PReD-Bench/PRed-Bench huggingface dataset:
Large cation ethylammonium incorporated perovskite for efficient and spectra stable blue light-emitting diodes
Authors: Jingbi You
Qiufeng Ye
Fei Ma
Huixiong Deng
Yang Zhao
Zema Chu
Cai-Xin Zhang
Xingwang Zhang
Feng Gao
Zhigang Yin
Junhua Meng
Journal: Nature Communications (2020)
Discipline: Multidisciplinary
Keywords: Perovskite light-emitting diodes; external quantum efficiency; blue emission; cation CH3CH2NH2+; bandgap
Affiliations: Key Laboratory of Semiconductor Materials Science, Institute of Semiconductors, Chinese Academy of Sciences, Beijing, 100083, P. R. China., Center of Materials Science and Optoelectronics Engineering, University of Chinese Academy of Sciences, Beijing, 100049, P. R. China., State Key Lab Superlattices & Microstruct, Beijing 100083, Institute of Semiconductors, Chinese Academy of Sciences, Beijing, 100083, P. R. China., Key Laboratory of Semiconductor Materials Science, Institute of Semiconductors, Chinese Academy of Sciences, Beijing, 100083, P. R. China. ., Center of Materials Science and Optoelectronics Engineering, University of Chinese Academy of Sciences, Beijing, 100049, P. R. China. .

Abstract:  Perovskite light-emitting diodes (PeLEDs) have showed significant progress in recent years; the external quantum efficiency (EQE) of electroluminescence in green and red regions has exceeded 20%, but the efficiency in blue lags far behind. Here, a large cation CH3CH2NH2+ is added in PEA2(CsPbBr3)2PbBr4 perovskite to decrease the Pb-Br orbit coupling and increase the bandgap for blue emission. X-ray diffraction and nuclear magnetic resonance results confirmed that the EA has successfully replaced Cs+ cations to form PEA2(Cs1-xEAxPbBr3)2PbBr4. This method modulates the photoluminescence from the green region (508 nm) into blue (466 nm), and over 70% photoluminescence quantum yield in blue is obtained. In addition, the emission spectra is stable under light and thermal stress. With configuration of PeLEDs with 60% EABr, as high as 12.1% EQE of sky-blue electroluminescence located at 488 nm has been demonstrated, which will pave the way for the full color display for the PeLEDs. 

Retracted: No

PubPeer comments:
 There is a obvious mistake in the manuscript, the large cation should be CH3CH2NH3+, instead of CH3CH2NH2+. Could the author double check? ![file] ![file] , 
 Dear Cophyla, Thank you so much for your kind remind and careful reading. Sorry for the typo, we will correct it. Best Regards Jingbi You ,
The hydrophobic cysteine-rich domain of SNAP25 couples with downstream residues to mediate membrane interactions and recognition by DHHC palmitoyl transferases
Authors: Masaki Fukata
Gerald R Prescott
Jennifer Greaves
Christine Salaun
Yuko Fukata
Luke H Chamberlain
Journal: Molecular Biology of the Cell (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SNAP25; membrane association; palmitoylation; DHHC palmitoyl transferases; syntaxin 1A
Affiliations: Centre for Integrative Physiology, School of Biomedical Sciences, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom., *Centre for Integrative Physiology, School of Biomedical Sciences, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom;, Division of Membrane Physiology, National Institute for Physiological Sciences, Okazaki 444-8787, Japan;, INSERM U845, Faculte de Medecine Paris Descartes–Site Necker, 75730 Paris Cedex 15, France

Abstract:  SNAP25 is synthesized as a soluble protein but must associate with the plasma membrane to function in exocytosis; however, this membrane-targeting pathway is poorly defined. SNAP25 contains a palmitoylated cysteine-rich domain with four cysteines, and we show that coexpression of specific DHHC palmitoyl transferases is sufficient to promote SNAP25 membrane association in HEK293 cells. siRNA-mediated knockdown of its SNARE partner, syntaxin 1A, does not affect membrane interaction of SNAP25 in PC12 cells, whereas specific cysteine-to-alanine mutations perturb membrane binding, which is restored by leucine substitutions. These results suggest a role for cysteine hydrophobicity in initial membrane interactions of SNAP25, and indeed other hydrophobic residues in the cysteine-rich domain are also important for membrane binding. In addition to the cysteine-rich domain, proline-117 is also essential for SNAP25 membrane binding, and experiments in HEK293 cells revealed that mutation of this residue inhibits membrane binding induced by coexpression with DHHC17, but not DHHC3 or DHHC7. These results suggest a model whereby SNAP25 interacts autonomously with membranes via its hydrophobic cysteine-rich domain, requiring only sufficient expression of partner DHHC proteins for stable membrane binding. The role of proline-117 in SNAP25 palmitoylation is one of the first descriptions of elements within substrate proteins that modulate DHHC specificity. 

Retracted: No

PubPeer comments:
 Figure 9. Much more similar than expected. ![file] ,
The Role, Function, and Mechanism of Long Intergenic Noncoding RNA1184 (linc01184) in Colorectal Cancer
Authors: Yan Yu
Dong-Li Zhao
Lin-Chuan Wang
Yan-Xia Sui
Journal: Disease Markers (2021)
Discipline: CLINICAL MEDICINE
Keywords: linc01184; colorectal cancer; tumorigenesis; expression pattern; mechanism
Affiliations: Department of Pathology, The First Affiliated Hospital of Xi'an Jiaotong University, Yan Ta Road No 277, Xi'an, Shaanxi Province 710061, China., Department of Radiotherapy, The First Affiliated Hospital of Xi'an Jiaotong University, Yan Ta Road No 277, Xi'an, Shaanxi Province 710061, China., Inspection Department of Hong-Hui Hospital, Xi'an Jiaotong University College of Medicine, Nan Guo Road No 76, Xi'an, Shaanxi Province 710041, China., Department of Clinical Laboratory, The First Affiliated Hospital of Xi'an Jiaotong University, Yan Ta Road No 277, Xi'an, Shaanxi Province 710061, China.

Abstract:  Background: Long intergenic noncoding RNA1184 (linc01184) has been recently discovered; however, its role in human diseases is limited to date. The present study is aimed at investigating the expression pattern and mechanism of linc01184 in colorectal cancer (CRC) tumorigenesis. Methods: The expression of linc01184 in CRC tissues and cell lines was compared with that in normal controls. The functions of linc01184 in CRC cells were identified by overexpression and small interfering RNA (siRNA) approaches in vitro. Meanwhile, the target gene prediction software, luciferase reporter, RNA pull-down, and western blotting assays were used to analyze the oncogenic mechanism. Results: We found that linc01184 was obviously upregulated in CRC tissues and cells when compared to normal controls, and its upregulation had a positive association with the CRC progression. linc01184 knockdown significantly suppressed CRC cell proliferation and invasion and promoted apoptosis. Besides, linc01184 acted as a competitive endogenous RNA (ceRNA) by directly binding to microRNA-331 (miR-331), and its overexpression resulted in notable increases of human epidermal growth factor receptor 2 (HER2), phosphorylated Ser/Thr kinases (p-Akt), and extracellular regulated protein kinase 1/2 (p-ERK1/2) at posttranscriptional levels in CRC cells, which were antagonized by miR-331. Conclusions: The findings reveal for the first time that linc01184 is an enhancer for the proliferation and invasion of CRC by functioning as a ceRNA through the linc01184-miR-331-HER2-p-Akt/ERK1/2 pathway regulatory network. 

Retracted: No

PubPeer comments:
 Figure 2C 5nM siRNA for SW480 and HCT-116 overlap, possibly at different focuses: ![file] , 
 ![file] ,
MiR-378 inhibits progression of human gastric cancer MGC-803 cells by targeting MAPK1 in vitro
Authors: Bojian Fei
Haorong Wu
Journal: Oncology research (2012)
Discipline: CLINICAL MEDICINE
Keywords: Gastric cancer; microRNAs; miR-378; cell proliferation; cell cycle progression
Affiliations: Department of General Surgery, The Second Affiliated Hospital of Soochow University, SooChow, Jiangsu, PR China.

Abstract:  Gastric cancer (GC) is one of the most common cancers and the leading cause of cancer-related deaths globally. The discovery of microRNAs (miRNAs) provides a new avenue for GC diagnostic and treatment regiments. Currently, a large number of miRNAs have been reported to be associated with the progression of GC, among which miR-378 has been examined to be downregulated in GC tissues and several cell lines. However, the function of miR-378 on GC cells and the mechanisms were less known. Here we found that ectopic expression of miR-378 could inhibit cell proliferation, cell cycle progression, cell migration as well as invasion, and induced cell apoptosis in GC cell line MGC-803. Moreover, we found that oncogene mitogen-activated protein kinase 1 (MAPK1) was a target gene of miR-378 in GC cells, and the tumor-suppressive role of miR-378 might be achieved by the direct interaction with MAPK1. Taken together, our results showed that miR-378 might act as tumor suppressors in GC, and it may provide novel diagnostic and therapeutic options for human GC clinical operation in the future. 

Retracted: No

PubPeer comments:
 Although the resolution of the images is low, there appears to be a number of duplications among the images in this paper. In flow cytometry ![file] In the cell cycle analysis ![file] In the cell invasion assay ![file] And in the scratch assays ![file] ,
Efficacy and tolerability of tapentadol prolonged release in the elderly and fragile patient: an observational study
Authors: M Zampi
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Chronic pain; elderly patients; tapentadol; analgesic treatment; dual mechanism of action
Affiliations: Azienda Ospedaliero-Universitaria Federico II, Naples, Italy. .

Abstract:  Objective: The incidence of chronic pain increases with age and comorbidities, a particularly relevant issue in the elderly over the age of 80 years. Thus, the choice of the best analgesic treatment is difficult to make. The therapeutic priority in elderly patients is to favor the least invasive route of administration, and the minimum effective dose, with a gradual and slow up-titration, if needed. Tapentadol with its dual mechanism of action, combining synergistically a reduced load (&lt;40% that of strong opioids) of μ-opioid receptor agonism (MOR) with noradrenaline reuptake inhibition (NRI), can be an interesting analgesic option for geriatric patients, because of its easy manageability, the lower rate of adverse effects, the good level of analgesia, and the ability of improving the overall quality of life of elderly patients. Patients and methods: A total of 49 elderly patients (&gt;80 years) with chronic pain from different etiologies received tapentadol PR daily over 8 weeks. Results: At the end of the study, responders to treatment were 43% (20/47 patients). Compared with baseline, pain intensity, both at rest and during loading, decreased by 60% and by 55%, respectively (p&lt;0.0001). Tolerability was high throughout the study period, with 92% of patients grading it either good or excellent during follow-up. In total, 16 episodes of side effects were reported, with five considered severe and leading to therapy discontinuation. Ten cases of therapy discontinuation occurred, most of them (five patients, 10%) due to the ineffectiveness of analgesic treatment. Conclusions: Tapentadol PR, adequately titrated according to patients' need, are safe and effective to control pain in most elderly patients. 

Retracted: Yes

PubPeer comments:
 This 2019 article has been withdrawn in 2020. The retraction notice just reads  This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause. ,
ExoSTING, an extracellular vesicle loaded with STING agonists, promotes tumor immune surveillance
Authors: Joyoti Dey
Douglas E Williams
Raymond J Moniz
Chang Ling Sia
Sriram Sathyanarayanan
Joanne Lim
Kyriakos D Economides
Ke Xu
Nikki L Ross
Scott Estes
William K Dahlberg
Tong Zi
Agata Villiger-Oberbek
Kelvin Zhang
Kevin Dooley
Nuruddeen Lewis
Rane A Harrison
Raymond Bourdeau
Marc Grenley
Su Chul Jang
Katherine Kirwin
Jorge Sanchez-Salazar
Christine McCoy
Journal: Communications Biology (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CDN; STING pathway; immune activation; tumor clearance; intratumorally
Affiliations: Codiak BioSciences Inc., Cambridge, MA, USA., Presage Biosciences, Seattle, WA, USA., Codiak BioSciences Inc., Cambridge, MA, USA. .

Abstract:  Cyclic dinucleotide (CDN) agonists of the STimulator of InterferoN Genes (STING) pathway have shown immune activation and tumor clearance in pre-clinical models. However, CDNs administered intratumorally also promote STING activation leading to direct cytotoxicity of many cell types in the tumor microenvironment (TME), systemic inflammation due to rapid tumor extravasation of the CDN, and immune ablation in the TME. These result in a failure to establish immunological memory. ExoSTING, an engineered extracellular vesicle (EV) exogenously loaded with CDN, enhances the potency of CDN and preferentially activates antigen presenting cells in the TME. Following intratumoral injection, exoSTING was retained within the tumor, enhanced local Th1 responses and recruitment of CD8+ T cells, and generated systemic anti-tumor immunity to the tumor. ExoSTING at therapeutically active doses did not induce systemic inflammatory cytokines, resulting in an enhanced therapeutic window. ExoSTING is a novel, differentiated therapeutic candidate that leverages the natural biology of EVs to enhance the activity of CDNs. 

Retracted: No

PubPeer comments:
 Animal exp done all at the same? How can author validate transferring the green line over all the graphs in fig 1def? How much cdn is lost after the incorporation of CDN into EVs last step of processing with centrifugation? Was cdn alone also processed in the same way with centrifugation to compare with ExoSTING. How to be sure of the amount being injected for consistency? Legend in figure 2b implies h E analysis are from subcutaneous tumors. Is this correct? The tissue does not look like B16F10 tumors. , 
 The authors should clarify whether the green curves in Figure 1D and Figure 1F are the same groups or animals presented twice or whether they are independent experiments. If they are not independent experiments, have the exoCDN2 been directly compared to CDN2? ,
Essential role of TAK1 in regulating mantle cell lymphoma survival
Authors: Anas Younes
Dorin Toader
Jamal Saeh
Daniela Buglio
Francisco Vega
Sattva S Neelapu
Kate Byth
Sangeetha Palakurthi
Journal: Blood (2012)
Discipline: CLINICAL MEDICINE
Keywords: TAK1; lymphoma; NF-κB; p38; apoptosis
Affiliations: Department of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA.

Abstract:  TGF-β-activated kinase 1 (TAK1), a member of the MAPK kinase family, plays a key role in B-cell growth and development. In the present study, we examined the potential role of TAK1 as a therapeutic target for lymphoma. Here, we show that the active phosphorylated form of TAK1 is abundantly expressed in a panel of lymphoma cell lines, including mantle cell, anaplastic large cell, and Hodgkin lymphoma cell lines. Silencing TAK1 expression via the use of siRNA inhibited the activation of NF-κB and p38 and induced apoptosis in lymphoma cell lines. Moreover, submicromolar concentrations of AZ-TAK1, a novel ATP-competitive small molecule inhibitor of TAK1, dephosphorylated TAK1, p38, and IκB-α in lymphoma cell lines. These molecular events were associated with the release of cytochrome c into the cytosol, down-regulation of X-linked inhibitor of apoptosis, activation of caspase 9, and induction of apoptosis. We also demonstrate that primary lymphoma cells express TAK1 and pTAK1 and were sensitive to AZ-TAK1-mediated cell death. Collectively, our data demonstrate an essential role for TAK1 in regulating critical survival mechanisms in lymphoma and suggest that it may serve as a therapeutic target. 

Retracted: No

PubPeer comments:
null, 
null, 
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null, 
null, 
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 #2 but not for figure 5. ,
Evidence for the existence of a secondary pathway for fibril growth during the aggregation of tau
Authors: Jayant B Udgaonkar
Gayathri Ramachandran
Journal: Journal of Molecular Biology (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: amyloid fibril formation; proteins; nucleation-dependent polymerization (NDP) model; kinetics; aggregation reactions
Affiliations: National Centre for Biological Sciences, Tata Institute of Fundamental Research, Bangalore 560065, India.

Abstract:  The mechanism of amyloid fibril formation by proteins has been classically described by the nucleation-dependent polymerization (NDP) model, which makes certain predictions regarding the kinetics of fibrillation. All proteins whose aggregation conforms to the NDP model display a t(2) time dependence for their initial reaction profile. However, there are proteins whose aggregation reactions have kinetic signatures of a flat lag phase followed by an exponential rise in fibril mass, which does not conform to the NDP model. Amyloid fibril formation by tau, a microtubule-associated protein whose aggregation to form neurofibrillary tangles is implicated in Alzheimer's disease and other tauopathies, in the presence of inducers such as heparin and fatty acid micelles, has always been traditionally described by a ligand-induced NDP model. In this study, the existence of a secondary pathway for fibril growth during the aggregation of the functional, repeat domain of tau in the presence of heparin has been established. Both kinetic and accessory evidence are provided for the existence of this pathway, which is shown to augment the primary homogeneous nucleation pathway. From the kinetic data, the main secondary pathway that is operative appears to be fibril fragmentation but other pathways such as branching or secondary nucleation may also be operative. 

Retracted: No

PubPeer comments:
 ![file] , 
 As stated in its caption, Figure 9 shows AFM images of fibrils formed by 25 micromolar protein at different time points. In Figure 9c, the time point is 55 mins. 55 mins is the lag time (t10 ) for 25 micromolar protein, as evident in Figure 2b inset. As stated in its caption, Figure 10 shows AFM images of fibrils formed at the end of the lag phase, ie at t10 , for different protein concentrations. Figure 10b shows fibrils formed by 25 micromolar protein at the end of its lag phase, ie at t10 = 55 mins. The images in Figures 9c and 10b are exactly the same because they are from the same experiment (not two independent experiments) at the exact same time point. As explained above, the end of the lag phase (the lag time or t10) for 25 micromolar concentration is 55 min. ,
Up-regulation of miR-34c-5p inhibits nasopharyngeal carcinoma cells by mediating NOTCH1
Authors: Xin Xu
Haomin Yan
Le Zhang
Jing Liu
Haoyu Cheng
Yu Huang
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MiR-34c-5p; NOTCH1; nasopharyngeal carcinoma.
Affiliations: Department of Otolaryngology, Yan'an Hospital of Kunming City, Yunnan 650031, P.R. China., Department of Hematology, Aerospace Center Hospital of Beijing, Beijing 100049, P.R. China.

Abstract:  Objective: To explore the correlation between miR-34c-5p and NOTCH1 in nasopharyngeal carcinoma (NPC). Materials and methods: qPCR was employed to quantify miR-34c-5p and NOTCH1 mRNA in NPC, and Western blot to detect NOTCH1. MiR-34c-5p mimics/inhibitor and NOTCH1 siRNA were constructed to analyze the role of miR-34c-5p/NOTCH1 on the biological function of NPC cells. Results: NPC cells showed lower miR-34c-5p expression and higher NOTCH1 expression than normal cells, and up-regulating miR-34c-5p or inhibiting NOTCH1 could strongly suppress the epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of NPC cells, and induce apoptosis in them. Up-regulating miR-34c-5p could inhibit NOTCH1, and miR-34c-5p was negatively correlated with NOTCH1. Rescue experiment results revealed that NOTCH1 up-regulation could counteract the changes of cell process induced by increased miR-34c-5p. Conclusion: MiR-34c-5p inhibits the growth of NPC by down-regulating NOTCH1, so up-regulating miR-34c-5p or down-regulating NOTCH1 may become the potential direction of NPC treatment. 

Retracted: Yes

PubPeer comments:
 Some of the Western blots panels - Figure 3 shown here - appear to share the same background. Could the authors please show the uncropped blots here? ![file] , 
 Retracted, [28 October 2021] . -------------------------- This article is being retracted from Bioscience Reports at the request of the Editor-in-Chief and the Editorial Board following receipt of a notification from a reader, alerting the Editorial Board to the backgrounds of the Western blots throughout the paper which unexplainedly contain the same features. The authors have been contacted in regards to the Retraction, and have not responded to the Journal s queries and the concerns raised. Given the extent of the issues raised, the Editorial Board stand by the decision to retract the article. ,
Immunoprecipitation of amyloid fibrils by the use of an antibody that recognizes a generic epitope common to amyloid fibrils
Authors: Fernando L Palhano
Jeffery W Kelly
Erin R Greiner
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Amyloid fibrils; Alzheimer's disease; isolation; purification; protocol
Affiliations: Departments of Chemistry and Molecular and Experimental Medicine and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, United States of America., Departments of Chemistry and Molecular and Experimental Medicine and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, United States of America; Instituto de Bioquímica Médica Leopoldo de Meis, Programa de Biologia Estrutural, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract:  Amyloid fibrils are associated with many maladies, including Alzheimer's disease (AD). The isolation of amyloids from natural materials is very challenging because the extreme structural stability of amyloid fibrils makes it difficult to apply conventional protein science protocols to their purification. A protocol to isolate and detect amyloids is desired for the diagnosis of amyloid diseases and for the identification of new functional amyloids. Our aim was to develop a protocol to purify amyloid from organisms, based on the particular characteristics of the amyloid fold, such as its resistance to proteolysis and its capacity to be recognized by specific conformational antibodies. We used a two-step strategy with proteolytic digestion as the first step followed by immunoprecipitation using the amyloid conformational antibody LOC. We tested the efficacy of this method using as models amyloid fibrils produced in vitro, tissue extracts from C. elegans that overexpress Aβ peptide, and cerebrospinal fluid (CSF) from patients diagnosed with AD. We were able to immunoprecipitate Aβ(1-40) amyloid fibrils, produced in vitro and then added to complex biological extracts, but not α-synuclein and gelsolin fibrils. This method was useful for isolating amyloid fibrils from tissue homogenates from a C. elegans AD model, especially from aged worms. Although we were able to capture picogram quantities of Aβ(1-40) amyloid fibrils produced in vitro when added to complex biological solutions, we could not detect any Aβ amyloid aggregates in CSF from AD patients. Our results show that although immunoprecipitation using the LOC antibody is useful for isolating Aβ(1-40) amyloid fibrils, it fails to capture fibrils of other amyloidogenic proteins, such as α-synuclein and gelsolin. Additional research might be needed to improve the affinity of these amyloid conformational antibodies for an array of amyloid fibrils without compromising their selectivity before application of this protocol to the isolation of amyloids. 

Retracted: No

PubPeer comments:
 Figure 5 appears to contain splices in some rows but not in others. Could the authors review and comment? Brought to my attention by another reader. *** ![file] ,
Astrocyte activation and neurotoxicity: A study in different rat brain regions and in rat C6 astroglial cells
Authors: Neeraj Joshi
Poonam Goswami
Sarika Singh
Sharad Sharma
Sonam Gupta
Journal: Environmental toxicology and pharmacology (2015)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Astrocyte activation; DNA damage; Melatonin; Nitrite level; Reactive oxygen species
Affiliations: Toxicology Division, CSIR-CDRI, Lucknow 226031, India; Academy of Scientific & Innovative Research (AcSIR), India., Department of Biochemistry and Biophysics, University of California, San Francisco, CA, USA., Toxicology Division, CSIR-CDRI, Lucknow 226031, India., Toxicology Division, CSIR-CDRI, Lucknow 226031, India; Academy of Scientific & Innovative Research (AcSIR), India. Electronic address: .

Abstract:  The present study was conducted to investigate the effect of rotenone on astrocytes activation, their viability and its effect on neuronal death in different brain regions. Rotenone was injected in rat brain by intracerebroventricularly (bilateral) route at dose of 6 μg and 12 μg. In vitro C6 cells were treated with rotenone at concentration of 0.1, 0.25, 0.5, 1 and 2 μM. Rotenone administration to rat brain caused significant astrocytes activation in frontal cortex, cerebellum, cerebellar nucleus, substantia nigra, hypothalamus and hippocampus regions of the rat brain. Rotenone administration also led to significant degeneration of cells in all the studied regions along with altered nuclear morphology assessed by hematoxylin-eosin and cresyl violet staining. Histological staining showed the significantly decreased number of cells in all the studied regions except cerebellar nucleus in dose and time dependant manner. Rotenone administration in the rat brain also caused significant decrease in glutathione levels and augmented nitrite levels. In vitro treatment of rotenone to astrocytic C6 cells caused significantly increased expression of glial fibrillar acidic protein (GFAP) and decreased viability in dose and time dependent manner. Rotenone treatment to C6 cells exhibited significant generation of reactive oxygen species, augmented nitrite level, impaired mitochondrial activity, apoptotic chromatin condensation and DNA damage in comparison to control cells. Findings showed that oxidative stress play a considerable role in rotenone induced astrocyte death that was attenuated with co-treatment of antioxidant melatonin. In conclusion, results showed that rotenone caused significant astrocytes activation, altered nuclear morphology, biochemical alteration and apoptotic cell death in different rat brain regions. In vitro observations in C6 cells showed that rotenone treatment exhibited oxidative stress mediated apoptotic cell death, which was attenuated with co treatment of melatonin. 

Retracted: No

PubPeer comments:
 **Duplications!** **Please also see the related link below:** [Link] ![file] ![file] ![file] ,
MiR-125b reduces porcine reproductive and respiratory syndrome virus replication by negatively regulating the NF-κB pathway
Authors: Liurong Fang
Huanchun Chen
Shaobo Xiao
Quangang Chen
Lu Cao
Dang Wang
Rui Luo
Kui Li
Zheng Xu
Yao Zhong
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Porcine reproductive and respiratory syndrome virus; miR-125b; replication; innate immunity; antiviral function
Affiliations: Division of Animal Infectious Diseases, State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.

Abstract:  Porcine reproductive and respiratory syndrome virus (PRRSV) is an Arterivirus that has been devastating the swine industry worldwide since the late 1980s. To investigate the impact of cellular microRNAs (miRNAs) on the replication of PRRSV, we screened 10 highly conserved miRNAs implicated in innate immunity or antiviral function and identified miR-125b as an inhibitor of PRRSV replication. Virus titer and western blot assays demonstrated that miR-125b reduced PRRSV replication and viral gene expression in a dose-dependent manner in both MARC-145 cell line and primary porcine alveolar macrophages. Mechanistically, miR-125b did not target the PRRSV genome. Rather, it inhibited activation of NF-κB, which we found to be required for PRRSV replication. PRRSV, in turn, down-regulated miR-125b expression post-infection to promote viral replication. Collectively, miR-125b is an antiviral host factor against PRRSV, but it is subject to manipulation by PRRSV. Our study reveals an example of manipulation of a cellular miRNA by an arterivirus to re-orchestrate host gene expression for viral propagation and sheds new light on targeting host factors to develop effective control measures for PRRS. 

Retracted: No

PubPeer comments:
 Figures S5C and S6B, more similar than expected. Could authors check please? ![file] , 
 Tubulin is the loading control we used for Western blots. We used the Tubulin because its level of expression does not change whatever the culture conditions. Therefore, a similar intensity of bands in the different lanes and blots is fully expected. When zooming on the bands in squares, it appears that the background around the Tubulin signals is not the same, indicating that it is not a duplicate. I thank you for having given me the opportunity to respond to this comment. ,
TGFβ1 protects myocardium from apoptosis and oxidative damage after ischemia reperfusion
Authors: A-H Shu
M Zhou
M Zhang
Y-Y Chu
F-G Xie
H-H Wen
Y-F Liu
X-Z Zhang
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Myocardial apoptosis; Ischemia-reperfusion injury; Transforming growth factor β1 (TGFβ1); Oxidative damage; Endogenous protective mechanism
Affiliations: Department of Anesthesiology, Three Gorges University People's Hospital, The First People's Hospital of Yichang, Yichang, Hubei, China. .

Abstract:  Objective: Myocardial apoptosis is an important pathologic basis of ischemia-reperfusion injury (I/R). Transforming growth factor β1 (TGFβ1) participates in the regulation of oxidative damage and apoptosis. TGFβ1 is upregulated in the repair process of I/R injury. It is speculated that TGFβ1 over-expression is involved in the endogenous protective mechanism of I/R injury. This study explores the significance of TGFβ1 in myocardial cell apoptosis after I/R. Materials and methods: Rat myocardial I/R injury model was established. Left ventricular ejection fraction (LVEF) and Left ventricular fractional shortening (LVFS) were detected by ultrasonic cardiogram. TGFβ1 expression in the myocardium was tested. H9C2 cells were cultured under ischemic hypoxic condition for 6 h, and then were treated by reoxygenation for 6 h to simulate I/R model. H9C2 cells were divided into three groups, including I/R+pIRES2-Blank, I/R+pIRES2 TGFβ1, and I/R+pIRES2-TGFβ1+LY364947. TGFβ1 mRNA and protein levels were evaluated. Cell apoptosis and reactive oxygen species (ROS) were determined by flow cytometry. Results: LVEF and LVFS significantly decreased in I/R group compared with Sham group. TGFβ1 mRNA and protein expressions in myocardium from I/R group up-regulated than the control. I/R treatment markedly elevated TGFβ1 mRNA and protein levels, increased ROS content, and enhanced cell apoptosis in H9C2 cells. Over-expression of TGFβ1 significantly weakened ROS production and apoptosis in H9C2 cells after I/R. TGFβ receptor inhibitor LY364947 restrained ROS production and apoptosis attenuation in H9C2 cells treated by TGFβ. Conclusions: TGFβ1 alleviates myocardial cell apoptosis after I/R. Blocking TGFβ1 attenuates the protective effect of TGFβ1 on I/R injury. 

Retracted: No

PubPeer comments:
 Figs 2B, 3B: ![file] Fig 4B: ![file] This is an example of what has elsewhere been labeled as  Papermill #2 , characterised by stylised WBs reminiscent of the blobs in a Miro painting, ![] ...and by a small repertoire of recurring FACS plots, slightly modified by artisanal stippling on each of their occurrences. ![] https: forbetterscience.com 2020 02 27 dark-satanic-papermills ,
Expression of ADAM15 in rheumatoid synovium: up-regulation by vascular endothelial growth factor and possible implications for angiogenesis
Authors: Isao Inoki
Eiji Ikeda
Yasunori Okada
Hideo Matsumoto
Koichiro Komiya
Yoshiaki Toyama
Satoko Okazaki
Eiko Ohuchi
Yoshinari Fujita
Hiroyuki Enomoto
Journal: Arthritis research & therapy (2005)
Discipline: CLINICAL MEDICINE
Keywords: ADAMs; metalloproteinases; cell-cell interaction; cell migration; signal transduction
Affiliations: Department of Pathology, School of Medicine, Keio University, Tokyo, Japan. 

Abstract:  ADAMs (a disintegrin and metalloproteinases) comprise a new gene family of metalloproteinases, and may play roles in cell-cell interaction, cell migration, signal transduction, shedding of membrane-anchored proteins and degradation of extracellular matrix. We screened the mRNA expression of 10 different ADAMs with a putative metalloproteinase motif in synovial tissues from patients with rheumatoid arthritis (RA) or osteoarthritis (OA). Reverse transcription PCR and real-time quantitative PCR analyses indicated that among the ADAMs, ADAM15 mRNA was more frequently expressed in the RA samples and its expression level was significantly 3.8-fold higher in RA than in OA (p &lt; 0.01). In situ hybridization, immunohistochemistry and immunoblotting demonstrated that ADAM15 is expressed in active and precursor forms in the synovial lining cells, endothelial cells of blood vessels and macrophage-like cells in the sublining layer of RA synovium. There was a direct correlation between ADAM15 mRNA expression levels and vascular density in the synovial tissues (r = 0.907, p &lt; 0.001; n = 20). ADAM15 was constitutively expressed in RA synovial fibroblasts and human umbilical vein endothelial cells (HUVECs), and the expression level was increased in HUVECs by treatment with vascular endothelial growth factor (VEGF)165. On the other hand, ADAM15 expression in RA synovial fibroblasts was enhanced with VEGF165 only if vascular endothelial growth factor receptor (VEGFR)-2 expression was induced by treatment with tumor necrosis factor-alpha, and the expression was blocked with SU1498, a specific inhibitor of VEGFR-2. These data demonstrate that ADAM15 is overexpressed in RA synovium and its expression is up-regulated by the action of VEGF165 through VEGFR-2, and suggest the possibility that ADAM15 is involved in angiogenesis in RA synovium. 

Retracted: No

PubPeer comments:
 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. , 
 I have identified some potentially repeated features in Figure 2. I did not attempt to locate them all. *** ![file] ,
A fourth IkappaB protein within the NF-kappaB signaling module
Authors: Alexander Hoffmann
Inder M Verma
Gourisankar Ghosh
Vinay Tergaonkar
Chris A Benedict
Ellen O&#x27;Dea
Soumen Basak
Shannon L Werner
Jeffrey D Kearns
Hana Kim
Carl F Ware
Journal: Cell (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NF-kappaB; RelA; IkappaB; p100; signaling
Affiliations: Department of Chemistry and Biochemistry, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

Abstract:  Inflammatory NF-kappaB/RelA activation is mediated by the three canonical inhibitors, IkappaBalpha, -beta, and -epsilon. We report here the characterization of a fourth inhibitor, nfkappab2/p100, that forms two distinct inhibitory complexes with RelA, one of which mediates developmental NF-kappaB activation. Our genetic evidence confirms that p100 is required and sufficient as a fourth IkappaB protein for noncanonical NF-kappaB signaling downstream of NIK and IKK1. We develop a mathematical model of the four-IkappaB-containing NF-kappaB signaling module to account for NF-kappaB/RelA:p50 activation in response to inflammatory and developmental stimuli and find signaling crosstalk between them that determines gene-expression programs. Further combined computational and experimental studies reveal that mutant cells with altered balances between canonical and noncanonical IkappaB proteins may exhibit inappropriate inflammatory gene expression in response to developmental signals. Our results have important implications for physiological and pathological scenarios in which inflammatory and developmental signals converge. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] Thank you for bringing this to our notice. We acknowledge that the first three lanes of the 10 ug ml of a-LTbR panel indeed had been inadvertently replicated under the TNF panel while assembling these figures. We sincerely apologize for this oversight. We have now retrieved the original gel image used for generating these panels and provided the corrected figure. This correction in the supplementary figure S1H does not, in any way, impact the conclusions drawn in the manuscript. We will also contact the journal office to rectify this unintended error in the online supplementary information section associated with the paper (Basak et al., 2007). ,
Identification and functional characterization of the BAG protein family in Arabidopsis thaliana
Authors: Martin B Dickman
John Reed
Elena V Doukhanina
Esther van der Zalm
Shaorong Chen
Adam Godzik
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: genes; programmed cell death; apoptosis-like cell death; plant homologs; regulators
Affiliations: Department of Plant Pathology, University of Nebraska, Lincoln, Nebraska 68583, USA.

Abstract:  The genes that control mammalian programmed cell death are conserved across wide evolutionary distances. Although plant cells can undergo apoptosis-like cell death, plant homologs of mammalian regulators of apoptosis have, in general, not been found. This is in part due to the lack of primary sequence conservation between animal and putative plant regulators of apoptosis. Thus, alternative approaches beyond sequence similarities are required to find functional plant homologs of apoptosis regulators. Here, we present the results of using advanced bioinformatic tools to uncover the Arabidopsis family of BAG proteins. The mammalian BAG (Bcl-2-associated athanogene) proteins are a family of chaperone regulators that modulate a number of diverse processes ranging from proliferation to growth arrest and cell death. Such proteins are distinguished by a conserved BAG domain that directly interacts with Hsp70 and Hsc70 proteins to regulate their activity. Our searches of the Arabidopsis thaliana genome sequence revealed seven homologs of the BAG protein family. We further show that plant BAG family members are also multifunctional and remarkably similar to their animal counterparts, as they regulate apoptosis-like processes ranging from pathogen attack to abiotic stress and development. 

Retracted: No

PubPeer comments:
 There are so many undeclared splice sites in the immunoblots in Figure S3 (blue arrowheads). many lanes of the blots are from different images. Some bands in red boxes or green boxes are very similar. Could the authors explain why? ![file] ,
Modulation of intracellular signaling pathways to induce apoptosis in prostate cancer cells
Authors: Zhi-Xiong J Xiao
Chang-Yan Chen
Jinjin Guo
Tongbo Zhu
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: prostate cancer; apoptosis; Ras signaling; protein kinase C; intracellular signaling pathways
Affiliations: Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

Abstract:  An understanding of the molecular pathways defining the susceptibility of prostate cancer, especially refractory prostate cancer, to apoptosis is the key for developing a cure for this disease. We previously demonstrated that up-regulating Ras signaling, together with suppression of protein kinase C (PKC), induces apoptosis. Dysregulation of various intracellular signaling pathways, including those governed by Ras, is the important element in the development of prostate cancer. In this study, we tested whether it is possible to modulate the activities of these pathways and induce an apoptotic crash among them in prostate cancer cells. Our data showed that DU145 cells express a high amount of JNK1 that is phosphorylated after endogenous PKC is suppressed, which initiates caspase 8 cleavage and cytochrome c release, leading to apoptosis. PC3 and LNCaP cells contain an activated Akt. The inhibition of PKC further augments Akt activity, which in turn induces ROS production and the accumulation of unfolded proteins in the endoplasmic reticulum, resulting in cell death. However, the concurrent activation of JNK1 and Akt, under the condition of PKC abrogation, dramatically augment the magnitude of apoptosis in the cells. Thus, our study suggests that Akt, JNK1, and PKC act in concert to signal the intracellular apoptotic machinery for a full execution of apoptosis in prostate cancer cells. 

Retracted: Yes

PubPeer comments:
 2007 retraction. http: www.jbc.org content 282 49 36132 This article has been withdrawn by the authors. ,
Cortical excitability correlates with the event-related desynchronization during brain–computer interface control
Authors: Ian Daly
Nicholas P Holmes
Caroline Blanchard
Journal: Journal of Neural Engineering (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Brain-computer interfaces; motor control; stroke rehabilitation; event-related desynchronization (ERD); neural correlate
Affiliations: Brain-Computer Interfaces and Neural Engineering Laboratory, School of Computer Science and Electronic Engineering, University of Essex, Colchester, CO4 3SQ, United Kingdom.

Abstract:  Objective: Brain-computer interfaces (BCIs) based on motor control have been suggested as tools for stroke rehabilitation. Some initial successes have been achieved with this approach, however the mechanism by which they work is not yet fully understood. One possible part of this mechanism is a, previously suggested, relationship between the strength of the event-related desynchronization (ERD), a neural correlate of motor imagination and execution, and corticospinal excitability. Additionally, a key component of BCIs used in neurorehabilitation is the provision of visual feedback to positively reinforce attempts at motor control. However, the ability of visual feedback of the ERD to modulate the activity in the motor system has not been fully explored. Approach: We investigate these relationships via transcranial magnetic stimulation delivered at different moments in the ongoing ERD related to hand contraction and relaxation during BCI control of a visual feedback bar. Main results: We identify a significant relationship between ERD strength and corticospinal excitability, and find that our visual feedback does not affect corticospinal excitability. Significance: Our results imply that efforts to promote functional recovery in stroke by targeting increases in corticospinal excitability may be aided by accounting for the time course of the ERD. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: As a control freak, it is hard to let others into the lab to play with my TMS toys! The first author Dr Daly is a great engineer, but I don t understand the maths or analysis he used in this paper. I just have to trust that it s OK... ,
Glandular mast cells with distinct phenotype are highly elevated in chronic rhinosinusitis with nasal polyps
Authors: Anju T Peters
Roderick Carter
Shigeharu Fujieda
Bruce K Tan
Robert P Schleimer
Lydia A Suh
Leslie C Grammer
David B Conley
James Norton
Robert C Kern
Rakesh K Chandra
Tetsuji Takabayashi
Atsushi Kato
Journal: Journal of Allergy and Clinical Immunology (2012)
Discipline: IMMUNOLOGY
Keywords: Chronic rhinosinusitis; nasal polyps; mast cells; T(H)2 inflammation; tryptase
Affiliations: Division of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Abstract:  Background: Although chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is characterized by T(H)2 inflammation, the role of mast cells is poorly understood. Objective: The objective of this study was to investigate the presence, localization, and phenotype of mast cells in patients with CRS. Methods: We collected nasal tissue and nasal lavage fluid from patients with CRS and control subjects. We analyzed mRNA for the mast cell proteases tryptase, chymase, and carboxypeptidase A3 by using real-time PCR and measured mast cell protease proteins by using ELISA, immunohistochemistry, and immunofluorescence. Results: Tryptase mRNA was significantly increased in nasal polyps (NPs) from patients with CRSwNP (P&lt; .001) compared with uncinate tissue from patients with CRS or control subjects. Tryptase protein was also elevated in NPs and in nasal lavage fluids from patients with CRSwNP. Immnohistochemistry showed increased numbers of mast cells in epithelium and glands but not within the lamina propria in NPs. The mast cells detected in the epithelium in NPs were characterized by the expression of tryptase and carboxypeptidase A3 but not chymase. Mast cells expressing all the 3 proteases were abundant within the glandular epithelium of NPs but were not found in normal glandular structures. Conclusions: Herein we demonstrated a unique localization of mast cells within the glandular epithelium of NPs and showed that mast cells in NPs have distinct phenotypes that vary by tissue location. Glandular mast cells and the diverse subsets of mast cells detected may contribute to the pathogenesis of CRSwNP. 

Retracted: No

PubPeer comments:
 Could the authors please check the original submission to the journal if the duplications shown below have been introduced by the  editor ? ![file] ,