PReD-Bench/PRed-Bench huggingface dataset:
Three-Dimensional Reconstruction of Cerebrovascular and Algorithm Realization
Authors: Linfeng Li
Xiao-Jing Jia
Journal: Journal of Healthcare Engineering (2021)
Discipline: Multidisciplinary
Keywords: CT cerebrovascular; medical image registration; optimization algorithm; relative position information; blood vessels
Affiliations: Affiliated Hospital of Beihua University, Jilin 132011, China

Abstract:  Objective: In the three-dimensional reconstruction of CT cerebrovascular medical image registration, a new optimization algorithm based on the relative position information between the contours of various blood vessels in the image is proposed. Methods: Using the rule that the center of gravity of the vascular tissue structure on the series of slices has continuity, find the registration relationship between the contours of the vessels in the two adjacent slices. Because the shape of cerebrovascular contour is relatively symmetrical, its center of gravity is slightly away from its geometric center. Therefore, the geometric center is used to replace the center of gravity, and the "mass" of each contour is calculated according to the area of each contour to achieve the registration of the blood vessel contour. Results: The method has the characteristics of global optimization and stronger robustness. Conclusion: The cerebrovascular image obtained by this method is more realistic and can be used for the import of various software, simulation training, and later research, which provides an effective method for preoperative simulation of cerebrovascular intervention surgery. 

Retracted: No

PubPeer comments:
 This paper is supposed to be about cerebrovascular and contains only 8 items in the reference list. Some cited papers are apparently irrelevant and associated with Shaofei Wu. ![file] , 
 It is hard to find the connection among the author name, affiliation, and provided contacting email account. ![file] ,
Corrigendum: l-Arginine Uptake by Cationic Amino Acid Transporter Promotes Intra-Macrophage Survival of Leishmania donovani by Enhancing Arginase-Mediated Polyamine Synthesis
Authors: Ruby Singh
Ajay Kumar
Pradeep Das
Abhishek Mandal
Sudha Verma
Ayan Kumar Ghosh
Saptarshi Roy
Abul Hasan Sardar
Sushmita Das
Kumar Abhishek
Bidyut Purkait
Savita Saini
Chitra Mandal
Ashish Kumar
Journal: Frontiers in Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: CAT-2; Leishmania; arginase; cytokine; l-arginine
Affiliations: Department of Molecular Biology, Rajendra Memorial Research Institute of Medical Sciences (ICMR), Patna, India., Department of Microbiology, All India Institute of Medical Sciences (AIIMS), Patna, India., Cancer Biology and Inflammatory Disorder Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India., Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Hajipur, India.

Abstract:  [This corrects the article DOI: 10.3389/fimmu.2017.00839.]. 

Retracted: No

PubPeer comments:
 A mega-correction; the latest addressed by this group. Paper not previously on PubPeer. u201c A Corrigendum on L-Arginine Uptake by Cationic Amino Acid Transporter Promotes Intra-Macrophage Survival of Leishmania donovani by Enhancing Arginase-Mediated Polyamine Synthesis by Mandal, A., Das, S., Kumar, A., Roy, S., Verma, S., Ghosh, A. K., et al. (2017). Front. Immunol. 8:839. doi: 10.3389 fimmu.2017.00839 In the original article, there were mistakes in Figure 2D, Figure 2E, Figure 7C, Figure 10 (blot image), Figure 11A and Figure 11C as published. The same image was unintentionally provided for (1) CAT-2 panel in Figure 2D and Figure 2E (2) Arg-1 panel in Figure 7C and Figure 10 (blot image) (3) GAPDH panel in Figure 11A and Figure 11C. The corrected Figures 2, 7, 10, and 11 appear below. The authors apologize for this error (sic) and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.u201d ,
Human embryonic stem cell-derived neural precursor transplants in collagen scaffolds promote recovery in injured rat spinal cord
Authors: Hossein Baharvand
Sahar Kiani
Nargess Zare Mehrjardi
Maryam Hatami
Katayoun Hemmesi
Hossein Azizi
Abdolhossein Shahverdi
Journal: Cytotherapy (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: neural progenitor cells; human embryonic stem cell-derived NPC; spinal cord injury; transplantation; collagen scaffolds
Affiliations: Department of Stem Cells, Cell Science Research Center, Royan Institute, Tehran, Iran.

Abstract:  Background aims: Several studies have reported functional improvement after transplantation of in vivo-derived neural progenitor cells (NPC) into injured spinal cord. However, the potential of human embryonic stem cell-derived NPC (hESC-NPC) as a tool for cell replacement of spinal cord injury (SCI) should be considered. Methods: We report on the generation of NPC as neural-like tubes in adherent and feeder-free hESC using a defined media supplemented with growth factors, and their transplantation in collagen scaffolds in adult rats subjected to midline lateral hemisection SCI. Results: hESC-NPC were highly expressed molecular features of NPC such as Nestin, Sox1 and Pax6. Furthermore, these cells exhibited the multipotential characteristic of differentiating into neurons and glials in vitro. Implantation of xenografted hESC-NPC into the spinal cord with collagen scaffold improved the recovery of hindlimb locomotor function and sensory responses in an adult rat model of SCI. Analysis of transplanted cells showed migration toward the spinal cord and both neural and glial differentiation in vivo. Conclusions: These findings show that transplantation of hESC-NPC in collagen scaffolds into an injured spinal cord may provide a new approach to SCI. 

Retracted: No

PubPeer comments:
 Figure 2B. * Blue boxes: The two Pax6 plots appear to look similar to each other. * Green boxes: It is not clear what the difference is between the two  Nestin  Stage 3 plots, but they look very similar to each other ![file] , 
 #1 Thank you for your concern. We have explained to the editor and asked to publish an Erratum to our manuscript to avoid any potential ambiguities in the future and they accepted. ,
Mechanism of anti-inflammatory effect of tricin, a flavonoid isolated from Njavara rice bran in LPS induced hPBMCs and carrageenan induced rats
Authors: A Helen
Ananthasankaran Jayalekshmi
V Shalini
Journal: Molecular Immunology (2015)
Discipline: IMMUNOLOGY
Keywords: Inflammation; Lipopolysaccharide; Signaling; Tricin.
Affiliations: Department of Biochemistry, University of Kerala Kariavattom Campus, Thiruvananthpuram, Kerala 695581, India. Electronic address: ., Chemical Sciences & Technology Division, National Institute for Interdisciplinary Science and Technology (NIIST), CSIR, Industrial Estate P.O., Thiruvananthapuram, Kerala 695019, India. Electronic address: .

Abstract:  Njavara is an indigenous medicinal rice variety traditionally used in Ayurvedic system of medicine practiced in Kerala, India. Tricin is a bioflavonoid present in significantly higher levels in rice bran of Njavara. Present study attempted to identify the molecular target of tricin in TLR mediated signaling pathways by using lipopolysaccharide (LPS) induced human peripheral blood mononuclear cells (hPBMCs) and carrageenan induced paw edema in rats as experimental models. Tricin acted upstream in the activation of inflammation cascade by interfering with TLR4 activation, preferably by blocking the LPS induced activation of TLR4, MYD88 and TRIF proteins in hPBMCs. Subsequently, tricin significantly blocked the activation of downstream kinases like p38MAPK, JNK1/2 and IRF3. Thus the inhibitory effect of tricin on NF-κB and IRF3 together confirms the specific inhibition of both MYD88 dependent and TRIF dependent pathways. Tricin treatment also inhibited the pro-inflammatory effect of LPS by blocking the TLR4 signaling mediated activation of cytosolic phospholipase A2 (cPLA2), which is confirmed by specific inhibition of COX-2. Results demonstrated that in addition to NF-κB, tricin can prevent the activation of STAT proteins by significantly inhibiting the activation of both STAT1 and STAT3 via the down regulation of upstream phosphorylating enzymes like JAK1 and JAK2. The protective anti-inflammatory effect of tricin was also confirmed by in vivo experiments. Thus, this study provides strong evidence that tricin exerts its anti-inflammatory effect via a mechanism involving the TLR4/NF-κB/STAT signaling cascade. 

Retracted: No

PubPeer comments:
 The lane 1 is same in another publication stating different treatment condition. Could the authors clarify? ![file] ,
IL-17 polarization of MAIT cells is derived from the activation of two different pathways
Authors: Laura Saieva
Giuliana Guggino
Marianna Lo Pizzo
Francesco Ciccia
Francesco Dieli
Riccardo Alessandro
Diana Di Liberto
Giovanni Triolo
Journal: European Journal of Immunology (2017)
Discipline: IMMUNOLOGY
Keywords: IL-17; IL-23; IL-7; MAIT cells; RORc
Affiliations: Dipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, Università di Palermo, Palermo, Italy., Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), Università di Palermo, Palermo, Italy., Dipartimento di Biotecnologie Mediche, Università di Palermo, Palermo, Italy.

Abstract:  MAIT cells are expanded in salivary glands of patients with Sjogren's syndrome and are IL-17 polarized. IL-7 and IL-23 induce IL-17 production activating two different pathways: IL-7 stimulation induces in fact a significant STAT3 and HIF1alpha upregulation, conversely, IL-23 stimulation significantly induces RORc overexpression in MAIT cells of patients with Sjogren's syndrome. 

Retracted: No

PubPeer comments:
 Part of some of the images in Figure 1A are remarkably similar considering they are supposed to be from different individuals (a patient and a control). (There is more there but the marked areas say enough) ![file] ![file] ,
MicroRNA-1179 inhibits the proliferation, migration and invasion of human pancreatic cancer cells by targeting E2F5
Authors: Yonglian Zeng
Fudi Zhong
Huizhao Su
Chengjie Lin
Zhigao Hu
Guandou Yuan
Songqing He
Zhenya Guo
Keqing Jiang
Journal: Chemico-Biological Interactions (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cell cycle arrest; MicroRNA; Pancreatic cancer; Proliferation.
Affiliations: Department of General Surgery, Xiangya Hospital Central South University, Changsha, Hunan, 410008, China., Department of General Surgery, Xiangya Hospital Central South University, Changsha, Hunan, 410008, China; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, 530021, China., Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, 530021, China., Department of General Surgery, Xiangya Hospital Central South University, Changsha, Hunan, 410008, China; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, 530021, China. Electronic address: .

Abstract:  Pancreatic cancer is one of deadly cancers and is responsible for significant mortality and morbidity across the globe. The unavailability of the efficient chemotheruptic drugs and the potent thereuprtic targets forms a bottleneck in the treatment of pancreatic cancer. In this study we explored the potential of MicroRNA-1179 as the therapeutic target for the treatment of pancreatic cancer. The results of this study indicated that the expression of miR-1179 was significantly downregulated in the pancreatic cancer cell lines as compared to the normal pancreatic cells. To unveil the potential role of miR-1179, it was overexpressed in the pancreatic cancer cells. It was observed that ectopic expression of miR-1179 caused reduction in the proliferation of pancreatic cancer cells by triggering G0/G1 cell cycle arrest. Further, overexpression of miR-1179 caused inhibition of the cell migration and invasion of the pancreatic cancer cells. To find out the potential target of miR-1179 in pancreatic cancer cells, we carried out bioinformatic analysis, the results showed that miR-1179 targets E2F transcription factor 5. This was also confirmed by western blotting analysis wherein in overexpression of miR-1179 was associated with the downregulation of the expression E2F5. Conversely, silencing of E2F5 had similar effects as that of miR-1179 suppression. Further, E2F5 overexpression could also nullify the effect on cell proliferation, migration and invasion in pancreatic cancer cells. Finally, miR-1179 overexpression could also inhibit tumor growth in vivo by suppressing the expression of E2F5. Taken together, we conclude that miR-1179 overexpression may prove beneficial for the treatment of pancreatic cancer. 

Retracted: No

PubPeer comments:
 Figure 8: The NS panel appears to show an overlap with the FG panel. Shown with red boxes. ![file] , 
 Note: This article has been corrected. Please see the link below: https: www.oncotarget.com article 27605 ,
Integrin-mediated muscle cell spreading. The role of protein kinase c in outside-in and inside-out signaling and evidence of integrin cross-talk
Authors: M H Disatnik
T A Rando
Journal: Journal of Biological Chemistry (1999)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Muscle cell survival; integrins; extracellular matrix proteins; alpha(5); alpha(7)
Affiliations: Department of Neurology and Neurological Sciences, Veterans Affairs Medical Center, Stanford, California 94305-5235, USA.

Abstract:  Muscle cell survival depends upon the presence of various integrins with affinities for different extracellular matrix proteins. The absence of either alpha(5) or alpha(7) integrins leads to degenerative disorders of skeletal muscle, muscular dystrophies. To understand the cell survival signals that are mediated by integrin engagement with matrix proteins, we studied the early signaling events initiated by the attachment of muscle cells to fibronectin, an interaction that is mediated primarily by alpha(5) integrins. Cells that express alpha(5) integrin rapidly spread on fibronectin, and this process is associated with the phosphorylation of focal adhesion kinase (FAK). Cells deficient in alpha(5) integrin failed to spread or promote FAK phosphorylation when plated on fibronectin. For alpha(5)-expressing cells, both spreading and FAK phosphorylation could be blocked by inhibitors of protein kinase C (PKC), indicating that PKC is necessary for this "outside-in signaling" mediated by alpha(5) integrin. Surprisingly, activators of PKC could promote spreading and FAK phosphorylation in alpha(5)-deficient muscle cells plated on fibronectin. This PKC-induced cell spreading appeared to be due to activation of alpha(4) integrins ("inside-out signaling") since it could be blocked by peptides that specifically inhibit alpha(4) integrin binding to fibronectin. A model of integrin signaling in muscle cells is presented in which there is a positive feedback loop involving PKC in both outside-in and inside-out signaling, and the activation of this cycle is essential for cell spreading and downstream signaling to promote cell survival. In addition, the data indicate a cross-talk that occurs between integrins in which the outside-in signaling via one integrin can promote the activation of another integrin via inside-out signaling. 

Retracted: No

PubPeer comments:
 Figure 1B. Horizontal splice in upper fibronectin panel not apparent in upper laminin panel. ![file] ,
Undecylprodigiosin induced apoptosis in P388 cancer cells is associated with its binding to ribosome
Authors: Meiyu Geng
Yuan-yuan Wang
Xin Qi
Ping Liu
QianQun Gu
Jing Li
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Prodigiosins; anticancer activity; molecular basis; UP; P388 cells
Affiliations: Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, China.

Abstract:  Prodigiosins (PGs) are a family of natural red pigments with anticancer activity, and one member of the family has entered clinical phase II trials. However, the anticancer mechanisms of PGs remain largely unclear. This study was designed to investigate the molecular basis of anticancer activity of UP, a derivative of PGs, in P388 cells. By introducing pharmacological inhibitors and utilizing a variety of analytical approaches including western blotting, flow cytometry and confocal laser microscopy, we found that UP inhibited proliferation of P388 via arresting cells at G2/M phase and inducing cells apoptosis, which was related to the activation of P38, JNK rather than ERK1/2 signaling. ROS regeneration and acidification in cells appear not involved in UP induced apoptosis. Furthermore, utilizing mass spectrometry, sucrose density gradient fractionation and immunofluorescence staining, we discovered that UP was apparently located at ribosome. These results together indicate that ribosome may be the potential target of UP in cancer cells, which opened a new avenue in delineating the anticancer mechanism of PGs. 

Retracted: No

PubPeer comments:
 Figure 3B * Red boxes: Lanes 1-2 in the Cyt C panel look similar to lanes 1-2 in the VDAC panel if one of the two panels is rotated 180 degrees. Reported to the journal in 2015. ![file] , 
 July 2020 correction, at https: journals.plos.org plosone article?id=10.1371 journal.pone.0236282 It reads: * After this article [1] was published, concerns were raised about Fig 3B. Specifically, the Blank and DMSO lanes of the Cyt C and VDAC panels for the Mitochondrial fraction appear similar, when rotated 180 degrees. *  *The authors commented that these experiments were repeated about three times at the time of the original experiments, and this duplication in the published figure may have arisen due to errors in preparing the figure. The authors have provided replacement data from a different replicate of the Mitochondrial fraction CytC and VDAC blot experiments, along with an updated version of the graph in Fig 3B showing quantification of the replacement blots. A member of PLOS ONEu2019s Editorial Board confirmed that the replacement blot images support the results and conclusions as reported in the article. *  *In addition, the authors clarified that in preparing Figs 3 and 5 they spliced a lane out of each blot image between the DMSO and UP lanes. They provided updated versions of these figures and the accompanying legends which indicate where images were spliced and which incorporate the replacement Mitochondrial Cyt C and VDAC data discussed above. * ,
Induction of the transcriptional repressor Yin Yang-1 by vascular cell injury. Autocrine/paracrine role of endogenous fibroblast growth factor-2
Authors: F S Santiago
H C Lowe
Y V Bobryshev
L M Khachigian
Journal: Journal of Biological Chemistry (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: YY1; transcription factor; growth factor; smooth muscle cells; injury
Affiliations: Center for Thrombosis and Vascular Research, The University of New South Wales, Sydney, New South Wales 2052, Australia.

Abstract:  Yin Yang-1 (YY1) is a multifunctional transcription factor that can repress the expression of many growth factor, hormone, and cytokine genes implicated in atherogenesis. YY1 expression is activated in rat vascular smooth muscle cells shortly after injury. YY1 DNA binding activity paralleled elevated protein levels in the nucleus. Smooth muscle cell injury triggered the rapid extracellular release of immunoreactive fibroblast growth factor-2 (FGF-2). YY1 induction after injury was blocked by neutralizing antibodies directed against FGF-2. This growth factor increased YY1 mRNA and protein expression and stimulated YY1 binding and transcriptional activity. Overexpression of YY1 inhibited smooth muscle cell replication. Immunohistochemical analysis demonstrated YY1 staining in medial smooth muscle cells, coincident with FGF-2 expression. Proliferating cell nuclear antigen staining, in contrast, was confined mainly to the atherosclerotic intima. This is the first demonstration that YY1 is induced by either injury or FGF-2, is differentially expressed in normal and diseased human arteries, and that its overexpression inhibits vascular smooth muscle but not endothelial cell replication. 

Retracted: No

PubPeer comments:
  Uninj and  Untrd lanes in Fig 1C and 2E appear very similar. ![file] ,
Self-assembled dihydroartemisinin nanoparticles as a platform for cervical cancer chemotherapy
Authors: Yun Lu
Bo Yang
Yue Chen
BiQiong Wang
Kang Xiong
Qian Wen
ShaoZhi Fu
ZhouXue Wu
Jia Luo
Journal: Drug Delivery (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Dihydroartemisinin; MPEG-PCL; cervical cancer; nanoparticles.
Affiliations: Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, China, Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, Luzhou, China, Department of Oncology, Three Gorges Central Hospital, Chongqing, China

Abstract:  Dihydroartemisinin (DHA) is a potent anti-cancer drug that has limited clinical applications due to poor water solubility and low bioavailability. We designed a biodegradable poly(ethylene glycol) methyl ether-poly(ε-caprolactone) (MPEG-PCL) micelle carrier for DHA using the self-assembly method. The DHA/MPEG-PCL nanoparticles were spherical with an average particle size of 30.28 ± 0.27 nm, and released the drug in a sustained manner in aqueous solution. The drug-loaded nanoparticles showed dose-dependent toxicity in HeLa cells by inducing cycle arrest and apoptosis. Furthermore, compared to free DHA, the DHA/MPEG-PCL nanoparticles showed higher therapeutic efficacy and lower toxicity in vivo, and significantly inhibited tumor growth and prolonged the survival of tumor-bearing nude mice. In addition, the tumor tissues of the DHA/MPEG-PCL-treated mice showed a marked decline in the in situ expression of proliferation and angiogenesis markers. Taken together, the self-assembled DHA/MPEG-PCL nanoparticles are a highly promising delivery system for targeted cancer treatment. 

Retracted: No

PubPeer comments:
 Figure 7 appears to have two images which overlap. Marked with blue boxes (apologies that they are difficult to see). *** ![file] ,
Epithelial progeny of estrogen-exposed breast progenitor cells display a cancer-like methylome
Authors: Kenneth P Nephew
John Quackenbush
Benjamin A T Rodriguez
Mathias Ehrich
Joseph Liu
Pearlly S Yan
Aedín C Culhane
Tim H-M Huang
Michael W Y Chan
Aejaz Nasir
Chinnambally R Venkataramu
Alfred S L Cheng
Timothy J Yeatman
Journal: Cancer Research (2008)
Discipline: CLINICAL MEDICINE
Keywords: Estrogen imprinting; endocrine disruptors; breast cancer risk; stem cells; progenitor cells
Affiliations: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA.

Abstract:  Estrogen imprinting is used to describe a phenomenon in which early developmental exposure to endocrine disruptors increases breast cancer risk later in adult life. We propose that long-lived, self-regenerating stem and progenitor cells are more susceptible to the exposure injury than terminally differentiated epithelial cells in the breast duct. Mammospheres, containing enriched breast progenitors, were used as an exposure system to simulate this imprinting phenomenon in vitro. Using MeDIP-chip, a methylation microarray screening method, we found that 0.5% (120 loci) of human CpG islands were hypermethylated in epithelial cells derived from estrogen-exposed progenitors compared with the non-estrogen-exposed control cells. This epigenetic event may lead to progressive silencing of tumor suppressor genes, including RUNX3, in these epithelial cells, which also occurred in primary breast tumors. Furthermore, normal tissue in close proximity to the tumor site also displayed RUNX3 hypermethylation, suggesting that this aberrant event occurs in early breast carcinogenesis. The high prevalence of estrogen-induced epigenetic changes in primary tumors and the surrounding histologically normal tissues provides the first empirical link between estrogen injury of breast stem/progenitor cells and carcinogenesis. This finding also offers a mechanistic explanation as to why a tumor suppressor gene, such as RUNX3, can be heritably silenced by epigenetic mechanisms in breast cancer. 

Retracted: No

PubPeer comments:
 Figure 2B, the bands are with too much similarity than expected. ![file] ,
A necrotic stimulus is required to maximize matrix-mediated myogenesis in mice
Authors: Drew Kuraitis
Erik J Suuronen
Maria Grazia Berardinelli
Antonio Musarò
Journal: Disease Models & Mechanisms (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Biomaterials; skeletal muscle; extracellular matrix; regeneration; ischemic muscle
Affiliations: Institute Pasteur Cenci-Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, Via Scarpa 14, Rome 00161, Italy., Institute Pasteur Cenci-Bolognetti, Rome, Italy, University of Ottawa Heart Institute, Ottawa, Canada;

Abstract:  Biomaterials that are similar to skeletal muscle extracellular matrix have been shown to augment regeneration in ischemic muscle. In this study, treatment with a collagen-based matrix stimulated molecular myogenesis in an mdx murine model of necrosis. Matrix-treated animals ran ≥ 40% further, demonstrating functional regeneration, and expressed increased levels of myogenic transcripts. By contrast, matrix treatment was unable to induce transcriptional or functional changes in an MLC/SOD1(G93A) atrophic mouse model. In vitro, satellite cells were cultured under standard conditions, on matrix, in the presence of myocyte debris (to simulate a necrotic-like environment) or with both matrix and necrotic stimuli. Exposure to both matrix and necrotic stimuli induced the greatest increases in mef2c, myf5, myoD and myogenin transcripts. Furthermore, conditioned medium collected from satellite cells cultured with both stimuli contained elevated levels of factors that modulate satellite cell activation and proliferation, such as FGF-2, HGF and SDF-1. Application of the conditioned medium to C2C12 myoblasts accelerated maturation, as demonstrated by increased mef2c, myf5 and myogenin transcripts and fusion indexes. In summary, the collagen matrix required a necrotic stimulus to enhance the maturation of satellite cells and their secretion of a myogenic cocktail. Considering that matrix treatment supports myogenesis only in in vivo models that exhibit necrosis, this study demonstrates that a necrotic environment is required to maximize matrix-mediated myogenesis. 

Retracted: No

PubPeer comments:
 unexpected image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Postsegregational Killing Mediated by the P1 Phage “Addiction Module” phd-doc Requires the Escherichia coli Programmed Cell Death System mazEF
Authors: M Reches
B Sat
R Hazan
H Engelberg-Kulka
Journal: Journal of Bacteriology (2001)
Discipline: MICROBIOLOGY
Keywords: Addiction modules; genes; toxin; phd-doc; P1 prophage
Affiliations: Department of Molecular Biology, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel., <!--label omitted: 1-->Department of Molecular Biology, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel

Abstract:  "Addiction modules" consist of two genes; the product of the second is long lived and toxic, while the product of the first is short lived and antagonizes the lethal action of the toxin. The extrachromosomal addiction module phd-doc, located on the P1 prophage, is responsible for the postsegregational killing effect (death of plasmid-free cells). The Escherichia coli chromosomal addiction module analogue, mazEF, is responsible for the induction of programmed cell death. Here we show that the postsegregational killing mediated by the P1 phd-doc module depends on the presence of the E. coli mazEF system. In addition, we demonstrate that under conditions of postsegregational killing, mediated by phd-doc, protein synthesis of E. coli is inhibited. Based on our findings, we suggest the existence of a coupling between the phd-doc and mazEF systems. 

Retracted: No

PubPeer comments:
 ![file] The highlighted colonies appear more similar than expected after rotation. Could the authors check ? ,
EGFR tyrosine kinase inhibitors activate autophagy as a cytoprotective response in human lung cancer cells
Authors: Jie Sun
Hongchuan Jin
Weidong Han
Yan Chen
Lifeng Feng
Xiaoying Lin
Hongming Pan
Xiaojia Wang
Weiting Ge
Xian Wang
Yanshan Wang
Jing Li
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Epidermal growth factor receptor; tyrosine kinase inhibitors; gefitinib; erlotinib; non-small-cell lung cancer
Affiliations: Department of Medical Oncology, Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

Abstract:  Epidermal growth factor receptor tyrosine kinase inhibitors gefitinib and erlotinib have been widely used in patients with non-small-cell lung cancer. Unfortunately, the efficacy of EGFR-TKIs is limited because of natural and acquired resistance. As a novel cytoprotective mechanism for tumor cell to survive under unfavorable conditions, autophagy has been proposed to play a role in drug resistance of tumor cells. Whether autophagy can be activated by gefitinib or erlotinib and thereby impair the sensitivity of targeted therapy to lung cancer cells remains unknown. Here, we first report that gefitinib or erlotinib can induce a high level of autophagy, which was accompanied by the inhibition of the PI3K/Akt/mTOR signaling pathway. Moreover, cytotoxicity induced by gefitinib or erlotinib was greatly enhanced after autophagy inhibition by the pharmacological inhibitor chloroquine (CQ) and siRNAs targeting ATG5 and ATG7, the most important components for the formation of autophagosome. Interestingly, EGFR-TKIs can still induce cell autophagy even after EGFR expression was reduced by EGFR specific siRNAs. In conclusion, we found that autophagy can be activated by EGFR-TKIs in lung cancer cells and inhibition of autophagy augmented the growth inhibitory effect of EGFR-TKIs. Autophagy inhibition thus represents a promising approach to improve the efficacy of EGFR-TKIs in the treatment of patients with advanced non-small-cell lung cancer. 

Retracted: No

PubPeer comments:
 Figure 3B and Figure 4B. When the two WB bands shown in red and blue boxes are subjected to enlargement and horizontal flip, respectively, they look more similar than expected. Could the authors provide the original WB image to rule out this concern? ![file] ,
Regulation of carbohydrate metabolism by indole-3-carbinol and its metabolite 3,3′-diindolylmethane in high-fat diet-induced C57BL/6J mice
Authors: Sankaran Mirunalini
Jayakumar Poornima
Journal: Molecular and Cellular Biochemistry (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Indole glucosinolates; indole-3-carbinol; 3,3'-diindolylmethane; carbohydrate metabolism; high-fat diet
Affiliations: Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, 608002, Tamil Nadu, India.

Abstract:  Indole glucosinolates, present in cruciferous vegetables have been investigated for their putative pharmacological properties. The current study was designed to analyse whether the treatment of the indole glucosinolates-indole-3-carbinol (I3C) and its metabolite 3,3'-diindolylmethane (DIM) could alter the carbohydrate metabolism in high-fat diet (HFD)-induced C57BL/6J mice. The plasma glucose, insulin, haemoglobin (Hb), glycosylated haemoglobin (HbA1c), glycogen and the activities of glycolytic enzyme (hexokinase), hepatic shunt enzyme (glucose-6-phosphate dehydrogenase), gluconeogenic enzymes (glucose-6-phosphatase and fructose-1,6-bisphosphatase) were analysed in liver and kidney of the treated and HFD mice. Histopathological examination of liver and pancreases were also carried out. The HFD mice show increased glucose, insulin and HbA1c and decreased Hb and glycogen levels. The elevated activity of glucose-6-phosphatase and fructose-1,6-bisphosphatase and subsequent decline in the activity of glucokinase and glucose-6-phosphate dehydrogenase were seen in HFD mice. Among treatment groups, the mice administered with I3C and DIM, DIM shows decreased glucose, insulin and HbA1c and increased Hb and glycogen content in liver when compared to I3C, which was comparable with the standard drug metformin. The similar result was also obtained in case of carbohydrate metabolism enzymes; treatment with DIM positively regulates carbohydrate metabolic enzymes by inducing the activity of glucokinase and glucose-6-phosphate dehydrogenase and suppressing the activity of glucose-6-phosphatase and fructose-1,6-bisphosphatase when compared to I3C, which were also supported by our histopathological observations. 

Retracted: No

PubPeer comments:
 Concern about Figure 1. In panels D and E, some structures appear to be visible multiple times. Shown with green, red, and blue circles. ![file] ,
Knockdown of HMGB1 inhibits growth and invasion of gastric cancer cells through the NF-κB pathway in vitro and in vivo
Authors: Jing Zhang
Shuang Li
Yu-Bin Kou
Jin-Shui Zhu
Wei-Xiong Chen
Journal: International Journal of Oncology (2014)
Discipline: CLINICAL MEDICINE
Keywords: HMGB1; gastric adenocarcinoma; tumor growth; invasion; metastasis
Affiliations: Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, P.R. China., Department of Gastroenterology, Baoshan Branch Hospital, Shuguang Hospital Affiliated with Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China.

Abstract:  High mobility group box 1 (HMGB1) as a novel inflammatory molecule has been shown to be involved in a variety of cell physiological and pathological behaviors including immune response, inflammation and cancer. Evidence suggests that HMGB1 plays a critical role in the development and progression of multiple malignancies. However, the underlying molecular mechanisms for the HMGB1-mediated growth and invasion of gastric cancer have not yet been elucidated. The present study investigated the expression of HMGB1 in gastric adenocarcinoma (GAC) and the mechanisms by which it contributes to tumor growth and invasion. The correlation between HMGB1 expression and clinicopathological characteristics of GAC patients was assessed by immunohistochemical assay through tissue microarray procedures. The RNA and protein expressions of HMGB1 and downstream factors were detected by quantitative PCR and western blot assays; cell proliferation and invasion were determined by MTT, wound-healing and 3D-Matregel assays, subcutaneous SGC-7901 tumor models were established to verify tumor growth in vivo. We demonstrated that, the expression of HMGB1 was significantly increased in the nucleus of GAC tissues compared with that in adjacent non-cancer tissues (88.6 vs.70.5%, P&lt;0.001), and correlated with the metastatic lymph node of GAC (P=0.018). Furthermore, knockdown of HMGB1 by shRNA inhibited cell proliferative activities and invasive potential, and downregulated the expression of NF-κB p65, PCNA and MMP-9 in GAC cells (SGC-7901 and AGS). The tumor volumes in SGC7901 subcutaneous nude mouse models treated with Lv-shHMGB1 was significantly smaller than those of the nonsense sequence group. Taken together, these findings suggest that increased expression of HMGB1 is associated with tumor metastasis of GAC, and knockdown of HMGB1 suppresses growth and invasion of GAC cells through the NF-κB pathway in vitro and in vivo, suggesting that HMGB1 may serve as a potential therapeutic target for GAC. 

Retracted: No

PubPeer comments:
 Figure 6. * The tumors in the NC group look much larger than would be approved by most animal ethics rules. They look like they might be limiting the animals movement a lot. * The error bars in Figure B at day 14 and C look very different, while the averages look the same.  This study was supported by National Nature Science Foundation of China (nos. 81302093 and 81272752). ![file] ,
The novel cancer-testis antigen A-kinase anchor protein 4 (AKAP4) is a potential target for immunotherapy of ovarian serous carcinoma
Authors: Shikha Saini
Nirmal Kumar Lohiya
Aruna Batra
Anil Suri
Nirmala Jagadish
Abdul S Ansari
Sumit Agarwal
Abhilasha Sinha
Archana Verma
Sushma Suri
Anju Gupta
Deepak Parashar
Journal: OncoImmunology (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: AKAP4; cancer-testis antigen; immunotherapy; ovarian serous carcinoma; vaccine.
Affiliations: Cancer Microarray; Genes and Proteins Laboratory; National Institute of Immunology; Aruna Asaf Ali Marg; New Delhi, India.

Abstract:  Ovarian cancer is one of the neoplasms affecting the reproductive tract associated with high mortality rate because of limited therapeutic options and an elevated incidence of chemoresistance and recurrence. In this context, immunotherapy may constitute a promising approach to improve survival rates and clinical outcome, raising the need for specific target antigens. Cancer-testis antigens (CTAs) are considered promising candidates in this sense because they are aberrant expressed by various malignancies but not by non-transformed tissue, with the exception of testes. Here, we examined the expression and potential to promote humoral immune responses of a novel CTA, A-kinase anchor protein 4 (AKAP4), among 38 ovarian carcinoma patients. Our results reveal that AKAP4 was expressed at both the mRNA and protein levels in 89% (34/38) of ovarian carcinoma tissue specimens but not in 21 matched adjacent non-cancerous tissues. In addition, a humoral response against AKAP4 was detected in 58% (22/38) of ovarian carcinoma patients by ELISA. In particular, 65% (22/34) patients bearing an AKAP4-expressing tumor exhibited circulating anti-AKAP4 antibodies. Interestingly, the majority of specimens were categorized as ovarian serous adenocarcinoma and serous papillary carcinoma, of which 93% (28/30) and 100% (6/6), respectively, expressed AKAP4. A humoral response against AKAP4 was detected in 79% (19/24) and 67% (4/6) of ovarian serous adenocarcinoma and serous papillary carcinoma patients, respectively. The presence of circulating anti-AKAP4 antibodies suggests the AKAP4 is highly immunogenic in ovarian serous carcinoma patients. Our study lays the foundations for exploring AKAP4 as a potential target for the immunotherapy of ovarian cancer. 

Retracted: No

PubPeer comments:
 Lanes 2 and 4 of Figure 4B appear to be the same. *** Enhanced contrast ![file] *** Original ![file] ,
Steering post-C–C coupling selectivity enables high efficiency electroreduction of carbon dioxide to multi-carbon alcohols
Authors: Yuanjie Pang
Cao Thang Dinh
Xue-Li Zheng
Phil De Luna
Bang-Jiao Ye
Edward H. Sargent
Rafael Quintero-Bermudez
David Sinton
Bo Zhang
Pei-Ning Chen
Yi Li
Fei Meng
Miao Zhong
Jun Li
Ali Seifitokaldani
Hongyan Liang
Shu-Hong Yu
Thomas Burdyny
Zhi-Qin Liang
Yimeng Min
Wen-Na Ge
Fanglin Che
Tao-Tao Zhuang
Journal: Nature Catalysis (2018)
Discipline: CHEMISTRY
Keywords: copper-based catalysts; high-value alcohols; C-C coupling; core-shell vacancy engineering catalysts; electrochemical CO2 reduction

Abstract: Engineering copper-based catalysts that favour high-value alcohols is desired in view of the energy density, ready transport and established use of these liquid fuels. In the design of catalysts, much progress has been made to target the C–C coupling step; whereas comparatively little effort has been expended to target post-C–C coupling reaction intermediates. Here we report a class of core–shell vacancy engineering catalysts that utilize sulfur atoms in the nanoparticle core and copper vacancies in the shell to achieve efficient electrochemical CO2 reduction to propanol and ethanol. These catalysts shift selectivity away from the competing ethylene reaction and towards liquid alcohols. We increase the alcohol-to-ethylene ratio more than sixfold compared with bare-copper nanoparticles, highlighting an alternative approach to electroproduce alcohols instead of alkenes. We achieve a C2+ alcohol production rate of 126\u2009±\u20095\u2009mA\u2009cm\u22122 with a selectivity of 32\u2009±\u20091% Faradaic efficiency. The conversion of carbon dioxide into multi-carbon alcohols would enable the synthesis of sustainable liquid fuels with high energy densities. Now, vacancy-engineered core–shell copper-based catalysts are able to shift the selectivity of electrochemical CO2 reduction into alcohols instead of alkenes, as obtained with bare-copper catalysts.

Retracted: No

PubPeer comments:
 In Figure 4b, multiple regions with unexpected similar background patterns are observed on the two bottom curves. Although the upper one looks like a little bit thicker than the bottom one (may use different line thickness), the shape and trend are indeed similar for the two different samples. ![file] , 
 #1 It is seems to be a bit worse. After scaling (94.1%) and rotation (-0.8 degree) the purple curve (Cu) is near-identical to the green curve (Cu2S-Cu) in noise. It is hard to imagine an experimental explanation for this. ![file] (click to animate) ![file] ,
Long noncoding RNA NEAT1 sponges miR‑125a‑5p to suppress cardiomyocyte apoptosis via BCL2L12
Authors: Hong Yan
Qianhuan Zhang
Dongli Chen
Huasheng Liang
Lie Liu
Journal: Molecular Medicine Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: NEAT1; cardiomyocytes; apoptosis; miR-125a-5p; BCL2L12
Affiliations: Department of Cardiology, Guangdong Cardiovascular Research Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510515, P.R. China.

Abstract:  Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. The present study indicated that NEAT1 expression is markedly downregulated in cardiomyocytes following ischemia/reperfusion injury in vivo and hydrogen peroxide treatment in vitro. Further experiments suggested that ectopic overexpression of NEAT1 suppresses cardiomyocyte apoptosis induced by hydrogen peroxide, as assessed by TUNEL assay and flow cytometry. In addition, using a dual‑luciferase reporter assay, NEAT1 was demonstrated to directly interact with microRNA (miR)‑125a‑5p and overexpression of miR‑125a‑5p efficiently reversed the stimulatory effect of NEAT1 on B‑cell lymphoma‑2‑like 12 (BCL2L12) expression. Furthermore, the results indicated that NEAT1 inhibits cardiomyocyte apoptosis via regulating the expression of BCL2L12, which appeared to be mediated via miR‑125a‑5p. In conclusion, the present study suggested that NEAT1 functions as a miR sponge to inhibit cardiomyocyte apoptosis and may be a novel therapeutic target for cardiomyocyte apoptosis‑associated heart diseases. 

Retracted: No

PubPeer comments:
 ![file] In **Fig.2B.** overly similar images from DAPI stained cell nuclei appear between conditions: H2O2+vector and H2O2+NEAT1. This similarity in DAPI staining is highly unlikely between these are 2 different experimental conditions. Could the authors explain and provide the **raw DAPI staining images** of these **2 different panels**? ,
Tripartite motif 16 suppresses breast cancer stem cell properties through regulation of Gli-1 degradation via the ubiquitin-proteasome pathway
Authors: Juntao Yao
Tao Xu
Xiao Fu
Tingting Shi
Suoni Li
Wenjuan Wang
Tao Tian
Yu Yao
Aili Suo
Zhiping Ruan
Hui Guo
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: Cancer stem cells; TRIM16; breast cancer; metastasis; prognosis
Affiliations: The Integrated Department of TCM and Western Medicine, Shaanxi Provincial Tumor Hospital, Xi'an, Shaanxi 710061, P.R. China., Department of Thoracic Surgery, The Center Hospital of Xi'an, Xi'an, Shaanxi 710061, P.R. China., Department of Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China., Department of Oncology, Shaanxi Provincial Tumor Hospital, Xi'an, Shaanxi 710061, P.R. China.

Abstract:  Cancer stem cells (CSCs) are responsible for cancer progression and patient prognosis. Tripartite motif 16 (TRIM16) is a proteasome coactivator that regulates proteolytic activity in eukaryotic cells. Abundant evidence has shown that TRIM16 is lowly expressed in a number of human carcinomas. In a previous study, we demonstrated that TRIM16 suppressed cancer malignancy and that TRIM16 expression levels were associated with favorable prognostic parameters of patients with cancer. However, the precise role of this motif in the pathogenesis of breast cancer remains unknown. In the present study, we examined 29 human breast cancer specimens, and found that TRIM16 was lowly expressed in breast cancers; thus, TRIM16 expression is negatively correlated with metastasis in breast cancer patients. Moreover, we showed that TRIM16 suppressed CSC properties in a population of breast cancer cells. TRIM16 depletion resulted in an increased proportion of CSCs relative to breast cancer cells when several assays were used to assess CSC properties. Finally, we demonstrated that TRIM16 directly regulated the degradation of Gli‑1 protein via the ubiquitin‑proteasome pathway. In conclusion, we propose that inhibition of CSC properties may be one of the functions of TRIM16 as a suppressor of breast cancer progression. 

Retracted: No

PubPeer comments:
 Figure 4E and 8C * Red boxes: Two panels that appear to be showing different cell lines and experiments appear to overlap ![file] ,