PReD-Bench/PRed-Bench huggingface dataset:
SP70-Targeted Imaging for the Early Detection of Lung Adenocarcinoma
Authors: Chunrong Gu
Jian Xu
Peijun Huang
Shichang Zhang
Wei Zhang
Ting Xu
Daqian Li
Lu Yang
Shiyang Pan
Min Gu
Yue Wang
Erfu Xie
Fang Wang
Jiexin Zhang
Bingfeng Zhang
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: monoclonal antibody; SP70 antigen; lung adenocarcinoma; targeted imaging; xenograft
Affiliations: Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University (Jiangsu Province Hospital), Nanjing, China., Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University (Jiangsu Province Hospital), Nanjing, China. .

Abstract:  NJ001 is a monoclonal antibody that can specifically recognize the SP70 antigen on lung adenocarcinoma cells. The goal of this study was to explore its utility in targeted imaging. Subcutaneous xenograft and orthotopic lung tumor implantation BALB/c mouse models were established. Near-infrared fluorescent CF750-labeled NJ001 was injected into two tumor mouse models. Mice that received orthotopic lung tumor implantation were also injected with NJ001-conjugated nanomagnetic beads intravenously, and then underwent micro-CT scanning. Meanwhile, mice with lung tumor were intravenously injected with normal saline and bare nanomagnetic beads as a control. Fluorescence could be monitored in the mice detected by anti-SP70 fluorescence imaging, which was consistent with tumor burden. Signal intensities detected with SP70-targeted micro-CT scans were greater than those in control mice. More importantly, orthotopic tumor lesions could be found on the fourth week with SP70-targeted imaging, which was 2 weeks earlier than detection in the control. Our results suggest that SP70 is a promising target for molecular imaging, and molecularly targeted imaging with an NJ001-labeled probe could be applied for the early detection of lung adenocarcinoma. 

Retracted: No

PubPeer comments:
 I think itu2019s possible that some of the animals in Figure 4A appear more than once. I have marked some for review by the authors and journal. *** ![file] , 
 Figure 5 may have similar issues. Could the authors please check? I have only marked two. *** ![file] ,
Tissue growth modeling in a wavy-walled bioreactor
Authors: Ericka M Bueno
Bahar Bilgen
Korkut Uygun
Philippe Sucosky
Gilda A Barabino
Journal: Tissue Engineering Part A (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bioreactors; Cartilage tissue engineering; Hydrodynamic environment; Wavy-walled bioreactor; Tissue growth model
Affiliations: Department of Orthopaedics, Alpert Medical School of Brown University and Rhode Island Hospital, Providence, Rhode Island., Center for Engineering in Medicine, Massachusetts General Hospital, Harvard Medical School, and Shriners Hospitals for Children, Boston, Massachusetts., Skeletal Biology Laboratory, Department of Orthopedic Surgery, Brigham and Women's Hospital, Boston, Massachusetts., Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia.

Abstract:  Bioreactors have played a crucial role in recent approaches to cartilage tissue engineering, providing an environment that promotes efficient cell seeding, nutrient and waste transport, and essential physical stimuli. This study employed a wavy-walled bioreactor to investigate the effects of the hydrodynamic environment on the properties of engineered cartilage. Its unique design provides multiple hydrodynamic environments within one setting. A tissue growth model was developed to characterize the tissue growth and extracellular matrix synthesis by chondrocytes seeded and cultivated on polyglycolic acid scaffolds in the wavy-walled bioreactor for a period of 4 weeks. This model consists of four components: 1) a computational fluid dynamics model, 2) a kinetic growth model, 3) an artificial neural network that empirically correlates hydrodynamic parameters with kinetic constants, and 4) a second artificial neural network that correlates the biochemical composition of constructs with their material properties. In tandem, these components enable the prediction of the dynamics of tissue growth, as well as the final compositional and mechanical properties of engineered cartilage. The growth model methodology developed in this study serves as a tool to predict the optimal bioprocessing conditions required to achieve desired tissue properties. 

Retracted: No

PubPeer comments:
 ![file] ![file] , 
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Therapeutic Effects of Bone Marrow-Derived Mesenchymal Stem Cells in Models of Pulmonary and Extrapulmonary Acute Lung Injury
Authors: Hongli He
Jingyuan Xu
Yi Yang
Shuling Hu
Yingzi Huang
Xiuping Xu
Airan Liu
Jibin Han
Ling Liu
Fengmei Guo
Haibo Qiu
Qihong Chen
Journal: Cell Transplantation (2015)
Discipline: CLINICAL MEDICINE
Keywords: Mesenchymal stem cells; acute lung injury; intrapulmonary; extrapulmonary; lipopolysaccharide
Affiliations: Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu, P. R. China., Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu, P. R. China

Abstract:  Bone marrow-derived mesenchymal stem cells (MSCs) offer a promising therapy for acute lung injury (ALI). However, whether the same MSC treatments possess similar potential for different ALI models is not fully clear. The present study evaluated the distribution and therapeutic effects of intravenous MSC administration for the treatment of intratracheal lipopolysaccharide (LPS)-induced intrapulmonary ALI and intravenous LPS/zymosan-induced extrapulmonary ALI, matched with lung injury severity, at 30 min and 1, 3, and 7 days. We found that MSC transplantation attenuated lung injury and inhibited lung inflammation in both ALI models. The benefits of MSCs were more significant in the intrapulmonary ALI mice. In vivo and ex vivo fluorescence imaging showed that MSCs primarily homed into the lung. However, more MSCs were recruited into the lungs of the intrapulmonary ALI mice than those of the extrapulmonary ALI mice over the time course. A few MSCs were also detected in the liver and spleen at days 3 and 7. In addition, the two ALI models showed different extrapulmonary organ dysfunction. A lower percentage of cell apoptosis and SDF-1α levels was found in the liver and spleen of the intrapulmonary ALI mice than in those of the extrapulmonary ALI mice. These results suggested that the two ALI models were accompanied with different degrees of extrapulmonary organ damage, which resulted in differences in the trafficking and accumulation of MSCs to the injured lung and consequently accounted for different therapeutic effects of MSCs for lung repair in the two ALI models. These data suggest that intravenous administration of MSCs has a greater potential for the treatment of intrapulmonary ALI than extrapulmonary ALI matched with lung injury severity; these differences were due to more recruitment of MSCs in the lungs of intrapulmonary ALI mice than those of extrapulmonary ALI mice. This finding may contribute to the clinical use of MSCs for the treatment of ALI. 

Retracted: No

PubPeer comments:
 Figure 1A appears to have two images which overlap. This seems to be a recurring issue in papers with a common author. *** ![file] , 
 Similar issue in Figure 2A (only a portion of the figure is shown). *** ![file] , 
 There appear to be some unexpected similarities in Figure 5. *** Brightness enhanced ![file] *** Original ![file] ,
Nanofiber-Based Multi-Tubular Conduits with a Honeycomb Structure for Potential Application in Peripheral Nerve Repair
Authors: Jiajia Xue
Haoxuan Li
Younan Xia
Journal: Macromolecular Bioscience (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Schwann cells; bone marrow stem cells; electrospun nanofibers; multi-tubular conduit; nerve tissue engineering.
Affiliations: The Wallace H. Coulter Department of Biomedical Engineering Georgia, Institute of Technology and Emory University, Atlanta, GA 30332, USA., School of Chemistry and Biochemistry, School of Chemical and Biomolecular Engineering, Georgia Institute of Technology, Atlanta, GA, 30332, USA.

Abstract:  Peripheral nerve injury is a large-scale problem and it is a great challenge to repair the long lesion in a thick nerve. The design of a multi-tubular conduit with a honeycomb structure by mimicking the anatomy of a peripheral nerve for the potential repair of large defects in thick nerves has been reported. A bilayer mat of electrospun nanofibers is rolled up to form a single tube, with the inner and outer layers comprised aligned and random nanofibers, respectively. Seven such tubes are then assembled into a hexagonal array and encased within the lumen of a larger tube to form the multi-tubular conduit. By introducing an adhesive to the regions between the tubes, the conduit is robust enough for handling during surgery. The seeded bone marrow stem cells (BMSCs) are able to proliferate in all the tubes with even circumferential and longitudinal distributions. Under chemical induction, the BMSCs are transdifferentiated into Schwann-like cells in all the tubes. While the cellular version holds great promise for peripheral nerve repair, the multi-tubular conduit can also be used to investigate the fundamental aspects involved in the development of peripheral nervous system and migration of cells. 

Retracted: No

PubPeer comments:
 Figure S5. * Yellow boxes: The proximal panels representing tubes 2 and 3 appear to share an overlap. The images appear to be shown at different exposures. ![file] ,
Role of interleukin-12 in determining differential kinetics of invariant natural killer T cells in response to differential burden of Listeria monocytogenes
Authors: Masashi Emoto
Robert Hurwitz
Stefan H E Kaufmann
Volker Brinkmann
Yoshiko Emoto
Izumi Yoshizawa
Journal: Microbes and Infection (2008)
Discipline: IMMUNOLOGY
Keywords: Invariant natural killer T cells; iNKT cells; Listeria monocytogenes infection; interleukin-12; liver
Affiliations: Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.

Abstract:  Invariant (i) natural killer (NK) T cells are unique T lymphocytes expressing NKR-P1B/C (NK1.1), which recognize glycolipids, notably alpha-galactosylceramide (alpha-GalCer) presented by CD1d. The characteristic phenotype of these iNKT cells undergoes dramatic changes following Listeria monocytogenes infection, and interleukin (IL)-12 is involved in these alterations. Here we show that liver iNKT cells in mice are differentially influenced by the load of infection. Liver alpha-GalCer/CD1d tetramer-reactive (alpha-GalCer/CD1d(+)) T cells expressing NK1.1 became undetectable by day 2 following L. monocytogenes infection and concomitantly cells lacking NK1.1 increased regardless of the severity of infection. Whereas alpha-GalCer/CD1d(+)NK1.1(+) T cells remained virtually undetectable on day 4 following low-dose infection, considerable numbers of these cells were detected in high-dose-infected mice. Whereas numbers of IL-12 producers in the liver on day 4 post infection were comparable in low- and high-dose-infected mice without in vitro restimulation with heat-killed Listeria, those were more prominent in low-dose-infected mice than in high-dose-infected mice after restimulation despite the fact that higher numbers of macrophages and granulocytes infiltrated the liver in high-dose-infected mice than in low-dose-infected mice. Our results indicate that NK1.1 surface expression on iNKT cells is differentially modulated by the burden of infection, and suggest that a high bacterial load probably causes loss of IL-12 production. 

Retracted: No

PubPeer comments:
 ![file] See also an an investigation carried out by Gunma University (http: www.gunma-u.ac.jp wp-content uploads 2017 10 chosakekka29.pdf ,
Nucleoside diphosphate kinase of Mycobacterium tuberculosis acts as GTPase-activating protein for Rho-GTPases
Authors: Anil Koul
Anil K Tyagi
Ramandeep Singh
Puneet Chopra
Harshavardhan Koduri
Yogendra Singh
Megha Ghildiyal
Kirti Sharma
Journal: FEBS Letters (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: bacterial pathogens; GTPase-activating proteins; Rho-GTPases; Mycobacterium tuberculosis; culture supernatant
Affiliations: Institute of Genomics and Integrative Biology, Mall Road, Delhi, India.

Abstract:  Several bacterial pathogens secrete proteins into the host cells that act as GTPase-activating proteins (GAPs) for Rho-GTPases and convert GTP-bound active form to GDP-bound inactive form. However, no such effector molecule has been identified in Mycobacterium tuberculosis. In this study, we show that culture supernatant of M. tuberculosis H(37)Rv harbors a protein that stimulates the conversion of GTP-bound Rho-GTPases to the GDP-bound form. Nucleoside diphosphate kinase (Ndk) was identified as this culture supernatant protein that stimulated in vitro GTP hydrolysis by members of Rho-GTPases. The histidine-117 mutant of Ndk, which is impaired for autophosphorylation and nucleotide-binding activities, shows GAP activity. These results suggest that Ndk of M. tuberculosis functions as a Rho-GAP to downregulate Rho-GTPases, and this activity may aid in pathogenesis of the bacteria. 

Retracted: No

PubPeer comments:
 ![file] Figure 4 : Panels B and C appear to originate from the same chromatogram with different exposures , 
 ![file] Figure 1 : Panels B C appear identical except for some horizontal resizing. , 
 Thanks for showing interest in our research work and for your observations. Paper that you have mentioned is 18 years old (2002).u00a0 I left institute in 2004 and joined pharma industry, similarly my Ph.D supervisor has also moved to a different university many years back. Therefore, it is difficult to retrive old note books to check the raw data and original TLC radiogram pictures. We are trying to reitrive the raw data to address your queries. As a first author of this study, i want to assure all the readers that data reported in this manuscript is scientifically correct. ,
A late-acting quality control process for mature eukaryotic rRNAs
Authors: Frederick J LaRiviere
Daniel J Ferullo
Sarah E Cole
Melissa J Moore
Journal: Molecular Cell (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Ribosome biogenesis; trans-acting factors; chemical reactions; RNA conformational changes; RNA-protein associations
Affiliations: Howard Hughes Medical Institute, Brandeis University, Waltham, Massachusetts 02454, USA.

Abstract:  Ribosome biogenesis is a multifaceted process involving a host of trans-acting factors mediating numerous chemical reactions, RNA conformational changes, and RNA-protein associations. Given this high degree of complexity, tight quality control is likely crucial to ensure structural and functional integrity of the end products. We demonstrate that ribosomal RNAs (rRNAs) containing individual point mutations, in either the 25S peptidyl transferase center or 18S decoding site, that adversely affect ribosome function are strongly downregulated in Saccharomyces cerevisiae. This downregulation occurs via decreased stability of the mature rRNA contained in fully assembled ribosomes and ribosomal subunits. Thus, eukaryotes possess a quality-control mechanism, nonfunctional rRNA decay (NRD), capable of detecting and eliminating the rRNA component of mature ribosomes. 

Retracted: No

PubPeer comments:
 Figure 3C u2013 more similar than expected (contrast enhanced) ![file] Supplemental Fig. S2B: More similar than expected (left panels galactose, right panel glucose). Could authors check please? ![file] ,
11,670 whole-genome sequences representative of the Han Chinese population from the CONVERGE project
Authors: Roseann E Peterson
Warren W Kretzschmar
Brien Riley
Tim B Bigdeli
Silviu Bacanu
Richard Mott
Na Cai
Bradley Todd Webb
Yihan Li
Kenneth S Kendler
Jonathan Flint
Qibin Li
Jieqin Liang
Jonathan Marchini
Jingchu Hu
Journal: Scientific data (2017)
Discipline: Multidisciplinary
Keywords: Genetic Epidemiology; Major Depressive Disorder; Han Chinese; Whole Genome Sequencing; Single Nucleotide Polymorphisms
Affiliations: Wellcome Trust Centre for Human Genetics, OX3 7BN Oxford, UK., Wellcome Trust Sanger Institute, Wellcome Genome Campus, CB10 1SA Hinxton, Cambridge, UK., European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, CB10 1SD Hinxton, Cambridge, UK., Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia 23298, USA., BGI-Shenzhen, Shenzhen, Guangdong 518083, China., Department of Statistics, University of Oxford, Oxford OX1 3TG, UK., UCL Genetics Institute, University College London, London WC1E 6BT, UK., Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, California 90095-1761, USA.

Abstract:  The China, Oxford and Virginia Commonwealth University Experimental Research on Genetic Epidemiology (CONVERGE) project on Major Depressive Disorder (MDD) sequenced 11,670 female Han Chinese at low-coverage (1.7X), providing the first large-scale whole genome sequencing resource representative of the largest ethnic group in the world. Samples are collected from 58 hospitals from 23 provinces around China. We are able to call 22 million high quality single nucleotide polymorphisms (SNP) from the nuclear genome, representing the largest SNP call set from an East Asian population to date. We use these variants for imputation of genotypes across all samples, and this has allowed us to perform a successful genome wide association study (GWAS) on MDD. The utility of these data can be extended to studies of genetic ancestry in the Han Chinese and evolutionary genetics when integrated with data from other populations. Molecular phenotypes, such as copy number variations and structural variations can be detected, quantified and analysed in similar ways. 

Retracted: Yes

PubPeer comments:
 ![file] The %ID g values in Fig 6A do not match the PET scans in Fig 6B? The liver seems very hot in the vehicle treated mice and lower in the gem-treated mice (6B), but in the ex vivo biodistribution they are both low ~4%ID g (6A). ,
Long non-coding RNA TTN-AS1 promotes the progression of lung adenocarcinoma by regulating PTEN/PI3K/AKT signaling pathway
Authors: Zheng Liu
Jiwen Luo
Journal: Biochemical and Biophysical Research Communications (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: LAD progression; PI3K/AKT pathway; PTEN stabilization; TTN-AS1.
Affiliations: Department of Thoracic Surgery, Mianyang Central Hospital, Mianyang, Sichuan, 621000, China. Electronic address: ., Department of Thoracic Surgery, Mianyang Central Hospital, Mianyang, Sichuan, 621000, China.

Abstract:  Long non-coding RNA (lncRNAs), which are increasingly identified to be dysregulated in cancers, has been verified to participate in tumorigenesis and cancer development. LncRNA TTN-AS1 has been validated as an oncogene in several cancers, such as esophageal squamous cell carcinoma and cervical cancer. Here, we studied the role of TTN-AS1 in lung adenocarcinoma (LAD). The online website UCSC, NCBI and NONCODE displayed that TTN-AS1 is poorly expressed in normal lung tissue. Furtherly, we found a remarkable increase of TTN-AS1 expression in LAD cell lines in comparison with BEAS-2B cells. Functionally, silencing TTN-AS1 resulted in inhibited cell proliferation and migration in LAD cells. Mechanically, TTN-AS1 knockdown enhanced the level of PTEN protein while reduced p-AKT level. Meanwhile, PTEN inhibition observably recovered the repressive effect of TTN-AS1 silence on the biological behaviors of A549 cells. What's more, we demonstrated that TTN-AS1 modulated PTEN expression not at mRNA level but protein level. Intriguingly, TTN-AS1 was uncovered to reduce PTEN stability via inhibiting the interactivity of PTEN with MAGI2. Jointly, our findings unveiled that TTN-AS1 plays a carcinogenic part in LAD progression through destabilizing PTEN protein so as to activate PI3K/AKT pathway, therefore indicating TTN-AS1 as a promising target for LAD treatment. 

Retracted: No

PubPeer comments:
 In Figure 2D, two flow cytometry dot plots are too similar. ![file] ,
Heterosandwich immunoswab assay for dengue virus Ns1 antigen detection
Authors: Advaita Ganguly
Ravindra B Malabadi
Raimer Loebenberg
Hoon H Sunwoo
Mavanur R Suresh
Journal: Diagnostic Microbiology and Infectious Disease (2014)
Discipline: IMMUNOLOGY
Keywords: Bispecific antibody; Dengue; Immunoswab; NS1 protein.
Affiliations: Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, 11304-89 Avenue, Edmonton, Alberta Canada, T6G 2 N8., Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, 11304-89 Avenue, Edmonton, Alberta Canada, T6G 2 N8. Electronic address: .

Abstract:  Dengue and the more severe dengue hemorrhagic fever have been a very critical public health problem globally. Millions of people especially in the tropical areas get infected with dengue. An efficient diagnostic is very important for early screening of dengue infection. In dengue-infected patients, the nonstructural protein NS1 is present on the surface of infected cells and secreted in plasma. The NS1 antigen is an important target for developing a quick diagnostic largely due to its long presence in the blood. We have developed a simple-to-use immunoswab-based diagnostic procedure employing monoclonal antibodies and the second-generation quadromas. The detection limit for NS1 has been established to be in the subnanogram range. The assay is very sensitive, has a visual end point, and also being extremely inexpensive. With this assay, screening time for a dengue-infected person would be very rapid. 

Retracted: No

PubPeer comments:
 Blue boxes: A panel in Figure 1 (Direct Immunoswab) looks very similar to a panel in Figure 2 (Heterosandwich immunoswab), if one of the two photos would be in mirror image. Reported to the journal in October 2015, with reminders in 2016 and 2017. ![file] Detail comparison: ![file] ,
Nonhomologous DNA End Joining of Nucleosomal Substrates in a Purified System
Authors: Go Watanabe
Michael R Lieber
Christina A Gerodimos
Journal: DNA Repair (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Artemis; DNA damage; DNA recombination; DNA repair; DNA-dependent serine/threonine protein kinase (DNA-PK)

Abstract:  The nonhomologous DNA end joining pathway is required for repair of most double-strand breaks in the mammalian genome. Here we use a purified biochemical NHEJ system to compare the joining of free DNA with recombinant mononucleosomal and dinucleosomal substrates to investigate ligation and local DNA end resection. We find that the nucleosomal state permits ligation in a manner dependent on the presence of free DNA flanking the nucleosome core particle. Local resection at DNA ends by the Artemis:DNA-PKcs nuclease complex is completely suppressed in all mononucleosome substrates regardless of flanking DNA up to a length of 14 bp. Like mononucleosomes, dinucleosomes lacking flanking free DNA are not joined. Therefore, the nucleosomal state imposes severe constraints on NHEJ nuclease and ligase activities. 

Retracted: No

PubPeer comments:
 Very interesting work. I wonder if the negative impact of DNA-PKcs on the ligation reaction could be due to competition of ATP consumption by two enzymes, DNA-PKcs and Lig4. It will be interesting to see if including an ATP regeneration system in the reaction affects the NHEJ efficiency in the presence of DNA-PKcs ,
Plasmodium falciparum enolase: stage-specific expression and sub-cellular localization
Authors: Shobhona Sharma
Ipsita Pal Bhowmick
Isabelle Coppens
Gotam K Jarori
Nirbhay Kumar
Journal: Malaria Journal (2009)
Discipline: CLINICAL MEDICINE
Keywords: Plasmodium falciparum; enolase; sub-cellular localization; immunofluorescence assay; immuno-gold electron microscopy
Affiliations: Department of Biological Sciences, Tata Institute of Fundamental Research, Homi Bhabha Road, Colaba, Mumbai-400005, India. 

Abstract:  Background: In an earlier study, it was observed that the vaccination with Plasmodium falciparum enolase can confer partial protection against malaria in mice. Evidence has also build up to indicate that enolases may perform several non-glycolytic functions in pathogens. Investigating the stage-specific expression and sub-cellular localization of a protein may provide insights into its moonlighting functions. Methods: Sub-cellular localization of P. falciparum enolase was examined using immunofluorescence assay, immuno-gold electron microscopy and western blotting. Results: Enolase protein was detected at every stage in parasite life cycle examined. In asexual stages, enolase was predominantly (&gt;or=85-90%) present in soluble fraction, while in sexual stages it was mostly associated with particulate fraction. Apart from cytosol, enolase was found to be associated with nucleus, food vacuole, cytoskeleton and plasma membrane. Conclusion: Diverse localization of enolase suggests that apart from catalyzing the conversion of 2-phosphoglycericacid into phosphoenolpyruvate in glycolysis, enolase may be involved in a host of other biological functions. For instance, enolase localized on the merozoite surface may be involved in red blood cell invasion; vacuolar enolase may be involved in food vacuole formation and/or development; nuclear enolase may play a role in transcription. 

Retracted: No

PubPeer comments:
 (a) The operator defined by eq.(4) is not order preserving with respect to the order relation introduced in Definition 4. (b) The operator defined by eq.(6) is not well defined because the $n$ arguments may not be ranked in a unique way according to the order relation introduced in Definition 4. The methods for multiple attribute decision making based on such operators are not sound ![file] ![file] ![file] , 
 A typical citation pattern of GW Wei, the first author of this paper. ![file] ![file] ![file] ![file] ,
ATP activates a reactive oxygen species-dependent oxidative stress response and secretion of proinflammatory cytokines in macrophages
Authors: Ana L M Ventura
Alessandra Rinna
Pedro M Persechini
Cristiane M Cruz
Henry Jay Forman
David M Ojcius
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: proinflammatory cytokines; interleukin-1beta; interleukin-18; microbial products; lipopolysaccharide
Affiliations: School of Natural Sciences, University of California, Merced, California 95344, USA.

Abstract:  Secretion of the proinflammatory cytokines, interleukin (IL)-1beta and IL-18, usually requires two signals. The first, due to microbial products such as lipopolysaccharide, initiates transcription of the cytokine genes and accumulation of the precursor proteins. Cleavage and secretion of the cytokines is mediated by caspase-1, in association with an inflammasome containing Nalp3, which can be activated by binding of extracellular ATP to purinergic receptors. We show that treatment of macrophages with ATP results in production of reactive oxygen species (ROS), which stimulate the phosphatidylinositol 3-kinase (PI3K) pathway and subsequent Akt and ERK1/2 activation. ROS exerts its effect through glutathionylation of PTEN (phosphatase and tensin homologue deleted from chromosome 10), whose inactivation would shift the equilibrium in favor of PI3K. ATP-dependent ROS production and PI3K activation also stimulate transcription of genes required for an oxidative stress response. In parallel, ATP-mediated ROS-dependent PI3K is required for activation of caspase-1 and secretion of IL-1beta and IL-18. Thus, an increase in ROS levels in ATP-treated macrophages results in activation of a single pathway that promotes both adaptation to subsequent exposure to oxidants or inflammation, and processing and secretion of proinflammatory cytokines. 

Retracted: No

PubPeer comments:
null, 
 The authors write:  Immunoblotting with an Ab against GSH revealed that a sizable fraction of PTEN exists in a monomeric form that can be recognized by the anti- GSH Ab even in untreated macrophages, with a smaller fraction of PTEN being found in a high molecular-weight complex (Fig. 5A). But the amount of PTEN in both the monomeric glutathionylated form and in the high molecular-weight complex increased significantly after a 3 minute incubation with ATP (Fig. 5A). Treatment of the immunoprecipitate with the reducing agent, DTT, before electrophoresis resulted in disappearance of both the monomeric and multimeric PTEN (Fig. 5A), demonstrating that the Ab recognized only the glutathionylated form of PTEN. However, the last lane (ATP+DTT) of Figure 5A appears to be splice or masking of the blot, as it does not have the same background and you can even see a small piece of adjacent band peeking out from underneath. Even if one accepts that the last lane is a splice from another blot, the authors claim it was a single blot that was re-probed to produce Figure 5B:  Reprobing the same membrane with an Ab against PTEN verified the presence of PTEN (60 kDa) in both the treated and untreated macrophages (Fig. 5B). ![file] ,
Docosahexaenoic acid inhibits development of hypoxic pulmonary hypertension: in vitro and in vivo studies
Authors: Yuchun Gu
Jinchuan Yan
Peijing Liu
Rui Chen
Journal: International Journal of Cardiology (2013)
Discipline: CLINICAL MEDICINE
Keywords: Docosahexaenoic acid; Hypoxic pulmonary hypertension; Pulmonary arterial smooth muscle cell; Vascular remodeling.
Affiliations: Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, China. Electronic address: .

Abstract:  Background: Hypoxic pulmonary hypertension (HPH) is initiated by acute hypoxic pulmonary vasoconstriction followed by vascular remodeling and right ventricular failure. Numerous studies have shown that long-term supplementation with docosahexaenoic acid (DHA) may have a role in preventing cardiovascular disease. However, the effects of DHA on HPH remain unclear. Extracellular signal-regulated kinase 1/2 (ERK1/2) is known to be involved in the proliferation and migration of various cell types. In this study, we determined the role of DHA in the prevention of HPH via the ERK1/2 signal pathway. Methods: Rats were intragastrically administered with saline or DHA (100 mg) daily before exposure to room air or chronic hypoxia (O(2) content was maintained at 10%) for 8 h a day for 3 weeks. At the end of study, we compared the right ventricular systolic pressure (RVSP), the weight ratio of right ventricular (RV) free wall to the left ventricular (LV) including the septum (S) free wall, the percent wall thickness (wt.%) of small pulmonary arteries and the area of α-smooth muscle actin (α-SMA)-positive pulmonary artery smooth muscle cells (PASMCs) in the pulmonary arteries among the rats. In vitro, the proliferation and migration of PASMCs were through an MTT assay and a Boyden chamber, respectively. The phenotype marker expression and ERK1/2 activation in the PASMCs were through real-time PCR and western blot analysis, respectively. Results: Under hypoxia, DHA treatment reduced the RVSP (20.41 mmHg ± 2.18 vs. 35.46 mmHg ± 3.21; P &lt; 0.05), the weight ratio of RV free wall to left ventricular and septal free wall [RV/(LV + S)] (0.27 ± 0.03 vs. 0.38 ± 0.05; P &lt; 0.05), wt.% (17.45 ± 1.58% vs. 59.65 ± 4.59%; P &lt; 0.05) and the percentage of SMA-positive vessels (55.42 ± 5.18% vs. 84.71 ± 6.22%; P &lt; 0.05) compared with those of the saline-treated rats. Hypoxia promoted the proliferation, migration and phenotype switching of PASMCs in vitro. However, DHA treatment suppressed the hypoxia-induced changes. Additionally, DHA attenuated the expression of hypoxia-activated ERK1/2 in the PASMCs. Conclusions: Our observations indicate that DHA may potentially prevent HPH. 

Retracted: No

PubPeer comments:
 ![file] ,
Adipogenic Differentiation of Thyroid Cancer Cells Through the Pax8-PPARγ Fusion Protein Is Regulated by Thyroid Transcription Factor 1 (TTF-1)
Authors: Jeffrey O&#x27;Donnell
Yanxiao Zhang
Bin Xu
Maureen A Sartor
Michael O&#x27;Donnell
Jingcheng Yu
Ronald J Koenig
Journal: Journal of Biological Chemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: cancer; differentiation; fusion protein; gene expression; thyroid.
Affiliations: From the Department of Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan Medical Center, Ann Arbor, Michigan 48109-5678 and ., From the Department of Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan Medical Center, Ann Arbor, Michigan 48109-5678 and., Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan 48109-2218.

Abstract:  A subset of thyroid carcinomas contains a t(2;3)(q13;p25) chromosomal translocation that fuses paired box gene 8 (PAX8) with the peroxisome proliferator-activated receptor γ gene (PPARG), resulting in expression of a PAX8-PPARγ fusion protein, PPFP. We previously generated a transgenic mouse model of PPFP thyroid carcinoma and showed that feeding the PPARγ agonist pioglitazone greatly decreased the size of the primary tumor and prevented metastatic disease in vivo The antitumor effect correlates with the fact that pioglitazone turns PPFP into a strongly PPARγ-like molecule, resulting in trans-differentiation of the thyroid cancer cells into adipocyte-like cells that lose malignant character as they become more differentiated. To further study this process, we performed cell culture experiments with thyrocytes from the PPFP mouse thyroid cancers. Our data show that pioglitazone induced cellular lipid accumulation and the expression of adipocyte marker genes in the cultured cells, and shRNA knockdown of PPFP eliminated this pioglitazone effect. In addition, we found that PPFP and thyroid transcription factor 1 (TTF-1) physically interact, and that these transcription factors bind near each other on numerous target genes. TTF-1 knockdown and overexpression studies showed that TTF-1 inhibits PPFP target gene expression and impairs adipogenic trans-differentiation. Surprisingly, pioglitazone repressed TTF-1 expression in PPFP-expressing thyrocytes. Our data indicate that TTF-1 interacts with PPFP to inhibit the pro-adipogenic response to pioglitazone, and that the ability of pioglitazone to decrease TTF-1 expression contributes to its pro-adipogenic action. 

Retracted: No

PubPeer comments:
 The cell morphology of different groups in red box appear to look similar in Fig 2B. ![file] ,
Differential diagnosis of membranous nephropathy with autoantibodies to phospholipase A2 receptor 1
Authors: Nora Hornig
Lars Komorowski
Wolfgang Schlumberger
Kai Fechner
Cornelia Dähnrich
Winfried Stöcker
Christian Probst
Sascha Lange
Journal: Autoimmunity Reviews (2014)
Discipline: IMMUNOLOGY
Keywords: Autoantibodies; ELISA; Indirect immunofluorescence; Membranous nephropathy; Nephrotic syndrome
Affiliations: Institute for Experimental Immunology, Euroimmun, Seekamp 31, 23560 Lübeck, Germany. Electronic address: .

Abstract:  Membranous nephropathy (MN) accounts for most cases of the nephrotic syndrome in adults. Recently, studies on the underlying pathomechanisms led to the identification of the podocyte M-type receptor for secretory phospholipase A2 (PLA2R1) as a target antigen of circulating autoantibodies. Autoantibodies to PLA2R1 may not only play a role in the development of primary MN, but also serve as a marker for diagnosis, disease activity and therapy monitoring. Antibody detection is crucial to discriminate between patients with primary MN and those with a secondary form of the disease, as both forms require different diagnostic approaches and treatment strategies. Standardized test systems based on recombinant PLA2R1 allow for the sensitive and specific analysis of anti-PLA2R1 autoantibodies. Further research into pathogenic mechanisms and other disease markers can pave the way for improved patient care. 

Retracted: No

PubPeer comments:
 Figure 1A shows an example of the Euroimmun Biochip mosaic, which features ten reaction fields, each with two biochips. However, the area around the biochips appears to contain many repetitive features. Could the authors please explain if this is a photo of a real Biochip device or a photocomposite design of a future product? ![file] , 
 This chip, for the detection of phospholipase A2, also shows unexpected similarity to  Hantavirus Mosaic biochips manufactured by Euroimmun as shown in Figure 1 of Lederer et al.  Indirect Immunofluorescence Assay for the Simultaneous Detection of Antibodies against Clinically Important Old and New World Hantaviruses in PLoS Negl Trop Dis 7(4): e2157, DOI: 10.1371 journal.pntd.0002157. Here is that Lederer et al. Figure 1. The bottom photo appears to show similarities to Schlumberger Figure 1 all over the slide, while the top slide appears to only show similarities in the outer parts of the slide, not in the center mosaics themselves. Note that the slides have a different assay name in the photos. ![file] , 
 The same product slide might be visible in another paper from partially the same authors. Here is Figure 1 from Niedrig et al., Clinical and vaccine immunology : CVI (2008), DOI: 10.1128 CVI.00078-07. In the Niedrig 2008 paper, the slide is designed to detect Yellow Fever Virus. ![file] ,
Comparison of improved laparoscopic peritoneal vaginoplasty and gasless laparoscopic ileal vaginoplasty in treatment of androgen insensitivity syndrome
Authors: Zhixin Huang
Guangnan Luo
Peishu Liu
Journal: Archives of Gynecology and Obstetrics (2014)
Discipline: CLINICAL MEDICINE
Keywords: Androgen insensitivity syndrome (AIS); laparoscopic peritoneal vaginoplasty; gasless laparoscopic ileal vaginoplasty; sexual function; Female Sexual Function Index (FSFI)
Affiliations: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, 107 Jinan Culture Road, Jinan, 250012, Shandong, China.

Abstract:  Purpose: To investigate a better approach for androgen insensitivity syndrome (AIS) treatment using laparoscopic peritoneal or ileal vaginoplasty. Method: Improved laparoscopic peritoneal vaginoplasty and gasless laparoscopic ileal vaginoplasty were, respectively, applied to AIS patients in vaginal reconstruction. The operation condition and surgical results were summarized and follow-up was performed from the 5th week after operation, then once a month. The sexual function was scored by Female Sexual Function Index (FSFI), and FSFI score &gt;30 represented a very good sexual function, 25-30 as good, and &lt;25 as bad. Result: The operation time (including gonadal resection and genital plastic surgery) of improved laparoscopic peritoneal vaginoplasty was 77.2 ± 18.9 (55-105) min, while of ileal vaginoplasty was 183.3 ± 30.1 (155-215) min, longer than peritoneal vaginoplasty, and the bleeding amount was 7.2 ± 13.0 (5-30) versus 50.0 ± 30.0 (20-80) mL, respectively. The surgery was successful in all 12 cases without complications. During 1 month to 7 years follow-up, the depth of artificial vagina was approximately 8-12 cm after peritoneal vaginoplasty, while 6-11 cm after ileal vaginoplasty. The vaginal mucosa appeared as normal in all cases. Besides, 4/9 cases had normal FSFI score after peritoneal vaginoplasty while only 1/3 case after ileal vaginoplasty. Conclusion: The peritoneal vaginoplasty seems better than the ileal vaginoplasty because of the shorter operation time, less bleeding, rapid recovery, less trauma and scar, easy operating and early sexual life without mold. But the treatment should be individualized and comprehensive considering the patient anatomical characteristics and other factors. 

Retracted: No

PubPeer comments:
 In this paper, 26 subjects with Androgen Insensitivity Syndrome (AIS) are described. These are described as XY patients who are female in gender, but vaginal hypoplasia. Twelve AIS patients underwent vaginal reconstruction. Table 1 presents the (presumed) last name and age of the patients. There is no word on consent by the patients to have their data published in this paper. Because AIS is a relatively rare disease, the patients thus appear to be identifiable. Two questions for the authors. 1. Did the patients give permission to have their last names and ages and their syndrome published in this paper? Can we see some proof of that, or did the authors show that to the editors? 2. Did the authors obtain an IRB approval for this new operation technique? ,
TRIM59 attenuates inflammation and apoptosis caused by myocardial ischemia reperfusion injury by activating the PI3K/Akt signaling pathway
Authors: C-Y Yang
Q-S Xing
Z-Q Lv
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Myocardial ischemia reperfusion injury; TRIM59 gene; oxidative stress; myocardial injury; ATPase
Affiliations: Qingdao University, Qingdao, China. .

Abstract:  Objective: Myocardial ischemia reperfusion injury (MIRI) is a common factor in heart-related diseases. The aim of this study was to explore the effect of TRIM59 gene on MIRI and its mechanism. Materials and methods: Rats were used to construct MIRI models, and TRIM59 gene was overexpressed in myocardium by Entranster technique to detect the effects of TRIM59 on myocardial oxidative stress, myocardial injury, and ATPase. In addition, rat myocardial H9c2 cells were cultured, and a hypoxia-reoxygenation model of H9c2 cells was constructed to detect the effect of TRIM59 overexpression on the inflammation and apoptosis of H9c2 cells. Finally, the PI3K/Akt signaling pathway inhibitor LY294002 was used to study the effect of TRIM59 on the PI3K/Akt signaling pathway. Results: Overexpression of TRIM59 in vivo effectively reduced the expressions of MDA, CK, and LDH, and increased the expression of SOD and the activity of Na+-K+-ATPase and Ca2+-Mg2+-ATPase. In addition, overexpression of TRIM59 in H9c2 cells significantly reduced the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and oxidative stress (ROS) levels. TRIM59 also significantly increased the activity of PI3K/Akt signaling pathway and promoted the phosphorylation of Akt. Conclusions: TRIM59 reduces the level of inflammation and apoptosis of myocardial cells caused by MIRI by activating the PI3K/Akt signaling pathway, thereby reducing myocardial injury. 

Retracted: Yes

PubPeer comments:
 This article has been  withdrawn from the authors - not sure what that means, but that is how it is stated on the notice here: https: www.europeanreview.org wp wp-content uploads 5192-5192.pdf The original article has been removed. ,
MERIT40 controls BRCA1-Rap80 complex integrity and recruitment to DNA double-strand breaks
Authors: Troy E Messick
Jeffrey Patterson-Fortin
Roger A Greenberg
Dan Feng
Yingqun Wang
Genze Shao
Niraj Shanbhag
Journal: Genes & Development (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Rap80; BRCA1; MERIT40; Abraxas; BRCC36
Affiliations: Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.

Abstract:  Rap80 targets the breast cancer suppressor protein BRCA1 along with Abraxas and the BRCC36 deubiquitinating enzyme (DUB) to polyubiquitin structures at DNA double-strand breaks (DSBs). These DSB targeting events are essential for BRCA1-dependent DNA damage response-induced checkpoint and repair functions. Here, we identify MERIT40 (Mediator of Rap80 Interactions and Targeting 40 kD)/(C19orf62) as a Rap80-associated protein that is essential for BRCA1-Rap80 complex protein interactions, stability, and DSB targeting. Moreover, MERIT40 is required for Rap80-associated lysine(63)-ubiquitin DUB activity, a critical component of BRCA1-Rap80 G2 checkpoint and viability responses to ionizing radiation. Thus, MERIT40 represents a novel factor that links BRCA1-Rap80 complex integrity, DSB recognition, and ubiquitin chain hydrolytic activities to the DNA damage response. These findings provide new molecular insights into how BRCA1 associates with independently assembled core protein complexes to maintain genome integrity. 

Retracted: No

PubPeer comments:
 ![file] ![file] Figure 1B and Figure 2D looks very similar to each other. ,
A homozygous PDE6D mutation in Joubert syndrome impairs targeting of farnesylated INPP5E protein to the primary cilium
Authors: Alessia Micalizzi
Marta Romani
Lydie Burglen
Stanislas Lyonnet
Michel Vekemans
Sophie Thomas
Iain A Drummond
Arnold Munnich
Joseph G Gleeson
Ferechté Encha-Ravazi
Avinash Abhyankar
Jean-Laurent Casanova
Nadia Elkhartoufi
Nicolas Chassaing
Nathalie Boddaert
Sophie Saunier
Mandy Kwong
Jeanne Amiel
Wolfgang Baehr
Tania Attié-Bitach
Enza Maria Valente
Julie Litzler
Peter K Jackson
Kevin J Wright
Julien Saada
Isabelle Perrault
Stéphanie Le Corre
Emilie Filhol
Journal: Human Mutation (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Joubert syndrome; cerebellar structural defect; molar tooth sign; genetic heterogeneity; cilia biogenesis

Abstract:  Joubert syndrome (JS) is characterized by a distinctive cerebellar structural defect, namely the &lt;&lt; molar tooth sign &gt;&gt;. JS is genetically heterogeneous, involving 20 genes identified to date, which are all required for cilia biogenesis and/or function. In a consanguineous family with JS associated with optic nerve coloboma, kidney hypoplasia, and polydactyly, combined exome sequencing and mapping identified a homozygous splice-site mutation in PDE6D, encoding a prenyl-binding protein. We found that pde6d depletion in zebrafish leads to renal and retinal developmental anomalies and wild-type but not mutant PDE6D is able to rescue this phenotype. Proteomic analysis identified INPP5E, whose mutations also lead to JS or mental retardation, obesity, congenital retinal dystrophy, and micropenis syndromes, as novel prenyl-dependent cargo of PDE6D. Mutant PDE6D shows reduced binding to INPP5E, which fails to localize to primary cilia in patient fibroblasts and tissues. Furthermore, mutant PDE6D is unable to bind to GTP-bound ARL3, which acts as a cargo-release factor for PDE6D-bound INPP5E. Altogether, these results indicate that PDE6D is required for INPP5E ciliary targeting and suggest a broader role for PDE6D in targeting other prenylated proteins to the cilia. This study identifies PDE6D as a novel JS disease gene and provides the first evidence of prenyl-binding-dependent trafficking in ciliopathies. 

Retracted: No

PubPeer comments:
 This paper describes the unique family affected with this type of Joubert syndrome. Unfortunately, the clinical description is poor. I would like some clinical precisions from the authors ![file] - What is the geographical origin of this family? - How do the authors define microphthalmia? (clinical examination, MRI, scanner?) - Could the authors precise the type of coloboma for JC-18b? For the fetal case ![file] - What is the histological procedure? - What is the staining used for this examination? - Could the authors precise magnification? ,