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Combining cardiopulmonary exercise testing with echocardiography: a multiparametric approach to the cardiovascular and cardiopulmonary systems. 心肺运动测试与超声心动图相结合:心血管和心肺系统的多参数方法。
Pub Date : 2023-08-18 eCollection Date: 2023-05-01 DOI: 10.1093/ehjimp/qyad021
Lavinia Del Punta, Nicolò De Biase, Silvia Armenia, Valerio Di Fiore, Davide Maremmani, Luna Gargani, Matteo Mazzola, Marco De Carlo, Alessandro Mengozzi, Tommaso Lomonaco, Gian Giacomo Galeotti, Frank L Dini, Stefano Masi, Nicola Riccardo Pugliese

Exercise intolerance is a prominent feature of several cardiovascular conditions. However, the physical effort requires the intertwined adaptation of several factors, namely the cardiovascular system, the lungs, and peripheral muscles. Several abnormalities in each domain may be present in a given patient. Cardiopulmonary exercise testing (CPET) has been used to investigate metabolic and ventilatory alterations responsible for exercise intolerance but does not allow for direct evaluation of cardiovascular function. However, this can readily be obtained by concomitant exercise-stress echocardiography (ESE). The combined CPET-ESE approach allows for precise and thorough phenotyping of the pathophysiologic mechanisms underpinning exercise intolerance. Thus, it can be used to refine the diagnostic workup of patients with dyspnoea of unknown origin, as well as improve risk stratification and potentially guide the therapeutic approach in specific conditions, including left and right heart failure or valvular heart disease. However, given its hitherto sporadic use, both the conceptual and technical aspects of CPET-ESE are often poorly known by the clinician. Improving knowledge in this field could significantly aid in anticipating individual disease trajectories and tailoring treatment strategies accordingly. Therefore, we designed this review to revise the pathophysiologic correlates of exercise intolerance, the practical principles of the combined CPET-ESE examination, and its main applications according to current literature.

运动不耐受是多种心血管疾病的一个显著特征。然而,体力劳动需要多个因素(即心血管系统、肺部和外周肌肉)的相互配合。在特定患者身上,每个领域都可能存在多种异常。心肺运动测试(CPET)已被用于研究导致运动不耐受的代谢和通气改变,但无法直接评估心血管功能。不过,通过同时进行运动负荷超声心动图(ESE)可以很容易地获得心血管功能评估结果。CPET-ESE 联合方法可对运动不耐受的病理生理机制进行精确而全面的表型分析。因此,它可用于完善不明原因呼吸困难患者的诊断工作,改善风险分层,并有可能指导特定病症(包括左右心衰或瓣膜性心脏病)的治疗方法。然而,由于 CPET-ESE 的使用尚属零星,临床医生往往对其概念和技术方面知之甚少。提高对这一领域的认识将大大有助于预测个体疾病的发展轨迹并相应地调整治疗策略。因此,我们设计了这篇综述,旨在根据当前的文献,重新审视运动不耐受的病理生理学相关性、CPET-ESE 联合检查的实用原则及其主要应用。
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引用次数: 0
Training doctors in perioperative medicine for older people undergoing surgery (POPS): an innovative foundation placement. 为接受手术的老年人培训围手术期医生(POPS):创新的基础实习。
IF 4.4 Pub Date : 2019-11-01 DOI: 10.7861/clinmed.2019-0256
Sarah Barber, Edward Singleton, Judith Sl Partridge, Jugdeep K Dhesi
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引用次数: 0
43 – Molecular Diagnosis of Lung Cancers 肺癌的分子诊断
Pub Date : 2017-08-01 DOI: 10.1016/J.CANCERGEN.2017.04.044
K. Goud, Kavitha Matam, Adi Mahalakshmi Madasu, R. Vempati, Sagarika Darepalli, Madhuri Pullemula
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引用次数: 0
HbA1c and the Prediction of Type 2 Diabetes in Children and Adults. HbA1c 与儿童和成人 2 型糖尿病的预测。
IF 14.8 Pub Date : 2017-01-01 Epub Date: 2016-11-03 DOI: 10.2337/dc16-1358
Pavithra Vijayakumar, Robert G Nelson, Robert L Hanson, William C Knowler, Madhumita Sinha

Objective: Long-term data validating glycated hemoglobin (HbA1c) in assessing the risk of type 2 diabetes in children are limited. HbA1c, fasting plasma glucose (FPG), and 2-h postload plasma glucose (2hPG) concentrations were measured in a longitudinal study of American Indians to determine their utility in predicting incident diabetes, all of which is thought to be type 2 in this population.

Research design and methods: Incident diabetes (FPG ≥126 mg/dL [7.0 mmol/L], 2hPG ≥200 mg/dL [11.1 mmol/L], HbA1c ≥6.5% [8 mmol/mol], or clinical diagnosis) was determined in 2,095 children without diabetes ages 10-19 years monitored through age 39, and in 2,005 adults ages 20-39 monitored through age 59. Areas under the receiver operating characteristic (ROC) curve for HbA1c, FPG, and 2hPG in predicting diabetes within 10 years were compared.

Results: During long-term follow-up of children and adolescents who did not initially have diabetes, the incidence rate of subsequent diabetes was fourfold (in boys) as high and more than sevenfold (in girls) as high in those with HbA1c ≥5.7% as in those with HbA1c ≤5.3%-greater rate ratios than experienced by adults in the same HbA1c categories. Analyses of ROCs revealed no significant differences between HbA1c, FPG, and 2hPG in sensitivity and specificity for identifying children and adolescents who later developed diabetes.

Conclusions: HbA1c is a useful predictor of diabetes risk in children and can be used to identify prediabetes in children with other type 2 diabetes risk factors with the same predictive value as FPG and 2hPG.

目的:验证糖化血红蛋白(HbA1c)在评估儿童罹患 2 型糖尿病风险方面的长期数据十分有限。在一项针对美国印第安人的纵向研究中测量了 HbA1c、空腹血浆葡萄糖(FPG)和负荷后 2 小时血浆葡萄糖(2hPG)的浓度,以确定它们在预测糖尿病发病中的作用,在这一人群中,所有糖尿病都被认为是 2 型糖尿病:对 2,095 名 10-19 岁无糖尿病的儿童(监测至 39 岁)和 2,005 名 20-39 岁的成年人(监测至 59 岁)进行了糖尿病发病率(FPG ≥126 mg/dL [7.0 mmol/L]、2hPG ≥200 mg/dL [11.1 mmol/L]、HbA1c ≥6.5% [8 mmol/mol] 或临床诊断)测定。比较了 HbA1c、FPG 和 2hPG 预测 10 年内糖尿病的接收器操作特征曲线下面积:结果:在对最初未患糖尿病的儿童和青少年进行长期随访期间,HbA1c ≥5.7%的儿童和青少年与 HbA1c ≤5.3%的儿童和青少年相比,后患糖尿病的发病率分别高出四倍(男孩)和七倍多(女孩)--与相同 HbA1c 类别的成年人相比,这一比率更高。ROC分析表明,HbA1c、FPG和2hPG在识别后来患糖尿病的儿童和青少年的灵敏度和特异性方面没有显著差异:结论:HbA1c 是预测儿童糖尿病风险的有效指标,可用于识别具有其他 2 型糖尿病风险因素的儿童中的糖尿病前期,其预测价值与 FPG 和 2hPG 相同。
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引用次数: 0
Arsenic Trioxide and Tretinoin (AsO/ATRA) for Acute Promyelocytic Leukemia (APL). 三氧化二砷和维甲酸(AsO/ATRA)治疗急性早幼粒细胞白血病(APL)。
IF 0.7 Pub Date : 2016-09-01 DOI: 10.1310/hpj5108-628
Erin Damery, Dominic A Solimando, J Aubrey Waddell

The complexity of cancer chemotherapy requires pharmacists be familiar with the complicated regimens and highly toxic agents used. This column reviews various issues related to preparation, dispensing, and administration of antineoplastic therapy, and the agents, both commercially available and investigational, used to treat malignant diseases. Questions or suggestions for topics should be addressed to Dominic A. Solimando, Jr., President, Oncology Pharmacy Services, Inc., 4201 Wilson Blvd #110-545, Arlington, VA 22203, e-mail: OncRxSvc@comcast.net; or J. Aubrey Waddell, Professor, University of Tennessee College of Pharmacy; Oncology Pharmacist, Pharmacy Department, Blount Memorial Hospital, 907 E. Lamar Alexander Parkway, Maryville, TN 37804, e-mail: waddfour@charter.net.

癌症化疗的复杂性要求药剂师熟悉复杂的方案和使用的高毒性药物。本专栏回顾了与抗肿瘤治疗的制备、分配和管理相关的各种问题,以及用于治疗恶性疾病的市售和研究用药物。有关主题的问题或建议应提交给肿瘤药物服务公司总裁Dominic A. Solimando, Jr.,地址:4201 Wilson Blvd #110-545, Arlington, VA 22203,电子邮件:OncRxSvc@comcast.net;或J. Aubrey Waddell,田纳西大学药学院教授;布朗特纪念医院肿瘤科药剂师,907 E. Lamar Alexander Parkway, Maryville, TN 37804, e-mail: waddfour@charter.net。
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引用次数: 2
Comparison of transport AC losses in an eight-strand YBCO Roebel cable and a four-tape YBCO stack 八股YBCO罗贝尔电缆和四带YBCO堆叠中传输交流损耗的比较
Pub Date : 2011-11-01 DOI: 10.1016/J.PHYSC.2011.05.109
Zhenan Jiang, K. Thakur, N. Long, R. Badcock, M. Staines
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引用次数: 27
GSTT1 copy number gain is a poor predictive marker for escalated-dose imatinib treatment in chronic myeloid leukemia: genetic predictive marker found using array comparative genomic hybridization GSTT1拷贝数增益是慢性髓性白血病伊马替尼增加剂量治疗的一个较差的预测标记:使用阵列比较基因组杂交发现的遗传预测标记
Pub Date : 2010-12-01 DOI: 10.1016/j.cancergencyto.2010.08.022
Youngil Koh , Dae-Young Kim , Sung-Hyo Park , Seung-Hyun Jung , Eunkyung Park , Hyeoung-Joon Kim , Sang Kyun Sohn , Young Don Joo , Seok Jin Kim , Ho-Jin Shin , Sung-Hyun Kim , Hong Suk Song , Jooseop Chung , Inho Kim , Sung-Soo Yoon , Byoung Kook Kim , Seung-Hun Shin , Yeun-Jun Chung , Seonyang Park

In a study population of 45 patients who were previously enrolled in an imatinib dose escalation trial, genome-wide screening for regions of genetic gains and losses was performed using array comparative genomic hybridization (aCGH). Early molecular response (EMR), defined as >50% reduction in the ratio of BCR-ABL1 to ABL1 within 6 months after dose escalation, was a major endpoint for analysis. After aCGH analysis, copy number change of four genes was investigated in 52 patients as a validation. Copy number gain in 16p11.2 was more frequently observed in patients with EMR than in patients who failed to achieve EMR (P = 0.034). A tendency for increased copy number in 22q11.23 in patients without EMR and for decreased copy number in 17q12 in patients with EMR was observed (P = 0.072 and P = 0.070, respectively). For GSTT1, in 22q11.23, copy number gain was observed in patients without EMR (P = 0.035). GSTT1 copy number gain was related to short time to treatment failure (TTFx) in patients without BCR–ABL1 mutations (P = 0.007). In multivariate analysis, GSTT1 copy number gain was an independent predictive factor for short TTFx (P = 0.020). We conclude that chromosome regions 16p11.2, 22q11.23, and 17q12 are potential locations related to response in imatinib dose escalation therapy for CML. GSTT1 copy number gain is a genetic change affecting outcome in this setting.

在先前参加伊马替尼剂量递增试验的45名患者的研究人群中,使用阵列比较基因组杂交(aCGH)对遗传增益和损失区域进行全基因组筛选。早期分子反应(EMR),定义为在剂量增加后6个月内BCR-ABL1与ABL1的比例减少50%,是分析的主要终点。在aCGH分析后,对52例患者的4个基因拷贝数变化进行了研究,作为验证。在EMR患者中,16p11.2基因拷贝数增加的频率高于未实现EMR的患者(P = 0.034)。无EMR患者的22q11.23拷贝数增加,有EMR患者的17q12拷贝数减少(P = 0.072和P = 0.070)。对于GSTT1,在22q11.23中,没有EMR的患者中观察到拷贝数增加(P = 0.035)。在无BCR-ABL1突变的患者中,GSTT1拷贝数增加与治疗失败的短时间(TTFx)相关(P = 0.007)。在多变量分析中,GSTT1拷贝数增益是短TTFx的独立预测因素(P = 0.020)。我们得出结论,染色体区域16p11.2, 22q11.23和17q12是与伊马替尼剂量递增治疗CML反应相关的潜在位置。在这种情况下,GSTT1拷贝数增加是一种影响结果的遗传变化。
{"title":"GSTT1 copy number gain is a poor predictive marker for escalated-dose imatinib treatment in chronic myeloid leukemia: genetic predictive marker found using array comparative genomic hybridization","authors":"Youngil Koh ,&nbsp;Dae-Young Kim ,&nbsp;Sung-Hyo Park ,&nbsp;Seung-Hyun Jung ,&nbsp;Eunkyung Park ,&nbsp;Hyeoung-Joon Kim ,&nbsp;Sang Kyun Sohn ,&nbsp;Young Don Joo ,&nbsp;Seok Jin Kim ,&nbsp;Ho-Jin Shin ,&nbsp;Sung-Hyun Kim ,&nbsp;Hong Suk Song ,&nbsp;Jooseop Chung ,&nbsp;Inho Kim ,&nbsp;Sung-Soo Yoon ,&nbsp;Byoung Kook Kim ,&nbsp;Seung-Hun Shin ,&nbsp;Yeun-Jun Chung ,&nbsp;Seonyang Park","doi":"10.1016/j.cancergencyto.2010.08.022","DOIUrl":"10.1016/j.cancergencyto.2010.08.022","url":null,"abstract":"<div><p>In a study population of 45 patients who were previously enrolled in an imatinib dose escalation trial, genome-wide screening for regions of genetic gains and losses was performed using array comparative genomic hybridization (aCGH). Early molecular response (EMR), defined as &gt;50% reduction in the ratio of <em>BCR-ABL1</em> to <em>ABL1</em> within 6 months after dose escalation, was a major endpoint for analysis. After aCGH analysis, copy number change of four genes was investigated in 52 patients as a validation. Copy number gain in 16p11.2 was more frequently observed in patients with EMR than in patients who failed to achieve EMR (<em>P</em> = 0.034). A tendency for increased copy number in 22q11.23 in patients without EMR and for decreased copy number in 17q12 in patients with EMR was observed (<em>P</em> = 0.072 and <em>P</em> = 0.070, respectively). For <em>GSTT1</em>, in 22q11.23, copy number gain was observed in patients without EMR (<em>P</em> = 0.035). <em>GSTT1</em> copy number gain was related to short time to treatment failure (TTFx) in patients without <em>BCR–ABL1</em> mutations (<em>P</em> = 0.007). In multivariate analysis, <em>GSTT1</em> copy number gain was an independent predictive factor for short TTFx (<em>P</em> = 0.020). We conclude that chromosome regions 16p11.2, 22q11.23, and 17q12 are potential locations related to response in imatinib dose escalation therapy for CML. <em>GSTT1</em> copy number gain is a genetic change affecting outcome in this setting.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 215-221"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29533577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
Letter to the Editor regarding the article “Chromosome abnormalities additional to the Philadelphia chromosome at the diagnosis of chronic myelogenous leukemia: pathogenic and prognostic implications” 致编辑关于文章“诊断慢性粒细胞白血病时费城染色体外的染色体异常:致病性和预后意义”的信
Pub Date : 2010-12-01 DOI: 10.1016/j.cancergencyto.2010.09.011
Vesna Najfeld Ph.D.
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引用次数: 1
Three rearrangements of chromosome 5 in a patient with myelodysplastic syndrome: an atypical deletion 5q, a complex intrachromosomal rearrangement of chromosome 5, and a paracentric inversion of chromosome 5 骨髓增生异常综合征患者5号染色体的三个重排:非典型缺失5q, 5号染色体的复杂染色体内重排和5号染色体的顺中心倒置
Pub Date : 2010-12-01 DOI: 10.1016/j.cancergencyto.2010.07.129
Nathalie Douet-Guilbert , Audrey Basinko , Jean-Richard Eveillard , Frédéric Morel , Marie-Josée Le Bris , Nadia Guéganic , Clément Bovo , Angèle Herry , Christian Berthou , Marc De Braekeleer

We report the case of a 74-year-old man who sought care for de novo myelodysplastic syndrome (RAEB-1). Conventional cytogenetic techniques showed a karyotype with two different deletions of the long arm of chromosome 5 distributed in three clones: 46,XY,del(1)(p34),del(5)(q14q23)[2]/46,XY,del(1)(p34),del(5)(q14q34)[10]/46,idem,inv(5)(q?11q?34)[7]. Precise characterization of the breakpoints, delineation of the deleted regions, identification of the complex intrachromosomal rearrangement of chromosome 5, and sequential accumulation of chromosomal abnormalities were elucidated by several fluorescence in situ hybridization analyses. We also assessed the clinical, biological, and cytogenetic evolution under lenalidomide treatment and after its interruption.

我们报告一例74岁的男性谁寻求照顾新生骨髓增生异常综合征(RAEB-1)。常规细胞遗传学技术显示,5号染色体长臂缺失的核型分布在3个克隆中:46,XY,del(1)(p34),del(5)(q14q23)[2]/46,XY,del(1)(p34),del(5)(q14q34)[10]/46,idem,inv(5)(q11q34)[7]。通过荧光原位杂交分析,精确描述了断点,缺失区域的描绘,鉴定了5号染色体的复杂染色体内重排,以及染色体异常的顺序积累。我们还评估了来那度胺治疗和中断治疗后的临床、生物学和细胞遗传学进化。
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引用次数: 6
Screening for DNA copy number aberrations in mucinous adenocarcinoma arising from the minor salivary gland: two case reports 小唾液腺粘液腺癌DNA拷贝数畸变的筛查:两例报告
Pub Date : 2010-12-01 DOI: 10.1016/j.cancergencyto.2010.08.027
Kenichiro Uchida , Atsunori Oga , Takamitsu Mano , Hitoshi Nagatsuka , Yoshiya Ueyama , Kohsuke Sasaki

Mucinous adenocarcinoma (MAC) is a rare malignancy in the minor salivary gland. To our knowledge, genomic alterations in this tumor have not been reported previously. To identify DNA copy number aberrations, we applied comparative genomic hybridization (CGH) to four samples of MAC in minor salivary gland derived from two patients: a primary tumor and two cervical metastatic lymph nodes from one patient, and a primary tumor from the other patient. Copy number increases were commonly detected in 1q21∼q31 and 20q13, and these may play an important role in MAC carcinogenesis. Copy number increases in 1q, 12p, 12q, and 20q were commonly detected in all three samples derived from patient 1, and gain of 7p and loss of chromosome 4 were additionally detected in the two samples derived from metastatic lymph nodes. Amplifications were also detected in the chromosomal regions 8q22∼qter, 12p11∼p12, 12q11∼q21, and 20q13. Amplification of MDM2 (12q15) and of AURKA (20q13) was detected with fluorescence in situ hybridization. The DNA copy number aberrations detected in MAC in minor salivary glands were different from those reported for colorectal MAC. The present findings are novel in identifying genomic alterations of MAC arising from the minor salivary gland.

摘要粘液腺癌是一种罕见的小唾液腺恶性肿瘤。据我们所知,这种肿瘤的基因组改变以前没有报道过。为了确定DNA拷贝数畸变,我们应用比较基因组杂交(CGH)对来自两名患者的小唾液腺MAC样本进行了分析:一名患者的原发肿瘤和两个宫颈转移淋巴结,另一名患者的原发肿瘤。拷贝数增加通常在1q21 ~ q31和20q13中检测到,这可能在MAC癌变中起重要作用。在患者1的所有三个样本中,1q、12p、12q和20q的拷贝数增加是常见的,在转移性淋巴结的两个样本中,另外还检测到7p的增加和4号染色体的缺失。在染色体区域8q22 ~ qter、12p11 ~ p12、12q11 ~ q21和20q13中也检测到扩增。荧光原位杂交检测MDM2 (12q15)和AURKA (20q13)基因的扩增。在小唾液腺MAC中检测到的DNA拷贝数畸变与结直肠MAC中检测到的DNA拷贝数畸变不同。本研究在鉴定小唾液腺引起的MAC基因组改变方面是新颖的。
{"title":"Screening for DNA copy number aberrations in mucinous adenocarcinoma arising from the minor salivary gland: two case reports","authors":"Kenichiro Uchida ,&nbsp;Atsunori Oga ,&nbsp;Takamitsu Mano ,&nbsp;Hitoshi Nagatsuka ,&nbsp;Yoshiya Ueyama ,&nbsp;Kohsuke Sasaki","doi":"10.1016/j.cancergencyto.2010.08.027","DOIUrl":"10.1016/j.cancergencyto.2010.08.027","url":null,"abstract":"<div><p>Mucinous adenocarcinoma (MAC) is a rare malignancy in the minor salivary gland. To our knowledge, genomic alterations in this tumor have not been reported previously. To identify DNA copy number aberrations, we applied comparative genomic hybridization (CGH) to four samples of MAC in minor salivary gland derived from two patients: a primary tumor and two cervical metastatic lymph nodes from one patient, and a primary tumor from the other patient. Copy number increases were commonly detected in 1q21∼q31 and 20q13, and these may play an important role in MAC carcinogenesis. Copy number increases in 1q, 12p, 12q, and 20q were commonly detected in all three samples derived from patient 1, and gain of 7p and loss of chromosome 4 were additionally detected in the two samples derived from metastatic lymph nodes. Amplifications were also detected in the chromosomal regions 8q22∼qter, 12p11∼p12, 12q11∼q21, and 20q13. Amplification of <em>MDM2</em> (12q15) and of <em>AURKA</em> (20q13) was detected with fluorescence in situ hybridization. The DNA copy number aberrations detected in MAC in minor salivary glands were different from those reported for colorectal MAC. The present findings are novel in identifying genomic alterations of MAC arising from the minor salivary gland.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 324-327"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29534022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
期刊
Cancer Genetics and Cytogenetics
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