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Xinyan Hu,1,&ast; Yanling Sui,1,&ast; Xinhao Yang,1 Zhengyu Yang,2 Qiuting Wang,2 Jiehong Yuan,2 Maoyu Li,1 Xiaotong Ma,1 Chengxuan Qiu,3 Qinjian Sun1 1Key Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People’s Republic of China; 2Department of Neurology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, People’s Republic of China; 3Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet-Stockholm University, Stockholm, Sweden&ast;These authors contributed equally to this workCorrespondence: Qinjian Sun, Key Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Neurology, Shandong Provincial Hospital affiliated to Shandong First Medical University, No. 324 Jingwu Weiqi Road, Jinan, Shandong, 250021, People’s Republic of China, Email sqj1210@163.comBackground: The inflammatory response is a pivotal factor in accelerating the progression of atherosclerosis. The high-sensitivity C-reactive protein-to-albumin ratio (CAR) has emerged as a novel marker of systemic inflammation. However, few studies have shown the CAR to be a promising prognostic marker for carotid atherosclerotic disease. This study aimed to analyse the predictive role of the CAR in carotid atherosclerotic disease.Methods: This community-based cohort study recruited 2003 participants from the Rose asymptomatic IntraCranial Artery Stenosis (RICAS) study who were free of stroke or transient ischemic attack. Carotid atherosclerotic plaques and their stability were identified via carotid ultrasound. Logistic regression models were utilized to investigate the association between CAR and the presence of carotid atherosclerotic plaques.Results: The prevalence of carotid atherosclerotic plaques was 38.79% in this study. After adjusting for clinical risk factors, including sex, age, dyslipidemia, hypertension, diabetes mellitus (DM), and smoking and drinking habits, a high CAR-level was independently associated with carotid plaque (odds ratio [OR] of upper: 1.46, 95% confidence interval [CI]: 1.13– 1.90, P = 0.004; P for trend = 0.011). The highest CAR tertile was still significantly associated with carotid plaques among middle-aged (40– 64 years) or female participants. Notably, an elevated CAR may be an independent risk factor for vulnerable carotid plaques (OR of upper: 2.06, 95% CI: 1.42– 2.98, P < 0.001; P for trend < 0.001).Conclusion: A high CAR may be correlated with a high risk of carotid plaques, particularly among mildly aged adults (40– 64 years) or females. Importantly, the CAR may be associated with vulnerable carotid plaques, suggesting that the CAR may be a new indicator for stroke prevention. Keywords: C-reactive protein, albumin, plaque, atherosclerotic, cohort study

Jie Du,1 Jing Niu,1 Lanxiang Ma,2 Yongjie Sui,1 Shuili Wang3 1Department of Health Examination Center, Shaanxi Provincial People Hospital, Xi’an, People’s Republic of China; 2Department of Cardiology, Shaanxi Provincial Corps Hospital, Chinese People’s Armed Police Forces, Xi’an, People’s Republic of China; 3Department of Respiratory Medicine, Shaanxi Provincial People Hospital, Xi’an, People’s Republic of ChinaCorrespondence: Lanxiang Ma, Department of Cardiology, Shaanxi Provincial Corps Hospital, Chinese People’s Armed Police Forces, Xi’an, People’s Republic of China, Tel +86-15991765901, Email mztjzx2250@163.comPurpose: High blood urea nitrogen (BUN) is associated with an elevated risk of mortality in various diseases, such as heart failure and pneumonia. Heart failure and pneumonia are common comorbidities of chronic obstructive pulmonary disease (COPD) exacerbation. However, data on the relationship of BUN levels with length of stay (LOS) in patients with pneumonic COPD exacerbation are sparse. The purpose of this study was to evaluate the correlation between BUN levels and LOS in a cohort of patients with pneumonic COPD exacerbation.Patients and Methods: The present study was a multicentre, retrospective cohort study. A total of 1226 patients with pneumonic COPD exacerbation were included through a validated algorithm derived from the 10th revision of the International Classification of Diseases and Related Health Problems (ICD-10). It should be noted that the entire study was completed by Shiroshita et al, who uploaded the data to the DATADRYAD website. The author only used these data for secondary analysis.Results: After adjusting for potential confounders (age, gender), a nonlinear relationship was detected between BUN levels less than 40 mg/dl and LOS. The effect sizes and the confidence intervals on the left and right sides of the inflection point were 0.27 (0.16, 0.39) and − 0.17 (− 0.34, 0.01), respectively.Conclusion: High levels of BUN in the hospital may be associated with increased LOS. BUN was positively related to LOS when BUN was less than 40 mg/dl.Keywords: pneumonia, chronic obstructive pulmonary disease, exacerbation, blood urea nitrogen, length of stay

Kun Lu, Yingli Sui, Lin Fu Institute of Chronic Disease, School of Basic Medicine, Qingdao University, Qingdao, Shandong, People’s Republic of ChinaCorrespondence: Lin FuInstitute of Chronic Disease, School of Basic Medicine, Qingdao University, No. 308 Ningxia Road, Qingdao City, Shandong Province, 266071, People’s Republic of ChinaTel +86 138 1804 8288Fax +86 532-85953085Email smilefulin@163.comBackground: Lung adenocarcinoma (LUAD) is the primary subtype of human lung cancer. The effectiveness of treatment and long-term survival of patients with LUAD are current suboptimal. Tripartite motif containing 56 (TRIM56) is a member of the TRIM protein family that have functions predominantly in immunity and cancer.Purpose: To investigate the expression of TRIM56 in LUAD, and explore the potential regulatory role of TRIM56 in the invasion and migration of LUAD cells.Methods: The Gene Expression Omnibus datasets and The Cancer Genome Atlas-LUAD cohort were used to analyze the mRNA expression of TRIM56 in LUAD. The differential expression profiles of miRNAs associated with TRIM56 were obtained from The Cancer Genome Atlas-LUAD cohort. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to determine the principal functions of miRNAs and interacting proteins. Transwell and wound healing were used to detect the effect of overexpression of TRIM56 on the invasion and migration of LUAD cells.Results: The expression of TRIM56 was decreased in LUAD and associated with poor prognosis. We determined the genome copy number, negatively correlated miRNA and potential transcription factors of TRIM56, and conducted enrichment analysis. Among them, hsa-mir-542 and hsa-mir-627 were the most likely to inhibit the expression of TRIM56. We also predicted the interacting proteins and potential ubiquitination substrate of TRIM56. Finally, we demonstrated that overexpression of TRIM56 inhibits the invasion and migration of LUAD cells.Conclusion: This study is the first to analyze the expression of TRIM56 and its inhibitory effect on the invasion and migration of LUAD. This evidence provides a new direction for further study of the reasons for the low expression of TRIM56 in LUAD and its regulatory mechanism.Keywords: TRIM56, lung adenocarcinoma, bioinformatics analysis, invasion, migration

Liang-qian Tong,1,* Yan-fang Sui,2,* Sheng-nan Jiang,1 Yan-hai Yin3 1Department of Nuclear Medicine, Central South University Xiangya School Affiliated Haikou Hospital, Haikou, Hainan, 570208, People’s Republic of China; 2Department of Rehabilitation Medicine, Central South University Xiangya School Affiliated Haikou Hospital, Haikou, Hainan, 570208, People’s Republic of China; 3Department of Nuclear Medicine, Hainan Medicine College Affiliated Hainan Hospital, Haikou, Hainan, 570311, People’s Republic of China*These authors contributed equally to this workCorrespondence: Sheng-nan JiangDepartment of Nuclear Medicine, Central South University Xiangya School Affiliated Haikou Hospital, No. 43 of Renmin Road, Meilan District, Haikou, Hainan, 570208, People’s Republic of ChinaTel/ Fax +86 0898 66151088Email jiang_ddueg@tom.comObjective: This study aimed to evaluate the relationship between fluorodeoxyglucose metabolism and smoking history in healthy adults by analyzing lung standardized uptake value (SUV).Methods: The 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) studies of 347 patients who did not show signs of having malignant diseases or lung inflammation were retrospectively evaluated. Four circular regions of interest (ROI) were manually drawn on the upper and lower lung regions. The averages of maximum SUV (SUVmax-avr) and mean SUV (SUVmean-avr) were calculated, and the mean values of each parameter for non-smokers, ex-smokers, and current smokers were compared. The correlation between SUVmax-avr and smoking history (tobacco burden and the duration of smoking cessation) was assessed based on present smoking status. The ex-smokers and current smokers were divided into three groups according to their tobacco burden, and the SUVmax-avrs of the two groups were compared.Results: Both the mean values of SUVmax-avr and SUVmean-avr increased based on smoking history, with non-smokers having the lowest values and current smokers the highest. Tobacco burden had a positive correlation with SUVmax-avr in current smokers (r = 0.474, P< 0.001). However, neither tobacco burden (r = 0171, P = 0.162) nor duration of smoking cessation (r = 0.212, P = 0.082) had a significant correlation with SUVmax-avr in ex-smokers. The mean SUVmax-avr of current smokers was significantly higher than that of ex-smokers in patients with a medium or large tobacco burden (P = 0.012, P< 0.001, respectively). Although there was no significant difference between the mean SUVmax-avrs of ex-smokers and current smokers in patients with a small tobacco burden (P = 0.888), the mean SUVmax-avrs of both ex-smokers and current smokers with a small tobacco burden were significantly higher than that of non-smokers (P< 0. 001, P< 0.001, respectively).Conclusion: The findings indicate that lung SUV increases in current heavy smokers and partially decreases after the cessation of smoking, which is in line with previous reports studied by analyzingfluorodeoxyglucose (FDG) metabolism of lung specimens.Keywords: smoking, lung, positron emission tomography/computed tomography, fluorodeoxyglucose

Inflammatory bowel disease (IBD) is a chronic illness characterized by dysregulated immune cascades in the intestines, in which the Th17 immune response plays an important role. We demonstrated that mice with intestinal epithelium–specific deletion of Krüppel-like factor 5 (Klf5) developed Th17-dependent colonic inflammation. In the absence of KLF5, there was aberrant cellular localization of phosphorylated STAT3, an essential mediator of the Th17-associated cytokine, IL-22, which is required for epithelial tissue regeneration. In contrast, mitigation of IL-17A with anti–IL-17A neutralizing antibody attenuated colitis in Klf5-deficient mice. There was also a considerable shift in the colonic microbiota of Klf5-deficient mice that phenocopied human IBD. Notably, the inflammatory response due to Klf5 deletion was alleviated by antibiotic treatment, implicating the role of microbiota in pathogenesis. Finally, human colitic tissues had reduced KLF5 levels when compared with healthy tissues. Together, these findings demonstrated the importance of KLF5 in protecting the intestinal epithelium against Th17-mediated immune and inflammatory responses. The mice described herein may serve as a potential model for human IBD.

Yang Zhao,1,* Tiantian Li,2,* Shuaiwei Tian,1,* Wei Meng,1 Yi Sui,2 Jian Yang,1 Baocheng Wang,1 Zhuangzhuang Liang,1 Heng Zhao,1 Yipeng Han,1 Yujie Tang,1,2 Lei Zhang,2 Jie Ma1 1Department of Pediatric Neurosurgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 2Key Laboratory of Cell Differentiation and Apoptosis of the National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jie MaDepartment of Pediatric Neurosurgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Yangpu District, Shanghai 200092, People’s Republic of ChinaTel +86- 13818138498Fax +86-21- 65795173Email majie@xinhuamed.com.cnLei ZhangKey Laboratory of Cell Differentiation and Apoptosis of the National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Huangpu, Shanghai 200025, People’s Republic of ChinaTel +86-13918539872Fax +86-21-6415 4900Email lei.zhang2012@sjtu.edu.cnPurpose: In medulloblastoma (MB), group 3 (G3) patients with MYC amplification tend to exhibit worse prognosis, thus creating a need for novel effective therapies. As the driver and crucial dependency for MYC-amplified G3-MB, MYC has been proven to be a prospective therapeutic target. Here, we aimed to identify novel effective therapeutic strategies against MYC-amplified G3-MB via targeting MYC translation.Materials and Methods: Major components of translation initiation complex eIF4F were subjected to MB tumor dataset analysis, and EIF4A1 was identified to be a potential therapeutic target of MYC-amplified G3-MB. Validation was performed through genetic or pharmacological approaches with multiple patient-derived tumor models of MYC-amplified G3-MB in vitro and in vivo. Underlying mechanisms were further explored by Western blot, quantitative real-time PCR and mass spectrometry (MS) analyses.Results: MB tumor datasets analyses showed that EIF4A1 was significantly up-regulated in G3-MB patients relative to normal cerebella, positively correlated with MYC in G3-MB at transcriptional level and a crucial cancer dependency in MYC-amplified G3-MB cells. Targeting EIF4A1 with a CRISPR/Cas9 approach or small-molecule inhibitor silvestrol effectively attenuated growth in multiple preclinical models of MYC-amplified G3-MB via blocking proliferation and inducing apoptosis. Mechanistically, EIF4A1 inhibition effectively impeded MYC expression at translational level, and its potency was positively associated with MYC level. Whole-proteome MS analysis of silvestrol-treated cells further unveiled other biological functions and pathways influenced by EIF4A1 inhibition.Conclusion: Our investigation shows that interrupting MYC translation by EIF4A1 inhibition could be a potential effective therapeutic approach when treating patients with MYC-amplified G3-MB.Keywords: eIF4F complex, EIF4A1, MYC-amplified group 3 medulloblastoma, Silvestrol, translation inhibition

Xuewen Wang,1,* Bing Chen,1– 3,* Danfen Xu,1 Zhijun Li,4 Yuxia Sui,5,6 Xinhua Lin1– 3 1Department of Pharmaceutical Analysis, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian, People’s Republic of China; 2Nano Medical Technology Research Institute, Fujian Medical University, Fuzhou, Fujian, People’s Republic of China; 3Higher Educational Key Laboratory for Nano Biomedical Technology of Fujian Province, Fujian Medical University, Fuzhou, Fujian, People’s Republic of China; 4School of Pharmacy, Fujian Medical University, Fuzhou 350180, Fujian, People’s Republic of China; 5Department of Pharmacy, Shengli Clinical Medical College of Fujian Medical University, Fuzhou 350001, People’s Republic of China; 6Department of Pharmacy, Fujian Provincial Hospital, Fuzhou 350001, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xinhua LinDepartment of Pharmaceutical Analysis, Fujian Medical University, No. 1 Xueyuan Road, University Town, Fuzhou 350122, People’s Republic of ChinaTel/Fax +86 13906909638Email xhlfz123454321@sina.comYuxia SuiDepartment of Pharmacy, Fujian Provincial Hospital, No. 134 Dong Street, Fuzhou 350001, People’s Republic of ChinaTel/Fax +86 15959090652Email suiyuxia123@163.comBackground: The incidence and mortality of lung cancer continue to increase around the world; in 2018, new lung cancer cases accounted for 11.6% of all cancer cases, and lung cancer deaths accounted for 18.4% of cancer deaths. Cisplatin (DDP) is a first-line chemotherapy drug for lung cancer; however, DDP resistance can lead to a poor prognosis in patients with lung cancer. Therefore, reversing DDP resistance is a treatment goal.Materials and Methods: Cell counting kit-8 (CCK8) assays, wound healing analyses, Transwell assays, in vitro tumor xenografts, and flow cytometry were used to detect the proliferation, migration, invasion, and apoptosis of multidrug resistant A549/DDP and PC9/DDP cells, respectively. Western blot was performed to detect protein levels of cleaved caspase-3, CHOP, and GRP78.Results: Delicaflavone inhibited DDP resistance of lung cancer cells and decreased proliferation in a dose- and time-dependent manner. It also decreased migration and invasion and enhanced apoptosis. Western blots showed that delicaflavone overcame DDP resistance by increasing the expression of GRP78 and CHOP and the apoptosis-related protein cleaved caspase-3.Conclusion: Delicaflavone can reverse DDP resistance in A549/DDP and PC9/DDP cells by inhibiting cell proliferation and migration and enhancing apoptosis and cleaved caspase-3 levels by increasing the expression of CHOP and GRP78 protein via the endoplasmic reticular stress pathway. It could be a useful therapeutic adjunct to treat DDP-resistant lung cancer.Keywords: delicaflavone, Cisplatin; DDP, lung cancer, endoplasmic reticulum stress

Inflammatory bowel disease (IBD) is a chronic immune-mediated disease of the gastrointestinal tract. While therapies exist, response can be limited within the patient population. Researchers have thus studied mouse models of colitis to further understand pathogenesis and identify new treatment targets. Flow cytometry and RNA-sequencing can phenotype immune populations with single-cell resolution but provide no spatial context. Spatial context may be particularly important in colitis mouse models, due to the simultaneous presence of colonic regions that are involved or uninvolved with disease. These regions can be identified on hematoxylin and eosin (H&E)-stained colonic tissue slides based on the presence of abnormal or normal histology. However, detection of such regions requires expert interpretation by pathologists. This can be a tedious process that may be difficult to perform consistently across experiments. To this end, we trained a deep learning model to detect 'Involved' and 'Uninvolved' regions from H&E-stained colonic tissue slides. Our model was trained on specimens from controls and three mouse models of colitis-the dextran sodium sulfate (DSS) chemical induction model, the recently established intestinal epithelium-specific, inducible Klf5ΔIND (Villin-CreERT2;Klf5fl/fl) genetic model, and one that combines both induction methods. Image patches predicted to be 'Involved' and 'Uninvolved' were extracted across mice to cluster and identify histological classes. We quantified the proportion of 'Uninvolved' patches and 'Involved' patch classes in murine swiss-rolled colons. Furthermore, we trained linear determinant analysis classifiers on these patch proportions to predict mouse model and clinical score bins in a prospectively treated cohort of mice. Such a pipeline has the potential to reveal histological links and improve synergy between various colitis mouse model studies to identify new therapeutic targets and pathophysiological mechanisms.

A well-established numerical approach to solve the Navier-Stokes equations for incompressible fluids is Chorin's projection method [1], whereby the fluid velocity is explicitly updated, and then an elliptic problem for the pressure is solved, which is used to orthogonally project the velocity field to maintain the incompressibility constraint. In this paper, we develop a mathematical correspondence between Newtonian fluids in the incompressible limit and hypo-elastoplastic solids in the slow, quasi-static limit. Using this correspondence, we formulate a new fixed-grid, Eulerian numerical method for simulating quasi-static hypo-elastoplastic solids, whereby the stress is explicitly updated, and then an elliptic problem for the velocity is solved, which is used to orthogonally project the stress to maintain the quasi-staticity constraint. We develop a finite-difference implementation of the method and apply it to an elasto-viscoplastic model of a bulk metallic glass based on the shear transformation zone theory. We show that in a two-dimensional plane strain simple shear simulation, the method is in quantitative agreement with an explicit method. Like the fluid projection method, it is efficient and numerically robust, making it practical for a wide variety of applications. We also demonstrate that the method can be extended to simulate objects with evolving boundaries. We highlight a number of correspondences between incompressible fluid mechanics and quasi-static elastoplasticity, creating possibilities for translating other numerical methods between the two classes of physical problems.

Fei Wu,1 Yujie Sui,2 Yinhuai Wang,1 Tianmin Xu,1 Limei Fan,1 He Zhu1 1Department of Gynecology and Obstetrics, The Second Hospital of Jilin University, Changchun 130041, People’s Republic of China; 2Medical Research Center, The Second Hospital of Jilin University, Changchun 130041, People’s Republic of ChinaCorrespondence: He ZhuDepartment of Gynecology and Obstetrics, The Second Hospital of Jilin University, 218 Ziqiang Road, Jilin, Changchun 130041, People’s Republic of ChinaTel +86 135 1440 0868Email zhuhe_jl@163.comPurpose: A long noncoding RNA called small nucleolar RNA host gene 7 (SNHG7) is known to be a key regulator of biological processes in multiple human cancer types. In this study, our aims were to determine the expression status of SNHG7 in cervical cancer, to figure out the detailed roles of SNHG7 in cervical cancer cells, and to identify the mechanism underlying the activity of SNHG7 in cervical cancer.Methods: Reverse-transcription quantitative PCR was performed to measure SNHG7 expression in cervical cancer. A Cell Counting Kit-8 assay, flow-cytometric analysis, cell migration and invasion assays, and a tumor xenograft experiment were conducted to respectively determine the effects of SNHG7 on cervical cancer cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo.Results: SNHG7 was found to be markedly upregulated in cervical cancer tissues and cell lines. Higher SNHG7 expression significantly correlated with FIGO stage, lymph node metastasis, the depth of cervical invasion, and shorter overall survival in patients with cervical cancer. Functional experiments indicated that a SNHG7 knockdown attenuated proliferation, migration, and invasiveness and promoted apoptosis of cervical cancer cells in vitro. The SNHG7 knockdown also slowed tumor growth in vivo. Further investigation showed that SNHG7 acts as a competing endogenous RNA for microRNA-485 (miR-485) in cervical cancer cells, and the inhibitory actions of the SNHG7 knockdown on the malignant phenotype were reversed by miR-485 inhibition. P21-activated kinase 4 (PAK4) was identified as a direct target gene of miR-485 in cervical cancer, and PAK4 expression was promoted by SNHG7.Conclusion: SNHG7 functions as an oncogenic RNA in cervical cancer, competitively binds to miR-485, and thereby upregulates PAK4. This SNHG7–miR-485–PAK4 regulatory network may provide insights into the pathogenesis of cervical cancer, and can help in the identification of novel diagnostic and therapeutic approaches for cervical cancer.Keywords: small nucleolar RNA host gene 7, P21-activated kinase 4

OBJECTIVE: The aim of this study was to screen the differential genes related to ferroptosis in osteoporosis patients. MATERIALS AND METHODS: GEO2R was used to screen the differential genes related to ferroptosis in osteoporosis patients by searching the relevant chips in the GEO database, and Spearman's correlation analysis was used to describe the correlation between quantitative variables without normal distribution. p-values lower than 0.05 were considered statistically significant. Another group of osteoporosis patients was selected in the GEO database to verify the significantly differentially expressed genes. RESULTS: The results showed that 10 samples in chip GSE35956 were identified as research objects, and a total of 5 ferroptosis differential genes were screened out: ATP5MC3, CDKN1A, MT1G, NCOA4, SLC1A5, of which 3 up-regulated genes (CDKN1A, MT1G, SLC1A5), 2 down-regulated genes (ATP5MC3, NCOA4). The above differential genes were placed in 19 samples of chip GSE35959 for verification, and the same expression trend was obtained, but only the MT1G difference was statistically significant. CONCLUSIONS: The gene correlation test found that MT1G and ATP5MC3 had a strong negative correlation. [ABSTRACT FROM AUTHOR]

Wu F, Sui Y, Wang Y, Xu T, Fan L, Zhu H. Onco Targets Ther. 2020;13:685–699. The Editor and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised regarding the integrity of the tumor data presented in Figure 7B and the alleged duplication of images in Figure 2C with similar images from unrelated studies, specifically: Figure 2C panel C-33A, si-NC appears to have been duplicated with a similar image in Figure 2C from Gao et al, 2020 (https://doi.org/10.1080/15384101.2020.1749466). The authors responded to our queries but were unable to provide an explanation for the alleged image duplication and could not provide the original raw data for their study and have therefore agreed to retract the article. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper