PReD-Bench/PRed-Bench huggingface dataset:
A Novel Structure of Blockchain Applied in Vaccine Quality Control: Double-Chain Structured Blockchain System for Vaccine Anticounterfeiting and Traceability
Authors: Zehuan Qiu
Yifan Zhu
Journal: Journal of Healthcare Engineering (2021)
Discipline: Multidisciplinary
Keywords: Vaccine; Anticounterfeiting; Blockchain-based transaction platform; Mixed-chains structured platform; Public chain
Affiliations: College of Cyberspace Security, Hangzhou Dianzi University, Hangzhou 310018, Zhejiang, China, London School of Hygiene & Tropical Medicine Keppel Street, London WC1E 7HT, UK

Abstract:  Background: Vaccine, as an irreplaceable means in herd immunization, is widely applied in prevention for communicable diseases. However, adverse impacts were frequently incurred by fake or expired vaccines in China. Given the necessity of vaccine anticounterfeiting, blockchain-based transaction platform could be practiced as a solution in addressing the issue; however, most of the available experiments focused on single-chain structured design with inventible limitations. Accordingly, exploration for the effectiveness and feasibility of mixed-chains structured platform for vaccine anticounterfeiting and tracing is essentially required. Methods: Both public chain and private chain were inserted in anticounterfeiting and tracing platform designing process, which were subsequently simulated in Ethereum environment. Results: By recording different information in public chain and private chain, partial information privacy protection requirements are realized. The transfer identification module realized the function of vaccine quality supervision and solves the problem of EPC label replication. Discussion. Compared with the traditional single-structured design, completeness information could be visited by all stakeholders in double-chain structure, including vaccine suppliers, National Medical Products Administration (NMPA), vaccine purchasers, and the vaccinated. Conclusion: Double-chain structured system for vaccine anticounterfeiting and tracing is more effective. 

Retracted: No

PubPeer comments:
 **3.3.4. Payment** If there are no abnormal adverse reactions due to vaccination during this period, the vaccine is considered to be qualified in quality [23]. 23. Y. X. Yang, H. Li, W. K. Zheng, Y. Bai, Z. M. Liu, and J. J. Zhang, u201cExperimental study on calcining process of secondary coated ceramsite solidified chromium contaminated soil,u201d Science of Advanced Materials, vol. 11, no. 7, pp. 208u2013214, 2019. Could the authors explain the relevance of Reference 23? ,
Automatic mental associations predict future choices of undecided decision-makers
Authors: Luciano Arcuri
Silvia Galdi
Bertram Gawronski
Journal: Science (2008)
Discipline: Multidisciplinary
Keywords: choice decisions; unconscious influences; automatic mental associations; future choices; self-report measures
Affiliations: Department of Developmental Psychology and Socialization, University of Padova, Via Venezia 8, 35131 Padova, Italy. 

Abstract:  Common wisdom holds that choice decisions are based on conscious deliberations of the available information about choice options. On the basis of recent insights about unconscious influences on information processing, we tested whether automatic mental associations of undecided individuals bias future choices in a manner such that these choices reflect the evaluations implied by earlier automatic associations. With the use of a computer-based, speeded categorization task to assess automatic mental associations (i.e., associations that are activated unintentionally, difficult to control, and not necessarily endorsed at a conscious level) and self-report measures to assess consciously endorsed beliefs and choice preferences, automatic associations of undecided participants predicted changes in consciously reported beliefs and future choices over a period of 1 week. Conversely, for decided participants, consciously reported beliefs predicted changes in automatic associations and future choices over the same period. These results indicate that decision-makers sometimes have already made up their mind at an unconscious level, even when they consciously indicate that they are still undecided. 

Retracted: No

PubPeer comments:
 This article has been cited a lot (157 times in WebofScience as of May 3 2021) because it was published in Science. However, the claims made in this article should not be trusted because the sample sizes are very small and the cross-lagged panel model produces artifacts that are entirely due to the stability of the measures over time. Even simulated data without lagged effects show significant coefficients. https: replicationindex.com 2020 08 22 cross-lagged The main claim in this article is that implicit measures predict future choice behavior for undecided participants better than explicit measures. This finding failed to replicate in a study with a larger sample of N = 303 undecided voters. https: www.ncbi.nlm.nih.gov pmc articles PMC3430672 pdf pone.0044130.pdf ,
HSP90 is a key for telomerase activation and malignant transition in pheochromocytoma
Authors: Brigitte Peters
Cuong Hoang-Vu
Regine Schneider-Stock
Hendrik Lehnert
Albert Roessner
Carsten Boltze
Journal: Endocrine (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: pheochromocytomas; telomerase; hTR; TP1; hTERT
Affiliations: Department of Pathology, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany. 

Abstract:  Recent studies on a limited number of pheochromocytomas (PCs) revealed a potential role of telomerase in the malignant transition of these tumors. Telomerase is a ribonucleoprotein complex that includes the telomerase RNA component (hTR), the telomerase-associated protein (TP1), the telomerase catalytic subunit (hTERT), and the heat-shock protein 90 (HSP90). The interactions between these subunits and the activation machinery of telomerase are still unclear. To test whether the expression and regulation of telomerase subunits are reflected in the malignant transition of PCs, we determined their mRNA and/or protein expression in 28 benign and 9 malignant PCs and compared the results with telomerase activity. Reverse transcriptase polymerase chain reaction analysis revealed that TP1 was ubiquitously expressed. hTR was found in all malignant (100%) and in 13/28 (46%) benign PCs. By contrast, hTERT was clearly associated with aggressive biologic behavior. All the malignant (100%) but only 2/28 benign (7%) PCs expressed hTERT. HSP90 was increased in malignant PCs but was also expressed at a lower level in benign tumors. High telomerase activity was measurable in only hTERT-positive tissues. Our data indicate that hTERT, HSP90, and telomerase activity are upregulated in malignant cells of the adrenal medulla. Overexpression of HSP90 is an important factor in the activation of telomerase via hTERT. The common expression of hTERT and telomerase activity thus represents an additional prognostic marker that may identify more aggressive tumors. 

Retracted: No

PubPeer comments:
null, 
 The Withdrawal notice is unfortunately behind a paywall. The original article is not listed as retracted, and Springer still charges $40 + tax to read it, without any warning it is withdrawn. Even worse, Springer charges another $40 + tax to read the withdrawal notice, which I will be happy to share here for free. Because that is how it should be. ![file] A post-mortem analysis for this paper appears to show more concerns than just similarity to another paper. Figure 1 appears to contain some duplicated areas which I have marked here with blue and red boxes. ![file] , 
 Third author. https: retractionwatch.com 2016 12 29 cancer-researcher-germany-loses-multiple-papers-misconduct-finding 4 retractions to date. http: retractiondatabase.org RetractionSearch.aspx#?auth%3dSchneider-Stock%252c%2bRegine , 
 The retraction note is open access and free to download: https: link.springer.com article 10.1007%2Fs12020-004-0002-4 ,
Serologic Testing of US Blood Donations to Identify Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)–Reactive Antibodies: December 2019–January 2020
Authors: Darbi Boulay
Bailey Alston
Shanna Bolcen
Heather Tatum
Yunlong Qin
Matthew R P Sapiano
So Hee Park
Mohammed Ata Ur Rasheed
Monica Epperson
Jan Drobeniuc
Rita Desai
Azaibi Tamin
Peter Browning
Carrie Reed
Susan Gerber
Muyiwa Ategbole
Ebenezer David
Lisa Mills
Sandra Lester
Palak Patel
Jarad Schiffer
Evelene Steward-Clark
Fiona Havers
Kimberly Moss
Natalie J Thornburg
Monica E Patton
Jennifer Harcourt
Brandi Freeman
Vera Semenova
Panagiotis Maniatis
Li Cronin
Sridhar V Basavaraju
Tao Jia
Andrew Vogan
Kacie Grimm
Han Li
Yamini Gorantla
Susan L Stramer
Kristina Ortiz
Megan Stumpf
Briana Zellner
Journal: Clinical Infectious Diseases (2021)
Discipline: IMMUNOLOGY
Keywords: SARS-CoV-2; antibody; blood donors.
Affiliations: Centers for Disease Control and Prevention, Atlanta, Georgia, USA., American Red Cross, Scientific Affairs, Gaithersburg, Maryland, USA., Synergy America, Inc, Atlanta, Georgia, USA., Eagle Global Scientific, Atlanta, Georgia, USA., IHRC, Atlanta, Georgia, USA., CFD Research Corporation, Huntsville, Alabama, USA., Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, USA.

Abstract:  Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19), was first identified in Wuhan, China, in December 2019, with subsequent worldwide spread. The first US cases were identified in January 2020. Methods: To determine if SARS-CoV-2-reactive antibodies were present in sera prior to the first identified case in the United States on 19 January 2020, residual archived samples from 7389 routine blood donations collected by the American Red Cross from 13 December 2019 to 17 January 2020 from donors resident in 9 states (California, Connecticut, Iowa, Massachusetts, Michigan, Oregon, Rhode Island, Washington, and Wisconsin) were tested at the Centers for Disease Control and Prevention for anti-SARS-CoV-2 antibodies. Specimens reactive by pan-immunoglobulin (pan-Ig) enzyme-linked immunosorbent assay (ELISA) against the full spike protein were tested by IgG and IgM ELISAs, microneutralization test, Ortho total Ig S1 ELISA, and receptor-binding domain/ACE2 blocking activity assay. Results: Of the 7389 samples, 106 were reactive by pan-Ig. Of these 106 specimens, 90 were available for further testing. Eighty-four of 90 had neutralizing activity, 1 had S1 binding activity, and 1 had receptor-binding domain/ACE2 blocking activity &gt;50%, suggesting the presence of anti-SARS-CoV-2-reactive antibodies. Donations with reactivity occurred in all 9 states. Conclusions: These findings suggest that SARS-CoV-2 may have been introduced into the United States prior to 19 January 2020. 

Retracted: No

PubPeer comments:
 This paper is one of several discussed in this thread. https: twitter.com Ayjchan status 1349163446143746052 , 
 https: twitter.com trvrb status 1333647437869633537 ,
Changes and significance of IL-25 in chicken collagen II-induced experimental arthritis (CIA)
Authors: Shen Pei
Xue Yuan
Xu Huaxi
Wang Kaiwen
Sandoghchian Shotorbani Siamak
Su Zhaoliang
Liu Yanfang
Huang Xinxiang
Wang Shengjun
Zhao Yinxia
Jiao Zhijun
Lu Liwei
Shao Qixiang
Yang Heng
Zheng Dong
Journal: Rheumatology International (2012)
Discipline: CLINICAL MEDICINE
Keywords: Rheumatoid arthritis; IL-25; autoimmune inflammatory disease; cytokine family; Th2 cells
Affiliations: Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, 212013 Zhenjiang, People's Republic China.

Abstract:  Rheumatoid arthritis (RA) is an autoimmune inflammatory disease. It is a systemic inflammatory disease, characterized by chronic, symmetrical, multi-articular synovial arthritis. IL-25 (IL-17E) is a member of the recently emerged cytokine family (IL-17s), which is expressed in Th2 cells and bone marrow-derived mast cells. Unlike the other members of this family, IL-25 is capable of inducing Th2-associated cytokines (IL-4, IL-5, and IL-13) and also promotes the release of some pro-immune factors (IL-6 and IL-8). IL-25 is also a pleiotropic factor, which constitutes a tissue-specific pathological injury and chronic inflammation. In this study, we used chicken collagen II-induced experimental arthritis (CIA) model in DBA/1 mice to investigate the relationship between IL-25 and other inflammatory factors, revealing the possible mechanism in CIA. Our results showed that the expression level of IL-25 was enhanced in the late stage of CIA, and IL-17 was increased in the early stage of the disease. It is well known that IL-17 has a crucial role in the development of RA pathogenesis, and IL-25 plays a significant role in humoral immune. For reasons given above, we suggested that the IL-25 inhibited IL-17 expression to some extent, while enhancing the production of IL-4. It was confirmed that IL-25 not only regulated the cellular immune, but also involved the humoral immune in rheumatoid arthritis. 

Retracted: No

PubPeer comments:
 Figure 3E * Cyan and blue boxes: Parts of the Onset of CIA and Peak of CIA plots appear to look quite similar, while the top right parts and the gated percentages are different. ![file] ,
MicroRNA-224 sustains Wnt/β-catenin signaling and promotes aggressive phenotype of colorectal cancer
Authors: Liuqing He
Zhiyuan Xiao
Tingting Li
Juanjuan Cai
Yanqing Ding
Wenting Liao
Li Liang
Hongli Jiao
Shuyang Wang
Qiuhua Lai
Yaping Ye
Danling Deng
Journal: Journal of Experimental & Clinical Cancer Research (2016)
Discipline: CLINICAL MEDICINE
Keywords: Wnt/β-catenin pathway; miR-224; CRC development; proliferation; metastasis
Affiliations: Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China. ., Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China. ., State Key Laboratory of Oncology in Southern China, Department of Experimental, Guangzhou, Guangdong, China. .

Abstract:  Background: Growing evidence suggests that Wnt/β-catenin pathway plays an important role in CRC development, progression and metastasis. Aberrant miR-224 expression has been reported in CRC. However, the mechanism of miR-224 promotes both proliferation and metastatic ability largely remains unclear. Methods: Real-time PCR was used to quantify miR-224 expression. Luciferase reporter assays were conducted to confirm the activity of Wnt/β-catenin pathway and target gene associations, and immunofluorescence staining assay was performed to observe the nuclear translocation of β-catenin. Bioinformatics analysis combined with in vivo and vitro functional assays showed the potential target genes, GSK3β and SFRP2, of miR-224. Specimens from forty patients with CRC were analyzed for the expression of miR-224 and the relationship with GSK3β/SFRP2 by real-time PCR and western blot. Results: Bioinformatics and cell luciferase function studies verified the direct regulation of miR-224 on the 3'-UTR of the GSK3β and SFRP2 genes, which leads to the activation of Wnt/β-catenin signaling and the nuclear translocation of β-catenin. In addition, knockdown of miR-224 significantly recovered the expression of GSK3β and SFRP2 and attenuated Wnt/β-catenin-mediated cell metastasis and proliferation. The ectopic upregulation of miR-224 dramatically inhibited the expression of GSK3β/SFRP2 and enhanced CRC proliferation and invasion. Conclusion: Our research showed mechanistic links between miR-224 and Wnt/β-catenin in the pathogenesis of CRC through modulation of GSK3β and SFRP2. 

Retracted: No

PubPeer comments:
 Figure 3C. *** ![file] , 
 Thanks for the comment regarding on our figure 3C. We read it carefully. We checked the raw data and found that we really made a mistake in preparing this figure. We are so sorry about this. We will contact the Journal editor and correct this as soon as possible. At last, we are so appreciated for you pointing out the problem. , 
 #2 Thank you. Could you post here the images for Supplemental file 3? The link on the journal website does not work for me. Additional file 3: Data S1. mRNA expression of miR-224, GSK3u03b2and SFRP2 in 20 CRC tissues. (DOC 15 kb) ,
MicroRNA-29a plays a suppressive role in non-small cell lung cancer cells via targeting LASP1
Authors: Yanhui Zhou
Shuang Wang
Kaiying Zhou
Changqi Li
Zhaolan Hu
Yanhui Cui
Xiaoqing Qiao
Journal: OncoTargets and Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: LIM and SH3 protein 1; invasion; microRNA-29a; migration; non-small cell lung cancer

Abstract:  MicroRNA (miR)-29a has been implicated in non-small cell lung cancer (NSCLC), but the mechanism remains largely unclear. LASP1, a cAMP- and cGMP-dependent signaling protein, was recently found to promote proliferation and aggressiveness in NSCLC. However, the regulatory mechanism of LASP1 expression in NSCLC, as well as the relationship between LASP1 and miR-29a, has never been previously studied. In this study, we found that miR-29a was remarkably downregulated and low expression of miR-29a was associated with the malignant progression of NSCLC. Moreover, the expression of LASP1 was markedly increased in NSCLC tissues and cell lines. Bioinformatics analysis and luciferase reporter assay data further identified LASP1 as a target gene of miR-29a, and the expression of LASP1 was negatively mediated by miR-29a at the post-transcriptional level in NSCLC cells. Overexpression of miR-29a reduced the proliferation, migration, and invasion of NSCLC cells, just as the effects of LASP1 knockdown. Moreover, overexpression of LASP1 attenuated the suppressive effect of miR-29a on the malignant phenotypes of NSCLC cells. In addition, upregulation of miR-29a decreased the growth of A549 cells in nude mice and protected the animals from tumor-induced death. Therefore, we demonstrate that miR-29a plays a suppressive role in NSCLC via targeting LASP1, suggesting that the miR-29a/LASP1 axis may become a promising therapeutic target for NSCLC. 

Retracted: No

PubPeer comments:
 There is a problem with the western blots in figure 1, with a critical issue regarding the loading control which seems to be reused innapropriately (orange boxes): ![file] Further problems appear with several splicings (blue arrows) across the whole blots, which are presented as coming from a unique membrane. , 
 This paper is truly amazing regarding the western blot figures. I am not sure how it is possible to quantify something that does not exist but apparently the authors managed to do it in Figure 2. https: journals.plos.org plosone article figure?id=10.1371 journal.pone.0100310.g002 First of all, the blots displayed are not labelled, which make it difficult to understand what are the conditions for each band. Second, both phospho Smad1,5,8 and phospho Smad2,3 are empty of any measurable signal. Yet, the authors provide quantification which does not seem to be possible with such a low amount of signal. More than this, they actually manage to get statistical significance. Finally, the authors provides a spliced gel for T-Smad. As this figure, like the first figure, seems central for this publication, it raises the question of the validity of the entire study. ,
<p>The inhibitive effect of sh-HIF1A-AS2 on the proliferation, invasion, and pathological damage of breast cancer via targeting miR-548c-3p through regulating HIF-1&alpha;/VEGF pathway in vitro and vivo</p>
Authors: Shenghai Lee
Xiao Guo
Peilong Cao
Journal: OncoTargets and Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: HIF-1α/VEGF; HIF1A-AS2; MCF-7; breast cancer; miR-548c-3p
Affiliations: Department of Breast Surgery, Central Clinical College of Gynecology Obstetrics, Tianjin Medical University, Tianjin 300110, China., Department of Surgery, Zhaoqing Medical College, Zhaoqing, Guangdong 526020, China., Department of Pathology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shanxi 710061, China, .

Abstract:  Background: Breast cancer (BC) has been the commonest malignant tumor with a low survival rate among woman. Long non-coding RNA hypoxia-inducible factor-1 alpha antisense RNA-2 (HIF1A-AS2) was correlated with various cancers. Purpose: The study aimed to investigate the roles and related underlying molecular mechanisms of HIF1A-AS2 in BC. Material and methods: Target relationships were speculated by Targetscan 7.0 and confirmed by dual luciferase reporter assay. Proteins levels were monitored by RT-qPCR, Western blot and immunohistochemistry assays. CCK-8 assay, SA-β-gal staining and transwell assay were used to detect proliferation, senescence and invasion, respectively. Xenograft nude mice were put into use to evaluate the tumor growth and motility. Results: The present study exhibited that HIF1A-AS2 and hypoxia-inducible factor-1 alpha (HIF-1α) were upregulated while miR-548c-3p was downregulated in MDA-MB-231, MCF-7, ZR-75-1, and BT-549 BC cell lines. Bioinformatics analysis showed HIF1A-AS2 and HIF-1α were two targets of miR-548c-3p, and the target relationship was further confirmed by dual luciferase reporter assay. Moreover, knockdown of HIF1A-AS2 by shRNA (sh-HIF1A-AS2) markedly elevated miR-548c-3p level, and the enhanced miR-548c-3p noticeably suppressed cell proliferation, invasion, and epithelial-mesenchymal transition, and promoted senescence in vitro. In addition, overexpression of HIF-1α promoted MCF-7 cell invasion. Intriguingly, low expression of HIF1A-AS2 reduced HIF-1α level by upregulating the expression of miR-548c-3p. Furthermore, experiment in xenograft nude mice has indicated that sh-HIF1A-AS2 inhibited tumor growth and motility by targeting miR-548c-3p through regulating HIF-1α/vascular endothelial growth factor (VEGF) pathway in vivo. Conclusion: The inhibitive effect of HIF-1α/VEGF pathway by sh-HIF1A-AS2 through targeting miR-548c-3p plays crucial regulatory roles in BC. Therefore, designing targeted drugs against HIF1A-AS2 provides a new direction for the treatment of BC. 

Retracted: Yes

PubPeer comments:
 Figure 4A: Two micrographs have been duplicated, modified and presented as something else in Figure 5D. ![file] , 
 Retracted [11 February 2021] . -------------------------------------------- The Editor and Publisher of OncoTargets and Therapy wish to retract the published article. The journal was notified of potential image duplication between Figures 4A and 5D: ,
Intercalant-independent transition temperature in superconducting black phosphorus
Authors: I V Grigorieva
R Zhang
J Waters
A K Geim
Journal: Nature communications (2017)
Discipline: Multidisciplinary
Keywords: Black phosphorus; superconductor; intercalation; alkali metals; alkali-earth
Affiliations: School of Physics and Astronomy, University of Manchester, Oxford Road, Manchester M13 9PL, UK., School of Earth, Atmospheric and Environmental Sciences, University of Manchester, Oxford Road, Manchester M13 9PL, UK.

Abstract:  Research on black phosphorus has been experiencing a renaissance over the last years, after the demonstration that few-layer crystals exhibit high carrier mobility and a thickness-dependent bandgap. Black phosphorus is also known to be a superconductor under high pressure exceeding 10 GPa. The superconductivity is due to a structural transformation into another allotrope and accompanied by a semiconductor-metal transition. No superconductivity could be achieved for black phosphorus in its normal orthorhombic form, despite several reported attempts. Here we describe its intercalation by several alkali metals (Li, K, Rb and Cs) and alkali-earth Ca. All the intercalated compounds are found to be superconducting, exhibiting the same (within experimental accuracy) critical temperature of 3.8±0.1 K and practically identical characteristics in the superconducting state. Such universal superconductivity, independent of the chemical composition, is highly unusual. We attribute it to intrinsic superconductivity of heavily doped individual phosphorene layers, while the intercalated layers of metal atoms play mostly a role of charge reservoirs. 

Retracted: No

PubPeer comments:
 This paper was proven to be wrong: https: www.sciencedirect.com science article pii S2542529317302316 In fact the authors just measured the superconductivity of Sn (Tc = 3.7 K) impurities in their sample. The Sn comes from the vapour transport grown crystals. This synthesis pathway requires Sn and SnI4. That s why they see only a very small superconducting volume fraction. All the standard characterization measurements (specific heat, resistivity, elemental analysis) of the samples are missing. ,
Circular RNA ACR relieves high glucose‐aroused RSC96 cell apoptosis and autophagy via declining microRNA‐145‐3p
Authors: Jing Kang
Xiaoqing Chen
Jingjing Yao
Ying Liu
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Retraction; Circular RNA ACR; High glucose; RSC96 cell; Apoptosis
Affiliations: Department of General Medicine, Heze Municipal Hospital, Heze, Shandong, China., Infectious Disease Department, Heze Infectious Disease Hospital, Heze, Shandong, China., Department of Endocrinology and Metabolism, Heze Municipal Hospital, Heze, Shandong, China.

Abstract:  Retraction: 'Circular RNA ACR relieves high glucose-aroused RSC96 cell apoptosis and autophagy via declining microRNA-145-3p', by Ying Liu, Xiaoqing Chen, Jingjing Yao, Jing Kang, J Cell Biochem. The above article, published online on 30 December 2019 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.29568), has been retracted by agreement between the the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction. 

Retracted: No

PubPeer comments:
 There is a typo in parafibromin forward primer, it should be  GAGAGAGTATGGAGGACACGAAC , and the results were not affected. There is a typo in GAPDH reverse primer, the correct sequence should be  GAGTCAACGGATTTGGTCGT . The primers provided in this paper were blasted in NCBI. The primers work fine and have been frequently used by us and others. , 
 Could authors explain letter u201cVu201d (yellow tag) indicated which nucleotide? ![file] , 
 There have some writing errors in the qPCR primer section. There is a typo in parafibromin forward primer, it should be  GAGAGAGTATGGAGGACACGAAC , and the results were not affected. There is a typo in GAPDH forward primer (the correct sequence should be  GAGTCAACGGATTTGGTCGT ). The results were not affected. ,
SIRT1 ameliorates oxidative stress induced neural cell death and is down-regulated in Parkinson’s disease
Authors: Christopher M Morris
Peter S Hanson
Preeti Singh
Journal: BMC Neuroscience (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alpha-synuclein; Cell survival; Oxidative stress; Parkinson’s disease; SIRT1.
Affiliations: Medical Toxicology Centre, and NIHR Health Protection Research Unit in Chemical and Radiation Threats and Hazards, Newcastle University, Wolfson Building, Claremont Place, Newcastle upon Tyne, NE2 4AA, UK., NIHR Biomedical Research Unit in Lewy Body Disorders, and Biomedical Research Centre in Ageing and Chronic Disease, Institute of Neuroscience, Newcastle University, Edwardson Building, Newcastle upon Tyne, NE4 5PJ, UK., Medical Toxicology Centre, and NIHR Health Protection Research Unit in Chemical and Radiation Threats and Hazards, Newcastle University, Wolfson Building, Claremont Place, Newcastle upon Tyne, NE2 4AA, UK. ., NIHR Biomedical Research Unit in Lewy Body Disorders, and Biomedical Research Centre in Ageing and Chronic Disease, Institute of Neuroscience, Newcastle University, Edwardson Building, Newcastle upon Tyne, NE4 5PJ, UK. .

Abstract:  Background: Sirtuins (SIRTs) are NAD+ dependent lysine deacetylases which are conserved from bacteria to humans and have been associated with longevity and lifespan extension. SIRT1, the best studied mammalian SIRT is involved in many physiological and pathological processes and changes in SIRT1 have been implicated in neurodegenerative disorders, with SIRT1 having a suggested protective role in Parkinson's disease. In this study, we determined the effect of SIRT1 on cell survival and α-synuclein aggregate formation in SH-SY5Y cells following oxidative stress. Results: Over-expression of SIRT1 protected SH-SY5Y cells from toxin induced cell death and the protection conferred by SIRT1 was partially independent of its deacetylase activity, which was associated with the repression of NF-кB and cPARP expression. SIRT1 reduced the formation of α-synuclein aggregates but showed minimal co-localisation with α-synuclein. In post-mortem brain tissue obtained from patients with Parkinson's disease, Parkinson's disease with dementia, dementia with Lewy bodies and Alzheimer's disease, the activity of SIRT1 was observed to be down-regulated. Conclusions: These findings suggests a negative effect of oxidative stress in neurodegenerative disorders and possibly explain the reduced activity of SIRT1 in neurodegenerative disorders. Our study shows that SIRT1 is a pro-survival protein that is downregulated under cellular stress. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than you would expect. https: imgur.com WwvXDiH ,
lncRNA GHET1 down-regulation suppresses the cell activities of glioma
Authors: Ren-Ping Li
Dong Hu
Fan Wen
Wei Ni
Xiao-Bing Xu
Lin Luo
Ping Zuo
Journal: Cancer Biomarkers (2018)
Discipline: CLINICAL MEDICINE
Keywords: GHET1; biological activities; lncRNAs; numb; vitro study
Affiliations: Department of Neurosurgery, The Third Affiliated Hospital of Kunming Medical University, Kunming 650118, Yunnan, China., Department of Neurosurgery, Yunnan Cancer Hospital, Kunming 650118, Yunnan, China., Department of Neurosurgery, Yunnan Cancer Center, Kunming 650118, Yunnan, China.

Abstract:  Long noncoding RNAs (lncRNAs) are emerging as new modulators in cancer origination and progression. The previous study found lncRNA gastric carcinoma highly expressed transcript 1 (GHET1) was significantly up-regulation in the gastric cancer. In our present study, we studied the GHET1 expression in glioma and its effects to biological activities of glioma in vitro and vivo studies. In the clinical analysis, the results were shown that lncRNA GHET1 was significantly up-regulation and the Numb protein expression was significantly down-regulation in glioma tissues. In vitro and vivo studies, the results were shown that lncRNA GHET1 knock-down had effects to inhibit biological activities by regulation Numb and down-stream genes P53 and MMP2/9. The results suggested that GHET1 is a novel tumor oncogene by Numb in glioma. LncRNA GHET1 may serve as a potential biomarker and therapeutic target for glioma. 

Retracted: No

PubPeer comments:
 Retracted.  The above article originally published in Cancer Biomarkers volume 23, number 1, 2018, pp. 9u201322 has been retracted in consultation between the corresponding author and the publisher of Cancer Biomarkers. It was found in further research that there are other more complex mechanisms involed in the LncRNA GHET1 regulation of development of glioma. In order to ensure the scientificity and integrity of the research, the journal has decided to retract it from its online catalogue. , 
 Perhaps this will shed some light on the concerns with paper, which is no longer available on the journal site. *** ![file] ,
Silencing CDK4 radiosensitizes breast cancer cells by promoting apoptosis
Authors: Harold I Saavedra
Xiangbin Zeng
Ruth M O&#x27;Regan
Katie R Hagen
Mi-Young Lee
Yuan Liu
Xingming Deng
Sandra S Zaky
Shannon Tucker Kahn
Mary Kathryn Harrison Pitner
Journal: Cell division (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: molecular markers; breast cancer subtypes; radiotherapy resistance; G1 phase regulatory machinery; CDK2
Affiliations: Department of Radiation Oncology, Emory University School of Medicine, Atlanta, USA., Department of Biostatistics and Bioinformatics, Emory University School of Public Health, Atlanta, USA.

Abstract:  Background: The discovery of molecular markers associated with various breast cancer subtypes has greatly improved the treatment and outcome of breast cancer patients. Unfortunately, breast cancer cells acquire resistance to various therapies. Mounting evidence suggests that resistance is rooted in the deregulation of the G1 phase regulatory machinery. Methods: To address whether deregulation of the G1 phase regulatory machinery contributes to radiotherapy resistance, the MCF10A immortalized human mammary epithelial cell line, ER-PR-Her2+ and ER-PR-Her2- breast cancer cell lines were irradiated. Colony formation assays measured radioresistance, while immunocytochemistry, Western blots, and flow cytometry measured the cell cycle, DNA replication, mitosis, apoptosis, and DNA breaks. Results: Molecular markers common to all cell lines were overexpressed, including cyclin A1 and cyclin D1, which impinge on CDK2 and CDK4 activities, respectively. We addressed their potential role in radioresistance by generating cell lines stably expressing small hairpin RNAs (shRNA) against CDK2 and CDK4. None of the cell lines knocked down for CDK2 displayed radiosensitization. In contrast, all cell lines knocked down for CDK4 were significantly radiosensitized, and a CDK4/CDK6 inhibitor sensitized MDA-MB-468 to radiation induced apoptosis. Our data showed that silencing CDK4 significantly increases radiation induced cell apoptosis in cell lines without significantly altering cell cycle progression, or DNA repair after irradiation. Our results indicate lower levels of phospho-Bad at ser136 upon CDK4 silencing and ionizing radiation, which has been shown to signal apoptosis. Conclusion: Based on our data we conclude that knockdown of CDK4 activity sensitizes breast cancer cells to radiation by activating apoptosis pathways. 

Retracted: No

PubPeer comments:
 Figure 1A. Much more similar than you would expect after slightly longer exposure. https: imgur.com nLAzBZZ , 
 This paper is not from my lab. ,
LncRNA AB073614 promotes tumor migration and invasion by repressing CDKN1A in non-small cell lung cancer
Authors: W-D Zhao
N Du
B-X Zhang
X-H Cui
J Zhang
Y-F Zhang
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; AB073614; metastasis; non-small cell lung cancer; RT-qPCR
Affiliations: Department of Oncosurgery, Weinan Central Hospital of Shannxi Province, Weinan, China. .

Abstract:  Objective: Some researches have showed that long noncoding RNAs (lncRNAs) take part in varieties of biological behaviors during the tumor progression. This study aims to determine whether lncRNA AB073614 functioned in the metastasis of non-small cell lung cancer (NSCLC). Patients and methods: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect AB073614 expression in NSCLC tissues. Besides, wound healing assay and transwell assay were conducted in NSCLC cells. Furthermore, the mechanism assays were performed to identify how AB073614 functioned in metastasis of NSCLC cells. Results: By comparing with the expression level in adjacent tissues, the AB073614 expression level in NSCLC samples was significantly higher. Moreover, after AB073614 was knocked down, invasion and migration of NSCLC cells were inhibited. And after AB073614 was overexpressed, invasion and migration of NSCLC cells were promoted. Also, mRNA and protein expression level of CDKN1A was upregulated via knockdown of AB073614, while mRNA and protein expression level of CDKN1A was downregulated via overexpression of AB073614. Besides, the expression of CDKN1A in NSCLC tissues was negatively correlated to the expression of AB073614. Conclusions: Our results indicated that AB073614 could enhance cell migration and cell invasion in NSCLC through repressing CDKN1A, which might offer a potential therapeutic choice for patients with NSCLC. 

Retracted: Yes

PubPeer comments:
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 #9 Figure 3(B). Much more similar than you would expect. https: imgur.com fUXzYia ,
Injectable alginate-O-carboxymethyl chitosan/nano fibrin composite hydrogels for adipose tissue engineering
Authors: R Jayakumar
K P Chennazhi
K M Sajesh
Shantikumar V Nair
S Soumya
Dhanya Jaikumar
T R Nimal
Journal: International Journal of Biological Macromolecules (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ADSCs; Alginate; Injectable hydrogel; O-carboxymethyl chitosan; PVA
Affiliations: Amrita Centre for Nanosciences and Molecular Medicine, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham University, Kochi, 682041 India., Amrita Centre for Nanosciences and Molecular Medicine, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham University, Kochi, 682041 India. Electronic address: .

Abstract:  Injectable, biodegradable scaffolds are required for soft tissue reconstruction owing to its minimally invasive approach. Such a scaffold can mimic the native extracellular matrix (ECM), provide uniform distribution of cells and overcome limitations like donor site morbidity, volume loss, etc. So, here we report two classes of biocompatible and biodegradable hydrogel blend systems namely, Alginate/O-carboxymethyl chitosan (O-CMC) and Alginate/poly (vinyl alcohol) (PVA) with the inclusion of fibrin nanoparticles in each. The hydrogels were prepared by ionic cross-linking method. The developed hydrogels were compared in terms of its swelling ratio, degradation profile, compressive strength and elastic moduli. From these preliminary findings, it was concluded that Alginate/O-CMC formed a better blend for tissue engineering applications. The potential of the formed hydrogel as an injectable scaffold was revealed by the survival of adipose derived stem cells (ADSCs) on the scaffold by its adhesion, proliferation and differentiation into adipocytes. Cell differentiation studies of fibrin incorporated hydrogel scaffolds showed better differentiation was confirmed by Oil Red O staining technique. These injectable gels have potential in soft tissue regeneration. 

Retracted: No

PubPeer comments:
 In Figure 6, panel B and D appear to show an area of overlap. Could the authors please comment? Shown here with red boxes. ![file] , 
 Corrigendum published [15 August 2019] . -------------------------- In the original manuscript, Fig. 6B inadvertently repeated as Fig. 6D. It has been rectified and the corrected Fig. 6 is presented below. ![] This change in the figure would not affect the conclusion from the figure nor the overall conclusion of the whole manuscript. The authors would like to apologize for any inconvenience caused. ,
A Method to Stop Analyzing Random Error and Start Analyzing Differential Responders to Exercise
Authors: Jeremy P Loenneke
Scott J Dankel
Journal: Sports Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: exercise response; responder categories; random error; intervention group; control group
Affiliations: Department of Health and Exercise Science, Exercise Physiology Laboratory, Rowan University, Glassboro, NJ, USA., Department of Health, Exercise Science, and Recreation Management, Kevser Ermin Applied Physiology Laboratory, The University of Mississippi, P.O. Box 1848, University, MS, 38677, USA. .

Abstract:  It is commonly stated that individuals respond differently to exercise even when the same exercise intervention is performed. This has led many researchers to conduct exercise interventions and subsequently categorize individuals into different responder categories to determine what causes individuals to respond differently. Some methods by which differential responders are categorized include percentile ranks, standard deviations from the mean, and cluster analyses. Notably, each of these methods will result in the presence of differential responders even in the absence of an exercise intervention, indicating that individuals may be categorized based on the presence of random error as opposed to true differences in the exercise response. Here we propose a method by which differential responders can be classified after accounting for the presence of random error that is quantified from a time-matched control group. Individuals who exceed random error from the mean response of the intervention group can be confidently labelled as high and low responders. Importantly, the number of differential responders will be proportional to the ratio of variance in the exercise and control groups. We provide easy-to-follow steps and examples to demonstrate how this technique can identify differential responders to exercise. We also detail the flaws in other classification methods by demonstrating the number of differential responders who would have been classified using the same data set. Our hope is that this method will help to avoid misclassifying individuals based on random error and, in turn, increase the replicability of differential responder studies. 

Retracted: No

PubPeer comments:
 From the Methods:  *Between January 2012 and December 2018, a total of 130 subjects aged 0u201318 years with previously untreated neuroblastoma (NB) were diagnosed in the affiliated hospital of Qingdao university. * The paper was submitted in January 2020, a bit more than a year since the last patients were enrolled. Yet, looking at Figures 1B and 1C the whole cohort of 130 subjects was followed for ca. 2,000 days = over 5 years. Could the authors please clarify? ![file] ,
NLRP3 Inflammasome Is Involved in Q-VD-OPH Induced Necroptosis Following Cerebral Ischemia-Reperfusion Injury
Authors: Hui Li
Xianping Tang
Deqin Geng
Yonggang Chen
Sheng Ding
Ying Zhang
Zhihan Liu
Tao Feng
Weiwei Chen
Xue Teng
Journal: Neurochemical Research (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Apoptosis; Brain ischemia; NLRP3 inflammasome; Necroptosis; Q-VD-OPH.
Affiliations: Xuzhou Medical University, Xuzhou, 221004, China., Neurology Department of Xuzhou Central Hospital, Xuzhou, 221009, China., Department of Rehabilitation Medicine, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, 221002, China., Jiangsu Key Laboratory of Brain Disease Bioinformation of Xuzhou Medical College, Xuzhou, 221009, China., Department of Clinical Pharmacy of Xuzhou Central Hospital, Xuzhou, 221009, China., Neurology Department of The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, China. .

Abstract:  Necroptosis is a manner of caspase-independent cell death,which accounts for delayed ischemic cerebral injury, and can be used as a novel tool to expand the treatment time window in ischemic cerebral injury. Q-VD-OPH, a novel pan caspase inhibitor, has been identified as an inducer of necroptosis. In this study, we determined the optimal dose of Q-VD-OPH, which induces necroptosis in rats by the middle cerebral artery occlusion, followed by reperfusion. Furthermore, we report that the NLRP3 inflammasome is involved in necroptosis, with levels of NLRP3 inflammasome proteins as well as inflammatory cytokines, such as IL-1β, being elevated. We also demonstrated that NLRP3 was not only expressed in microglia and vascular endothelial cell, but also in neurons when necroptosis is induced with Q-VD-OPH. Inhibition of NLRP3 by glyburide strongly suppressed the expression of NLRP3 inflammasome proteins and IL-1β, and markedly reduced brain tissue damage. Our findings provide evidence that pretreatment with Q-VD-OPH suppresses apoptosis and induces necroptosis in the cerebral ischemia-reperfusion model. We also identified that the NLRP3 inflammasome plays an important role in neuronal necroptosis, and that NLRP3 inflammasome deficiency reduces brain tissue damage after cerebral ischemia-reperfusion injury in rats. 

Retracted: No

PubPeer comments:
 I noticed a discrepancy between the abstract and full text: The authors write in the abstract:  We also demonstrated that NLRP3 was not only expressed in microglia and vascular endothelial cell . However, there is no mentioning of microglia or endothelial cells in the rest of the manuscript. The only staining is Fig. 2 on p. 5 and the sentence about this is  In addition, immunofluorescence analysis on NLRP3, caspase-3 and caspase-1 reveals cytoplasmic localization within cortical neurons. (p. 4). In addition, Fig. 2B, Fig. 3, Fig. 4: n=3, sample size is too low and certainly not sufficient to perform parametric tests (ANOVA). The authors did not report on normality and variance heterogeneity, which is necessary to decide whether a parametric test can be used or not. ,
Investigating the role of group-based morality in extreme behavioral expressions of prejudice
Authors: Mohammad Atari
Gwenyth Portillo-Wightman
Brendan Kennedy
Morteza Dehghani
Aida Mostafazadeh Davani
Joe Hoover
Leigh Yeh
Journal: Nature Communications (2021)
Discipline: Multidisciplinary
Keywords: motivations; hatred; extreme behavioral expressions of prejudice (EBEPs); marginalized groups; moral values

Abstract:  Understanding motivations underlying acts of hatred are essential for developing strategies to prevent such extreme behavioral expressions of prejudice (EBEPs) against marginalized groups. In this work, we investigate the motivations underlying EBEPs as a function of moral values. Specifically, we propose EBEPs may often be best understood as morally motivated behaviors grounded in people's moral values and perceptions of moral violations. As evidence, we report five studies that integrate spatial modeling and experimental methods to investigate the relationship between moral values and EBEPs. Our results, from these U.S. based studies, suggest that moral values oriented around group preservation are predictive of the county-level prevalence of hate groups and associated with the belief that extreme behavioral expressions of prejudice against marginalized groups are justified. Additional analyses suggest that the association between group-based moral values and EBEPs against outgroups can be partly explained by the belief that these groups have done something morally wrong. 

Retracted: No

PubPeer comments:
 https: twitter.com MortezDehghani status 1420806243757686784 Authors cut: https: psyarxiv.com 359me ,