PReD-Bench/PRed-Bench huggingface dataset:
Chemotherapeutic potential of curcumin-bearing microcells against hepatocellular carcinoma in model animals
Authors: Qamar Zia
Mohammad Owais
Aijaz Ahmad Khan
Beenu Joshi
Mohammad Farazuddin
Bhavyata Dua
Journal: International Journal of Nanomedicine (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Curcuma longa; cancer; carcinogenesis; diferuloylmethane; microparticle

Abstract:  Curcumin (diferuloylmethane) is found in large quantities in the roots of Curcuma longa. It possesses strong antioxidant and anti-inflammatory properties, and inhibits chemically-induced carcinogenesis in the skin, forestomach, colon, and liver. Unfortunately, the poor bioavailability and hydrophobicity of curcumin pose a major hurdle to its use as a potent anticancer agent. To circumvent some of these problems, we developed a novel, dual-core microcell formulation of curcumin. The encapsulation of curcumin in microcells increases its solubility and bioavailability, and facilitates slow release kinetics over extended periods. Besides being safe, these formulations do not bear any toxicity constraints, as revealed by in vitro and in vivo studies. Histopathological analysis revealed that curcumin-bearing microcells helped in regression of hepatocellular carcinoma and the maintenance of cellular architecture in liver tissue. Free curcumin had a very mild effect on cancer suppression. Empty (sham) microcells and microparticles failed to inhibit cancer cells. The novel curcumin formulation was found to suppress hepatocellular carcinoma efficiently in Swiss albino mice. 

Retracted: No

PubPeer comments:
 Figure 9. * Blue boxes. Panels A (healthy control) and G (PLGA microparticles) appear to show an overlap if one of the panels is rotated 180 degrees. ![file] ,
Four lncRNAs associated with breast cancer prognosis identified by coexpression network analysis
Authors: Xiaoran Ma
Cun Liu
Yan Yao
Huayao Li
Lijuan Liu
Chundi Gao
Xiaoming Zhang
Jie Li
Lingyu Qi
Kejia Wang
Chao Zhou
Jia Li
Changgang Sun
Jing Zhuang
Xue Wang
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: breast cancer; gene coexpression; lncRNA.
Affiliations: College of First Clinical Medicine, Shandong University of Traditional Chinese MedicineJinan Shandong P. R. China, College of Traditional Chinese Medicine, Shandong University of Traditional Chinese MedicineJinan Shandong P. R. China, Department of OncologyWeifang Traditional Chinese HospitalWeifang Shandong P. R. China, Department of OncologyAffiliated Hospital of Weifang Medical UniversityWeifang Shandong P. R. China, Clinical Medical Colleges, Weifang Medical UniversityWeifang Shandong P. R. China, College of Basic Medicine, Qingdao UniversityQingdao Shandong P. R. China

Abstract:  Previous studies on long noncoding RNA (lncRNA) have made breakthroughs in the treatment of several tumors, and these findings have brought attention to the lncRNA signature of breast cancer. Increased understanding of genomic architecture and achievement of innovative therapeutic strategies has prompted creation of a novel oncological model for the treatment of solid cancers. In this study, we systematically analyzed the transcriptome of breast cancer tissues to gain more in-depth knowledge of tumor biology. Gene coexpression relationships were studied in 206 samples from The Cancer Genome Atlas database, and nine coexpression modules were identified. After screening and analysis, we identified four important prognosis-related lncRNAs (HOTAIR, SNHG16, HCP5, and TINCR), and constructed a prognostic model, one (HCP5) of which has not previously been identified in the context of breast cancer. Importantly, an understanding of prognosis facilitates precise disease risk assessment and advances the selection of strategies for risk-adaptive management. These findings broaden the landscape of carcinogenic lncRNAs in breast cancer, providing insights into the biological significance and clinical application of lncRNAs in breast cancer. 

Retracted: No

PubPeer comments:
 Why does the gene heatmap presented in Figure 1 show repetitive unusual patterns? The ROC curves in Figure 9 also need some attention. ![file] ,
Thermostable direct hemolysin downregulates human colon carcinoma cell proliferation with the involvement of E-cadherin, and β-catenin/Tcf-4 signaling
Authors: Nibedita Mahata
Debasis Pore
Manoj K Chakrabarti
Pinki Chowdhury
Amit Pal
Poulomee Karmakar
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Colon cancers; bacterial toxins; Thermostable direct hemolysin (TDH); Vibrio parahaemolyticus; calcium
Affiliations: Division of Pathophysiology, National Institute of Cholera and Enteric Diseases, Beliaghata, Kolkata, India.

Abstract:  Background: Colon cancers are the frequent causes of cancer mortality worldwide. Recently bacterial toxins have received marked attention as promising approaches in the treatment of colon cancer. Thermostable direct hemolysin (TDH) secreted by Vibrio parahaemolyticus causes influx of extracellular calcium with the subsequent rise in intracellular calcium level in intestinal epithelial cells and it is known that calcium has antiproliferative activity against colon cancer. Key results: In the present study it has been shown that TDH, a well-known traditional virulent factor inhibits proliferation of human colon carcinoma cells through the involvement of CaSR in its mechanism. TDH treatment does not induce DNA fragmentation, nor causes the release of lactate dehydrogenase. Therefore, apoptosis and cytotoxicity are not contributing to the TDH-mediated reduction of proliferation rate, and hence the reduction appears to be caused by decrease in cell proliferation. The elevation of E-cadherin, a cell adhesion molecule and suppression of β-catenin, a proto-oncogene have been observed in presence of CaSR agonists whereas reverse effect has been seen in presence of CaSR antagonist as well as si-RNA in TDH treated cells. TDH also triggers a significant reduction of Cyclin-D and cdk2, two important cell cycle regulatory proteins along with an up regulation of cell cycle inhibitory protein p27(Kip1) in presence of CaSR agonists. Conclusion: Therefore TDH can downregulate colonic carcinoma cell proliferation and involves CaSR in its mechanism of action. The downregulation occurs mainly through the involvement of E-cadherin-β-catenin mediated pathway and the inhibition of cell cycle regulators as well as upregulation of cell cycle inhibitors. 

Retracted: No

PubPeer comments:
 ![file] Visible splicing ,
Chitosan and lactic acid-grafted chitosan nanoparticles as carriers for prolonged drug delivery
Authors: Narayan Bhattarai
Miqin Zhang
Hassna R Ramay
Shinn-Huey Chou
Journal: International Journal of Nanomedicine (2006)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Nanoparticles; Chitosan; Lactic acid; Drug loading; Drug release
Affiliations: Department of Material Science and Engineering, University of Washington, Seattle,WA 98195, USA.

Abstract:  Nanoparticles of approximately 10nm in diameter made with chitosan or lactic acid-grafted chitosan were developed for high drug loading and prolonged drug release. A drug encapsulation efficiency of 92% and a release rate of 28% from chitosan nanoparticles over a 4-week period were demonstrated with bovine serum protein. To further increase drug encapsulation, prolong drug release, and increase chitosan solubility in solution of neutral pH, chitosan was modified with lactic acid by grafting D,L-lactic acid onto amino groups in chitosan without using a catalyst. The lactic acid-grafted chitosan nanoparticles demonstrated a drug encapsulation efficiency of 96% and a protein release rate of 15% over 4 weeks. With increased protein concentration, the drug encapsulation efficiency decreased and drug release rate increased. Unlike chitosan, which is generally soluble only in acid solution, the chitosan modified with lactic acid can be prepared from solutions of neutral pH, offering an additional advantage of allowing proteins or drugs to be uniformly incorporated in the matrix structure with minimal or no denaturization. 

Retracted: No

PubPeer comments:
 Figure 3 https: imgur.com a smRJVI4 ,
Securin induces genetic instability in colorectal cancer by inhibiting double-stranded DNA repair activity
Authors: J A Franklyn
M J O Wakelam
A L Stratford
H N Pemberton
J C Watkinson
A Warfield
D S Kim
T Ishmail
C J McCabe
V E Smith
Journal: Carcinogenesis (2006)
Discipline: CLINICAL MEDICINE
Keywords: Genetic instability; Securin; Tumor development; Colorectal tumors; Dukes' stage
Affiliations: Division of Medical Sciences, Institute of Biomedical Research, University of Birmingham B15 2TH, UK.

Abstract:  Genetic instability (GI) is a hallmark feature of tumor development. Securin, also known as pituitary tumor transforming gene (PTTG), is a mitotic checkpoint protein which is highly expressed in numerous cancers, is associated with tumor invasiveness, and induces GI in thyroid cells. We used fluorescence inter-simple sequence repeat PCR to assess GI caused primarily by DNA breakage events in 19 colorectal tumors. GI values ranged significantly, with Dukes' stage C&amp;D colorectal tumors exhibiting greater GI and higher securin expression than Dukes' stage A&amp;B tumors. Consistent with these findings, we observed a dose-dependent increase in GI in HCT116 cells in response to securin overexpression, as well as in non-transformed human fibroblasts. As securin has been implicated in a novel DNA repair pathway in fission yeast, we investigated its potential role in chemotoxic DNA damage response pathways in mammalian cells, using host cell reactivation assays. Securin overexpression in HCT116 cells inhibited etoposide-induced double-stranded DNA damage repair activity, and repressed Ku heterodimer function. Additionally, we observed that securin and Ku70 showed a reciprocal cytosol-nuclear translocation in response to etoposide-induced dsDNA damage. Our data suggest that, by repressing Ku70 activity and inhibiting the non-homologous end-joining dsDNA repair pathway, securin may be a critical gene in the development of GI in colorectal cancer. 

Retracted: No

PubPeer comments:
 Figures 2B and 5C. Much more similar than you would expect. https: imgur.com A6A2EZm ,
Fluoxetine protects against methamphetamine‑induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats
Authors: Yun Wang
Yang Bai
Huai-Liang Wang
Ming Liu
Yu-Han Gu
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Methamphetamine abuse; fluoxetine; pulmonary inflammation; nuclear factor erythroid 2-related factor 2 (Nrf2); antioxidative stress
Affiliations: Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning 110122, P.R. China., Department of Drug Control, China Criminal Police University, Shenyang, Liaoning 110035, P.R. China.

Abstract:  Methamphetamine (MA) abuse is a major public health and safety concern throughout the world and a growing burden on healthcare costs. The purpose of the present study was to investigate the protective effect of fluoxetine against MA‑induced chronic pulmonary inflammation and to evaluate the potential role of nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidative stress. Wistar rats were divided into control, MA and two fluoxetine‑treated groups. Rats in the MA and the two fluoxetine‑treated groups were treated daily with intraperitoneal injection of 10 mg/kg MA twice daily. Rats in the two fluoxetine‑treated groups were injected intragastrically with fluoxetine (2 and 10 mg/kg) once daily, respectively. After 5 weeks, the rats were euthanized and hematoxylin and eosin staining, immunohistochemistry, western blot analysis and redox assay were performed. It was demonstrated that chronic exposure to MA can induce pulmonary inflammation in rats, with the symptoms of inflammatory cell infiltration, crowded lung parenchyma, thickened septum and a reduced number of alveolar sacs. Fluoxetine attenuated pulmonary inflammation and the expression of interleukin‑6 and tumor necrosis factor‑α in rat lungs. Fluoxetine inhibited MA‑induced increases in the expression levels of serotonin transporter (SERT) and p‑p38 mitogen‑activated protein kinase (MAPK), and reversed the MA‑induced decrease in nuclear Nrf2 and human heme oxygenase‑1 in lungs. Fluoxetine at 10 mg/kg significantly reversed the reduced glutathione (GSH) level, the ratio of GSH/oxidized glutathione, and the reactive oxygen species level in rat lungs from the MA group. These findings suggested that fluoxetine, a SERT inhibitor, has a protective effect against MA‑induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats. 

Retracted: No

PubPeer comments:
 There is an instance of image duplication in this paper. Figure 1B and 1C are taken from the same image - see the green boxes. ![file] ,
The circ_0021977/miR-10b-5p/P21 and P53 regulatory axis suppresses proliferation, migration, and invasion in colorectal cancer
Authors: Dawei Rong
Bingqing Hui
Chaoxi Dong
Weiwei Tang
Hongyong Cao
Wei Jiang
Kai Fu
Chen Lu
Journal: Journal of cellular physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: P21; P53; circ_0021977; colorectal cancer; invasion
Affiliations: Department of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China., The Third Clinical Medical College, Nanjing Medical University, Nanjing, Jiangsu, China., Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China., The First Clinical Medical College, Nanjing Medical University, Nanjing, Jiangsu, China.

Abstract:  An in-depth understanding of circular RNAs (circRNAs) indicates that they are abundant in the eukaryotic transcriptome. Many circRNAs act as microRNA sponges; thus, they represent a new type of regulatory factor. However, the role of circRNA in colorectal cancer (CRC) remains largely unknown. Low circ_0021977 expression in patients with CRC is associated with higher tug-lymph node metastasis (TNM) stage and poorer prognosis compared with patients with high circ_0021977 expression. Moreover, miR-10b-5p was shown to be a target of circ_0021977, and p21 and p53 are suggested to be putative target genes of miR-10b-5p. The results showed that the circ_0021977/miR-10b-5p/p21&amp;p53 regulatory axis suppresses proliferation, migration, and invasion by CRC cells. This evidence reveals new relationships and brings new highlights to the treatment of CRC. 

Retracted: No

PubPeer comments:
 Figure 5C * Green boxes: The HCT116 miR-10b-5p panels appears to show an overlap with the SW480 miR-10b-5p panel. ![file] , 
 Corrigendum, October 2020: https: onlinelibrary.wiley.com doi 10.1002 jcp.30072  In (Lu et al., 2020) the following error was published on page 1084 in Figures 1h and 5c. The authors would like to correct Figures 1h and 5c, as errors were introduced in the preparation of these figures for publication. The authors declare that these corrections do not change the results or conclusions of this paper. The corrected figure appears below. The authors apologize for the mistake. ,
Biological characteristics and effect of human umbilical cord mesenchymal stem cells (hUC-MSCs) grafting with blood plasma on bone regeneration in rats
Authors: Zhiguo Qu
Libin Guo
Zhenghong Cui
Ying Liu
Shengnan Guo
Guojun Fang
Journal: Cell Biochemistry and Biophysics (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: hUC-MSCs; bone regeneration; rat tibia nonunion; blood plasma; stem cell transplantation
Affiliations: Department of Orthopaedic Surgery, Siping Central Hospital, Siping, Jilin, China.

Abstract:  We evaluated the biological characteristics/effect of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) grafting with blood plasma on bone regeneration in rat tibia nonunion. SD rats (142) were randomly divided into four groups: fracture group (positive control); nonunion group (negative control); hUC-MSCs grafting with blood plasma group; and hUC-MSCs grafting with saline group. Rats were administered tetracycline (30 mg/kg) and calcein blue (5 mg/kg) 8 days before killing. The animals were killed under deep anesthesia at 4 and 8 weeks post fracture for radiological evaluation and histological/immunohistological studies. The hUC-MSCs grafting with blood plasma group was similar to fracture group: the fracture line blurred in 4 weeks and disappeared in 8 weeks postoperatively. Histological/immunohistological studies showed that hUC-MSCs were of low immunogenicity which merged in rat bone tissue, differentiated into osteogenic lineages, and completed the healing of nonunion. After stem cell transplantation, regardless of whether plasma or saline was used, new multi-center bone formation was observed; fracture site density was better in stem cell grafting with blood plasma group. We, therefore, concluded that the biological characteristics of hUC-MSCs-treated nonunion were different from the standard fracture healing process, and the proliferative and localization capacity of hUC-MSCs might benefit from the use of blood plasma. 

Retracted: No

PubPeer comments:
 Figure 3 appears to include a repeated image, representing two different time points. *** Original ![file] *** Enhanced brightness ![file] ,
Fhit interaction with ferredoxin reductase triggers generation of reactive oxygen species and apoptosis of cancer cells
Authors: Francesco Trapasso
Rami I Aqeilan
Hiroshi Okumura
Rodolfo Iuliano
Eugenio Gaudio
Marco Gaspari
Kari Green-Church
Flavia Pichiorri
David E Birk
Salvatore Venuta
Luigi G Spagnoli
Kay Huebner
Carlo M Croce
Tiziana Palumbo
Cinzia Raso
Muller Fabbri
Giampiero Di Leva
Journal: Journal of Biological Chemistry (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Fhit protein; tumorigenicity; apoptosis; proteomics; Hsp60
Affiliations: Ohio State University, Comprehensive Cancer Center, Columbus, Ohio 43210, USA.

Abstract:  Fhit protein is lost in most cancers, its restoration suppresses tumorigenicity, and virus-mediated FHIT gene therapy induces apoptosis and suppresses tumors in preclinical models. We have used protein cross-linking and proteomics methods to characterize a Fhit protein complex involved in triggering Fhit-mediated apoptosis. The complex includes Hsp60 and Hsp10 that mediate Fhit stability and may affect import into mitochondria, where it interacts with ferredoxin reductase, responsible for transferring electrons from NADPH to cytochrome P450 via ferredoxin. Viral-mediated Fhit restoration increases production of intracellular reactive oxygen species, followed by increased apoptosis of lung cancer cells under oxidative stress conditions; conversely, Fhit-negative cells escape apoptosis, carrying serious oxidative DNA damage that may contribute to an increased mutation rate. Characterization of Fhit interacting proteins has identified direct effectors of the Fhit-mediated apoptotic pathway that is lost in most cancers through loss of Fhit. 

Retracted: Yes

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
 2017 retraction. http: www.jbc.org content 292 34 14279 , 
  This work was supported, in whole or in part, by National Institutes of Health Grants CA77738 and CA78890.  , 
 Paper on same molecule by same group corrected 2016. https: pubpeer.com publications 6093A3FE962827D8104FFC912725C7 , 
 http: radio.wosu.org post amid-ethics-concerns-ohio-state-stands-behind-researcher-carlo-croce#stream 0 , 
 http: retractionwatch.com 2017 08 29 carlo-croce-osu-cancer-researcher-investigation-retracts-paper , 
null, 
 https: retractionwatch.com 2021 02 04 litigious-osu-professor-loses-appeal-in-federal-defamation-case ,
Localisation of PGK1 determines metabolic phenotype to balance metastasis and proliferation in patients with SMAD4-negative pancreatic cancer
Authors: Si Shi
Qingcai Meng
Chen Liang
Bo Zhang
Jie Hua
Jin Xu
Xian-Jun Yu
Qiangshen Hu
Shunrong Ji
Yi Qin
Journal: Gut (2020)
Discipline: CLINICAL MEDICINE
Keywords: PGK1; SMAD4; metabolic phenotype; metastasis; pancreatic cancer.
Affiliations: Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China., Department of Oncology, Shanghai Medical College Fudan University, Shanghai, China., Pancreatic Cancer Institute, Fudan University, Shanghai, China., Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China .

Abstract:  Objective: Pancreatic ductal adenocarcinoma (PDAC) is the most aggressive type of GI tumour, and it possesses deregulated cellular energetics. Although recent advances in PDAC biology have led to the discovery of recurrent genetic mutations in Kras, TP53 and SMAD4, which are related to this disease, clinical application of the molecular phenotype of PDAC remains challenging. Design: We combined molecular imaging technology (positron emission tomography/CT) and immunohistochemistry to evaluate the correlation between the maximum standardised uptake value and SMAD4 expression and examined the effect of SMAD4 on glycolysis through in vitro and in vivo experiments. Furthermore, we identified the effect of SMAD4 on metabolic reprogramming by metabolomics and glucose metabolism gene expression analyses. Dual luciferase reporter assays and chromatin immunoprecipitation were performed to identify whether SMAD4 functioned as a transcription factor for phosphoglycerate kinase 1 (PGK1) in PDAC cells. Proliferative and metastatic assays were performed to examine the effect of PGK1 on the malignant behaviour of PDAC. Results: We provide compelling evidence that the glycolytic enzyme PGK1 is repressed by transforming growth factor-β/SMAD4. Loss of SMAD4 induces PGK1 upregulation in PDAC, which enhances glycolysis and aggressive tumour behaviour. Notably, in SMAD4-negative PDAC, nuclear PGK1 preferentially drives cell metastasis via mitochondrial oxidative phosphorylation induction, whereas cytoplasmic PGK1 preferentially supports proliferation by functioning as a glycolytic enzyme. The PDAC progression pattern and distinct PGK1 localisation combine to predict overall survival and disease-free survival. Conclusion: PGK1 is a decisive oncogene in patients with SMAD4-negative PDAC and can be a target for the development of a therapeutic strategy for SMAD4-negative PDAC. 

Retracted: No

PubPeer comments:
 Figure 4. Cell migration 0h sample images of u201cindependent experimentsu201d appear to repeat and or overlap with orientation changes. Red images appear identical, yellow images are flipped. See marked features. Caption included for convenience. *** ![file] , 
 Figures 4C and 5D appear to have an image which overlaps. I believe there are more image issues in this paper. *** ![file] ![file] ,
Microfluidic Immunoassays for Sensitive and Simultaneous Detection of IgG/IgM/Antigen of SARS-CoV-2 within 15 min
Authors: Liling Liu
Jilie Kong
Xueen Fang
Donghua Wen
Jing Wu
Wenjuan Wu
Qiuyuan Lin
Journal: Analytical Chemistry (2020)
Discipline: CHEMISTRY
Keywords: SARS-CoV-2; microfluidic immunoassay system; IgG; IgM; Antigen
Affiliations: Shanghai Suxin Biotechnology Co. Ltd., Shanghai 201318, P. R. China., NingBo iGeneTec Technology Co. Ltd., Ningbo 315000, P. R. China., Department of Chemistry and Institutes of Biomedical Sciences, Fudan University, Shanghai 200433, P. R. China., Department of Laboratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200123, P. R. China.

Abstract:  The outbreak of SARS-CoV-2 is posing serious global public health problems. Facing the emergence of this pandemic, we established a portable microfluidic immunoassay system for easy-to-use, sensitive, rapid (&lt;15 min), multiple, and on-site detection of IgG/IgM/Antigen of SARS-CoV-2 simultaneously. This integrated method was successfully applied for detecting SARS-CoV-2 IgM and IgG antibodies in clinical human serum as well as SARS-CoV-2 antigen in pharyngeal swabs from 26 patients with COVID-19 infection and 28 uninfected people. The assay demonstrated high sensitivity and specificity, which is promising for the diagnosis and monitoring as well as control of SARS-CoV-2 worldwide. 

Retracted: No

PubPeer comments:
 There seems to be a problem with references, as references 17-20 (at least) do not match the text they are appended to. ,
Retraction: Walach et al. The Safety of COVID-19 Vaccinations—We Should Rethink the Policy. Vaccines 2021, 9, 693
Authors: Vaccines Editorial Office
Journal: Vaccines (2021)
Discipline: IMMUNOLOGY
Keywords: COVID-19 Vaccinations; Safety; Misinterpretation; Data; Errors
Affiliations: MDPI, St. Alban-Anlage 66, 4052 Basel, Switzerland.

Abstract:  The journal retracts the article, The Safety of COVID-19 Vaccinations-We Should Rethink the Policy [1], cited above. Serious concerns were brought to the attention of the publisher regarding misinterpretation of data, leading to incorrect and distorted conclusions. The article was evaluated by the Editor-in-Chief with the support of several Editorial Board Members. They found that the article contained several errors that fundamentally affect the interpretation of the findings. These include, but are not limited to: The data from the Lareb report (https://www.lareb.nl/coronameldingen) in The Netherlands were used to calculate the number of severe and fatal side effects per 100,000 vaccinations. Unfortunately, in the manuscript by Harald Walach et al. these data were incorrectly interpreted which led to erroneous conclusions. The data was presented as being causally related to adverse events by the authors. This is inaccurate. In The Netherlands, healthcare professionals and patients are invited to report suspicions of adverse events that may be associated with vaccination. For this type of reporting a causal relation between the event and the vaccine is not needed, therefore a reported event that occurred after vaccination is not necessarily attributable to vaccination. Thus, reporting of a death following vaccination does not imply that this is a vaccine-related event. There are several other inaccuracies in the paper by Harald Walach et al. one of which is that fatal cases were certified by medical specialists. It should be known that even this false claim does not imply causation, which the authors imply. Further, the authors have called the events 'effects' and 'reactions' when this is not established, and until causality is established they are 'events' that may or may not be caused by exposure to a vaccine. It does not matter what statistics one may apply, this is incorrect and misleading. The authors were asked to respond to the claims, but were not able to do so satisfactorily. The authors were notified of the retraction and did not agree. 

Retracted: No

PubPeer comments:
 Listed as #3 at https: www.the-scientist.com news-opinion the-top-retractions-of-2021-69533 See https: pubpeer.com publications EFDB755C20C351E0077D38D67B933F for backgrounds. ,
Downregulation of microRNA-122 promotes proliferation, migration, and invasion of human hepatocellular carcinoma cells by activating epithelial&ndash;mesenchymal transition
Authors: Nanyao Wang
Xiangming Cao
Dan Wu
Dong Shen
Qiong Wang
Xia Sun
Journal: OncoTargets and Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: HepG2 cells; Wnt1; epithelial mesenchymal transition; invasion; microRNA-122
Affiliations: Department of Oncology, The Affiliated Jiangyin Hospital, School of Medicine, Southeast University, Jiangyin, Jiangsu, People's Republic of China.

Abstract:  Objective: To investigate the effects of microRNA-122 (miR-122) on proliferation, migration, and invasion in human hepatocellular carcinoma (HCC) cells by activating epithelial-mesenchymal transition (EMT) pathways. Methods: miR-122 mimics, miR-122 inhibitors, relevant control oligonucleotides, and Wnt1 were transfected into HepG2 and huh7 cell lines which were then divided into six groups: miR-122 group, anti-miR-122 group, miR-negative control (NC) group, anti-miR-NC group, miR-122 + Wnt1 group, and miR-122 + vector group. The miR-122 expressions and mRNA expressions of Wnt1 and EMT-related genes (E-cadherin, vimentin, β-cadherin, and N-cadherin) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR). Protein expression levels of Wnt1, E-cadherin, vimentin, β-cadherin, and N-cadherin were measured by Western blot. Cell proliferation, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, wound-healing assay, and Transwell assay, respectively. Results: Dual luciferase reporter gene results showed that Wnt1 is a direct target gene of miR-122 in both HepG2 and huh7 cell lines. Compared to miR-NC, anti-miR-NC, and miR-122 + Wnt1 groups, miR-122 expression was markedly higher in the miR-122 group and miR-122 + vector group, but was sharply decreased in anti-miR-122 group (both P&lt;0.05), and the mRNA and protein levels of Wnt1, vimentin, β-cadherin, and N-cadherin decreased significantly; also E-cadherin increased, and cell proliferation, migration, and invasion decreased in the miR-122 group and miR-122 + vector group (all P&lt;0.05), but the situation was totally reversed in the anti-miR-122 group (all P&lt;0.05). Conclusion: Downregulation of miR-122 promoted proliferation, migration, and invasion of human HCC cells by targeting Wnt1 and regulating Wnt/β-catenin pathway which activated the EMT pathways. 

Retracted: No

PubPeer comments:
 There are multiple examples of repeated features within and between images in this art project, including some areas that look like alien crop circles (not identified). TAM. It appears that the PubPeer system has the corresponding authoru2019s given name wrong. *** Figure 6 ![file] *** Figure 8D ![file] ,
Contribution of the P2X4 Receptor in Rat Hippocampus to the Comorbidity of Chronic Pain and Depression
Authors: Shangdong Liang
Guilin Li
Runan Yang
Jingjian Yang
Xiumei Xu
Zijing Li
Guodong Li
Minghao Sun
Rolf-Detlef Treede
Baoe Liu
Wolfgang Greffrath
Shuangmei Liu
Yuting Zou
Lin Li
Journal: ACS Chemical Neuroscience (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: P2X4 receptor; comorbidity of pain and depression; hippocampus; neuropathic pain; unpredictable chronic mild stress.
Affiliations: Neuropharmacology Laboratory of Physiology Department, Basic Medical College of Nanchang University, Nanchang 330006, People’s Republic of China, Medical School of Nanchang University, Nanchang, Jiangxi 330006, People’s Republic of China, Queen Marie College of Nanchang University, Medical College of Nanchang University, Nanchang, 330008, People’s Republic of China, Department of Neurophysiology, Centre for Biomedicine and Medical Technology Mannheim, Heidelberg University, Mannheim 68167, Germany

Abstract:  The hippocampus is an important region for the interaction between depression and pain. Studies show that the P2X4 receptor plays key role in neuropathic pain. This work investigated the potential implication of the P2X4 receptor in the hippocampus in comorbidity of chronic pain and depression. The rat model induced by chronic constriction injury (CCI) plus unpredictable chronic mild stress (UCMS) was used in this study. Our data showed that CCI plus UCMS treatment resulted in abnormal changes in pain and depressive-like behaviors in the rat, accompanied by the upregulated expression of P2X4, NLRP3 (NOD-like receptor protein 3) inflammasome, and interleukin-1β and the activation of p38 MAPK in the hippocampus. The P2X4 antagonist 5-BDBD reversed these abnormal changes in the hippocampus, relieved hippocampal neuronal damage, and alleviated the abnormal pain and depressive-like behaviors in the CCI plus UCMS treated rats. These findings suggest that the P2X4 receptor in the hippocampus may mediate and significantly contribute to the pathological processes of comorbid pain and depression. 

Retracted: No

PubPeer comments:
 Figure 1H: two micrographs have been duplicated and presented as something else. Figure 2D: a micrograph has been duplicated and presented as something else. ![file] ,
Long intergenic non-protein coding RNA 960 regulates cancer cell viability, migration and invasion through modulating miR-146a-5p/interleukin 1 receptor associated kinase 1 axis in pancreatic ductal adenocarcinoma
Authors: Qingqing Yan
Yaoxing Huang
Danchun Yu
Xiaojuan Sun
Shuman Jiang
Weidong Li
Lin Jia
Journal: Bioengineered (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: IRAK1; LINC00960; miR-146a-5p; pancreatic ductal adenocarcinoma.
Affiliations: Department of Gastroenterology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology , Guangzhou, China.

Abstract:  Long non-coding RNAs (lncRNAs) are considered as crucial regulatory factors in cancer biology. However, the biological function of long intergenic non-protein coding RNA 960 (LINC00960) in the tumorigenesis of pancreatic ductal adenocarcinoma (PDAC) is still unknown. The goal of this study is to investigate the role of LINC00960 in PDAC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression levels of LINC00960 in PDAC tissues and cell lines. After transfection, the loss-of-function models of LINC00960 or interleukin 1 receptor-associated kinase 1 (IRAK1) were established with BxPC-3 cells and Colo357 cells, and the malignant phenotypes of BxPC-3 cells and Colo357 cells were detected by CCK-8 assay, BrdU assay and Transwell assay, respectively. The interactions among LINC00960, miR-146a-5p and IRAK1 were predicted by bioinformatics analysis, and verified by luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. The regulatory functions of LINC00960 and miR-146a-5p on IRAK1 were detected by Western blot. We demonstrated that the LINC00960 expression was increased in PDAC tissues and cell lines. Knocking down LINC00960 or IRAK1 could repress the viability, migration, and invasion of BxPC-3 and Colo357 cells. LINC00960 functioned as a molecular sponge for miR-146a-5p, and IRAK1 was verified as a target gene of miR-146a-5p. Additionally, LINC00960 could up-regulate IRAK1 expression via repressing miR-146a-5p, and the oncogenic properties of LINC00960 were partly reversed by miR-146a-5p. Our findings reveal that LINC00960 is a promoter of PDAC progression through regulating miR-146a-5p/IRAK1axis. 

Retracted: No

PubPeer comments:
 Figure 5e appears to include a constructed image. The corresponding authoru2018s email address bears no resemblance to their name. *** ![file] , 
 #1 As well as the rotated duplication within the upper-left panel, I am concerned about the sharp-edged rectangular discontinuity in the upper-right panel. ![] ,
EMMPRIN, SP1 and microRNA-27a mediate physcion 8-O-β-glucopyranoside-induced apoptosis in osteosarcoma cells
Authors: Huilin Yang
Zhaohong Wang
Journal: American journal of cancer research (2016)
Discipline: CLINICAL MEDICINE
Keywords: EMMPRIN; Physcion 8-O-β-glucopyranoside; ROS; Sp1; miR-27a
Affiliations: Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University No 188, Shizi Street, Suzhou 215006, China.

Abstract:  Physcion 8-O-β-glucopyranoside (PG), the main active ingredient of Rumex japonicus, induces apoptosis and causes cell cycle arrest in human lung cancer cells. However, its anti-tumor effects are not fully understood. In this study, we explored the mechanisms underlying PG induced apoptosis in the osteosarcoma cell line MG-63. Our results showed that PG exerted anti-proliferative effects and induced apoptosis in MG-63 cells via the intrinsic mitochondrial pathway, accompanied by loss of mitochondrial membrane potential (MMP) and cytochrome C release from the mitochondria. In addition, physcion treatment significantly inhibited extracellular matrix metalloproteinase inducer (EMMPRIN) expression in MG-63 cells, in a dose-dependent manner; meanwhile, EMMPRIN protein overexpression markedly reduced PG-induced apoptosis. Moreover, our findings suggested that the modulatory effects of PG on EMMPRIN were due, at least in part, to regulation of an ROS-miR-27a/ZBTB10-Sp1 transcription factor pathway. 

Retracted: Yes

PubPeer comments:
  Figure 4 PG modulates EMMPRIN expression by regulation Sp1 . Unexpected similarities in 4(E), flow-cytometry plots. ![file] , 
 Below: Fig 7A,  In vivo anti-[osteosarcoma] tumor effect of PG . Above: Fig 7B from [Liu et al (2017)] :  AF suppresses ovarian tumor growth in vivo. ... B. Tumor volume measurement showed that AF suppressed tumor growth in a dose-dependent manner. ![file] Different cancer, treatment, and authors. Same mice. , 
 Retracted [1 July 2020] .  A large portion of the data and the text in this article was copied from another source as disclosed by a knowledgeable informant and subsequently confirmed by the Editorial Office. Therefore, the entire article has been retracted in accordance with this journalu2019s policy and editorial decision. ,
Adipose derived mesenchymal stem cells alleviated osteoarthritis and chondrocyte apoptosis through autophagy inducing
Authors: Jun Zhou
Yu Wang
Fan Lian
Hanjiang Zeng
Hanshi Xu
Yiming Liu
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: adipose derived mesenchymal stem cell; apoptosis; autophagy; osteoarthritis.
Affiliations: Department of Rheumatology &amp; Clinical ImmunologyThe First Affiliated Hospital of Sun Yat‐sen UniversityGuangzhou China, Department of Interventional OncologyThe First Affiliated Hospital of Sun Yat‐sen UniversityGuangzhou China

Abstract:  Objective: We aim to explore the effect of adipose derived mesenchymal stem cells (ADMSCs) on a knee osteoarthritis rat model and analyze how ADMSCs affect chondrocyte apoptosis. Materials and methods: A surgically induced rat knee osteoarthritis (OA) model was constructed. ADMSCs were engrafted into the right knee cavity. Hematoxylin and eosin (H&amp;E), Masson, and Safranin O were used to compare the histopathology of synovial membrane and cartilage. Immunohistochemical (IHC) was used to measure MMP-13, Collagen 2 (Col-2), Caspase-3 (Cas-3), PARP, p62, LC3b, DDR-2, FGFR-1, Wnt, P-AKT/AKT, p-CAMKII/CAMKII, and p-Smad1/Smad1 expression in the articular cartilage. qPCR and Western blot analysis were used to detect mRNA and protein levels of markers in chondrocytes. TUNEL and Annexin-V were used to assess apoptosis. Results: Histological analysis showed that ADMSCs alleviated the deterioration of cartilage and osteoarthritis. ADMSCs coculture increase the expression of Col2 and Sox-9, while down regulated MMP-13 in IL-1β stimulated chondrocytes. ADMSCs decreased proinflammatory cytokines IL-1β, IL-6, and TNF-α. ADMSCs enhanced the viability of IL-1β stimulated chondrocytes. ADMSC attenuated chondrocyte apoptosis. The pretreatment of 3-methyladenine (3-MA) reversed the reduction of Caspase-3 caused by ADMSCs, showing that the antiapoptotic effect was associated with autophagy inducing. ADMSCs significantly reduced the expression of FGFR-1, DDR-2, and Wnt in IL-1β stimulated chondrocytes. ADMSCs reduced the ratio of p-Smad1/Smad1 and p-CAMK II/CAMKII, and increased the ratio of p-AKT/AKT. Conclusions: ADMSCs treatment alleviate osteoarthritis in rat OA models. AMDSCs reduced the secretion of proinflammatory cytokines and protected against apoptosis through autophagy inducing. ADMSCs' function could be related to multiple signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 7B. Some panels appear to look more similar than expected. Shown with blue and red boxes. ![file] ,
Effects of ultrasound-guided stellate-ganglion block on sleep and regional cerebral oxygen saturation in patients undergoing breast cancer surgery: a randomized, controlled, double-blinded trial
Authors: Feng Jin
Hong Ma
A-Yong Tian
Huang-Wei Lu
Wen-Fei Tan
Bo Fang
Xiao-Qian Li
Journal: Journal of clinical monitoring and computing (2018)
Discipline: CLINICAL MEDICINE
Keywords: Regional cerebral oxygen saturation; Sleep; Stellate ganglion block.
Affiliations: Department of Anaesthesiology, The First Hospital of China Medical University, 155# Nanjingbei Street, Shenyang, China., Department of Anaesthesiology, The First Hospital of China Medical University, 155# Nanjingbei Street, Shenyang, China. .

Abstract:  Numerous factors could contribute to sleep disturbances in women with breast cancer. We hypothesized that stellate ganglion block (SGB) during surgery would preserve sleep after surgery and increase intraoperative regional cerebral oxygen saturation (rSO2) on the blocked side in patients undergoing breast cancer surgery. A randomized, double-blinded, controlled trial was conducted at the First Hospital of China Medical University from January 2016 to September 2016. Ninety-six patients who underwent radical breast cancer surgery requiring general anaesthesia were randomly assigned to one of two study groups: a control group that received a saline SGB and a block group that received a 0.25% ropivacaine hydrochloride SGB. The primary outcome measure was the postoperative sleep profile, which was assessed using the bispectral index on the first postoperative night. The secondary outcome measure was the intraoperative rSO2, monitored was throughout surgery using near-infrared spectroscopy. A total of 91 female patients (mean age: 45 years; range 24-51 years) were included in the study. The duration of sleep was significantly increased by 66.3 min in the ropivacaine-SGB group compared with the saline-SGB group. No differences in rSO2 were observed on either the left or right side of the patients in either group 50 min after anaesthesia induction. We conclude that ropivacaine-SGB combined with general anaesthesia might increase the first postoperative sleep duration without influencing the intraoperative rSO2 in female patients undergoing elective breast cancer surgery. Clinical trials.gov identifier NCT02651519. 

Retracted: No

PubPeer comments:
 Fig.6a with XPS spectrum of Pt is identical to Figure 7a in another paper. https: pubpeer.com publications 748500DB9FAB0D07C81A0CD8F73613 Both papers are about Pt nanoparticles but surfactants used to prepare these nanoparticles are different. ![file] , 
 Anhydrous THF and anhydrous tetrahydrofuran are different? , 
 #2 You are right. I assumed all samples were prepared using octanethiol. Sample I actually was prepared using hexanethiol as in the other paper. I apologize for the mistake. The same sample might have been used in both studies submitted with 3 months interval. ,
Overexpression of Abl2 predicts poor prognosis in hepatocellular carcinomas and is associated with cancer cell migration and invasion
Authors: Chun-Mei Qu
Gang Wang
Quan-Tai Xing
Journal: OncoTargets and Therapy (2014)
Discipline: CLINICAL MEDICINE
Keywords: Abl2; Arg; HCC; metastasis; prognosis.
Affiliations: Department of Infectious Diseases, Qilu Hospital of Shandong University, Jinan, People's Republic of China.

Abstract:  Introduction: Abl2 nonreceptor tyrosine kinase (Arg, c-abl oncogene 2) has recently been identified as being recurrently amplified at DNA levels and overexpressed at mRNA levels in hepatocellular carcinomas (HCCs), and might be a potential oncogenic driver and therapeutic target for HCC. Methods: In this study, we investigated the Abl2 expression in a series of HCC tumors by immunohistochemistry and further evaluated its clinicopathological and prognostic significance. We also performed an in vitro experiment to validate the effect of Abl2 gene silencing on the migration and invasion abilities of human liver cancer HepG2 cells. Results: It has been demonstrated that Abl2 was unregulated in 37.3% (28/75) of primary HCC tissues, and was significantly associated with a shorter overall survival time (P=0.0005). In addition, Abl2 gene silencing in HepG2 cells significantly attenuated its migration and invasion abilities in vitro. We also found that the phosphorylation of metastasis-associated gene cortactin was markedly decreased by Abl2 silencing. Conclusion: We propose that Abl2 might be a potential candidate therapeutic target for HCCs and that targeted therapies against Abl2 in the treatment of HCCs deserve further investigation in the future. 

Retracted: No

PubPeer comments:
 This paper has several fundamental issues unfortunately, and very surprising to see that it was published in Nature Materials. 1) The bonding shown in the unit cell in Figure 1 completely wrong and you cannot bend the bonds in such a manner. 2) The whole discussion on the buckling and electromechanic nonsense and most of the paper are based on Raman measurements.  we rank it as a significant descriptive characteristic for ionic transport modifications under strainu2014connecting lattice near-order bond changes to transport and strain. But the shifts they observe are within the spectral resolution of their instrument which is also given in their experimental part  Micro-Raman spectroscopy spectra (WITec CRM200) were acquired by a high-resolution microscope, equipped with a 532 nm wavelength excitation laser and a spectral resolution of 0.7 cmu22121. , making the shifts they observe = 0.7 cm-1 meaningless and most of the manuscript useless and unreliable. ![file] , 
 also oxygen vacancy is randomly placed in the unit cell shown. One cannot make such a prediction with the characterization they presented. , 
 #1 is quite right about the Raman data. Raman peak widths are way over few cm-1 and 0.7cm-1 shifts they claimed are not there to see. ![file] it appears to be wishful thinking. , 
 Raman peak widths are way over few cm-1, so the effects and shifts claimed to be see are too forced. ![file] ,
Mutations in GluCl associated with field ivermectin-resistant head lice from Senegal
Authors: George Diatta
Nadia Amanzougaghene
Didier Raoult
Cheikh Sokhna
Oleg Mediannikov
Florence Fenollar
Journal: International Journal of Antimicrobial Agents (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: GluCl; Head lice; Ivermectin; Resistance; Senegal.
Affiliations: Aix-Marseille Université, IRD, AP-HM, MEPHI, IHU-Méditerranée Infection, Marseille, France., Aix Marseille Université, IRD, AP-HM, SSA, VITROME, IHU-Méditerranée Infection, Marseille, France., Aix Marseille Université, IRD, AP-HM, SSA, VITROME, IHU-Méditerranée Infection, Marseille, France; VITROME, Campus International UCAD-IRD, Dakar, Senegal., Aix-Marseille Université, IRD, AP-HM, MEPHI, IHU-Méditerranée Infection, Marseille, France. Electronic address: .

Abstract:  Through its unique mode of action, ivermectin represents a relatively new and very promising tool to fight against human lice, especially in cases of resistance to commonly used pediculicides. However, ivermectin resistance in the field has already begun to be reported. Therefore, understanding the mechanisms involved is a key step in delaying and tackling this phenomenon. In this study, field head lice with confirmed clinical resistance to ivermectin in rural human populations from Senegal were subjected to genetic analysis targeting the GluCl gene, the primary target of ivermectin known to be involved in resistance. Through DNA-polymorphism analysis, three relevant non-synonymous mutations in GluCl which were found only in ivermectin-resistant head lice (76 head lice tested), were identified. The A251V mutation found in the TM3 transmembrane domain was the most prevalent (allelic frequency of 0.33), followed by the S46P mutation (0.28) located at the N-terminal extracellular domain. The H272R was in the M3-M4 linker transmembrane region of GluCl and has shown the lowest frequency (0.18). Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) diagnostic assays were also developed for their accurate genotyping. Our study is the first to report the presence of GluCl point mutations in clinical ivermectin-resistant head lice occurring in rural human populations of Senegal. 

Retracted: No

PubPeer comments:
 Fig 5c.  images of cell invasion in each group . ![file] The orange rectangle marks an overlap with Fig 8A of [Li et al (2017)] : ![] Fig 6 of [Liu et al (2017)] . ![] A small clump of cells (pink oval) also appears in Fig 6 of [Dai Cai (2017)] . ![file] , 
 Figs 7D; 8B D; 9G H. ![file] These Western Blots have a curiously stylised appearance, devoid of background, with no variation in the general shape of the bands between gels or within each gel. Is it possible to upload scans of the original blots? ,