PReD-Bench/PRed-Bench huggingface dataset:
Manipulation of the dephasing time by strong coupling between localized and propagating surface plasmon modes
Authors: Tomoya Oshikiri
Jinghuan Yang
Kosei Ueno
Qihuang Gong
Quan Sun
Hiroaki Misawa
Xu Shi
Journal: Nature Communications (2018)
Discipline: Multidisciplinary
Keywords: Strong coupling; resonance modes; hybrid modes; localized surface plasmon resonance; surface plasmon polariton Bloch wave
Affiliations: State Key Laboratory for Mesoscopic Physics and Collaborative Innovation Center of Quantum Matter, Department of Physics, Peking University, Beijing, 100871, China., Research Institute for Electronic Science, Hokkaido University, Sapporo, 001-0021, Japan., Research Institute for Electronic Science, Hokkaido University, Sapporo, 001-0021, Japan. ., Center for Emergent Functional Matter Science, National Chiao Tung University, Hsinchu, 30010, Taiwan. ., State Key Laboratory for Mesoscopic Physics and Collaborative Innovation Center of Quantum Matter, Department of Physics, Peking University, Beijing, 100871, China. ., Collaborative Innovation Center of Extreme Optics, Shanxi University, Taiyuan, Shanxi, 030006, China. .

Abstract:  Strong coupling between two resonance modes leads to the formation of new hybrid modes exhibiting disparate characteristics owing to the reversible exchange of information between different uncoupled modes. Here, we realize the strong coupling between the localized surface plasmon resonance and surface plasmon polariton Bloch wave using multilayer nanostructures. An anticrossing behavior with a splitting energy of 144 meV can be observed from the far-field spectra. More importantly, we investigate the near-field properties in both the frequency and time domains using photoemission electron microscopy. In the frequency domain, the near-field spectra visually demonstrate normal-mode splitting and display the extent of coupling. Importantly, the variation of the dephasing time of the hybrid modes against the detuning is observed directly in the time domain. These findings signify the evolution of the dissipation and the exchange of information in plasmonic strong coupling systems and pave the way to manipulate the dephasing time of plasmon modes, which can benefit many applications of plasmonics. 

Retracted: No

PubPeer comments:
 Figure 2. peaks in these spectra are growing and shifting but noise remains the same.  ,
The bromodomain protein Brd4 insulates chromatin from DNA damage signalling
Authors: Amanda M Del Rosario
Jonathan Rameseder
Clark C Chen
Qiuying Huang
Ian G Cannell
Fred C Lam
Richard Ho
Anna Fydrych
Emily J Blake
Scott M Clarke
Forest M White
Anne E Carpenter
Scott R Floyd
Grace C Chen
William C Hahn
Michael J Lee
Michael E Pacold
Michael B Yaffe
James E Bradner
David E Root
Bryan D Bryson
Amanda Maffa
Benjamin A Greenberger
David M Sabatini
Journal: Nature (2013)
Discipline: Multidisciplinary
Keywords: DNA damage; signalling network; cell-cycle progression; DNA repair factors; senescence
Affiliations: Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.

Abstract:  DNA damage activates a signalling network that blocks cell-cycle progression, recruits DNA repair factors and/or triggers senescence or programmed cell death. Alterations in chromatin structure are implicated in the initiation and propagation of the DNA damage response. Here we further investigate the role of chromatin structure in the DNA damage response by monitoring ionizing-radiation-induced signalling and response events with a high-content multiplex RNA-mediated interference screen of chromatin-modifying and -interacting genes. We discover that an isoform of Brd4, a bromodomain and extra-terminal (BET) family member, functions as an endogenous inhibitor of DNA damage response signalling by recruiting the condensin II chromatin remodelling complex to acetylated histones through bromodomain interactions. Loss of this isoform results in relaxed chromatin structure, rapid cell-cycle checkpoint recovery and enhanced survival after irradiation, whereas functional gain of this isoform compacted chromatin, attenuated DNA damage response signalling and enhanced radiation-induced lethality. These data implicate Brd4, previously known for its role in transcriptional control, as an insulator of chromatin that can modulate the signalling response to DNA damage. 

Retracted: No

PubPeer comments:
 Supplemental Fig. S1c u2013 more similar than expected  Supplemental Fig. S2c u2013 more similar than expected  Could the authors check it please? ,
Resistance Training Volume Enhances Muscle Hypertrophy but Not Strength in Trained Men
Authors: Jozo Grgic
James Krieger
Andrew Alto
Brad J Schoenfeld
Ramon Belliard
Bret Contreras
Kenneth Delcastillo
Journal: Medicine and science in sports and exercise (2019)
Discipline: CLINICAL MEDICINE
Keywords: muscular adaptations; resistance training protocols; resistance-trained men; low-volume; moderate-volume
Affiliations: Department of Health Sciences, CUNY Lehman College, Bronx, NY., Sport Performance Research Institute, AUT University, Auckland, NEW ZEALAND., Weightology, LLC, Redmond, WA., Institute for Health and Sport (IHES), Victoria University, Melbourne, AUSTRALIA.

Abstract:  Purpose: The purpose of this study was to evaluate muscular adaptations between low-, moderate-, and high-volume resistance training protocols in resistance-trained men. Methods: Thirty-four healthy resistance-trained men were randomly assigned to one of three experimental groups: a low-volume group performing one set per exercise per training session (n = 11), a moderate-volume group performing three sets per exercise per training session (n = 12), or a high-volume group performing five sets per exercise per training session (n = 11). Training for all routines consisted of three weekly sessions performed on nonconsecutive days for 8 wk. Muscular strength was evaluated with one repetition maximum (RM) testing for the squat and bench press. Upper-body muscle endurance was evaluated using 50% of subjects bench press 1RM performed to momentary failure. Muscle hypertrophy was evaluated using B-mode ultrasonography for the elbow flexors, elbow extensors, mid-thigh, and lateral thigh. Results: Results showed significant preintervention to postintervention increases in strength and endurance in all groups, with no significant between-group differences. Alternatively, while all groups increased muscle size in most of the measured sites from preintervention to postintervention, significant increases favoring the higher-volume conditions were seen for the elbow flexors, mid-thigh, and lateral thigh. Conclusions: Marked increases in strength and endurance can be attained by resistance-trained individuals with just three 13-min weekly sessions over an 8-wk period, and these gains are similar to that achieved with a substantially greater time commitment. Alternatively, muscle hypertrophy follows a dose-response relationship, with increasingly greater gains achieved with higher training volumes. 

Retracted: No

PubPeer comments:
 https: p70s6k.com 2018 09 28 some-thoughts-on-resistance-training-volume-and-hypertrophy , 
 Another commentary on this paper: https: bodyrecomposition.com research a-response-to-james-krieger , 
  Link to full-text: https: journals.lww.com acsm-msse Fulltext 2019 09000 Statistical_Power_in_a_Recent_Study_by_Schoenfeld.22.aspx  Link to full-text: https: journals.lww.com acsm-msse Fulltext 2019 09000 Response.23.aspx ,
Camptothecin Regulates Microglia Polarization and Exerts Neuroprotective Effects via Activating AKT/Nrf2/HO-1 and Inhibiting NF-Œ∫B Pathways In Vivo and In Vitro
Authors: Dewei He
Dianfeng Liu
Yingchun Su
Xiyu Gao
Bingxu Huang
Shoupeng Fu
Yufei Zhang
Ang Zhou
Jian Du
Journal: Frontiers in Immunology (2021)
Discipline: IMMUNOLOGY
Keywords: M1/M2; Parkinson‚Äôs disease; camptothecin; microglia polarization; neuroinflammation.
Affiliations: College of Animal Science and Veterinary Medicine, Jilin University, Changchun, China.

Abstract:  Microglia, the main immune cells in the brain, participate in the innate immune response in the central nervous system (CNS). Studies have shown that microglia can be polarized into pro-inflammatory M1 and anti-inflammatory M2 phenotypes. Accumulated evidence suggests that over-activated M1 microglia release pro-inflammatory mediators that damage neurons and lead to Parkinson's disease (PD). In contrast, M2 microglia release neuroprotective factors and exert the effects of neuroprotection. Camptothecin (CPT), an extract of the plant Camptotheca acuminate, has been reported to have anti-inflammation and antitumor effects. However, the effect of CPT on microglia polarization and microglia-mediated inflammation responses has not been reported. In our study we found that CPT improved motor performance of mice and reduced the loss of neurons in the substantia nigra (SN) of the midbrain in LPS-injected mice. In the mechanism study, we found that CPT inhibited M1 polarization of microglia and promotes M2 polarization via the AKT/Nrf2/HO-1 and NF-Œ∫B signals. Furthermore, CPT protected the neuroblastoma cell line SH-SY5Y and dopaminergic neuron cell line MN9D from damage mediated by microglia activation. In conclusion, our results demonstrate that CPT regulates the microglia polarization phenotype via activating AKT/Nrf2/HO-1 and inhibiting NF-Œ∫B pathways, inhibits neuro-inflammatory responses, and exerts neuroprotective effects in vivo and in vitro. 

Retracted: No

PubPeer comments:
 Dear authors, Fig.4M contains a WB image with a potentially spliced band. Could you please provide the uncropped original image for this particular WB for reviewing? Contrast enhanced:  , 
 Dear Heterochasta Lasioplaca, Thanks for your comments. After receiving your comments, we carefully checked our original results.In Figure 4, the image of Ym-1 was indeed in the form presented in the paper, without splicing. We have provided the uncropped original image for this particular WB for reviewing, as shown below:  , 
 Dear Dianfeng, Thank you for providing the original blot image and for the transparency. It is indeed from the same blot. , 
 #3 Dear Heterochasta, Thank you for your reply. Your comments help us do better. ,
Adenosine A2A receptor: a target for regulating renal interstitial fibrosis in obstructive nephropathy
Authors: Nan Yang
Wei Liu
Liang-Yi Si
Gang Meng
Xing Chen
Ren-Ping Xiong
Ping Li
Yuan-Guo Zhou
Hang Xiao
Hai-Ying Shen
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Renal interstitial fibrosis; epithelial-mesenchymal transition; inflammation; adenosine A2A receptor; RIF
Affiliations: Department of Geriatrics, Southwest Hospital, Third Military Medical University, Chongqing, China.

Abstract:  Renal interstitial fibrosis (RIF) is the common pathological process of chronic kidney diseases leading inevitably to renal function deterioration. RIF and its preceding epithelial-mesenchymal transition (EMT) are commonly triggered by an early occurring renal inflammation. However, an effective approach to prevent EMT and RIF is still lacking and of urgent need. Recently, the adenosine A2A receptor (A2AR) emerges as a novel inflammation regulator, therefore manipulation of A2AR may suppress the EMT process and as such protect against RIF. To test this hypothesis we applied a unilateral ureteral obstruction (UUO) model of RIF on A2AR knockout mice and their wild-type littermates, combined with the intervention of a selective A2AR agonist, CGS 21680. On days 3, 7 and 14 post-UUO we evaluated the effects of A2AR manipulation on the molecular pathological progresses of RIF, including the cellular component of interstitial infiltration, expression of profibrotic factors, cellular biomarkers of EMT, and collagen deposition of extracellular matrix. Our data demonstrated that activation of A2AR significantly suppressed the deposition of collagen types I and III, reduced the infiltration of CD4+ T lymphocytes, and attenuated the expression of TGF-Œ≤1 and ROCK1, which in turn inhibited and postponed the EMT progress. Conversely, genetic inactivation of A2AR exacerbated the aforementioned pathological processes of UUO-induced RIF. Together, activation of A2AR effectively alleviated EMT and RIF in mice, suggesting A2AR as a potential therapeutic target for the treatment of RIF. 

Retracted: No

PubPeer comments:
 Figure 2A. * Red boxes: Two panels appear to look similar to each other. Reported to the journal in 2015, with a friendly reminder in 2016, but no response so far.  ,
The gender gap in cystic fibrosis
Authors: Natalie Healey
Journal: Nature (2020)
Discipline: Multidisciplinary
Keywords: advances; therapies; genetic disease; women; outcomes

Abstract: Despite advances in therapies for people with the genetic disease, women seem to have poorer outcomes. Despite advances in therapies for people with the genetic disease, women seem to have poorer outcomes.

Retracted: No

PubPeer comments:
 Nature has added a plainly false claim to this article: (Nature recognizes that sex and gender are not the same, and are neither fixed nor binary.) This is beyond bizarre and directly contradicts elementary biology. There are an uncountable number of articles in Nature which report to the sex of cells and organisms as male or female. Many of those articles would make much less sense if the sex of those cells was not fixed or not binary. Just look back a few years in Nature: [Janine A. Clayton and Francis S. Collins unveil policies to ensure that preclinical research funded by the US National Institutes of Health considers females and males.] [Researchers are using state-of-the-art molecular biology to delve into the sex chromosomes, particularly the X. Their findings are feeding into a new way of thinking about how the X and Y chromosomes make the two sexes different] Nature has clearly claimed credit for the bizarre false claim in this  editorially independent supplement and can t point to their (clearly entirely unproblematic) acceptance of financial support from third parties. This article is part of Nature Outlook: Cystic fibrosis, an editorially independent supplement produced with the financial support of third parties. [Hilton et al. have written pointing out the harms from this type of open anti-intellectualism.] Perhaps reincarnation, resurrection and transubstantiation are next for Nature. Perhaps intelligent design ? What an exciting future! , 
 Can pubpeer provide any explanation as to why my comment was moderated? There was no breaking of any guideline, just the clear demonstration that sex is not binary and not fixed is false. ,
6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3
Authors: Tuo Zhang
Wei Quan
Mingyang Kang
Chunyang Kang
Yingying Han
Jian Gao
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 6-gingerols; BNIP3; MiR-103; cell apoptosis; cell autophagy
Affiliations: a Department of Neurology , China-Japan Union Hospital of Jilin University , Changchun , China., b Department of Spine Surgery , The Second Hospital of Jilin University , Changchun , China., c Northeast Normal University , Changchun , China., d Department of Neurosurgery , China-Japan Union Hospital of Jilin University , Changchun , China.

Abstract:  Finding novel therapeutic agent for the treatment of cerebral ischemia is urgently required. These experiments explored the potential roles of 6-Gingerols (6G) in hypoxia-stimulated rat PC-12 cells. Cell viability, apoptosis and its related proteins were studied by the approaches of MTT assay, flow cytometry assay and Western blot analysis, respectively. In addition, whether 6G achieved its functions in hypoxia-induced injury through miR-103 was illustrated. Moreover, the associated signalling pathways were investigated. Obviously, hypoxia treatment blocked cell viability and enhanced apoptosis while this trend was ameliorated by 6G. Then we observed that hypoxia administration up-regulated miR-103 expression and 6G could further increase miR-103 expression in hypoxia-stimulated PC-12 cells. Inhibition of miR-103 attenuated the neuroprotective effects of 6G on hypoxia-treated PC-12 cells. Moreover, Bcl2/adenovirus EIB 19kD-interacting protein 3 (BNIP3) was a target of miR-103 and BNIP3 upregulation also attenuated the neuroprotective impact of 6G on hypoxia-treated PC-12 cells. Hypoxia activated the p38MAPK and JNK pathways were inactivated by 6G. To sum up, 6G protected hypoxia-stimulated PC-12 cells through miR-103-mediatated down-regulation of BNIP3 by inhibiting p38 MAPK and JNK pathways. Highlights 6-Gingerols (6G) is a promising agent for cerebral ischemia therapy. The neuroprotective effects of 6G are mediated by miR-103 and BNIP3. Up-regulation of miR-103 exerts neuroprotective effects. 

Retracted: No

PubPeer comments:
 To plagiarise a comment from another thread:  The Western blots and other figures in this paper have an interesting layout that appears to be shared with many other papers, as discussed in a January 2020 post on Leonid Schneider s blog: https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing In almost all papers, Western blot panels within the same figure, and across figures and papers, appear to share the same background, while the bands are regularly spaced, all have similar rounded edges without the usual smudges and specks, and with some bands showing a recognizable  jumping sardine shape.  ,
Downregulation of microRNA-17-5p improves cardiac function after myocardial infarction via attenuation of apoptosis in endothelial cells
Authors: Shuo Yang
Hong Jiang
Jing Chen
Qi Hu
Bofang Zhang
Weipan Xu
Tao Fan
Jian Yang
Changwu Xu
Journal: Molecular Genetics and Genomics (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Apoptosis; Endothelial cells; MicroRNA-17-5p; Myocardial infarction.
Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, 238 JieFang Road, Wuhan, 430060, China., Department of Thoracic Surgery, Remin Hospital of Wuhan University, Wuhan, China., Department of Cardiology, Huangshi Central Hospital, Huangshi, China., Department of Cardiology, Yichang Central People's Hospital, Yichang, China., Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, 238 JieFang Road, Wuhan, 430060, China. .

Abstract:  MicroRNA-17-5p (miR-17-5p) was indicated to suppress the formation of blood vessels, which is associated with cardiac function after myocardial infarction. In this study, the relationship between miR-17-5p and cardiac function was researched. Human umbilical vein endothelial cells were infected with adenoviruses. Apoptosis was determined by Annexin V-7AAD/PI. Real-time RT-PCR was used to evaluate miR-17-5p and ERK levels. Western blotting was used to determine the levels of ERK, the anti-apoptosis protein bcl-2 and apoptosis proteins, including bax, caspase 3, and caspase 9. An in vivo acute myocardial infarction (AMI) model was established in SD male rats. Heart function was evaluated by echocardiography prior to inducing AMI and after 7 and 28 days later. The heart was removed to perform histological examination, real-time RT-PCR, and western blotting, as described above. The result indicated that the ERK pathway was activated by miR-17-5p downregulation and an increase in the level of the anti-apoptosis protein bcl-2; however, the levels of apoptosis proteins (bax/caspase 3/caspase 9) were decreased. The results were completely reversed when miR-17-5p was up-regulated. At 7 and 28 days after the induction of AMI, in the miR-17-5p inhibition group, the infarction areas and collagen fibers were decreased, apoptosis in cardiac tissues was inhibited, and the endothelial growth process was promoted. Therefore, MiR-17-5p silencing protects heart function after AMI through decreasing the rate of apoptosis and repairing vascular injury. 

Retracted: No

PubPeer comments:
 Figure 4C has 2 images which appear to be the same with different dimensions. Some shared features indicated. *** Contrast adjusted  ,
Ostreolysin induces browning of adipocytes and ameliorates hepatic steatosis
Authors: Katerina Staikin
Irena Peri
Lili Nimri
Betty Schwartz
Einav Yehuda-Shnaidman
Journal: Journal of Gastroenterology and Hepatology (2018)
Discipline: CLINICAL MEDICINE
Keywords: browning; inflammation; non-alcoholic fatty liver disease; ostreolysin; steatosis.
Affiliations: Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot, Israel., Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and EnvironmentThe Hebrew University of Jerusalem Rehovot Israel

Abstract:  Background and aim: Non-alcoholic fatty liver disease (NAFLD) is associated with all features of the metabolic syndrome. Deposition of excess triglycerides in liver cells, a hallmark of NAFLD, is associated with loss of insulin sensitivity. Ostreolysin (Oly) is a 15-kDa fungal protein known to interact with cholesterol-enriched raft-like membrane domains. We aim to test whether a recombinant version of Oly (rOly) can induce functional changes in vitro in adipocytes or in vivo in mice fed a high-fat diet (HFD). Methods: White preadipocyte 3T3-L1 cells or mouse primary adipocytes treated with rOly. Male C57BL/6 mice were fed a control or HFD and treated with saline or with rOly (1 mg/kg BW) every other day for 4 weeks. Results: White preadipocyte 3T3-L1 cells or mouse primary adipocytes treated with rOly acquire a browning phenotype through activation of 5' adenosine monophosphate-activated protein kinase and downregulation of tumor necrosis factor Œ±-mediated activation of IŒ∫B kinase Œµ and TANK-binding kinase 1. HFD-fed mice treated with rOly showed a 10% reduction in BW and improved glucose tolerance, which paralleled improved expression of liver and adipose functionality, metabolism, and inflammation status, mimicking the in vitro findings. Conclusion: This study provides first evidence of rOly's prevention of HFD-induced NAFLD by stimulating liver and adipose muscle tissue functionality and oxidative potential, improving glucose tolerance, and ameliorating the metabolic profile of diet-induced obese mice. 

Retracted: No

PubPeer comments:
 Figure 2. * Red boxes: The b-Actin panel in A (3T3-L1 adipocytes) looks similar to the b-actin panel in E (primary epididymal fat pad adipocytes). * Blue boxes: In the PGC1a panel in Figure 2A, lanes 1 and 2 look similar to lanes 3 and 4.  ,
Elemene displays anti-cancer ability on laryngeal cancer cells in vitro and in vivo
Authors: Liang Zhou
Min Yao
Luying Zheng
Lei Tao
Journal: Cancer Chemotherapy and Pharmacology (2006)
Discipline: CLINICAL MEDICINE
Keywords: Elemene; Laryngeal cancer cells; Inhibitory effects; Mechanism; Growth
Affiliations: Department of otolaryngology-HNS, Eye, Ear, Nose and Throat Hospital of Fudan University, 83 Fenyang Road, Shanghai, 200031, China.

Abstract:  Purpose: The goal of this study is to investigate the inhibitory effects and mechanism of elemene on the growth of laryngeal cancer cells in vitro and in vivo. Methods: Laryngeal cancer cells (HEp-2 cells) were grown in elemene, cisplatin, or a combination of the drugs. The cytotoxic, or apoptotic, effects of elemene on the cells were evaluated by a 3-[4,5-dimethylthiazol-2yl]-2,5-diphenyltetrazolium bromide assay, flow cytometry, and a caspase-3 activity assay. A Western blot was used to semi-quantify the protein expression of eukaryotic initiation factors (eIF4E and eIF4G), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF); RT-PCR analysis semi-quantified the mRNA transcript expression of bFGF and VEGF. The HEp-2 cells were transplanted subcutaneously to BALB/c nude mice to produce solid tumors. Elemene and cisplatin were administered to the mice either as individual drugs or in combination. The tumors were excised and immunostained to determine the effect each drug had on tumor size, eIF levels, angiogenic factors, and microvessel density (MVD). Results: Elemene inhibited the growth of HEp-2 cells in vitro in a dose- and time-dependent manner with an IC(50) of 346.5 microM (24 h incubation). Increased apoptosis was observed in elemene-administered cells. Elemene is suspected to enhance caspase-3 activity, and thus inhibit protein expression of eIFs (4E, 4G), bFGF, and VEGF. In vivo, the growth of HEp-2 cell-transplanted tumors in nude mice was inhibited by intraperitoneal injection of elemene. Compared with control groups, elemene significantly inhibited the protein expression of eIFs (4E and 4G), bFGF, and VEGF and decreased the MVD. Conclusions: Elemene inhibits the growth of HEp-2 cells in vitro and in vivo. These data provide useful information for further clinical study on the treatment of LSCC by elemene. 

Retracted: No

PubPeer comments:
 Figure 2A: * Rounded boxes of the same color highlight areas that look repetitive within or between panels Figure 3AB: * Rectangular boxes of the same color highlight lanes that look more similar than expected Reported to the journal together with 28 other papers in the summer of 2015, with a friendly reminder in April 2017, but no answer. With the exception of one paper, the journal did not correct or retract a single paper from this set.  ,
Œë-synuclein induces microglial cell migration through stimulating HIF-1Œ± accumulation
Authors: Ni Zhang
Zhonghen Wu
Qiaojun Zhang
Wenjuan Li
Xijing He
Dong Wang
Hongfei Qiao
Yanping Hui
Libo Li
Journal: Journal of neuroscience research (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: HIF-1Œ±; caveolin-1; microglial cell; spinal cord injury; toll-like receptor 7/8.
Affiliations: Departments of Rehabilitation Medicine, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China., Departments of Orthopedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Abstract:  Microglial cell migration and infiltration plays a critical role in spinal cord injury after thoracoabdominal aortic surgery. In our previous study, Œ±-synuclein, a presynaptic protein was shown to be released from injured neurons and cause microglial cell activation. Here, we aimed to explore the effect of Œ±-synuclein on microglial cell migration. Primary microglial cells were isolated from Sprague-Dawley rats and then exposed different doses (0.2, 0.4, and 0.6 ŒºM) of Œ±-synuclein oligomers. The mRNA and protein levels of HIF-1Œ± were then analyzed by qRT-PCR and Western blot. Cell migration was examined by a 96-well Boyden chamber. Moreover, toll-like receptor (TLR) 2-expression as well as TLR7/8-expression was inhibited by specific siRNA transfection. HIF-1Œ± was overexpressed by Ad-HIF-1Œ± transfection. In the results, Œ±-synuclein was found to stimulate HIF-1Œ± accumulation in microglial cells in a dose-dependent manner. Silencing HIF-1Œ± expression dampened Œ±-synuclein induced microglial cell migration. Furthermore, blockade of TLR7/8 expression but not TLR2 expression reduced HIF-1Œ± accumulation in microglial cells. In addition, overexpressed HIF-1Œ±, along with Src, prompted caveolin-1 expression and phosphorylation, as well as migration in microglial cells. Œë-synuclein acts via TLR7/8 and enhances HIF-1Œ± expression, which might play a regulatory role in microglial cell migration. ¬© 2017 Wiley Periodicals, Inc. 

Retracted: No

PubPeer comments:
 This article seems to have multiple image duplications Figure 1E demonstrating concentrations of 0.4 and 0.6 show different parts of the same area (green circle). Arrows show patchwork.  Figure 4C: control and adHIF-1a (middle row) is the continuation of the same picture  ,
Recombinant Adeno-associated Virus Serotypes 2‚Ä?and 5‚ÄìMediated Gene Transfer in the Mammalian Brain: Quantitative Analysis of Heparin Co-infusion
Authors: Robert M Kotin
Matthew J During
Kristin Baer
Mihail Y Mastakov
Journal: Molecular Therapy (2002)
Discipline: CLINICAL MEDICINE
Keywords: Recombinant adeno-associated viruses; gene delivery; CNS; transduction levels; injection parameters

Abstract:  Recombinant adeno-associated viruses (rAAVs) are among the most promising vectors for gene delivery into the CNS. However, a major hurdle for gene transfer to the mammalian brain is to achieve high transduction levels in target cells beyond the immediate injection site. Therefore, building upon the optimization of injection parameters on which we have recently reported, it is important to define additional methods to increase the volume of distribution. Here, we establish an optimal heparin concentration, and show that co-injection of heparin together with rAAV2 leads to a significantly higher and more homogeneous distribution of transduced cells. In contrast, the diffusion pattern of rAAV serotype 5 differs from that of rAAV2, in that its distribution is less homogeneous, more variable, and patchy. Furthermore, this study illustrates the influence of receptor binding on the expression pattern following injection of rAAV in the CNS. In addition to improvements in expression cassettes and viral titers and the use of very slow infusion rates, gene transfer studies in the CNS where the goal is to obtain widespread transduction should consider co-injecting the viral vector rAAV2 with heparin to maximize transduction efficiency and viral spread. 

Retracted: No

PubPeer comments:
 An image in Figure 2 appears to have a region which is duplicated, although there are both similarities (several identified by ellipses) *and* differences in the seemingly repeated region. Difficult to understand how this could occur by chance. ***  *** Here s a closeup without the internal features annotated  ,
Abundant DNA 6mA methylation during early embryogenesis of zebrafish and pig
Authors: Yanan Yue
Yuanxiang Zhu
Hang Yin
Dali Han
Guan-Zheng Luo
Yizhen Wang
Kai Chen
Xin Zong
Ye Fu
Xiaona Wang
Dahua Chen
Xinxia Wang
Chuan He
Jianzhao Liu
Journal: Nature communications (2016)
Discipline: Multidisciplinary
Keywords: DNA modification; N6-methyldeoxyadenosine; epigenetic roles; embryogenesis; vertebrates
Affiliations: Department of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, The University of Chicago, 929 East 57th Street, Chicago, Illinois 60637, USA., State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China., Key Laboratory of Animal Nutrition and Feed Sciences, Ministry of Agriculture, College of Animal Sciences, Zhejiang University, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.

Abstract:  DNA N6-methyldeoxyadenosine (6mA) is a well-known prokaryotic DNA modification that has been shown to exist and play epigenetic roles in eukaryotic DNA. Here we report that 6mA accumulates up to ‚à?.1-0.2% of total deoxyadenosine during early embryogenesis of vertebrates, but diminishes to the background level with the progression of the embryo development. During this process a large fraction of 6mAs locate in repetitive regions of the genome. 

Retracted: No

PubPeer comments:
 The major conclusion of this paper was just reports to be an artifact of bacterial contamination in early zebrafish embryos. The evidence that the DNA 6mA methylation occurs in zebrafish DNA is weak. https: bmcgenomics.biomedcentral.com articles 10.1186 s12864-019-5754-6 , 
 Bacterial contamination was the source of abundant 6mA in early zebrafish embryogenesis https: bmcgenomics.biomedcentral.com articles 10.1186 s12864-019-5754-6 , 
 Authors should check another recent well executed study showing that previous reports of 6mA in higher organisms are artifactual: No evidence for DNA N6-methyladenine in mammals https: advances.sciencemag.org content 6 12 eaay3335 ,
Inflammation, but not hypoxia, mediated HIF-1alpha activation depends on COX-2
Authors: David R O&#x27;Brien
Zaver M Bhujwalla
Ioannis Stasinopoulos
Journal: Cancer biology & therapy (2009)
Discipline: CLINICAL MEDICINE
Keywords: COX pathway; pharmaceutical intervention; inflammatory component; asthma; Alzheimer's
Affiliations: The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

Abstract:  The COX pathway has been a target for pharmaceutical intervention in diseases with a high inflammatory component ranging from asthma and Alzheimer's to arthritis and cancer. A major transcriptional promoter of the malignant phenotype, HIF-1alpha, has been observed to be regulated by the COX-2 product PGE2. Here we show that HIF-1alpha protein significantly accumulated in human breast cancer MDA-MB-231 cells in response to the pro-inflammatory cytokine IL-1beta, but not in COX-2-silenced MDA-MB-231 cells. In contrast HIF-1alpha expression could be detected in COX-2- silenced cells in response to the hypoxia-mimetic agent CoCl(2) and hypoxia. Gene expression profiling in COX-2-containing and COX-2-silenced cells showed that the hypoxia-induced transcriptional response is largely unaffected by COX-2 silencing. These data suggest that the profound effects of COX-2 silencing on inhibiting invasion, tumor growth and metastasis from MDA-MB-231 cells are dependent on the induction of IL-1beta-dependent COX-2 and HIF-1alpha but are independent of hypoxia 

Retracted: No

PubPeer comments:
 Much more similar than you wuld expect for different samples. Figure 1A. https: imgur.com EqG1bQ0 Figure 1B. https: imgur.com iFZXMUd , 
 It is difficult to see the similarities in the images. Can the images be enlarged and compared side by side. It appears that the Pooled samples of the western results were spliced in. Perhaps the authors can comment on this please? ,
microRNA-223 promotes the growth and invasion of glioblastoma cells by targeting tumor suppressor PAX6
Authors: Xiao-Bo Li
Yang Han
Bai-Sheng Huang
Li-Jun Cao
Li-Xiang Wu
Qi-Zhi Luo
Journal: Oncology Reports (2013)
Discipline: CLINICAL MEDICINE
Keywords: Glioblastoma; microRNAs; miR-223; PAX6; cell invasiveness
Affiliations: Department of Physiology, Xiangya School of Medicine, Central South University, Changsha 410078, P.R. China.

Abstract:  Glioblastoma is the most common primary central nervous system malignancy and its unique invasiveness hinders effective treatment. Its high invasiveness may be controlled partly by microRNAs (miRNAs, miRs) and their target genes. In the present study, we found that increased miR-223 expression and reduced PAX6 expression coexisted in glioblastoma as detected by quantitative PCR or tissue microarrays. We confirmed that miR-223 directly targets PAX6 through binding to its 3'-UTR using dual luciferase reporter assay. In U251 and U373 glioblastoma cells, overexpression of miR-223 decreased PAX6 mRNA and protein expression; however, inhibition of miR-223 increased PAX6 mRNA and protein expression. Moreover, overexpression of miR-223 led to effects similar to those of PAX6 knockdown: increased cell viability, increased percentage of cells in the G1 phase and increased cell invasiveness parallel with increased MMP2, MMP9 and VEGFA expression. In addition, inhibition of miR-223 resulted in effects similar to those of PAX6 overexpression: decreased cell viability, decreased percentage of cells in the G1 phase and decreased cell invasiveness parallel with reduced MMP2, MMP9 and VEGFA expression. The data presented here suggest that miR-223 promotes the growth and invasion of U251 and U373 glioblastoma cells by targeting PAX6, which serves as a tumor suppressor in glioblastoma exerting the functions of inhibition of cell cycle transition, and the expression of MMP2, MMP9 and VEGFA. In conclusion, the present study supports miR-223 and PAX6 as novel therapeutic targets for glioblastoma. 

Retracted: No

PubPeer comments:
 FIG 4 duplication  , 
 #1 Dear Mss. Thank you very much for the appreciation. This is a clear figure montage error, which has not been detected by the authors or the reviewers of the manuscript. Today I will send a letter warning of the error and the correct figure 4 (panel I) to the editorial team of Respiratory research.  , 
 Thank you for the correction. ,
Inhibition of Sp1 prevents ER homeostasis and causes cell death by lysosomal membrane permeabilization in pancreatic cancer
Authors: Bhuwan Giri
Vikas Dudeja
Patricia Dauer
Alice Nomura
Vineet K Gupta
Sulagna Banerjee
Ashok K Saluja
Olivia McGinn
Nikita S Sharma
Nivedita Arora
Journal: Scientific reports (2017)
Discipline: Multidisciplinary
Keywords: Endoplasmic reticulum stress; unfolded protein response; pancreatic ductal adenocarcinoma; specificity protein 1; chronic ER stress
Affiliations: Department of Pharmacology, University of Minnesota, Minneapolis, MN, 55455, USA., Department of Surgery, University of Miami, Miami, FL, 33136, USA., Department of Surgery, University of Miami, Miami, FL, 33136, USA. .

Abstract:  Endoplasmic reticulum (ER) stress initiates an important mechanism for cell adaptation and survival, named the unfolded protein response (UPR). Severe or chronic/prolonged UPR can breach the threshold for survival and lead to cell death. There is a fundamental gap in knowledge on the molecular mechanism of how chronic ER stress is stimulated and leads to cell death in pancreatic ductal adenocarcinoma (PDAC). Our study shows that downregulating specificity protein 1 (Sp1), a transcription factor that is overexpressed in pancreatic cancer, activates UPR and results in chronic ER stress. In addition, downregulation of Sp1 results in its decreased binding to the ER stress response element present in the promoter region of Grp78, the master regulator of ER stress, thereby preventing homeostasis. We further show that inhibition of Sp1, as well as induction of ER stress, leads to lysosomal membrane permeabilization (LMP), a sustained accumulation of cytosolic calcium, and eventually cell death in pancreatic cancer. 

Retracted: No

PubPeer comments:
 Could the authors clarify whether the control images marked in red are intended to be the same? I note that the control bars in the chart appear to have different values for controls. ***  , 
 Controls for panel B and C are the same. They have just been represented as separate panels for ease of explanation. They show staining for Cathepsin B and Lysotracker. Figure panel A and C and representations of cytosolic cathepsin B activity assay and not a quantitation of the figure. hence the control values are slightly different between the two treatments. This difference however is not significant. ,
Evaluation of anti-apoptotic activity of different dietary antioxidants in renal cell carcinoma against hydrogen peroxide
Authors: Rajeev K Tyagi
Suresh P Vyas
Neeraj K Garg
Sharad Mangal
Abhinav Mehta
Tejram Sahu
Journal: Asian Pacific Journal of Tropical Biomedicine (2011)
Discipline: CLINICAL MEDICINE
Keywords: Anticancer; Antioxidants; Apoptosis; Hydrogen peroxide; RCC-26

Abstract:  Objective: To evaluate the anti-apoptotic and radical scavenging activities of dietary phenolics, namely ascorbic acid,Œ±-tocopherol acetate, citric acid, salicylic acid, and estimate H2O2-induced apoptosis in renal cell carcinoma cells. Methods: The intracellular antioxidant potency of antioxidants was investigated. H2O2-induced apoptosis in RCC-26 was assayed with the following parameters: cell viability (% apoptosis), nucleosomal damage and DNA fragmentation, bcl-2 levels and flow cytometery analysis (ROS production evaluation). Results: The anticancer properties of antioxidants such as ascorbic acid, Œ±-tocopherol acetate, citric acid, salicylic acid with perdurable responses were investigated. It was observed that these antioxidants had protective effect (anti-apoptotic activity) against hydrogen peroxide (H2O2) in renal cell carcinoma (RCC-26) cell line. Conclusions: This study reveals and proves the anticancer properties. However, in cancer cell lines anti-apoptotic activity can indirectly reflect the cancer promoter activity through radicals scavenging, and significantly protect nucleus and bcl-2. 

Retracted: No

PubPeer comments:
null, 
 #1  In Figure 9, identical cells appear to be visible multiple times in different panels, even though each panel represents different experimental conditions. Peer 1 s original illustrations 2 and 3 were lost in the Great Changeover from PubPeer 1.0 to 2.0. Here s my own version of some of the issues with Fig 9:  , 
 #1  In Figure 6, two lane appear to be visible multiple times, albeit stretched different ways. Lanes VII and X appear very similar to each other (shown in yellow boxes) Lanes II, V, AI, VIII, IX, and XI also appear to be very similar to each other (shown in red boxes). In addition, the bottom part of lane IV appear similar to these other lanes as well. I have not drawn the yellow and red boxes to match Peer 1 s description, but here is Figure 6 for readers to judge for themselves.  ,
DDB2, an essential mediator of premature senescence
Authors: Carmen Dominguez-Brauer
Hyun Jung Park
Nilotpal Roy
Tanya Stoyanova
Srilata Bagchi
Pradip Raychaudhuri
Journal: Molecular and cellular biology (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Reactive oxygen species; premature senescence; nucleotide excision repair protein DDB2; ROS accumulation; antioxidant genes
Affiliations: Center of Molecular Biology of Oral Diseases (M/C 860), College of Dentistry, Cancer Center, University of Illinois at Chicago, 801 S. Paulina Ave., Chicago, IL 60612, USA., Department of Biochemistry and Molecular Genetics (M/C 669), Cancer Center, University of Illinois at Chicago, 900 S. Ashland Ave., Chicago, Illinois 60607, Center of Molecular Biology of Oral Diseases (M/C 860), College of Dentistry, Cancer Center, University of Illinois at Chicago, 801 S. Paulina Ave., Chicago, Illinois 60612

Abstract:  Reactive oxygen species (ROS) is critical for premature senescence, a process significant in tumor suppression and cancer therapy. Here, we reveal a novel function of the nucleotide excision repair protein DDB2 in the accumulation of ROS in a manner that is essential for premature senescence. DDB2-deficient cells fail to undergo premature senescence induced by culture shock, exogenous oxidative stress, oncogenic stress, or DNA damage. These cells do not accumulate ROS following DNA damage. The lack of ROS accumulation in DDB2 deficiency results from high-level expression of the antioxidant genes in vitro and in vivo. DDB2 represses antioxidant genes by recruiting Cul4A and Suv39h and by increasing histone-H3K9 trimethylation. Moreover, expression of DDB2 also is induced by ROS. Together, our results show that, upon oxidative stress, DDB2 functions in a positive feedback loop by repressing the antioxidant genes to cause persistent accumulation of ROS and induce premature senescence. 

Retracted: Yes

PubPeer comments:
null, 
 These were the problems reported to the journal in September 2016. * Purple boxes: Two panels in Figure 5A appear to show an overlap * Red boxes: Three panels in Figure 6B appear to show an overlap, some are rotated * Green, pink, orange, moss, brown, blue, etc rounded boxes: Several bands in Figure 8 appear to be visible multiple times.  This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
Restoration of SHIP-1 activity in human leukemic cells modifies NF-kappaB activation pathway and cellular survival upon oxidative stress
Authors: E Charlier
C Erneux
G Gloire
J Piette
C Volanti
S Rahmouni
A Chariot
Journal: Oncogene (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NF-kappaB; redox regulation; leukemic cells; hydrogen peroxide; IKK
Affiliations: Virology-Immunology Unit, University of Li√®ge, Li√®ge, Belgium.

Abstract:  Nuclear factor-kappa B (NF-kappaB) is an important prosurvival transcription factor activated in response to a large array of external stimuli, including reactive oxygen species (ROS). Previous works have shown that NF-kappaB activation by ROS involved tyrosine phosphorylation of the inhibitor IkappaBalpha through an IkappaB kinase (IKK)-independent mechanism. In the present work, we investigated with more details NF-kappaB redox regulation in human leukemic cells. By using different cell lines (CEM, Jurkat and the subclone Jurkat JR), we clearly showed that NF-kappaB activation by hydrogen peroxide (H2O2) is cell-type dependent: it activates NF-kappaB through tyrosine phosphorylation of IkappaBalpha in Jurkat cells, whereas it induces an IKK-mediated IkappaBalpha phosphorylation on S32 and 36 in CEM and Jurkat JR cells. We showed that this H2O2-induced IKK activation in CEM and Jurkat JR cells is mediated by SH2-containing inositol 5'-phosphatase 1 (SHIP-1), a lipid phosphatase that is absent in Jurkat cells. Indeed, the complementation of SHIP-1 in Jurkat cells made them shift to an IKK-dependent mechanism upon oxidative stress stimulation. We also showed that Jurkat cells expressing SHIP-1 are more resistant to H2O2-induced apoptosis than the parental cells, suggesting that SHIP-1 has an important role in leukemic cell responses to ROS in terms of signal transduction pathways and apoptosis resistance, which can be of interest in improving ROS-mediated chemotherapies. 

Retracted: No

PubPeer comments:
 Figure 5b. Much more similar than you would expect. https: imgur.com yIEjCnP , 
 Figure 6. Much more similar than you would expect. https: imgur.com w9VDMWM , 
 Anti-SHIP1 blots were done for normalization purposes. Indeed, both highlighted in blue are identical. The anti-SHIP1 D672A blot illustrated in Figure 5B is mislabeled and is actually a mistake as it should not have been illustrated there. The correct loading control cannot be provided since the cellular extracts are not available anymore. Figure 6 is showing IKK kinase assays controlled with GST IkBa coomassie blue gels. This is not the most sensitive way to control western blots. A better way would have been the use of anti-GST or anti IkBa antibodies. This mistake does not have any influence on the conclusions raised in both figures. ,