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摘要: 肠道微生态是由原核微生物(细菌)、真核微生物(包括真菌以及原生动物)和病毒构成的强大“器官”，在机体营养代谢、维持肠道黏膜上皮屏障的完整性、免疫调节中发挥至关重要的作用。已有研究表明，肠道微生态与多种疾病的发病机制相关，如神经精神性疾病、自身免疫性疾病、癌症以及慢性代谢性疾病等。近年来的研究发现，肠道微生态能够通过氧化三甲胺和短链脂肪酸及其受体途径对血流动力学发挥调控作用; 同时，肠道微生态失调、易位激活机体炎症反应可影响机体血流动力学的稳定。本文梳理二者之间的关系，以期为进一步开展相关研究提供借鉴。Abstract: The gut microbiota is a powerful "organ" composed of prokaryotic organisms (bacteria), eukaryotic microorganisms (including fungi and protozoa) and viruses, which plays a crucial role in the nutrition metabolism, maintenance of the integrity of intestinal mucosal barrier, and immune regulation of the body. Researches have shown that intestinal microecology is related to the pathogenesis of many diseases, such as neuropsychiatric diseases, autoimmune diseases, cancer and chronic metabolic diseases. Recent studies have found that gut microbiota can regulate hemodynamics through the oxidation of trimethylamine and short chain fatty acids. At the same time, gut microbiota disorder and translocation can activate the body's inflammatory response, affecting the stability of the body's hemodynamics.In this article, we summarize the relationship between gut microbiota and hemodymamics, in order to provide reference for further research.
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Keywords:
- gut microbiota /
- hemodynamics /
- critical care
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无偿献血是一项事关广大人民群众身体健康和生命安全的社会公益事业。在党和国家的高度重视下，我国无偿献血制度、血液管理法制体系和血站采供血服务体系日趋完善[1-2]。但时有非法卖血行为发生，对我国血液管理制度造成严重破坏，对用血安全造成严重干扰[3]。非法组织卖血罪是指违反国家有关规定，非法组织出卖他人血液的行为。其严重扰乱医疗机构诊疗秩序，威胁血液质量安全，应予以严厉打击。本研究对近年来北京地区发生的非法组织卖血罪案件进行总结，旨在为针对性预防措施的出台提供参考，为首都健康公益事业保驾护航。
1. 资料与方法
1.1 资料来源
2020年11月18日于中国裁判文书官方网站(https://wenshu.court.gov.cn)以“北京”和“非法组织卖血罪”为关键词，检索2013—2019年北京地区非法组织卖血罪的裁判文书。以全部裁判文书为研究对象进行分析。
1.2 方法
对裁判文书涉及的案件资料进行分类汇总，包括罪犯个人信息与判决结果、犯罪时间、犯罪区域与地点等。
1.3 统计学处理
采用Microsoft Excel 2007软件进行资料整理和图表绘制。计数资料以频数(百分数)的形式进行描述。
2. 结果
2.1 案件总体情况
共检索2013—2019年北京地区非法组织卖血罪的裁判文书58份，涉及58起案件和115名罪犯。58起案件涉及北京8个城区，共组织638人卖血，非法卖血13 600 mL，卖血价格为400~600元/400 mL。共5份裁判文书记述招募卖血者方式，其中散发小广告2份(40.0%)、随机打电话2份(40.0%)、利用互联网媒介发布信息2份(40.0%)、上门问询1份(20.0%)等。关于罪犯判决情况，最轻的刑罚为拘役三个月缓刑六个月，并处罚金人民币二千元，最重的判决为有期徒刑一年八个月，并处罚金人民币五千元。
2.2 罪犯个人信息及判决结果
115名罪犯，男性99人(86.1%)，女性16人(13.9%)；罪犯年龄18~61岁，平均年龄33岁。其中20~29岁年龄段人数最多(42.6%，49/115)，其次为30~39岁(24.3%，28/115)；有违法记录25人(21.7%)，无违法记录90人(78.3%)。判处拘役、缓刑并处罚金10人(8.7%)，有期徒刑、缓刑并处罚金8人(7.0%)，有期徒刑并处罚金97人(84.3%)，详情见表 1。
表 1 58起非法组织卖血犯罪案件涉及罪犯判决结果[n(%)]指标 拘役、缓刑、处罚金 有期徒刑、缓刑、处罚金 有期徒刑、处罚金 合计 性别 男性 8(8.1) 4(4.0) 87(87.9) 99(86.1) 女性 2(12.5) 4(25.0) 10(62.5) 16(13.9) 年龄(岁) ＜20 0(0) 1(16.7) 5(83.3) 6(5.2) 20~29 2(4.1) 3(6.1) 44(89.8) 49(42.6) 30~39 1(3.6) 2(7.1) 25(89.3) 28(24.3) 40~49 5(26.3) 0(0) 14(73.7) 19(16.5) 50~59 2(16.7) 2(16.7) 8(66.7) 12(10.4) ≥60 0(0) 0(0) 1(100) 1(0.9) 违法记录 有 0(0) 1(4.0) 24(96.0) 25(21.7) 无 10(11.1) 7(7.8) 73(81.1) 90(78.3) 2.3 犯罪时间分布
2013—2019年北京地区非法组织卖血犯罪案件频次总体呈波动下降趋势，其中2015年出现较大反弹，案件发生频次最高(34.5%, 20/58)，2018年案件发生频次最低(0)。组织卖血人数变化趋势与案件频次变化趋势基本一致，2015年最高(62.1%，396/638)，2018年最低(0)，见图 1。
从案件发生所处的月份上看，1月发生的案件频次最高(32.8%，19/58)，其次为6月(15.5%，9/58)，而4、5月均无非法组织卖血犯罪案件发生。关于案件涉及的卖血人数，1月占比最高(61.6%，393/638)，12月次之(13.6%，87/638)，见图 2。
2.4 犯罪区域与地点
58起非法组织卖血罪案件发生区域涉及北京8个城区，其中海淀区占比最高(62.1%，36/58)，其次为房山区(22.4%，13/58)，余6区案件频次占比均较低。发生于房山区的案件涉及的组织卖血人数最多(50.2%, 320/638)，其次为海淀区(20.2%, 129/638)，见图 3。
从犯罪地点上看，发生于医院的案件占比55.2%(32/58)，组织卖血人数占比61.2%(390/638)；发生于血液中心(包括采血站)的案件占比44.8%(26/58)，组织卖血人数占比38.8%(248/638)，见图 4。
3. 讨论与建议
3.1 讨论
无偿献血是传递爱心的公益事业，同时也是满足医疗服务需求，完善血液供应保障机制的重要组成部分，事关人民福祉和社会稳定，必须保障人民群众用血安全，维持采供血机制完善。非法组织卖血的行为干扰了血液供应机制的正常运行，社会危害极大，应严厉杜绝。本研究对2013—2019年北京地区58起非法组织卖血犯罪的特征进行了总结，探究其规律和特征，以实现精准预防。
首先从案件的年度分布上看，2013—2019年案件频次和涉及的卖血人数整体均呈下降趋势，间接反映出在各级党委、政府和相关部门的组织领导和有力推动下，北京血液管理体系和血站采供血机制逐渐完善，取得了显著成绩。积极推进无偿献血事业的进程，必须在坚持中发展。为净化供血环境，保障临床用血安全，2015年1月30日北京市公安局曾联合多部门对位于房山区某第一医院的非法组织卖血活动进行专项集中整治，打掉犯罪团伙11个，形成裁判文书11份，可能是2015年案件频次出现较大波动的原因。
对案件发生所处的月份进行分析，发现1、6月为案件高发期，而4、5月均无相关案件发生。临床用血来源主要依靠无偿献血，学生与进城务工人员等流动性人员是无偿献血的主体人群之一。受寒暑假期间流动性人口返乡以及酷热、严寒对其出行的影响，可能导致寒暑期间血液采集量大为减少。北京地区临床用血量较多，不可避免地发生季节性“血荒”[4]，为非法组织卖血人员提供了可乘之机。1月份临近春节，部分经济拮据的人可能为增加经济收入，而参与非法卖血。
关于案件发生的区域与地点，海淀区与房山区为非法组织卖血案件高发区，发生地点主要为医院，其次为血液中心。医院为主要用血单位，故非法人员瞄准医院而开展非法卖血行为。海淀区域分布广，医院和血液中心多，以致非法组织卖血案件高发。房山区为城乡结合处，外来人员多，卫生防护意识相对差，可能为非法组织卖血人员实施犯罪提供了机会。
3.2 建议
首先，司法机关应坚决打击非法组织卖血犯罪案件，尤其集团化犯罪团伙，组织卖血人员众多、影响巨大的案件予以严厉刑罚，以形成强大威慑力，实现刑罚特殊预防和一般预防的效果。本研究58起案件共涉及115名罪犯，其中判有期徒刑并罚金97名，对于减少此类案件的发生可能具有积极作用。
其次，公安机关建立非法组织卖血资料数据库，特别是案件高发的海淀区与房山区，可利用大数据实施精准打击，实现有效预防。对于血液中心、医院等高发场所，保卫部门与当地派出所建立联动机制，利用人脸识别系统实现动态监测，营造持续高压态势，发现一起，查处一起。
再次，加强血液储备和区域间血液调动，确保血液供应及时、充足，保障公民临床急救用血的需求。
最后，加强无偿献血、血液安全健康宣教，增强人民群众的法律意识。可适当建立无偿献血激励机制，积极动员广大群众至正规场所进行无偿献血，彻底铲除犯罪的土壤。
4. 小结
血液是宝贵的医疗资源，无偿献血是一种无私奉献、救死扶伤的崇高行为，保障用血安全意义重大。受利益驱动，一些不法人员进行非法组织卖血，其行为对正常的血液安全管理体系和公共卫生秩序造成了严重干扰。本研究通过对北京地区非法组织卖血案件的特征进行了总结，为今后对此类案件的预防提供了借鉴。
作者贡献：潘晓俊负责文献查阅及论文撰写; 陈德昌负责选题设计、审核及修订。利益冲突：所有作者均声明不存在利益冲突 -
[1] Socała K, Doboszewska U, Szopa A, et al. The role of microbiota-gut-brain axis in neuropsychiatric and neurological disorders[J]. Pharmacol Res, 2021, 172: 105840. DOI: 10.1016/j.phrs.2021.105840
[2] Xiao L, Liu Q, Luo M, et al. Gut Microbiota-Derived Metabolites in Irritable Bowel Syndrome[J]. Front Cell Infect Microbiol, 2021, 11: 729346. DOI: 10.3389/fcimb.2021.729346
[3] Doroszkiewicz J, Groblewska M, Mroczko B. The Role of Gut Microbiota and Gut-Brain Interplay in Selected Diseases of the Central Nervous System[J]. Int J Mol Sci, 2021, 22: 10028. DOI: 10.3390/ijms221810028
[4] Hou H, Chen D, Zhang K, et al. Gut microbiota-derived short-chain fatty acids and colorectal cancer: Ready for clinical translation?[J]. Cancer Lett, 2022, 526: 225-235. DOI: 10.1016/j.canlet.2021.11.027
[5] Zaky A, Glastras SJ, Wong MYW, et al. The Role of the Gut Microbiome in Diabetes and Obesity-Related Kidney Disease[J]. Int J Mol Sci, 2021, 22: 9641. DOI: 10.3390/ijms22179641
[6] Cai J, Sun L, Gonzalez FJ. Gut microbiota-derived bile acids in intestinal immunity, inflammation, and tumori-genesis[J]. Cell Host Microbe, 2022, 30: 289-300. DOI: 10.1016/j.chom.2022.02.004
[7] Adhikari AA, Ramachandran D, Chaudhari SN, et al. A Gut-Restricted Lithocholic Acid Analog as an Inhibitor of Gut Bacterial Bile Salt Hydrolases[J]. ACS Chem Biol, 2021, 16: 1401-1412. DOI: 10.1021/acschembio.1c00192
[8] Campbell C, McKenney PT, Konstantinovsky D, et al. Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells[J]. Nature, 2020, 581: 475-479. DOI: 10.1038/s41586-020-2193-0
[9] Jin WB, Li TT, Huo D, et al. Genetic manipulation of gut microbes enables single-gene interrogation in a complex microbiome[J]. Cell, 2022, 185: 547-562. e522. DOI: 10.1016/j.cell.2021.12.035
[10] Franzosa EA, Sirota-Madi A, Avila-Pacheco J, et al. Gut microbiome structure and metabolic activity in inflammatory bowel disease[J]. Nat Microbiol, 2019, 4: 293-305. DOI: 10.1038/s41564-018-0306-4
[11] Gadaleta RM, Garcia-Irigoyen O, Cariello M, et al. Fibroblast Growth Factor 19 modulates intestinal microbiota and inflammation in presence of Farnesoid X Receptor[J]. EBioMedicine, 2020, 54: 102719. DOI: 10.1016/j.ebiom.2020.102719
[12] Doden HL, Wolf PG, Gaskins HR, et al. Completion of the gut microbial epi-bile acid pathway[J]. Gut Microbes, 2021, 13: 1-20.
[13] Turner JR. Intestinal mucosal barrier function in health and disease[J]. Nat Rev Immunol, 2009, 9: 799-809. DOI: 10.1038/nri2653
[14] Tang WHW, Li DY, Hazen SL. Dietary metabolism, the gut microbiome, and heart failure[J]. Nat Rev Cardiol, 2019, 16: 137-154. DOI: 10.1038/s41569-018-0108-7
[15] Rajilić-Stojanović M, de Vos WM. The first 1000 cultured species of the human gastrointestinal microbiota[J]. FEMS Microbiol Rev, 2014, 38: 996-1047. DOI: 10.1111/1574-6976.12075
[16] Kamada N, Seo SU, Chen GY, et al. Role of the gut microbiota in immunity and inflammatory disease[J]. Nat Rev Immunol, 2013, 13: 321-335. DOI: 10.1038/nri3430
[17] Stanley EG, Bailey NJ, Bollard ME, et al. Sexual dimorphism in urinary metabolite profiles of Han Wistar rats revealed by nuclear-magnetic-resonance-based metabonomics[J]. Anal Biochem, 2005, 343: 195-202. DOI: 10.1016/j.ab.2005.01.024
[18] Tang WHW, Bäckhed F, Landmesser U, et al. Intestinal Microbiota in Cardiovascular Health and Disease: JACC State-of-the-Art Review[J]. J Am Coll Cardiol, 2019, 73: 2089-2105.
[19] Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease[J]. Nature, 2011, 472: 57-63. DOI: 10.1038/nature09922
[20] Zhu W, Buffa JA, Wang Z, et al. Flavin monooxygenase 3, the host hepatic enzyme in the metaorganismal trimethyla-mine N-oxide-generating pathway, modulates platelet responsiveness and thrombosis risk[J]. J Thromb Haemost, 2018, 16: 1857-1872. DOI: 10.1111/jth.14234
[21] Bergeron N, Williams PT, Lamendella R, et al. Diets high in resistant starch increase plasma levels of trimethylamine-N-oxide, a gut microbiome metabolite associated with CVD risk[J]. Br J Nutr, 2016, 116: 2020-2029. DOI: 10.1017/S0007114516004165
[22] Hauet T, Baumert H, Gibelin H, et al. Noninvasive monitoring of citrate, acetate, lactate, and renal medullary osmolyte excretion in urine as biomarkers of exposure to ischemic reperfusion injury[J]. Cryobiology, 2000, 41: 280-291. DOI: 10.1006/cryo.2000.2291
[23] Griffin JL, Wang X, Stanley E. Does our gut microbiome predict cardiovascular risk? A review of the evidence from metabolomics[J]. Circ Cardiovasc Genet, 2015, 8: 187-191. DOI: 10.1161/CIRCGENETICS.114.000219
[24] Seldin MM, Meng Y, Qi H, et al. Trimethylamine N-Oxide Promotes Vascular Inflammation Through Signaling of Mitogen-Activated Protein Kinase and Nuclear Factor-κB[J]. J Am Heart Assoc, 2016, 5.
[25] Makrecka-Kuka M, Volska K, Antone U, et al. Trimethylamine N-oxide impairs pyruvate and fatty acid oxidation in cardiac mitochondria[J]. Toxicol Lett, 2017, 267: 32-38. DOI: 10.1016/j.toxlet.2016.12.017
[26] Savi M, Bocchi L, Bresciani L, et al. Trimethylamine-N-Oxide (TMAO)-Induced Impairment of Cardiomyocyte Function and the Protective Role of Urolithin B-Glucuronide[J]. Molecules, 2018, 23.
[27] Jacobs J, Braun J. Host genes and their effect on the intestinal microbiome garden[J]. Genome Med, 2014, 6: 119. DOI: 10.1186/s13073-014-0119-x
[28] Moron R, Galvez J, Colmenero M, et al. The Importance of the Microbiome in Critically Ⅲ Patients: Role of Nutrition[J]. Nutrients, 2019, 11.
[29] Valdés-Duque BE, Giraldo-Giraldo NA, Jaillier-Ramírez AM, et al. Stool Short-Chain Fatty Acids in Critically Ⅲ Patients with Sepsis[J]. J Am Coll Nutr, 2020, 39: 706-712. DOI: 10.1080/07315724.2020.1727379
[30] Arpaia N, Campbell C, Fan X, et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation[J]. Nature, 2013, 504: 451-455. DOI: 10.1038/nature12726
[31] Pluznick J. A novel SCFA receptor, the microbiota, and blood pressure regulation[J]. Gut Microbes, 2014, 5: 202-207. DOI: 10.4161/gmic.27492
[32] Pluznick JL, Protzko RJ, Gevorgyan H, et al. Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation[J]. Proc Natl Acad Sci U S A, 2013, 110: 4410-4415. DOI: 10.1073/pnas.1215927110
[33] Samuel BS, Shaito A, Motoike T, et al. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41[J]. Proc Natl Acad Sci U S A, 2008, 105: 16767-16772. DOI: 10.1073/pnas.0808567105
[34] Maslowski KM, Vieira AT, Ng A, et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43[J]. Nature, 2009, 461: 1282-1286. DOI: 10.1038/nature08530
[35] Le Poul E, Loison C, Struyf S, et al. Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation[J]. J Biol Chem, 2003, 278: 25481-25489. DOI: 10.1074/jbc.M301403200
[36] Tazoe H, Otomo Y, Karaki S, et al. Expression of short-chain fatty acid receptor GPR41 in the human colon[J]. Biomed Res, 2009, 30: 149-156. DOI: 10.2220/biomedres.30.149
[37] Samuel BS, Gordon JI. A humanized gnotobiotic mouse model of host-archaeal-bacterial mutualism[J]. Proc Natl Acad Sci U S A, 2006, 103: 10011-10016. DOI: 10.1073/pnas.0602187103
[38] Durazzi F, Sala C, Castellani G, et al. Comparison between 16S rRNA and shotgun sequencing data for the taxonomic characterization of the gut microbiota[J]. Sci Rep, 2021, 11: 3030. DOI: 10.1038/s41598-021-82726-y
[39] Osuka A, Shimizu K, Ogura H, et al. Prognostic impact of fecal pH in critically ill patients[J]. Crit Care, 2012, 16: R119. DOI: 10.1186/cc11413
[40] Yamada T, Shimizu K, Ogura H, et al. Rapid and Sustained Long-Term Decrease of Fecal Short-Chain Fatty Acids in Critically Ill Patients With Systemic Inflammatory Response Syndrome[J]. JPEN J Parenter Enteral Nutr, 2015, 39: 569-577. DOI: 10.1177/0148607114529596
[41] Ladopoulos T, Giannaki M, Alexopoulou C, et al. Gastrointestinal dysmotility in critically ill patients[J]. Ann Gastroenterol, 2018, 31: 273-281.
[42] Imhann F, Bonder MJ, Vich Vila A, et al. Proton pump inhibitors affect the gut microbiome[J]. Gut, 2016, 65: 740-748. DOI: 10.1136/gutjnl-2015-310376
[43] Rogers MAM, Aronoff DM. The influence of non-steroidal anti-inflammatory drugs on the gut microbiome[J]. Clin Microbiol Infect, 2016, 22: 178. e171-e178. e179.
[44] Habes QLM, van Ede L, Gerretsen J, et al. Norepinephrine Contributes to Enterocyte Damage in Septic Shock Patients: A Prospective Cohort Study[J]. Shock, 2018, 49: 137-143. DOI: 10.1097/SHK.0000000000000955
[45] Fink MP. Intestinal epithelial hyperpermeability: update on the pathogenesis of gut mucosal barrier dysfunction in critical illness[J]. Curr Opin Crit Care, 2003, 9: 143-151. DOI: 10.1097/00075198-200304000-00011
[46] De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of gluta-mine[J]. Crit Care Med, 2005, 33: 1125-1135. DOI: 10.1097/01.CCM.0000162680.52397.97
[47] Wang C, Li Q, Ren J. Microbiota-Immune Interaction in the Pathogenesis of Gut-Derived Infection[J]. Front Immunol, 2019, 10: 1873. DOI: 10.3389/fimmu.2019.01873
[48] Andriamihaja M, Lan A, Beaumont M, et al. The deleteri-ous metabolic and genotoxic effects of the bacterial metabolite p-cresol on colonic epithelial cells[J]. Free Radic Biol Med, 2015, 85: 219-227. DOI: 10.1016/j.freeradbiomed.2015.04.004
[49] Simonen M, Dali-Youcef N, Kaminska D, et al. Conjugated bile acids associate with altered rates of glucose and lipid oxidation after Roux-en-Y gastric bypass[J]. Obes Surg, 2012, 22: 1473-1480. DOI: 10.1007/s11695-012-0673-5
[50] le Roux CW, Bloom SR. Why do patients lose weight after Roux-en-Y gastric bypass?[J]. J Clin Endocrinol Metab, 2005, 90: 591-592. DOI: 10.1210/jc.2004-2211
[51] Ince C, Mayeux PR, Nguyen T, et al. The Endothelium in Sepsis[J]. Shock, 2016, 45: 259-270. DOI: 10.1097/SHK.0000000000000473
[52] Kakihana Y, Ito T, Nakahara M, et al. Sepsis-induced myocardial dysfunction: pathophysiology and management[J]. J Intensive Care, 2016, 4: 22. DOI: 10.1186/s40560-016-0148-1
[53] Hollenberg SM. Understanding stress cardiomyopathy[J]. Intensive Care Med, 2016, 42: 432-435. DOI: 10.1007/s00134-015-4018-4
[54] Stanzani G, Duchen MR, Singer M. The role of mitochondria in sepsis-induced cardiomyopathy[J]. Biochim Biophys Acta Mol Basis Dis, 2019, 1865: 759-773. DOI: 10.1016/j.bbadis.2018.10.011
[55] Yin J, Liao SX, He Y, et al. Dysbiosis of Gut Microbiota With Reduced Trimethylamine-N-Oxide Level in Patients With Large-Artery Atherosclerotic Stroke or Transient Ischemic Attack[J]. J Am Heart Assoc, 2015, 4: e002699. DOI: 10.1161/JAHA.115.002699
[56] Wang F, Li Q, Wang C, et al. Dynamic alteration of the colonic microbiota in intestinal ischemia-reperfusion injury[J]. PLoS One, 2012, 7: e42027. DOI: 10.1371/journal.pone.0042027
[57] Nagatomo Y, Tang WH. Intersections Between Microbiome and Heart Failure: Revisiting the Gut Hypothesis[J]. J Card Fail, 2015, 21: 973-980. DOI: 10.1016/j.cardfail.2015.09.017
[58] Harikrishnan S. Diet, the Gut Microbiome and Heart Failure[J]. Card Fail Rev, 2019, 5: 119-122. DOI: 10.15420/cfr.2018.39.2
[59] Wozniak H, Beckmann TS, Fröhlich L, et al. The central and biodynamic role of gut microbiota in critically ill patients[J]. Crit Care, 2022, 26: 250. DOI: 10.1186/s13054-022-04127-5
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