PReD-Bench/PRed-Bench huggingface dataset:
Anti-cancer effect of R3V6 peptide-mediated delivery of an anti-microRNA-21 antisense-oligodeoxynucleotide in a glioblastoma animal model
Authors: Minhyung Lee
Hojung Song
Sung-Hee Ihm
Jungju Oh
Binna Oh
Gyeungyun Kim
Dahee Lee
Journal: Journal of Drug Targeting (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Antisense-oligodeoxynucleotide; R3V6 peptide; gene therapy; glioblastoma; microRNA-21.

Abstract:  MicroRNA-21 (miR-21) expression in glioblastoma inhibits the expression of pro-apoptotic genes, thereby promoting tumor growth. A previous study showed that the amphiphilic R3V6 peptide is an efficient carrier of the anti-miR-21 antisense oligodeoxynucleotide (antisense-ODN) into cells in vitro. In the current study, in vivo delivery of antisense-ODN using the R3V6 peptide was evaluated in a glioblastoma animal model. In vitro transfection showed that the R3V6 peptide delivered antisense-ODN more efficiently than polyethylenimine (25 kDa, PEI25k) in C6 glioblastoma cells. For in vivo evaluation, antisense-ODN/R3V6 complex was injected intratumorally into a C6 glioblastoma xenograft animal model. Tumor growth was suppressed by the injection of the antisense-ODN/R3V6 complex, compared with the antisense-ODN/PEI25k and scrambled-antisense-ODN (scr-antisense-ODN)/R3V6 complexes. Real-time RT-PCR showed that miR-21 levels were reduced most efficiently by the antisense-ODNR3V6 complex in tumors. Due to inhibition of miR-21, expression of the programed cell death 4 (PDCD4) gene was promoted in tumors, resulting in the induction of apoptosis of tumor cells. These results suggest that delivery of antisense-ODN using R3V6 peptides may be useful for the development of antisense-ODN therapy for glioblastoma. 

Retracted: No

PubPeer comments:
 In Figure 7, a micrograph has been duplicated and presented as something else.  , 
 Thank you for your comments on the images of TUNEL assays. Surely, in the process of compiling the images, an image for Scr-antisense-ODN R3V6 was used for naked antisense-ODN again by accident. We apologize for our mistake. We have images for naked antisense-ODN and will propose correction to the journal soon. Thank you for your comments again. ,
How Did Life Begin?
Authors: Jack Szostak
Journal: Nature (2018)
Discipline: Multidisciplinary
Keywords: Nanoscience and technology.

Abstract: Untangling the origins of organisms will require experiments at the tiniest scales and observations at the vastest. Untangling the origins of organisms will require experiments at the tiniest scales and observations at the vastest.

Retracted: No

PubPeer comments:
 One may question if it is a good idea to have sponsored content without editorial correction. Surely, an editor, or any researcher in the field, would find this a poor representation of origins research, its viewpoints, open questions and criticisms. These critiques are not new to the author. In years preceding the sponsored content the following commentary by Walker and Cronin even calls into question the scientific validity of the whole approach that would somehow produce the picture painted by Szostak. 10.1126 science.aaf6310 25 researchers from 21 institutes have collectively called for a stop to such continuing acts of division, and stress a future where bridges must be built in an intellectually safe and honest environment https: pubmed.ncbi.nlm.nih.gov 32110893 who thinks this sponsored opinion is simply the viewpoint of researchers alligned with RNA-world is not quite correct. Very few think this. See e.g. Krishnamurtyu2019s 10.1002 chem.201801847 ,
Targeting activation of specific NF-Œ∫B subunits prevents stress-dependent atherothrombotic gene expression
Authors: Marina Pizzi
Muhammed Kashif
Florian Bea
Markus Schwaninger
David Piel
Markus Hecker
Thomas Fleming
Stephan Herzig
Angelika Bierhaus
R√ºdiger von Bauer
Martin Zeier
Sajjad Muhammad
Peter P Nawroth
Zdenka Djuric
Berend Isermann
Journal: Molecular Medicine (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Psychosocial stress; atherosclerosis; NF-Œ∫B; gene expression; in vitro
Affiliations: Department of Medicine I and Clinical Chemistry, University of Heidelberg, Heidelberg, Germany.

Abstract:  Psychosocial stress has been shown to be a contributing factor in the development of atherosclerosis. Although the underlying mechanisms have not been elucidated entirely, it has been shown previously that the transcription factor nuclear factor-Œ∫B (NF-Œ∫B) is an important component of stress-activated signaling pathway. In this study, we aimed to decipher the mechanisms of stress-induced NF-Œ∫B-mediated gene expression, using an in vitro and in vivo model of psychosocial stress. Induction of stress led to NF-Œ∫B-dependent expression of proinflammatory (tissue factor, intracellular adhesive molecule 1 [ICAM-1]) and protective genes (manganese superoxide dismutase [MnSOD]) via p50, p65 or cRel. Selective inhibition of the different subunits and the respective kinases showed that inhibition of cRel leads to the reduction of atherosclerotic lesions in apolipoprotein(-/-) (ApoE(-/-)) mice via suppression of proinflammatory gene expression. This observation may therefore provide a possible explanation for ineffectiveness of antioxidant therapies and suggests that selective targeting of cRel activation may provide a novel approach for the treatment of stress-related inflammatory vascular disease. 

Retracted: No

PubPeer comments:
 Is experiment A using the same controls as experiment B?  Did the authors confuse ACC with ASS? Why are vitamin E and C leading to identical bands?  ,
Differential Regulation of MAPK Phosphorylation in the Dorsal Hippocampus in Response to Prolonged Morphine Withdrawal-Induced Depressive-Like Symptoms in Mice
Authors: Ying Du
Jianguo Shi
Wei Dang
Jianhua Wang
Bin Wu
Qiong Zhou
Rui Liu
Rui Zhang
Wei Jia
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Depression; Opiate addiction; MAPK; MKP; Morphine withdrawal
Affiliations: Methadone Maintenance Treatment Clinic, Xi'an Mental Health Center, Xi'an, China.

Abstract:  Depression is one of the most frequent neuropsychiatric comorbidities associated with opiate addiction. Mitogen activated protein kinase (MAPK) and MAPK phosphatase (MKP) are involved in drug addiction and depression. However, the potential role of MAPK and MKP in depression caused by morphine withdrawal remains unclear. We utilized a mouse model of repeated morphine administration to examine the molecular mechanisms that contribute to prolonged withdrawal induced depressive-like behaviors. Depressive-like behaviors were significant at 1 week after withdrawal and worsened over time. Phospho-ERK (extracellular signal-regulated protein kinase) was decreased and MKP-1 was elevated in the hippocampus, and JNK (c-Jun N-terminal protein kinase), p38 (p38 protein kinase) and MKP-3 were unaffected. A pharmacological blockade of MKP-1 by intra-hippocampal sanguinarine (SA) infusion prevented the development of depressive-like behaviors and resulted in relatively normal levels of MKP-1 and phospho-ERK after withdrawal. Our findings support the association between hippocampal MAPK phosphorylation and prolonged morphine withdrawal-induced depression, and emphasize the MKP-1 as an negative regulator of the ERK phosphorylation that contributes to depression. 

Retracted: No

PubPeer comments:
 This paper has a September 2013 correction for an error in the affiliation. Here are additional concerns about Figure 7. Two of these concerns were notified to the journal in October 2015. * Blue boxes: The 2h ERK panel and the week 1 ERK panel appear to look similar. * Orange boxes: The 2h b-actin panel and the week 1 b-actin panel appear to look similar. * Green boxes: Lanes 1-2 in the 2h p-ERK panel look similar to lanes 2-3 in the week 1 p-ERK panel.  ,
Genetic interactions among Brca1, Brca2, Palb2, and Trp53 in mammary tumor development
Authors: Pier Selenica
Amar H Mahdi
Xin Pei
Ying Chen
Britta Weigelt
David N Brown
Nicola J Barnard
Kelly Kyker-Snowman
Nadeem Riaz
Bing Xia
Thais Basili
Arnaud Da Cruz Paula
Tao Li
Rahul Kumar
Yongmei Tan
Fresia Pareja
Yanying Huo
Yu-Xiu Huang
Jorge S Reis-Filho
Journal: npj Breast Cancer (2021)
Discipline: CLINICAL MEDICINE
Keywords: BRCA1; BRCA2; PALB2; mammary tumor suppression; conditional knockout
Affiliations: Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Stomatological Hospital of Guangzhou Medical University, Guangzhou, China., The First Affiliated Hospital of Fujian Medical University, Fuzhou, China., Department of Pathology and Laboratory Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA., Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. ., Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA. .

Abstract:  Inherited mutations in BRCA1, BRCA2, and PALB2 cause a high risk of breast cancer. Here, we conducted parallel conditional knockout (CKO) of Brca1, Palb2, and Brca2, individually and in combination, along with one copy of Trp53, in the mammary gland of nulliparous female mice. We observed a functional equivalence of the three genes in their basic tumor-suppressive activity, a linear epistasis of Palb2 and Brca2, but complementary roles of Brca1 and Palb2 in mammary tumor suppression, as combined ablation of either Palb2 or Brca2 with Brca1 led to delayed tumor formation. Whole-exome sequencing (WES) revealed both similarities and differences between Brca1 and Palb2 or Brca2 null tumors. Analyses of mouse mammary glands and cultured human cells showed that combined loss of BRCA1 and PALB2 led to high levels of reactive oxygen species (ROS) and increased apoptosis, implicating oxidative stress in the delayed tumor development in Brca1;Palb2 double CKO mice. The functional complementarity between BRCA1 and PALB2/BRCA2 and the role of ROS in tumorigenesis require further investigation. 

Retracted: No

PubPeer comments:
 The description of the figure 3d in the text: _ we found that B1P tumors had signiufb01cantly higher levels of telomeric allelic imbalance (NtAI)33 than B2P tumors, while P2P tumors showed an intermediate phenotype (Fig. 3d). _ does not seem to match the figure, where B1P vs B2P comparison is labeled as non-significant, and B1P vs P2P is not labelled but does not look significant either :  ,
In vitro and in vivo double-enhanced suicide gene therapy mediated by generation 5 polyamidoamine dendrimers for PC-3 cell line
Authors: Deling Kong
Yong Xu
Gang Wang
Yue Chen
Zhihong Zhang
Kuo Yang
Weiming Zhao
Ranlu Liu
Journal: World Journal of Surgical Oncology (2012)
Discipline: CLINICAL MEDICINE
Keywords: suicide gene therapy; HSV-TK/GCV; Cx43; gemcitabine; non-viral vector
Affiliations: Department of Urology, Second Hospital of TianJin Medical University, TianJin Institute of Urology, Tianjin, China.

Abstract:  Background: One of the most frequently used and efficient suicide gene therapies for prostate cancer is HSV-TK/GCV system, but its application has been limited due to lack of favorable gene vector and the reduction of "bystander effect". We investigated the effect of a novel combination of HSV-TK/GCV fused with Cx43 and gemcitabine using non-viral vector generation 5 polyamidoamine dendrimers (G5-PAMAM-D) on PC-3 cells. Methods: RT-PCR and Western blot were used to detect TK and Cx43 expression. Cell viability and proliferation were measured by using MTT assay. Cell apoptosis was detected with double-staining of Annexin V-FITC and propidium iodide (PI) by flow cytometry. Nude mice models were established to evaluate the therapeutic effect in vivo. Results: G5-PAMAM-D efficiently delivered recombinant plasmids into PC-3 cells and HSV-TK and Cx43 could be expressed successfully. With gemcitabine, G5-PAMAM-D mediated HSV-TK and Cx43 expression effectively inhibited prostate cancer PC-3 cell proliferation, leading to more cellular apoptosis and inhibiting PC-3 tumor growth in nude mice models. Conclusions: This study illustrates that this new suicide gene system mediated by G5-PAMAM-D is effective in decreasing PC-3 cell proliferation and inducing cell apoptosis, and inhibiting tumor growth in vivo. In a word, our study could provide a potential approach for gene therapy of prostate cancer. 

Retracted: No

PubPeer comments:
 repeated image areas  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. , 
 #1 I agree with this automated finding and would further note that the images appear to have been resized, suggesting that this did not occur solely as a mistake during figure assembly. In addition, Figure 1 appears to have some repeated lanes, visible after contrast brightness adjustment. *** False color  *** Original  ,
Eukaryote culturomics of the gut reveals new species
Authors: Nina Gouba
Didier Raoult
Michel Drancourt
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: microeukaryotes; human gut; fungal species; protists; PCR-sequencing
Affiliations: Aix Marseille Universit√©, URMITE, UMR63, CNRS 7278, IRD 198, Inserm 1095, Marseille, France.

Abstract:  The repertoire of microeukaryotes in the human gut has been poorly explored, mainly in individuals living in northern hemisphere countries. We further explored this repertoire using PCR-sequencing and culture in seven individuals living in four tropical countries. A total of 41 microeukaryotes including 38 different fungal species and three protists were detected. Four fungal species, Davidiella tassiana, Davidiella sp., Corticiaceae sp., and Penicillium sp., were uniquely detected by culture; 27 fungal species were uniquely detected using PCR-sequencing and Candida albicans, Candida glabrata, Trichosporon asahii, Clavispora lusitaniae, Debaryomyces hansenii, Malassezia restricta, and Malassezia sp. were detected using both molecular and culture methods. Fourteen microeukaryotes were shared by the seven individuals, whereas 27 species were found in only one individual, including 11 species in Amazonia, nine species in Polynesia, five species in India, and two species in Senegal. These data support a worldwide distribution of Malassezia sp., Trichosporon sp., and Candida sp. in the gut mycobiome. Here, 13 fungal species and two protists, Stentor roeseli and Vorticella campanula, were observed for first time in the human gut. This study revealed a previously unsuspected diversity in the repertoire of human gut microeukaryotes, suggesting spots for further exploring this repertoire. 

Retracted: No

PubPeer comments:
 In this paper, stool samples were collected from *three individuals from Polynesia (Iles Raietea, rural area), two individuals from Amazonia (Manaus, urban area, forest area), one individual from Senegal (Nu2019Diop, rural area) and one individual in India (New Dheli).* The Methods state that *The study was approved by the local ethics committee of the Institut Federatif de Recherche 48 (IFR 48, Marseille, France; agreement number 09u2013022).* But there is no word about obtaining IRB approval e.g. on consent wording with the local authorities. In addition, all authors are from France, without giving a chance for local researchers to contribute. Could the authors please explain how the research was being performed, and why local researchers were not given a chance to participate? How were these individuals selected? How did the authors manage to store the samples at -80C if they were collected in rural areas such as the Amazon? Were they transported back to France in -80C containers and extracted in France, or were the samples extracted locally? Did local researchers or authorities participate? ,
PPARŒ≤/Œ¥ and Œ≥ in a rat model of Parkinson's disease: possible involvement in PD symptoms
Authors: Loredana Cristiano
Marcello Alecci
Annamaria Cimini
Antonio Giordano
Tiziana Marilena Florio
Andrea Antonosante
Erica Di Giacomo
Roberta Falcone
Elisabetta Benedetti
Mara Massimi
Rodolfo Ippoliti
Alessia Fidoamore
Journal: Journal of Cellular Biochemistry (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LIPID PEROXIDATION; MOOD DISORDERS; NEUROTROPHINS; PPARs.
Affiliations: Department of Life, Health andÔª?Environmental Sciences, University of L'Aquila, Italy., Department of Life, Health andÔª?Environmental Sciences; University of L'Aquila; Italy, Italian National Institute for Nuclear Physics (INFN); L'Aquila Italy, Department of Medicine, Surgery and Neurosciences; University of Siena; Italy, Sbarro Institute for Cancer Research and Molecular Medicine and Center for Biotechnology; Temple University; Philadelphia Pennsylvania

Abstract:  Parkinson's disease is one of the most common neurologic disorder, affecting about 1-4% of persons older than 60 years. Among the proposed mechanisms of PD generation, free radical damage is believed to play a pivotal role in the development and/or progression of the disease. Recently, PPARs, a class of transcription factors involved in several pathways both in physiological and pathological conditions, have been linked by us and others to neurodegeneration. Particularly, PPARŒ≥ and its ligands have been indicated as potential therapeutic targets for the treatment of several pathological conditions associated with neuroinflammation within the CNS. The anti-inflammatory function of PPARŒ≥ has attracted attention since agonists exert a broad spectrum of protective effects in several animal models of neurological diseases, including psychiatric diseases. On the other hand a detrimental role for PPARŒ≤/Œ¥ has been proposed in Alzheimer, being closely related to the decrease of BDNF and Trkfl. On these bases, in this work we used a 6-OHDA hemi-lesioned rat model, inducing loss of dopaminergic neurons, to study the effects of the lesion at three time points from the lesion (1, 2, and 3 weeks), in relevant areas of PD motor symptoms, such as substantia nigra and globus pallidus and in the area of reward and mood control, the nucleus accumbens. In particular, it was studied: (i) the expression of BDNF and its downstream signals; (ii) the modulation of PPARs levels. The results obtained indicate the possible use of a dual PPARŒ≤/Œ¥ antagonist/PPARŒ≥ agonist to counteract primary and secondary signs of PD neurodegeneration. 

Retracted: No

PubPeer comments:
 In Figure 3G, a micrograph has been duplicated and presented as something else.  ,
Neurotoxicity of prion peptides mimicking the central domain of the cellular prion protein
Authors: Oriol Nicol√°s
Rosalina Gav√≠n
Silvia Vilches
Cristina Vergara
Sonia Var√≥n
Miriam Royo
Jos√© A Del R√≠o
Sandra Merino
Gloria Sanclimens
Gerardo A Acosta
Fernando Albericio
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: PrP(C); synthetic peptides; neurotoxic; central domain; charge cluster
Affiliations: Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia, Barcelona, Spain.

Abstract:  The physiological functions of PrP(C) remain enigmatic, but the central domain, comprising highly conserved regions of the protein may play an important role. Indeed, a large number of studies indicate that synthetic peptides containing residues 106-126 (CR) located in the central domain (CD, 95-133) of PrP(C) are neurotoxic. The central domain comprises two chemically distinct subdomains, the charge cluster (CC, 95-110) and a hydrophobic region (HR, 112-133). The aim of the present study was to establish the individual cytotoxicity of CC, HR and CD. Our results show that only the CD peptide is neurotoxic. Biochemical, Transmission Electron Microscopy and Atomic Force Microscopy experiments demonstrated that the CD peptide is able to activate caspase-3 and disrupt the cell membrane, leading to cell death. 

Retracted: No

PubPeer comments:
 Concern about Figure 2, reported to the journal five years ago, in October 2015, but still unaddressed. * Red boxes: Panels J (CC 48h) and NN (CC 0h) appear to show an overlap  , 
 Figure 3E. * Yellow boxes: In the Tuj1 row, the PBS and HR treatment photos appear to be very similar. Are these showing the same sample?  ,
Spinal translocator protein alleviates chronic neuropathic pain behavior and modulates spinal astrocyte‚Äìneuronal function in rats with L5 spinal nerve ligation model
Authors: Yi Jin
Zhuqiang Cheng
Xiaoming Liu
Weiyan Li
Weiliang Xia
Zongxiang Tang
Hongjun Liu
Shuangshuang Xu
Journal: Pain (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: TSPO; chronic neuropathic pain; astrocytes; Ro5-4864; CXCL1
Affiliations: Pain Management Center, Department of Anesthesiology, Nanjing Jinling Hospital, Nanjing, China Laboratory of Medical Neurobiology, School of Basic Medical Science, Nanjing University of Traditional Chinese Medicine, Nanjing, China School of Bio-medical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.

Abstract:  Recent studies reported the translocator protein (TSPO) to play critical roles in several kinds of neurological diseases including the inflammatory and neuropathic pain. However, the precise mechanism remains unclear. This study was undertaken to explore the distribution and possible mechanism of spinal TSPO against chronic neuropathic pain (CNP) in a rat model of L5 spinal nerve ligation (SNL). Our results showed that TSPO was upregulated in a time-related manner in the spinal dorsal horn after SNL. Spinal TSPO was predominately expressed in astrocytes. A single intrathecal injection of TSPO agonist Ro5-4864, but not TSPO antagonist PK11195, alleviated the mechanical allodynia in a dose-dependent manner. A single intraspinal injection of TSPO overexpression lentivirus (LV-TSPO), but not TSPO inhibited lentivirus (LV-shTSPO), also relieved the development of CNP. Intrathecal administration of 2 Œºg Ro5-4864 on day 3 induced a significant increase of TSPO protein content at the early stage (days 5-7) while inhibited the TSPO activation during the chronic period (days 14-21) compared with the control group. Ro5-4864 suppressed the astrocytes and p-JNK1 activation and decreased the CXCL1 expression in both in vivo and in vitro studies. Ro5-4864 also attenuated the spinal CXCR2 and p-ERK expressions. These results suggested that early upregulation of TSPO could elicit potent analgesic effects against CNP, which might be partly attributed to the inhibition of CXCL1-CXCR2-dependent astrocyte-to-neuron signaling and central sensitization. TSPO signaling pathway may present a novel strategy for the treatment of CNP. 

Retracted: No

PubPeer comments:
 figure 7, duplicate pictures in CXCR2 and control groups.  ,
Multimeric recombinant M2e protein-based ELISA: a significant improvement in differentiating avian influenza infected chickens from vaccinated ones
Authors: Farshid Hadifar
Sophie Putland
Simson Tarigan
Abdulghaffar Ownagh
Andrea McWhorter
Farhid Hemmatzadeh
Noor Haliza Hasan
Jagoda Ignjatovic
Esmaeil Ebrahimie
Risa Indriani
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: avian influenza virus; H5N1; DIVA test; M2 protein; ELISA
Affiliations: School of Animal and Veterinary Sciences, The University of Adelaide, South Australia, Adelaide, Australia., School of Veterinary Science, The University of Melbourne, Melbourne, Victoria, Australia., Indonesian Research Centre for Veterinary Science, Bogor, West Java, Indonesia., School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia, Australia., Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.

Abstract:  Killed avian influenza virus (AIV) vaccines have been used to control H5N1 infections in countries where the virus is endemic. Distinguishing vaccinated from naturally infected birds (DIVA) in such situations however, has become a major challenge. Recently, we introduced the recombinant ectodomain of the M2 protein (M2e) of H5N1 subtype as a novel tool for an ELISA based DIVA test. Despite being antigenic in natural infection the monomer form of the M2e used in ELISA had limited antigenicity and consequently poor diagnostic capability. To address this shortcoming, we evaluated the use of four tandem copies of M2e (tM2e) for increased efficiency of M2e antibody detection. The tM2e gene of H5N1 strain from Indonesia (A/Indonesia/CDC540/2006) was cloned into a pMAL- p4x expression vector and expressed in E.coli as a recombinant tM2e-MBP or M2e-MBP proteins. Both of these, M2e and tM2e antigens reacted with sera obtained from chickens following live H5N1 infection but not with sera from vaccinated birds. A significantly stronger M2e antibody reaction was observed with the tM2e compared to M2e antigen. Western blotting also supported the superiority of tM2e over M2e in detection of specific M2e antibodies against live H5N1 infection. Results from this study demonstrate that M2e tetramer is a better antigen than single M2e and could be more suitable for an ELISA based DIVA test. 

Retracted: No

PubPeer comments:
 Figure 2. * Blue boxes: Lane 4 appears to show some unexpected repetitive elements. Can the authors please provide an explanation? Image made darker to bring out details.  ,
Effects of the Particulate Matter‚Ç?‚Ç?(PM‚Ç?‚Ç? on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity
Authors: Inho Choi
Jihoe Kim
Eun-Young Lee
Jae-Yong Kim
Kyung-Hyun Cho
Journal: Molecules and cells (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: embryo; glycation; lipoprotein; oxidation; particulate matter 2.5
Affiliations: School of Biotechnology, Korea.

Abstract:  Particulate matter2.5 (PM2.5) is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which PM2.5 aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism. Collected PM2.5 from Seoul, Korea was dissolved in water, and the water extract (final 3 and 30 ppm) was treated to human serum lipoproteins, macrophages, and dermal cells. PM2.5 extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared. PM2.5 treatment (final 30 ppm) also induced cellular uptake of oxidized LDL (oxLDL) into macrophages, especially in the presence of fructose (final 50 mM). Uptake of oxLDL along with production of reactive oxygen species was accelerated by PM2.5 solution in a dose-dependent manner. Further, PM2.5 solution caused cellular senescence in human dermal fibroblast cells. Microinjection of PM2.5 solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins. 

Retracted: No

PubPeer comments:
 Could the authors comment on the apparent splice in Figure 1A? *** Contrast enhanced  ,
Activation of mitogen-activated protein kinase pathway by the antiandrogen hydroxyflutamide in androgen receptor-negative prostate cancer cells
Authors: George Wilding
Franky L Chan
Jiaoti Huang
Wen-Jye Lin
Yi-Fen Lee
Edward M Messing
Chawnshang Chang
Journal: Cancer Research (2002)
Discipline: CLINICAL MEDICINE
Keywords: hydroxyflutamide; antiandrogen withdrawal syndrome; androgen receptor; prostate cancer; phospho-extracellular signal-regulated kinase 1/2
Affiliations: George Whipple Laboratory for Cancer Research, Department of Pathology, and The Cancer Center, University of Rochester Medical Center, New York 14642, USA.

Abstract:  Whereas hydroxyflutamide (HF) has been used as an antiandrogen to block androgen-stimulated prostate tumor growth, the antiandrogen withdrawal syndrome that allows antiandrogens to stimulate prostate tumor growth still occurs in many patients treated with androgen ablation therapy. This was previously explained by mutations in the androgen receptor (AR) and/or modulation from AR coregulators, so that HF becomes an AR agonist. Using immunohistochemical analysis, we analyzed four prostate cancer patients undergoing androgen ablation therapy with flutamide and compared their phospho-extracellular signal-regulated kinase 1/2 levels in prostate cancer biopsies before receiving HF and after experiencing disease progression while taking HF. We found a significant increase of activated mitogen-activated protein (MAP) kinase in prostate tumors from patients receiving HF during androgen ablation therapy. In vitro studies showed that HF induced a rapid activation of the Ras/MAP kinase pathway in human prostate cancer DU145 cells which lack the AR, as well as in PC-3AR2 and CWR22 cells which express the AR. Cycloheximide failed to inhibit this activation, but both AG1478, an inhibitor of the epidermal growth factor receptor (EGF-R), and an EGF-R-neutralizing antibody blocked this HF-mediated activation of MAP kinase, which suggests that the activation of Ras/MAP kinase by HF is a membrane-initiated, non-AR-mediated, and nongenomic action. The consequence of this activation may result in increasing cell proliferation and cyclin D1 expression. This raises a concern for using HF in the complete-androgen-ablation therapy in prostate cancer treatment and provides a possible pathway that might contribute to the HF withdrawal syndrome. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes. Lanes 1-7 of the ERK1 2 panel in Figure 4A look similar to the ERK1 2 panel in Figure 4B (and possibly also with that of Figure 2A). Could the authors please check?  ,
Optimization of a Deep Learning Algorithm for Security Protection of Big Data from Video Images
Authors: Qiang Geng
Xingru Lu
Huifeng Yan
Journal: Computational Intelligence and Neuroscience (2022)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: communication technology; digital technology; security; encryption algorithm; neural cryptography
Affiliations: School of Big Data & Software Engineering, Chongqing College of Mobile Communication, Chongqing 401520, China, School of Software Engineering, Chongqing University of Posts and Telecommunications, Chongqing 400065, China

Abstract:  With the rapid development of communication technology, digital technology has been widely used in all walks of life. Nevertheless, with the wide dissemination of digital information, there are many security problems. Aiming at preventing privacy disclosure and ensuring the safe storage and sharing of image and video data in the cloud platform, the present work proposes an encryption algorithm against neural cryptography based on deep learning. Primarily, the image saliency detection algorithm is used to identify the significant target of the video image. According to the significant target, the important region and nonimportant region are divided adaptively, and the encrypted two regions are reorganized to obtain the final encrypted image. Then, after demonstrating how attackers conduct attacks to the network under the ciphertext attack mode, an improved encryption algorithm based on selective ciphertext attack is proposed to improve the existing encryption algorithm of the neural network. Besides, a secure encryption algorithm is obtained through detailed analysis and comparison of the security ability of the algorithm. The experimental results show that Bob's decryption error rate will decrease over time. The average classification error rate of Eve increases over time, but when Bob and Alice learn a secure encryption network structure, Eve's classification accuracy is not superior to random prediction. Chosen ciphertext attack-advantageous neural cryptography (CCA-ANC) has an encryption time of 14s and an average speed of 69mb/s, which has obvious advantages over other encryption algorithms. The self-learning secure encryption algorithm proposed here significantly improves the security of the password and ensures data security in the video image. 

Retracted: No

PubPeer comments:
 Reference [10] is a research ethics paper completely not related to the content of the paper. , 
 Is u201cEuropean distanceu201d a misspelling of [u201cEuclidian distanceu201d] ? _Rhipidura albiventris_ noticed that this phrase is [surprisingly frequent] .  Found with the [_Problematic Paper Screener_] . ,
While K- ras Is Essential for MouseDevelopment, Expression of the K- ras 4A Splice VariantIsDispensable
Authors: David W Melton
Jennifer Doig
Martin L Hooper
D James Williamson
Mark J Arends
Sarah J Plowman
Ann-Marie Ritchie
David J Harrison
Charles E Patek
Maureen J O&#x27;Sullivan
Journal: Molecular and Cellular Biology (2003)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ras genes; K-ras 4A; K-ras 4B; mouse development; gene targeting
Affiliations: Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, Scotland, U.K., Division of Pathology, University of Edinburgh Medical School, Edinburgh EH89AG, Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, Western General Hospital, Edinburgh EH42XU, Department of Pathology, Addenbrooke‚Äôs Hospital, University of Cambridge, Cambridge CB2 2QQ, United Kingdom

Abstract:  In mammals, the three classical ras genes encode four highly homologous proteins, N-Ras, H-Ras, and the isoforms K-Ras 4A and 4B. Previous studies have shown that K-ras is essential for mouse development and that while K-ras 4A and 4B are expressed during development, K-ras 4A expression is regulated temporally and spatially and occurs in adult kidney, intestine, stomach, and liver. In the present study, the pattern of K-ras 4A expression was examined in a wide range of wild-type adult mouse tissues, and gene targeting was used to generate K-ras 4A-deficient mice to examine its role in development. It was found that K-ras 4A is also expressed in uterus, lung, pancreas, salivary glands, seminal vesicles, bone marrow cells, and cecum, where it was the major K-Ras isoform expressed. Mating between K-ras(tmDelta4A/+) mice produced viable K-ras(tmDelta4A/tmDelta4A) offspring with the expected Mendelian ratios of inheritance, and these mice expressed the K-ras 4B splice variant only. K-ras(tmDelta4A/tmDelta4A) mice were fertile and showed no histopathological abnormalities on inbred (129/Ola) or crossbred (129/Ola x C57BL/6) genetic backgrounds. The results demonstrate that K-Ras 4A, like H- and N-Ras, is dispensable for normal mouse development, at least in the presence of functional K-Ras 4B. 

Retracted: No

PubPeer comments:
 Figure 4, middle panel, much more similar than expected.  , 
 Figure 2A. Much more similar than expected.  , 
 #1 Figure 4, middle panel, continued. Much more similar than expected.  , 
 #3 Figure 4. Bottom panel. Much more similar than expected.  ,
Expression of neuropeptide Y and cholecystokinin in the rat brain by chronic mild stress
Authors: Hye-Jung Lee
Wei-Whan Whang
Kwang-Ho Pyun
Dae-Hyun Hahm
Insop Shim
Hyunyoung Kim
Sun-Young Cho
Hyun-Taek Kim
Journal: Brain Research (2003)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Neuropeptide Y; cholecystokinin; chronic mild stress; depression; sucrose intake

Abstract:  Neuropeptide Y (NPY) and cholecystokinin (CCK) are known to play important roles in the response to stress and the control of anxiety. In order to investigate the role of NPY and CCK in chronic mild stress (CMS), an animal model of depression, we examined the effects of CMS on sucrose intake as a measure of anhedonia, and expression of NPY and CCK in the rat brain utilizing immunohistochemistry. Sprague-Dawley rats were exposed to a variety of chronic unpredictable mild stressors for 8 weeks. CMS rats significantly reduced the consumption of sucrose intake and gained body weight more slowly, compared to control rats. CMS dramatically produced a decrease in NPY expression in several diencephalic regions including the parvocellular subregion of the paraventricular hypothalamic nucleus (PVN), the periventricular hypothalamic nucleus (PE), the paraventricular thalamic nucleus (PV) and the arcuate nucleus (ACN). In contrast, CCK-like immunoreactivity throughout these areas was substantially increased in chronic mild stressed rats. These results clearly demonstrated that exposure of chronic mild stress upregulated CCK synthesis and downregulated NPY synthesis within the hypothalamus. The present results demonstrated that there was an inverse relationship between NPY and CCK in mediating stress response in an animal model of depression. These findings suggest that CCK and NPY systems may play important roles in expressing the symptopathology of the chronic stress responses such as depression, abnormality of food intake or anxiety-related disorders. 

Retracted: No

PubPeer comments:
 Two of the images in Figure 3 are of the same histology slide. I have highlighted the overlapping regions.  Given the relative placement of the grids - since we now know how they relate to one-another - I am a bit confused. The square in A is listed as the PVN and the square in D is listed as the periventricular hypothalamic nucleus. This seems like a weird relative placement. Would the authors care to comment? ,
Human pregnane X receptor is expressed in breast carcinomas, potential heterodimers formation between hPXR and RXR-alpha
Authors: Francisco J Gonz√°lez
Mar√≠a I Arenas
Emilio Alba
Isabel Conde
Mar√≠a V T Lobo
Julio P√©rez
Ricardo Paniagua
Benito Fraile
Javier Zamora
Journal: BMC Cancer (2008)
Discipline: CLINICAL MEDICINE
Keywords: hPXR; RXRs; breast tissues; breast cancer; recurrent disease
Affiliations: Department of Cell Biology and Genetics, University of Alcal√°, 28871 Alcal√° de Henares, Madrid, Spain. 

Abstract:  Background: The human pregnane X receptor (hPXR) is an orphan nuclear receptor that induces transcription of response elements present in steroid-inducible cytochrome P-450 gene promoters. This activation requires the participation of retinoid X receptors (RXRs), needed partners of hPXR to form heterodimers. We have investigated the expression of hPXR and RXRs in normal, premalignant, and malignant breast tissues, in order to determine whether their expression profile in localized infiltrative breast cancer is associated with an increased risk of recurrent disease. Methods: Breast samples from 99 patients including benign breast diseases, in situ and infiltrative carcinomas were processed for immunohistochemistry and Western-blot analysis. Results: Cancer cells from patients that developed recurrent disease showed a high cytoplasmic location of both hPXR isoforms. Only the infiltrative carcinomas that relapsed before 48 months showed nuclear location of hPXR isoform 2. This location was associated with the nuclear immunoexpression of RXR-alpha. Conclusion: Breast cancer cells can express both variants 1 and 2 of hPXR. Infiltrative carcinomas that recurred showed a nuclear location of both hPXR and RXR-alpha; therefore, the overexpression and the subcellular location changes of hPXR could be considered as a potential new prognostic indicator. 

Retracted: No

PubPeer comments:
 Fig 3F and I have identical areas  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. ,
The protein kinase TOUSLED is required for maintenance of transcriptional gene silencing in Arabidopsis
Authors: Jian-Kang Zhu
Junguo Wang
Ran Xia
Jun Liu
Xuhui Hong
Jie Shen
Yu Wang
Zhizhong Gong
Rui Cao
Journal: EMBO reports (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TOUSLED-like kinases; transcriptional gene silencing; TOUSLED; TSL; ros1
Affiliations: State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University  Yuanmingyuan Xilu #2, Haidai Dist Beijing 100094 China, Department of Botany and Plant Sciences, Institute of Integrative Genome Biology  2150 Batchelor Hall, University of California, Riverside California 92521 USA

Abstract:  TOUSLED-like kinases (TLKs) are highly conserved in plants and animals, but direct evidence linking TLKs and transcriptional gene silencing is lacking. We isolated two new alleles of TOUSLED (TSL). Mutations of TSL in ros1 reactivate the transcriptionally silent 35S-NPTII transgene and the transcriptionally silent endogenous loci TSI (TRANSCRIPTIONAL SILENCING INFORMATION). Chromatin immunoprecipitation (ChIP) analysis shows that histone H3Lys9 dimethylation is decreased in the reactivated transgene and endogenous TSI loci in the tsl ros1 mutant. However, there is no change in DNA methylation in the affected loci. Western blot and ChIP assay suggest that TSL might not be responsible for histone H3Ser10 phosphorylation. The tsl seedlings were more sensitive to DNA damage reagent methyl methanesulphonate and UV-B light. Our results provide direct evidence for a crucial role of the TOUSLED protein kinase in the maintenance of transcriptional gene silencing in some genomic regions in a DNA-methylation-independent manner in Arabidopsis. 

Retracted: No

PubPeer comments:
 Figure 4C, sensitive comparison of C24 WT, *ros1*, *tsl4 ros1* and *tsl4* seedlings grown on medium containing **0.0075%** and **0.01%** methyl methanesulphonate. It appears as thereu2019s an image duplication (yellow boxes). Could the authors please check?  , 
 Thanks for pointing out the duplicated image. We think that this image was maded by wrongly copying the image. We found out the original files. The wrong ones are in the middle of 0.0075% for tsl-4ros1 and tsl-4. These seedlings are cultured in the liquid medium and the seedlings were then taken out from the medium and put on plates for taking pictures. Please see the original images and the corrected one. We are very sorry for this mistake. If anyone needs the original files, we can provide them.  , 
 #2 Thank you for your reply and for clarifying this matter. May I ask whether you are planning to issue a correction? Best regards. , 
 #3 The authors are working with EMBO reports to resolve this issue. ,
Dermatofibrosarcoma protuberans-derived fibrosarcoma: clinical history, biological profile and sensitivity to imatinib
Authors: Elena Palassini
Elena Conca
Paola Collini
Tiziana Negri
Alessandro Gronchi
Florence Pedeutour
Frederique Keslair
Paolo G Casali
Andrea Marrari
Carlo Morosi
Silvia Stacchiotti
Silvana Pilotti
Journal: International Journal of Cancer (2011)
Discipline: CLINICAL MEDICINE
Keywords: Dermatofibrosarcoma Protuberans; DFSP; COL1A1/PDGFB fusion-gene; PDGFRB activation; Fibrosarcomatous transformation
Affiliations: Adult Sarcoma Medical Oncology Unit, Department of Cancer Medicine, Fondazione IRCCS Istituto Nazionale Tumori, Milan, Italy. 

Abstract:  Dermatofibrosarcoma Protuberans (DFSP) carries a translocation resulting in the COL1A1/PDGFB fusion-gene, responsible for platelet derived growth factor beta receptor (PDGFRB) activation. Fibrosarcomatous (FS) transformation in DFSP rarely occur. The fusion-gene and PDGFRB expression/activation pattern and imatinib role in DFSP-derived FS is less defined. We reviewed all consecutive patients operated for localized DFSP at our institution from 1994 to 2009, selecting cases with FS component. We also reviewed patients treated with imatinib for advanced FS-DFSP over the same period. When cryopreserved material was available, biochemical/molecular analyses were performed. Of 275 DFSPs, 13 (4.7%) showed a FS component. Fifteen percent of these patients developed metastases, one to the brain. Four patients with DFSP-derived FS received imatinib, with a Response Evaluation Criteria in Solid Tumor Partial Response. Response was followed by early secondary progression in two. One died for brain metastases. Three patients underwent surgery after imatinib. The fusion-gene was detected in all cases in both the classical and FS component, before and after imatinib. PDGFRB expression/activation was confirmed in all cases. mTOR was switched-off, despite the phosphorylation of its effectors. However, a strong phosphorylation of S6 and 4EBP1 was restricted to the FS component. In conclusion, DFSP-derived FS maintains the fusion-gene, being sensitive to imatinib. However, responses are short-lasting. Secondary resistance to imatinib is not related to PDGFRB. 

Retracted: No

PubPeer comments:
 There are some unexpected similarities between pictures in Figures 1 and 2.   ,
Cardiac-Specific Expression of ŒîH2-R15 Mini-Dystrophin Normalized All Electrocardiogram Abnormalities and the End-Diastolic Volume in a 23-Month-Old Mouse Model of Duchenne Dilated Cardiomyopathy
Authors: Dongsheng Duan
Nalinda B Wasala
Federica Montanaro
Jin-Hong Shin
Yongping Yue
Yi Lai
Journal: Human Gene Therapy (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DMD; Duchenne muscular dystrophy; cardiomyopathy; dystrophin; mini-dystrophin
Affiliations: Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, Missouri., Dubowitz Neuromuscular Centre, Molecular Neurosciences Section, Developmental Neurosciences Programme, UCL Great Ormond Street Institute of Child Health, London, United Kingdom., Department of Neurology, School of Medicine, The University of Missouri, Columbia, Missouri., Department of Bioengineering, The University of Missouri, Columbia, Missouri., Department of Biomedical Sciences, College of Veterinary Medicine, The University of Missouri.

Abstract:  Heart disease is a major health threat for Duchenne/Becker muscular dystrophy patients and carriers. Expression of a 6-8 kb mini-dystrophin gene in the heart holds promise to change the disease course dramatically. However, the mini-dystrophin gene cannot be easily studied with adeno-associated virus (AAV) gene delivery because the size of the minigene exceeds AAV packaging capacity. Cardiac protection of the ŒîH2-R19 minigene was previously studied using the cardiac-specific transgenic approach. Although this minigene fully normalized skeletal muscle force, it only partially corrected electrocardiogram and heart hemodynamics in dystrophin-null mdx mice that had moderate cardiomyopathy. This study evaluated the ŒîH2-R15 minigene using the same transgenic approach in mdx mice that had more severe cardiomyopathy. In contrast to the ŒîH2-R19 minigene, the ŒîH2-R15 minigene carries dystrophin spectrin-like repeats 16 to 19 (R16-19), a region that has been suggested to protect the heart in clinical studies. Cardiac expression of the ŒîH2-R15 minigene normalized all aberrant electrocardiogram changes and improved hemodynamics. Importantly, it corrected the end-diastolic volume, an important diastolic parameter not rescued by ŒîH2-R19 mini-dystrophin. It is concluded that that ŒîH2-R15 mini-dystrophin is a superior candidate gene for heart protection. This finding has important implications in the design of the mini/micro-dystrophin gene for Duchenne cardiomyopathy therapy. 

Retracted: No

PubPeer comments:
 Authors may want to check 2 images (marked in red below) in Figure 2B. Although very difficult to see in original, with brightness or contrast adjusted there appear to be several areas of similarities. Apologies if I misunderstood something. Top: showing images of concern; Bottom: original Figure 1B. ***  ***  , 
 #1 Hi, Thank you very much for your comments. Your observation is correct. We will submit an erratum to Human Gene Therapy with the correct images. Nalinda and Dongsheng , 
 Attached please see the correct image. ,