Academic literature on the topic 'YI 2362'

In order to explore how ethnic minorities in China reshape their perception of themselves today, I conducted field research in K Village in southwest China. In this anthropological research about this village which has a majority of Yi minorities, I did in-depth interviews, discourse analysis, and participatory observance to examine the conflicts between three different identities, the tensions behind the contemporary society, the history of Christianity in this village, and the meaning of different identities to individuals. Based on the analysis of this cultural phenomena in K Village, I interpret the cultural meaning of Christianity there––Yi minorities in this village are using Christianity as a tool to reconcile their modern political identities and cultural or religious identities. This research not only contributes to the understanding of ethnic minorities’ bodily practices of negotiating various cultures, but also assists governments in developing better ethnic policies.

Abstract Cells release molecules through vesicles or into specific locations through exocytosis. Extracellular vesicle is divided into ectosomes and exosomes. Exosomes has been the main mechanism of discussion in recent studies and cancer research. As Exosomes with a diameter of ~30-160 nm (with an average diameter of 100 nm) carries intracellular molecules such as DNA, RNA, miRNA, proteins, and lipids. The physiological function of exosomes is not fully understood at present, it is important to understand the role of exosome in cancer. Src is highly activated in colon cancer and Src inhibition is the potential treatment strategy in colon cancer. In this study, colon cancer cells HT-29 were used to investigate the difference sizes of exosomes that response to Src inhibitor treatment. In the preliminary results, the exosome from HT-29 cultured medium were isolated and examined by transmission electron microscopy (TEM). The micrograph showed the average size of exosome is around 100 nm. When HT-29 were treated with Dasatinib (DST) the Src inhibitor, the drug resistant (DSTR) cells were grown, the secreted exosome from DSTR were collected and demonstrated the bigger size of exosome with average diameter of 130 nm. The role of the size changes of exosome in response to Dasatinib resistant will be further investigated, however, this study provides the clues that exosome detection can be applied in monitoring drug resistance. Citation Format: Hui Min Koo, Yi-Wen Lu, Yu-Chi Tseng, Kai-Yu Tseng, Yen-Tse Lu, Wei-Ting Chao. Visualizing exosome structure in Dasatinib resistant colon cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2365.

Abstract Despite the success of PD-1 blockade in melanoma and other cancers, effective treatment strategies to overcome resistance to cancer immunotherapy are lacking. We identified the innate immune kinase TANK-binding kinase 1 (TBK1) as a candidate immune evasion gene in a pooled genetic screen. Using a suite of genetic and pharmacologic tools across multiple experimental model systems, we confirm a role for TBK1 as an immune evasion gene. Targeting TBK1 enhances response to PD-1 blockade by lowering the cytotoxicity threshold to effector cytokines (TNF𝛂/IFN𝛄). TBK1 inhibition in combination with PD-1 blockade also demonstrated efficacy using patient-derived tumor models, with concordant findings in matched patient-derived organotypic tumor spheroids (PDOTS) and matched patient-derived organoids (PDOs). Tumor cells lacking TBK1 are primed to undergo RIPK- and caspase-dependent cell death in response to TNF𝛂/IFN𝛄 in a JAK/STAT-dependent manner. Taken together, our results demonstrate that targeting TBK1 is a novel and effective strategy to overcome resistance to cancer immunotherapy. Citation Format: Yi Sun, Or-yam Revach, Seth Anderson, Robert T. Manguso, Russell W Jenkins. Targeting TBK1 to overcome resistance to cancer immunotherapy [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr B28.

Abstract Recent advances in single-cell RNA sequencing have revealed heterogeneous cell types and gene expression states in the non-cancerous cells in tumors. The integration of multiple scRNA-seq datasets across tumors can reveal common cell types and states in the tumor microenvironment (TME). However, tumor scRNA analysis relies on clustering cells and annotating with markers from experts. Subsequent challenges include inconsistent cell type and state definition, different marker usage among studies, and that clustering doesn’t find continuous cell states. We developed a data-driven framework, MetaTiME, to overcome the limitations in resolution and consistency that result from manual labeling using known gene markers. Using millions of TME single cells, MetaTiME learns meta-components that encode independent components of gene expression observed across cancer types. The meta-components are biologically interpretable as cell types, cell states, and signaling activities. For example, the T cell co-signaling meta-component reflects co-expressed gene modules of multiple immune checkpoint blockade targets. Also, the tumor-infiltrating macrophage meta-components found macrophage states in different metabolism preferences, rather than the pro-inflammatory versus anti-inflammatory classifications. We also observed certain macrophage states associated with tumor prognosis and cancer immunotherapy response. By projecting onto the MetaTiME space, we provide a tool to annotate cell states and signature continuums for TME scRNA-seq data. Lastly, leveraging epigenetics data, MetaTiME reveals critical transcriptional regulators for the cell states. Overall, MetaTiME learns data-driven meta-components that depict cellular states and gene regulators for tumor immunity and cancer immunotherapy. Citation Format: Yi Zhang, Guanjue Xiang, Yijia Alva Jiang, Allen Lynch, Zexian Zeng, Chenfei Wang, Wubing Zhang, Jingyu Fan, Jiajinlong Kang, Shengqing Gu, Changxin Wan, Boning Zhang, Shirley Liu, Myles Brown, Clifford Meyer. MetaTiME: meta-components of the tumor immune microenvironment [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr B65.

The study examines the Republic of Korea’s (ROK) history politics under Park Chung Hee rule (1961-1979). The author argues that it’s possible to identify two stages of the development of policy toward Korea’s national heritage: 1) the early stage (1961 to mid 1960s), during which the government of the ROK managed to create the legal basis of the state policy on the protection of cultural heritage and the Office of Cultural Properties and 2) the late stage (the late 1960’s to 1979), when the regime carried out large-scale propaganda of Korean traditional culture. The article covers such problems as historical views of Park Chung Hee, restoration of Korean places of military glory, measures to perpetuate the memory of Korean outstanding historical figures - admiral Yi Sun-sin and king Sejong the Great, glorification of the ancient Korean kingdom Silla, promotion of Confucian values. The author concludes that President Park Chung Hee sought to strengthen the national consciousness of South Koreans in order to mobilize them to implement national tasks and unite the population around the authorities. The main emphasis was placed on the heroic pages of the military history of Korea and the history of Silla, the first unified Korean state. In the 1970s, the state actively promoted Confucian values to ensure the loyalty of the population to the authoritarian regime of Park Chung Hee. Despite the democratization of the Republic of Korea since 1987, Park Chung Hee’s cultural policy has played a significant role in shaping the historical identity of modern South Koreans. The research is based on Park Chung Hee’s works, ROK’s official documents and materials of South Korean researchers.

Abstract Increased tumor associated tissue eosinophilia (TATE) is associated with better prognosis in colorectal cancers, melanoma, and prostate cancer, however, the mechanisms which regulate TATE and how it impacts tumor biology remain largely unexplored. Eosinophils within tumors have been shown to secrete cytotoxic granular contents that induce necrosis and lead to the recruitment of other immune cells which together inhibit tumor growth. Interestingly, estrogens have been shown to increase eosinophilia in several disease settings although it has not been established if and how estrogens impact eosinophilia in various cancers. Thus, we have explored the role of estrogens in regulating TATE, and its impact on tumor progression, in preclinical models of breast cancer and melanoma. To this end eight weeks old female C57BL6 mice were ovariectomized and supplemented with either placebo or 17β-estradiol (E2) (clamping E2 levels) before tumor implantation. In this manner it was determined that E2 accelerated tumor growth in multiple models of TNBC (triple-negative breast cancer) and melanoma and that this was associated with a significant decrease in TATE. Eosinophil depletion studies were performed the results of which confirmed a role for these immune cells in suppressing tumor growth in these disease relevant models. Mechanistically, it was determined that E2 treatment decreased the levels of cytokines that facilitate eosinophil migration and survival in tumors. The direct effects of E2 on eosinophil recruitment into tumors was confirmed using adoptively transferred eosinophils. Moreover, E2 decreased the survival and cytotoxicity of eosinophils differentiated from bone-marrow progenitors. Altogether, these data indicated that E2 has direct and indirect effects on eosinophils wherein they affect eosinophil differentiation in bone marrow as well as modulate the tumor microenvironment resulting in decreased TATE resulting in increased tumor growth. Analysis of the Metabric and TCGA databases revealed a survival advantage for patients with TNBC whose tumors exhibit a higher expression of an eosinophil signature. Importantly, a selective estrogen receptor modulator (SERM), lasofoxifene, a drug which is in late-stage clinical development for metastatic breast cancer, antagonized E2 actions and reversed the negative impact of E2 on TATE and reduced tumor growth. Given the widespread use of SERMs and other endocrine therapies in the treatment of estrogen receptor positive breast cancer, our findings may inform new therapeutic strategies that exploit eosinophil-mediated antitumor response for the treatment of breast cancer and other cancers where the presence of TATE is beneficial. Citation Format: Sandeep Artham, Aditi Goyal, Jovita Byemerwa, Ching-Yi Chang, Donald Patrick Mcdonnell. Estrogens regulate tumor associated tissue eosinophilia to promote tumor growth [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr B02.

Abstract Small cell lung cancer (SCLC), which comprises about 15% of lung cancer cases, is the most aggressive and deadliest type of lung cancer with extremely poor clinical outcomes (about 6% of 5-year overall survival). For about the last three decades, combinatory chemotherapy of etoposide and platinum (EP) treatment has been used as the standard first-line treatment for SCCL. While tumors are generally responsive to the EP treatment, in most cases, they rapidly relapse and acquire resistance after the treatment. However, detailed mechanisms underlying the acquired chemoresistance are not well understood. In this study, we constructed a SCLC comprehensive regulatory network using 135 SCLC tumors, projected chemo-resistant signature genes derived from patient-derived xenografts and genetically engineered mouse models on the network, and identified Granulin (GRN) as a key regulator of the chemo-resistant genes. In multiple independent SCLC datasets, expression levels of GRN and its associated genes increase with the EP treatment and show anti-correlation with neuroendocrine (NE) features of SCLC. Yap activation in a SCLC mouse model increases Grn expression suggesting Yap1 as a potential upstream regulator of Grn. But, on the other hand, the expression levels of GRN and its associated genes are up-regulated in EP treated patient-derived CDX models compared to treatment naïve ones, in which YAP1 expression is depleted in both groups, suggesting YAP1 independent GRN functions associated with chemoresistance. Our observations were validated using 4 SCLC cell lines having different GRN expressions (GRNhigh: SHP77 and H841 and GRNlow: H524 and H2081). The GRNlow showed better responses to the EP treatment compared to the GRNhigh cells (IC50: GRNhigh > 1𝜇M; GRNlow ≈ 1nM). Furthermore, the GRNlow cells with GRN over-expression acquired resistance to the treatment suggesting that GRN expression in SCLC is sufficient for chemo-resistance regardless of YAP1 activation. When we stratified SCLC patients using GRN and its associated genes, the patients in the GRN low group received clear benefits of the chemotherapy with better survival than ones without the treatment (LRT p=0.004) while there were no survival differences among patients regardless of the treatment in the GRN high group. Interestingly, immune checkpoint blockade marker genes were significantly up-regulated in patients from the GRN high group (p= 1.8×10-5, 4.8×10-5, 3.5×10-5, and 0.0002 for PDCD1, CD274, PDCD1LG2, and CTLA4, respectively). Combining this with an observation of that GRN and its associated genes were associated with high PDL1 expression in non-NE SCLC mouse models, immunotherapies might be a potentially effective treatment option for the GRN high group. Our study suggests GRN as a novel key regulator modulating chemo-resistance as well as a potential biomarker for immunotherapy response in SCLC and, hence, provide valuable information in the clinical decisions for better diagnosis, prognosis, and treatment for the purpose of precision medicine. Citation Format: Seungyeul Yoo, Ayushi Patel, Yi Zhong, Feng Jiang, Wenhui Wang, Hideo Watanabe, Jun Zhu. Molecular network analysis identifies GRN as a key regulator of chemotherapy resistance in small cell lung cancer [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr B53.

Background:People with Axial Spondyloarthritis (axSpA) experience a diagnostic delay between 7 to 10 years. (1-5) This delay contributes to increased depression and desperation in searching for an appropriate diagnosis. (6) Consequently, people with axSpA experience impaired physical function, structural damage, and overall worsened quality of life than those who experience a timely diagnosis. (7)Objectives:To gain knowledge and understand patients’ experiences with healthcare providers in diagnosis of axSpA.Methods:Using qualitative study design, we conducted six focus groups, with a total of 26 participants with a confirmed diagnosis of axSpA by rheumatologists from three different geographic locations: Worcester, MA, Aurora, CO and Philadelphia, PA. Focus groups were audio recorded and approximately 2 hours in duration. The focus groups were transcribed, deidentified, cleaned and stored in a secure location. NVivo software was used to code the data using a coding scheme which emerged from the focus group discussion topics. For intercoder reliability, two researchers coded the data and generated summary reports for data analysis.Results:Patients described their frustrating journeys to diagnosis and attributed the lengthy diagnosis delays to a multitude of factors. These elements include, lack of definitive diagnostic test, disease characteristics, lack of primary care providers’ awareness of axSpA, time, and trust. Patients felt that their physicians dismissed their complaints or would describe their symptoms as psychosomatic. The health care system also contributed to their diagnostic delays, including the lengthy referral process to a rheumatologist and the short clinical appointments. Patients believe that to reduce diagnostic delay, physicians must work with their patients; listening and believing their patients while allotting time for patients to discuss their experiences. In addition, patients believe earlier referral to a rheumatologist, and HLA-B27 genetic testing would decrease the diagnostic delay of axSpA.Conclusion:In this study, patients desire definitive testing in clinical practice for earlier diagnosis of axSpA. Additionally, more education regarding the guidelines to diagnose axSpA and earlier referral to rheumatologists might be needed. Until this is feasible, patients seek clinicians who will work with them until a diagnosis is made, listening, and believing their experiences and symptoms.References:[1]Deodhar A, Mease P, Reveille J, Curtis J, Karunaratne P, Malhotra K. Prevalence of axial spondyloarthritis among undiagnosed chronic back pain patients in the United States [abstract]. Ann Rheum Dis. 2014;73:198-199.[2]Deodhar A, Mease PJ, Reveille JD, et al. Frequency of Axial Spondyloarthritis Diagnosis Among Patients Seen by US Rheumatologists for Evaluation of Chronic Back Pain. Arthritis Rheumatol. 2016;68(2326-5205 (Electronic)):1669–1676.[3]Garrido-Cumbrera M, Poddubnyy D, Gossec L, et al. The European Map of Axial Spondyloarthritis: Capturing the Patient Perspective-an Analysis of 2846 Patients Across 13 Countries. Curr Rheumatol Rep. 2019;21(1534-6307 (Electronic)):19.[4]Redeker I, Callhoff J, Hoffmann F, et al. Determinants of diagnostic delay in axial spondyloarthritis: an analysis based on linked claims and patient-reported survey data. Rheumatology (Oxford) 2019;58(1462-0332 (Electronic)):1634–1638.[5]Strand V, Singh JA. Evaluation and Management of the Patient With Suspected Inflammatory Spine Disease. Mayo Clin Proc 2017;92(1942-5546 (Electronic)):555–564.[6]Martindale J. The impact of delay in diagnosing ankylosing spondylitis/axial SpA. . Rheumatology. 2014;53.[7]Yi EA-O, Ahuja A, Rajput T, George AT, Park Y. Clinical, Economic, and Humanistic Burden Associated With Delayed Diagnosis of Axial Spondyloarthritis: A Systematic Review. Rheumatol Ther 2020(2198-6576 (Print)):65-87.Disclosure of Interests:Kate Lapane: None declared, Catherine Dubé Grant/research support from: Novartis, as personnel on such studies, Katarina Ferrucci: None declared, Sara Khan: None declared, Kristine A. Kuhn Consultant of: UCB, Eli Lilly, Novartis, Grant/research support from: Pfizer, Alexis Ogdie Consultant of: Abbvie, Amgen, BMS, Celgene, Corrona, Gilead, Janssen, Lilly, Novartis, Pfizer, UCB, Grant/research support from: Pfizer to Penn, Novartis to Penn, Amgen to Forward/NDB, Esther Yi Employee of: Novartis Pharmaceuticals, Jonathan Kay Consultant of: AbbVie, Inc.; Boehringer Ingelheim GmbH; Celltrion Healthcare Co. Ltd.; Jubilant Radiopharma; Merck & Co.,Inc.; Pfizer Inc.; Samsung Bioepis; Sandoz Inc.; Scipher Medicine; UCB, Inc., Grant/research support from: (paid to UMass Medical School) Gilead Sciences Inc.; Novartis Pharmaceuticals Corp.; Pfizer Inc., Shao-Hsien Liu Grant/research support from: Novartis

We use orthogonal and biorthogonal projections to post-process the gradient of the finite element solution produced by a non-conforming finite element approach. This leads to a better approximation property of the recovered gradient. We use an L2-projection, where the trial and test spaces are different but form a biorthogonal system. This leads to an efficient numerical approach. We also modify our projection by applying the boundary modification method to obtain a higher order approximation on the boundary patch. Numerical examples are presented to demonstrate the efficiency and optimality of the approach. References R. E. Bank and J. Xu. Asymptotically exact a posteriori error estimators, Part I: Grids with superconvergence. SIAM J. Numer. Anal. 41 (2003), pp. 2294–2312. doi: 10.1137/S003614290139874X J. H. Bramble and A. H. Schatz. Higher order local accuracy by averaging in the finite element method. Math. Comput. 31 (1977), pp. 94–111. doi: 10.1090/S0025-5718-1977-0431744-9. M. Crouzeix and P.-A. Raviart. Conforming and nonconforming finite element methods for solving the stationary Stokes equations I. RAIRO 7.R3 (1973), pp. 33–75. doi: 10.1051/m2an/197307R300331 H. Guo and Z. Zhang. Gradient recovery for the Crouzeix–Raviart element. J. Sci. Comput. 64.2 (2015), pp. 456–476. doi: 10.1007/s10915-014-9939-5. B.-O. Heimsund, X.-C. Tai, and J. Wang. Superconvergence for the gradient of finite element approximations by L2 projections. SIAM J. Numer. Anal. 40.4 (2002), pp. 1263–1280. doi: 10.1137/S003614290037410X Y. Huang and N. Yi. The superconvergent cluster recovery method. J. Sci. Comput. 44 (2010), pp. 301–322. doi: 10.1007/s10915-010-9379-9 M. Ilyas, B. P. Lamichhane, and M. H. Meylan. A gradient recovery method based on an oblique projection and boundary modification. Proceedings of the 18th Biennial Computational Techniques and Applications Conference, CTAC-2016. Ed. by J. Droniou, M. Page, and S. Clarke. Vol. 58. ANZIAM J. 2017, pp. C34–C45. doi: 10.21914/anziamj.v58i0.11730 M. Kˇríˇzek and P. Neittaanmäki. Superconvergence phenomenon in the finite element method arising from averaging gradients. Numer. Math. 45 (1984), pp. 105–116. doi: 10.1007/BF01379664 B. P. Lamichhane, R. P. Stevenson, and B. I. Wohlmuth. Higher order mortar finite element methods in 3D with dual Lagrange multiplier bases. Numer. Math. 102 (2005), pp. 93–121. doi: 10.1007/s00211-005-0636-z A. Naga and Z. Zhang. A posteriori error estimates based on the polynomial preserving recovery. SIAM J. Numer. Anal. 42.4 (2004), pp. 1780–1800. doi: 10.1137/S0036142903413002 R. Rannacher and S. Turek. Simple nonconforming quadrilateral Stokes element. Num. Meth. Part. Diff. Eq. 8.2 (1992), pp. 97–111. doi: 10.1002/num.1690080202 Z. Zhang and A. Naga. A new finite element gradient recovery method: Superconvergence property. SIAM J. Sci. Comput. 26.4 (2005), pp. 1192–1213. doi: 10.1137/S1064827503402837 O. C. Zienkiewicz and J. Z. Zhu. The superconvergent patch recovery and a posteriori error estimates. Part 1: The recovery technique. Int. J. Num. Meth. Eng. 33 (1992), pp. 1331–1364. doi: 10.1002/nme.1620330702

Abstract We examined rural-urban differences in the prevalence of cancer risk factors and screening behaviors across U.S. census regions to better understand variations within and between geographic regions and inform strategies to address rural cancer inequities. Using an ecological cross-sectional design, we examined rural-urban differences in the self-reported prevalence of county-level cancer risk factors (i.e., obesity, physical inactivity, alcohol consumption) and cancer screening behaviors (i.e., breast, colorectal and cervical) ascertained from the Behavioral Risk Factor Surveillance System and National Health Interview Survey (2008-2013) across four U.S. census regions (Northeast, Midwest, South, and West). County-level rurality was defined using 2013 U.S. Office of Management and Budget rural-urban classification codes, and the U.S. Department of Agriculture, Economic Research Service’s rural-urban continuum codes. Chi-square tests assessed differences in the mean prevalence of county-level cancer risk factors and cancer screening behaviors in each geographic region. Analysis of variance (ANOVA) models estimated the p-values for trends in cancer risk factors and screening prevalence across the rural-urban continuum. Within each geographic region, rural counties had a higher prevalence of smoking, obesity and physical inactivity. Yet, rural-urban differences in cancer risk factors were not statistically significant in all geographic regions (e.g., prevalence of obesity for Western rural vs. urban counties was 26.5% vs. 25.7% [p=0.08] and physical inactivity for Northeastern rural vs. urban counties was 23.2% vs. 22.5% [p=0.15]). Moreover, the mean prevalence of obesity was higher in urban areas of the Midwest (31%) and South (31.3%) compared to rural areas in the West (26.5%) and Northeast (29.5%). Binge alcohol use was higher in rural vs. urban counties in the West (19.8% vs. 17.7%; p<0.001) and Midwest (22.3% vs. 21.5%; p=0.006), but lower in the South (13.5% vs. 15.2%; p<0.001). Obesity and smoking prevalence increased with increasing rurality across all regions (ptrend<0.045). Breast, cervical and colorectal cancer screening prevalence were lower in rural vs. urban counties in each geographic region (all p-values<0.04). However, the overall prevalence of screening across all cancer sites was higher in rural Northeast counties compared to both rural and urban counties in the South and West regions. Across all regions, cervical and breast cancer screening decreased with increasing rurality (all ptrend<0.001). A significant inverse trend in prevalence of colorectal cancer screening with increasing rurality was observed in all regions except the Northeast (ptrend=0.17). Our findings suggest notable variations in rural-urban cancer risk factors and screening disparities across U.S. geographic regions. Further exploration of the source of this geographic variation is warranted to ensure the development and implementation of relevant cancer control interventions targeting rural populations most in need. Citation Format: Kelly A. Hirko, Huiwen Xu, Laura Q. Rogers, Michelle Y. Martin, Siddhartha Roy, Kimberly M. Kelly, Shannon M. Christy, Kimlin Tam Ashing, Jean C. Yi, Marquita W. Lewis-Thames, Cathy D. Meade, Qian Lu, Clement K. Gwede, Rachel M. Ceballos, Usha Menon, Katie Cueva, Karen Yeary, Lisa Klesges, Monica L. Baskin, Kassandra I. Alcaraz, Sabrina Ford. Rural-urban disparities in cancer risk factors and screening by United States census region [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr B053.