PReD-Bench/PRed-Bench huggingface dataset:
MiRNALet‐7a mediates prostate cancer PC‐3 cell invasion, migration by inducing epithelial‐mesenchymal transition through CCR7/MAPK pathway
Authors: Ruoyang Du
Guanlin Tang
Zhaobing Tang
Youlin Kuang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CCR7; EMT; Let-7a; MAPK; invasion
Affiliations: Chongqing Medical University, Chongqing, China., Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Abstract:  Prostate cancer is one of the most common malignancies in older men. Recent evidence has demonstrated microRNA (miRNA) Let-7a expression decreased in prostate cancer, while the expression of CC chemokine receptor type 7 (CCR7) increased. In this study, we investigated whether CCR7 overexpression was associated with a decrease in the expression of miRNA Let-7a in invasion and metastasis of prostate cancer cell. Synthetic Let-7a mimics and Let-7a inhibitors were transfected into prostate cancer PC-3 cells, respectively. Then Western blot was used to detect the expression of CCR7, ERK, p38, MMP-9, and Epithelial-Mesenchymal Transition (EMT)-related proteins. Matrigel invasion assays were performed to assess the migratory and invasive activities of PC3 cells. To confirm the fact that 3'UTR of CCR7 is a direct target of Let-7a, a luciferase assay for the reporter gene expressing the Let-7a binding sites of CCR7 3'UTR was used. Synthetic Let-7a mimics decreased prostate cancer cell migration and invasion, as well as the expression of CCR7, phospho-p38, phospho-ERK1/2, MMP-9, N-cadherin, and Snail in PC-3 cells. The Let-7a inhibitors reversed the effects of Let-7a on PC-3 cells. The 3'UTR of CCR7 was confirmed as a direct target of Let-7a by using the luciferase assay. All findings demonstrated that Let-7a/CCR7 axis regulated EMT progress in prostate cancer cells and mediated the tumor cell invasion and migration process via activation of P38/ERK signal pathway. Our results suggested that the therapeutic potential of Let-7a as an antitumor and antimetastatic manager in prostate cancer and CCR7 may be regarded as a therapeutic target for the prostate cancer treatment. 

Retracted: No

PubPeer comments:
 Figure 2. * Red boxes: The NC panel in Figure 2A (invasion) appears to show an overlap with the Let-7a mimics con panel in Figure 2C (migration). ![file] , 
 Figure 4. * Blue boxes: The E-cadherin panel in Figure 4A (SB203850 treatment) appears to look very similar to the E-cadherin panel in Figure 4B (PD98059 treatment), albeit stretched differently. ![file] ,
miR‐150 functions as a tumour suppressor in human colorectal cancer by targeting c‐Myb
Authors: Yu Wang
Yanlei Ma
Junlan Feng
Peng Zhang
Huanlong Qin
Yongzhi Yang
Feng Wang
Journal: Journal of Cellular and Molecular Medicine (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: c-Myb; colorectal cancer; miR-150.
Affiliations: Department of Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China., Department of GI Surgery Shanghai Tenth People's Hospital Affiliated to Tongji University Shanghai China, Department of Surgery Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai China

Abstract:  Our previously published study documented a deregulation of the microRNA miR-150 in colorectal cancer. Here, we investigated further, in vitro and in vivo, the potential molecular mechanisms underlying the involvement of miR-150 in colorectal cancer, using the appropriate molecular biological methods. We report that miR-150 is a key regulator in the tumourigenesis and progression of colorectal cancer, by acting as a tumour suppressor targeting c-Myb. The current findings suggest that miR-150 may have important roles in the pathogenesis of colorectal cancer. 

Retracted: No

PubPeer comments:
 Figures 2E and 5E: * Red boxes: Two panels that appear to show different experiments show an area of overlap. ![file] , 
 Dear Dr. Bik, Thank you very much for comment on our published work. Please allow me to express my sincere thanks on your great work on checking the data in published papers to improve the quality of publications. After receiving your comments, we have carefully checked the indicated PCNA immunoreactivity images in Figures 2E and 5E and confirmed errors in these figure panels. We have checked our original data carefully and found we misused the image in mimics group due to the wrong labeling during obtaining data. To reflect our rigorous attitude to this article, the corrected image and original data of PCNA image in Figure 2E have been shown below. This mistake doesnu2019t affect any conclusions we made in our paper. We will contact the editor office and publish a corrigendum as soon as possible. Thanks again for your kind pointing-out the mistake in our paper. We will keep a more cautious attitude towards our future research work. Sincerely yours, Huanlong. , 
 ![file] ,
Morphine alleviates myocardial ischemia/reperfusion injury in rats by inhibiting TLR4/NF-κB signaling pathway
Authors: H-W Zhao
Y Wang
J-H Li
F-Z Zhang
L Wang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Morphine; myocardial ischemia/reperfusion injury; TLR4/NF-κB signaling pathway; rats; cardiac dysfunction
Affiliations: Department of Anesthesioiogy, People's Hospital of Rizhao, Rizhao, China. .

Abstract:  Objective: The aim of this study was to investigate the effect of morphine on myocardial ischemia/reperfusion (I/R) injury in rats and its underlying mechanism, thereby providing a reference for the prevention and treatment of myocardial I/R injury in clinical practice. Materials and methods: A total of 60 male Sprague-Dawley (SD) rats were randomly divided into 3 groups, including: Sham group (n=20), I/R group (n=20) and I/R + morphine group (n=20) using a random number table. The left anterior descending coronary artery (LAD) of rat was ligated and re-canalized, and the I/R model was established in rats. Rats in I/R + sevoflurane (SEV) group were pretreated with 2.5% SEV. Infarction area of heart in each group was detected using triphenyltetrazolium chloride (TTC) test. Ejection fraction % (EF%) and fraction shortening % (FS%) were determined by echocardiography. Hematoxylin-eosin (HE) staining assay was performed to detect the morphological changes of cardiac myocardial cells in each group. Meanwhile, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) staining was adopted to detect the apoptosis of myocardial cells and fibroblasts. In addition, the expression levels of toll-like receptor 4 (TLR4) and p65 in heart samples of rats in each group were measured via immuno-histochemical staining. Finally, the influence of morphine on TLR4/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway was detected using Western blotting. Results: Morphine significantly alleviated I/R-induced cardiac dysfunction in rats, whereas significantly increased EF% and FS% (p&lt;0.05). In addition, morphine evidently inhibited myocardial infarction caused by I/R injury. Meanwhile, it reduced the infarction area from [(59.61±3.41) %] to [(26.67±3.62) %] (p&lt;0.05). The results of HE staining showed that compared with I/R group, I/R + morphine group exhibited remarkably tidier cardiac myofilament, less degradation and necrosis, as well as significantly relieved cellular edema. Immuno-histochemical staining results revealed that morphine overtly reversed decreased expressions of TLR4 and p65 induced by I/R in rats (p&lt;0.05). Furthermore, Western blotting found that morphine significantly inhibited the protein expressions of TLR4 and phosphorylated p65. Conclusions: Morphine clearly alleviates I/R-induced myocardial injury in rats. The possible mechanism may be associated with the inhibition on TLR4/NF-κB signaling pathway. 

Retracted: No

PubPeer comments:
 Sharp change in the background suggesting irregular splicing in Figure 4A ![file] , 
 Sharp change in the background in Figure 4C ![file] ,
Canstatin inhibits Akt activation and induces Fas-dependent apoptosis in endothelial cells
Authors: David J Panka
James W Mier
Journal: Journal of Biological Chemistry (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Canstatin; apoptosis; angiogenesis; Akt; focal adhesion kinase
Affiliations: Division of Oncology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachussetts 02215, USA.

Abstract:  Canstatin, a 24-kDa peptide derived from the C-terminal globular non-collagenous (NC1) domain of the alpha2 chain of type IV collagen, was previously shown to induce apoptosis in cultured endothelial cells and to inhibit angiogenesis in vitro and in vivo. In this report, we demonstrate that canstatin inhibits the phosphorylation of Akt, focal adhesion kinase, mammalian target of rapamycin, eukaryotic initiation factor-4E-binding protein-1, and ribosomal S6 kinase in cultured human umbilical vein endothelial cells. It also induces Fas ligand expression, activates procaspases 8 and 9 cleavage, reduces mitochondrial membrane potential, and increases cell death (as determined by propidium iodide staining). Canstatin-induced activation of procaspases 8 and 9 as well as the induced reduction in mitochondrial membrane potential and cell viability were attenuated by the forced expression of FLICE-inhibitory protein. Canstatin-induced procaspase 8 activation and cell death were also inhibited by a neutralizing anti-Fas antibody. Collectively, these data indicate that canstatin-induced apoptosis is associated with phosphatidylinositol 3-kinase/Akt inhibition and is dependent upon signaling events transduced through membrane death receptors. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
 I agree there is an unexpected amount of repetition in the background. Given that other papers with common authors have been retracted (albeit, without unanimous agreement by all authors), and [ORI found misconduct] elsewhere, perhaps one of the authors could comment here. *** Inverted, false color ![file] ,
Inhaled lactonase reduces Pseudomonas aeruginosa quorum sensing and mortality in rat pneumonia
Authors: Hubert Lepidi
Julien Hiblot
Eric Chabriere
Sami Hraiech
Fabienne Bregeon
John Lafleur
Janek Bzdrenga
Didier Raoult
Laurent Papazian
Mikael Elias
Mark W Silby
Jean-Marc Rolain
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Antibiotic molecules; Pseudomonas aeruginosa pneumonia; bacterial resistance; quorum sensing; lactonases
Affiliations: Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes, UMR CNRS-IRD 6236, IFR48, Aix-Marseille Université, Marseille, France; Réanimation - Détresses Respiratoires et Infections Sévères, APHM, CHU Nord, Marseille, France., Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes, UMR CNRS-IRD 6236, IFR48, Aix-Marseille Université, Marseille, France., Department of Biology, University of Massachusetts Dartmouth, Dartmouth, Massachusetts, United States of America; Department of Emergency Medicine, Alpert School of Medicine, Providence, Rhode Island, United States of America., Weizmann Institute of Science, Biological Chemistry, Rehovot, Israel., Department of Biology, University of Massachusetts Dartmouth, Dartmouth, Massachusetts, United States of America.

Abstract:  Rationale: The effectiveness of antibiotic molecules in treating Pseudomonas aeruginosa pneumonia is reduced as a result of the dissemination of bacterial resistance. The existence of bacterial communication systems, such as quorum sensing, has provided new opportunities of treatment. Lactonases efficiently quench acyl-homoserine lactone-based bacterial quorum sensing, implicating these enzymes as potential new anti-Pseudomonas drugs that might be evaluated in pneumonia. Objectives: The aim of the present study was to evaluate the ability of a lactonase called SsoPox-I to reduce the mortality of a rat P. aeruginosa pneumonia. Methods: To assess SsoPox-I-mediated quorum quenching, we first measured the activity of the virulence gene lasB, the synthesis of pyocianin, the proteolytic activity of a bacterial suspension and the formation of biofilm of a PAO1 strain grown in the presence of lactonase. In an acute lethal model of P. aeruginosa pneumonia in rats, we evaluated the effects of an early or deferred intra-tracheal treatment with SsoPox-I on the mortality, lung bacterial count and lung damage. Measurements and primary results: SsoPox-I decreased PAO1 lasB virulence gene activity, pyocianin synthesis, proteolytic activity and biofilm formation. The early use of SsoPox-I reduced the mortality of rats with acute pneumonia from 75% to 20%. Histological lung damage was significantly reduced but the lung bacterial count was not modified by the treatment. A delayed treatment was associated with a non-significant reduction of mortality. Conclusion: These results demonstrate the protective effects of lactonase SsoPox-I in P. aeruginosa pneumonia and open the way for a future therapeutic use. 

Retracted: No

PubPeer comments:
 The ACTIN panel (red box) was reused in different cell types in Figure 3A. ![file] ,
Correlation of Covid-19 With Stomatognathic System With Homeopathic Proposal for Adjunct Treatment to Increase Oral and General Health
Authors: Leila C Mourão
Andrea Padre
Journal: Alternative therapies in health and medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: SARS-CoV-2; COVID-19; ACE2; salivary glands; oral cavity

Abstract:  Context: SARS-CoV-2 is a new virus responsible for the outbreak of COVID-19. Studies have shown that the expression of ACE2 was found in the smaller salivary glands was higher than that in the lungs, suggesting that salivary glands may be a potential target of the virus. This may indicate that one of the main gateways to coronavirus infection is the oral cavity. Objective: This review intended to evaluate the comorbidities of the oral cavity and their relationships to COVID-19 and to show the benefits of homeopathic therapies as adjuvant treatments to increase oral and general health and mitigate the devastating effects of the coronavirus. Design: The authors conducted a narrative review of articles published in indexed journals and websites of dental institutions and the WHO. They were selected oral pathological manifestations, sleep disorders, mood, orofacial pain and bruxism, associated with the oral-facial manifestations of Covid-19 and articles of evidence of homeopathy in dentistry. Setting: Study done in Brazil with research professors in Homeopathy and Periodontics in universities. Results: Some studies report that patients who are more susceptible to anxiety and stress during the pandemic, due to social confinement, may have disorders in the stomatognathic system such as: neuralgic pain in the face and teeth, fractures of teeth and dental prostheses, nibbled mucosa, stomatitis, ulcers, pain in the Temporal Mandibular Joint, otalgias, dental tightening, bruxism, xerostomia, peeling of the mucous membranes and skin, facial paralysis. Conclusions: The researchers concluded that homeopathy is a safe and viable therapy for the control of COVID-19 symptoms, as scientific evidence has proven its benefits through clinical trials and use in previous epidemics. In dentistry, this therapy allows the dentist to act fully in the promotion of oral health and in the prevention of oral and systemic diseases. 

Retracted: No

PubPeer comments:
 ![file] ,
Expression of Fas and Fas-related molecules in human hepatocellular carcinoma
Authors: J J Jang
M S Shin
W S Park
H S Lee
J H Lee
H K Lee
J Y Park
S Y Kim
S H Kim
M Joo
S H Lee
H S Kim
Y K Kang
R R Oh
N J Yoo
J Y Lee
J H Bae
S Y Han
Journal: Human Pathology (2001)
Discipline: CLINICAL MEDICINE
Keywords: tumor cells; hepatocellular carcinoma; Fas; Fas ligand; apoptosis
Affiliations: Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Abstract:  Many tumor cells, including hepatocellular carcinoma (HCC), express both Fas and its ligand on their surfaces, and it has remained a mystery why such cells do not spontaneously become apoptotic. In the current study, we analyzed the alterations of Fas structure and the expression of Fas and Fas ligand (FasL) and of Fas pathway inhibitors, including soluble Fas (sFas), Fas-associated phosphatase-1 (FAP-1), and bcl-2, in 50 cases of human HCC. Monoallelic loss of the Fas gene, as determined by loss of heterozygosity with intragenic polymorphisms, was observed in 5 of the 34 informative cases (15%), but none of the 50 cases showed Fas gene mutation. Expression of Fas and FasL was detected in 44 (88%) and 50 (100%) cases, respectively. sFas messenger RNA, as analyzed by in situ reverse-transcription polymerase chain reaction was expressed in 42 of the 50 cases (84%), and FAP-1 expression was observed in 40 of the 50 cases (80%). In contrast, none of the 50 cases showed bcl-2 expression. Our results showed that the majority of the HCCs (88%) coexpressed a death receptor, Fas and its cognate ligand, FasL, but all HCCs showed one or more alterations of the Fas pathway molecules known to inhibit Fas-mediated apoptosis. These findings suggest that the expression of sFas and FAP-1 and, in part, loss of Fas expression, rather than Fas gene alteration or bcl-2 expression, may be involved in the Fas resistance of HCC in vivo and that these mechanisms may play important roles in the pathogenesis of human HCC. HUM PATHOL 32:250-256. 

Retracted: No

PubPeer comments:
 The same figure was also used in another paper [Hum Pathol . 2001 Mar;32(3)250-6] ![file] , 
 I am the corresponding author of the papers. I can confirm that the SSCP of these Figures are same. The issue have already been reported in the https: pubpeer.com publications B13A8ED914FDF13715925084CD12C2. The figures show allelic losses in the gene that is known to be frequent in many cancers including lung, liver and bladder cancer. As the manuscript said that it was a u201cRepresentative results of SSCP analysisu201d. However, we did not declare the details and should not have used the same images without notification. However, I believe that it was a mistake probably during the arrangement with a lot of number of cases, and that it was not intentional. Once, again, I sincerely apologize to have made this error. ,
Bisphenol-A Mediated Inhibition of Hippocampal Neurogenesis Attenuated by Curcumin via Canonical Wnt Pathway
Authors: Shashi Kant Tiwari
Swati Agarwal
Anurag Tripathi
Rajnish Kumar Chaturvedi
Journal: Molecular Neurobiology (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Bisphenol A (BPA); Curcumin; Hippocampus; Neural stem cells (NSC); Neurogenesis
Affiliations: Developmental Toxicology Division, Systems Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), 80 MG Marg, Lucknow, 226001, India., Academy of Scientific and Innovative Research (AcSIR), New Delhi, India., Food, Drugs and Chemical Toxicology Group, CSIR-IITR, 80 MG Marg, Lucknow, 226001, India., Developmental Toxicology Division, Systems Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), 80 MG Marg, Lucknow, 226001, India. ., Academy of Scientific and Innovative Research (AcSIR), New Delhi, India. .

Abstract:  Bisphenol A (BPA) is an environmental xenoestrogenic endocrine disruptor, utilized for production of consumer products, and exerts adverse effects on the developing nervous system. Recently, we found that BPA impairs the finely tuned dynamic processes of neurogenesis (generation of new neurons) in the hippocampus of the developing rat brain. Curcumin is a natural polyphenolic compound, which provides neuroprotection against various environmental neurotoxicants and in the cellular and animal models of neurodegenerative disorders. Here, we have assessed the neuroprotective efficacy of curcumin against BPA-mediated reduced neurogenesis and the underlying cellular and molecular mechanism(s). Both in vitro and in vivo studies showed that curcumin protects against BPA-induced hippocampal neurotoxicity. Curcumin protects against BPA-mediated reduced neural stem cells (NSC) proliferation and neuronal differentiation and enhanced neurodegeneration. Curcumin also enhances the expression/levels of neurogenic and the Wnt pathway genes/proteins, which were reduced due to BPA exposure in the hippocampus. Curcumin-mediated neuroprotection against BPA-induced neurotoxicity involved activation of the Wnt/β-catenin signaling pathway, which was confirmed by the use of Wnt specific activators (LiCl and GSK-3β siRNA) and inhibitor (Dkk-1). BPA-mediated increased β-catenin phosphorylation, decreased GSK-3β levels, and β-catenin nuclear translocation were significantly reversed by curcumin, leading to enhanced neurogenesis. Curcumin-induced protective effects on neurogenesis were blocked by Dkk-1 in NSC culture treated with BPA. Curcumin-mediated enhanced neurogenesis was correlated well with improved learning and memory in BPA-treated rats. Overall, our results conclude that curcumin provides neuroprotection against BPA-mediated impaired neurogenesis via activation of the Wnt/β-catenin signaling pathway. 

Retracted: No

PubPeer comments:
 ![file] Partial image duplication found. The cells highlighted in red box are common in both the experimental groups. , 
 ![file] Another partial image duplication found.The cells highlighted in red box are common in both the experimental groups. Some features are also erased in the images. ,
Triplex PCR using new primers for the detection of Toxoplasma gondii
Authors: Rahmah Noordin
Anizah Rahumatullah
Boon Yin Khoo
Journal: Experimental Parasitology (2012)
Discipline: MICROBIOLOGY
Keywords: Molecular methods; Toxoplasma gondii; triplex PCR; B1 gene; ITS1 region
Affiliations: Institute for Research in Molecular Medicine, Universiti Sains Malaysia, Penang, Malaysia. 

Abstract:  Molecular methods are used increasingly for the detection of Toxoplasma gondii infection. This study developed a rapid, sensitive, and specific conventional triplex PCR for the detection of the B1 gene and ITS1 region of T. gondii using newly designed primers and an internal control based on the Vibrio cholerae HemM gene. The annealing temperature and concentrations of the primers, MgCl(2), and dNTPs were optimized. Two sets of primers (set 1 and 2) were tested, which contained different segments of the T. gondii B1 gene, 529 repeat region and ITS1 region. A series of sensitivity tests were performed using parasite DNA, whole parasites, and spiked human body fluids. Specificity tests were performed using DNA from common protozoa and bacteria. The newly developed assay based on set 2 primers was found to be specific and sensitive. The test was capable of detecting as little as 10 pg T. gondii DNA, 10(4) tachyzoites in spiked body fluids, and T. gondii DNA in the organ tissues of experimentally infected mice. The assay developed in this study will be useful for the laboratory detection of T. gondii infection. 

Retracted: No

PubPeer comments:
 In this paper, 14 PCR gels are presented over four figures. As we shall see, the total number of PCR gels in the paper will actually work out at a tad less than 14. In Figure 1, the PCRs in (b) and (c) were annealed at different temperatures. Perhaps this is why the same gel is repeated at different grey scales? ![image] , 
 In Fig. 4, (b)(ii) is a stretchy version of (a)(ii). Here they are compared after (b)(ii) was vertically destretched ![image] , 
 The gel in Fig. 3 (B) reappears with an extra lane as Fig. 4 (C)(i) for a different experiment. ![image] , 
 Completing the PCR reuses, the gel in Fig. 3 (c) reappears as Fig. 4 (c)(ii) for a different experiment. ![image] ,
Long noncoding RNA LUCAT1 promotes cervical cancer cell proliferation and invasion by upregulating MTA1
Authors: M-Q Wang
J Du
Q-X Pang
A-H Wang
J-M Zhao
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; LUCAT1; cervical cancer; proliferation; invasion
Affiliations: Yan'an Key Laboratory of Cancer Prevention and Treatment, School of Medicine, Yan'an University, Yan'an, China. .

Abstract:  Objective: Recent researches have revealed the role of long noncoding RNAs (lncRNAs) in the development of tumors. In this study, lncRNA LUCAT1 was explored to identify how it affected the progression of cervical cancer. Patients and methods: Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect LUCAT1 expression in both cervical cancer cells and tissue samples. Moreover, the associations between LUCAT1 expression level and patients' overall survival rate were explored, respectively. In addition, cell proliferation assay and transwell assay were conducted. Furthermore, the underlying mechanism was explored via performing qRT-PCR and Western blot assay. Results: By comparing with the expression level in corresponding ones, the LUCAT1 expression level in cervical cancer samples was significantly higher. Moreover, expression level of LUCAT1 was negatively correlated with patients' overall survival time. In addition, after LUCAT1 was overexpressed, cell proliferation, cell invasion and migration capacities were promoted in vitro. In addition, the mRNA and protein expressions of MTA1 were upregulated after LUCAT1 was overexpressed. Furthermore, it was found that the expression level of MTA1 was positively related to LUCAT1 expression level in cervical cancer tissues. Conclusions: We showed that LUCAT1 could enhance proliferation, invasion and migration of cervical cancer cells through upregulating MTA1, which might offer a potential therapeutic choice for patients with cervical cancer. 

Retracted: Yes

PubPeer comments:
 ![file] ![file] In this article, some panel of Figure2A and Figure4A are identical, however, the experiment group is different. , 
 ![file] ![file] Some panels of these two figures are identical. , 
 ![file] ,
Locating primary somatosensory cortex in human brain stimulation studies: systematic review and meta-analytic evidence
Authors: Nicholas Paul Holmes
Luigi Tamè
Journal: Journal of Neurophysiology (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: MRI; S1; SI; TDCS; TMS.
Affiliations: School of Psychology, University of Nottingham, University Park , Nottingham , United Kingdom., Department of Psychological Sciences, Birkbeck University of London , London , United Kingdom.

Abstract:  Transcranial magnetic stimulation (TMS) over human primary somatosensory cortex (S1), unlike over primary motor cortex (M1), does not produce an immediate, objective output. Researchers must therefore rely on one or more indirect methods to position the TMS coil over S1. The "gold standard" method of TMS coil positioning is to use individual functional and structural magnetic resonance imaging (f/sMRI) alongside a stereotactic navigation system. In the absence of these facilities, however, one common method used to locate S1 is to find the scalp location that produces twitches in a hand muscle (e.g., the first dorsal interosseus, M1-FDI) and then move the coil posteriorly to target S1. There has been no systematic assessment of whether this commonly reported method of finding the hand area of S1 is optimal. To do this, we systematically reviewed 124 TMS studies targeting the S1 hand area and 95 fMRI studies involving passive finger and hand stimulation. Ninety-six TMS studies reported the scalp location assumed to correspond to S1-hand, which was on average 1.5-2 cm posterior to the functionally defined M1-hand area. Using our own scalp measurements combined with similar data from MRI and TMS studies of M1-hand, we provide the estimated scalp locations targeted in these TMS studies of the S1-hand. We also provide a summary of reported S1 coordinates for passive finger and hand stimulation in fMRI studies. We conclude that S1-hand is more lateral to M1-hand than assumed by the majority of TMS studies. 

Retracted: No

PubPeer comments:
 Fig 1 - more similar than expected (contrast enhanced) ![file] ,
Heat shock factor 1 upregulates transcription of Epstein–Barr Virus nuclear antigen 1 by binding to a heat shock element within the BamHI-Q promoter
Authors: Feng-Wei Wang
Wen-Ju Liu
Shi-Juan Mai
Yong-Sheng Zong
Mu-Sheng Zeng
Sheng Lin
Xian-Rui Wu
Yi-Ji Liao
Yi-Xin Zeng
Dan Xie
Journal: Virology (2011)
Discipline: MICROBIOLOGY
Keywords: Epstein-Barr virus; EBNA1; heat treatment; transcription; Cp
Affiliations: The State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou, China.

Abstract:  Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) is essential for maintenance of the episome and establishment of latency. In this study, we observed that heat treatment effectively induced EBNA1 transcription in EBV-transformed B95-8 and human LCL cell lines. Although Cp is considered as the sole promoter used for the expression of EBNA1 transcripts in the lymphoblastoid cell lines, the RT-PCR results showed that the EBNA1 transcripts induced by heat treatment arise from Qp-initiated transcripts. Using bioinformatics, a high affinity and functional heat shock factor 1 (HSF1)-binding element within the -17/+4 oligonucleotide of the Qp was found, and was determined by electrophoretic mobility shift assay and chromatin immunoprecipitation assay. Moreover, heat shock and exogenous HSF1 expression induced Qp activity in reporter assays. Further, RNA interference-mediated HSF1 gene silencing attenuated heat-induced EBNA1 expression in B95-8 cells. These results provide evidence that EBNA1 is a new target for the transcription factor HSF1. 

Retracted: No

PubPeer comments:
null, 
 This article was selected for a replication project that replicated social science studies published in Science and Nature. The main finding did not replicate in a much larger sample. Thus, this article should not be cited as evidence for the claims made in this article. Camerer CF, Dreber A, Holzmeister F, Ho T-H, Huber J, Johannesson M, et al. Evaluating the replicability of social science experiments in Nature and Science between 2010 and 2015. Nat Hum Behav. 2018; 2: 637u2013644. https: doi.org 10.1038 s41562-018-0399-z Peers also had low confidence in the replicability of this study (38%). Gordon M, Viganola D, Dreber A, Johannesson M, Pfeiffer T (2021) Predicting replicabilityu2014Analysis of survey and prediction market data from large-scale forecasting projects. PLoS ONE 16(4): e0248780. https: doi.org 10.1371 journal.pone.0248780 ,
A novel biocompatible, simvastatin-loaded, bone-targeting lipid nanocarrier for treating osteoporosis more effectively
Authors: Shan Tao
Fang-Ying Yu
Wen-Tao Zhou
Guo-Xi Qiu
Hong Yuan
Lu Bao
Fu-Qiang Hu
Qing Qiao
Jian-Wei Wang
Shao-Qing Chen
Journal: RSC Advances (2020)
Discipline: CHEMISTRY
Keywords: Osteoporosis treatment; Simvastatin; Lipid nanoparticles; Bone-targeting moieties; BMP-Smad signaling pathway
Affiliations: College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China, Anesthesia Department, Zhejiang University School of Medicine, Sir Run Run Shaw Hospital, Department of Orthopaedics, The Second Affiliated Hospital of Zhejiang University School of Medicine

Abstract:  An insufficient drug concentration at the target site and drug efflux resulting in poor efficacy are recognized as important obstacles in osteoporosis treatment. Simvastatin (SIM), which can treat osteoporosis by promoting osteoblast differentiation and mineralization through the bone morphogenetic proteins (BMP)-Smad signaling pathway, has lower bioavailability, and less bone tissue distribution. Herein, novel lipid nanoparticles (LNPs) delivering SIM (SIM/LNPs) for osteoporosis therapy were developed with aspartic oligopeptide (ASP n , here ASP6)-based bone-targeting moieties grafted to the nanoparticles (SIM/ASP6-LNPs) in an attempt to increase the concentration of SIM in bones with a relatively low dose to minimize adverse effects. In vivo experiments indicated that the ASP6-LNPs exhibited ideal bone-targeting characteristics, and in vitro cell evaluation experiments showed LNPs have good biocompatibility with MC3T3-E1 cells. The cell mineralization experiment revealed that the SIM-loaded LNPs induced osteoblast differentiation and the formation of mineralized nodules in MC3T3-E1 cells, achieving the same efficacy as that of SIM. Pharmacodynamic experiments revealed that SIM/ASP6-LNPs improved the efficacy of SIM on the recovery of bone mineral density when compared to SIM/LNPs or to SIM alone. Therefore, SIM/ASP6-LNPs may represent a potential bone-targeting drug delivery system (DDS) that contributes to the development of a novel osteoporosis treatment. 

Retracted: No

PubPeer comments:
 Some mistakes were made it seems for Figure 7 and 9. ![file] , 
 #1 Dear Dicksonia Gigantea: We greatly appreciate your carefulness and we are very sorry for our negligence. For Figure7, we took the wrong slice of the SIM ASP6-LNPs group, that is ,we regarded the Sham group as the SIM ASP6-LNPs group. We re-observed the SIM ASP6-LNPs group under a light microscope (Nikon, ECLIPSE Ni) and we have readjusted Figure7 in the attached file.![file] For Figure 9, We are so sorry because of our carelessness that we added the wrong image and we also rescaled Figure 9 in the attached file. ![file] These changes will not influence the framework and conclusion of the paper. Once again, thank you very much for your comments . Best regards, Sincerely yours Hong Yuan, Ph. D. Professor College of Pharmaceutical Sciences, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, China E-mail: yuanhong70@zju.edu.cn ,
LncRNA LINC01503 aggravates the progression of cervical cancer through sponging miR-342-3p to mediate FXYD3 expression
Authors: Jinyu Gao
Yumei Zhang
Xing Peng
Chunyan Cai
Journal: Bioscience reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CC; FXYD3; LINC01503; miR-342-3p.
Affiliations: Department of Gynaecology, the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No.6 Beijing West Road, Huaian, 223300, Jiangsu, China.

Abstract:  Cervical cancer (CC), an aggressive malignancy, has a high risk of relapse and death, mainly occurring in females. Accumulating investigations have confirmed the critical role of long noncoding RNAs (lncRNAs) in diverse cancers. LncRNA LINC01503 has been reported as an oncogene in several cancers. Nonetheless, its role and molecular mechanism in CC have not been explored. In the present study, we found that FXYD3 expression was considerably up-regulated in CC tissues and cells. Moreover, FXYD3 deficiency conspicuously hampered cell proliferation and migration while facilitated cell apoptosis in CC cells. Subsequently, molecular mechanism experiments implied that FXYD3 was a downstream target gene of miR-342-3p, and FXYD3 expression was reversely mediated by miR-342-3p. Moreover, we discovered that LINC01503 acted as the endogenous sponge for miR-342-3p. Besides, LINC01503 negatively regulated miR-342-3p expression and positively regulated FXYD3 expression in CC. Rescue assays revealed that LINC01503 depletion-induced repression on CC progression could be partly recovered by miR-342-3p inhibition, and then the co-transfection of sh-FXYD3#1 rescued this effect. Conclusively, LINC01503 aggravated CC progression through sponging miR-342-3p to mediate FXYD3 expression, providing promising therapeutic targets for CC patients. 

Retracted: No

PubPeer comments:
 Sorry, I retract my comment. Not sure how to delete. ,
Transcriptional regulation of th2 differentiation by inducible costimulator
Authors: Umberto Dianzani
Chen Dong
Hiroko Kishikawa
Roza I Nurieva
I cheng Ho
Richard A Flavell
Julie Duong
Jose M Rojo
Journal: Immunity (2003)
Discipline: IMMUNOLOGY
Keywords: Helper T cell differentiation; transcriptional changes; costimulatory receptors; ICOS; Th2 differentiation
Affiliations: Department of Immunology, University of Washington School of Medicine, Seattle, WA 98195, USA.

Abstract:  Helper T (Th) cell differentiation is accompanied by complex transcriptional changes. Although costimulatory receptors are important in Th differentiation, the underlying mechanisms are poorly understood. Here we examine the transcriptional mechanisms by which ICOS regulates Th2 differentiation and selective IL-4 expression by effector T cells. We found impaired expression of c-Maf transcription factor functionally associated with the IL-4 defect in ICOS(-/-) cells. c-Maf expression in effector cells was regulated by IL-4 levels during Th differentiation. ICOS costimulation potentiated the T cell receptor (TcR)-mediated initial IL-4 production, possibly through the enhancement of NFATc1 expression. These data indicate that ICOS, by enhancing TcR signals at an early stage of T cell activation, regulates IL-4 transcription and T cell function in effector cells. 

Retracted: No

PubPeer comments:
 Retracted [6 December 2021] . Part of a collection on  [Big Data and Intelligent Computing Techniques in Geosciences]  , edited by Ahmed Farouk.  The Editor-in-Chief and the Publisher have retracted this article because the content of this article is nonsensical. The peer review process was not carried out in accordance with the Publisher s peer review policy. The author has not responded to correspondence regarding this retraction. ,
Fluorescence in situ hybridization microscopic detection of Bacilli Calmette Guérin mycobacteria in aortic lesions: A case report
Authors: Nadia Saidani
Florent Darriet
Paola Bernioles
Carole Eldin
Michel Drancourt
Ahmed Loukil
Journal: Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: BCG; arterial aneurysm; diagnosis; intravesical instillation; vaccine
Affiliations: Microbiology Laboratory Infectious Disease Department, Assistance Publique -Hôpitaux de Marseille Aix-Marseille University, Institut de Recherche pour le Développement, Microbes, Evolution, Phylogénie, Infections, Institut Hospitalier Universitaire Méditerranée-Infection, Marseille, France.

Abstract:  Rationale: To improve the diagnosis of life-threatening Bacilli Calmette Guérin (BCG) arterial aneurysm in patients treated by intravesical instillation of BCG vaccine as adjunctive therapy for non-muscular bladder carcinoma, is a life-threatening condition. Its diagnosis remains cumbersome. Patient concerns: One patient with a history of intravesical BCG installation presented with aortic aneurysm with routine microscopic examination after Ziehl-Neelsen staining remaining negative. Diagnoses: We used fluorescence in situ hybridization (FISH) to target the Mycobacterium tuberculosis complex rpob gene in a fresh aortic specimen. FISH yielded fluorescent mycobacteria in aortic lesions; mycobacteria were further confirmed as Mycobacterium bovis BCG mycobacteria by polymerase chain reaction (PCR) sequencing. Interventions: The patient benefited from an antituberculous treatment combining rifampicin, isoniazid, and ethambunol. Outcome: A 9-month follow-up indicated a favorable outcome. Lessons: This case report teaches that FISH targeting the M tuberculosis complex rpoB gene should be incorporated in the laboratory investigation of aortic aneurysm in patients with a history of bladder carcinoma. 

Retracted: No

PubPeer comments:
 Fig 2a . Detection of TH level in the substantia nigra of rats in each group by immunohistochemistry . I have marked some overlaps between panels, undermining trust in the scale bars. Of special interest is the partial overlap between the Normal and sh-BACE1-AS panels, where the overlap **should** continue below the red boxes, but does not. ![file] , 
 Fig 2d. Repeated graphic elements in one panel do not inspire trust in the other panels. ![file] ![file] , 
 Fig 3. I have concerns. ![file] Some panels of 3a... ![file] Three more panels, with an overlap and an internal repetition. ![file] Two panels of Fig 3c. I have marked one repeated pair of cells, and increased contrast to make the  cloning halos around some of the other repetitions even more obvious. ![file] The right-hand panel of 3c. I could continue, but I have probably already spent more time on this figure than was spent in creating it. ![file] , 
  Acknowledgments We would like to acknowledge the reviewers for their helpful comments on this pap. *[sic]* Imagine what Figures 2 and 3 of the pap looked like before the reviewers helpful comments. ,
Intraperitoneal Tenckhoff catheter for the treatment of recurrent lymphoceles after kidney transplantation: our early experience
Authors: D Montanaro
G L Adani
P Tulissi
A Risaliti
V Bresadola
D Lorenzin
M Sponza
E Benzoni
U Baccarani
D De Anna
D Gasparini
Journal: Transplantation proceedings (0)
Discipline: CLINICAL MEDICINE
Keywords: Lymphocele; Kidney transplantation; Percutaneous drainage; Tenckhoff catheter; Recurrence
Affiliations: Department of Surgery & Transplantation, Udine University School of Medicine, Udine, Italy. 

Abstract:  Lymphoceles may occur as frequently as 16% of the time after kidney transplantation, becoming clinically evident between 18 and 180 days after surgery. The management of lymphoceles is unclear. Percutaneous needle aspiration and external drainage are associated with high recurrence and complications. Surgical intraperitoneal marsupialization of lymphocele is considered the treatment of choice, but requires hospital admission, general anesthesia, and sometimes extensive surgical dissection. We discuss our experience in the treatment of recurrent symptomatic lymphocele intraperitoneally drained using a Tenckhoff catheter in 7 consecutive patients. Clinical manifestations became evident between 26 and 90 days after transplantation. The diagnosis was obtained with abdominal ultrasound in all cases; mean lymphocele diameter was 14 +/- 6 cm. After percutaneous drainage, performed to differentiate urinoma/lymphocele and to rule out infections, the lymphocele recurred within 1 month. Thereafter, we decided to treat recurrent lymphatic collection using a Tenckhoff catheter. The lymphocele was located during the operative procedure using a sterile 3.5-MHz ultrasound probe. With the patient under local anesthesia, we performed 2 vertical 1-cm incisions to the lymphocele and peritoneum, respectively. The Tenckoff catheter was first positioned into the lymphocele and the tunneled inside the peritoneal cavity. One cuff of the Tenckhoff was fixed to the fascia to avoid possible delocalization. The patients were discharged the same day. The catheter was removed 6 months later with no evidence of lymphocele recurrence. 

Retracted: No

PubPeer comments:
 This article reports the same results as another paper published by the same team: **Adani GL, Baccarani U, Risaliti A, et al. Treatment of recurrent symptomatic lymphocele after kidney transplantation with intraperitoneal Tenckhoff catheter. Urology. 2007;70(4):659-661. doi:[10.1016 j.urology.2007.05.018] ** Did the authors inform the editors-in-chief of Transplantation Proceedings and Urology about submitting the same results in slightly different manuscripts to both journals which seems to be against their policies? Was potential self-plagiarism verified? ,
<p>Tizanidine (Hydrochloride) Inhibits A549 Lung Cancer Cell Proliferation and Motility Through Regulating Nischarin</p>
Authors: Liang Zhao
Gefei Zhao
Qi Xue
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: A549; AKT pathway; Tizanidine; apoptosis; lung cancer.
Affiliations: Department of Thoracic Surgery, Cancer Hospital, Chinese Academy of Medical Sciences, Beijing 100021, People's Republic of China.

Abstract:  Purpose: Tizanidine hydrochloride (TZN) is a centrally acting α2-adrenergic agonist. In this study, we aimed to explore the role of TZN on human lung cancer and to elucidate its underlying mechanisms. Methods: The effect of TZN treatment in A549 cell proliferation, migration, invasion and apoptosis was evaluated by CCK8, transwell and flow cytometer assays. The expression of apoptosis-related proteins and the activation of AKT and Wnt3a/β-catenin pathways were detected by Western blot. From the data of DrugBank, TZN could act as an agonist to target Nischarin in humans. We next investigated the function of Nischarin receptor in lung cancer and its role in the anti-tumor activity of TZN. Results: The treatment of TZN inhibited the proliferation, migration and invasion of A549 cells, and induced apoptosis. These results were further confirmed by that TZN treatment increased the Bax/Bcl-2 ratio in A549 cells. We also observed that TZN treatment changed the expression and phosphorylation of proteins of AKTand Wnt3a/β-catenin signaling pathway members. By bioinformatics analysis, we found that Nischarin was down-regulated in human lung cancer tissues and patients with high Nischarin expression had a better survival. Moreover, Nischarin functioned as a tumor suppressor in the survival and metastasis of A549 cells through the regulation of AKT and Wnt3a/β-catenin pathways. Knockdown of Nischarin promoted the proliferation, invasion, migration of A549 cells and inhibited the apoptosis, which were reversed by the TZN treatment. Conclusion: Summary, our data revealed that treatment of TZN inhibited the growth of lung cancer cell line A549 and may be used as a novel strategy for lung cancer therapy. 

Retracted: No

PubPeer comments:
 Figure1D and Figure1E ![file] ,
JNK contributes to the tumorigenic potential of human cholangiocarcinoma cells through the mTOR pathway regulated GRP78 induction
Authors: Chunyan Zhang
Run Chen
Yuxiao Li
Mei Wei
Xianming Xia
Youping Liu
Chunhong Feng
Song Su
Kai He
Chun-Yan Duan
Shaokun Chen
Rongyang Dai
Bo Li
Hong Li
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: JNK; cholangiocarcinoma; mTOR; GRP78; eIF2α
Affiliations: Department of Hepatobiliary Surgery of the Affiliated Hospital, Luzhou Medical College, Luzhou, Sichuan, China., Department of Biochemistry and Molecular Biology, Luzhou Medical College, Luzhou, Sichuan, China., Department of Public Health, Luzhou Medical College, Luzhou, Sichuan, China., Affiliated Hospital of Chinese Traditional Medicine, Luzhou Medical College, Luzhou, Sichuan, China., Department of Hepatobiliary Surgery of the Affiliated Hospital, Luzhou Medical College, Luzhou, Sichuan, China ; Department of Biochemistry and Molecular Biology, Luzhou Medical College, Luzhou, Sichuan, China.

Abstract:  Less is known about the roles of c-Jun N-terminal kinase (JNK) in cholangiocarcinoma (CCA). Here, we report that JNK exerts its oncogenic action in human CCA cells, partially due to the mammalian target of rapamycin (mTOR) pathway regulated glucose-regulated protein 78 (GRP78) induction. In human CCA cells, the phosphorylation of eukaryotic initiation factor alpha (eIF2α) results in the accumulation of activating transcription factor 4 (ATF4) and GRP78 independent of unfolded protein response (UPR). Suppression of GRP78 expression decreases the proliferation and invasion of human CCA cells. It's notable that mTOR is required for eIF2α phosphorylation-induced ATF4 and GRP78 expression. Importantly, JNK promotes eIF2α/ATF4-mediated GRP78 induction through regulating the activity of mTOR. Thus, our study implicates JNK/mTOR signaling plays an important role in cholangiocarcinogenesis, partially through promoting the eIF2α/ATF4/GRP78 pathway. 

Retracted: No

PubPeer comments:
 * Blue and red arrows: Possible vertical splices and rectangular patches appear to be visible in Figures 1 and 6 * Green boxes: In the p-p70S6K RBE panel in Figure 6A, the same two dots appear to be visible multiple times * Cyan boxes: In the p-p70S6K HCCC-9810 panel in Figure 6A, the same lane appears to be visible twice * Orange boxes: Two adjacent lanes in the mTOR panel in Figure 6B appear to look more similar to each other than expected Reported to the journal in October 2015, but no action taken as of today. ![file] ,