PReD-Bench/PRed-Bench huggingface dataset:
Biomarkers of periodontitis in oral fluids
Authors: Rajnish Jain
Simmi Kharb
Balwant Rai
Suresh C Anand
Journal: Journal of Oral Science (2008)
Discipline: CLINICAL MEDICINE
Keywords: Matrix metalloproteinases; GCF; MMP-2; MMP-9; MMP-8
Affiliations: Department of Dentistry, Government Dental College, Rohtak, India. 

Abstract:  Matrix metalloproteinases (MMPs), the key enzymes responsible for matrix degradation, are derived from polymorphonuclear leukocytes during the early stages of periodontitis. The present study determined the levels of GCF matrix metalloproteinase-2 (MMP-2) and metalloproteinase-9 (MMP-9) and salivary MMP-8 in patients with gingivitis and periodontitis and in healthy controls. Levels of crevicular MMP-2, MMP-9 and salivary MMP-8 were determined by ELISA in subjects with healthy gingiva (n = 15), gingivitis (n = 18) and periodontitis (n = 20). Significantly higher salivary MMP-8 and crevicular MMP-9 were observed in cases of periodontitis compared to gingivitis and healthy adults. On the other hand, crevicular MMP-2 levels in periodontitis subjects were lower than those in gingivitis and healthy subjects. The three MMP levels were highly correlated to probing depth, and bleeding on probing. Salivary MMP-8, crevicular MMP- 2 and 9 may serve as biomarkers of periodontal disease and aid in early detection of periodontitis or gingivitis. 

Retracted: No

PubPeer comments:
 In Table 1, the authors report some clinical parameters of the study subjects, such as age range and probing depth. Some of these values are expected to be measured as whole numbers, such as number of teeth present, or number of teeth with periodontitis. However, several of the reported mean values for such measurements have decimals that appear to be impossible. In particular, all three values reported under  number of teeth with periodontitis appear impossible according to the GRIM test developed by James Heathers and Nicholas Brown (see: https: peerj.com preprints 2064v1 and http: www.prepubmed.org grim_test) 2.12; inconsistent with an n=15 2.32; inconsistent with an n=18 9.31; inconsistent with an n=20. ![file] Could the authors please comment? Maybe I am misunderstanding something. , 
 Measurements in Tables 1 and 2 from this 2008 paper look remarkably similar to values in a newer paper by some of the same authors, i.e. Balwant Rai et al., The Saudi Dental Journal, doi: 10.1016 j.sdentj.2010.04.006 - https: pubpeer.com publications 5FDB04ECCF5F47FF54A80E4FE976E4 In particular the reported standard deviations are remarkably similar, even though the patient groups are different in size. Tables 1 compared: ![file] Tables 2 compared: ![file] , 
 The data in Tables 1 and 2 of this paper are also similar to those in another paper by some of the same authors, i.e. Balwant Rai et al., Pesquisa Brasileira em Odontopediatria e Clu00ednica Integrada (2008), doi: 10.4034 1519.0501.2008.0083.0014 - https: pubpeer.com publications 0FCDA571D67C9C6745643A3C4FEC28 Here are Tables 1 and 2 from that 2008 paper for comparison with the screenshots given above. ![file] ,
Phenelzine, a small organic compound mimicking the functions of cell adhesion molecule L1, promotes functional recovery after mouse spinal cord injury
Authors: Sudhanshu Sahu
Rong Li
Melitta Schachner
Journal: Restorative Neurology and Neuroscience (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: L1; inflammation; mouse; phenelzine; regeneration
Affiliations: Center for Neuroscience, Shantou University Medical College, Shantou, Guangdong, China, Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA

Abstract:  Background: Neural cell adhesion molecule L1 contributes to nervous system development and maintenance by promoting neuronal survival, neuritogenesis, axonal regrowth/sprouting, myelination, and synapse formation and plasticity. L1 also enhances recovery after spinal cord injury and ameliorates neurodegenerative processes in experimental rodent models. Aiming for clinical translation of L1 into therapy we screened for and functionally characterized in vitro the small organic molecule phenelzine, which mimics characteristic L1 functions. Objective: The present study was designed to evaluate the potential of this compound in vivo in a mouse model of spinal cord injury. Methods and results: In mice, intraperitoneal injection of phenelzine immediately after severe thoracic compression, and thereafter once daily for 6 weeks, improved hind limb function, reduced astrogliosis and promoted axonal regrowth/sprouting at 4 and 5 weeks after spinal cord injury compared to vehicle control-treated mice. Phenelzine application upregulated L1 expression in the spinal cord and stimulated the cognate L1-mediated intracellular signaling cascades in the spinal cord tissue. Phenelzine-treated mice showed decreased levels of pro-inflammatory cytokines, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α in the injured spinal cord during the acute phase of inflammation. Conclusions: This study provides new insights into the role of phenelzine in L1-mediated neural functions and modulation of inflammation. The combined results raise hopes that phenelzine may develop into a therapeutic agent for nervous system injuries. 

Retracted: No

PubPeer comments:
 The panel shown in figure 4C(i) is highly similar to that in figure 6A(i) of doi: 10.1016 j.jnutbio.2018.01.016 . While both panels are to represent MBP staining of the control condition, mice are described to have undergone slightly different treatments: 1% DMSO in PBS orally in Sahu et al., 2018 and PBS only, presumably by IP injection as the experimental drug, in Li et al., 2018. ![file] , 
 We apologize again for our oversight. The HNK-1 and L1 mimetic papers were initially combined and sent to a journal. But due its extensiveness, we were asked to split. Since no difference observed with PBS and DMSO, one representative panel was added to the figure and we mentioned in the manuscript. While we split the paper we forgot to put the corresponding control figure. ,
Laminin-111 derived peptides AG73 and C16 regulate invadopodia activity of a human adenoid cystic carcinoma cell line
Authors: Vanessa M Freitas
Adriane S de Siqueira
João J V Pinheiro
Camila F Nascimento
Ruy G Jaeger
Journal: Experimental Cell Research (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Adenoid cystic carcinoma; invadopodia; laminin-111 peptides; AG73; C16
Affiliations: Department of Cellular and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, Brazil.

Abstract:  Adenoid cystic carcinoma is a frequently occurring malignant salivary gland neoplasm with high level of recurrence and distant metastasis long time after treatment. Metastatic tumor cells that actively migrate and invade surrounding tissues rely on invadopodia to degrade extracellular matrix (ECM) barriers. Invadopodia are actin-rich membrane protrusions that localize enzymes required for ECM degradation. Breakdown of ECM macromolecules releases fragments and bioactive peptides. We have already demonstrated that laminin-111 and its derived peptides regulate migration, invasion and protease activity of adenocarcinoma cells. Here we addressed the role of laminin-111 peptides AG73 and C16 in invadopodia activity of cells (CAC2) derived from human adenoid cystic carcinoma. CAC2 cells were treated by AG73 and C16, and subjected to fluorescent gelatin substrate degradation assay. In this assay invadopodia activity areas appear as black dots in a fluorescent background. Both peptides significantly increased invadopodia formation and activity compared to controls. We analyzed putative receptors and signaling pathways related to peptide effects. β1 integrin silencing by siRNA decreased AG73- and C16-induced invadopodia. Furthermore inhibition of Rac1 and ERK signaling pathways decreased both C16- and AG73-related invadopodia activities. We propose that laminin-111 peptides AG73 and C16 increase invadopodia activity in CAC2 cells through β1 integrin. Rac1 and ERK1/2 signaling pathways would transduce signals generated by both peptides. 

Retracted: No

PubPeer comments:
 2021 retraction. https: academic.oup.com carcin advance-article doi 10.1093 carcin bgab029 6262656 This article is being retracted at the request of the authors. Recent research (1) has identified the potential for an analytical artefact associated with the use of gas chromatography that could have contributed to the levels of N-nitrosodimethylamine (NDMA) measured in urine samples containing ranitidine in this study. Given this artefact, the authors have informed the journal that their NDMA measurements are not reliable. References 1.tUnited States Food and Drug Administration (FDA). U. S. FDA Updates and Press Announcements on NDMA in Zantac (ranitidine). FDA Provides Update on Testing of Ranitidine for NDMA Impurities. https: www.fda.gov drugs drug-safety-and-availability fda-updates-and-press-announcements-ndma-zantac-ranitidine , 
 See also https: retractionwatch.com 2021 06 15 widely-covered-paper-on-ranitidine-cancer-link-retracted ,
An NKT-mediated autologous vaccine generates CD4 T-cell–dependent potent antilymphoma immunity
Authors: Chen Dong
Hong Qin
Chang-Yuil Kang
Larry W Kwak
Sanghee Kim
Yeonseok Chung
Journal: Blood (2007)
Discipline: CLINICAL MEDICINE
Keywords: lymphoma; vaccination; NKT cells; tumor-specific immunity; alpha-galactosylceramide
Affiliations: Department of Immunology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

Abstract:  Relapses occurring in most patients with lymphoma after antibody or chemotherapy highlight a need for effective vaccination approaches. Autologous tumors are ideal sources of patient-specific tumor antigens for vaccines; however, their poor immunogenicity has been a major obstacle in practice. Natural killer T (NKT) cells have recently emerged as crucial regulators of autoimmunity and tumor immunosurveillance. Here, we show that an autologous lymphoma vaccine that activates NKT cells generated tumor-specific protective immunity in experimental mice. Single vaccination with alpha-galactosylceramide (alphaGC)-loaded A20 lymphoma cells elicited effective antitumor immunity against tumor challenge. This vaccination strategy also induced significant tumor regression in A20-bearing mice. Importantly, the survivors from primary tumor inoculation were all resistant to tumor rechallenge, indicative of established adaptive memory immunity. Depletion as well as adoptive transfer studies revealed an exclusive role of conventional CD4(+) but not CD8(+) T cells in mediating antitumor immunity. In addition, we found normal hematopoietic compartments in the vaccinated mice. Therefore, NKT ligand-loaded lymphoma elicits long-lasting and effective antitumor immunity, which can be further developed as patient- and tumor-specific immunotherapy against human lymphomas. 

Retracted: No

PubPeer comments:
 In Figure 1A, the gatings for frequency calculation are unexpectedly different among each other. Could the others explain why the gatings were different? ![file] , 
 In this experiment, we determined the kinetics of iNKT cell population in mice after vaccination with A20 lymphoma treated with an iNKT cell ligand, alpha-galactosyl ceramide. iNKT cell staining can be defined by TCRbeta+CD1d-tetramer+, and we could define a clear iNKT cell population in each staining. The staining patterns of iNKT cells can differ depending on the levels of TcR, particularly after activation by ligand. Considering that the vaccination with A20 aGC induces the activation of iNKT cells in vivo, one can expect that the TCRbeta+CD1d-tetramer+ staining pattern will be changed a little bit. Therefore, we believe the gatings were reasonable and correct ones; if the same gating was used without considering the nature of TCR expression upon activation, one can lose iNKT cell population or include non-iNKT cell population in the analysis. -Yeonseok Chung and Chen Dong ,
Scalable efficient expansion of mesenchymal stem cells in xeno free media using commercially available reagents
Authors: Jason Reneau
Marialaura Madrigal
Kathya de Cupeiro
Sergio Ruiz
Francisco Silva
Amit N Patel
Nelsy Sanchez
Neil H Riordan
Natalia Jiménez
Thomas E Ichim
Journal: Journal of translational medicine (2015)
Discipline: CLINICAL MEDICINE
Keywords: mesenchymal stem cells; fetal calf serum; XcytePLUS™ media; human platelet lysate; expansion
Affiliations: Medistem Panama, Inc., Building 221, City of Knowledge, Clayton, Panama City, Republic of Panama. ., Indicasat AIP Panama, City of Knowledge, Rep. of Panama. ., Acharya Nagarjuna University, Guntur, India. ., Amniotic Therapies, LLC, Farmers Branch, TX, USA. ., Coma Research Institute, La Jolla, CA, USA. ., University of Utah School of Medicine, Salt Lake City, UT, USA. .

Abstract:  Background: The rapid clinical translation of mesenchymal stem cells (MSC) has resulted in the development of cell-based strategies for multiple indications. Unfortunately one major barrier to widespread implementation of MSC-based therapies is the limited supply of fetal calf serum (FCS) used to expand cells to therapeutic numbers. Additionally, the xenogeneic element of fetal calf serum has been previously demonstrated to stimulate antibody mediated reactions and in some cases sensitization leading to anaphylaxis. Method: XcytePLUS™ media, a human platelet lysate based product, was used to supplement the culture medium at 5, 7.5 and 10% and compared to fetal calf serum at 10%, for human umbilical cord MSC expansion. Properties of the expanded cells were investigated. Results: This study demonstrated equivalent or superior effects of human platelet lysate compared to standard FCS supplemented media, based on doubling rate, without loss of identity or function, as demonstrated with flow cytometry characterization. Differentiation into osteocytes, adipocytes and chondrocytes was comparable from cells expanded in either media supplement. Conclusions: These data support the implementation of human platelet lysate supplemented media as an alternative to xenogeneic containing preparations which may lead to safer MSC products with therapeutic uses. 

Retracted: No

PubPeer comments:
 Figure 6. * Yellow boxes: In the top row, panels b (5% XcytePLUS) and c (7.5% XcytePLUS) appear to show a small area of overlap. ![file] , 
 I have sent this to NH Riordan who can help clarify your question ,
Single-Walled Carbon Nanotube Supported PtNi Nanoparticles (PtNi@SWCNT) Catalyzed Oxidation of Benzyl Alcohols to the Benzaldehyde Derivatives in Oxygen Atmosphere
Authors: Kemal Cellat
Fatih Şen
Haydar Göksu
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: oxidation; benzyl alcohol; benzaldehyde; PtNi@SWCNT; nanocatalyst
Affiliations: Kaynasli Vocational College, Düzce University, Düzce, 81900, Turkey. ., Sen Research Group, Department of Biochemistry, Dumlupınar University, 43100, Kütahya, Turkey., Sen Research Group, Department of Biochemistry, Dumlupınar University, 43100, Kütahya, Turkey. .

Abstract:  This study reports a developed process which is a general and facile method for the oxidation of benzyl alcohol (BnOH) compounds to the benzaldehyde (BA) derivatives, under mild conditions. The oxidation of BnOH species catalyzed by PtNi@SWCNT in toluene (3 ml) at 80 °C under a continuous stream of O2. Single wall carbon nanotube supported PtNi (PtNi@SWCNT) nanoparticles were synthesized using a single-step modified reduction process. The characterization of PtNi@SWCNT nanocatalyst was performed by transmission electron microscope (TEM), X-ray diffraction (XRD), X-ray Photoelectron Spectroscopy (XPS), and elemental analysis by ICP-OES. A variety of BnOH compounds were oxidized by the PtNi@SWCNT catalyst and all the expected oxidation products were obtained in high efficiency in 2 hours of reaction time. TLC was used to monitoring the reaction progress, and the products were identified by 1H/13C-NMR analysis. 

Retracted: No

PubPeer comments:
 This paper appears to be one of a set of at least 2 papers by the same research group that both appear to share the same photo. In both papers, this photo is used as a zoomed-in inset representing the high-resolution transmission electron microscopy (HRTEM) analysis of the  atomic lattice fringe and particle size of the nanoparticles. Of concern, the same photo, which I have called  Inset 4 , is used to represent a different type of nanoparticle in each of these papers. The two papers using the  Inset 4 photo are: * Betuu0308l Su0327en et al. - DOI: 10.1038 s41598-020-68773-x - PdCo@AC * Haydar Gou0308ksu et al. - DOI: 10.1038 s41598-020-66492-x - PtNi@SWCNT Here is a comparison of both  Inset 4 photos: ![file] ![file] Here is a close-up view of both inset photos with red boxes marking the similar-looking areas. ![file] Of note, this is a different set of papers than the 30 papers by the same group that all appear to use another HRTEM image called  Inset 1 . For an example of that photo and the list of those 30 papers, see DOI 10.1016 j.ijhydene.2018.03.175 https: pubpeer.com publications 8AD71F4A32472314CCE9983D47E36F It is also a different set of papers than the 14 papers by the same group that all appear to use another HRTEM image called  Inset 2 . For an example of that photo and the list of those 14 papers, see DOI: 10.1016 j.ijhydene.2017.05.113 https: pubpeer.com publications CAD2F16435F6C639F5DE6851A2E61D ,
MiR-122 Promotes the Development of Colon Cancer by Targeting ALDOA In Vitro
Authors: Junwei Sun
Rui Xiong
Zhao Jin
Zilin Li
Xinhua Zhang
Hong Li
Chuanyi Duan
Tao Yin
Journal: Technology in Cancer Research & Treatment (2019)
Discipline: CLINICAL MEDICINE
Keywords: ALDOA; colon cancer; invasion ability; miR-10; miR-122
Affiliations: Hubei Cancer Hospital, Wuhan, Hubei, China, Xinhua Zhang is the co-first author., Zhongnan Hospital of Wuhan University

Abstract:  Non-coding RNAs, originally considered junk gene products, have taken center stage in view of their significant involvement in a spectrum of biological processes during human development, thereby offering novel therapeutic targets for improvement of treatment options. Accumulating evidence has demonstrated non-coding RNA dysfunction across various human cancers. In particular, microRNAs have emerged as key regulatory molecules in cancer biology. MicroRNAs are noninvasive, readily accessible biomarkers that can be effectively applied for diagnosis and prognosis of different tumor types, including colon cancer. In this study, we reanalyzed the available data with bioinformatics tools to identify differentially expressed microRNAs in colon cancer cells. The top 3 upregulated microRNAs (miR-10, miR-199, and miR-122) in colon cancer cells were further validated in tissues of clinical patients via reverse transcription-quantitative polymerase chain reaction. Our results showed that miR-122 significantly promotes the proliferation and invasion ability of SW480 and SW620 cells through inhibition of Aldolase, Fructose-Bisphosphate A (ALDOA) expression. We further summarized recent advances in our understanding of the functional relevance of microRNAs in cancer development and discussed the possible implications of specific microRNAs in colon cancer. This study extends our knowledge of microRNA involvement in colon cancer biology and presents novel candidates for the development of attractive therapeutic strategies. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have two images which overlap. Of concern, the dimensions appear different, so this is not a simple matter of the selection of the wrong image during figure assembly. Notes: 1) The email address for the corresponding author bears no resemblance to the authoru2019s name; 2) The authors appear to have only one or two papers (including this one); 3) Only one author appears to have a PhD, the others are MDs. These issues are regularly found with papermill or outsourced papers. *** ![file] *** ![file] ,
A deep facial recognition system using computational intelligent algorithms
Authors: Mohamed Taha
Diaa Salama AbdELminaam
Abdulrhman M Almansori
Elsayed Badr
Journal: PLoS ONE (2020)
Discipline: Multidisciplinary
Keywords: Biometric applications; Facial recognition; Smart cities; Algorithms; Transfer learning
Affiliations: Department of Information Systems, Faculty of Computers and Artificial Intelligence, Benha University, Benha City, Egypt., Department of Computer Science, Faculty of Computers and Artificial Intelligence, Benha University, Benha City, Egypt., Department of Scientific Computing, Faculty of Computers and Artificial Intelligence, Benha University, Benha City, Egypt.

Abstract:  The development of biometric applications, such as facial recognition (FR), has recently become important in smart cities. Many scientists and engineers around the world have focused on establishing increasingly robust and accurate algorithms and methods for these types of systems and their applications in everyday life. FR is developing technology with multiple real-time applications. The goal of this paper is to develop a complete FR system using transfer learning in fog computing and cloud computing. The developed system uses deep convolutional neural networks (DCNN) because of the dominant representation; there are some conditions including occlusions, expressions, illuminations, and pose, which can affect the deep FR performance. DCNN is used to extract relevant facial features. These features allow us to compare faces between them in an efficient way. The system can be trained to recognize a set of people and to learn via an online method, by integrating the new people it processes and improving its predictions on the ones it already has. The proposed recognition method was tested with different three standard machine learning algorithms (Decision Tree (DT), K Nearest Neighbor(KNN), Support Vector Machine (SVM)). The proposed system has been evaluated using three datasets of face images (SDUMLA-HMT, 113, and CASIA) via performance metrics of accuracy, precision, sensitivity, specificity, and time. The experimental results show that the proposed method achieves superiority over other algorithms according to all parameters. The suggested algorithm results in higher accuracy (99.06%), higher precision (99.12%), higher recall (99.07%), and higher specificity (99.10%) than the comparison algorithms. 

Retracted: No

PubPeer comments:
 The GAPDH band in Figure 2G has a very different appearance than the other bands in this figure, which is odd if these were imaged at the same time on the same membrane. Could the authors please post the original uncropped scans to reassure readers that these originated on a single membrane? *** ![file] *** ![file] , 
 April 7, 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Individual overexpression of five subunits of human translation initiation factor eIF3 promotes malignant transformation of immortal fibroblast cells
Authors: Lili Zhang
Xiaoyu Pan
John W B Hershey
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: transcriptional regulation; post-transcriptional regulation; tumorigenesis; translation; eIF3
Affiliations: Department of Biochemistry and Molecular Medicine, School of Medicine, University of California, Davis, California 95616, USA.

Abstract:  Transcriptional and post-transcriptional regulatory mechanisms are commonly accepted paradigms of tumorigenesis. The view is emerging that deregulation of translation contributes importantly to cancer development, a role not generally appreciated before. Eukaryotic initiation factor eIF3 contains at least thirteen non-identical subunits, named from eIF3a to eIF3m, and plays an essential role in the rate-limiting initiation phase of translation. Increased mRNA and protein levels of the eIF3a, -3b, -3c, -3h, and -3i subunits have been detected in a wide variety of human tumors and are frequently identified as prognostic biomarkers for poor clinical outcome. However, it remains to be established whether up-regulation of eIF3 subunits is a consequence or a cause of the malignant phenotypes. Here we report that ectopic expression of eIF3a, -3b, -3c, -3h, or -3i in stably transfected NIH3T3 cells leads to a number of oncogenic properties: decreased doubling times, increased clonogenicity and viability, facilitated S-phase entry, attenuation of apoptosis, formation of transformed foci, and anchorage-independent growth. Only overexpression of the transforming subunits results in a stimulation of initiation and global protein synthesis rates and enhanced translation of poorly translated mRNAs that encode growth-regulating proteins, including cyclinD1, c-Myc, fibroblast growth factor-2, and ornithine decarboxylase, which may be responsible for oncogenic malignancy in the transformed cell lines. Based on these results, we hypothesize that eIF3 contributes to hyperactivation of the translation initiation machinery and thereby may play an important role in neoplasia. Cancer cells appear to require an aberrantly activated translational state to survive, suggesting that the initiation factors may be promising therapeutic targets for treating cancer. 

Retracted: No

PubPeer comments:
 The flow cytometry dot plots in red boxes appear to look similar in Fig 4A. But the percentages of cells are different. ![file] ,
Silencing lncRNA PVT1 inhibits activation of astrocytes and increases BDNF expression in hippocampus tissues of rats with epilepsy by downregulating the Wnt signaling pathway
Authors: Teng Zhao
Ying Ding
Min Li
Weihong Lin
Chunkui Zhou
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PVT1; Wnt signaling pathway; astrocytes; epilepsy; hippocampal
Affiliations: Department of Neurology, The First Hospital of Jilin University, Changchun, China., Department of Radiology, The First Hospital of Jilin University, Changchun, China.

Abstract:  The aim of this study is to investigate the effects of long-chain noncoding RNA plasmacytoma variant translocation 1 (PVT1) on the activation of astrocytes and the expression of brain-derived neurotrophic factor (BDNF) in hippocampus tissues of epileptic rats. The epilepsy rat model was induced by intraperitoneal injection of lithium chloride-pilocarpine. Successfully modeled rats were grouped, and their spatial learning and memory, neuronal loss, number of TdT-mediated dUTP nick labeling (TUNEL)-positive cells, and the expression of cleaved-caspase-3, pro-caspase-3, Bax, Bcl-2, GFAP, BDNF, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, axin, and cyclin D1 in hippocampus tissues were evaluated. Increased expression of PVT1 was found in hippocampus tissues of epileptic rats. Silencing of PVT1 improved spatial learning and memory, decreased neuronal loss, decreased the number of TUNEL-positive cell, decreased the expression of cleaved-caspase-3 and Bax while increased pro-caspase-3 and Bcl-2 expression, decreased the expression of GFAP, increased the expression of BDNF, decreased the expression of TNF-α, IL-1β, and IL-6, and decreased the expression of axin and cyclin D1 in hippocampus tissues in epileptic rats. Our study provides evidence that the inhibition of PVT1 may decrease the loss of neurons, inhibit the activation of astrocytes, and increase the expression of BDNF in hippocampus by downregulating the Wnt signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 5. The backgrounds of bands are so clear that nothing changed in high contrast. ![file] Figure 7. Picture scaling and cropping. ![file] , 
 Thanks so much for your comments. I attach great importance to all your questions. I m also asking my team to call the original pictures for verification urgently. Thank you again for your suggestions for the improvement of my work. , 
 Figure 3 appears to have similar issues. I will contact the journal. *** ![file] ,
MicroRNA-625-3p promotes the proliferation, migration and invasion of thyroid cancer cells by up-regulating astrocyte elevated gene 1
Authors: Lei Fang
Dedi Kong
Wei Xu
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Astrocyte elevated gene 1; Cell proliferation; MicroRNA-625-3p; Thyroid cancer; Wnt/β-catenin
Affiliations: Department of Thyroid Breast Surgery, Jining NO.1 People's Hospital, Jining, 272011, Shandong, China., Department of Thyroid Breast Surgery, Jining NO.1 People's Hospital, Jining, 272011, Shandong, China. Electronic address: .

Abstract:  Background: Thyroid cancer is the most common malignancy in human endocrine system. This study aimed to investigate the effects of microRNA-625-3p (miR-625-3p) on thyroid cancer cell proliferation, migration, invasion and apoptosis, as well as underlying potential mechanism. Methods: The relative expressions of miR-625-3p in tumor tissues and adjacent normal tissues of 20 patients with papillary thyroid cancer (PTC) were assessed using qRT-PCR. Cell transfection was used to up-regulate or down-regulate the expressions of miR-625-3p in thyroid cancer SW579 and TPC-1 cells. Effects of miR-625-3p overexpression or suppression on SW579 and TPC-1 cell viability, migration, invasion and apoptosis were detected respectively. The regulatory effect of miR-625-3p on astrocyte elevated gene 1 (AEG-1) expression was also analyzed. Then, the roles of AEG-1 in SW579 and TPC-1 cell proliferation, migration, invasion and apoptosis, as well as Wnt/β-catenin and c-Jun N-terminal kinase (JNK) pathways activation, were evaluated. Results: miR-625-3p had high expressions in tumor tissues, compared to adjacent normal tissues. Overexpression of miR-625-3p significantly promoted SW579 and TPC-1 cell proliferation, migration and invasion but had no influence on cell apoptosis. Knockdown of miR-625-3p had opposite effects, but induced cell apoptosis. AEG-1 was up-regulated by miR-625-3p overexpression and participated in the effects of miR-625-3p on SW-579 and TPC-1 cells. In addition, overexpression of AEG-1 induced the activation of Wnt/β-catenin and JNK pathways in SW579 and TPC-1 cells. Conclusion: miR-625-3p promoted proliferation, migration and invasion of thyroid cancer cells by enhancing the expression of AEG-1 and activating downstream Wnt/β-catenin and JNK pathways. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is Axxx 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable , 
 This paper is A106 ,
Modulation of myocardin function by the ubiquitin E3 ligase UBR5
Authors: Michelle Henderson
Jiliang Zhou
Xiaobo Wang
Amanda J Russell
Guoqing Hu
Darren N Saunders
B Paul Herring
Journal: Journal of Biological Chemistry (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: smooth muscle cells; myocardin; UBR5; transcription factor; protein degradation
Affiliations: Center for Cardiovascular Sciences, Albany Medical College, Albany, New York 12208, USA.

Abstract:  Fully differentiated mature smooth muscle cells (SMCs) are characterized by the presence of a unique repertoire of smooth muscle-specific proteins. Although previous studies have shown myocardin to be a critical transcription factor for stimulating expression of smooth muscle-specific genes, the mechanisms regulating myocardin activity are still poorly understood. We used a yeast two-hybrid screen with myocardin as bait to search for factors that may regulate the transcriptional activity of the myocardin. From this screen we identified a HECT domain-containing protein UBR5 (ubiquitin protein ligase E3 component n-recognin 5) as a myocardin-binding protein. Previous studies have shown that HECT domain-containing proteins are ubiquitin E3 ligases that play an important role in protein degradation. UBR5 has, however, also been shown to regulate transcription independent of its E3 ligase activity. In the current study we demonstrated that UBR5 localized in the nuclei of SMCs and forms a complex with myocardin in vivo and in vitro. We also show that UBR5 specifically enhanced trans-activation of smooth muscle-specific promoters by the myocardin family of proteins. In addition, UBR5 significantly augmented the ability of myocardin to induce expression of endogenous SMC marker genes independent on its E3 ligase function. Conversely, depletion of endogenous UBR5 by small interfering RNA in fibroblast cells attenuated myocardin-induced smooth muscle-specific gene expression, and UBR5 knockdown in SMCs resulted in down-regulation of smooth muscle-specific genes. Furthermore, we found that UBR5 can attenuate myocardin protein degradation resulting in increased myocardin protein expression without affecting myocardin mRNA expression. The effects of UBR5 on myocardin requires only the HECT and UBR1 domains of UBR5. This study reveals an unexpected role for the ubiquitin E3 ligase UBR5 as an activator of smooth muscle differentiation through its ability to stabilize myocardin protein. 

Retracted: No

PubPeer comments:
 ![file] , 
 The MRTF band looks like it has been hand drawn, and is obscuring the correct band below. ,
Designing slow water-releasing alginate nanoreserviors for sustained irrigation in scanty rainfall areas
Authors: S K Shukla
R B Shrivastava
Somen Acharya
A K Bajpai
Raineesh Sharma
Jaya Bajpai
Journal: Carbohydrate polymers (2014)
Discipline: CHEMISTRY
Keywords: Agriculture; Alginate; Deswelling; Nanoparticles; Slow release.
Affiliations: Bose Memorial Research Laboratory, Department of Chemistry, Government Autonomous Science College, Jabalpur, M.P. 482001, India., Bose Memorial Research Laboratory, Department of Chemistry, Government Autonomous Science College, Jabalpur, M.P. 482001, India. Electronic address: ., Defence Institute of High Altitude Research, Leh-Laddakh, J&K, India., Central Water Commission, Ministry of Water Resources, Nagpur, MH, India.

Abstract:  In this study, water absorbing Ca(2+) ion cross-linked alginate nanoparticles were prepared and their water holding capacity was assessed. The prepared nanoparticles were characterized by Fourier transform infra red (FTIR) and X-ray diffraction (XRD) spectroscopy, field emission scanning electron microscopy (FESEM), and Zeta potential measurements to gain insights into their structural and morphological features and to see if the nanoparticles carried a charge over them. The swelling experiments were performed for different compositions of prepared nanoparticles at varied pH and temperatures. The capacity of the nanoparticles to retain imbibed water was evaluated by conducting deswelling studies of the pre-swollen nanoparticles. These particles were mixed with soil and soil-pot experiments were conducted. In order to assess the sustained water release potential of nanoparticles in agricultural fields, the seeds were planted in both native and nanoparticle-mixed soil pots, and moisture content of the soil was measured periodically and growth of the plants was observed. 

Retracted: No

PubPeer comments:
 At left here, Fig 2,  XRD spectra of alginate nanoparticles . At right, Fig 8 from [Singh et al (2015)] ,  XRD images of a CNPs and b CCIONPs . ![file] The vertical axis of Fig 8 is clearly incorrectly labeled. I am also wondering whether Fig 2 and Fig 8(B) represent alginate NPs, or  casein-coated iron oxide nanostructures (CCIONPs) . ,
c-Cbl ubiquitin ligase regulates focal adhesion protein turnover and myofibril degeneration induced by neutrophil protease cathepsin G
Authors: Steven R Houser
Mikhail A Kolpakov
Abdelkarim Sabri
Khadija Rafiq
Jianfen Guo
Liudmila Vlasenko
Archana Sanjay
Xinji Guo
Journal: Journal of Biological Chemistry (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Neutrophil-derived serine protease; Cathepsin G; Myocyte detachment; Apoptosis; Anoikis
Affiliations: Cardiovascular Research Center, Department of Physiology, Temple University Medical School, Philadelphia, Pennsylvania 19140, USA.

Abstract:  The neutrophil-derived serine protease, cathepsin G (Cat.G), has been shown to induce myocyte detachment and apoptosis by anoikis through down-regulation of focal adhesion (FA) signaling. However, the mechanisms that control FA protein stability and turnover in myocytes are not well understood. Here, we have shown that the Casitas b-lineage lymphoma (c-Cbl), adaptor protein with an intrinsic E3 ubiquitin ligase activity, is involved in FA and myofibrillar protein stability and turnover in myocytes. Cat.G treatment induced c-Cbl activation and its interaction with FA proteins. Deletion of c-Cbl using c-Cbl knock-out derived myocytes or inhibition of c-Cbl ligase activity significantly reduced FA protein degradation, myofibrillar degeneration, and myocyte apoptosis induced by Cat.G. We also found that inhibition of the proteasome activity, but not the lysosome or the calpain activity, markedly attenuated FA and myofibrillar protein degradation induced by Cat.G. Interestingly, c-Cbl activation induced by Cat.G was mediated through epidermal growth factor receptor (EGFR) transactivation as inhibition of EGFR kinase activity markedly attenuated c-Cbl phosphorylation and FA protein degradation induced by Cat.G. These findings support a model in which neutrophil protease Cat.G promotes c-Cbl interaction with FA proteins, resulting in enhanced c-Cbl-mediated FA protein ubiquitination and degradation, myofibril degradation, and subsequent down-regulation of myocyte survival signaling. 

Retracted: No

PubPeer comments:
 A closer look at the presented tumors in Figure 6b is enough to conclude that this paper is a falsification. Most probably a papermill product, due to other typical indications like the blurry appearance of the Western immunoblot bands. ![file] , 
 I have not tried to find all the repeated graphic elements in Fig 2d,e. ![file] ,
Brn-3b enhances the pro-apoptotic effects of p53 but not its induction of cell cycle arrest by cooperating in trans-activation of bax expression
Authors: Sonia Lee
Elizabeth Ensor
David S Latchman
Peter J Morris
Vishwanie S Budhram-Mahadeo
Samantha Bowen
Christina Perez-Sanchez
Journal: Nucleic Acids Research (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Brn-3a; Brn-3b; transcription factor; neuroblastoma cells; differentiation
Affiliations: Medical Molecular Biology Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK. 

Abstract:  The Brn-3a and Brn-3b transcription factor have opposite and antagonistic effects in neuroblastoma cells since Brn-3a is associated with differentiation whilst Brn-3b enhances proliferation in these cells. In this study, we demonstrate that like Brn-3a, Brn-3b physically interacts with p53. However, whereas Brn-3a repressed p53 mediated Bax expression but cooperated with p53 to increase p21cip1/waf1, this study demonstrated that co-expression of Brn-3b with p53 increases trans-activation of Bax promoter but not p21cip1/waf1. Consequently co-expression of Brn-3b with p53 resulted in enhanced apoptosis, which is in contrast to the increased survival and differentiation, when Brn-3a is co-expressed with p53. For Brn-3b to cooperate with p53 on the Bax promoter, it requires binding sites that flank p53 sites on this promoter. Furthermore, neurons from Brn-3b knock-out (KO) mice were resistant to apoptosis and this correlated with reduced Bax expression upon induction of p53 in neurons lacking Brn-3b compared with controls. Thus, the ability of Brn-3b to interact with p53 and modulate Bax expression may demonstrate an important mechanism that helps to determine the fate of cells when p53 is induced. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
 #1 Correction. That should read figure 5A, not 6A. , 
 #4 ![file] ,
Overexpression of SMARCA2 or CAMK2D is associated with cisplatin resistance in human epithelial ovarian cancer
Authors: Tianning Shao
Zhiguo Zheng
Lanlan Jia
Qinqing Tu
Xiaoli Xu
Hong Xu
Shasha Suo
Yuejin Hua
Bowen Liu
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: SWI/SNF related matrix associated actin dependent regulator of chromatin subfamily A member 2; calcium/calmodulin dependent protein kinase IIδ; cisplatin resistance; ovarian cancer; quantitative proteomics
Affiliations: Institute of Nuclear‑Agricultural Sciences, Zhejiang University, Hangzhou, Zhejiang 310029, P.R. China, Institute of Zhejiang Cancer Research, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, P.R. China

Abstract:  Ovarian cancer is one of the most lethal types of gynecological cancer. Drug resistance is a major underlying cause of treatment failure, which has lead to continued poor mortality and morbidity rates in patients. In the present study, highly sensitive transcriptome sequencing was performed to systematically identify differentially expressed mRNAs in cisplatin-sensitive (A2780) and -resistant (A2780-DR) cells. Calcium/calmodulin dependent protein kinase IIδ (CAMK2D) and SWI/SNF related matrix associated actin dependent regulator of chromatin subfamily A member 2 (SMARCA2) were identified as exhibiting increased expression in cisplatin-resistant cells. Overexpression of either SMARCA2 or CAMK2D led to a significant increase in the survival rates of A2780 and SKVO3 cells following cisplatin treatment. To further verify the contribution of these two genes in the development of drug resistance, the RNA levels in tissues with different recurrence-free survival (RFS) rates were compared. An increased mRNA level of CAMK2D was detected in samples with shorter RFS rates. An apoptosis assay revealed that overexpression of SMARCA2 or CAMK2D increased the resistance of ovarian cancer cells to cisplatin, as indicated by the decreased apoptotic cell populations. The levels of these two genes also affected the cell cycle and apoptosis-associated protein expression. Quantitative proteomic analyses revealed that overexpression of SMARCA2 or CAMK2D influences multiple metabolism and cancer-associated signaling pathways, which are critical for responses to cisplatin treatment and drug resistance development. 

Retracted: No

PubPeer comments:
 Interesting work. However, in Figure 3E, looks like the siRNA knockdown of CAMK2D and SMARCA2 didn t work at all in the western blot results. Could the authors clarify? Thanks. ,
Type 1 interferons as a potential treatment against COVID-19
Authors: France Mentre
Nathan Peiffer-Smadja
François-Xavier Lescure
Erwan Sallard
Yazdan Yazdanpanah
Journal: Antiviral Research (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: COVID-19; Interferon; SARS-CoV-2.
Affiliations: École Normale Supérieure de Paris, 45 Rue D'Ulm, 75005, Paris, France., Université de Paris, IAME, INSERM, F-75018, Paris, France; Department of Infectious and Tropical Diseases, Assistance Publique - Hôpitaux de Paris, Bichat-Claude Bernard University Hospital, 75018, Paris, France., Université de Paris, IAME, INSERM, F-75018, Paris, France., Université de Paris, IAME, INSERM, F-75018, Paris, France; Department of Infectious and Tropical Diseases, Assistance Publique - Hôpitaux de Paris, Bichat-Claude Bernard University Hospital, 75018, Paris, France. Electronic address: .

Abstract:  Type 1 interferons have a broad antiviral activity in vitro and are currently evaluated in a clinical trial to treat MERS-CoV. In this review, we discuss preliminary data concerning the potential activity of type 1 interferons on SARS-CoV-2, and the relevance of evaluating these molecules in clinical trials for the treatment of COVID-19. 

Retracted: No

PubPeer comments:
 In this article Yazdanpanah did not declare any competing interest. However, he has some ![file] , 
 In this article Yazdanpanah did not declare any competing interests. However he has some. ![file] ,
Knockdown of STMN1 enhances osteosarcoma cell chemosensitivity through inhibition of autophagy
Authors: Zili Wang
Rongzhen He
Song Wu
Yu Wei
Hansong Xia
Journal: Oncology Letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: autophagy; chemoresistance; osteosarcoma; paxilitaxel; stathmin 1.
Affiliations: Department of Orthopaedic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.

Abstract:  Chemoresistance is a major cause for the poor prognosis of osteosarcoma (OS) patients. However, our understanding of mechanisms underlying chemoresistance in OS are limited. The present study aimed to investigate the effect of stathmin 1 (STMN1) on paclitaxel-induced chemoresistance, as well as the underlying mechanism. Western blot analysis data revealed that the expression level of STMN1 was dramatically increased in OS cell lines (HOS, Saos-2, U-2OS and MG-63), when compared to normal osteoblast hFOB1.19 cells. Furthermore, treatment with paclitaxel led to upregulation of STMN1 in U-2OS cells, accompanied by activation of autophagy, which may attenuate the cytotoxicity of paclitaxel in OS cells. Following knockdown of STMN1 expression, paclitaxel-induced autophagy was significantly reduced, accompanied by increased cytotoxicity of paclitaxel to U-2OS cells. In addition, blockade of mammalian target of rapamycin signaling attenuated the inhibitory effect of STMN1 knockdown on autophagy in OS cells. In conclusion, the present study demonstrated that knockdown of STMN1 enhances osteosarcoma cell chemosensitivity to paclitaxel through inhibition of autophagy. Therefore, STMN1 may be a potential target for the treatment of chemoresistant OS. 

Retracted: No

PubPeer comments:
 Image concerns in this paper were found during a systematic search of papers in Spandidos journals for possible duplicated images. Figures 2D, 3B, 5A, and 5C. Two bands appear to be visible at least four times in the paper, while representing different proteins or experiments. Note a little air bubble at the bottom of the left band. ![file] , 
 Fig 1B,  western blot analysis were performed to determine the ... protein levels of STMN1 in four osteosarcoma cell lines (HOS, Saos-2, U-2OS and MG-63, as well as normal osteoblast cell line hFOB1.19). ![file] Could the authors comment on the similarity of the control band to Figs 1B from [Chen et al (2014)] ... ![] ... Fig 6C from [Sui et al (2017)] ... ![] ... *[left]* Fig 6B from [Ying et al (2017)] .  The expression of Wnt5a, b-catenin, and pGSK3b protein was measured by Western blot after the indicated treatment and quantified ? ![] ,