PReD-Bench/PRed-Bench huggingface dataset:
Viral RNA intermediates as targets for detection and discovery of novel and emerging mosquito-borne viruses
Authors: Daniel Watterson
Mah-Lee Ng
Alice Wei Yee Yam
Caitlin A O&#x27;Brien
Natalie A Prow
Sonja Hall-Mendelin
David Warrilow
Agathe M G Colmant
Roy A Hall
Jody Hobson-Peters
Alexander A Khromykh
Breeanna J McLean
Journal: PLoS Neglected Tropical Diseases (2015)
Discipline: IMMUNOLOGY
Keywords: Mosquito-borne viruses; Viral RNA replication; Double-stranded RNA; Monoclonal antibodies; Immunofluorescence assay
Affiliations: Australian Infectious Disease Research Centre, School of Chemical and Molecular Biosciences, The University of Queensland, St. Lucia, Queensland, Australia., Public Health Virology Laboratory, Forensic and Scientific Services, Department of Health, Archerfield, Queensland, Australia., Department of Microbiology, National University Health System, National University of Singapore, Singapore.

Abstract:  Mosquito-borne viruses encompass a range of virus families, comprising a number of significant human pathogens (e.g., dengue viruses, West Nile virus, Chikungunya virus). Virulent strains of these viruses are continually evolving and expanding their geographic range, thus rapid and sensitive screening assays are required to detect emerging viruses and monitor their prevalence and spread in mosquito populations. Double-stranded RNA (dsRNA) is produced during the replication of many of these viruses as either an intermediate in RNA replication (e.g., flaviviruses, togaviruses) or the double-stranded RNA genome (e.g., reoviruses). Detection and discovery of novel viruses from field and clinical samples usually relies on recognition of antigens or nucleotide sequences conserved within a virus genus or family. However, due to the wide antigenic and genetic variation within and between viral families, many novel or divergent species can be overlooked by these approaches. We have developed two monoclonal antibodies (mAbs) which show co-localised staining with proteins involved in viral RNA replication in immunofluorescence assay (IFA), suggesting specific reactivity to viral dsRNA. By assessing binding against a panel of synthetic dsRNA molecules, we have shown that these mAbs recognise dsRNA greater than 30 base pairs in length in a sequence-independent manner. IFA and enzyme-linked immunosorbent assay (ELISA) were employed to demonstrate detection of a panel of RNA viruses from several families, in a range of cell types. These mAbs, termed monoclonal antibodies to viral RNA intermediates in cells (MAVRIC), have now been incorporated into a high-throughput, economical ELISA-based screening system for the detection and discovery of viruses from mosquito populations. Our results have demonstrated that this simple system enables the efficient detection and isolation of a range of known and novel viruses in cells inoculated with field-caught mosquito samples, and represents a rapid, sequence-independent, and cost-effective approach to virus discovery. 

Retracted: No

PubPeer comments:
 Figure 7 appears to have a repeated image. Could the authors please confirm whether this is intentional? *** ![file] ,
Glucose-dependent insulinotropic peptide receptor expression in the hippocampus and neocortex of mesial temporal lobe epilepsy patients and rats undergoing pilocarpine induced status epilepticus
Authors: Eduardo L G Moreira
Nelson de Mello
Rodrigo Medeiros
Bruno Lobão-Soares
Cláudia P Figueiredo
Gabriella Di Giunta
Katia Lin
Tânia L Mazzuco
Victor L S Antunes
Marcelo Linhares
Rui D S Prediger
Roger Walz
Journal: Peptides (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: glucose-dependent insulinotropic peptide receptor; GIPR; neuroplasticity; epilepsy; immunohistochemistry
Affiliations: Programa de Pós-graduação em Neurociências, Departamento Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil.

Abstract:  The glucose-dependent insulinotropic peptide receptor (GIPR) has been implicated with neuroplasticity and may be related to epilepsy. GIPR expression was analyzed by immunohistochemistry in the hippocampus (HIP) and neocortex (Cx) of rats undergoing pilocarpine induced status epilepticus (Pilo-SE), and in three young male patients with left mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE-HS) treated surgically. A combined GIPR immunohistochemistry and Fluoro-Jade staining was carried out to investigate the association between the GIPR expression and neuronal degeneration induced by Pilo-SE. GIPR was expressed in the cytoplasm of neurons from the HIP CA subfields, dentate gyrus (DG) and Cx of animals and human samples. The GIPR expression after the Pilo-SE induction increases significantly in the HIP after 1h and 5 days, but not after 12h or 50 days. In the Cx, the GIPR expression increases after 1h, 12h and 5 days, but not 50 days after the Pilo-SE. The expression of GIPR 12h after Pilo-SE was inversely proportional to the Fluoro-Jade staining intensity. In the human tissue, GIPR expression patterns were similar to those observed in chronic Pilo-SE animals. No Fluoro-Jade stained cells were observed in the human sample. GIPR is expressed in human HIP and Cx. There was a time and region dependent increase of GIPR expression in the HIP and Cx after Pilo-SE that was inversely associated to neuronal degeneration. 

Retracted: No

PubPeer comments:
 Figure 1A and Figure 2A: More similar than expected. Could authors check please? ![file] Figure 4: More similar than expected, could authors check please? ![file] , 
 Thank you for identifying the mistake and bringing it to our attention. We are currently attempting to retrieve the original data to correct the figure, and we will contact the journal to fix the issue. ,
Association of Serotonin Transporter Gene (5-HTTLPR/rs25531) Polymorphism with Comorbidities of Panic Disorder
Authors: Hisanobu Kaiya
Shunsuke Tanahashi
Yuji Okazaki
Tsukasa Sasaki
Hisashi Tanii
Mamoru Tochigi
Motohiro Okada
Takeshi Otowa
Yoshiaki Konishi
Journal: Neuropsychobiology (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: 5-HTTLPR; Agoraphobia; Comorbidity; Depression; Panic disorder.
Affiliations: Division of Neuroscience, Department of Psychiatry, Graduate School of Medicine, Brain Science and Animal Model Research Center, Mie University, Tsu, Japan., Division of Neuroscience, Department of Psychiatry, Graduate School of Medicine, Brain Science and Animal Model Research Center, Mie University, Tsu, Japan, ., Center for Physical and Mental Health, Mie University, Tsu, Japan, ., Department of Neuropsychiatry, NTT Medical Center Tokyo, Tokyo, Japan., Laboratory of Health Education, Graduate School of Education, The University of Tokyo, Tokyo, Japan., Department of Psychiatry, Teikyo University School of Medicine, Tokyo, Japan., Department of Psychiatry, Koseikai Michinoo Hospital, Nagasaki, Japan., Panic Disorder Research Center, Warakukai Medical Corporation, Tokyo, Japan.

Abstract:  Introduction: Panic disorder (PD) has many comorbidities such as depression, bipolar disorder (BPD), and agoraphobia (AG). PD is a moderately heritable anxiety disorder whose pathogenesis is not well understood. Recently, a tri-allelic serotonin transporter (5-HTTLPR/rs25531) polymorphism was reported to be more sensitive to personality traits compared to the bi-allelic 5-HTTLPR polymorphism. We hypothesized that the 5-HTTLPR/rs25531 polymorphism may lead to a pathological anxious state depending on the presence or absence of a comorbidity in PD. Methods: In this study, we investigated the relationship between comorbidities in PD and tri-allelic 5-HTTLPR polymorphisms. A total of 515 patients with PD (148 males, 367 females) were genotyped, and the Revised NEO Personality Inventory as well as anxiety-related psychological tests were administered. Depression, BPD, and AG were diagnosed as comorbidities. Results: For the tri-allele 5-HTTLPR genotype, a significant interaction effect was found between openness to experience and comorbid depression. Examination of the interaction between AG and the tri-allelic 5-HTTLPR genotype revealed that L' allele carriers are associated with higher trait anxiety than the S'S' genotype group in PD without AG. Conclusion: Some anxiety and personality traits can be characterized by the tri-allelic gene effect of 5-HTTLPR. These results suggest that tri-allelic 5-HTTLPR genotypes have genetic effects on the presence of comorbidities of PD. 

Retracted: No

PubPeer comments:
 ![file] According to describing, the data (Fig1 and supple Table 3) was analyzed by ANCOVA. F value of ANCOVA =0.37 (Not significant) , 
 ![file] According to describing, the data (Fig2 and supple Table 4) was analyzed by ANCOVA. F value of ANCOVA =0.94 (Not significant) ,
The regulation of survival and differentiation of neural stem cells by miR-124 via modulating PAX3
Authors: Kui Li
Zuneng Lu
Chunxia Wei
Lanfen Ren
Journal: Neuroscience Letters (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Akt-GSK3β signaling pathway; Neural stem cells; PAX3; TUBB3; miR-124.
Affiliations: Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China., Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China., Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China. Electronic address: .

Abstract:  MicroRNAs (miRNAs) have crucial functions in the regulation of proliferation and differentiation of neural stem cells (NSCs). MiR-124 has been reported to be implicated in neurogenesis. However, the precise function and mechanism of miR-124 still need further verification. In this study, we identified paired box 3 (PAX3) as a potential target of miR-124 using bioinformatics approaches. Next, we found PAX3 had reversed expression pattern with miR-124 as well as TUBB3 and GFAP. Dual-luciferase assay showed that miR-124 could bind to the 3'-UTR of PAX3 mRNA and restrain its expression. It was demonstrated that overexpression and knocking down of miR-124 in NSCs could promote the survival and suppress the apoptosis of NSCs. Meanwhile, miR-124 enhanced the expression of TUBB3 and GFAP via impairing PAX3 expression. Mechanistic study revealed that augmented Akt-GSK3β signaling pathway was the driving-force for the regulatory functions of miR-124 in NSCs. In summary, this study for the first time uncovered that miR-124 could suppress PAX3 expression, which in turn regulated the differentiation of NSCs. 

Retracted: Yes

PubPeer comments:
 Figure 1 appears to have two images which overlap, this appears to extend to the merged column as well. *** Enhanced brightness ![file] *** Original ![file] , 
 Retraction dated [13 July 2022] .  This article has been retracted at the request of the Editor in Chief. It has come to our attention that Figs. 1A and 5A in this paper include duplicate panels, i.e. panels appearing elsewhere in this paper and labeled as showing different experiments. The authors have explained that this is an error of negligence and have requested that we issue a corrigendum which replaces these figures with new ones that represent their original data. The Editor in Chief has serious concerns about the overall integrity of the data in this article and has decided that this paper should be retracted. ,
The decreased N-methyladenine DNA modification in cancer cells
Authors: Li-He Zhang
Hong Wang
Huahu Guo
Quan Du
Wei Song
Xianhua Zhang
Zhiping Hu
Min Ye
Zhenjun Yang
Xin Xiong
Da Liang
Suodi Zhai
Journal: Biochemical and Biophysical Research Communications (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cancer; DNA modification; Epigenetic.
Affiliations: State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Department of Obstetrics and Gynecology, Peking University Third Hospital, Peking University, Beijing, 100191, China., Department of Pharmacy, Peking University Third Hospital, Peking University, Beijing, 100191, China., Department of Hepatobiliary Surgery, Peking University People's Hospital, Beijing 100044, China., State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Department of Obstetrics and Gynecology, Peking University Third Hospital, Peking University, Beijing, 100191, China. Electronic address: .

Abstract:  N6-methyladenine (6 mA) is a recently characterized DNA modification in mammalian genomes, although its biological importance remains to be resolved. Using a highly sensitive HPLC/MS/MS approach, here we report regulation of 6 mA modification in mammalian cells. To these aspects, down-regulation of 6 mA modification was first characterized in human cancer cells and tissues, relative to their normal controls. In contrast to the relative stable 5 mC modification, a dramatic decrease of 6 mA modification was found, showing that 6 mA is the most regulated DNA modification in cancers. In addition to the regulation in cancer cells, a hundreds-fold increase of 6 mA modification was found for in vitro cultured human cells, relative to the in vivo cells. This up-regulation was also confirmed with in vitro cultured mouse cells. Taken together, our study revealed distinct 6 mA modification profiles in the cancer and cultured cells. Considering its distinct regulation from that of 5 mC, our study suggests that 6 mA DNA modification may play a crucial role in cell fate transition of mammalian cells. 

Retracted: No

PubPeer comments:
 Authors should note another well executed study showing that previous reports of 6mA in mammals are artifactual: No evidence for DNA N6-methyladenine in mammals https: advances.sciencemag.org content 6 12 eaay3335  Unfortunately, in the absence of a 6mdA detection technique robust to the multiple sources of error that we have outlined, we conclude that the evidence published to date is not sufficient to support the presence of 6mdA in mammals. ,
Cysteinyl Leukotriene Synthesis via Phospholipase A2 Group IV Mediates Exercise-induced Bronchoconstriction and Airway Remodeling
Authors: Akira Saito
Yosuke Kimura
Masachika Hayashi
Hiroyuki Takeuchi
Hiroshi Ueno
Masaaki Arakawa
Takashi Hasegawa
Keisuke Tsukioka
Toshiyuki Koya
Toshiaki Kikuchi
Satoshi Watanabe
Journal: American Journal of Respiratory Cell and Molecular Biology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: airway hyperresponsiveness; airway remodeling; cysteinyl-leukotriene; exercise-induced bronchoconstriction; phospholipase A2 group IV.
Affiliations: Department of Respiratory Medicine and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan., Department of General Medicine, Niigata University Medical and Dental Hospital, Niigata, Japan; and., Niigata Institute for Health and Sports Medicine, Niigata, Japan.

Abstract:  It is well known that the prevalence of asthma is higher in athletes, including Olympic athletes, than in the general population. In this study, we analyzed the mechanism of exercise-induced bronchoconstriction by using animal models of athlete asthma. Mice were made to exercise on a treadmill for a total duration of 1 week, 3 weeks, or 5 weeks. We analyzed airway responsiveness, BAL fluid, lung homogenates, and tissue histology for each period. In mice that were treated (i.e., the treatment model), treatments were administered from the fourth to the fifth week. We also collected induced sputum from human athletes with asthma and analyzed the supernatants. Airway responsiveness to methacholine was enhanced with repeated exercise stimulation, although the cell composition in BAL fluid did not change. Exercise induced hypertrophy of airway smooth muscle and subepithelial collagen deposition. Cysteinyl-leukotriene (Cys-LT) levels were significantly increased with exercise duration. Montelukast treatment significantly reduced airway hyperresponsiveness (AHR) and airway remodeling. Expression of PLA2G4 (phospholipase A2 group IV) and leukotriene C4 synthase in the airway epithelium was upregulated in the exercise model, and inhibition of PLA2 ameliorated AHR and airway remodeling, with associated lower levels of Cys-LTs. The levels of Cys-LTs in sputum from athletes did not differ between those with and without sputum eosinophilia. These data suggest that AHR and airway remodeling were caused by repeated and strenuous exercise. Cys-LTs from the airway epithelium, but not inflammatory cells, may play an important role in this mouse model. 

Retracted: No

PubPeer comments:
 Use of same controls in different experiments statistical analysis. ![file] ,
Adenoviral-mediated RNA interference targeting URG11 inhibits growth of human hepatocellular carcinoma
Authors: Ping Mo
Yongquan Shi
Yongzhan Nie
Xue Zou
Jie Liu
Yanglin Pan
Zhaorui Lian
Lina Zhao
Xiaohua Li
Wenqi Du
Rui Fan
Rui Du
Daiming Fan
Mark A Feitelson
Lin Xia
Guanhong Luo
Journal: International Journal of Cancer (2011)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocellular carcinoma; gene therapy; URG11; siRNA; carcinogenesis
Affiliations: State Key Laboratory of Cancer Biology, Xijing Hospital of Digestive Diseases, The Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.

Abstract:  Hepatocellular carcinoma (HCC) is the second most common malignancy in Asia, with a 5-year survival rate of less than 5% due to high recurrence after surgery and resistance to chemotherapy. A variety of therapeutic interventions to treat HCC, particularly gene therapy, have recently been investigated in tumor model systems to provide a more complete understanding of hepatocarcinogenesis and effectively design therapeutic strategies to treat this disease. In our study, we constructed an adenoviral vector expressing small interfering RNA (siRNA) targeting a newly discovered gene named upregulated gene 11 (URG11). We introduced this vector into HCC cells to investigate the role of URG11 in HCC carcinogenesis. We observed that upon URG11 knockdown, HCC cell proliferation was inhibited through downregulation of several G1-S phase related molecules including cyclin D1 and apoptosis was induced as a result of Bcl-2 downregulation. Besides decreased expression of cyclin D1, CDK4, pRb and Bcl-2, URG11 also suppressed several other proteins including CAPN9, which was identified by cDNA microarray and 2D gel electrophoresis. Moreover, Ad-URG11-siRNA significantly suppressed HCC tumor growth in nude mice. In conclusion, Ad-URG11-siRNA can significantly suppress HCC tumor growth in vitro and in vivo by silencing the URG11 gene, and the use of this vector for gene therapy may represent a novel strategy to treat human HCC. 

Retracted: No

PubPeer comments:
 Fig. 2c and Fig. 2d contain two WB bands that look more similar than expected. ![file] , 
 There appears to be a potential splicing in the actin band in Fig. 2a. ![file] ,
RETRACTED: Genetically reducing mTOR signaling rescues central insulin dysregulation in a mouse model of Alzheimer's disease
Authors: Antonella Caccamo
Salvatore Oddo
Ramona Belfiore
Journal: Neurobiology of Aging (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: AD; Amyloid beta; Aβ; Diabetes; Glucose
Affiliations: The Arizona State University-Banner, Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA., The Arizona State University-Banner, Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA; Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy., The Arizona State University-Banner, Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA; School of Life Sciences, Arizona State University, Tempe, AZ, USA.

Abstract:  Alzheimer's disease (AD) is the most common neurodegenerative disease. The causes of sporadic AD, which represents more than 95% of AD cases, are unknown. Several AD risk factors have been identified and among these, type 2 diabetes increases the risk of developing AD by 2-fold. However, the mechanisms by which diabetes contributes to AD pathogenesis remain elusive. The mammalian target of rapamycin (mTOR) is a protein kinase that plays a crucial role in the insulin signaling pathway and has been linked to AD. We used a crossbreeding strategy to remove 1 copy of the mTOR gene from the forebrain of Tg2576 mice, a mouse model of AD. We used 20-month-old mice to assess changes in central insulin signaling and found that Tg2576 mice had impaired insulin signaling. These impairments were mTOR dependent as we found an improvement in central insulin signaling in mice with lower brain mTOR activity. Furthermore, removing 1 copy of mTOR from Tg2576 mice improved cognition and reduced levels of Aβ, tau, and cytokines. Our findings indicate that mTOR signaling is a key mediator of central insulin dysfunction in Tg2576. These data further highlight a possible role for mTOR signaling in AD pathogenesis and add to the body of evidence indicating that reducing mTOR activity could be a valid therapeutic approach for AD. 

Retracted: Yes

PubPeer comments:
 2021 retraction. https: www.sciencedirect.com science article pii S0197458021001196?via%3Dihub This article has been retracted at the request of the Editor-in-Chief and the authors. An institutional inquiry concluded that two authors (A.C and S.O.) misrepresented data in Figures 3A, 4A and 6A, and that the report s conclusions are not reliable. The other author (R.B.) was not found at fault. The authors regret this and apologize to readers of Neurobiology of Aging. ,
Actin-independent exclusion of CD95 by PI3K/AKT signalling: implications for apoptosis
Authors: Patrick Moreau
Patrick Legembre
Sophie Daburon
Hariniaina Rampanarivo
Michel Castroviejo
Benjamin Chaigne-Delalande
Sébastien Tauzin
Mathieu Pizon
Jean-François Moreau
Journal: European Journal of Immunology (2011)
Discipline: IMMUNOLOGY
Keywords: immune system; CD95; FADD; caspases; death-inducing signalling complex
Affiliations: CNRS UMR 5164, Bordeaux, France.

Abstract:  The immune system eliminates infected or transformed cells through the activation of the death receptor CD95. CD95 engagement drives the recruitment of the adaptor protein Fas-associated death domain protein (FADD), which in turn aggregates and activates initiator caspases-8 and -10. The CD95-mediated apoptotic signal relies on the capacity to form the CD95/FADD/caspases complex termed the death-inducing signalling complex (DISC). Cells are classified according to the magnitude of DISC formation as either type I (efficient DISC formation) or type II (inefficient). CD95 localised to lipid rafts in type I cells, whereas the death receptor was excluded from these domains in type II cells. Here, we show that inhibition of both PI3K class IA and serine-threonine kinase Akt in type II cells promoted the redistribution of CD95 into lipid rafts, DISC formation and the initiation of the apoptotic signal. Strikingly, these molecular events took place independently of CD95L and the actin cytoskeleton. Overall, these findings highlight that the oncogenic PI3K/Akt signalling pathway participates in maintaining cells in a type II phenotype by excluding CD95 from lipid rafts. 

Retracted: No

PubPeer comments:
 Some flow cytometry histograms appear to be identical, but these are supposed to have been obtained from different cell lines. ![file] , 
 It looks like there is a re-use of already published data from the same group in Figure S1A and B (this re-use is not mentioned in the text): compare to S3A and B from doi: 10.1158 1541-7786.mcr-07-0331 There is also a PubPeer thread about the older Molecular Cancer Research article: https: pubpeer.com publications 9029374011752067C7DC1C917E0F1C ![file] ,
CD55 in rat male reproductive tissue: differential expression in testis and expression of a unique truncated isoform on spermatozoa
Authors: Rossen M Donev
Claire L Harris
Masashi Mizuno
B Paul Morgan
Journal: Molecular Immunology (2007)
Discipline: IMMUNOLOGY
Keywords: CD55; complement activation; alternative splicing; reproductive tissues; immunohistochemistry
Affiliations: Complement Biology Group, Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.

Abstract:  CD55 is a key regulator of complement activation, expressed on most tissues and cells in man and other mammals. In the rat, alternative splicing in the gene encoding CD55 yields GPI-anchored (GPI-CD55) and transmembrane (TM-CD55) forms. Published Northern blot analysis indicated that while GPI-CD55 was broadly expressed, TM-CD55 was primarily expressed in the testis, although the precise site of expression was not identified. To clarify the distribution of CD55 isoforms in rat reproductive tissues, we first performed immunohistochemistry and Western blot analysis with an anti-rat CD55 mAb that recognized all reported CD55 isoforms, and a polyclonal immunoglobulin specific for TM-CD55. CD55 was absent in testis prior to puberty. Post-puberty, CD55 was expressed at high levels on all spermiogenic cells from step 6 spermatid onward, and on mature spermatozoa focussed on the acrosome, but was absent from support cells and early progenitors. Enzymatic digestion revealed that GPI-CD55 was predominant in testis and spermatozoa. Staining for TM-CD55 with specific immunoglobulin confirmed its absence from mature sperm and expression on spermatids only between steps 11 and 14 of development. GPI-CD55 on spermatozoa was of lower molecular weight than that in testis and other tissues; sequencing from spermatozoal mRNA identified a unique isoform of GPI-CD55 missing short consensus repeat 4. The predominant acrosome expression and presence of a unique, truncated isoform of CD55 on spermatozoa provides further support for the hypothesis that the acrosome is a highly specialized region in which closely regulated complement activation may contribute to reproductive function. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] , 
 https: retractionwatch.com 2014 01 06 fourth-retraction-results-from-cardiff-investigation ,
Decontamination of ambient RNA in single-cell RNA-seq with DecontX
Authors: Shiyi Yang
Yusuke Koga
Masanao Yajima
W Evan Johnson
Zhe Wang
Joshua D Campbell
Sean E Corbett
Journal: Genome biology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bayesian mixture model; Decontamination; Single cell; scRNA-seq.
Affiliations: Division of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA., Department of Mathematics & Statistics, Boston University, Boston, MA, USA., Division of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA. .

Abstract:  Droplet-based microfluidic devices have become widely used to perform single-cell RNA sequencing (scRNA-seq). However, ambient RNA present in the cell suspension can be aberrantly counted along with a cell's native mRNA and result in cross-contamination of transcripts between different cell populations. DecontX is a novel Bayesian method to estimate and remove contamination in individual cells. DecontX accurately predicts contamination levels in a mouse-human mixture dataset and removes aberrant expression of marker genes in PBMC datasets. We also compare the contamination levels between four different scRNA-seq protocols. Overall, DecontX can be incorporated into scRNA-seq workflows to improve downstream analyses. 

Retracted: No

PubPeer comments:
 Unfortunately it is not compared to SoupX (another method published on [BiorXiv Feb 2020] ). Did the authors or others compared (comparing the corrected expression matrices, not just the estimated fraction). Comments appreciated! ,
Long-term curcumin treatment antagonizes masseter muscle alterations induced by chronic unpredictable mild stress in rats
Authors: Min Cui
Qiang Li
Ya-Juan Zhao
Min Zhang
Yong-Jin Chen
Fei Huang
Journal: Archives of Oral Biology (2014)
Discipline: CLINICAL MEDICINE
Keywords: CUMS; Curcumin; Masseter muscle; Metabolic disorder; Oxidative stress.

Abstract:  Objective: To investigate the correlation between psychological stress and masseter muscle (MM) alterations, and explore the therapeutic agents for restoring the impaired masticatory muscle. Design: We established a chronic unpredictable mild stress (CUMS) animal model and observed the changes of ultrastructure, redox homeostasis and energy metabolism in MM in rats with and without curcumin treatment. Results: The depressive-like behavior in stressed rats was confirmed by the evidences of altered behaviors in sucrose preference test and open field test; while these phenomena were eased by curcumin. Except for the pathological changes in ultrastructure, decreased SOD, GSH-Px, CAT, Na(+)-K(+)ATPase, and Ca(2+)-Mg(2+)ATPase activities as well as increased MDA and LD content and LDH activity were also observed in MM in stressed rats. However, curcumin was capable of reversing CUMS-induced MM disorder by improving the activities of the examined anti-oxidant enzymes and energy metabolism enzymes. Additionally, the increased MDA content, LD content, and LDH activity in stressed rats were reduced by curcumin. Conclusion: All the findings indicate the adverse effects of CUMS on MM function in rats, and raise the possibility of developing curcumin as a potential therapeutic agent for psychological stress-induced masseter dysfunction. 

Retracted: No

PubPeer comments:
 It is said  The characteristic diffraction peak of Co2(CO3)(OH)2 (JCPDS, PDF 48-0083)(Lee et al., 2018) was observed in the XRD pattern of CC@LDH . The problem is that a more recent work (2019) has established the crystal structure corresponding to that 48-0083 JCPDS card, and the chemical composition as well as the symmetry were previously completely wrong... See : http: scripts.iucr.org cgi-bin paper?S2053229618017734 ![file] ,
Treatment of MCF-7 cells with taxol and etoposide induces distinct alterations in the expression of apoptosis-related genes BCL2, BCL2L12, BAX, CASPASE-9 and FAS
Authors: Hellinida Thomadaki
Andreas Scorilas
Maroulio Talieri
Journal: Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: mRNA expression; BCL2; BCL2L12; BAX; FAS
Affiliations: Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Athens, Panepistimiopolis, and Department of Biochemistry and Molecular Biology, Papanikolaou Cancer Research Centre, St. Savas Hospital, Athens, Greece.

Abstract:  We studied alterations in the mRNA expression levels of BCL2 (Bcl-2), BCL2L12, BAX, FAS and CASPASE-9 genes in the MCF-7 breast cancer cell line in response to treatment with two anticancer drugs. Cell toxicity was evaluated by the MTT method, trypan blue staining and DNA laddering, whereas the expression levels of the apoptosis-related genes were analysed by RT-PCR using gene-specific primers. In the case of etoposide, down-regulation of the BCL2L12-A gene variant and of CASPASE-9, as well as upregulation of BAX, was observed, whereas treatment of MCF-7 cells with taxol led to down-regulation of the mRNA levels of all genes examined. Our results support the idea that after long-term clinical studies, mRNA expression analysis of BCL2L12 and other members of the BCL2 gene family may serve as useful molecular markers predicting chemotherapy response in breast cancer. 

Retracted: No

PubPeer comments:
 Figure 3. * Cyan boxes: Two lanes representing different exposures and time points appear to look similar. ![file] ,
Wogonin inhibits tumor angiogenesis via degradation of HIF-1α protein
Authors: Jing Yao
Li Zhao
Mi Zhou
Zhiyu Li
Hu Wang
Fei Wang
Yuxin Zhou
Libin Wei
Xiuming Song
Qinglong Guo
Na Lu
Journal: Toxicology and applied pharmacology (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Angiogenesis; CAM; CHX; ChIP; DMOG
Affiliations: State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, People's Republic of China.

Abstract:  Wogonin, a plant-derived flavone, has been shown recently to have antitumor effects. However, the mechanisms that wogonin inhibits tumor angiogenesis are not well known. In this study, we investigated the effects of wogonin on expression of hypoxia-inducible factor-1α (HIF-1α) and secretion of vascular endothelial growth factor (VEGF) in tumor cells. We found that wogonin decreased the expression of HIF-1α by affecting its stability and reduced the secretion of VEGF, which suppressed angiogenesis in cancer. Wogonin promoted the degradation of HIF-1α by increasing its prolyl hydroxylation, which depended on prolyl hydroxylase (PHD) and the von Hippel-Lindau tumor suppressor (VHL). Intriguingly, wogonin impeded the binding between heat-shock protein 90 (Hsp90) and HIF-1α. In addition, wogonin down-regulated the Hsp90 client proteins EGFR, Cdk4 and survivin, but did not affect the level of Hsp90. Wogonin also increased ubiquitination of HIF-1α and promoted its degradation in proteasome. We also found that wogonin could inhibit nuclear translocation of HIF-1α. Electrophoresis mobility shift assay (EMSA) showed that wogonin decreased the binding activity of exogenous consensus DNA oligonucleotide with HIF-1α in nuclear extracts from MCF-7 cells. Chromatin immunoprecipitation (ChIP) assay also revealed that HIF-1α directly binded to endogenous hypoxia-responsive element (HRE) and this binding was significantly decreased in MCF-7 cells treated with wogonin. Preliminary results indicated in vivo activity of wogonin against xenograft-induced angiogenesis in nude mice. Taken together, the results suggested that wogonin was a potent inhibitor of HIF-1α and provided a new insight into the mechanisms of wogonin against cancers. 

Retracted: No

PubPeer comments:
 In Figure 2A, part of a micrograph has been duplicated and presented as something different: ![file] , 
 Corrigendum 14 September 2019 [1 December 2019] :  The authors regret there was a mistake in Fig. 2A. During figure fomation, the image of control group under normal oxygen in transwell assay was accidentally wrong used. We have provided a correct image in Fig. 2, which showed no influence to the results. ![]  The authors would like to apologise for any inconvenience caused. ,
In vivo delivery of adenoviral vector containing interleukin-17 receptor a reduces cardiac remodeling and improves myocardial function in viral myocarditis leading to dilated cardiomyopathy
Authors: Tianqing Peng
Xian Zhang
Yingzhen Yang
Ruizhen Chen
Xinggang Wang
Yuquan Xie
Junbo Ge
Yunzeng Zou
Haozhu Chen
Minghui Li
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Th17 cells; IL-17A; viral myocarditis; dilated cardiomyopathy; adenoviral transfer
Affiliations: Key Laboratory of Viral Heart Diseases, Ministry of Public Health, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China ; Department of Cardiology, Xinhua Hospital affiliated to Shanghai Jiaotong University, Shanghai, China.

Abstract:  Th17 cells have been implicated in the pathogenesis of myocarditis. Interleukin (IL)-17A produced by Th17 cells is dispensable for viral myocarditis but essential for the progression to dilated cardiomyopathy (DCM). This study investigated whether the adenoviral transfer of the IL-17 receptor A reduces myocardial remodeling and dysfunction in viral myocarditis leading to DCM. In a mouse model of Coxsackievirus B3 (CVB3)-induced chronic myocarditis, the delivery of the adenovirus-containing IL-17 receptor A (Ad-IL17RA:Fc) reduced IL-17A production and decreased the number of Th17 cells in the spleen and heart, leading to the down-regulation of systemic TNF-α and IL-6 production. Cardiac function improved significantly in the Ad-IL17R:Fc- compared with the Ad-null-treated mice 3 months after the first CVB3 infection. Ad-IL17R:Fc reduced the left ventricle dilation and decreased the mortality in viral myocarditis, leading to DCM (56% in the Ad-IL17R:Fc versus 76% in the Ad-null group). The protective effects of Ad-IL17R-Fc on remodeling correlated with the attenuation of myocardial collagen deposition and the reduction of fibroblasts in CVB3-infected hearts, which was accompanied by the down-regulation of A distintegrin and metalloprotease with thrombospondin type 1 motifs (ADAMTS-1), Matrix metalloproteinase-2(MMP-2), and collagen subtypes I and III in the heart. Moreover, in cultured cardiac fibroblasts, IL-17A induced the expression of ADAMTS-1, MMP-2, and collagen subtypes I and III and increased the proliferation of fibroblasts. We determined that the delivery of IL-17-RA:Fc reduces cardiac remodeling, improves function, and decreases mortality in viral myocarditis leading to DCM, possibly by suppressing fibrosis. Therefore, the adenoviral transfer of the IL-17 receptor A may represent an alternative therapy for chronic viral myocarditis and its progression to DCM. 

Retracted: No

PubPeer comments:
 Figure 5 and 6. * Red arrows: Two lanes in the GAPDH panels appear to look similar, if one of the two panels is rotated 180 degrees. Reported to the journal in October 2015, but no action as of today. ![file] ,
Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin
Authors: Felicia Permatasari
Jia-An Zhang
Dan Luo
Yang Xu
Bing-Rong Zhou
Di Wu
Juan Liu
Li-Wen Ma
Journal: Oxidative Medicine and Cellular Longevity (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Soy oligopeptides; UVB-induced photodamage; Skin protection; Erythema index; Melanin index
Affiliations: Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Abstract:  Aim. We explored the effects of soy oligopeptides (SOP) in ultraviolet B- (UVB-) induced acute photodamage of human skin in vivo and foreskin ex vivo. Methods. We irradiated the forearm with 1.5 minimal erythemal dose (MED) of UVB for 3 consecutive days, establishing acute photodamage of skin, and topically applied SOP. Erythema index (EI), melanin index, stratum corneum hydration, and transepidermal water loss were measured by using Multiprobe Adapter 9 device. We irradiated foreskin ex vivo with the same dose of UVB (180 mJ/cm(2)) for 3 consecutive days and topically applied SOP. Sunburn cells were detected by using hematoxylin and eosin staining. Apoptotic cells were detected by using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Cyclobutane pyrimidine dimers (CPDs), p53 protein, Bax protein, and Bcl-2 protein were detected by using immunohistochemical staining. Results. Compared with UVB group, UVB-irradiated skin with topically applied SOP showed significantly decreased EI. Compared with UVB group, topical SOP significantly increased Bcl-2 protein expression and decreased CPDs-positive cells, sunburn cells, apoptotic cells, p53 protein expression, and Bax protein expressions in the epidermis of UVB-irradiated foreskin. Conclusion. Our study demonstrated that topical SOP can protect human skin against UVB-induced photodamage. 

Retracted: No

PubPeer comments:
 2020 retraction. https: www.hindawi.com journals omcl 2020 8265810 Oxidative Medicine and Cellular Longevity has retracted the article titled u201cProtective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skinu201d [1]. The article was found to contain duplicated images as follows: (i)tThe fourth image in Figure 6A is the same as the third image in Figure 7B (ii)tThe third image in Figure 6C is the same as the first image in Figure 6D, if slightly rotated anticlockwise The authors apologized for this mistake and stated that it was out of carelessness and they asked to correct the duplicated images. However, the Editorial Board recommended retraction. The authors agree to retraction. References B.-r. Zhou, L.-w. Ma, J. Liu et al., u201cProtective Effects of Soy OligoPeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin,u201d Oxidative Medicine and Cellular Longevity, vol. 2016, Article ID 5846865, 13 pages, 2016. ,
Caffeine targets TOR complex I and provides evidence for a regulatory link between the FRB and kinase domains of Tor1p
Authors: Ted Powers
Aaron Reinke
Sofia Aronova
Jenny C-Y Chen
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: TOR kinase; growth regulation; eukaryotic cells; budding yeast; TORC1
Affiliations: Section of Molecular and Cellular Biology, College of Biological Sciences, University of California, Davis, California 95616, USA.

Abstract:  The target of rapamycin (TOR) kinase is an important regulator of growth in eukaryotic cells. In budding yeast, Tor1p and Tor2p function as part of two distinct protein complexes, TORC1 and TORC2, where TORC1 is specifically inhibited by the antibiotic rapamycin. Significant insight into TORC1 function has been obtained using rapamycin as a specific small molecule inhibitor of TOR activity. Here we show that caffeine acts as a distinct and novel small molecule inhibitor of TORC1: (i) deleting components specific to TORC1 but not TORC2 renders cells hypersensitive to caffeine; (ii) rapamycin and caffeine display remarkably similar effects on global gene expression; and (iii) mutations were isolated in Tor1p, a component specific to TORC1, that confers significant caffeine resistance both in vivo and in vitro. Strongest resistance requires two simultaneous mutations in TOR1, the first at either one of two highly conserved positions within the FRB (rapamycin binding) domain and a second at a highly conserved position within the ATP binding pocket of the kinase domain. Biochemical and genetic analyses of these mutant forms of Tor1p support a model wherein functional interactions between the FRB and kinase domains, as well as between the FRB domain and the TORC1 component Kog1p, regulate TOR activity as well as contribute to the mechanism of caffeine resistance. 

Retracted: No

PubPeer comments:
 Figure 3D u2013 more similar than expected ![file] , 
 Thank you for catching this error in our preparation of this figure. It appears we inadvertently used the image for the I1954V mutant grown on the -5-FOA plate twice, including for the TOR1-1 mutant. Below I have included the original plates that were cropped to produce the figure for the manuscript. I have provided a key and labels and have boxed in red the correct image of the TOR1-1 strain that should have been used instead. This error, though regrettable, does not change any of the conclusions in the manuscript. -Ted Powers ![file] ,
Cleavage of CAD inhibitor in CAD activation and DNA degradation during apoptosis
Authors: H Sakahira
S Nagata
M Enari
Journal: Nature (1998)
Discipline: Multidisciplinary
Keywords: apoptosis; caspase 3; CAD; ICAD; DNA degradation
Affiliations: Department of Genetics, Osaka University Medical School, Suita, Japan.

Abstract:  Various molecules such as cytokines and anticancer drugs, as well as factor deprivation, rapidly induce apoptosis (programmed cell death), which is morphologically characterized by cell shrinkage and the blebbing of plasma membranes and by nuclear condensation. Caspases, particularly caspase 3, are proteases that are activated during apoptosis and which cleave substrates such as poly(ADP-ribose) polymerase, actin, fodrin, and lamin. Apoptosis is also accompanied by the internucleosomal degradation of chromosomal DNA. In the accompanying Article, we have identified and molecularly cloned a caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD). Here we show that caspase 3 cleaves ICAD and inactivates its CAD-inhibitory effect. We identified two caspase-3 cleavage sites in ICAD by site-directed mutagenesis. When human Jurkat cells were transformed with ICAD-expressing plasmid, occupation of the receptor Fas, which normally triggers apoptosis, did not result in DNA degradation. The ICAD transformants were also resistant to staurosporine-induced DNA degradation, although staurosporine still killed the cells by activating caspase. Our results indicate that activation of CAD downstream of the caspase cascade is responsible for internucleosomal DNA degradation during apoptosis, and that ICAD works as an inhibitor of this process. 

Retracted: No

PubPeer comments:
null, 
 September 2015 Corrigendum, which reads: *Recently, it has come to our attention that in Fig. 1a of this Letter, lanes 1 and 5 appear to be duplicated and lanes 6 and 10 appear to be duplicated. It is unclear how this happened. We have repeated the experiment (see Fig. 1 of this Corrigendum) and the results were as described in the original Letter. The Supplementary Information to this Corrigendum contains the source data used to generate the corrected Fig. 1. Our conclusions are unaffected.* Here is the original Figure 1 as reported in May 2015. ![file] ,
Psychological impacts of “screen time” and “green time” for children and adolescents: A systematic scoping review
Authors: Alice R Rumbold
Tassia K Oswald
Vivienne M Moore
Sophie G E Kedzior
Journal: PLoS ONE (2020)
Discipline: Multidisciplinary
Keywords: screen time; green time; psychological outcomes; young children; schoolchildren
Affiliations: School of Public Health, Faculty of Health & Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia., Robinson Research Institute, Faculty of Health & Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Abstract:  Technological developments in recent decades have increased young people's engagement with screen-based technologies (screen time), and a reduction in young people's contact with nature (green time) has been observed concurrently. This combination of high screen time and low green time may affect mental health and well-being. The aim of this systematic scoping review was to collate evidence assessing associations between screen time, green time, and psychological outcomes (including mental health, cognitive functioning, and academic achievement) for young children (&lt;5 years), schoolchildren (5-11 years), early adolescents (12-14 years), and older adolescents (15-18 years). Original quantitative studies were identified in four databases (PubMed, PsycInfo, Scopus, Embase), resulting in 186 eligible studies. A third of included studies were undertaken in Europe and almost as many in the United States. The majority of studies were cross-sectional (62%). In general, high levels of screen time appeared to be associated with unfavourable psychological outcomes while green time appeared to be associated with favourable psychological outcomes. The ways screen time and green time were conceptualised and measured were highly heterogeneous, limiting the ability to synthesise the literature. The preponderance of cross-sectional studies with broadly similar findings, despite heterogeneous exposure measures, suggested results were not artefacts. However, additional high-quality longitudinal studies and randomised controlled trials are needed to make a compelling case for causal relationships. Different developmental stages appeared to shape which exposures and outcomes were salient. Young people from low socioeconomic backgrounds may be disproportionately affected by high screen time and low green time. Future research should distinguish between passive and interactive screen activities, and incidental versus purposive exposure to nature. Few studies considered screen time and green time together, and possible reciprocal psychological effects. However, there is preliminary evidence that green time could buffer consequences of high screen time, therefore nature may be an under-utilised public health resource for youth psychological well-being in a high-tech era. 

Retracted: No

PubPeer comments:
 Figure 2 - two identical XRD patterns for different samples. ![file] ,