PReD-Bench/PRed-Bench huggingface dataset:
SATB1-Binding Sequences and Alu -Like Motifs Define a Unique Chromatin Context in the Vicinity of Human Immunodeficiency Virus Type 1 Integration Sites
Authors: Ramesh R Bhonde
Pavan P Kumar
Dimple Notani
Prabhat Kumar Purbey
Sameet Mehta
Ranveer S Jayani
Dhananjay V Raje
Hemant J Purohit
Debashis Mitra
Sanjeev Galande
Dyavar S Ravi
Journal: Journal of Virology (2007)
Discipline: MICROBIOLOGY
Keywords: Retroviral integration; chromatin; Alu-like motifs; human immunodeficiency virus type 1 (HIV-1); SATB1
Affiliations: National Centre for Cell Science, NCCS Complex, Ganeshkhind, Pune 411007, India., National Centre for Cell Science, Ganeshkhind, Pune 411007, India, Environmental Genomics Unit, National Environmental Engineering Research Institute, Nagpur 440020, India

Abstract:  Retroviral integration has recently been shown to be nonrandom, favoring transcriptionally active regions of chromatin. However, the mechanism for integration site selection by retroviruses is not clear. We show here the occurrence of Alu-like motifs in the sequences flanking the reported viral integration sites that are significantly different from those obtained from the randomly picked sequences from the human genome, suggesting that unique primary sequence features exist in the genomic regions targeted by human immunodeficiency virus type 1 (HIV-1). Additionally, these sequences were preferentially bound by SATB1, the T lineage-restricted chromatin organizer, in vitro and in vivo. Alu repeats make up nearly 10% of the human genome and have been implicated in the regulation of transcription. To specifically isolate sequences flanking the viral integration sites and also harboring both Alu-like repeats and SATB1-binding sites, we combined chromatin immunoprecipitation with sequential PCRs. The cloned sequences flanking HIV-1 integration sites were specifically immunoprecipitated and amplified from the pool of anti-SATB1-immunoprecipitated genomic DNA fragments isolated from HIV-1 NL4.3-infected Jurkat T-cell chromatin. Moreover, many of these sequences were preferentially partitioned in the DNA associated tightly with the nuclear matrix and not in the chromatin loops. Strikingly, many of these regions were disfavored for integration when SATB1 was silenced, providing unequivocal evidence for its role in HIV-1 integration site selection. We propose that definitive sequence features such as the Alu-like motifs and SATB1-binding sites provide a unique chromatin context in vivo which is preferentially targeted by the HIV-1 integration machinery. 

Retracted: No

PubPeer comments:
 Figure 1F appears to have an undisclosed splice. *** Inverse image ![file] *** Original image ![file] , 
 Much more similar than expected ![file] , 
 Figure 1C, more similar than expected after resizing. *** Enhanced sharpness to illustrate similar features ![file] *** Original ![file] ,
Quality of life in elderly patients following coronary artery bypass grafting
Authors: Ewelina Bak
Czesław Marcisz
Journal: Patient preference and adherence (2014)
Discipline: CLINICAL MEDICINE
Keywords: activities of daily living; cognitive function; coronary heart disease; depression.
Affiliations: Faculty of Health Sciences, University of Bielsko-Biała, Bielsko-Biała, Poland., Department of Gerontology and Geriatric Nursing, School of Health Sciences, Medical University of Silesia, Katowice, Poland.

Abstract:  Background: Surgical revascularization of the coronary arteries leads to changes in quality of life (QoL) for patients with coronary heart disease. The aim of this work was to monitor QoL, considering cognitive function, depression, and activities of daily living in elderly patients after coronary artery bypass grafting (CABG). Methods: This study included 65 patients (29 women and 36 men) aged 61-74 years with stable coronary heart disease who underwent CABG. The control group included 29 women and 36 men aged 61-74 years who were not suffering from coronary heart disease. The questionnaires used in the study canvassed QoL (Nottingham Health Profile), cognitive function, depression, and basic and instrumental activities of daily living. The research was conducted before surgery and repeated 6 and 12 months after surgery. Results: QoL was comparable between women and men and was lower than in the control group (P&lt;0.05). After CABG, the values for particular domains of QoL improved more in men than in women. There was a reduction in the severity of depression 6 months after surgery in men and 12 months after surgery in women. Conclusion: Elderly patients with coronary heart disease have decreased QoL, which normalizes in men and improves in women after CABG. 

Retracted: No

PubPeer comments:
 The authors reported in the abstract 29 women and 36 men in the control group, however, on page 290 they reported 27 women and 38 men. Then, tables 1 and 3 reported that there was 38 females and 27 males. ,
Protective effects of baicalin on rabbit articular chondrocytes in vitro
Authors: Liqin Wang
Xianyuan Huang
Huayu Wu
Jinmin Zhao
Li Zheng
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: baicalin; bioactivities; chondrocytes; joint disease; proliferation.
Affiliations: Guangxi Engineering Center in Biomedical Materials for Tissue and Organ Regeneration, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China., The Medical and Scientific Research Center, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China., Department of Cell Biology and Genetics, School of Premedical Sciences, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China., Department of Radiology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510275, P.R. China., Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

Abstract:  Drug therapy is one of the typical treatments for post-injury inflammation of cartilage. Traditional Chinese herbs have potential as treatments, as their long history of clinical application has demonstrated they are effective and induce minimal side effects. Baicalin is a traditional Chinese medicine that has been used to treat inflammation, fever, ulcers and cancer for hundreds of years. Previous studies have demonstrated that baicalin may decrease levels of interleukin-1β and suppress the expression of type-I collagen, thus attenuating cartilage degeneration. In the present study, the effect of baicalin on chondrocytes was assessed by examining the morphology, proliferation, extracellular matrix (ECM) synthesis and cartilage-specific gene expression of chondrocytes. The results indicated that baicalin may promote the proliferation of articular chondrocytes, secretion of cartilage ECM and collagen type II, aggrecan and SRY box (Sox) 9 gene upregulation. The expression of collagen I, a marker of chondrocyte dedifferentiation, was downregulated by baicalin; therefore, baicalin may maintain the phenotype of chondrocytes. Within the recommended concentrations of baicalin ranging from 0.625-6.25 µmol/l cell proliferation was increased and a 1.25 µmol/l dose of baicalin exerted the most positive effect on articular chondrocytes. The results of the present study may therefore indicate that baicalin may be used as a novel agent promoting the repair of articular cartilage damage. 

Retracted: No

PubPeer comments:
 Figure 5: Two micrographs have been duplicated: Day4; control vs 2.5 u00b5mol l (one of them has been modified). Day4; 0.625 u00b5mol l vs 1.25 u00b5mol l. ![file] , 
 Figure 3. ![file] , 
 #2 The **difference** between the duplicated slides is very localised It includes a red spot in the right-hand version, denoting a dead chondrocyte. ![file] ,
Immunohistochemical expression of hard tissue related factors in the mouse dental pulp after immediate teeth separation
Authors: N Okafuji
A Nabeyama
A Yamamoto
S Saito
Toshiyuki Kawakami
K Nakano
E Kasahara
M Sato
Journal: European journal of medical research (2011)
Discipline: CLINICAL MEDICINE
Keywords: Runx2; ALP; tooth pulp; teeth separation; immunohistochemistry
Affiliations: Matsumoto Dental University Graduate School of Oral Medicine, Shiojiri, Japan.

Abstract:  We examined change of Runx2 and ALP expression in mouse tooth pulp which exposed to teeth separation experiment by immunohistochemistry as a model for conservative dentistry treatment. 8-week-old 36 male ddY mice were used and wedge was inserted between upper 1st and 2nd molars. The wedge was removed 30 minutes as well as 3 hours after the insertion and the samples were prepared extending up to 1 week of time period for regular histopathological and immunohistochemical examinations for ALP and Runx2 expression. The opposite sides without wedge insertion were taken as controls. In the control group pulp, weak expressions of Runx2 and ALP in the vessel endothelial cells as well as the pulp cells were revealed, suggesting the appearance of these genes upon mechanical stress induced by mastication and tongue pressure etc. On the other hand in the experiment group, Runx2 expression increased both in 30-minute and 3-hour teeth separation group. The expression became maximum at 24 hours. Then it gradually decreased and became similar level with the control group at 1-week after the wedge insertion. Similarly ALP expression increased after the wedge insertion and was maximum at 24 hours and then gradually decreased to the levels similar with the control group. These results suggest that when immunohistochemical expression of Runx2 as well as ALP was used as an index, no severe damage occur upon clinical application of wedge insertion. 

Retracted: No

PubPeer comments:
 unexpected image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
RETRACTED ARTICLE: A compact photometer based on metal-waveguide-capillary: application to detecting glucose of nanomolar concentration
Authors: Bo Qu
Ji Zhang
Jian Hao
Hui Huang
Haibo Wu
Min Bai
Journal: Scientific Reports (2015)
Discipline: Multidisciplinary
Keywords: Trace analysis; liquid samples; photometer; metal-waveguide-capillary (MWC); absorbance detection
Affiliations: Department of Electronic Science and Technology, Faculty of Electronic Information and Electrical Engineering, Dalian University of Technology, Dalian 116024, China., Jordan Valley Semiconductors UK Ltd, Shanghai 201206, China.

Abstract:  Trace analysis of liquid samples has wide applications in life science and environmental monitor. In this paper, a compact and low-cost photometer based on metal-waveguide-capillary (MWC) was developed for ultra-sensitive absorbance detection. The optical-path can be greatly enhanced and much longer than the physical length of MWC, because the light scattered by the rippled and smooth metal sidewall can be confined inside the capillary regardless of the incident-angle. For the photometer with a 7 cm long MWC, the detection limit is improved ~3000 fold compared with that of commercial spectrophotometer with 1 cm-cuvette, owing to the novel nonlinear optical-path enhancement as well as fast sample switching, and detecting glucose of a concentration as low as 5.12 nM was realized with conventional chromogenic reagent. 

Retracted: Yes

PubPeer comments:
 2021 retraction. https: www.nature.com articles s41598-021-91478-8 Retraction of: Scientific Reports https: doi.org 10.1038 srep10476, published online 28 May 2015 The authors have retracted this article. In the study described in our article, the metal-waveguide-capillary (MWC)-based photometer was applied to two samples: the red-ink solution (RIS) and the glucose solution. However, we recently found that the detection results with the RIS cannot be reproduced. This may be due to contamination of the RIS, as the reagent bottles used for the RIS measurement were not clean. In light of this, the performance metrics and optical-path enhancement reported are incorrect, as well as the suggested mechanism of light scatter. All authors agree to this retraction. ,
Activation of peroxisome proliferator-activated receptor delta induces fatty acid beta-oxidation in skeletal muscle and attenuates metabolic syndrome
Authors: Yasutoshi Uchiyama
Masashi Yanagisawa
Joji Yamamoto
Mitsuhiro Watanabe
Ryoichi X Ioka
Kenta Magoori
Johan Auwerx
Toshiya Tanaka
Yuichiro Watanabe
Makoto Naito
Juro Sakai
Sadayoshi Ito
Hiroshi Asaba
Takefumi Doi
Keisuke Tachibana
Yukio Ikeda
Koichi Sumi
Hiroki Hamura
Tatsuhiko Kodama
Satoshi Iwasaki
Takao Hamakubo
Haruhisa Iguchi
Journal: Proceedings of the National Academy of Sciences of the United States of America (2003)
Discipline: Multidisciplinary
Keywords: PPARdelta; metabolic homeostasis; fatty acid oxidation; skeletal muscle; GW501516
Affiliations: Laboratory for Systems Biology and Medicine, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan.

Abstract:  In this study, we defined the role of peroxisome proliferator-activated receptor beta/delta (PPARdelta) in metabolic homeostasis by using subtype selective agonists. Analysis of rat L6 myotubes treated with the PPARdelta subtype-selective agonist, GW501516, by the Affymetrix oligonucleotide microarrays revealed that PPARdelta controls fatty acid oxidation by regulating genes involved in fatty acid transport, beta-oxidation, and mitochondrial respiration. Similar PPARdelta-mediated gene activation was observed in the skeletal muscle of GW501516-treated mice. Accordingly, GW501516 treatment induced fatty acid beta-oxidation in L6 myotubes as well as in mouse skeletal muscles. Administration of GW501516 to mice fed a high-fat diet ameliorated diet-induced obesity and insulin resistance, an effect accompanied by enhanced metabolic rate and fatty acid beta-oxidation, proliferation of mitochondria, and a marked reduction of lipid droplets in skeletal muscles. Despite a modest body weight change relative to vehicle-treated mice, GW501516 treatment also markedly improved diabetes as revealed by the decrease in plasma glucose and blood insulin levels in genetically obese ob/ob mice. These data suggest that PPARdelta is pivotal to control the program for fatty acid oxidation in the skeletal muscle, thereby ameliorating obesity and insulin resistance through its activation in obese animals. 

Retracted: No

PubPeer comments:
 The merged micrograph in Figure 6C does not correspond with the single staining micrographs. ![file] ,
miR-873 suppresses H9C2 cardiomyocyte proliferation by targeting GLI1
Authors: Yue Zhao
Jing-Shu Zhang
Jun-Xia Ruan
Tian-Xing Gong
Pei-Yan Liu
Nan Wan
Yue-Ling Sun
Guang-Rong Qiu
Yuan Lv
Journal: Gene (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cardiomyocyte; Congenital heart disease; GLI1; miR-873.
Affiliations: Department of Medical Genetics, College of Basic Medical Science, China Medical University, Shenyang, PR China; Sino-Dutch Biomedical and Information Engineering School, Northeastern University, Shenyang, PR China., Sino-Dutch Biomedical and Information Engineering School, Northeastern University, Shenyang, PR China., Liaoning Centre for Prenatal Diagnosis, Department of Gynecology & Obstetrics, Shengjing Hospital Affiliated to China Medical University, Shenyang, PR China., Key Laboratory of Systems Biomedicine (Ministry of Education), Collaborative Innovation Center of Systems Biomedicine, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, PR China., Department of Medical Genetics, College of Basic Medical Science, China Medical University, Shenyang, PR China; Women and Children's Hospital of Linyi City, Linyi, PR China., Department of Medical Genetics, College of Basic Medical Science, China Medical University, Shenyang, PR China; Department of Laboratory Medicine, No. 202 Hospital of PLA, Shenyang, PR China., Department of Laboratory Medicine, General Hospital of Shenyang Military Region, Shenyang, PR China., Department of Medical Genetics, College of Basic Medical Science, China Medical University, Shenyang, PR China. Electronic address: .

Abstract:  MicroRNAs (miRNAs) are a class of endogenous, non-coding small RNAs that regulate the expression of target genes. Previous studies have suggested that miRNAs are key regulators in cardiovascular systems. This study investigated the role of miR-873 in H9C2 cardiomyocytes by targeting glioma-associated oncogene 1 (GLI1). miR-873 was significantly up-regulated in serum samples from congenital heart disease (CHD) patients compared with those from normal individuals. Furthermore, miR-873 over-expression suppressed H9C2 proliferation and induced cell cycle arrest. Bioinformatic algorithms revealed a predicted target site for miR-873 in the 3'-untranslated region (3'UTR) of GLI1, which was verified using a dual-luciferase reporter assay. qPCR and western blot analysis also showed that miR-873 negatively regulated GLI1 mRNA and protein expression in H9C2 cells. Conversely, GLI1 over-expression partially reversed the growth-inhibitory effect of miR-873. To summarize, our data suggest that miR-873 is a novel miRNA that regulates H9C2 cell proliferation via targeting GLI1, and miR-873 may serve as a new potential biomarker diagnosis in CHD in the future. 

Retracted: No

PubPeer comments:
 Could the authors explain how the a-tubulin blots look identical for and across 4 different experimental conditions and samples? ![file] ,
MicroRNA-378 Alleviates Cerebral Ischemic Injury by Negatively Regulating Apoptosis Executioner Caspase-3
Authors: Junfa Li
Song Han
Yun Li
Yanling Yin
Jie Zhong
Nan Zhang
Journal: International journal of molecular sciences (2016)
Discipline: CHEMISTRY
Keywords: apoptosis; caspase-3; cerebral ischemic injury; ischemic stroke; miRNA-378.
Affiliations: Department of Human Anatomy, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China. ., Department of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, China. .

Abstract:  miRNAs have been linked to many human diseases, including ischemic stroke, and are being pursued as clinical diagnostics and therapeutic targets. Among the aberrantly expressed miRNAs in our previous report using large-scale microarray screening, the downregulation of miR-378 in the peri-infarct region of middle cerebral artery occluded (MCAO) mice can be reversed by hypoxic preconditioning (HPC). In this study, the role of miR-378 in the ischemic injury was further explored. We found that miR-378 levels significantly decreased in N2A cells following oxygen-glucose deprivation (OGD) treatment. Overexpression of miR-378 significantly enhanced cell viability, decreased TUNEL-positive cells and the immunoreactivity of cleaved-caspase-3. Conversely, downregulation of miR-378 aggravated OGD-induced apoptosis and ischemic injury. By using bioinformatic algorithms, we discovered that miR-378 may directly bind to the predicted 3'-untranslated region (UTR) of Caspase-3 gene. The protein level of caspase-3 increased significantly upon OGD treatment, and can be downregulated by pri-miR-378 transfection. The luciferase reporter assay confirmed the binding of miR-378 to the 3'-UTR of Caspase-3 mRNA and repressed its translation. In addition, miR-378 agomir decreased cleaved-caspase-3 ratio, reduced infarct volume and neural cell death induced by MCAO. Furthermore, caspase-3 knockdown could reverse anti-miR-378 mediated neuronal injury. Taken together, our data demonstrated that miR-378 attenuated ischemic injury by negatively regulating the apoptosis executioner, caspase-3, providing a potential therapeutic target for ischemic stroke. 

Retracted: No

PubPeer comments:
 There seems to be an image duplication in Figure 2. The authors should probably contact the journal for a correction. ![file] , 
 Dear Dr. Coniochaeta malacotricha, We thank you for the critical comment on Figure 2A. After careful examination of the original images of TUNEL staining, we have to admit the mistake of duplication in Figure 2A. We have asked the IJMS editorial office to give us an opportunity to make correction. Thank you again, Nan Zhang Nan Zhang, Ph.D. Department of Neurobiology Capital Medical University E-mail: nanzhang@mail.ccmu.edu.cn ,
MUC1 confers radioresistance in head and neck squamous cell carcinoma (HNSCC) cells
Authors: Zheng Cui
Ya-Nan Bi
Yi-Chuan Huang
Tian-Qiao Huang
Jin-Ping Guan
Journal: Bioengineered (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DNA double-strand break; Head and neck squamous cell carcinoma; MUC1; X-ray irradiation; radioresistance.
Affiliations: Department of Otolaryngology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China, Operating Room, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China, Endoscopy, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China, Emergency Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China

Abstract:  Mucin 1 (MUC1), a transmembrane glycoprotein, has shown to be as the possible prognostic marker to predict the risk of aggressive head and neck squamous cell carcinoma (HNSCC). In the present study, we investigated the effect of MUC1 in HNSCC cells and the response to X-ray irradiation (IR). Here, we examined the impact of MUC1 overexpression or downexpression on clonogenic survival and apoptosis in response to X-ray irradiation (IR). Radioresistance and radiosensitivity were also observed in HNSCC cells that are MUC1 overexpression and MUC1 downexpression. This enhanced resistance to IR in MUC1-overexpressing cells is primarily due to increased the number of radiation-induced γH2AX/53BP1-positive foci and DNA double-strand break (DSB) repair kinetics. MUC1 overexpression repaired more than 90% of DSBs after 2 Gy radiation by 24 h compared to the empty vector overexpressing cells with less than 50% of DSB repair. However, MUC1 downexpression repaired less than 20% of DSBs compared to the empty vector-overexpresing cells. MUC1 overexpression inhibited proapoptotic protein expression, such as caspase-3, caspase-8, and caspase-9, and induced antiapoptotic protein Bcl-2, followed by resistance to IR-induced apoptosis. Our results showed that targeting MUC1 may be as a promising strategy to counteract radiation resistance of HNSCC cells. 

Retracted: No

PubPeer comments:
 Figure 5a. Row of NC. The merge does not seem to be the merge of the 53BP1 and the u03b3H2AX images ![file] , 
 NC a 53bp1 H2AX was Edited by mistakeu3002 , 
 ![file] , 
 #3 Thank you Dr. Huang for your prompt explanation. A colleague of mine pointed out that the green dot (arrow) close to the lower-right corner in the merge is not seen in any of the single channels. ![file] , 
 #4 ![](http: )![file] , 
 #5 #5![file] , 
 If you deepen the dyeing, we can see it. ,
Piracetam Attenuates LPS-Induced Neuroinflammation and Cognitive Impairment in Rats
Authors: Pankaj Paliwal
Alok Tripathi
Sairam Krishnamurthy
Journal: Cellular and Molecular Neurobiology (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Amyloid beta; Cognition; Lipopolysaccharide; Mitochondrial dysfunction; Neuroinflammation
Affiliations: Neurotherapeutics Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P., 221 005, India., Neurotherapeutics Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P., 221 005, India. .

Abstract:  The present study was performed to investigate the effect of piracetam on neuroinflammation induced by lipopolysaccharide (LPS) and resulting changes in cognitive behavior. Neuroinflammation was induced by a single dose of LPS solution infused into each of the lateral cerebral ventricles in concentrations of 1 μg/μl, at a rate of 1 μl/min over a 5-min period, with a 5-min waiting period between the two infusions. Piracetam in doses of 50, 100, and 200 mg/kg i.p. was administered 30 min before LPS infusion and continued for 9 days. On ninth day, the behavioral test for memory and anxiety was done followed by blood collection and microdissection of the hippocampus (HIP) and prefrontal cortex brain regions. Piracetam attenuated the LPS-induced decrease in coping strategy to novel environment indicating anxiolytic activity. It also reversed the LPS-induced changes in the known arm and novel arm entries in the Y-maze test indicating amelioration of spatial memory impairment. Further, piracetam moderated LPS-induced decrease in the mitochondrial complex enzyme activities (I, II, IV, and V) and mitochondrial membrane potential. It ameliorated changes in hippocampal lipid peroxidation and nitrite levels including the activity of superoxide dismutase. Piracetam region specifically ameliorated LPS-induced increase in the level of IL-6 in HIP indicating anti-neuroinflammatory effect. Further, piracetam reduced HIP Aβ (1-40) and increased blood Aβ level suggesting efflux of Aβ from HIP to blood. Therefore, the present study indicates preclinical evidence for the use of piracetam in the treatment of neuroinflammatory disorders. 

Retracted: No

PubPeer comments:
 Figure 6A. Some bands appear to be visible multiple times within the same panel, albeit sometimes in mirror image. Arrows of the same color show similarities and orientation. Image contrast slightly adjusted to bring out details. ![file] , 
 Figure 7A. Some bands appear to be visible multiple times within the same panel or across panels, albeit sometimes in mirror image. Arrows of the same color show similarities and orientation. Image contrast slightly adjusted to bring out details. ![file] , 
 Figure 8A. Some bands appear to be visible multiple times within the same panel, albeit sometimes in mirror image. Arrows of the same color show similarities and orientation. Image contrast slightly adjusted to bring out details. ![file] ,
miR-18a impairs DNA damage response through downregulation of ataxia telangiectasia mutated (ATM) kinase
Authors: Jueheng Wu
Hui Gong
Yong Zeng
Mengfeng Li
Chuyong Lin
Jun Li
Zhiqiang Wu
Libing Song
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: DNA damage response; ATM Kinase; miR-18a; breast cancer; DNA repair
Affiliations: State Key Laboratory of Oncology in Southern China, Department of Experimental Research, Cancer Center, Sun Yat-sen University, Guangzhou, Guangdong, China.

Abstract:  The DNA damage response (DDR) encompasses multi-step processes by which cells evolve to sense DNA damage, transduce the signal and initiate the repair of damaged DNA. Ataxia Telangiectasia Mutated (ATM) Kinase, which functions as the primary sensor and transducer of DNA damage signal, has been demonstrated to play an important role in the DDR and cancer prevention. Hence, understanding the molecular mechanisms underlying the regulation of ATM has received much attention. Here, we found that miR-18a was upregulated in both cell lines and patients' tissue samples of breast cancer. Furthermore, we demonstrated that ectopically expressing miR-18a downregulated ATM expression by directly targeting the ATM-3'-UTR and abrogated the IR-induced cell cycle arrest. Similar to the effect of ATM siRNA, overexpressing miR-18a in breast cancer cells reduced the DNA damage repair ability and the efficiency of homologous recombination-based DNA repair (HRR) and sensitized cells to γ-irradiation (IR) treatment. However, inhibition of miR-18a led to augmentation of DNA damage repair, increase of HRR efficiency and reduced cellular radiosensitivity. Moreover, we showed that the phorsphorylation level and nuclear foci formation of H2AX and 53BP1, the downstream substrates of ATM kinase, were significantly deceased in miR-18a overexpressing cells. Taken together, our results uncover a new regulatory mechanism of ATM expression and suggest that miR-18a might be a novel therapeutic target. 

Retracted: No

PubPeer comments:
 Supplemental Figure 2 contains two WB bands which appear more similar than expected, with one subjected to vertical flipping. ![file] , 
 Dear Lecithocera Eumenopis Thanks for pointing this out. We are currently checking the original data of these Figures, and will make response as soon as possible. Jun Li , 
 #2 Could the authors please post the uncropped original scans when they locate them? Thank you. ,
Novel role of c-jun N-terminal kinase in regulating the initiation of cap-dependent translation
Authors: Manish R Patel
Robert A Kratzke
Peter B Bitterman
Faris Farassati
Tanawat Jirakulaporn
Blake A Jacobson
Ahad A Sadiq
Joe Jay-Dixon
Journal: International Journal of Oncology (2011)
Discipline: CLINICAL MEDICINE
Keywords: protein translation; mRNA cap; cell growth; proliferation; cap-dependent translation
Affiliations: University of Minnesota Medical School, Division of Hematology, Oncology, and Transplantation, Minneapolis, MN 55455, USA.

Abstract:  Initiation of protein translation by the 5' mRNA cap is a tightly regulated step in cell growth and proliferation. Aberrant activation of cap-dependent translation is a hallmark of many cancers including non-small cell lung cancer. The canonical signaling mechanisms leading to translation initiation include activation of the Akt/mTOR pathway in response to the presence of nutrients and growth factors. We have previously observed that inhibition of c-jun N-terminal kinase (JNK) leads to inactivation of cap-dependent translation in mesothelioma cells. Since JNK is involved in the genesis of non-small cell lung cancer (NSCLC), we hypothesized that JNK could also be involved in activating cap-dependent translation in NSCLC cells and could represent an alternative pathway regulating translation. In a series of NSCLC cell lines, inhibition of JNK using SP600125 resulted in inhibition of 4E-BP1 phosphorylation and a decrease in formation of the cap-dependent translation complex, eIF4F. Furthermore, we show that JNK-mediated inhibition of translation is independent of mTOR. Our data provide evidence that JNK is involved in the regulation of translation and has potential as a therapeutic target in NSCLC. 

Retracted: No

PubPeer comments:
 Figure 1B. Much more similar than expected. https: imgur.com MX3Re6a ,
Chimeric cytokine receptor enhancing PSMA-CAR-T cell-mediated prostate cancer regression
Authors: Shao Weimin
Asimujiang Abula
Wang Wenguang
Ding Qianghong
Journal: Cancer Biology & Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: Chimeric antigen receptor T; effector cells; prostate cancer; prostate specific membrane antigen; xenograft.
Affiliations: Reproductive medicine Center, The First Affiliated Hospital of Xinjiang Medical University, China., Department of Urology, The First Affiliated Hospital of Xinjiang Medical University, China., Department of Urology, Fourth People's Hospital of Shenzhen Longgang District, Shenzhen, China.

Abstract:  Objective: Chimeric antigen receptor T (CAR-T) cell therapy has demonstrated an unprecedented therapeutic efficacy in hematological malignancies; however, its effectiveness in solid tumors remains elusive. In order to enable CAR-T cells more effective to solid tumors, a inverted chimeric cytokine receptor (ICR) was designed, which is consists of the TGF-β extracellular domain, IL-7 receptor intracellular domain, and co-expression on CAR-T cells.Materials and Methods: We selected prostate specific membrane antigen (PSMA) as a target for CAR-T cells, constructed corresponding effector cells, and verified the anti-tumor activity of this enhanced PSMA-CAR-T cell by a series of repeated target cell stimulation experiments in vitro and the anti-tumor capabilities by using mice xenograft model in vivo.Results: In vitro experiments showed that co-expression of ICR could significantly enhance sustained anti-tumor capabilities of PSMA-CAR-T cells. Moreover, in vivo experiments also confirmed that the enhanced PSMA-CAR-T cells exhibited significant superior anti-tumor capabilities and could prolong the survival time in the xenograft and PDX models of prostate cancer.Conclusions: PSMA-CAR-T cells co-expressing ICR can be envisaged as a new therapeutic strategy for prostate cancer and support the translation of this enhanced approach in the clinical setting. 

Retracted: No

PubPeer comments:
 Figure 2C. Much more similar than expected. https: imgur.com ObLqPRx , 
 Figure 3A. Much more similar than expected. https: imgur.com P4rW7k6 , 
 Figure 4C. Much more similar than expected. https: imgur.com Lnm6QVJ ,
MicroRNA-338-3p inhibits thyroid cancer progression through targeting AKT3
Authors: Xi Zhen
Feng Guo
Qiang Luo
Dan Fei
Guo-Qing Sui
Shuai Yin
Hui Wang
Journal: American journal of cancer research (2017)
Discipline: CLINICAL MEDICINE
Keywords: AKT3; Thyroid cancer; invasion; miR-338-3p; proliferation.
Affiliations: Department of Ultrasound, The China-Japan Union Hospital of Jilin UniversityChangchun 130033, China.

Abstract:  microRNA-338-3p (miR-338-3p) has been implicated in tumor development and progression in many types of cancers. However, the function and mechanism underlying the action of miR-383-3p in thyroid cancer remain unclear and were therefore investigated in this study by in vitro and in vivo experiments. We found that miR-338-3p was downregulated in thyroid cancer tissues and cell lines. miR-338-3p expression was significantly associated with the clinical stage and lymph node metastasis of thyroid cancer. Forced expression of miR-338-3p suppressed thyroid cancer cell proliferation, clonogenicity, migration, and invasion in vitro and inhibited tumorigenesis in a nude mouse xenograft model system. Moreover, AKT3, a known oncogene, was confirmed as a direct target of miR-383-3p in thyroid cancer cells, as evidenced by the fact that ectopic miR-383 expression suppressed AKT3 expression and its downstream pathway (AKT pathway). In addition, AKT3 silencing by siRNA mimicked the effect of ectopic miR-338-3p on the growth and invasion of thyroid cancer cells. In contrast, AKT3 overexpression attenuated the inhibitory effect induced by miR-338-3p overexpression in thyroid cancer cells. These results suggest that miR-338-3p functions as a novel tumor suppressor that blocks thyroid cancer cell growth through targeting AKT3. 

Retracted: No

PubPeer comments:
 Fig 2E.  Tumor images for the miR-338-3p and miR-NC groups . ![file] I assume from the variability of shadows and lighting direction that the image is a composite of tumors photographed separately. Could the authors confirm whether this is the case, or correct my error if I am mistaken? ,
Overexpression of long noncoding RNA HOTTIP promotes tumor invasion and predicts poor prognosis in gastric cancer
Authors: Kun Liu
Keqing Qian
Heng Ye
Journal: OncoTargets and Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: HOTTIP; gastric cancer; long noncoding RNA; prognosis.
Affiliations: Department of Oncology, The Affiliated Hospital of Nanjing Medical University, Changzhou No 2 People's Hospital, Changzhou, Jiangsu, People's Republic of China., Department of General Surgery, The Affiliated Hospital of Nanjing Medical University, Changzhou No 2 People's Hospital, Changzhou, Jiangsu, People's Republic of China.

Abstract:  Purpose: Long noncoding RNAs have been proved to play important roles in the tumorigenesis and development of human gastric cancer (GC). Our study aims to investigate the expression and function of Homeobox A transcript at the distal tip (HOTTIP) in GC. Methods: HOTTIP expression was detected in GC tissues and cell lines by using quantitative reverse transcription polymerase chain reaction. Association between HOTTIP levels and clinicopathological factors and patient prognosis was also analyzed. MTT, flow cytometry, and transwell invasion and migration assays were used to investigate the role of HOTTIP in the regulation of biological behaviors of GC cells. Results: HOTTIP expression was remarkably increased in GC tissues and cell lines compared with that in the normal control. Clinicopathologic analysis revealed that high HOTTIP expression correlated with larger tumor size, deeper invasion depth, positive lymph node metastasis, advanced TNM stage, and shorter overall survival. Multivariate regression analysis identified HOTTIP overexpression as an independent unfavorable prognostic factor in GC patients. Moreover, HOTTIP downregulation by si-HOTTIP transfection impaired GC cell proliferation, promoted cell apoptosis, and reduced cell invasion and migration. Conclusion: These findings suggested that HOTTIP may contribute to GC initiation and progression, and would be not only a novel prognostic marker but also a potential therapeutic target for this disease. 

Retracted: No

PubPeer comments:
 *[left]* Fig 2.  Kaplanu2013Meier survival curves of gastric cancer patients based on HOTTIP expression status. *[right]* Fig 2 from [Cui, Zheng Kong (2016)] .  Kaplan-Meier survival curves of 106 gastric cancer patients based on miR-198 expression status . ![file] Table 1 from the present paper, and from Cui, Zheng Kong. ![file] Table 2 from the present paper, and from Cui, Zheng Kong. ![file] The Cui-Zheng-Kong paper belongs to a network of 11 papers, apparently the output of a papermill. The similarities here suggest that the present paper has the same provenance. , 
 What does [SimTexter] have to say about the similarity of the two papers? ![file] ![file] ![file] ![file] , 
 *[right]* Fig 3D E. *[left]* Fig 2 from [Gong et al (2015)] . ![file] , 
 *[left]* Fig 3C. *[right]* Fig 3C from [Han et al (2015)] . ![file] ,
Virtual Rehabilitation Training System Based on Surface EMG Feature Extraction and Analysis
Authors: Qiang Meng
Jianjun Zhang
Xi Yang
Journal: Journal of Medical Systems (2019)
Discipline: CLINICAL MEDICINE
Keywords: EMG feature extraction; Function evaluation; Rehabilitation training system; Virtual technology.
Affiliations: Department of Physical Education, Physical Education College of Zhengzhou University, Zhengzhou, China. ., Department of Physical Education, Physical Education College of Zhengzhou University, Zhengzhou, China.

Abstract:  Aiming at the characteristics that electromyography (EMG) signals can reflect the human body's motive intention and the information of muscle's motive state, this paper makes a thorough study on the evaluation of surface electromyography signals' motive state. At the same time, EMG signals can reflect the characteristics of limb movement and its changing rules, and can acquire the functional characteristics of limb movement so as to accurately evaluate the rehabilitation status of patients. In this paper, EMG signal analysis and feedback control are introduced into the virtual rehabilitation system to study the methods of EMG parameter identification and dynamic feature extraction, and obtain the EMG characteristics and variation rules related to human motion patterns. In this paper, a rehabilitation training system based on EMG feedback and virtual reality is built, and the validity of the system is verified by patient experiment. The feasibility of the system is verified by the methods of validity of the algorithm, recognition rate of the system action pattern and fatigue evaluation. 

Retracted: No

PubPeer comments:
null, 
 Note: This article has been corrected. Please see the link below: https: www.oncotarget.com article 27755 ,
3-N-butylphthalide inhibits neuronal apoptosis in rats with cerebral infarction via targeting P38/MAPK
Authors: Y Zhong
W Liao
L-F Dong
W Cheng
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: 3-n-butylphthalide (NBP); neuronal apoptosis; cerebral infarction; p38; mitogen-activated protein kinase (MAPK)
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou, China. .

Abstract:  Objective: To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway. Materials and methods: A total of 30 rats were divided into control group (healthy rats, n=10), model group (CI rat model, n=10), and NBP group (CI rat model + intraperitoneal injection of NBP, n=10). Then, the neurological function, degree of cerebral ischemia, apoptosis of brain tissues, the protein and messenger ribonucleic acid (mRNA) expressions of p-p38 and MAPK in brain tissues were detected using the neurological score, 2,3,5-triphenyltetrazolium chloride (TTC) staining, Reverse Transcription-Polymerase Chain Reaction (RT-PCR), terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and Western blotting, respectively. Results: In NBP group, the neurological score was significantly lower than in model group, and the difference was statistically significant (p&lt;0.05). The results of TTC staining revealed that the area of the white region in brain slices was significantly larger in model group than in control group, indicating the successful establishment of middle cerebral artery occlusion (MCAO) model. Compared with model group, NBP group had a smaller area and lighter color of the white region in brain slices, suggesting that NBP markedly reduces the MCAO-induced CI. The apoptosis rate in NBP group was higher than in control group (p&lt;0.05), but lower than in model group (p&lt;0.05), while it was higher in model group than in control group (p&lt;0.05). The protein expressions of p38 and MAPK in NBP group were higher than in control group (p&lt;0.05), but lower than in model group (p&lt;0.05), while they were higher in model group than in control group (p&lt;0.05). Moreover, the mRNA expressions of p38 and MAPK were lower in control group than in model group (p&lt;0.05), while they were higher in model group than in NBP group (p&lt;0.05), but there was no significant difference in the mRNA expression of p38 between NBP group and control group (p&gt;0.05). Conclusions: NBP alleviates neuronal apoptosis in CI by down-regulating the p38 signal and inhibiting the expression of MAPK, thereby treating CI. 

Retracted: No

PubPeer comments:
 Figure 2.  Effect of NBP on MCAO-induced neuronal apoptosis in brain tissues detected via TUNEL assay. A, Number of apoptotic cells . Why is the NBP image populated with repeated graphic elements? ![file] ,
The Role of microRNAs in the Tumorigenesis of Ovarian Cancer
Authors: Gianpiero Di Leva
Carlo M Croce
Journal: Frontiers in oncology (2013)
Discipline: CLINICAL MEDICINE
Keywords: miRNA profiles; miRNA profiling; microRNA; noncoding RNA; ovarian cancer.
Affiliations: Department of Molecular Virology, Immunology, and Medical Genetics, Comprehensive Cancer Center, The Ohio State University Columbus, OH, USA.

Abstract:  Epithelial ovarian cancer (EOC) is a complex disease, with multiple histological subtypes recognized. There have been major advances in the understanding of the cellular and molecular biology of this human malignancy, however the survival rate of women with EOC has changed little since platinum-based-treatment was introduced more than 30 years ago. Since 2006, an increasing number of studies have indicated an essential role for microRNAs (miRNAs) in ovarian-cancer tumorigenesis. Several miRNA profiling studies have shown that they associate with different aspects of ovarian cancer (tumor subtype, stage, histological grade, prognosis, and therapy resistance) and pointed to a critical role for miRNAs in the pathogenesis and progression of EOC. In this review, we discuss the current data concerning the accumulating evidence of the modulated expression of miRNAs in EOC, their role in diagnosis, prognosis, and prediction of response to therapy. Given the heterogeneity of this disease, it is likely that increases in long-term survival might be also achieved by translating the recent insights of miRNAs involvement in EOC into novel targeted therapies that will have a major impact on the management of ovarian cancer. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: www.frontiersin.org articles 10.3389 fonc.2020.00585 full Retraction: The role of microRNAs in the tumorigenesis of ovarian cancer Frontiers Editorial Office* A Retraction of the Review Article The role of microRNAs in the tumorigenesis of ovarian cancer by Di Leva, G., and Croce, C. M. (2013). Front. Oncol. 3:153. doi: 10.3389 fonc.2013.00153 The journal retracts the June 13, 2013 article cited above. Following publication, the authors contacted the Editorial Office to request that their article be corrected because of the inappropriate manner in which the article was written, which specifically involved improper reuse of text from previous articles. An investigation was conducted in accordance with our established procedures that confirmed the extensive and dispersed nature of the overlap; therefore, the article has been retracted. This retraction was approved by the Chief Editors of Frontiers in Oncology and the Editor-in-Chief of Frontiers. The authors did not agree to this retraction. , 
 https: retractionwatch.com 2020 05 01 litigious-osu-cancer-researcher-earns-his-11th-retraction ,
Downregulation of miR‐1225‐5p is pivotal for proliferation, invasion, and migration of HCC cells through NFκB regulation
Authors: Weiguo Zhang
Xiangsu Xu
Lin Liu
Yujing Hu
Liangliang Ma
Journal: Journal of Clinical Laboratory Analysis (2020)
Discipline: CLINICAL MEDICINE
Keywords: NFκB p65; hepatocellular carcinoma; invasion; miR-1225; migration
Affiliations: Department of Oncology Hematology, People's Hospital of Linzi District, Zibo, China., Department of General Surgery, Tianjin Fifth Central Hospital, Tianjin, China., Department of Obstetric Area 3, Shandong Qilu Hospital Pingyi Branch (Pingyi County People's Hospital), Linyi, China., Department of Hepatolibiary Surgery, Jining No.1 People's Hospital, Jining, China.

Abstract:  Background: As one of the most frequently seen malignancies, hepatocellular carcinoma (HCC) serves as the second largest contributor to malignancy-specific mortality worldwide. MicroRNA-1225-5p (miR-1225) exerts an essential impact on the growth and metastasis of many malignancies. However, the contribution of miR-125 to HCC and the molecular mechanism of cancer cell viability and apoptosis are still unclear. We focused our research on exploring the function and molecular mechanism of miR-1225 in regulating HCC cell growth, migration, and invasion. Material: Quantitative PCR data showed that miR-1225 expression was repressed in HCC cell lines and in the tissues of HCC patients, compared to that in normal human hepatic cells and tissues. Transfection of a miR-1225 mimic inhibited cell viability and proliferation as indicated by CCK-8 staining and MTT assay. Transwell invasion, wound healing assay, and Western blotting were performed to assess whether miR-1225 repressed the metastasis and invasion of HCC cells, and decreased matrix metalloproteinase 9 (MMP9) expression. Further bioinformatic prediction and dual-luciferase reporter assay suggested that miR-1225 targeted the 3'-UTR of NFκB p65. Results: Overexpression of p65 protein counteracted the repressive impact of miR-1225 on invasion, migration, and proliferation of HCC cells. Conclusion: This research provided new evidences that miR-1225 inhibits the viability, migration, and invasion of HCC cells by downregulation of p65. 

Retracted: No

PubPeer comments:
 Figure 5J appears to have two images that overlap. *** ![file] ,