PReD-Bench/PRed-Bench huggingface dataset:
Vascular endothelial cells facilitated HCC invasion and metastasis through the Akt and NF-κB pathways induced by paracrine cytokines
Authors: Dong-Mei Gao
Zheng-Gang Ren
Jie Chen
Yin-Ying Dong
Jie-Feng Cui
Rong-Xin Chen
Zhi-Ming Wang
Wei-Min Wang
Xiao-Ying Xie
Yao-Hui Wang
Journal: Journal of Experimental & Clinical Cancer Research (2013)
Discipline: CLINICAL MEDICINE
Keywords: cancer cells; angiogenic factors; endothelial cells; HCC cell growth; migration
Affiliations: Liver Cancer Institute, Zhongshan Hospital, Fudan University and Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, PR China.

Abstract:  Background: It is well documented that cancer cells secrete angiogenic factors to recruit and sustain tumor vascular networks. However, little is known about the effects of endothelial cells on the behavior of tumor cells. The study here was to determine the roles of endothelial cells in HCC cell growth, migration and invasion. Methods: A mixture of highly metastatic MHCC97H cells and HUVEC cells, as well as MHCC97H cells alone were subcutaneously injected into nude mice to observe the effects of HUVECs on HCC growth. The biological characteristics of MHCC97H cells respectively treated with conditioned medium (CM) derived from HUVECs and endothelial cell basal medium (EBM) in vitro, such as proliferation, migration and invasion, invasion/metastasis associated gene expression, were comparatively analyzed. Differential cytokines between CM and EBM were screened and identified using human cytokine array. Effects of the interested differential cytokine CCL2, IL-8 and CXCL16 and its related signaling pathways were further investigated in HCC cells. Results: Subcutaneous tumorigenicity of MHCC97H cells in nude mice was promoted by HUVECs and its invasion/metastasis associated genes were significantly upregulated. The in vitro, proliferation, migration and invasion of HCC cells treated with CM were all significantly enhanced as compared to those with EBM stimulation. Simultaneously, PI3K/Akt and ERK1/2 pathway in HCC cells were activated by CM. Total of 25 differential cytokines were identified between CM and EBM such as angiopoietin-2, CCL2 (MCP-1), uPA, endostatin, CXCL16, IL-8, pentraxin 3 etc. The selected differential cytokines CCL2, IL-8 and CXCL16 all modulated the expressions of HCC invasion/metastasis genes, especially MMP2 and MMP9. In exposure to CCL2 or CXCL16 alone, upregulation in AKT phosphorylation but no change in ERK phosphorylation were found in MHCC97H cells, moreover the contents of nuclear transcription factor NF-κB were increased as compared to the control. However, no effects on the activation of Akt and ERK pathway in MHCC97H were found in exposure to IL-8. Conclusion: This study expands the contribution of endothelial cells to the progression of HCC. It unveils a new paradigm in which endothelial cells function as initiators of molecular crosstalks that enhance survival, migration and invasion of HCC cells. 

Retracted: No

PubPeer comments:
 Blots of Akt would never align with blots in other rows (Fig. 3A) ![file] ,
Targeting autophagy as a novel strategy for facilitating the therapeutic action of potentiators on ΔF508 cystic fibrosis transmembrane conductance regulator
Authors: Alberto Luini
Valeria Raia
Marco Silano
Massimo Pettoello-Mantovani
Luigi Maiuri
Manuela Gavina
Speranza Esposito
Valeria Rachela Villella
Guido Kroemer
Ilaria Russo
Bob Scholte
Antonella De Matteis
Stefano Guido
Rosa Carnuccio
Alessandro Luciani
Maria Chiara Maiuri
Journal: Autophagy (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CFTR potentiators; autophagy; cystamine; cystic fibrosis; therapy.
Affiliations: European Institute for Research in Cystic Fibrosis, San Raffaele Scientific Institute, Milan, Italy.

Abstract:  Channel activators (potentiators) of cystic fibrosis (CF) transmembrane conductance regulator (CFTR), can be used for the treatment of the small subset of CF patients that carry plasma membrane-resident CFTR mutants. However, approximately 90% of CF patients carry the misfolded ΔF508-CFTR and are poorly responsive to potentiators, because ΔF508-CFTR is intrinsically unstable at the plasma membrane (PM) even if rescued by pharmacological correctors. We have demonstrated that human and mouse CF airways are autophagy deficient due to functional sequestration of BECN1 and that the tissue transglutaminase-2 inhibitor, cystamine, or antioxidants restore BECN1-dependent autophagy and reduce SQSTM1/p62 levels, thus favoring ΔF508-CFTR trafficking to the epithelial surface. Here, we investigated whether these treatments could facilitate the beneficial action of potentiators on ΔF508-CFTR homozygous airways. Cystamine or the superoxide dismutase (SOD)/catalase-mimetic EUK-134 stabilized ΔF508-CFTR at the plasma membrane of airway epithelial cells and sustained the expression of CFTR at the epithelial surface well beyond drug withdrawal, overexpressing BECN1 and depleting SQSTM1. This facilitates the beneficial action of potentiators in controlling inflammation in ex vivo ΔF508-CFTR homozygous human nasal biopsies and in vivo in mouse ΔF508-CFTR lungs. Direct depletion of Sqstm1 by shRNAs in vivo in ΔF508-CFTR mice synergized with potentiators in sustaining surface CFTR expression and suppressing inflammation. Cystamine pre-treatment restored ΔF508-CFTR response to the CFTR potentiators genistein, Vrx-532 or Vrx-770 in freshly isolated brushed nasal epithelial cells from ΔF508-CFTR homozygous patients. These findings delineate a novel therapeutic strategy for the treatment of CF patients with the ΔF508-CFTR mutation in which patients are first treated with cystamine and subsequently pulsed with CFTR potentiators. 

Retracted: No

PubPeer comments:
 Figure 1A - more similar than expected. Could authors check it please? ![file] , 
 I m sorry, but because of the contrast enhancement, the details of the image were lost. Below, I post my concerns in the original image ![file] ,
Oestrogen causes ATBF1 protein degradation through the oestrogen-responsive E3 ubiquitin ligase EFP
Authors: Dan Su
Xue-Yuan Dong
Xiaoying Fu
Jin-Tang Dong
Songqing Fan
Peng Guo
Journal: Biochemical Journal (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ATBF1; EFP; oestrogen-ERα signalling; breast cancer cells; autoregulatory feedback loop
Affiliations: Department of Hematology and Medical Oncology, School of Medicine, Winship Cancer Institute, Emory University, 1365-C Clifton Road, Atlanta, GA 30322, USA. , Department of Hematology and Medical Oncology, School of Medicine, Winship Cancer Institute, Emory University, 1365-C Clifton Road, Atlanta, GA 30322, U.S.A., Department of Pathology, the Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, China

Abstract:  We reported previously that the tumour suppressor ATBF1 (AT motif-binding factor 1) formed an autoregulatory feedback loop with oestrogen-ERα (oestrogen receptor α) signalling to regulate oestrogen-dependent cell proliferation in breast cancer cells. In this loop ATBF1 inhibits the function of oestrogen-ERα signalling, whereas ATBF1 protein levels are fine-tuned by oestrogen-induced transcriptional up-regulation as well as UPP (ubiquitin-proteasome pathway)-mediated protein degradation. In the present study we show that EFP (oestrogen-responsive finger protein) is an E3 ubiquitin ligase mediating oestrogen-induced ATBF1 protein degradation. Knockdown of EFP increases ATBF1 protein levels, whereas overexpression of EFP decreases ATBF1 protein levels. EFP interacts with and ubiquitinates ATBF1 protein. Furthermore, we show that EFP is an important factor in oestrogen-induced ATBF1 protein degradation in which some other factors are also involved. In human primary breast tumours the levels of ATBF1 protein are positively correlated with the levels of EFP protein, as both are directly up-regulated ERα target gene products. However, the ratio of ATBF1 protein to EFP protein is negatively correlated with EFP protein levels. Functionally, ATBF1 antagonizes EFP-mediated cell proliferation. These findings not only establish EFP as the E3 ubiquitin ligase for oestrogen-induced ATBF1 protein degradation, but further support the autoregulatory feedback loop between ATBF1 and oestrogen-ERα signalling and thus implicate ATBF1 in oestrogen-dependent breast development and carcinogenesis. 

Retracted: No

PubPeer comments:
 Figure S4A may have a differential splice in one band. *** Contrast enhanced ![file] *** ![file] ,
Functional interaction of STAT3 transcription factor with the coactivator NcoA/SRC1a
Authors: Olivier Coqueret
Sylvie Avril
David M Heery
Hugues Gascan
Sandrine Giraud
Frédéric Bienvenu
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: STAT3; transcription factors; gene activation; cytokine receptor; phosphorylation
Affiliations: INSERM EMI-U 9928, 4 rue Larrey, CHU Angers, Angers Cedex 49033, France.

Abstract:  Signal transducer and activator of transcription 3 (STAT3) transcription factors are cytoplasmic proteins that induce gene activation in response to cytokine receptor stimulation. Following tyrosine phosphorylation, STAT3 proteins dimerize, translocate to the nucleus, and activate specific target genes. This transcriptional activation by STAT3 proteins has been shown to require the recruitment of coactivators such as CREB-binding protein (CBP)/p300. In the present study, we show that steroid receptor coactivator 1, NcoA/SRC1a, originally identified as a nuclear receptor coactivator, also functions as a coactivator of STAT3 proteins. In coimmunoprecipitations, NcoA/SRC1a was found to associate with STAT3 following IL-6 stimulation of HepG2 hepatoma cells. Pull-down experiments indicated that the N-terminal part of NcoA/SRC1a associates with the activation domain of STAT3. Overexpression of NcoA/SRC1a or its SRC1e isoform enhanced transcriptional activation by STAT3 proteins in transient transfection experiments. This ability of NcoA/SRC1a to enhance STAT3 activity is dependent upon the presence of the CBP-interacting domain, activation domain 1. Using chromatin immunoprecipitation assays, we found that STAT3, NcoA/SRC1a, and CBP/p300 are simultaneously recruited to the p21(waf1) promoter following interleukin-6 stimulation. Taken together, these data suggest that CBP/p300 and NcoA/SRC1a may function in a common pathway to regulate STAT3 transcriptional activity. 

Retracted: No

PubPeer comments:
null, 
 Exactly, the panel of Stat3 was unexpectedly similar to the panel of Stat3-Tyr705. ![file] , 
 #1 ![file] ,
A synergistic therapeutic scheme for hyperglycemia and nephrotic disorders in diabetes
Authors: Xing Zhang
Baosan Han
Kanglai Tang
Zhiren Fu
Jianzhong Xu
Hao Yin
Qingyi He
Journal: Theranostics (2014)
Discipline: CLINICAL MEDICINE
Keywords: diabetes; electrospinning; islet transplantation; pioglitazone; scaffolds..
Affiliations: 2. Department of Orthopedic Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China 400038., 3. School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138 USA., 4. Department of Surgery, Shanghai Xinhua Hospital, Shanghai, China 200003., 1. Department of Surgery, Organ Transplant Center, Shanghai Changzheng Hospital, Shanghai Second Military Medical University, Shanghai, China 200003., 1. Department of Surgery, Organ Transplant Center, Shanghai Changzheng Hospital, Shanghai Second Military Medical University, Shanghai, China 200003. ; 5. Department of surgery, University of Chicago, Chicago, IL 60637 USA.

Abstract:  We previously demonstrated that the utilization of an electrospun scaffold could boost functional outputs of transplanted islets. In this study, we aim to develop a drug-eluting scaffold with a payload of pioglitazone to simultaneously rein in hyperglycemia and recoup lost renal functions in diabetic mice that underwent islet transplantation. The in vivo proliferation of islets was measured by a non-invasive bio-imaging technology whereas the blood insulin, blood glucose and renal proteins were assayed. The local stimulation of transplanted islets by pioglitazone saw an accelerated in vivo proliferation without apoptosis caused by the drug-eluting scaffold. In addition, pioglitazone contributed to an increased secretion of insulin and C-peptide 2, giving rise to an accelerated rein-in of hyperglycemia and enhanced tolerance of sudden oral glucose challenge. Moreover, the accelerated decrease of blood creatinine, urine creatinine and blood urea nitrogen suggested that pioglitazone contributed to the recovery of renal functions compromised by diabetes. Our bioengineering strategy effectively ameliorated hyperglycemia and associated nephrotic disorders, and shed a new light on an engineering approach to combat diabetes. 

Retracted: No

PubPeer comments:
 Dr. Yin, I am very interested to know that why some of the Fig. 3B images reappear in a different paper of your team (PMID-24600221, Fig3B)uff1f ![file] , 
 Too many duplications of in vivo images by the same team! ![file] , 
 ![file] Figure 7 B demonstated muine albumin depletion by urine in 24 hrs. Could the author explain how to collect all murine urine in a whole day? It seems to be an impossible mission. ,
A comprehensive review of recent developments in 3D printing technique for ceramic membrane fabrication for water purification
Authors: Saikat Sinha Ray
Shiao-Shing Chen
Hitesh Dommati
Jia-Chang Wang
Journal: RSC Advances (2019)
Discipline: CHEMISTRY
Keywords: Additive manufacturing; 3D printing; filtration; water treatment; nanofibers
Affiliations: Department of Mechanical Engineering, National Taipei University of Technology, Taiwan, Additive Manufacturing Center for Mass Customization Production, Institute of Environmental Engineering and Management

Abstract:  Additive manufacturing (AM), which is also commonly known as 3D printing, provides flexibility in the manufacturing of complex geometric parts at competitive prices and within a low production time. However, AM has not been used to a large extent in filtration and water treatment processes. AM results in the creation of millions of nanofibers that are sublayered on top of each other and compressed into a thin membrane. AM is a novel technique for fabricating filtration membranes with different shapes, sizes and controlled porosity, which cannot be achieved using conventional process such as electrospinning and knife casting. In this paper, we review the advantages and limitations of AM processes for fabricating ceramic membranes. Moreover, a brief background of AM processes is provided, and their future prospects are examined. Due to their potential benefits for fabrication and flexibility with different materials, AM methods are promising in the field of membrane engineering. 

Retracted: No

PubPeer comments:
 Hi authors, I m from Malaysia and am intrigued by your paper on  A comprehensive review of recent developments in 3D printing technique for ceramic membrane fabrication for water purification . I only have one question, correct me if i m wrong but for section 3.1, classification of AM techniques, I believe the image for ii. binder jetting is for i. which is vat photo polymerization and for the explanation on the paper, PBF is for number v, and material extrusion, iv. Can you clarify for the first and second image? Thank you.!![file] ,
Production and characterization of novel recombinant adeno-associated virus replicative-form genomes: a eukaryotic source of DNA for gene transfer
Authors: Richard H Smith
Cyriaque Beley
Emilios K Dimitriadis
Zhenhua Yuan
Robert M Kotin
Juan Li
Luis Garcia
Yu Yang
Lina Li
Chunping Qiao
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: non-viral gene transfer; eukaryotic vector DNA; adeno-associated virus (AAV); CELiD DNA; Sf9 insect cells
Affiliations: Laboratory of Molecular Virology and Gene Therapy, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.

Abstract:  Conventional non-viral gene transfer uses bacterial plasmid DNA containing antibiotic resistance genes, cis-acting bacterial sequence elements, and prokaryotic methylation patterns that may adversely affect transgene expression and vector stability in vivo. Here, we describe novel replicative forms of a eukaryotic vector DNA that consist solely of an expression cassette flanked by adeno-associated virus (AAV) inverted terminal repeats. Extensive structural analyses revealed that this AAV-derived vector DNA consists of linear, duplex molecules with covalently closed ends (termed closed-ended, linear duplex, or "CELiD", DNA). CELiD vectors, produced in Sf9 insect cells, require AAV rep gene expression for amplification. Amounts of CELiD DNA produced from insect cell lines stably transfected with an ITR-flanked transgene exceeded 60 mg per 5 × 10(9) Sf9 cells, and 1-15 mg from a comparable number of parental Sf9 cells in which the transgene was introduced via recombinant baculovirus infection. In mice, systemically delivered CELiD DNA resulted in long-term, stable transgene expression in the liver. CELiD vectors represent a novel eukaryotic alternative to bacterial plasmid DNA. 

Retracted: No

PubPeer comments:
 I m not entirely sure about this, but Figure 2B seems to have a sharp vertical transition between lanes 2 and 3 of the GAPDH band. Could the authors please provide the original uncropped scan to remove any doubt? *** ![file] *** Inverse image ![file] , 
 No, the data are not in doubt. there is no inconsistency with the background pixels and this was a single image of a blot that was not spliced or manipulated in any way. , 
 #2 Dr. Kotin: I appreciate the response. Is the original scan available? , 
 i left the NIH 7 yrs ago and the lab notebooks are warehoused. if you alleging misconduct, please take it up with the office of scientific integrity. professional assessment of the published images will demonstrate no manipulation, etc. ,
Prostratin antagonizes HIV latency by activating NF-kappaB
Authors: Dwayne Bisgrove
Lin-Feng Chen
Samuel A Williams
Hakju Kwon
Eric Verdin
David Fenard
Warner C Greene
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: quiescent memory CD4 T cells; HIV; proviruses; immune activating agents; prostratin
Affiliations: Gladstone Institute of Virology and Immunology, University of California, San Francisco, San Francisco, California 94141, USA.

Abstract:  A subset of quiescent memory CD4 T cells harboring integrated but transcriptionally silent proviruses poses a currently insurmountable barrier to the eradication of the human immunodeficiency virus (HIV) in infected patients. Induction of HIV gene expression in these latently infected cells by immune activating agents has been proposed as one approach to confer sensitivity to antiretroviral therapy. Interest has recently focused on the non-tumor-promoting phorbol ester, prostratin, as a potential agent to activate latent HIV proviruses. Using multiple Jurkat T cell lines containing integrated but transcriptionally latent HIV proviruses (J-Lat cells), we now demonstrate that prostratin effectively activates HIV gene expression in these latently infected cells. We further show that prostratin acts by stimulating IKK-dependent phosphorylation and degradation of IkappaBalpha, leading to the rapid nuclear translocation of NF-kappaB and activation of the HIV-1 long terminal repeat in a kappaB enhancer-dependent manner. In contrast, NFAT and AP-1 are not induced by prostratin. Using chromatin immunoprecipitation assays to identify host transcription factors recruited to the latent HIV-1 promoter in living cells, we find that prostratin induces RelA binding. Analysis of potential upstream signal transducers demonstrates that prostratin stimulates membrane translocation of classical, novel, and atypical protein kinase C (PKC) isoforms. Studies with isoform-specific PKC inhibitors suggest that the novel PKCs play a particularly prominent role in the prostratin response. These findings provide new insights into the molecular pathway through which prostratin antagonizes HIV latency highlighting a central role for the action of NF-kappaB. 

Retracted: No

PubPeer comments:
 Figure 4A. * Red boxes: In the Tubulin row, two lanes displaying different experiments appear to look identical. ![file] This paper was found during a systematic screen of biomedical papers for image duplications, as published in Bik et al., mBio (2016), doi: 10.1128 mBio.00809-16, https: journals.asm.org doi 10.1128 mBio.00809-16. This issue was reported to the journal in December 2014, but it has not yet been addressed by the journal, more than seven years later. ,
Metabolic Response to Mulberry Extract Supplementation in Patients With Diabetic Nephropathy: a Randomized Controlled Trial
Authors: Mohsen Taghizadeh
Alireza Moravveji
Zatollah Asemi
Majid Dastorani
Nasrin Sharifi
Narjes Farzin
Alireza Soleimani
Elahe Amirani
Afshin Naseri
Fereshteh Bahmani
Amir Asadi
Journal: Iranian journal of kidney diseases (2017)
Discipline: CLINICAL MEDICINE
Keywords: mulberry extract; insulin metabolism; lipid concentrations; inflammation; oxidative stress
Affiliations: Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran. .

Abstract:  Introduction: This study aimed to evaluate the effects of mulberry extract administration on markers of insulin metabolism, lipid concentrations, and biomarkers of inflammation and oxidative stress in patients with diabetic nephropathy (DN). Materials and methods: Sixty patients were randomly allocated into 2 groups to receive either 300 mg/d of mulberry extract (n = 30) or placebo (n = 30), twice per day for 12 weeks. Fasting blood samples were taken at the onset of the study and 12 weeks after supplementation to examine markers of insulin metabolism, lipid concentrations, and biomarkers of inflammation and oxidative stress. Results: Mulberry extract, compared to placebo, resulted in significant reductions in serum triglycerides (-37.3 ± 64.7 mg/dL versus 3.0 ± 78.8 mg/dL, P = .03) and very low-density lipoprotein cholesterol (-7.4 ± 12.9 mg/dL versus 0.6 ± 15.8 mg/dL, P = .03), and a significant increase in high-density lipoprotein cholesterol concentration (0.5 ± 4.0 mg/dL versus -2.0 ± 5.0 mg/dL, P = .03). Other significant changes were in serum high-sensitivity C-reaction protein (-2.3 ± 4.5 µg/mL versus -0.1 ± 2.2 µg/mL, P = .02), plasma glutathione (87.8 ± 159.7 µmol/L versus -24.2 ± 138.8 µmol/L, P = .005) and malondialdehyde (-0.03 ± 0.5 µmol/L versus 0.7 ± 1.0 µmol/L, P &lt; .001). Conclusions. These findings showed that mulberry extract administration had favorable effects on serum lipids, HSCRP, glutathione, and malondialdehyde levels in DN patients; however, it did not affect markers of insulin metabolism or biomarkers of inflammation and oxidative stress. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A118 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Evaluation of cloned cells, animal model, and ATRA sensitivity of human testicular yolk sac tumor
Authors: Le Qin
Hua Zhang
Xiaokun Lin
Wenqiang Lu
Jie Lin
Jinhui Shen
Congde Chen
Junfeng Zhao
Xiaoming Chen
Xiaozhou Bao
Xiangdong Wang
Haochuan Zhang
Journal: Journal of Translational Medicine (2012)
Discipline: CLINICAL MEDICINE
Keywords: Testicular yolk sac tumor; TYST; in vitro; in vivo models; sensitivity
Affiliations: Department of Pediatric Surgery, the Second Hospital, Wenzhou Medical College, Wenzhou, China.

Abstract:  The testicular yolk sac tumor (TYST) is the most common neoplasm originated from germ cells differentiated abnormally, a major part of pediatric malignant testicular tumors. The present study aimed at developing and validating the in vitro and vivo models of TYST and evaluating the sensitivity of TYST to treatments, by cloning human TYST cells and investigating the histology, ultra-structure, growth kinetics and expression of specific proteins of cloned cells. We found biological characteristics of cloned TYST cells were similar to the yolk sac tumor and differentiated from the columnar to glandular-like or goblet cells-like cells. Chromosomes for tumor identification in each passage met nature of the primary tumor. TYST cells were more sensitive to all-trans-retinoic acid which had significantly inhibitory effects on cell proliferation. Cisplatin induced apoptosis of TYST cells through the activation of p53 expression and down-regulation of Bcl- expression. Thus, we believe that cloned TYST cells and the animal model developed here are useful to understand the molecular mechanism of TYST cells and develop potential therapies for human TYST. 

Retracted: No

PubPeer comments:
 Figure 1. * How big is the tumor shown in Figure 1B? It appears to be bigger than 2 cm in diameter, which (at least in the US) is the size where an animal should be euthanized. * How many mice were included in each group? Should Figure 1A have error bars? Or was there just 1 mouse per group? ![file] ,
A SRCF cell line from snowtrout, Schizothorax richardsonii: development and characterization
Authors: S N Bahuguna
N S Nagpure
M Goswami
B S Sharma
W S Lakra
Journal: Tissue & cell (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Schizothorax richardsonii; snowtrout; cell line; SRCF; Leibovitz's L-15 medium
Affiliations: National Bureau of Fish Genetic Resources, Canal Ring Road, PO Dilkusha, Lucknow 226002, India. 

Abstract:  Schizothorax richardsonii, commonly called snowtrout, is an important indigenous coldwater fish of the Himalayas, India with high commercial values as food and game fish. A cell line named as SRCF was developed from the caudal fin tissue of S. richardsonii. The cell line has been maintained in Leibovitz's L-15 medium supplemented with 10% fetal bovine serum (FBS) at 24°C. The cells showed fibroblastic morphology, high plating efficiency and cell doubling time of 48h. Chromosomal analysis of SRCF cells revealed a diploid count of 98 chromosomes. The origin of the cell line was confirmed by the amplification of 655 and 578bp of cytochrome oxidase subunit I (COI) and 16S rRNA of mitochondrial DNA (mt-DNA) genes, respectively. Transfection of SRCF cells with pEGFP-C1 plasmid resulted in bright fluorescent signals, suggesting the application of cell line in transgenic and genetic improvement programme. In addition, genotoxicity assessment illustrated the utility of the cell line as an in vitro model for aquatic toxicological studies. 

Retracted: No

PubPeer comments:
 Figure 5 appears to show some sharp transitions when the image brightness is adjusted. *** ![file] *** Original ![file] ,
Lack of macrophage fatty-acid–binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis
Authors: MacRae F Linton
Jill Suttles
Vladimir R Babaev
K Teoman Uysal
Rex A Parker
Kazuhisa Maeda
Sergio Fazio
Jeffrey B Boord
Liza Makowski
Gökhan S Hotamisligil
Maureen A Morgan
Journal: Nature Medicine (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: adipocyte fatty-acid-binding protein; aP2; macrophages; atherosclerosis; Apolipoprotein E
Affiliations: Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA., Departments of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA., Bristol-Myers Squibb PRI, Department of Metabolic Research, Princeton, New Jersey, USA., Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky, USA., Pathology, Vanderbilt University Medical Center, Nashville, Tennessee, USA., Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Abstract:  The adipocyte fatty-acid-binding protein, aP2, has an important role in regulating systemic insulin resistance and lipid metabolism. Here we demonstrate that aP2 is also expressed in macrophages, has a significant role in their biological responses and contributes to the development of atherosclerosis. Apolipoprotein E (ApoE)-deficient mice also deficient for aP2 showed protection from atherosclerosis in the absence of significant differences in serum lipids or insulin sensitivity. aP2-deficient macrophages showed alterations in inflammatory cytokine production and a reduced ability to accumulate cholesterol esters when exposed to modified lipoproteins. Apoe-/- mice with Ap2+/+ adipocytes and Ap2-/- macrophages generated by bone-marrow transplantation showed a comparable reduction in atherosclerotic lesions to those with total aP2 deficiency, indicating an independent role for macrophage aP2 in atherogenesis. Through its distinct actions in adipocytes and macrophages, aP2 provides a link between features of the metabolic syndrome and could be a new therapeutic target for the prevention of atherosclerosis. 

Retracted: No

PubPeer comments:
 Figure 2: Much more similar than expected. Could authors check it please? ![file] ,
Bone marrow mesenchymal stem cell-derived exosomal miR-21 protects C-kit+ cardiac stem cells from oxidative injury through the PTEN/PI3K/Akt axis
Authors: Ranzhun Zhao
Wenwen Deng
Zhenglong Wang
Bei Shi
Yan Wang
Xianping Long
Journal: PLoS ONE (2018)
Discipline: Multidisciplinary
Keywords: Stem cell therapy; Ischemic cardiomyopathy; Exosomes; MicroRNAs; lncRNAs
Affiliations: Department of Cardiology, Affiliated Hospital of Zunyi Medical College, Zunyi, China.

Abstract:  Stem cell (SC) therapy for ischemic cardiomyopathy is hampered by poor survival of the implanted cells. Recently, SC-derived exosomes have been shown to facilitate cell proliferation and survival by transporting various proteins and non-coding RNAs (such as microRNAs and lncRNAs). In this study, miR-21 was highly enriched in exosomes derived from bone marrow mesenchymal stem cells (MSCs). Interestingly, exosomes collected from hydrogen peroxide (H2O2)-treated MSCs (H-Exo) contained higher levels of miR-21 than exosomes released from MSCs under normal conditions (N-Exo). The pre-treatment of C-kit+ cardiac stem cells (CSCs) with H-Exos resulted in significantly increased levels of miR-21 and phosphor-Akt (pAkt) and decreased levels of PTEN, which is a known target of miR-21. AnnexinV-FITC/PI analysis further demonstrated that the degree of oxidative stress-induced apoptosis was markedly lower in H-Exo-treated C-kit+ CSCs than that in N-Exo-treated cells. These protective effects could be blocked by both a miR-21 inhibitor and the PI3K/Akt inhibitor LY294002. Therefore, exosomal miR-21 derived from H2O2-treated MSCs could be transported to C-kit+ cardiac stem cells to functionally inhibit PTEN expression, thereby activating PI3K/AKT signaling and leading to protection against oxidative stress-triggered cell death. Thus, exosomes derived from MSCs could be used as a new therapeutic vehicle to facilitate C-kit+ CSC therapies in the ischemic myocardium. 

Retracted: No

PubPeer comments:
 ![file] Re-use of the same microscopy images across 4 different Figures of the same article. (Redundant) Duplications or allowed? , 
 Thanksuff0cbecause those the same groupsuff0cWe donu2019t know could not use the same images, we will pay attention in next article.All original data can be found in the attachment. Thanks again. ,
Inhibition of hydrogen sulfide generation contributes to gastric injury caused by anti-inflammatory nonsteroidal drugs
Authors: Elisabetta Antonelli
Renata Zanardo
Stefano Fiorucci
John L Wallace
Antonio Morelli
Barbara Renga
Giuseppe Cirino
Andrea Mencarelli
Giovanni Rizzo
Stefano Orlandi
Moses Di Sante
Eleonora Distrutti
Journal: Gastroenterology (2005)
Discipline: CLINICAL MEDICINE
Keywords: Hydrogen sulfide; NSAID gastropathy; Cystathionine beta-synthase; Cystathionine-gamma-lyase; Gastric blood flow
Affiliations: Dipartimento di Medicina Clinica, Patologia, Clinica di Gastroenterologia ed Endoscopia Digestiva, University of Perugia, Italy. 

Abstract:  Background &amp; aims: Hydrogen sulfide (H(2)S), an endogenous gaseous mediator that causes vasodilation, is generated in mammalian tissues by cystathionine beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). Here, we have investigated the role of H(2)S in a rodent model of nonsteroidal anti-inflammatory drug (NSAID) gastropathy. Methods: Rats were given acetyl salycilic acid (ASA) or an NSAID alone or in combination with NaHS, an H(2)S donor, and killed 3 hours later. Gastric blood flow was measured by laser-Doppler flowmetry, whereas intravital microscopy was used to quantify adhesion of leukocytes to mesenteric postcapillary endothelium. Results: At a dose of 100 micromol/kg, NaHS attenuated by 60%-70% the gastric mucosal injury, and tumor necrosis factor (TNF)-alpha, intercellular adhesion molecule (ICAM)-1, and lymphocyte function-associated antigen (LFA)-1 mRNA up-regulation induced by NSAIDs (P &lt; .05) NaHS administration prevented the associated reduction of gastric mucosal blood flow (P &lt; .05) and reduced ASA-induced leukocyte adherence in mesenteric venules. NaHS did not affect suppression of prostaglandin E(2) (PGE(2)) synthesis by NSAIDs. Glibenclamide, a K(ATP) channel inhibitor, and DL-propargylglycine, a CSE inhibitor, exacerbated, whereas pinacidil, a K(ATP) opener, attenuated gastric injury caused by ASA. Exposure to NSAIDs reduced H(2)S formation and CSE expression (mRNA and protein) and activity by 60%-70%. By promoter deletion and mutation analysis, an Sp1 consensus site was identified in the CSE promoter. Exposure to NSAIDs inhibits Sp1 binding to its promoter and abrogates CSE expression in HEK-293 cells transfected with a vector containing the core CSE promoter. Exposure to NSAIDs inhibits Sp1 and ERK phosphorylation. Conclusions: These data establish a physiologic role for H(2)S in regulating the gastric microcirculation and identify CSE as a novel target for ASA/NSAIDs. 

Retracted: No

PubPeer comments:
 Parts of Fig 5C in this paper PMID 16230075 Gastroenterology 129:1210-1224 look very similar to parts of Fig 9C in PMID 15521018 Gastroenterology 127:1497-1512, yet they are supposed to represent different samples, and the tops of the images look different. ![file] , 
 ![file] Part of figures 5C and 9 C from two different papers are strikingly similar, although they supposedly represent different samples...can the authors explain? ,
Reverse Correlation between MicroRNA-145 and FSCN1 Affecting Gastric Cancer Migration and Invasion
Authors: Jian-chun Cai
Jia-jia Chen
Gang Chen
Qi-cong Luo
Na Li
Xue-wen Liu
Wang-yu Cai
Wei-feng Huang
Journal: PLoS ONE (2015)
Discipline: Multidisciplinary
Keywords: MicroRNAs; miR-145; gene expression; tumorigenesis; tumor development
Affiliations: Department of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, China; Institute of Gastrointestinal Oncology, Medical College of Xiamen University, Xiamen, Fujian, China., Department of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, China.

Abstract:  MicroRNAs (miRs) play important roles in modulating gene expression during the processes of tumorigenesis and tumor development. Previous studies have found that miR-145 is down-regulated in the stomach neoplasm and is related to tumor migration and invasion. However, both the molecular mechanism and function of miR-145 in gastric cancer remain unclear. The present study is the first demonstration of the significant down-regulation of miR-145 expression in infiltrative gastric cancer compared to expanding gastric cancer. Additionally, correlation analyses revealed strong inverse correlations between miR-145 and FSCN1 expression levels in infiltrative gastric cancer. Furthermore, we demonstrated that miR-145 directly targets FSCN1 and suppresses cell migration and invasion in gastric cancer. Knocking down the expression of FSCN1 led to the suppression of migration and invasion in gastric cancer cells, and re-expressing FSCN1 in miR-145-overexpressing cells reversed their migration and invasion defects. Thus, we concluded that miR-145 regulates cell migration and invasion in gastric cancer primarily by directly targeting FSCN1. 

Retracted: No

PubPeer comments:
 Figure 5C appears to have a duplicated image ![file] ,
RETRACTED: The mouse complement regulator CD59b is significantly expressed only in testis and plays roles in sperm acrosome activation and motility
Authors: Rossen M Donev
Baalasubramanian Sivasankar
Masashi Mizuno
B Paul Morgan
Journal: Molecular Immunology (2008)
Discipline: IMMUNOLOGY
Keywords: CD55; CD59; complement regulators; duplication; CD59a
Affiliations: Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK. 

Abstract:  In mouse, genes encoding complement regulators CD55 and CD59 have been duplicated. The first described form of CD59, CD59a, is broadly distributed in mouse tissues, while the later identified CD59b was originally described as testis specific. Subsequent studies have been contradictory, some reporting widespread and abundant expression of CD59b. Resolution of the distribution patterns of the CD59 isoforms is important for interpretation of disease studies utilising CD59 knockout mice. Here we have performed a comprehensive distribution study of the CD59 isoforms at the mRNA and protein levels. These data confirm that expression of CD59b is essentially restricted to adult testis; trace expression in other tissues is a consequence of contamination with blood cells, shown previously to express CD59b at low level. In testis, onset of expression of CD59b coincided with puberty and was predominant on the spermatozoal acrosome. Ligation of CD59b, but not CD59a, markedly reduced spermatozoal motility, suggesting a specific role in reproductive function. 

Retracted: Yes

PubPeer comments:
null, 
null, 
 Prepared by another reader. *** ![file] , 
 https: retractionwatch.com 2014 01 06 fourth-retraction-results-from-cardiff-investigation ,
Antiherpes activity of glucoevatromonoside, a cardenolide isolated from a Brazilian cultivar of Digitalis lanata
Authors: Rodrigo Maia de Pádua
Célia Regina Monte Barardi
Cláudia Maria Oliveira Simões
Fernão Castro Braga
Jéssica Wildgrube Bertol
Caroline Rigotto
Wolfgang Kreis
Journal: Antiviral Research (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cardiac glycosides; antiviral activity; HSV; nucleoside analogs; drug-resistance
Affiliations: Departamento de Ciências Farmacêuticas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil.

Abstract:  Cardiac glycosides, known ligands of the sodium pump, are widely used in the treatment of heart failure, such as digoxin and digitoxin. Besides this important activity, other biological activities, such as the antiviral activity, have been described for this group. HSV are responsible for many infections of oral, ocular and genital regions. Treatment with nucleoside analogs such as acyclovir is effective in most cases; however drug-resistance may arise due to prolonged treatment mainly in immunocompromised individuals. In this study, an antiherpes screening was performed with 65 cardenolide derivatives obtained from different sources, and one natural cardenolide, glucoevatromonoside, inhibited HSV-1 and HSV-2 replication at very low concentrations. This cardenolide showed viral inhibitory effects if added up to 12h p.i. and these effects appear to take place by the inhibition of viral proteins synthesis (ICP27, U(L)42, gB, gD), the blockage of virus release and the reduction of viral cell-to-cell spread. This compound also showed synergistic antiviral effects with acyclovir and anti-Na(+)K(+)ATPase activity, suggesting that cellular electrochemical gradient alterations might be involved in the mechanism of viral inhibition. These results suggest that cardenolides might be promising for future antiviral drug design. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have an image duplication ![file] ,
Antitumor and immunomodulating activity of a polysaccharide from Sophora flavescens Ait
Authors: Li-Li Zhao
Li-Jun Shi
Bao-Shan Yang
Guang Song
Tie-Fu Liu
Lu Bai
Ai-Min Jiang
Li-Ying Zhu
Yong Liu
Journal: International Journal of Biological Macromolecules (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Sophora flavescens polysaccharide; immunostimulatory activity; tumor growth inhibition; splenocyte proliferation; macrophages
Affiliations: Gastroenterology Department, The Fourth Hospital of Harbin Medical University, Harbin 150001, China.

Abstract:  The immunostimulatory activity of Sophora flavescens polysaccharide (SFPW1) was evaluated by using in vitro cell models and in vivo animal models. The results demonstrated that SFPW1 could effectively inhibit the tumor growth in H22 tumor-bearing mice and promote the splenocyte proliferation, thus resulting in a prolonged life survival. For assay in vitro, SFPW1 significantly strengthened peritoneal macrophages to devour H22 tumor cells and stimulated macrophages to produce nitric oxide (NO) via up-regulation of inducible NO synthase (iNOS) activity. However, no direct cytotoxicity against H22 tumor cells was observed in vitro. These results suggest that SFPW1 might be a strong natural immunomodulator and the antitumor effect of this polysaccharide is associated with its potent immunostimulating effect. 

Retracted: No

PubPeer comments:
 The above article, first published online on 14 September 2011 in Wiley Online Library , has been retracted by agreement with the journal Editoru2010inu2010Chief and Wileyu2010VCH Verlag GmbH Co KGaA. The retraction has been agreed due to duplicated images in some of the figures appearing in the article. Figure 5 contains several duplicated panels and Figure 6 contains reu2010arranged western blot bands. As these figures comprise a significant proportion of the results, the Editoru2010inu2010Chief does not consider the results and conclusions reliable. Jasmine George, Amit Kumar Srivastava, Richa Singh, Yogeshwer Shukla, Proteomics 2011, 11, 4411. , 
 #1 Original thread here: https: pubpeer.com publications A384A6D53974AF627FC83477C2D43E ,
Osteopontin-induced brown adipogenesis from white preadipocytes through a PI3K-AKT dependent signaling
Authors: Teng Li
Xiao-Dan Shen
Guo-Hua Zeng
Ming He
Guo-Qiang Yan
Meng-Qing Wu
Ying Kong
Qi-Ren Huang
Jian-Bing Wen
Xiao-Juan Zhong
Dan Liu
Jia-Jia Chu
Journal: Biochemical and Biophysical Research Communications (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Adipocyte; Differentiation; Obesity; Osteopontin; PRDM16.
Affiliations: Jiangxi Provincial Key Laboratory of Basic Pharmacology, Nanchang University, Nanchang 330006, PR China; Department of Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang 330006, PR China., Jiangxi Provincial Key Laboratory of Basic Pharmacology, Nanchang University, Nanchang 330006, PR China; Department of Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang 330006, PR China. Electronic address: .

Abstract:  Recent studies have shown that OPN (osteopontin) plays critical roles in cell survival, differentiation, bio-mineralization, cancer and cardiovascular remodeling. However, its roles in the differentiation of brown adipocytes and the underlying mechanisms remain unclear. Therefore, the aim of this study was to investigate the roles of OPN in the brown adipogenesis and the underlying mechanisms. It was shown that the OPN successfully induced the differentiation of 3T3-L1 white preadipocytes into the PRDM16(+) (PRD1-BF1-RIZ1 homologous domain containing 16) and UCP-1(+) (uncoupling protein-1) brown adipocytes in a concentration and time-dependent manner. Also, activation of PI3K (phosphatidylinositol 3-kinase)-AKT pathway was required for the OPN-induced brown adipogenesis. The findings suggest OPN plays an important role in promoting the differentiation of the brown adipocytes and might provide a potential novel therapeutic approach for the treatment of obesity and related disorders. 

Retracted: No

PubPeer comments:
  Fig. 4. Fluorescence micrographs of the nasal tissue of mice excised following administration of ... (C) FITC-HBsAg encapsulated in plain liposomes or (D) FITC-HBsAg encapsulated in HA complexed liposomes. (D) is an enlarged detail of (C), rotated through 180 deg and with some additional light specks added. ![file] , 
 At right: Fig 3,  Molecular characterization of antigen-(A) SDS-PAGE analysis-Lane A: pure HBsAg; Lane B: encapsulated HBsAg in liposome; Lane C: pure HA; Lane D: HA complexed liposomes formulation. At left: Figure 4 from [Tiwari et al (2011)] ,  SDS-PAGE of protein antigen from different liposomal formulations. Lane A, molecular weight marker; lane B, pure antigen HBsAg; lane C, antigen HBsAg from plain liposomal formulation; lane D, protein HBsAg and antibody IgG from antibody conjugated liposomal formulation. ![file] Blots are the same in the same three right-hand lanes. Has one or other been edited? , 
 #2 I guess you meant  same three left-hand lanes? , 
 #3 Whoops. You re right. ![file] ,
MicroRNA-21 Inhibits the Apoptosis of Osteosarcoma Cell Line SAOS-2 via Targeting Caspase 8
Authors: Bin Xu
Zhihong Wang
Hehuan Xia
Yongsheng Lin
Junming Cao
Yipeng Yang
Journal: Oncology research (2017)
Discipline: CLINICAL MEDICINE
Keywords: miR-21; osteosarcoma; apoptosis; caspase 8; cell viability

Abstract:  Currently, multiple microRNAs (miRNAs) have been found to play vital roles in the pathogenesis of osteosarcoma. This study aimed to investigate the role of miR-21 in osteosarcoma. The level of miR-21 in 20 pairs of osteosarcoma and corresponding adjacent tissues was monitored by qPCR. Human osteosarcoma cell line SAOS-2 was transfected with either miR-21 mimic or miR-21 inhibitor, and then cell viability, survival, and apoptosis were measured by MTT, colony formation assay, and flow cytometry. A target of miR-21 was predicted by the microRNA.org database and verified in vitro by using luciferase reporter, qPCR, and Western blot analyses. Finally, cells were cotransfected with siRNA against caspase 8 and miR-21 inhibitor, and the apoptotic cell rate was determined again. Results showed that the mRNA level of miR-21 was highly expressed in osteosarcoma tissues compared with adjacent tissues. Overexpression of miR-21 improved cell viability and survival but suppressed apoptosis. Caspase 8 was a direct target of miR-21, and it was negatively regulated by miR-21. Moreover, miR-21 suppression attenuated caspase 8 silencing and induced the decrease in apoptosis. In conclusion, overexpression of miR-21 suppressed SAOS-2 cell apoptosis via directly targeting caspase 8. 

Retracted: No

PubPeer comments:
 The Western blots and other figures in this paper have an interesting layout that appears to be shared with many other papers, as discussed in a January 2020 post on Leonid Schneider s blog: https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing In almost all papers, Western blot panels within the same figure, and across figures and papers, appear to share the same background, while the bands are regularly spaced, all have similar rounded edges without the usual smudges and specks, and with some bands showing a recognizable  jumping sardine shape. In some of these papers, including this one, flow cytometry plots show an unnaturally dense and well defined  hairball of events in Q3 with a few regularly spaced events in Q1 and Q2, and a rectangular block of events in Q4. This paper does not share, however, the recognizable layout of the bar graphs. Perhaps because this might be one of the earlier papers from this set. To illustrate the recognizable layout of the blots and graphs in this paper, here is Figure 4. ![file] And here is a screenshot of Figure 5A to show the layout of the flow cytometry plots. ![file] ,