4 (CTLA-4), programed cell death 1 (PD-1), or its ligand (PD-L1) have become the mainstay for advanced malignancies. The incidence of endocrine adverse events provoked by these immune checkpoint inhibitors (ICI) is based on data from randomized controlled trials, which have their drawbacks. PubMed was searched through August 22nd, 2017, by 2 reviewers independently (J.d.F. and C.E.A.). Early phase I/II, phase III experimental trials, prospective and retrospective observational studies were included. The weighted incidence and risk ratio were estimated for hypophysitis, primary thyroid disease, primary adrenal insufficiency, and diabetes mellitus. Their management is discussed in a systematic review. A total of 101 studies involving 19 922 patients were included. Ipilimumab-treated patients experienced hypophysitis in 5.6% (95% CI, 3.9–8.1), which was higher than nivolumab (0.5%; 95% CI, 0.2–1.2) and pembrolizumab (1.1%; 95% CI, 0.5–2.6). PD-1/PD-L1 inhibitors had a higher incidence of thyroid dysfunction – particularly hypothyroidism (nivolumab, 8.0%; 95% CI, 6.4–9.8; pembrolizumab, 8.5%; 95% CI, 7.5–9.7; PD-L1, 5.5%; 95% CI, 4.4–6.8; ipilimumab, 3.8%; 95% CI, 2.6–5.5). Combination therapy was associated with a high incidence of hypothyroidism (10.2–16.4%), hyperthyroidism (9.4–10.4%), hypophysitis (8.8–10.5%), and primary adrenal insufficiency (5.2–7.6%). Diabetes mellitus and primary adrenal insufficiency were less frequent findings on monotherapy. Our meta-analysis shows a high incidence of endocrine adverse events provoked by single agent checkpoint blockade, further reinforced by combined treatment.

We utilized 5-s changes of neck pressure and neck suction (from 40 to -80 Torr) to alter carotid sinus transmural pressure in seven men with peak oxygen uptake (VO2peak) of 41.4 +/- 3.6 ml O2.kg-1.min-1. Peak responses of heart rate (HR) and mean arterial pressure (MAP) to each carotid sinus perturbation were used to construct open-loop baroreflex curves at rest and during exercise at 25.7 +/- 1.1 and 47.4 +/- 1.9% VO2peak. The baroreflex curves were fit to a logistic function describing the sigmoidal nature of the carotid sinus baroreceptor reflex. Maximal gain for baroreflex control of HR (-0.31 +/- 0.05 beats.min-1.mmHg-1) and MAP (-0.30 +/- 0.08 mmHg/mmHg) at rest was the same as during exercise at 25 and 50% VO2peak (-0.30 +/- 0.05, -0.39 +/- 0.13 beats.min-1.mmHg-1 for HR, P = NS; -0.23 +/- 0.04, -0.60 +/- 0.38 mmHg/mmHg for MAP, P = NS). Resetting of the baroreflex occurred during exercise at 50% VO2peak. The centering point, threshold, and saturation pressures were significantly increased for baroreflex control of HR (delta pressure = 26.3 +/- 6.8, 19.6 +/- 10.4, 33.0 +/- 5.6 mmHg, P < 0.05) and MAP (delta pressure = 27.1 +/- 7.7, 16.1 +/- 14.8, 38.2 +/- 8.5 mmHg, P < 0.05). The operating point (steady-state HR and MAP) was shifted closer to threshold of the baroreflex during exercise at 50% VO2peak, as reflected by differences in HR and MAP between the centering and operating points (delta HR = 12.5 +/- 4.7 beats/min, P = 0.10; delta MAP = 7.6 +/- 1.3 mmHg, P < 0.05). These findings suggest a resetting of the carotid baroreflex during exercise with no attenuation in maximal sensitivity. A shift in operating point toward threshold of the baroreflex enables effective buffering of elevations in systemic blood pressure via reflex alterations in HR and MAP.

The aim: Develop a classification of post-traumatic soft tissue defects of the hand to standardize the care of this group of patients. And in order to simplify the choice of plastic technic for post-traumatic soft tissue defects of the hand by surgeons and traumatologists. Materials and methods: We analyzed the treatment of 54 patients with hand injury and PTSTD. 14 physicians used AFC in the choice of surgical method for the closure of PTSTDH. The practical application of AFC and effectiveness of providing medical care to patients with PTSTDH was performed on a ten-point scale by anonymous questioning immediately at the time of discharge from the hospital and 6 months after the injury. Results: The results of the practical application analysis of AFC by physicians were as follows: «convenience» – 8.7 ± 0.6; «usefulness» is 9.4 ± 0.2. The results of treatment for 54 patients were: hands «functionality» – 8,3 ± 0,4, «aesthetics» – 7,6 ± 1,7. The results in the retrospective group, in which the AFC was not applied, were as follows: «functionality» – 6.8 ± 0.7, and «aesthetics» – 5.6 ± 1.1 Conclusions: The proposed AFC of PTSTDH help to choose the proper method of surgical management and get good results.

AbstractObjectiveTo determine the prevalence of high weight at different characteristics, understand the perceptions and behaviours towards high body weight, and determine potential influencing factors of body weight misperception among high-weight adults in Jilin Province.DesignA cross-sectional survey with complex sampling design was conducted. We described the prevalence and perception of high body weight.SettingNortheast China in 2012.SubjectsAdults (n 20 552) aged 18–79 years.ResultsOf overweight individuals, 37·4 % considered themselves as ‘normal weight’, 4·8 % reported themselves as being ‘very thin’ and only 53·1 % were aware of their own weight being ‘overweight’. About 1·8 % of both male and female obese individuals perceived themselves as ‘very thin’. Only 29·1 % of obese people thought of themselves as ‘too fat’. Nearly 30·0 % of centrally obese men and women perceived that their waist circumference was about right and they were of ‘normal weight’; 5·7 % of the centrally obese even perceived themselves as being ‘very thin’. Only 51·8 and 12·5 % of centrally obese individuals reported themselves to be ‘overweight’ or ‘too fat’. Body weight misperception was more common in rural residents (OR; 95 % CI: 1·340; 1·191, 1·509). The prevalence of body weight misperception increased with age (middle age: 1·826; 1·605, 2·078; old people: 3·101; 2·648, 3·632) and declined with increased education level (junior middle school: 0·628; 0·545, 0·723; senior middle school: 0·498; 0·426, 0·583; undergraduate and above: 0·395; 0·320, 0·487).ConclusionsBody weight misperception was common among adults from Jilin Province.

e22519 Background: Global actions on pediatric cancer control is targeting to improve the survival rates in low and middle income countries which already exceeded 80% in high income countries. Almost 300.000 pediatric cancer cases annually are expected in children and adolescents aged 0-14 globally. Pediatric cancer registry must be a priority within the pediatric cancer control programs. Here, we present the most updated results of the pediatric cancer registry in Turkey. Methods: Pediatric cancer registry has been established by the Turkish Pediatric Oncology Group and Turkish Pediatric Hematology Association in 2002. The childhood cancer cases registered between 2009-2020 was included in this analysis. International Childhood Cancer Classification System was used for the classification. Essential demographic findings, ICD-O-3 morphology and topography codes were recorded for each case. Results: During the 12 years from 2009 to 2020, 21792 cases were registered. For all cases, median age was 6.7 year (0-19; M/F 12198/9584, 4 hermaphrodite, 6 unknown). Age distribution was 0-4 yrs, 40.9%; 5-9 yrs, 23.7%; 10-14 yrs, 23.4%; 15-19 yrs, 12.0%) The distribution of the tumor types were [number of cases, percentage of total, median age yrs, M/F]: Leukemia (5208, 23.9%, 5.5, 3004/2204); Lymphoma & other RES tumors (4103, 18.8%, 9.8, 2733/1367, 1 hermaphrodite & 2 unknown); CNS [brain & spinal] (3269, 15.0%, 6.8, 1794/1474, 1 unkown); Symphatetic system (1794, 8.2%, 2.4, 933/861); Retinoblastoma (610, 2.8%, 1.4, 339/271); Renal (1079, 5.0%, 3.1, 524/553, 1 hermaphrodite & 1 unknown); Liver (376, 1.7%, 2.2, 216/160); Malignant bone (1448, 6.6%, 12.5, 787/661); Soft tissue sarcomas (1554, 7.1%, 7.6, 888/666); Germ cell (1461, 6.7%, 9.3, 547/910, 2 hermaphrodite, 2 unknown); Carcinoma & other malignant epithelial (745, 3.4%, 13.5, 362/383); Other/non-specific malignant (145, 0.7%, 7.9, 71/74). Five year survival rate was found as 72%. Conclusions: This registry shows the imrovement of survival rates to 72% in Turkey which is comparable with middle income countries. The pediatric cancer control community is investing on the control of childhood cancer for further improvement and this registry became a valuable source for pediatric oncology community at national and international level.

11085 Background: Gene-expression signatures were shown to be prognostic and predictive for breast cancer but their performances over time have not been investigated. Methods: Recurrence score (RS) of oncotype, 70-gene profile (SGP) of Mammaprint, intrinsic subtype (IS) and wound signature (WS) were analyzed using a single dataset of 295 samples from Fan et al. (Fan et al. N Engl J of Med 2006; 355:560–9). Time-varying coefficient Cox models were used to estimate the time-dependent hazard ratios (HR) for relapse-free survival (RFS). Annualized RFS hazard rates were estimated using cubic splines. Concordance between RS and SGP was calculated for different intrinsic subtypes in all 295 samples and was evaluated in a subset of 173 ER+ samples not in the training set of SGP for unbiased comparison. Results: For the high risk groups of RS, SGP, IS and WS, hazard rates peaked around the 2nd year from surgery and decreased rapidly over time. For the low risk groups, hazard rates also peaked around the 2nd yr but remained fairly constant over time. Hazard ratios of high vs. low risk groups of RS at yr 2, 5 and 10 were 17.0 (8.4–34.0), 4.0 (2.0–8.0), 1.7 (0.83–3.4). For intermediate vs. low risk groups of RS, the corresponding HRs were 2.7 (1.1–7.0), 5.0 (1.1–7.4), 1.6 (0.63–4.2). Poor vs. good groups of SVP had HRs of 7.4 (4.5–12.1), 3.6 (2.2–5.9), 2.0 (1.2–3.3) at yr 2, 5, 10. HRs of Luminal B (LB), Basal-like (BL), HER2/ER- (HER2), Normal-like (NL) vs. Luminal A (LA) of Intrinsic Subtypes were 6.8 (4.0–11.5), 5.7 (3.2–10.0), 7.6 (4.0–14.1) and 1.7 (0.9–3.3) at yr 2. HRs at yr 5 were 4.0 (2.3–6.8), 0.7 (0.4–1.2), 1.1 (0.6–2.0) and 2.3 (1.2–4.4) respectively. For WS, HRs at yr 2, 5, 10 were 6.3 (3.3–11.9), 2.9 (1.6–5.6) and 2.2 (1.2–4.1) respectively. Concordance rates of RS and SVP were 1.0, 0.91, 0.86, 0.72 and 0.62 for BL, HER2, LB, LA, NL of Intrinsic Subtypes. In 173 ER+ samples not present in the SGP training set, concordance rate between RS and SVP was 0.77 (Cramer's V = 0.56); the same as in the whole set of 225 ER+ patients (Fan et al. N Engl J of Med 2006; 355:560–9). Conclusions: Prognostic values of gene-expression signatures decrease over time. They can best predict breast cancer relapse during the first 5 years. Concordance between RS and SPV is highest in the basal-like tumors and lowest in the Luminal B and Normal-like subtypes. No significant financial relationships to disclose.

Objective To determine risk factors affecting time-to-death ≤90 and >90 days in children who underwent a modified Blalock-Taussig shunt (MBTS). Methods Data from a retrospective cohort study were obtained from children aged 0–3 years who experienced MBTS between 2005 and 2016. Time-to-death (prior to Glenn/repair), time-to-alive up until December 2017 without repair, and time-to-progression to Glenn/repair following MBTS were presented using competing risks survival analysis. Demographic, surgical and anesthesia-related factors were recorded. Time-to-death ≤90 days and >90 days was analyzed using multivariate time-dependent Cox regression models to identify independent predictors and presented by adjusted hazard ratios (HR) and 95% confidence intervals (CI). Results Of 380 children, 119 died, 122 survived and 139 progressed to Glenn/repair. Time-to-death probability (95% CI) within 90 days was 0.18 (0.14–0.22). Predictors of time-to-death ≤90 days (n = 63) were low weight (<3 kg) (HR 7.6, 95% CI:2.8–20.4), preoperative ventilator support (HR 2.7, 95% CI:1.3–5.6), postoperative shunt thrombosis (HR 5.0, 95% CI:2.4–10.4), bleeding (HR 4.5, 95% CI:2.1–9.4) and renal failure (HR 4.1, 95% CI:1.5–10.9). Predictors of time-to-death >90 days (n = 56) were children diagnosed with pulmonary atresia with ventricular septal defect and single ventricle (compared to tetralogy of fallot) (HR 3.2, 95% CI:1.2–7.7 and HR 3.1, 95% CI:1.3–7.6, respectively), shunt size/weight ratio >1.1 vs <0.65 (HR 6.8, 95% CI:1.4–32.6) and longer duration of mechanical ventilator (HR 1.002, 95% CI:1.001–1.004). Shunt size/weight ratio ≥1.0 (vs <1.0) and ≥0.65 (vs <0.65) were predictors for overall time-to-death in neonates and toddlers, respectively (HR 13.1, 95% CI:2.8–61.4 and HR 7.8, 95% CI:1.7–34.8, respectively). Conclusions Perioperative factors were associated with time-to-death ≤90 days, whereas particular cardiac defect, larger shunt size/weight ratio, and longer mechanical ventilation were associated with time-to-death >90 days after receiving MBTS. Larger shunt size/weight ratio should be reevaluated within 90 days to minimize the risk of shunt over flow.

Maddox Dairy, located in Riverdale, CA, USA, is a Holstein herd that milks 3500 cows with a 305-day mature-equivalent milk production of 12 800 kg, and they have been producing high genetic animals by embryo transfer (ET) since the early 1980s. Invivo-derived embryos from Holstein donors were transferred fresh (grade 1 or 2) or frozen (grade 1), at morula (4), early blastocyst (5), or blastocyst (6) stage, to virgin heifers (VH, natural oestrus, 13-15 months old) or lactating cows (LC, Presynch-Ovsynch, 86 days in milk, first or second lactation) 6 to 9 days after oestrus. Pregnancy diagnosis was done by transrectal ultrasonography at 32-46 days in VH and by the IDEXX PAG test at 30 days in LC. June, July, August, September, and October were called critical months (first service AI conception rate drops below 44%) and compared with the other months. The data from 32 503 ETs between January 2008 and December 2018 are summarised on Table 1. Pregnancy rates (PR) are lower for LC recipients than for VH. Embryo transfers performed 7 or 8 days after oestrus had higher PR in both types of recipients and embryos, but Day 6 and 9 oestrus are also used with fair results. The season does not seem to affect PR. There is not enough difference in the combination of stage and days from oestrus for invivo-derived embryos. These numbers do not belong to a planned experiment. Several management changes during the years were made, which make it very difficult to apply statistical methods to analyse the data correctly. They are used as a tool to make decisions in an attempt to improve future results. Table 1.Pregnancy rate (PR) of virgin heifers (top) and lactating cows (bottom)-fresh (SH) and frozen (OZ) invivo-derived embryo transfer1 Heat-months SH-ST4 SH-ST5 SH-ST6 SH-All OZ-ST4 OZ-ST5 OZ-ST6 OZ-All PR% n PR% n PR% n PR% n PR% n PR% n PR% n PR% n Heifers 6 d-CM 62 934 66 243 68 69 63 1246 56 473 58 219 62 42 57 734 6 d-OM 62 1623 67 489 69 211 64 2323 56 600 55 296 48 137 55 1033 6 d-T 62 2557 67 732 69 280 63 3569 56 1073 57 515 51 179 56 1767 7 d-CM 64 1506 68 495 67 221 65 2222 60 822 62 340 63 156 61 1318 7 d-OM 66 2723 68 1021 69 510 67 4254 57 1120 59 581 57 231 58 1932 7 d-T 66 4229 68 1516 69 731 67 6476 58 1942 60 921 60 387 59 3250 8 d-CM 65 1348 64 518 67 322 65 2188 59 595 64 258 63 108 61 961 8 d-OM 66 2166 68 886 70 510 67 3562 61 770 60 364 51 130 60 1264 8 d-T 66 3514 67 1404 69 832 66 5750 60 1365 62 622 56 238 60 2225 9 d-CM 60 109 56 43 70 20 60 172 60 5 33 6 50 4 47 15 9 d-OM 58 129 63 57 60 40 60 226 63 16 50 18 75 4 58 38 9 d-T 59 238 60 100 63 60 60 398 62 21 46 24 63 8 55 53 All-CM 64 3897 66 1299 67 632 65 5828 58 1895 61 823 63 310 60 3028 All-OM 65 6641 67 2453 69 1271 66 10 365 58 2506 58 1259 53 502 58 4267 All-T 65 10 538 67 3752 69 1903 66 16 193 58 4401 60 2082 57 812 59 7295 Lactating cows 6 d-CM 54 265 48 86 50 12 53 363 38 141 31 77 50 10 36 228 6 d-OM 49 463 52 203 45 56 50 723 46 101 48 54 59 27 48 182 6 d-T 51 728 51 289 46 68 51 1086 41 242 38 131 57 37 42 410 7 d-CM 54 755 59 274 56 103 55 1137 43 928 48 450 43 192 45 1570 7 d-OM 55 914 66 367 54 109 58 1393 46 1052 45 564 47 353 46 1969 7 d-T 55 1669 63 641 55 212 57 2530 45 1980 46 1014 46 545 45 3539 8 d-CM 63 252 68 82 76 33 65 368 48 219 56 80 42 33 50 332 8 d-OM 61 257 64 161 53 47 61 466 50 191 53 77 56 16 51 284 8 d-T 62 509 65 243 63 80 63 834 49 410 55 157 47 49 50 616 All-CM 56 1272 58 442 60 148 57 1868 44 1288 47 607 43 235 45 2130 All-OM 55 1634 62 731 51 212 56 2582 47 1344 46 695 48 396 47 2435 All-T 55 2906 60 1173 55 360 57 4450 45 2632 47 1302 46 631 46 4565 1ST=stage; CM=critical months (June, July, August, September, and October); OM=other months.

This research aims to study the hydrolysis of passion fruit peel using cellulase and its evaluation for ethanol production. Passion fruit peel is a fruit processing waste that has not been utilized properly. Passion fruit peel contains holo-cellulose (64% w/w), which can be converted into ethanol through hydrolysis followed by fermentation. Hydrolysis using cellulase is more efficient and its fermentation using yeast to produce ethanol is common. The hydrolysis is carried out at various enzyme ratios (3, 5, 7, and 9% v/v) and at temperature 30 oC, material concentration 5 g/100 mL, pH 4-5, and shaking speed 160 rpm. The kinetics chosen were heterogeneous models; they were the fractal model by Valjamae and Kopelman. Before being hydrolyzed, the essential oil and pectin in passion fruit peel were extracted, because the compositions were quite high; the results were around 16.23 and 11.36% w/w, respectively. The effect of the enzyme ratio to the sugar concentration by hydrolysis is very significant. At 9 h, the glucose concentration reached 45.38, 51.86, 60.50, 66.00 g/L at various enzyme ratios of 3, 5, 7, 9% v/v. During the hydrolysis, the glucose concentration continues to increase and starts to decrease after 9 h. Hydrolyzate solution fermentation obtained from hydrolysis in various enzyme ratios showed consistent results; the higher the enzyme ratio and glucose, and the higher the ethanol will be (5.6, 6.8, 7.6, and 8.9% v/v). The kinetics model by Valjamae is more appropriate to describe the enzymatic hydrolysis mechanism of passion fruit peel than Kopelman. The fractal exponent values obtained from Valjamae and Kopelman models were 0.28 and 0.27. In Valjamae model, the enzyme ratio rises, from 3 to 9% v/v, the rate constant rises from 0.22 to 0.53 1/h. In Kopelman model, the rate constant rises too, from 0.21 to 0.51 1/h.Keywords: bio-ethanol; cellulase; enzymatic hydrolysis; fractal kinetic; passion fruit peel

The aim of the study was to identify the peculiarities of neuropsychological indices disorders depending on changes in the level of constant potential in patients with occupational diseases as a result of physical factors.Materials and methods. The study involved 60 patients with vibration disease caused by local vibration (group I), 106 patients with vibration disease caused by combined exposure to local and general vibration (group II), 101 civil aviation pilots with an established diagnosis of professional sensorineural hearing loss (group III), and 50 healthy men (group IV, comparison group) who were not exposed to vibration and noise due to the specifics of their professional activities. Methods of neuro-energy mapping and neuropsychological testing were used.Results. In groups I–II, compared with group IV, an increase in local levels of constant potential (DC-potential level) in the central, right temporal, and central frontal parts of the brain (2.3 (6.5–3.8) mV; –0.3 (–2.1–2.1); 2.1 (–3.4–6.8) and –0.3 (–3.1–4.3); –2.24 (–6.4–3.8); 0.9 (–3.1–8.5) mV at p = 0.005, 0.007 and 0.004 respectively). Differences in the values of DC-potential level gradients in individuals of group III when compared with group IV reached the level of significance in the central, temporal, occipital leads relative to the central frontal (–5.0 (–13.1–3.8); –4.1 (–9.4–5.1); –2.1 (–10.9–6.6); –6.3 (–15.3–1.8) and 2.9 (–3.0–10.6); 2.2 (–4.5–13.8); 5.6 (–7.6–14.1); –1.4 (–7.5–3.9) mV at p = 0.008; 0.009; 0.009, and 0.007 respectively). Cognitive disorders in patients of groups I–III when compared with group IV correspond to a mild disorder of dynamic, constructive praxis and expressive speech (1.40 (0–1,6); 1.43 (0–1,7); 1.2 (0–1,5) and 0.3 (0–1); 0.2 (0–1); 0.06 (0–1) points at p = 0.008, 0.008 and 0.009 respectively).Conclusions. A common neurofunctional sign of a mild impairment of the cognitive sphere in occupational diseases caused by physical factors is an increase in direct current potential level in the frontal-central and parieto-occipital regions, predominantly of the left hemisphere of the brain.

Abstract Background Anti-TNFs antibodies are the first biologic treatment option in inflammatory bowel disease (IBD). The long-term effectiveness of this strategy at the population level is poorly known, particularly in pediatric-onset IBD. Methods All patients diagnosed with Crohn’s disease (CD) or ulcerative colitis (UC) before the age of 17 between 1988 and 2011 in a population-based registry were followed retrospectively until 2013. Among patients treated with anti-TNFs, the cumulative probabilities of anti-TNF failure defined by primary failure, loss of response or intolerance were evaluated. Factors associated with anti-TNF failure were investigated by a Cox model. Results Among a total of 1007 patients with CD (median disease duration, 3.2 years IQR (1.2–7.6) and median follow-up 8.8 years (IQR, 4.6–14.2)) and 337 patients with UC (median disease duration, 2.5 years IQR [1.1–4.5] and median follow-up 7.2 years (IQR, 3.8–13.0)), respectively 481 (48%) and 81 (24%) were treated with anti-TNFs. Median age at anti-TNF initiation was 17.4 years (IQR, 15.1–20.9). Median duration of anti-TNF therapy was 20.4 months (IQR, 6.0–59.9). In CD, the probability of failure of 1st line anti-TNF therapy at 1, 3 and 5 years was respectively 29.3%, 47.0% and 54.6% for infliximab (n = 397) and 22.6%, 37.7% and 48.0% for adalimumab (n = 83). In UC, the probability of failure of 1st line anti-TNF therapy at 1, 3 and 5 years was respectively 37.3%, 49.0% and 61.0% for infliximab (n = 71) and 12.5% for these 3 timepoints for adalimumab (n = 10). In CD, probabilities of primary failure, loss of response and intolerance at 5 years were 10.4%, 36.7% and 6.8% (n = 480), respectively; in UC, these same probabilities were 7.5%, 39.2% and 11.3% (n = 81), respectively. Female sex (Hazard Ratio (HR) 1.43, 95% CI 1.09–1.87; p = 0.010) and intestinal resection prior anti-TNF initiation (HR 1.73, 95% CI 1.21–2.47, p = 0.003) were associated with anti-TNF failure in multivariate analysis. Conclusion In a population-based study of pediatric-onset IBD, approximately half of anti-TNFs users discontinue use within 5 years. Loss of response account for around two-thirds of failure, both for CD and UC.

Abstract Objectives We examined the effects of the Lifestyle Eating and Performance (LEAP) program to alleviate fibromyalgia-related symptoms. Methods The retrospective study included de-identified data of 33 subjects with fibromyalgia. Dietitians used the in-vitro Leukocyte Activation Assay-MRT (LAA-MRT) blood test results to develop the tailored LEAP program for each subject. The LAA-MRT measures white blood cells reactivity to scale the degree of an adverse immune response to 150 food and food-chemical antigens. The LEAP program is based on the principles of the oligoantigenic dietary approach which is built in a nutritionally balanced manner and takes into consideration the subject's eating habits. Body Mass Index (BMI) was calculated as weight in kg/height in m2. A symptom survey was used to evaluate the severity and frequency of 13 domains of symptoms associated with fibromyalgia. The survey was quantified on a scale of 0 - 4 with a range score from 0 to 248 points. Descriptive statistics and linear mixed models were performed using SPSS version 25. The study received approval from an independent Institutional Review Board (IRB). Results Subjects' age was 47.7 ± 12.4 years, BMI of 27.9 ± 3.8 kg/m,2 and 29 (88%) were female. The follow-up time seen by the dietitian was 76.0 ± 60.7 days. Linear mixed models indicated a significant reduction in overall mean (standard error) scores of fibromyalgia symptoms pre- versus post-intervention (98.3 ± 5.7 vs. 54.2 ± 6.3, P &lt; 0.001) and for each of the 13 domains [constitutional (12.9 ± 0.8 vs. 7.0 ± 0.8, P &lt; 0.001); emotional/mental (12.9 ± 1.0 vs. 7.5 ± 1.0, P = 0.001); head/ears (6.7 ± 0.8 vs. 4.3 ± 0.6, P = 0.018); skin (3.5 ± 0.6 vs. 1.9 ± 0.3, P = 0.030); nasal/sinus (9.3 ± 0.7 vs. 5.6 ± 0.8, P = 0.002); mouth/throat (4.7 ± 0.7 vs. 2.2 ± 0.3, P = 0.004); lungs (3.4 ± 0.7 vs. 1.5 ± 0.4, P = 0.026); eyes (6.2 ± 0.6 vs. 3.9 ± 0.6, P = 0.009); genitourinary (2.2 ± 0.3 vs. 1.1 ± 0.2, P = 0.017); musculoskeletal (12.5 ± 0.7 vs. 8.1 ± 1.0, P = 0.001); cardiovascular (1.7 ± 0.3 vs. 0.9 ± 0.2, P = 0.046); digestive (15.3 ± 1.2 vs. 7.6 ± 1.2, P &lt; 0.001); and weight management (6.8 ± 0.7 vs. 2.4 ± 0.5, P &lt; 0.001)]. Conclusions This study showed the beneficial improvements in fibromyalgia symptoms by the LEAP program and the potential as a tailored dietary option in the clinical management of fibromyalgia. Funding Sources Oxford Biomedical Technologies, Inc.

Abstract Introduction: High-dose chemotherapy followed by autologous hematopoietic stem cell transplantation (auto-HCT) is the standard of care for younger patients with newly diagnosed multiple myeloma (MM). In approximately 15% of MM patients the monoclonal (M) spike consists of k or l light chains only as opposed to heavy + light chains. It remains unclear whether light chain (LC) MM has a different prognosis compared to other monoclonal protein subtypes after an auto-HCT. Methods: We retrospectively analyzed 1067 patients with MM who underwent auto-HCT between January 1, 2004 and January 1, 2011 at our institution. We evaluated the outcome of newly diagnosed patients with LCMM and compared it to patients with IgG or IgA MM, who underwent an auto-HCT after induction therapy. Primary endpoints were complete remission (CR), progression-free survival (PFS) and overall survival (OS) from the date of auto-HCT. Kaplan-Meier analysis with the log-rank test was performed for univariate comparison of survival. Cox proportional hazards regression method was used for univariate and multivariate analyses. Results: Of 1067 patients who underwent auto-SCT during the period, 223 underwent auto-SCT after relapse, and were excluded. From the remaining 844 who underwent auto-SCT in first remission, we excluded 102 patients (AL amyloidosis 60, POEMS and other plasma cell disorders 10, non-secretory MM 15, IgD 10, IgM 6 and IgE 1) from the analysis. The remaining 742 patients were divided as follows: IgA, 162 patients (22%); IgG, 444 (60%) and LC, 136 (18%). Baseline patient characteristics are described in Table 1. Patients with LCMM were younger and had a higher CR rate to induction. Median follow-up for the entire cohort after auto-HCT was 38 months (range, 0.2-87.0). Post auto-HCT, 28% with IgG/IgA MM and 38% with LCMM achieved a CR (p=0.015). Median PFS was 26.0 months and 27.7 months in IgG/IgA MM and LCMM groups, respectively (p= 0.742). Median OS was not reached and 71.1 months in IgG/IgA MM and LCMM groups, respectively (p= 0.18, Figure 1). Multivariate Cox regression analysis for PFS identified <PR after auto-SCT, non-diploid karyotype, and induction chemotherapy without thalidomide or bortezomib as adverse prognostic factors. Multivariate Cox regression analysis for OS identified presence of hypodiploidy or monosomy 13/del13, higher lactate dehydrogenase pre-transplant, lower hemoglobin pre-transplant, and <PR after auto-HCT as adverse prognostic factors. M protein subtype did not affect PFS (hazard ratio [HR], 1.040; 95% confidence interval [CI], 0.825-1.311; p=0.742) or OS (HR, 1.313; 95% CI, 0.874-1.971; p=0.190). Conclusions: Patients with LCMM have a higher CR rate after auto-HCT, but their PFS and OS were similar to patients with IgG/IgA MM. Table 1. Patient Characteristics Variables, No. (%)/median (range) IgG/IgA myelomaN= 606 Light chain myelomaN= 136 P Median age at transplant, (y) 59 (31-80) 56 (32-78) .004 Age >65 years 138 (23) 23 (17) .134 Male 357 (59) 74 (54) .337 Ethnicity .731 Caucasian 399 (66) 94 (69) African American 99 (16) 22 (16) Mixed 87 (14) 18 (13) Asian 16 (3) 2 (2) Cytogenetic abnormalities at diagnosis by conventional cytogenetics Diploid 180 (30) 36 (27) .159 Hyperdiploid 93 (15) 9 (7) .008 Hypodiploid 27 (5) 11 (8) .082 t(11;14) 4 (1) 3 (2) .092 Monosomy 13 / del 13 44 (7) 9 (7) .789 Other high-risk abnormalities 2 (0) 1 (1) .456 Induction chemotherapy Bortezomib or IMiD-based 507 (84) 123 (90) .046 Pre-transplant evaluation Bone marrow plasma cell, (%) 2 (0-71) 2 (0-50) .136 Bone marrow plasma cell >10% 90 (15) 18 (13) .735 Hemoglobin, (g/dL) 11.3 (4.4-16.0) 10.8 (6.8-15.3) .025 Lactate dehydrogenase, (IL/L) 526 (221-5062) 526 (239-2748) .522 Calcium, (mg/dL) 9.0 (7.6-10.4) 9.0 (7.5-11.0) .055 Creatinine, (mg/dL) 0.9 (0.4-12.5) 0.9 (0.5-9.8) .017 Beta-2 microglobulin (mg/dL) 2.4 (1.1-40.0) 2.8 (1.2-33.8) .001 Time from diagnosis to auto-HCT (month) 8.0 (1.9-174.4) 6.8 (2.4-44.6) .001 Pre-transplant disease status .004 ≥ CR 24 (4) 15 (11) VGPR/PR 545 (90) 109 (80) SD/PD 37 (6) 12 (9) Conditioning regimen .008 Melphalan alone 508 (84) 126 (93) Melphalan-based regimen 98 (16) 10 (7) Final response after transplant .080 ≥ CR 168 (28) 52 (38) VGPR/PR 353 (58) 70 (52) SD/PD 81 (13) 14 (10) Figure 1. a) Progression-free survival, b) Overall survival in patients with light chain myeloma compared to those with IgG/IgA myeloma Figure 1. a) Progression-free survival, b) Overall survival in patients with light chain myeloma compared to those with IgG/IgA myeloma Disclosures Shah: Celgene: Consultancy, Research Funding. Thomas:Novartis, Celgene, Acerta Pharmaceuticals, Idera Pharmaceuticals: Research Funding.

Abstract Abstract 2112 Poster Board II-89 (Purpose) Asian populations have a wide variety of genetics and circumstances. Therefore, immune responses to allo-antigens may differ from those that are common among American and European populations. However, we have little information from Asian populations, and collaborative international study is required to improve the success of blood transfusions and transplantations. Therefore, we tried to analyze allo-antibodies (Abs) to erythrocyte antigens in patients from Asian countries. (Method) Forty-eight institutes, including those in Japan (29), Korea (15), Hong Kong (1), Singapore (1), Malaysia (1) and Thailand (1), participated to this cooperative study of allo-antibodies to erythrocyte antigens in Asian populations. We investigated the number of blood grouping tests, cross matching tests, and erythrocyte irregular Ab analyses as well as information of institutes including total number of bed, operations and transfusions performed. We also investigated methods adopted for screening and detecting irregular Abs to erythrocyte antigens. Furthermore, we studied the frequencies of irregular Abs to erythrocytes (D, C ,c, E, e, f, Ce, P1, M, N, S, s, Mia, Lea, Leb, Jka, Jkb, Jk3, Fya, Fyb,K, k, Kpa, Kpb, Jsa, Jsb, Dia, Dib, Lua, Lub, Xga and H), and compared them among Asian countries. The total number of independent cases included more than 866,000 patients. If a case was analyzed multiple times, we counted it as one case. Multiple antibodies detected in a patient were separately summarized. (Results) Ab screening methods adopted in these institutes included gel columns, beads columns, traditional tubes or some combination of these three. There was no difference in the methods including the erythrocyte panel adopted. Among the serum of 8,880 patients (male /female: 1 /1.55) 10,069 antibodies were detected. The numbers of these patients registered in each country are as follows; 4,222 in Japan, 2,423 in Korea, 975 in Malaysia, 622 in Thailand, 612 in Hong Kong and 26 in Singapore. On average, anti-E Ab was detected in 25.7% (min-max country, 14.3-32.2%) of patients, anti-Lea 20.9 % (3.2-30.4), anti-Mia 7.3% (0-49.4), anti-P1 6.6 % (0-10.6), anti-M 5.6 % (0-7.0), ant-c+E 4.9 % (1.6-8.5), anti-Leb 4.3 % (0-7.6), anti-D 4.0 % (0-16.2), anti-Fyb 2.2 % (0-3.7), anti-Dia 1.9 % (0-3.3), anti-Jka 1.7 % (0.8-7.7), anti-C+e 1.5 % (0-3.3), anti-Lea+Leb 1.4 % (0-5.8), anti-S 1.1 % (0-1.9), anti-c 1.1 % (0-2.3) and other Abs 9.9 %. Anti-D Ab was frequently observed in patients from Korea and Malaysia compared to Thailand, Hong Kong and Japan. Anti-Lea Ab was frequently observed in patients from Malaysia, Japan, Singapore and Korea. Anti-Dia Ab was observed in patients from Japan and Korea. Anti-Mia Ab was frequently observed in patients from Thailand and Hong Kong, followed by Malaysia and Singapore, and rarely from Japan and Korea. (Conclusion) This is the first international collaborative study on allo-immunity to erythrocyte antigens in Asian populations. There are some important differences among Asian countries with regard to the presence of anti-D, -Lea, -Dia and -Mia Abs. Further, the proportions of detected Abs, (such as anti-K, -D and -MiaAbs) differ from those reported in previous studies of patients from US and European counties (Winters et al, Hoeltge et al, Walker et al, etc). These new data will contribute to the advancement in successful blood transfusion in Asia and the world. Furthermore, the study will strengthen the network of international collaboration in future. Disclosures: No relevant conflicts of interest to declare.

Abstract Abstract 5014 Exposure to toxic compounds and pesticides leads to an increased risk to develop Multiple Myeloma (MM). The metabolism and the excretion of xenobiotics are mediated by the enzymes and transporters acting in the detoxifying/elimination process. The nuclear receptors NR1I2 (or PXR) and NR1I3 (or CAR) act as xenosensor activating the detoxifying/elimination process in response to the intracellular levels of xenobiotics. It has been hypothesized that part of the individual variability in drug metabolism efficiency could be due to the genetic variations within these regulator genes affecting their expression and/or function. To investigate the impact of genetic variation within these genes on MM susceptibility, we selected and genotyped 10 tag Single Nucleotide Polymorphisms (SNPs) in the PXR gene and 7 tag SNPs in the CAR gene in 627 MM cases (320 males and 307 females) and 883 (459 males and 424 females) controls from different European populations. All the SNPs were in Hardy-Weinberg equilibrium (p>0.001), with the exception of the PXR SNP rs2461818 that was therefore excluded from the analysis. We found no association of any of the genotyped SNPs with MM risk. In the same way, haplotype distribution showed no differences between cases and controls. This was the first comprehensive investigation of genetic variation in xenobiotic regulators genes PXR and CAR in relation to MM risk and our data suggest that common variants in these genes have no impact in modifying MM risk. Table I. Genotype distribution of the PXR and CAR SNPs among MM cases and controls. SNP (rs) Cases (%) Controls (%) OR* 95%C.I. p-value p-trend PXR C/C 429 (69.5) 623 (70.7) 1.00 Ref 0.423 rs10511395 A/C 160 (25.9) 228 (25.9) 1.02 0.81 – 1.30 0.851 A/A 28 (4.6) 30 (3.4) 1.38 0.81 – 2.35 0.232 PXR C/C 452 (74.0) 656 (74.8) 1.00 Ref 0.451 rs1054190 C/T 137 (22.4) 200 (22.8) 1.00 0.78 – 1.28 0.993 T/T 22 (3.6) 21 (2.4) 1.56 0.84 – 2.88 0.155 PXR C/C 412 (65.9) 591 (67.2) 1.00 Ref 0.819 rs11917714 C/T 190 (30.4) 250 (28.5) 1.07 0.85 – 1.35 0.535 T/T 23 (3.7) 38 (4.3) 0.84 0.49 – 1.44 0.536 PXR C/C 223 (36.3) 296 (33.7) 1.00 Ref 0.126 rs12488820 C/T 289 (47.0) 407 (46.4) 0.93 0.74 – 1.18 0.574 T/T 103 (16.7) 175 (19.9) 0.79 0.58 – 1.06 0.119 PXR G/G 430 (69.6) 593 (67.4) 1.00 Ref 0.807 rs13071341 A/G 166 (26.9) 269 (30.6) 0.85 0.67 – 1.07 0.158 A/A 22 (3.5) 18 (2.0) 1.70 0.90 – 3.22 0.102 PXR A/A 352 (58.7) 516 (39.4) 1.00 Ref 0.981 rs3237359 A/G 209 (34.8) 291 (33.5) 1.04 0.83 – 1.30 0.720 G/G 39 (6.5) 62 (7.1) 0.90 0.59 – 1.37 0.619 PXR C/C 255 (41.2) 383 (43.6) 1.00 Ref 0.815 rs13059232 C/T 299 (48.3) 390 (44.4) 1.16 0.93 – 1.44 0.192 T/T 65 (10.5) 106 (12.0) 0.94 0.66 – 1.33 0.711 PXR A/A 300 (48.7) 437 (49.7) 1.00 Ref 0.258 rs3732357 A/G 240 (39.0) 361 (41.0) 0.94 0.75 – 1.17 0.589 G/G 76 (12.3) 82 (9.3) 1.31 0.92 – 1.85 0.130 PXR T/T 328 (53.6) 463 (52.9) 1.00 Ref 0.424 rs1357459 C/T 249 (40.7) 345 (39.4) 1.02 0.82 – 1.27 0.850 C/C 35 (5.7) 67 (7.7) 0.75 0.49 – 1.17 0.206 CAR A/A 218 (35.4) 335 (38.1) 1.00 Ref 0.571 rs3003596 A/G 296 (48.0) 393 (44.7) 1.16 0.93 – 1.46 0.191 G/G 102 (16.6) 151 (17.2) 1.04 0.77 – 1.41 0.799 CAR G/G 264 (42.7) 371 (42.0) 1.00 Ref 0.642 rs3813627 G/T 276 (44.7) 392 (44.4) 0.98 0.79 – 1.23 0.882 T/T 78 (12.6) 120 (13.6) 0.91 0.66 – 1.26 0.581 CAR A/A 441 (73.1) 635 (73.5) 1.00 Ref 0.911 rs11265571 A/T 147 (24.4) 207 (24.0) 1.01 0.79 – 1.29 0.911 T/T 15 (2.5) 22 (2.5) 0.97 0.49 – 1.89 0.921 CAR T/T 404 (64.2) 575 (65.7) 1.00 Ref 0.836 rs2307418 G/T 193 (31.1) 268 (30.6) 1.02 0.81 – 1.27 0.879 G/G 23 (3.7) 32 (3.7) 1.05 0.60 – 1.83 0.863 CAR C/C 348 (56.6) 508 (57.7) 1.00 Ref 0.527 rs2502805 C/T 220 (35.8) 313 (35.6) 1.05 0.84 – 1.30 0.693 T/T 47 (7.6) 59 (6.7) 1.16 0.77 – 1.74 0.484 CAR A/A 245 (39.8) 346 (39.4) 1.00 Ref 0.770 rs4073054 A/C 291 (47.2) 412 (46.9) 0.98 0.78 – 1.22 0.855 C/C 80 (13.0) 120 (13.7) 0.94 0.68 – 1.31 0.720 CAR C/C 360 (57.6) 524 (59.8) 1.00 Ref 0.391 rs4233368 A/C 225 (36.0) 302 (34.4) 1.09 0.88 – 1.36 0.439 A/A 40 (6.4) 51 (5.8) 1.15 0.74 – 1.78 0.538 Genotype distribution among MM cases and controls in the overall population. * OR are adjusted for age, gender and region of origin. Differences in samples numbers are due to failures in genotyping. Disclosures: No relevant conflicts of interest to declare.

Abstract Introduction: Novel therapeutic agents such as immune checkpoint inhibitor (ICI) and brentuximab vedotin (BV) are active in classic Hodgkin lymphoma (cHL), including in patients that relapse after autologous stem cell transplant (ASCT). However, optimal management strategy is unclear for patients with relapsed or refractory (RR) cHL post-ASCT. The aim of the study is to determine the impact of novel agents relative to conventional therapy and allogeneic stem cell transplant (allo-SCT) on survival outcomes of patients with cHL who relapsed after ASCT. Methods: Patients with RR cHL who underwent ASCT between 06/1993 and 10/2017 at 3 Mayo Clinic sites were included. Clinical characteristics, treatment information, and outcome data were abstracted. For patients who relapsed after ASCT, the post-relapse progression free survival (PFS) and overall survival (OS) were analyzed using the Kaplan-Meier method and Cox proportional hazards models. Statistical analyses were done in JMP v15.2.1 and EZR v1.54. Results: A total of 332 patients with RR cHL who underwent salvage therapy and ASCT were identified. After a median post-ASCT follow-up of 8.6 years (range 6.8-9.7), 136 (41%) patients had a relapse or disease progression after ASCT. Patient characteristics of the 136 cases are summarized in the Table. The median age at post-ASCT relapse was 34 years (range 20-73), and 77 (57%) were male. 59 (43%) relapsed within 6 months and 77 (57%) relapsed after 6 months following ASCT. 59 (45%) had an extranodal site involvement at relapse. 14 (10%) had therapy with ICI or BV as salvage therapy prior to ASCT or maintenance therapy post-ASCT. The median post-relapse PFS and OS was 0.8 (95% CI 0.6-1.1) and 3.2 years (95% CI 2.2-5.5) years, respectively. Compared to patients who relapse after 6 months, patients who relapsed within 6 months of ASCT had worse post-relapse PFS (median 0.5 [0.3-0.7] vs 1.3 [0.9-1.9] years, p=0.0003) and OS (median 1.3 [0.5-2.2] vs 6.4 [3.7-10.4] years, p=0.0003). Extranodal site involvement at relapse was not associated with post-relapse PFS (median 0.7 [0.5-1.2] vs 0.9 [0.6-1.3] years, p=0.28) but was associated with worse post-relapse OS (median 2.7 [1.5-4.2] vs 6.4 [2.6-NA] years, p=0.006). Prior therapy with ICI or BV was not associated with post-relapse PFS (median 0.6 [0.3-NA] vs 0.8 [0.6-1.1] year, p=0.8) and OS (median NR [1.0-NA] vs 3.2 [2.2-5.5] years, p=0.5). After post-ASCT relapse, the median lines of subsequent therapy were 2 (range 1-12). For first post-ASCT salvage therapy, novel agents (ICI or BV), compared to other therapies, were associated with superior post-relapse PFS (median 1.7 [0.7-3.6] vs 0.7 [0.5-1.0] years, p=0.004) and OS (median 7.6 [4.7-NA] vs 3.2 [2.2-5.6], p=0.02). Allo-SCT following first post-ASCT relapse (n=9) was not associated with improvement in post-relapse PFS (median 2.2 years [0.3-NA] vs 0.8 [0.6-1.1] years, p=0.1) or OS (median NR [0.5-NA] vs 5.1 [3.2-7.3] years, p=0.7). Patients who received ICI or BV at any point post-ASCT relapse had significantly better post-relapse OS (median 7.6 [4.3-16.7] vs 2.2 [1.4-3.7] years, p=0.004) compared to those who never received any novel agent (Figure 1A). In contrast, allo-SCT at any point post-ASCT relapse (n=27) did not improve post-relapse OS (median 5.6 [2.7-NA] vs 4.7 [2.7-7.3] years, p=0.3) (Figure 1B). In multivariate Cox regression models adjusted for age and sex, exposure to ICI and/or BV was associated with superior post-relapse OS (HR 0.5, 95% CI 0.3-0.8, p=0.007); however, allo-SCT was not associated with improvement in post-relapse OS (HR 0.8, 95% CI 0.4-1.5, p=0.5). Conclusions: Patients relapsing within 6 months of ASCT and those with extranodal involvement at relapse had inferior OS after post-ASCT relapse. Prior therapy with novel agents did not impact post-relapse survival outcomes. In the setting of post-ASCT relapse, novel therapeutic agents significantly improved survival outcomes while allo-SCT did not. Future multicenter studies are needed to explore the role of novel agents and allo-SCT in patients with RR cHL post-ASCT relapse. Figure 1 Figure 1. Disclosures Wang: Eli Lilly: Membership on an entity's Board of Directors or advisory committees; InnoCare: Research Funding; MorphoSys: Research Funding; Genentech: Research Funding; Novartis: Research Funding; LOXO Oncology: Membership on an entity's Board of Directors or advisory committees, Research Funding; Incyte: Membership on an entity's Board of Directors or advisory committees, Research Funding; TG Therapeutics: Membership on an entity's Board of Directors or advisory committees. Paludo: Karyopharm: Research Funding. Tun: Gossamer Bio, Acrotech: Consultancy; Mundipharma, Celgene, BMS, Acrotech, TG therapeutics, Curis, DTRM: Research Funding. Cerhan: Regeneron Genetics Center: Other: Research Collaboration; Genentech: Research Funding; Celgene/BMS: Other: Connect Lymphoma Scientific Steering Committee, Research Funding; NanoString: Research Funding. Habermann: Tess Therapeutics: Other: Data Monitoring Committee; Morphosys: Other: Scientific Advisory Board; Incyte: Other: Scientific Advisory Board; Seagen: Other: Data Monitoring Committee; Loxo Oncology: Other: Scientific Advisory Board; Eli Lilly & Co.,: Other: Scientific Advisor. Witzig: Karyopharm Therapeutics, Celgene/BMS, Incyte, Epizyme: Consultancy, Membership on an entity's Board of Directors or advisory committees; Celgene/BMS, Acerta Pharma, Kura Oncology, Acrotech Biopharma, Karyopharm Therapeutics: Research Funding. Nowakowski: Celgene, MorphoSys, Genentech, Selvita, Debiopharm Group, Kite/Gilead: Consultancy, Membership on an entity's Board of Directors or advisory committees; Celgene, NanoString Technologies, MorphoSys: Research Funding. Ansell: Bristol Myers Squibb, ADC Therapeutics, Seattle Genetics, Regeneron, Affimed, AI Therapeutics, Pfizer, Trillium and Takeda: Research Funding.

Abstract Abstract 1109 Poster Board I-131 The main objective of the CML-Registry of the European Treatment and Outcome Study (EUTOS) is to collect diagnostic, treatment and outcome data of CML-patients in Europe in order to allow for the analysis of prognostic factors, the evaluation of the quality of care and the comparative assessment of outcomes. Methods Eligibility criteria were: diagnosis of chronic phase Ph+ or bcr/abl positive CML between 2002 and 2006, age ≥ 18 years, and start with any kind of imatinib-based treatment in a prospective study within six months after first diagnosis. For hematologic (HR), cytogenetic (CgR), and molecular (MR) remission the ELN criteria were used. Competing risk estimations and Landmark analyses were applied when indicated. Patients from the FI-LMC-group in France (n=526), Germany (n=644), Italy (n=513), The Netherlands (n=119), the Nordic Countries (Denmark, Finland, Norway, Sweden, n=140)) and Switzerland (n=13) were included (date: 07/11/2009), for an overall n of 1955 patients. Results Median age was 52.5 years and 45% were female. The Euro prognostic score profile was for 38% of the patients low, for 51% intermediate and for 11% high risk. Imatinib 400 mg was allocated to 41%, Imatinib 600 mg to 8%, Imatinib 800 mg to 17%, and Imatinib-based combinations with IFN or Ara C to 34% of the patients. Median observation time was 24 months (range: 1-81). Complete hematologic remission (CHR) was finally achieved by 97%, complete cytogenetic remission (CCgR) by 94%, and major molecular remission (MMR) after 18 months by 62%. Overall survival (OS) after 60 months was 92%. Euro score clearly separated high risk vs. non high risk patients with regard to CHR (p=.0002), CCgR (p=.0023), but not for MMR, whereas Sokal score did so for CCgR (p<.0001). Deletion 9q did not show any impact on CHR, CCgR or MMR. Using Landmark-analysis with those 1012 patients who provided complete data for CHR, CCgR and MMR, CHR within 6 months from day 1 of imatinib treatment showed an impact on the chance to achieve CCgR (96.1% vs. 87.5% p=.0003) and MMR at 18 month (56.1% vs. 48.5%, p=.087). CHR within 3 months did not show a relevant impact on CCgR and MMR. Partial CgR (Ph+ < 35%, n=725)) within 6 months was associated with a higher chance to achieve MMR at 18 month (62.8% vs. 51.4% p=.0003). Patients who did not achieve CCgR within 3 (93%), 6 (70%), 12 (29%) or 18 (18%) months experienced an increasing risk for disease progression of 6%, 7%, 11% and 14% respectively but still showed a chance to eventually achieve CCgR of 87%, 83%, 60%, and 36%. Conclusions: This combined analysis of multinational European data showed very good response data regarding CHR, CCgR, MMR, and OS. Current prognostic CML scores seem to not separate prognosis of CML-patients sufficiently well. Early response markers like CHR and CgR after 6 months allow to differentiate the prognosis with regard to MMR but their clinical relevance may be questioned. Patients without CCgR within 6 months have a higher risk for disease progression and thus a closer follow up is indicated. With accumulating observation time the European CML Registry will allow to answer many clinically relevant questions about the prognostic value of early response markers. Disclosures Hasford: Novartis Pharma: Research Funding. Rosti:Novartis Pharma, Bristol Myers Squibb: Consultancy, Speakers Bureau. Baccarani:Novartis Pharma, Bristol Myers Squibb, Merck Sharp & Dome, Pfizer: Consultancy, Speakers Bureau. Montrucchio:Novartis Pharma : Employment. Rancati:Novartis Pharma: Employment. Simonsson:Novartis, BMS, Schering-Plough: Consultancy, Honoraria, Research Funding. Ossenkoppele:Novartis Pharma, BMS: Consultancy. Hehlmann:Novartis Pharma: Research Funding.

Background:Osteosarcopenia is defined as osteoporosis combined with sarcopenia. Both osteoporosis and sarcopenia are risk factors for falls and fractures in healthy individuals1. The relationships of falls and fractures to osteosarcopenia in rheumatoid arthritis (RA) patients are unknown.Objectives:The synergistic effect of osteoporosis and sarcopenia and the impact of osteosarcopenia on falls and fractures in RA patients were investigated using four years of data from a longitudinal study.Methods:The data from a prospective, observational study (CHIKARA study: UMIN000023744) were examined. The patients were divided into four groups according to their baseline status: no sarcopenia and osteoporosis (SP-OP-); only sarcopenia (SP+OP-); only osteoporosis (SP-OP+); and both sarcopenia and osteoporosis (SP+OP+). Sarcopenia was diagnosed by the criteria of the Asia Working Group on Sarcopenia 20142. Patients with osteoporosis were defined as those having a therapeutic intervention for osteoporosis. The survival rate and Cox hazard ratio were analyzed using falls and fractures as endpoints, adjusted by age, sex, and body mass index.Results:A total of 100 RA patients (female 78%, mean age 66.1 years) were enrolled. The number of SP-OP-, SP+OP-, SP-OP+, and SP+OP+ patients was 45, 17, 27, and 11, respectively. Their baseline characteristics are shown in Table 1. A total of 35 patients had falls, and 19 patients had fractures during the four-year follow-up. The fall-free survival rate in the SP-OP-, SP+OP-, SP-OP+, and SP+OP+ groups was 75.6%, 64.7%, 51.9%, and 36.4%, respectively; that of the SP+OP+ group was significantly lower than that of the other groups (P=0.021) (Figure 1). The fracture-free survival rate in the SP-OP-, SP+OP-, SP-OP+, and SP+OP+ groups was 86.7%, 82.4%, 81.5%, and 54.5%, respectively. That of the SP+OP+ group was relatively lower than that of the other groups (P=0.121). The hazard ratio of falls was significantly increased in the SP+OP+ group by 3.32-fold (95%CI: 1.01-10.9) compared to that in the SP-OP- group, whereas that in the SP+OP- and SP-OP+ groups was 2.58-fold (95%CI: 0.75-8.8) and 2.29-fold (95%CI: 0.94-5.6) higher, respectively. There were no significant differences compared to the SP-OP- group. The hazard ratio of fractures in the SP+OP+ group was increased 2.73-fold (95%CI: 0.61-12.2) compared to that in the SP-OP- group.Table 1.Baseline characteristics of the four groupsSA-OP-SA+OP-SA-OP+SA+OP+P value*Female, %73.358.888.91000.027Age, years63 (49, 72)69 (60, 79)73 (64, 75)73 (65, 81)0.008Disease duration, years4.4 (1.0, 8.4)4.0 (1.3, 8.9)7.6 (1.5, 14.5)10.5 (3.2, 26.5)0.035DAS28-ESR3.14 (2.66, 3.70)3.55 (3.01, 4.65)3.93 (3.28, 4.63)3.53 (2.48, 3.89)0.01mHAQ0.25 (0, 0.375)0.375 (0.125, 0.875)0.375 (0.125, 0.875)0.5 (0.125, 0.875)0.065MTX, mg/week, rate (%)8.4 ± 2.9 (86.7)8.7 ± 3.5 (70.6)8.3 ± 2.8 (92.6)6.8 ± 1.0 (90.9)0.388Glucocorticoid, mg/day, rate (%)3.7 ± 1.9 (20.0)6.3 ± 1.8 (11.8)4.0 ± 1.7 (44.4)3.8 ± 1.8 (18.2)0.400Body mass index, kg/m223.4 ± 3.819.2 ± 2.321.7 ± 2.419.2 ± 2.0<0.001Data are shown as mean ± standard deviation (SD) or median (25th, 75th percentile).*: compared in four groups by Kruskal-Walls test.Figure 1.Fall-free survival rates of the four groups.Conclusion:The survival rates with the endpoints of falls and fractures in RA patients with osteosarcopenia were lower during the four-year follow-up. In particular, the risk of falls increased with the synergistic effect of osteoporosis and sarcopenia in RA patients.References:[1]Dennison, E. M. et al. Fracture risk following intermission of osteoporosis therapy. Osteoporos Int30, 1733-1743, doi:10.1007/s00198-019-05002-w (2019).[2]Chen, L. K. et al. Sarcopenia in Asia: consensus report of the Asian Working Group for Sarcopenia. J Am Med Dir Assoc15, 95-101, doi:10.1016/j.jamda.2013.11.025 (2014).Disclosure of Interests:None declared.

Целью данной работы является синтез и исследование свойств синтетического айкинита, PbCuBiS3.Синтез проводили в откачанных кварцевых ампулах в течение 7–8 ч, максимальная температура составляла 1250–1325 К. Далее образцы охлаждали и выдерживали при 600 К в течение недели. Потом ампулы вскрывали, образцы тщательно перетирали и после плавки отжигали при 600–800 К в зависимости от состава не менее двух недель для приведения образцов в равновесное состояние. Отожженные образцы исследовали методами дифференциально-термического (ДТА), рентгенофазового (РФА), микроструктурного (МСА) анализов, а также измерением микротвердости и определением плотности. РФА проводили на рентгеновском приборе модели Д 2 PHASER с использованием CuKa- излучении Ni-фильтр.Комплексом методов физико-химического анализа изучены разрезы CuBiS2–PbS, Cu2S–PbCuBiS3, Bi2S3–PbCuBiS3, PbBi2S4–PbCuBiS3, PbBi4S7–PbCuBiS3 квазитройной системы Cu2S–Bi2S3–PbS и построены их фазовые диаграммы.Установлено, что кроме сечения PbBi2S4–PbCuBiS3 все разрезы квазибинарные и характеризуются наличием ограниченных областей растворимости на основе исходных компонентов.При изучении разреза CuBiS2–PbS установлено образование четверного соединения состава PbCuBiS3, встречающееся в природе в виде минерала айкинита, плавящегося конгруэнтно при 980 К. Установлено, что соединение PbCuBiS3 кристаллизуется в ромбической сингонии с параметрами решетки: а = 1.1632, b = 1.166, с = 0.401 нм, прост. группа Pnma, Z = 4. Методами ДТА и РФА установлено, что соединение PbCuBiS3 является фазой переменного состава с областью гомогенности от 45 до 52 мол. % PbS. 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Abstract Introduction: The optimal management of relapsed/refractory lymphoma is a significant clinical challenge. Early phase clinical trials are primarily designed to assess safety but also represent options for patients with limited therapeutic choices. Outcomes for lymphoma patients on early phase trials have previously been reported as single centre cohorts or grouped analyses with other malignancies. We performed a novel meta-analysis of publically available reports of early phase trials in lymphoma and compared the outcomes with those from our early phase trials unit. Methods: The outcomes of lymphoma patients enrolled on early phase trials at a UK tertiary centre were reviewed. AEs were graded according to CTCAE v4.0 and response criteria evaluated per protocol. Patient and therapy characteristics, AEs and best clinical responses were summarised by descriptive statistics. Individual-patient survival data were analysed using Kaplan-Meier method and survival curves compared with the log-rank test. A systematic literature review was performed using EMBASE, MEDLINE and clinicaltrials.gov to identify publicly available reports of early phase clinical trials reported in 2016-2017 and data was extracted by two independent reviewers. Meta-analyses of ORRs were performed using random-effect models. Results: 50 patients were enrolled onto 9 Phase I and I/II trials between March 2012 and June 2018, Four patients participated in 2 trials, considered separate events. 5 IMPs were small molecular inhibitors, 4 immunotherapies, 4 first in human and 8 investigated as monotherapy. Diagnoses included 42 aggressive NHL (aNHL) [30 DLBCL, 3 PMBCL, 3 Richters, 1 MCL, 5 T cell], 10 indolent NHL (5 WM, 2 FL, 2 MZL, 1 CLL/SLL) and 2 HL. Median age was 54 yr (27-83), 72% male, with a median time from diagnosis of 22.5 months and median 3 prior lines of therapy (range 1-8). Patients received a median number of 2 cycles of IMP (range 1-28) over 57.5 days (IQR: 37-116). 42.6% experienced grade 3-4 toxicity and 31.5% required dose interruptions of >7 days. ORR and clinical benefit rate (≥SD) were 28% and 47% respectively (CR 4%, PR 24%, SD 19%). Patients were followed up for a median of 11.4 months. Median PFS and OS were 2.3 and 6.8 months respectively, with PFS and OS at 3, 6 and 12 months being 45.8%, 34.4%, 26.5% and 58.4%, 45.4% and 38.8%. Median OS was greater for those who received <4 vs ≥ 4 prior lines of treatment (9.6 vs 5.2 months, p-value log-rank test = 0.1) and those with indolent lymphoma vs aNHL (8.2 vs 6.4 months). Patients with DLBCL had a median OS of 6.8 months; ABC subtype had inferior median OS vs GC (3.4 versus 17.6 months [p-value 0.1]). Study withdrawal was due to disease progression, toxicity and allogeneic stem cell transplantation. After trial, 5.6% proceeded to SCT, 33.3% patients received other treatment, 38.9% received palliation (subsequent outcome unknown in 16.7%). 164 lymphoma trial reports were included in the meta-analysis detailing outcomes of 4537 patients (Table 2). All studies were Phase I (72.6%) or I/II and 78% included only patients with lymphoma (all other trials included reported subgroup analysis of lymphoma patients). 95.7% of trials evaluated a single IMP, 52.4% used combinations of agents. IMPs most frequently investigated were small molecule inhibitors (25.6%), antibody-drug conjugates (11.6%) and epigenetic modifiers (10.4%). Immunotherapy trials comprise 36.1% of studies, including ADCs, checkpoint inhibitors (7.32%), naked antibodies (9.2%) and cellular therapies including CAR-T (7.93%). The ORR of all patients was 54.2% (95% CI 49.6% - 58.8%). Subset analysis showed that cellular therapies studies reported a pooled ORR of 62.5% (50.9 - 72.8) and antibody therapies 58.3 (46.7 - 69.2). Conclusion: The outcomes of lymphoma patients on early phase trials is historically perceived as very poor, partly due to the grouping of analysis with other malignancies. Our cohort had an ORR of 28% and OS at 6 months of 58.4%. The meta-analysis of global studies reporting lymphoma specific outcomes, revealed an ORR of 54.2%. This included all histological subtypes and some previously untreated patients. Our cohort was enriched for relapsed aNHL, which may account for the inferior ORR in our cohort. Together, both data sets indicate improved outcomes compared to historical reports and support enrolment of suitable patients into phase I trials when conventional options are exhausted. Disclosures Ardeshna: Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Other: Travel, Accommodations, Expenses; Roche: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Other: Travel, Accommodations, Expenses; Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Other: Travel, Accommodations, Expenses; Roche: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Other: Travel, Accommodations, Expenses; Takeda: Membership on an entity's Board of Directors or advisory committees; Takeda: Membership on an entity's Board of Directors or advisory committees; ADC Therapeutics: Membership on an entity's Board of Directors or advisory committees, Research Funding; ADC Therapeutics: Membership on an entity's Board of Directors or advisory committees, Research Funding. Popat:Amgen: Honoraria. Townsend:Gilead: Consultancy, Honoraria; Roche: Consultancy, Honoraria.

Nickel (Ni) laterites are regolith materials derived from ultramafic rocks and play an important role in the world's Ni production. Ni-laterite deposits are the supergene enrichment of Ni formed from the intense chemical and mechanical weathering of ultramafic parental rocks. In Vietnam, the weathering profile containing Ni laterite was first discovered in the Ha Tri massive (Cao Bang). This profile develops on the Ha Tri serpentinized peridotite rocks classified to the Cao Bang mafic-ultramafic complex (North Vietnam) and exhibits thick weathered zone (10 - 15m). This work carried out a detailed study of the weathering profile at the center of Ha Tri massive. Samples from different horizons of the profile were collected and analyzed in detail by XRF, XRD and SEM-EDX methods to establish the relationship between the Ni-rich supergene products and the parental peridotites (lherzolite) rocks in Ha Tri massive. The results show that the saprolite horizon is most Ni-rich in the weathering profile in Ha Tri. In this horizon, Ni-silicate minerals of garnierite group such as pimelite, nepouite and other Mg-Ni silicates have been found. The appearance of minerals of garnierite group is due to the exchange of Mg by Ni during weathering of peridotite minerals, especially olivine, which leads to the enrichment of the supergene Ni. The occurrence of Ni silicates suggests the existence of the supergene Ni ore in the weathering profile of the Ha Tri massive.References Bosio N.J., Hurst J.V., Smith R.L., 1975. Nickelliferousnontronite, a 15 Å garnierite, at Niquelandia, Goias Brazil. Clays Clay Miner., 23, 400-403. Brand N.W., Butt C.R.M., Elias M., 1998. Nickel Laterites: Classification and features. AGSO Journal of Australian Geology & Geophysics, 17(4), 81-88. Bricker O.P., Nesbitt H.W. and Gunter W.D., 1973. The stability of talc. American Mineralogist, 58, 64-72. Brindley G.W. and Hang P.T., 1973. 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Abstract Background: Total lymphocyte count (TLC) has been shown to correlate with outcomes in patients (pts) with acute leukemia. The clinical correlation to TLC in pts with chronic myeloid leukemia in chronic phase (CML-CP) who were treated with a tyrosine-kinase inhibitor (TKI) is unclear. Methods: Lymphocyte data in pts with newly diagnosed CML-CP who were enrolled in consecutive or parallel clinical trials with front-line imatinib (IM), nilotinib (Nilo), or dasatinib (Dasa) were collected at the time of diagnosis, and 3 and 6 months (M) after the start of TKI. Relative lymphocytrosis (RLC) was defined as lymphocyte >150% at 3 or 6M compared with baseline at diagnosis. Absolute lymphocytosis (ALC) was defined as lymphocyte > 4,000 /µL at 3 or 6M after the start of TKI. Pts were assessed for response, overall survival (OS), event-free survival (EFS), transformation-free survival (TFS), and failure-free survival (FFS) based on ALC and RLC. The Kaplan-Meier method was used to calculate OS, EFS, TFS, and FFS. A log-rank test and Cox regression were used for univariate (UVA) and multivariate analysis (MVA), respectively. Results: A total of 483 pts were enrolled in this study: 271 in IM, 105 in Nilo, and 107 in Dasa. Patient characteristics and outcomes are summarized in Table 1. Median age at diagnosis was 48 years, and median follow-up was 85M and ongoing (5-154+). Time from diagnosis to start of TKI, Sokal risk score, and ALC at baseline between groups did not differ clinically. Of 481 pts, 93 (19%) developed RLC at 3 or 6M; IM, 38 (14%); Nilo, 23 (22%); Dasa, 32 (30%) (p= .001). ALC at 3 or 6M was observed in 15 (3%); IM, 3 (1%); Nilo, 1 (1%); Dasa, 11 (10%) (p<.001). Overall, cumulative incidence of complete cytogenetic response (CCyR) at 6M, major molecular response (MMR) at 12M, molecular response with 4.5 log reduction by IS (MR4.5) at 24M did not differ significantly between RLC and non-RLC (3 or 6M), or between ALC and non-ALC (3 or 6M). 5-y TFS, EFS and OS in ALC group were significantly worse than those in non-ALC group (p= .002, p=.016, p=.008, respectively). By UVA and MVA related to OS, age [p <.001; Hazard ratio (HR), 1.062; 95% confidence interval (95%CI), 1.036-1.089], presence of ALC at 3 or 6M [p = .028; HR, 10.948; 95%CI, 1.297-92.415], absence of MMR at 24M [p=.016; HR, 2.263; 95%CI, 1.165-4.393] were identified as adverse prognostic factors for OS. Conclusion: The presence of ALC ≥4,000/µL at 3 or 6M of TKI therapies is rare but is adversely associated with overall survival. Table 1. Patient Characteristics and Outcomes (N=483)a Overall [n= 481] IM [n= 271] Nilo [n= 105] Dasa [n= 107] Age, (year) 48 (15-85) 48 (15-85) 49 (17-82) 48 (16-83) Sokal Risk, No. (%) Low 334 (69) 175 (65) 79 (75) 80 (75) Intermediate 114 (24) 74 (27) 18 (17) 22 (21) High 32 (7) 20 (7) 8 (8) 4 (4) Time from diagnosis to start of TKI, (M) 0.9 (0-12.6) 1.0 (0-12.6) 0.5 (0-5.6) 0.7 (0.1-7.8) ALC at baseline, (/109L) 2.5 (0-86.6) 2.4 (0-16.7) 2.6 (0.4-9.2) 2.7 (0.3-86.6) Incidence of Relative Lymphocytosis, No. (%) At 3M 65 (14) 25 (9) 16 (15) 24 (22) At 6M 76 (16) 32 (12) 20 (19) 24 (22) Overall 93 (19) 38 (14) 23 (22) 32 (30) Incidence of Absolute Lymphocytosis, No. (%) At 3M 8 (2) 1 (0) 0 7 (7) At 6M 11 (2) 3 (1) 1 (1) 7 (7) Overall 15 (3) 3 (1) 1 (1) 11 (10) Outcomes of RLC and ALC at any time in each group, +/- (%/%) (p) <10% BCR-ABL/ABL at 3M RLC 36/40 (.596) 22/44 (.213) 50/37 (.280) 31/38 (.537) ALC 38/39 (.952) 0/42 (.394) 100/39 (.214) 36/35 (.952) Cumulative CCyR at 6M RLC 75/75 (.288) 50/66 (.063) 96/90 (.413) 90/87 (.628) ALC 67/75 (.711) 33/64 (.276) 0/92 (.001) 82/89 (.599) Cumulative MMR at 12M RLC 67/74 (.406) 53/70 (.030) 83/82 (.921) 72/74 (.903) ALC 60/73 (.488) 33/68 (.197) 0/83 (.033) 73/74 (.745) Cumulative MR4.5 at 24M RLC 46/52 (.564) 37/50 (.139) 57/55 (.889) 50/57 (.729) ALC 33/52 (.332) 33/48 (.610) 0/56 (.264) 36/57 (.252) 5-y FFS RLC 61/71 (.133) 56/69 (.167) 62/70 (.710) 61/74 (.285) ALC 50/69 (.076) 0/68 (<.001) 0/70 (<.001) 71/70 (.974) 5-y TFS RLC 90/93 (.369) 88/93 (.597) 91/88 (.115) 91/99 (.213) ALC 72/93 (.002) 67/93 (.014) 0/90 (<.001) 80/97 (.121) 5-y EFS RLC 80/86 (.213) 71/83 (.154) 84/87 (.450) 86/93 (.486) ALC 64/85 (.016) 33/82 (<.001) 0/87 (<.001) 80/92 (.574) 5-y OS RLC 89/93 (.068) 81/94 (.007) 100/84 (.126) 96/99 (.207) ALC 82/93 (.008) 67/93 (.001) 100/88 (.847) 83/99 (.040) a Two in IM and 1 in Dasa were not evaluable due to lack of differential data at 3 and 6M. Figure 1. OS in Pts with ALC Figure 1. OS in Pts with ALC Disclosures O'Brien: Amgen, Celgene, GSK: Consultancy; CLL Global Research Foundation: Membership on an entity's Board of Directors or advisory committees; Emergent, Genentech, Gilead, Infinity, Pharmacyclics, Spectrum: Consultancy, Research Funding; MorphoSys, Acerta, TG Therapeutics: Research Funding.

RESUMENLos monasterios femeninos nacen en beaterios en muchos casos. Así los beaterios son el primer paso de la reclusión pero, al mismo tiempo el modelo de rechazo. Por otro lado, con el Concilio de Trento, la Contrarreforma fue la imposición de la reforma religiosa con una renovación espiritual, pero reproduce la subordinación femenina y la clausura. Nuevamente se renuevan los rechazos en este caso el modelo son los conventos de Toledo y el monasterio de San Clemente. Este estudio examina la importancia de los beaterios en las fundaciones conventuales en Toledo.Y analiza la oposición y acciones de rechazo de las beatas y monjas de las distintas comunidades monásticas y mendicantes frente a las reformas de vida claustral, incluido la normativa del Concilio de Trento. Utilizando para ello las fuentes documentales localizadas durante la elaboración de mi tesis doctoral.PALABRAS CLAVE: Beaterios, conventos, oposición, Toledo, Edad ModernaABSTRACTWomen’s monasteries often began as beatorios. These beaterios were thus the first step in confinement but at the same time the model of rejection. Meanwhile the Council of Trent and Counterreformation represented the imposition of religious reform with spiritual renewal, but reproduced female subordination and cloister. Again renew rejects in this case the model are convents in Toledo and the monastery of Saint Clemens. This study examines the importance of beaterios in the founding of convents in Toledo. And it analyses how pious women and nuns of the different monastic and mendicant orders opposed and rejected resist reforms of cloistered life, including the Council of Trent legislation. 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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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This paper presents a brief review on the ternary phase equilibria in the ternary AV–BVI–I systems (AV = Sb, Bi; BVI = S, Se, Te). These systems includes the series of ternary compounds those are very attractive source materials for photo-, thermos- and ferroelectric energy transformation along the recently discovered semiconductors that exhibit Rashba-type spin splitting in their surface states. In the Rashba semiconductors, a unique toroidal 3D Fermi surface appears on the crystal surface, which leads to unusual properties that make it possible to realize unique electronic devices based on these compounds. The thorough knowledge on the ternary phase diagram of these systems shed light on the chemical and structural design of new multifunctional materials with tunable properties. This knowledge is very important whenfocusing on the chemistry of such multifunctional materials based on complex element systems. REFERENCES Audzijonis A., Sereika R., Ћaltauskas R. 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The debate about diagnoses and treatment of attention deficit hyperactive disorder (ADHD) in children continue to range on between the developmental and biological perspectives. While there is increasing evidence that support the biological susceptibility of the disorder, a number of researches also emphasized the significant effect of environment on the syndrome. This study used developmental perspectives to evaluate and bring together various bio-psychosocial factors that impact on children diagnosed with ADHD. The study explored and integrated the existing and advancing study on ADHD to a more refined pattern that embraced developmental perspectives. The study also discussed how the linkage in childhood ADHD fits within the developmental psychopathology perspective. 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e4360011The objective of this research was to analyze how official documents and educational legislation present the subject of ethnic-racial diversity, and also reflect on their impact on reality through the National Household Sample Survey (PNAD) data. To this end, we conducted an analysis of legislation and official documents created for Brazilian education, from 1988 to 2018, based on the Bardin Content Analysis technique. Subsequently, this analysis was compared with the data available in the PNAD to verify the impact of publications regarding 1) average years of study by color/race in the period; 2) average years of study by color/race, considering the situation of poverty (extremely poor, vulnerable, poor and non-poor); and 3) average years of study in regions of Brazil with a higher percentage of black people. The prescriptions related to the education of ethnic-racial relations of the 12 files analyzed were described, as well as their categories and characteristics. After this process, were established the relations between the categories and the PNAD data. The results allowed us to conclude that the reduction in the average time difference between blacks and whites was a little less than 5 months. Despite the relevance of the efforts, the implementation of policies aimed at combating racial inequality in education is still far from achieving the expected effectiveness.ResumoO objetivo dessa pesquisa foi analisar como são tratadas, em documentos oficiais e na legislação educacional, as questões relativas à diversidade étnico-racial e refletir sobre o seu impacto na realidade por meio dos dados da Pesquisa Nacional por Amostra de Domicílios (PNAD). Para tanto, foi realizada uma análise das legislações e documentos oficiais criados para a educação brasileira, do período de 1988 a 2018, pautada na técnica da Análise de Conteúdo da Bardin. Subsequentemente, essa análise foi comparada com os dados disponíveis na PNAD para verificar o impacto das publicações com relação a: 1) média de anos de estudo por cor/raça, no período; 2) média de anos de estudo por cor/raça, considerando a situação de pobreza (extremamente pobres, vulneráveis, pobres e não pobres); e 3) média de anos de estudo em regiões do Brasil com percentual maior de pessoas negras. As prescrições relacionadas à educação das relações étnico-raciais dos 12 arquivos analisados foram descritas, assim como as categorias e as características que as compõem. Após esse processo, foram estabelecidas as relações entre as categorias e os dados da PNAD. Os resultados permitiram concluir que a redução da diferença de tempo médio de estudo entre brancos e negros foi de pouco menos de 5 meses. Apesar da relevância dos esforços, a implementação das políticas que visam o combate à desigualdade racial na educação ainda se apresenta longe de alcançar a eficácia esperada.Palavras-chave: Relações étnico-raciais, Legislação educacional, Desigualdades raciais, Análise de conteúdo.Keywords: Ethnic-Racial relations, Educational legislation, Racial inequalities, Content analysis.ReferencesAGUIAR, Márcia Angela Da S. Avaliação do plano nacional de educação 2001-2009: questões para reflexão. Educação Sociedade, Campinas, v. 31, n. 112, p. 707-727, set. 2010.ARTES, Amelia; MENA-CHALCO, Jesús Pascual. O Programa de Bolsas da Fundação Ford: 12 anos de atuação no Brasil. Educação e Realidade, Porto Alegre, v.44, n.3, p.1-22, 2019.BARDIN, Laurence. Análise de conteúdo. 4. ed. Lisboa: Edições 70, 2011, 279 p.BARROS, Marilisa Berti de Azevedo; FRANCISCO, Priscila Maria Stolses Bergamo; ZANCHETTA, Luane Margarete; CESAR, Chester Luiz Galvão. 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AbstractLiver stiffness measurement (LSM) by transient elastography (TE) is a non-invasive assessment for diagnosing and staging liver fibrosis in non-alcoholic fatty liver disease (NAFLD). Evidence on its role as a longitudinal monitoring tool is lacking. This study aims to evaluate the role of TE in monitoring NAFLD improvement following bariatric surgery. This study prospectively recruited 101 morbidly obese patients undergoing laparoscopic bariatric surgery for intraoperative liver biopsy. Thirty-seven patients of the cohort received perioperative TE. Postoperative anthropometric, biochemical and LSM data were collected annually for 5 years. In 101 patients receiving liver biopsy (mean age 40.0 ± 10.3 years, mean body-mass-index (BMI) 40.0 ± 5.7 kg/m2), NASH and liver fibrosis were diagnosed in 42 (41.6%) and 48 (47.5%) patients respectively. There were 29 (28.7%) stage 1, 11 (10.9%) stage 2, 7 (6.9%) stage 3, and 1 (1.0%) stage 4 fibrosis. In 37 patients receiving TE (mean age 38.9 ± 10.8 years, mean BMI 41.1 ± 5.6 kg/m2), the percentages of total weight loss were 21.1 ± 7.6% at 1 year, 19.7 ± 8.3% at 3 years, and 17.1 ± 7.0% at 5 years after surgery. The mean LSM reduced significantly from 9.8 ± 4.6 kPa at baseline to 6.9 ± 3.4 kPa at 1 year, 7.3 ± 3.0 kPa at 3 years, and 6.8 ± 2.6 kPa at 5 years (P = 0.002). Using pre-defined LSM cut-offs, the rates of significant fibrosis, advanced fibrosis and cirrhosis being ruled out at 5 years improved from baseline values of 43.7 to 87.5% (P < 0.001), 56.8 to 91.7% (P < 0.001), and 64.9 to 91.7% (P < 0.001), respectively. TE was a useful monitoring tool in demonstrating the improvement of liver fibrosis following bariatric surgery.

Abstract BACKGROUND: National population data on thyroid disease in women comes largely from NHANES. Prior research utilizing data from NHANES 1999-2002 indicated a 3.1% prevalence of hypothyroidism and 0.6% prevalence of hyperthyroidism among reproductive aged women. In this dataset, Mexican Americans had a similar risk of hypothyroidism but a slightly higher rate of hyperthyroidism when compared to non-Hispanic whites. We present data from a prospective cohort study of reproductive aged Hispanic women residing in the United States (US) in order to examine thyroid disease prevalence in this population. Methods: The Environment, Leiomyomas, Latinas and Adiposity Study (ELLAS) is a prospective NIMHD funded longitudinal cohort study of reproductive age Latinas/Latinx females in Southeast Michigan. Demographic and health data were collected via bilingual interviewers. Height, weight, and body composition were measured by trained staff using a Tanita MC780U scale. Fasting morning venipuncture was performed and samples were collected in a serum separating tube and sent to a commercial lab (Labcorp – Burlington, NC) for TSH electrochemiluminescence immunoassay [normal reference range 0.45-4.5 mIU/L]. The data were analyzed using SAS version 9.4 (Cary, NC). Results: 516 patients have enrolled in ELLAS and 450 of these have completed the first study visit. Mean age, BMI, and body fat % were 37.7 ± 7.0 years, 29.9 ± 6.8 kg/m2, 36.3% ± 6.6% (mean ± SD) respectively. Reported countries of birth were Mexico (76.2%), US (9.8%), Central America (6.7%), South America (5.6%), and the Caribbean Islands (0.7%). 34 (7.6%) participants reported a pre-existing thyroid condition. Of those, 28 reported they had been treated for a thyroid condition in the past, and 14 were currently taking prescription medication for thyroid disease. TSH levels were available on 418 women. Of those with a known thyroid condition, 6.5% had TSH values &lt; 0.45 and 16.1% had elevated TSH values (&gt; 4.5) at the time of their study visit, compared to 1.7% and 7.4% overall. 0.2% had TSH &gt; 10. Among those without a known history of thyroid disease, 1.3% had TSH &lt; 0.45 and 6.7% had TSH &gt; 4.5 at their visit. BMI, body fat %, and country of birth were not associated with TSH levels, but there was a small yet significant effect of age on TSH (p=0.009). Conclusion: In this US cohort of Hispanic women of reproductive age, we observed a high prevalence of thyroid dysfunction in those without pre-existing disease. In women with a known thyroid condition, the prevalence of abnormal TSH values was also high, representing both under- and over-treatment with thyroid hormone. Screening for thyroid disease in this population is important and presents a potential opportunity for intervention in an often underserved population.

Abstracts: Introduction: studying the percentage of display and dimensions of the middle cerebral artery and some related arteries on on 256 MSCT data. Methods: A cross-sectional study, with sample size of 261. Results: The percentage of display of middle cerebral artery is 100%; the posterior artery is 76.4; Internal Carotid Artery is 100%. The average diameter, average length are (mm) M1T respectively: 3.25 ± 0.43 and 19.98 ± 6.10; M1 P: 3.26 ± 0.46 and 19.68 ± 6.28; M2T left 2.10 ± 0.48 and 22.85 ± 13.18; M2T right 2.09 ± 0.49 and 23.42 ± 11.89; M2D left 2.48 ± 0.49 and 31.73-16.36; M2D right 2.55 ± 0.49 and 29.11 ± 15.31. PCoA T 1.29 ± 0.63 and 11.87 ± 4.87; PCoA P 1.26 ± 0.66 and 14.02 ± 9.13; Conclusions: The size of the middle cerebral artery and some related arteries were accurately evaluated in the study, the image of vascular anatomy was display clearly. Keywords Middle cerebral artery, cerebral angiography, multi-slices computed tomography ... References [1] H.V. Cúc. To the study of arterial blood supply vessels for Vietnamese adults, Ministry of Health research project, Hanoi Medical University, Hanoi, Vietnam (2000) (in Vietnamese).[2] H.M.Tú. To the study of cerebral artery anatomy on MSCT 64 image, Master's thesis in Medicine, Hanoi Medical University, Hanoi, Vietnam (2011) (in Vietnamese).[3] Ogeng'o, J.A. Geometric features of Vertebrobasilar arterial system in adult Black Kenyans, Int. J. Morphol, 36(2) (2018) 544 - 50. [4] KrzyżewsKi, R.M.. Variation of the anterior communicating artery complex and occurrence of anterior communicating artery aneurysm: A2 segment consideration, Folia medica cracoviensia, LIV (1) (2014) 13 - 20.[5] Jiménez-Sosa, M.S. Anatomical variants of Anterior cerebral arterial circle. A study by Multidetector computerized 3D tomographic angiography, Int J. Morphol 35(3) 1121 – 28.[6] Hamidi, C. (2013). Display with 64-detector MDCT angiography of cerebral vascular variations, Surg Radiol Anat 35 (2017) 729 – 36.[7] Dimmick, S.J., et al. Normal variations of the cerebral circulation at multidetector CT angiography, Radiographics 29(4) (2009) 1027 – 43.[8] P.T.Hà. To the study of Willis polygonal anatomy on MSCT 128 image of patients with cerebral aneurysm, Specialish level 2 thesis in Hanoi Medical University, Hanoi, Vietnam.[9] Saha, A. (2013). Variation of posterior communicating artery in human brain: a morphological study, Gomal Journal of Medical Sciences 11(1) (2018). 42 – 6.[10] Gullari, G. K. The branching pattern of the middle cerebral artery: is the intermediate trunk real or not? An anatomical study correlating with simple angiography, J.Neurosurg, 116 (2012) 1024 - 34.[11] Canaz, H., el al Morphometric analysis of the arteries of Willis Polygon, Romanian Neurosurgery, XXXII (1) (2018) 56 - 64.[12] Pedroza, A. (1987). Microanatomy of the Posterior Communicating Artery, Neurosurgery 20(2) (2018) 229 – 35.[13] Keeranghat, P. P., et al. Evaluation of normal variants of circle of Willis at MRI, Int.J. Res Med Sci, 6(5) (2018) 1617 - 22.[14] Tao, X., Yu, et al. Microsurgical anatomy of the anterior communicating artery complex in adult Chinese heads, Surgical Neurology 65 (2006) 155 – 61.[15] Krejza, J., et al. Carotid artery diameter in Men and Women and the relation to body and neck size, Stroke, 37 (2006) 1103 - 5.[16] Masatoukawashima. Microsurgical anatomy of cerebral revascularization. Part I: Anterior circulation, J.Neurosurg, 102 (2005) 116 – 31.[17] Jeyakumar.R., et al, Study of Anatomical Variations in Middle Cerebral Artery, Int.J.Sci Stud 5(12) (2018) 5-10. [18] Brzegowy, P, et al Middle cerebral artery anatomical variations and aneurysms: a retrospective study based on computed tomography angiography findings, Folia Morphol, 77(3) (2018) 434 – 40.[19] Rohan, V., et al, Length of Occlusion predicts recanalization and outcome after intravenous thrombolysis in middle cerebral artery stroke, Stroke, 45 (2014) 2010 - 17.[20] Vijaywargiya, M., et al. Anatomical study of petrous and cavernous parts of internal carotid artery, Anat Cell Biol, 50 (2017) 163 - 70.[21] Bouthillier, et al Segments of the internal carotid artery: a new classification, Neurosurgery, 38(3), (1996) 425 - 32.

Abstract Introduction Currently, enhanced external counterpulsation (EECP) is one of the safest non-invasive treatments for patients with coronary artery disease (CAD). In combination with traditional drug therapy, EECP can significantly improve the quality of life of patients by increasing coronary perfusion, improving myocardial contractile function, and improving endothelial function. Aim To study the effect of EECP on clinical status, quality of life (QL) and structural-functional state of blood vessels in patients with stable coronary artery disease. Materials and methods In the present study 67 CAD patients were included (average age 65.7±5.66 years; men 71.9%, angina pectoris of functional class II-III (FC)). All patients were on optimal medical therapy (ACE inhibitors, beta-blockers, antiplatelet agents, statins, nitrates), which remained unchanged during the follow-up. Patients were given a course of EECP (35 procedures 220–280 mmHg.art.). Test 6-minute walk (T6MW), QL (Minnesota Satisfaction Questionnaire (MSQ)), echocardiography (ejection fraction of the left ventricle (LVEF)) were performed at baseline and after 6 months. In addition, all the patients underwent laser photoplethysmography (Stiffness index (SI, m/s), phase shift (PS m/s) occlusion index (OI), nail fold videocapillaroscopy (capillary density at rest, after reactive hyperemia and venous occlusion (CDr, CDrh, CDvo, respectively, cap/mm2) and applanation tonometry (central aortic systolic pressure (CASP), (radial augmentation index (RAI)) in order to assess structural and functional characteristics of blood vessels. Results In six months after EECP, significant improvement in patient's condition was found. T6MW distance (212±32 vs 251±29 m, p&lt;0.05), QL MSQ (20.1±6.2 vs 41,6±7,1, p&lt;0.05) and LVEF (40.9±7,6% vs 45.2±10.1%, p&lt;0.05) increased significantly. Stiffness of large vessels was found to be decreased. CASP, RAI and SI decreased significantly, (CASP: 131±15.8 vs 129±14.8 mmHg, p&lt;0.05), (RAI: 97.2±25.1 vs 97±21.6%, p&lt;0.05), (SI: 8.9±1.5 vs 8.8±,1.6 m/s, p&lt;0.05), Functional characteristics of large blood vessels significantly improved (PS (5.6±1.2 vs 6.8±1.4 m/s, p&lt;0.05). Microcirculation - Reflection index (106.7 vs 95.3%, p&lt;0.05) and OI (1.5±0.3 vs 1.66±0.26, p&lt;0.05) for all. Increase CDrest (44±12.2–44.6±11.5 capillaries, p&gt;0.05), in samples with CDrh (45±14 vs 57±16 capillaries, p&lt;0.05) and CDvo (55±15–56 vs 4±14.2 capillaries, p&lt;0.05). Conclusion ECCP treatment of patients with stable CAD, in addition to optimal drug therapy, led to an increase in load tolerance and improvement of the QL, myocardial contractile function, accompanied by improvement of the structural and functional state of large vessels and microcirculatory bed. Funding Acknowledgement Type of funding sources: None.

Abstract Background Cardiac amyloidosis (CA) remains an underdiagnosed entity. Atrial fibrillation (AF) is common in patients with CA, likely owing to direct amyloid deposition in the left atrium. However, the prevalence of AF in CA and its association with in-hospital outcomes has not been studied in large populations. Purpose Our aim was to study the trends, baseline characteristics, and clinical impact of AF in patients with CA in the United States using the Healthcare Cost and Utilization Project (HCUP) National) Inpatient Sample (NIS) from 1999 to 2014. Methods We queried the NIS and identified CA using ICD-9-CM codes 277.39 and 425.7. AF in CA patients was identified using the ICD-9-CM code of 427.31. Statistical Analysis System (SAS) 9.4 was used for analysis of data. Results There were a total of 145,920 CA hospitalizations between 1999 and 2014 in the United States, of which 37,070 (25.4%) had AF. The prevalence of AF remained consistent from 27.5% in 1999 to 27.4% in 2014. The mean age of patients with AF was 72.9±28.2 years and for patients without AF was 67±31.9 years (p&lt;0.0001). The majority of the patients with AF were male (60.3%) and the study group was predominantly white (62.8% in patients with AF and 56.4% in patients without AF). CA patients with AF suffered more from thyroid-related disease (22.5% vs 16.1%), heart failure (62.9% vs 36.5%) and renal failure (34.7% vs 30.5%) and less from hypertension (29.3% vs 34.0%) and diabetes mellitus (23.2% vs 25.2%) (p&lt;0.0001). There was no significant difference in the Charlson comorbidity score between the groups. Inpatient mortality was significantly higher in CA patients with AF (10.4% vs 6.5%, p&lt;0.001). However, in-patient mortality has been decreasing over the years from 10.3% in 1999 to 7.6% in 2014. Furthermore, cardiogenic shock was significantly higher in CA patients with AF (2.1% vs 1.2%, p&lt;0.001), yet the use of mechanical circulatory support was not significantly different between the groups (0.42% vs 0.35%, p=0.375). Pacemaker implantation was also noted to be higher in CA patients with AF compared to patients without AF (2.8% vs 1.2%, p&lt;0.0001). There was no significant difference between CA patients with and without AF in mean cost of hospitalization ($58222±10752 vs $57695±545, p=0.081) or length of stay (7.9±0.1 vs 7.7±0.1 days, p=0.7089). Conclusion CA with atrial fibrillation is a well-recognized entity, and our large scale retrospective analysis found significant association with worse in-hospital outcomes and cardiogenic shock. Interestingly, trend of in-patient mortality in CA has been decreasing over the years, likely owing to improved imaging modalities for diagnosis. Optimal management of AF in CA is imperative to improve outcomes in this population. Funding Acknowledgement Type of funding source: None

The TRP superfamily of channels (nomenclature as agreed by NC-IUPHAR [159, 997]), whose founder member is the Drosophila Trp channel, exists in mammals as six families; TRPC, TRPM, TRPV, TRPA, TRPP and TRPML based on amino acid homologies. TRP subunits contain six putative TM domains and assemble as homo- or hetero-tetramers to form cation selective channels with diverse modes of activation and varied permeation properties (reviewed by [679]). Established, or potential, physiological functions of the individual members of the TRP families are discussed in detail in the recommended reviews and in a number of books [371, 635, 1064, 236]. The established, or potential, involvement of TRP channels in disease is reviewed in [412, 634] and [637], together with a special edition of Biochemica et Biophysica Acta on the subject [634]. Additional disease related reviews, for pain [585], stroke [1050], sensation and inflammation [919], itch [117], and airway disease [284, 977], are available. The pharmacology of most TRP channels has been advanced in recent years. Broad spectrum agents are listed in the tables along with more selective, or recently recognised, ligands that are flagged by the inclusion of a primary reference. See Rubaiy (2019) for a review of pharmacological tools for TRPC1/C4/C5 channels [751]. Most TRP channels are regulated by phosphoinostides such as PtIns(4,5)P2 although the effects reported are often complex, occasionally contradictory, and likely to be dependent upon experimental conditions, such as intracellular ATP levels (reviewed by [939, 638, 747]). Such regulation is generally not included in the tables.When thermosensitivity is mentioned, it refers specifically to a high Q10 of gating, often in the range of 10-30, but does not necessarily imply that the channel's function is to act as a 'hot' or 'cold' sensor. In general, the search for TRP activators has led to many claims for temperature sensing, mechanosensation, and lipid sensing. All proteins are of course sensitive to energies of binding, mechanical force, and temperature, but the issue is whether the proposed input is within a physiologically relevant range resulting in a response. TRPA (ankyrin) familyTRPA1 is the sole mammalian member of this group (reviewed by [268]). TRPA1 activation of sensory neurons contribute to nociception [382, 829, 555]. Pungent chemicals such as mustard oil (AITC), allicin, and cinnamaldehyde activate TRPA1 by modification of free thiol groups of cysteine side chains, especially those located in its amino terminus [529, 51, 336, 531]. Alkenals with α, β-unsaturated bonds, such as propenal (acrolein), butenal (crotylaldehyde), and 2-pentenal can react with free thiols via Michael addition and can activate TRPA1. However, potency appears to weaken as carbon chain length increases [23, 51]. Covalent modification leads to sustained activation of TRPA1. Chemicals including carvacrol, menthol, and local anesthetics reversibly activate TRPA1 by non-covalent binding [391, 470, 1005, 1004]. TRPA1 is not mechanosensitive under physiological conditions, but can be activated by cold temperatures [392, 193]. The electron cryo-EM structure of TRPA1 [688] indicates that it is a 6-TM homotetramer. Each subunit of the channel contains two short ‘pore helices’ pointing into the ion selectivity filter, which is big enough to allow permeation of partially hydrated Ca2+ ions. TRPC (canonical) familyMembers of the TRPC subfamily (reviewed by [261, 726, 15, 4, 84, 410, 687, 60]) fall into the subgroups outlined below. TRPC2 is a pseudogene in humans. It is generally accepted that all TRPC channels are activated downstream of Gq/11-coupled receptors, or receptor tyrosine kinases (reviewed by [713, 887, 997]). A comprehensive listing of G-protein coupled receptors that activate TRPC channels is given in [4]. Hetero-oligomeric complexes of TRPC channels and their association with proteins to form signalling complexes are detailed in [15] and [411]. TRPC channels have frequently been proposed to act as store-operated channels (SOCs) (or compenents of mulimeric complexes that form SOCs), activated by depletion of intracellular calcium stores (reviewed by [689, 15, 718, 764, 1037, 141, 675, 55, 142]). However, the weight of the evidence is that they are not directly gated by conventional store-operated mechanisms, as established for Stim-gated Orai channels. TRPC channels are not mechanically gated in physiologically relevant ranges of force. All members of the TRPC family are blocked by 2-APB and SKF96365 [319, 318]. Activation of TRPC channels by lipids is discussed by [60]. Important progress has been recently made in TRPC pharmacology [751, 571, 400, 92]. TRPC channels regulate a variety of physiological functions and are implicated in many human diseases [270, 61, 825, 958]. TRPC1/C4/C5 subgroup TRPC1 alone may not form a functional ion channel [210]. TRPC4/C5 may be distinguished from other TRP channels by their potentiation by micromolar concentrations of La3+. TRPC2 is a pseudogene in humans, but in other mammals appears to be an ion channel localized to microvilli of the vomeronasal organ. It is required for normal sexual behavior in response to pheromones in mice. It may also function in the main olfactory epithelia in mice [1034, 672, 673, 1035, 496, 1075, 1030].TRPC3/C6/C7 subgroup All members are activated by diacylglycerol independent of protein kinase C stimulation [319].TRPM (melastatin) familyMembers of the TRPM subfamily (reviewed by [252, 318, 689, 1062]) fall into the five subgroups outlined below. TRPM1/M3 subgroupIn darkness, glutamate released by the photoreceptors and ON-bipolar cells binds to the metabotropic glutamate receptor 6 , leading to activation of Go . This results in the closure of TRPM1. When the photoreceptors are stimulated by light, glutamate release is reduced, and TRPM1 channels are more active, resulting in cell membrane depolarization. Human TRPM1 mutations are associated with congenital stationary night blindness (CSNB), whose patients lack rod function. TRPM1 is also found melanocytes. Isoforms of TRPM1 may present in melanocytes, melanoma, brain, and retina. In melanoma cells, TRPM1 is prevalent in highly dynamic intracellular vesicular structures [368, 657]. TRPM3 (reviewed by [663]) exists as multiple splice variants which differ significantly in their biophysical properties. TRPM3 is expressed in somatosensory neurons and may be important in development of heat hyperalgesia during inflammation (see review [876]). TRPM3 is frequently coexpressed with TRPA1 and TRPV1 in these neurons. TRPM3 is expressed in pancreatic beta cells as well as brain, pituitary gland, eye, kidney, and adipose tissue [662, 875]. TRPM3 may contribute to the detection of noxious heat [947].TRPM2TRPM2 is activated under conditions of oxidative stress (respiratory burst of phagocytic cells) and ischemic conditions. However, the direct activators are ADPR(P) and calcium. As for many ion channels, PIP2 must also be present (reviewed by [1018]). Numerous splice variants of TRPM2 exist which differ in their activation mechanisms [219]. The C-terminal domain contains a TRP motif, a coiled-coil region, and an enzymatic NUDT9 homologous domain. TRPM2 appears not to be activated by NAD, NAAD, or NAADP, but is directly activated by ADPRP (adenosine-5'-O-disphosphoribose phosphate) [900]. TRPM2 is involved in warmth sensation [788], and contributes to neurological diseases [66]. Recent study shows that 2'-deoxy-ADPR is an endogenous TRPM2 superagonist [253]. TRPM4/5 subgroupTRPM4 and TRPM5 have the distinction within all TRP channels of being impermeable to Ca2+ [997]. A splice variant of TRPM4 (i.e.TRPM4b) and TRPM5 are molecular candidates for endogenous calcium-activated cation (CAN) channels [301]. TRPM4 is active in the late phase of repolarization of the cardiac ventricular action potential. TRPM4 deletion or knockout enhances beta adrenergic-mediated inotropy [546]. Mutations are associated with conduction defects [374, 546, 819]. TRPM4 has been shown to be an important regulator of Ca2+ entry in to mast cells [924] and dendritic cell migration [43]. TRPM5 in taste receptor cells of the tongue appears essential for the transduction of sweet, amino acid and bitter stimuli [494] TRPM5 contributes to the slow afterdepolarization of layer 5 neurons in mouse prefrontal cortex [471]. Both TRPM4 and TRPM5 are required transduction of taste stimuli [226].TRPM6/7 subgroupTRPM6 and 7 combine channel and enzymatic activities (‘chanzymes’). These channels have the unusual property of permeation by divalent (Ca2+, Mg2+, Zn2+) and monovalent cations, high single channel conductances, but overall extremely small inward conductance when expressed to the plasma membrane. They are inhibited by internal Mg2+ at ~0.6 mM, around the free level of Mg2+ in cells. Whether they contribute to Mg2+ homeostasis is a contentious issue. When either gene is deleted in mice, the result is embryonic lethality. The C-terminal kinase region is cleaved under unknown stimuli, and the kinase phosphorylates nuclear histones. TRPM7 is responsible for oxidant- induced Zn2+ release from intracellular vesicles [3] and contributes to intestinal mineral absorption essential for postnatal survival [574]. TRPM8Is a channel activated by cooling and pharmacological agents evoking a ‘cool’ sensation and participates in the thermosensation of cold temperatures [54, 161, 205] reviewed by [941, 516, 420, 599]. TRPML (mucolipin) familyThe TRPML family [729, 1047, 723, 1008, 173] consists of three mammalian members (TRPML1-3). TRPML channels are probably restricted to intracellular vesicles and mutations in the gene (MCOLN1) encoding TRPML1 (mucolipin-1) cause the neurodegenerative disorder mucolipidosis type IV (MLIV) in man. TRPML1 is a cation selective ion channel that is important for sorting/transport of endosomes in the late endocytotic pathway and specifically, fission from late endosome-lysosome hybrid vesicles and lysosomal exocytosis [765]. TRPML2 and TRPML3 show increased channel activity in low extracellular sodium and are activated by similar small molecules [293]. A naturally occurring gain of function mutation in TRPML3 (i.e. A419P) results in the varitint waddler (Va) mouse phenotype (reviewed by [729, 639]). TRPP (polycystin) familyThe TRPP family (reviewed by [197, 195, 275, 986, 345]) or PKD2 family is comprised of PKD2 (PC2), PKD2L1 (PC2L1), PKD2L2 (PC2L2), which have been renamed TRPP1, TRPP2 and TRPP3, respectively [997]. It should also be noted that the nomenclature of PC2 was TRPP2 in old literature. However, PC2 has been uniformed to be called TRPP2 [317]. PKD2 family channels are clearly distinct from the PKD1 family, whose function is unknown. PKD1 and PKD2 form a hetero-oligomeric complex with a 1:3 ratio. [843]. Although still being sorted out, TRPP family members appear to be 6TM spanning nonselective cation channels. TRPV (vanilloid) familyMembers of the TRPV family (reviewed by [926]) can broadly be divided into the non-selective cation channels, TRPV1-4 and the more calcium selective channels TRPV5 and TRPV6.TRPV1-V4 subfamilyTRPV1 is involved in the development of thermal hyperalgesia following inflammation and may contribute to the detection of noxius heat (reviewed by [710, 822, 858]). Numerous splice variants of TRPV1 have been described, some of which modulate the activity of TRPV1, or act in a dominant negative manner when co-expressed with TRPV1 [786]. The pharmacology of TRPV1 channels is discussed in detail in [303] and [945]. TRPV2 is probably not a thermosensor in man [684], but has recently been implicated in innate immunity [503]. TRPV3 and TRPV4 are both thermosensitive. There are claims that TRPV4 is also mechanosensitive, but this has not been established to be within a physiological range in a native environment [114, 488].TRPV5/V6 subfamily TRPV5 and TRPV6 are highly expressed in placenta, bone, and kidney. Under physiological conditions, TRPV5 and TRPV6 are calcium selective channels involved in the absorption and reabsorption of calcium across intestinal and kidney tubule epithelia (reviewed by [982, 185, 601, 248]).

The TRP superfamily of channels (nomenclature as agreed by NC-IUPHAR [159, 999]), whose founder member is the Drosophila Trp channel, exists in mammals as six families; TRPC, TRPM, TRPV, TRPA, TRPP and TRPML based on amino acid homologies. TRP subunits contain six putative TM domains and assemble as homo- or hetero-tetramers to form cation selective channels with diverse modes of activation and varied permeation properties (reviewed by [679]). Established, or potential, physiological functions of the individual members of the TRP families are discussed in detail in the recommended reviews and in a number of books [371, 635, 1066, 236]. The established, or potential, involvement of TRP channels in disease is reviewed in [412, 634] and [637], together with a special edition of Biochemica et Biophysica Acta on the subject [634]. Additional disease related reviews, for pain [585], stroke [1052], sensation and inflammation [921], itch [117], and airway disease [284, 979], are available. The pharmacology of most TRP channels has been advanced in recent years. Broad spectrum agents are listed in the tables along with more selective, or recently recognised, ligands that are flagged by the inclusion of a primary reference. See Rubaiy (2019) for a review of pharmacological tools for TRPC1/C4/C5 channels [751]. Most TRP channels are regulated by phosphoinostides such as PtIns(4,5)P2 although the effects reported are often complex, occasionally contradictory, and likely to be dependent upon experimental conditions, such as intracellular ATP levels (reviewed by [941, 638, 747]). Such regulation is generally not included in the tables.When thermosensitivity is mentioned, it refers specifically to a high Q10 of gating, often in the range of 10-30, but does not necessarily imply that the channel's function is to act as a 'hot' or 'cold' sensor. In general, the search for TRP activators has led to many claims for temperature sensing, mechanosensation, and lipid sensing. All proteins are of course sensitive to energies of binding, mechanical force, and temperature, but the issue is whether the proposed input is within a physiologically relevant range resulting in a response. TRPA (ankyrin) familyTRPA1 is the sole mammalian member of this group (reviewed by [268]). TRPA1 activation of sensory neurons contribute to nociception [382, 831, 555]. Pungent chemicals such as mustard oil (AITC), allicin, and cinnamaldehyde activate TRPA1 by modification of free thiol groups of cysteine side chains, especially those located in its amino terminus [529, 51, 336, 531]. Alkenals with α, β-unsaturated bonds, such as propenal (acrolein), butenal (crotylaldehyde), and 2-pentenal can react with free thiols via Michael addition and can activate TRPA1. However, potency appears to weaken as carbon chain length increases [23, 51]. Covalent modification leads to sustained activation of TRPA1. Chemicals including carvacrol, menthol, and local anesthetics reversibly activate TRPA1 by non-covalent binding [391, 470, 1007, 1006]. TRPA1 is not mechanosensitive under physiological conditions, but can be activated by cold temperatures [392, 193]. The electron cryo-EM structure of TRPA1 [688] indicates that it is a 6-TM homotetramer. Each subunit of the channel contains two short ‘pore helices’ pointing into the ion selectivity filter, which is big enough to allow permeation of partially hydrated Ca2+ ions. TRPC (canonical) familyMembers of the TRPC subfamily (reviewed by [261, 726, 15, 4, 84, 410, 687, 60]) fall into the subgroups outlined below. TRPC2 is a pseudogene in humans. It is generally accepted that all TRPC channels are activated downstream of Gq/11-coupled receptors, or receptor tyrosine kinases (reviewed by [713, 889, 999]). A comprehensive listing of G-protein coupled receptors that activate TRPC channels is given in [4]. Hetero-oligomeric complexes of TRPC channels and their association with proteins to form signalling complexes are detailed in [15] and [411]. TRPC channels have frequently been proposed to act as store-operated channels (SOCs) (or compenents of mulimeric complexes that form SOCs), activated by depletion of intracellular calcium stores (reviewed by [689, 15, 718, 765, 1039, 141, 675, 55, 142]). However, the weight of the evidence is that they are not directly gated by conventional store-operated mechanisms, as established for Stim-gated Orai channels. TRPC channels are not mechanically gated in physiologically relevant ranges of force. All members of the TRPC family are blocked by 2-APB and SKF96365 [319, 318]. Activation of TRPC channels by lipids is discussed by [60]. Important progress has been recently made in TRPC pharmacology [751, 571, 400, 92]. TRPC channels regulate a variety of physiological functions and are implicated in many human diseases [270, 61, 827, 960]. TRPC1/C4/C5 subgroup TRPC1 alone may not form a functional ion channel [210]. TRPC4/C5 may be distinguished from other TRP channels by their potentiation by micromolar concentrations of La3+. TRPC2 is a pseudogene in humans, but in other mammals appears to be an ion channel localized to microvilli of the vomeronasal organ. It is required for normal sexual behavior in response to pheromones in mice. It may also function in the main olfactory epithelia in mice [1036, 672, 673, 1037, 496, 1077, 1032].TRPC3/C6/C7 subgroup All members are activated by diacylglycerol independent of protein kinase C stimulation [319].TRPM (melastatin) familyMembers of the TRPM subfamily (reviewed by [252, 318, 689, 1064]) fall into the five subgroups outlined below. TRPM1/M3 subgroupIn darkness, glutamate released by the photoreceptors and ON-bipolar cells binds to the metabotropic glutamate receptor 6 , leading to activation of Go . This results in the closure of TRPM1. When the photoreceptors are stimulated by light, glutamate release is reduced, and TRPM1 channels are more active, resulting in cell membrane depolarization. Human TRPM1 mutations are associated with congenital stationary night blindness (CSNB), whose patients lack rod function. TRPM1 is also found melanocytes. Isoforms of TRPM1 may present in melanocytes, melanoma, brain, and retina. In melanoma cells, TRPM1 is prevalent in highly dynamic intracellular vesicular structures [368, 657]. TRPM3 (reviewed by [663]) exists as multiple splice variants which differ significantly in their biophysical properties. TRPM3 is expressed in somatosensory neurons and may be important in development of heat hyperalgesia during inflammation (see review [878]). TRPM3 is frequently coexpressed with TRPA1 and TRPV1 in these neurons. TRPM3 is expressed in pancreatic beta cells as well as brain, pituitary gland, eye, kidney, and adipose tissue [662, 877]. TRPM3 may contribute to the detection of noxious heat [949].TRPM2TRPM2 is activated under conditions of oxidative stress (respiratory burst of phagocytic cells) and ischemic conditions. However, the direct activators are ADPR(P) and calcium. As for many ion channels, PIP2 must also be present (reviewed by [1020]). Numerous splice variants of TRPM2 exist which differ in their activation mechanisms [219]. The C-terminal domain contains a TRP motif, a coiled-coil region, and an enzymatic NUDT9 homologous domain. TRPM2 appears not to be activated by NAD, NAAD, or NAADP, but is directly activated by ADPRP (adenosine-5'-O-disphosphoribose phosphate) [902]. TRPM2 is involved in warmth sensation [789], and contributes to neurological diseases [66]. Recent study shows that 2'-deoxy-ADPR is an endogenous TRPM2 superagonist [253]. TRPM4/5 subgroupTRPM4 and TRPM5 have the distinction within all TRP channels of being impermeable to Ca2+ [999]. A splice variant of TRPM4 (i.e.TRPM4b) and TRPM5 are molecular candidates for endogenous calcium-activated cation (CAN) channels [301]. TRPM4 is active in the late phase of repolarization of the cardiac ventricular action potential. TRPM4 deletion or knockout enhances beta adrenergic-mediated inotropy [546]. Mutations are associated with conduction defects [374, 546, 821]. TRPM4 has been shown to be an important regulator of Ca2+ entry in to mast cells [926] and dendritic cell migration [43]. TRPM5 in taste receptor cells of the tongue appears essential for the transduction of sweet, amino acid and bitter stimuli [494] TRPM5 contributes to the slow afterdepolarization of layer 5 neurons in mouse prefrontal cortex [471]. Both TRPM4 and TRPM5 are required transduction of taste stimuli [226].TRPM6/7 subgroupTRPM6 and 7 combine channel and enzymatic activities (‘chanzymes’). These channels have the unusual property of permeation by divalent (Ca2+, Mg2+, Zn2+) and monovalent cations, high single channel conductances, but overall extremely small inward conductance when expressed to the plasma membrane. They are inhibited by internal Mg2+ at ~0.6 mM, around the free level of Mg2+ in cells. Whether they contribute to Mg2+ homeostasis is a contentious issue. When either gene is deleted in mice, the result is embryonic lethality. The C-terminal kinase region is cleaved under unknown stimuli, and the kinase phosphorylates nuclear histones. TRPM7 is responsible for oxidant- induced Zn2+ release from intracellular vesicles [3] and contributes to intestinal mineral absorption essential for postnatal survival [574]. TRPM8Is a channel activated by cooling and pharmacological agents evoking a ‘cool’ sensation and participates in the thermosensation of cold temperatures [54, 161, 205] reviewed by [943, 516, 420, 599]. TRPML (mucolipin) familyThe TRPML family [729, 1049, 723, 1010, 173] consists of three mammalian members (TRPML1-3). TRPML channels are probably restricted to intracellular vesicles and mutations in the gene (MCOLN1) encoding TRPML1 (mucolipin-1) cause the neurodegenerative disorder mucolipidosis type IV (MLIV) in man. TRPML1 is a cation selective ion channel that is important for sorting/transport of endosomes in the late endocytotic pathway and specifically, fission from late endosome-lysosome hybrid vesicles and lysosomal exocytosis [766]. TRPML2 and TRPML3 show increased channel activity in low extracellular sodium and are activated by similar small molecules [293]. A naturally occurring gain of function mutation in TRPML3 (i.e. A419P) results in the varitint waddler (Va) mouse phenotype (reviewed by [729, 639]). TRPP (polycystin) familyThe TRPP family (reviewed by [197, 195, 275, 988, 345]) or PKD2 family is comprised of PKD2 (PC2), PKD2L1 (PC2L1), PKD2L2 (PC2L2), which have been renamed TRPP1, TRPP2 and TRPP3, respectively [999]. It should also be noted that the nomenclature of PC2 was TRPP2 in old literature. However, PC2 has been uniformed to be called TRPP2 [317]. PKD2 family channels are clearly distinct from the PKD1 family, whose function is unknown. PKD1 and PKD2 form a hetero-oligomeric complex with a 1:3 ratio. [845]. Although still being sorted out, TRPP family members appear to be 6TM spanning nonselective cation channels. TRPV (vanilloid) familyMembers of the TRPV family (reviewed by [928]) can broadly be divided into the non-selective cation channels, TRPV1-4 and the more calcium selective channels TRPV5 and TRPV6.TRPV1-V4 subfamilyTRPV1 is involved in the development of thermal hyperalgesia following inflammation and may contribute to the detection of noxius heat (reviewed by [710, 824, 860]). Numerous splice variants of TRPV1 have been described, some of which modulate the activity of TRPV1, or act in a dominant negative manner when co-expressed with TRPV1 [787]. The pharmacology of TRPV1 channels is discussed in detail in [303] and [947]. TRPV2 is probably not a thermosensor in man [684], but has recently been implicated in innate immunity [503]. TRPV3 and TRPV4 are both thermosensitive. There are claims that TRPV4 is also mechanosensitive, but this has not been established to be within a physiological range in a native environment [114, 488].TRPV5/V6 subfamily TRPV5 and TRPV6 are highly expressed in placenta, bone, and kidney. Under physiological conditions, TRPV5 and TRPV6 are calcium selective channels involved in the absorption and reabsorption of calcium across intestinal and kidney tubule epithelia (reviewed by [984, 185, 601, 248]).

Concentrations of 16 polycyclic aromatic hydrocarbons (PAHs) were determined in settled house dust and road dust samples collected from a core urban area of Hanoi. Levels of PAHs ranged from 830 to 3500 (median 2000) ng/g in house dust, and from 1400 to 4700 (median 1700) ng/g in road dust. Concentrations of PAHs in dust samples of this study were within the moderate range as compared with those from other countries in the world. Toxic equivalents to benzo[a]pyrene (BaP-EQs) in our samples ranged from 81 to 850 (median 330) ng BaP-EQ/g with principal contributors as BaP and dibenz[a,h]anthracene, which accounted for 69% to 93% of BaP-EQs. In almost all the samples, proportions of high-molecular-weight PAHs (HMW-PAHs with 4–6 rings) were higher than those of low-molecular-weight PAHs (LMW-PAHs with 2–3 rings), suggesting emission sources from combustion processes rather than direct contamination by petrogenic sources. 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Malignant hyperthermia (MH) is a clinical response happened to patient who is sensitive with inhaled anesthesia drug that could cause suddently death. Many previous studies showed that malignant hyperthermia strongly related to genetic background of patients including RYR1, CACNA1S or STAC3 gene polymorphisms. With the development of high technology such as next generation sequencing, scientists found that 37 to 86 percents of MH cases had RYR1 mutations and approximately 1 percent of those had CACNA1S mutations. Gene analysis testing was recommended to apply for patient with MH medical history or MH patient’s family relations. Keywords Malignant hyperthermia, inhaled anesthesia, RYR1, CACNA1S, STAC3. References [1] G. Torri, Inhalation anesthetics: a review, Minerva Anestesiologica 76 (2010) 215–228. [2] N. Kassiri, S. Ardehali, F. Rashidi, S. Hashemian, Inhalational anesthetics agents: The pharmacokinetic, pharmacodynamics, and their effects on human body, Biomed. Biotechnol. Res. 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