PReD-Bench/PRed-Bench huggingface dataset:
Heterogeneous nuclear ribonucleoprotein A1 is a novel cellular target of atrial natriuretic peptide signaling in renal epithelial cells
Authors: Kumar U Kotlo
Robert S Danziger
Bahar Hesabi
Journal: Cellular Signalling (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: guanylyl cyclases; cGMP; compartmentalization; ANP; NO

Abstract:  Two classes of guanylyl cyclases (GC) form intracellular cGMP. One is a receptor for atrial natriuretic peptide (ANP) and the other for nitric oxide (NO). The ANP receptor guanylyl cyclase (GC-A) is a membrane-bound, single subunit protein. Nitric oxide activated or soluble guanylyl cyclases (NOGC) are heme-containing heterodimers. These have been shown to be important in cGMP mediated regulation of arterial vascular resistance and renal sodium transport. Recent studies have shown that cGMP produced by both GCs is compartmentalized in the heart and vascular smooth muscle cells. To date, however, how intracellular cGMP generated by ANP and NO is compartmentalized and how it triggers specific downstream targets in kidney cells has not been investigated. Our studies show that intracellular cGMP formed by NO is targeted to cytosolic and cytoskeletal compartments whereas cGMP formed by ANP is restricted to nuclear and membrane compartments. We used two dimensional difference in gel electrophoresis and MALDI-TOF/TOF to identify distinct sub-cellular targets that are specific to ANP and NO signaling in HK-2 cells. A nucleocytoplasmic shuttling protein, heterogeneous nuclear ribonucleo protein A1 (hnRNP A1) is preferentially phosphorylated by ANP/cGMP/cGK signaling. ANP stimulation of HK-2 cells leads to increased cGK activity in the nucleus and translocation of cGK and hnRNP A1 to the nucleus. Phosphodiestaerase-5 (PDE-5 inhibitor) sildenafil augmented ANP-mediated effects on hnRNPA1 phosphorylation, translocation to nucleus and nuclear cGK activity. Our results suggest that cGMP generated by ANP and SNAP is differentially compartmentalized, localized but not global changes in cGMP, perhaps at different sub-cellular fractions of the cell, may more closely correlate with their effects by preferential phosphorylation of cellular targets. 

Retracted: No

PubPeer comments:
 The left panel in Fig. 6 appears to be composed of several parts.![file] ,
LncRNA MIR205HG Drives Esophageal Squamous Cell Carcinoma Progression by Regulating miR-214/SOX4 Axis
Authors: Chang Wang
Jinxiu Sheng
Zimo Jia
Lijun Yang
Huiqing Yin
Jinlin Jia
Fucheng He
Junhu Wan
Weiwei Meng
Jie Chu
Hongle Li
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: ESCC; MIR205HG; SOX4; lncRNA; miR-214.
Affiliations: Department of Molecular Pathology, The Henan Cancer Hospital, Zhengzhou, Henan, People's Republic of China., Department of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China., Department of Blood Transfusion, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China., Department of Medical Laboratory, Hebei Medical University, Shijiazhuang, People's Republic of China.

Abstract:  Background: Esophageal squamous cell carcinoma (ESCC) is a common and fatal malignancy, which has posed a great challenge to public health, especially in China. Dysregulation of long non-coding RNAs is involved in the occurrence, development, invasion, and metastasis of multiple cancers including ESCC. However, little is known about the function of MIR205HG in ESCC. Methods: We used qRT-PCR to detect the expression level of MIR205HG, miR-214, and SOX4 in human ESCC tissues and cell lines. Loss-of-functional assays were performed to test the impact of MIR205HG on cell proliferation, metastasis, and apoptosis process via CCK-8, transwell, and flow cell cytometry assays. Additionally, the downstream molecular mechanism of MIR205HG in ESCC was explored. Results: Here, we found MIR205HG was substantially up-regulated in ESCC, and there was a positive correlation between MIR205HG expression and tumor size and lymphatic metastasis of ESCC patients. Inhibition of MIR205HG attenuated cell proliferation, migration, and invasion. Silencing MIR205HG increased G1 phase cell counts and decreased S phase cell counts, along with increased apoptotic cell populations. Notably, the rescue assays indicated that miR-214 could partly reverse the influence of MIR205HG on ESCC cell migration. We also found that SOX4 was a direct target mRNA of miR-214, and MIR205HG could act as a molecular sponge to regulate SOX4 expression in ESCC. Conclusion: Taken together, our findings demonstrate that MIR205HG promotes ESCC progression by regulating the miR-214/SOX4 axis. MIR205HG may be a novel candidate target for ESCC diagnosis and therapy. 

Retracted: No

PubPeer comments:
 The study authors point out in the *Measures* section that  ***Taking action*** was assessed with two questions about whether the participant talked to neighbors or the landlord about not smoking in the past 6 months (e.g., u201cSince the last survey, about 6 months ago, did you talk to your landlord about protecting your apartment from secondhand smoke?u201d; u03b1=0.60). This outcome seems to be missing from the *Results* and *Discussion* section. ,
Expression of the SMADIP1 gene during early human development
Authors: Tania Attié-Bitach
Stanislas Lyonnet
Michel Vekemans
Arnold Munnich
Joëlle Augé
Férechté Encha-Razavi
Yolanda Espinosa-Parrilla
Jeanne Amiel
Journal: Mechanisms of development (2002)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SMADIP1; embryogenesis; neural crest cells; differentiation; malformations

Abstract:  The smad binding protein 1 gene (SMADIP1, MIM 605802) has been recently identified as a disease causing gene in a polytopic embryonic defect (MIM 235730) including midline anomalies, facial dysmorphic features and enteric nervous system malformation (Hirschsprung disease). To confirm the pleiotropic role of SMADIP1 during embryogenesis and investigate its role in neural crest cell derivatives differentiation, we performed RNA in situ hybridization at early stages of human development. According to the spectrum of malformations observed in patients, expression of SMADIP1 is observed in neural crest derived cells (peripheric nervous system, enteric nervous system, facial neurectoderm and cranial nerve ganglia), central nervous system, genital tubercle, muscles and kidneys. Surprisingly, SMADIP1 expression is also found in limbs and developing eye. Although congenital heart defects are frequently observed in patients with either a SMADIP1 large scale deletion or truncating mutation, no SMADIP1 expression could be detected in the developing heart at the stages studied. 

Retracted: No

PubPeer comments:
 A paper devoted to gene expression pattern in humans. Numerous errors. ![file] Clearly sections A and B cannot be adjacent. ![file] The prosencephalon (Pro) does not exist at that stage. it is replaced by diencephalon and telencephalon. The neural domain of expression is wrong. ![file] The expression by the enteric nervous system cannot be observed on this section. ![file] ![file] I guess the authors refer to mesectoderm and not neurectoderm. terminology is important. ![file] My arrow points to the pituitary stalk. The gene is expressed more rostrally. Are the authors trained in developmental biology? , 
 Thank you Kudoa Ciliatae #1 for pointing these inaccuracies in this paper. Terminology is really bad: ![file] Perichondrum does not exist but perichondrium. ![file] Submucose does not exist but submucosa ![file] What is considered as submucose (submucosa) in the esphagus is in fact both chorion (that belongs to mucosa) and submucosa. ![file] This is the same for the intestine. ![file] For the eye, choroid is the membrane that lines the pigmentary retina. Such is not the case here. ![file] What is called the mesencephalon (mes) has a very thin roof. this is specific for rhombencephalon and not mesencephalon. In my opinion this expression pattern should be removed from the literature because of so many inaccuracies. ,
NFκB is a central regulator of protein quality control in response to protein aggregation stresses via autophagy modulation
Authors: Stéphanie Simon
Maëlenn Fournier
Baptiste Guey
Carole Kretz-Remy
Mathieu Nivon
Emma Richet
Loïc Fort
André-Patrick Arrigo
Julie D Atkin
Claudio Hetz
Pascale Muller
Journal: Molecular Biology of the Cell (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Protein misfolding; Protein aggregates; Protein conformational diseases; NFκB transcription factor; Autophagy
Affiliations: Université de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France., Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, 70086 Santiago, Chile Center for Geroscience, Brain Health and Metabolism, 70086 Santiago, Chile., Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW 2109, Australia., Université de Lyon, 69622 Lyon, France CNRS, UMR 5310, INSERM U1217, Institut NeuroMyoGène, Université Lyon 1, 69100 Villeurbanne, France .

Abstract:  During cell life, proteins often misfold, depending on particular mutations or environmental changes, which may lead to protein aggregates that are toxic for the cell. Such protein aggregates are the root cause of numerous diseases called "protein conformational diseases," such as myofibrillar myopathy and familial amyotrophic lateral sclerosis. To fight against aggregates, cells are equipped with protein quality control mechanisms. Here we report that NFκB transcription factor is activated by misincorporation of amino acid analogues into proteins, inhibition of proteasomal activity, expression of the R120G mutated form of HspB5 (associated with myofibrillar myopathy), or expression of the G985R and G93A mutated forms of superoxide dismutase 1 (linked to familial amyotrophic lateral sclerosis). This noncanonical stimulation of NFκB triggers the up-regulation of BAG3 and HspB8 expression, two activators of selective autophagy, which relocalize to protein aggregates. Then NFκB-dependent autophagy allows the clearance of protein aggregates. Thus NFκB appears as a central and major regulator of protein aggregate clearance by modulating autophagic activity. In this context, the pharmacological stimulation of this quality control pathway might represent a valuable strategy for therapies against protein conformational diseases. 

Retracted: No

PubPeer comments:
 Fig. 2C and Fig. 2E: More similar than expected. Could authors check please? ![file] ,
SNHG7 mediates cisplatin-resistance in non-small cell lung cancer by activating PI3K/AKT pathway
Authors: L Luo
M Suotesiyali
K Chen
H Zhang
Y Zou
A Abuduwufuer
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNAs; SNHG7; cisplatin-resistant; NSCLC; drug-resistance
Affiliations: Department of Thoracic, Xinjiang Uygur Autonomous Region People's Hospital, Urumqi, China. .

Abstract:  Objective: The aim of this study was to clarify the function of long noncoding ribonucleic acids (lncRNAs) small nucleolar RNA host gene 7 (SNHG7) in cisplatin-resistant non-small cell lung cancer (NSCLC), and to explore the potential mechanism. Patients and methods: SNHG7 expression in NSCLC and para-cancerous tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, the correlation between SNHG7 expression with clinical stage and cisplatin-resistance in NSCLC patients was analyzed. After transfection of si-SNHG7 or p-complementary deoxyribonucleic acid (pcDNA)-SNHG7, changes in cellular behaviors of A549/DDP cells were evaluated, including cell viability, apoptosis, migration, invasion and cell cycle. The regulatory effects of SNHG7 on the expressions of genes were determined by qRT-PCR as well. Furthermore, Western blot was conducted to determine the protein expressions of drug-resistance genes minimal residual disease1 (MRD1), P-glycoprotein (P-gp), BCRP and relative genes in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway. Results: Compared with adjacent normal tissues, SNHG7 was highly expressed in NSCLC tissues. Moreover, SNHG7 expression was significantly higher in advanced-stage NSCLC patients than those in early-stage. SNHG7 level remained significantly higher in DDP-resistant NSCLC tissues and cell lines as well. Knockdown of SNHG7 remarkably enhanced cisplatin-resistance in NSCLC cells, manifesting as decreased cell viability, migratory and invasive rates, DNA synthesis capacity, and promoted apoptosis. Meanwhile, SNHG7 knockdown down-regulated the mRNA levels of matrix metalloprotein2 (MMP2), MMP7 and MMP9 in vitro. After SNHG7 knockdown, the expressions of drug-resistant and relative genes in the PI3K/AKT pathway were notably down-regulated. Conclusions: SNHG7 induces the development of cisplatin-resistance in NSCLC through upregulating MRD1 and BCRP via PI3K/AKT pathway. 

Retracted: No

PubPeer comments:
 Figure 2C. * Boxes of the same color highlight some of the remarkable similarities between the two panels. ![file] ,
Immune Response Is Key to Genetic Mechanisms of SARS-CoV-2 Infection With Psychiatric Disorders Based on Differential Gene Expression Pattern Analysis
Authors: Minghong Gan
Hua Li
Yaping Li
Yang Bai
Li Gu
Shuhan Chen
Jing Xia
Jiashuo Wu
Lu Gao
Clare Colette Prohaska
Dongfang Zhang
Journal: Frontiers in Immunology (2022)
Discipline: IMMUNOLOGY
Keywords: COVID-19; SARS-CoV-2; differentially expressed gene; functional enrichment; psychiatric illness.
Affiliations: Department of Pharmacognosy, School of Pharmacy, China Medical University, Shenyang, China., Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China., Division of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, United States., Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.

Abstract:  Existing evidence demonstrates that coronavirus disease 2019 (COVID-19) leads to psychiatric illness, despite its main clinical manifestations affecting the respiratory system. People with mental disorders are more susceptible to COVID-19 than individuals without coexisting mental health disorders, with significantly higher rates of severe illness and mortality in this population. The incidence of new psychiatric diagnoses after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is also remarkably high. SARS-CoV-2 has been reported to use angiotensin-converting enzyme-2 (ACE2) as a receptor for infecting susceptible cells and is expressed in various tissues, including brain tissue. Thus, there is an urgent need to investigate the mechanism linking psychiatric disorders to COVID-19. Using a data set of peripheral blood cells from patients with COVID-19, we compared this to data sets of whole blood collected from patients with psychiatric disorders and used bioinformatics and systems biology approaches to identify genetic links. We found a large number of overlapping immune-related genes between patients infected with SARS-CoV-2 and differentially expressed genes of bipolar disorder (BD), schizophrenia (SZ), and late-onset major depressive disorder (LOD). Many pathways closely related to inflammatory responses, such as MAPK, PPAR, and TGF-β signaling pathways, were observed by enrichment analysis of common differentially expressed genes (DEGs). We also performed a comprehensive analysis of protein-protein interaction network and gene regulation networks. Chemical-protein interaction networks and drug prediction were used to screen potential pharmacologic therapies. We hope that by elucidating the relationship between the pathogenetic processes and genetic mechanisms of infection with SARS-CoV-2 with psychiatric disorders, it will lead to innovative strategies for future research and treatment of psychiatric disorders linked to COVID-19. 

Retracted: No

PubPeer comments:
 Figure 1 panels A and C look remarkably similar or identical, which one would not expect from data collected from two different groups. ,
The contribution of linear perspective cues and texture gradients in the perceptual rescaling of stimuli inside a Ponzo illusion corridor
Authors: Christine Kettle
Philippe A Chouinard
Gizem Y Yildiz
Irene Sperandio
Journal: PLoS ONE (2019)
Discipline: Multidisciplinary
Keywords: linear perspective cues; texture gradients; perceptual rescaling; stimuli; Ponzo illusion
Affiliations: Department of Psychology and Counselling, School of Psychology and Public Health, La Trobe University, Melbourne, Australia., School of Psychology, University of East Anglia, Norwich, United Kingdom., Department of Pharmacy and Biomedical Sciences, School of Molecular Sciences, La Trobe University, Melbourne, Australia.

Abstract:  We examined the influence of linear perspective cues and texture gradients in the perceptual rescaling of stimuli over a highly-salient Ponzo illusion of a corridor. We performed two experiments using the Method of Constant Stimuli where participants judged the size of one of two rings. In experiment 1, one ring was presented in the upper visual-field at the end of the corridor and the other in the lower visual-field at the front of the corridor. The perceived size of the top and bottom rings changed as a function of the availability of linear perspective and textures. In experiment 2, only one ring was presented either at the top or the bottom of the image. The perceived size of the top but not the bottom ring changed as a function of the availability of linear perspective and textures. In both experiments, the effects of the cues were additive. Perceptual rescaling was also stronger for the top compared to the bottom ring. Additional eye-tracking revealed that participants tended to gaze more in the upper than the lower visual-field. These findings indicate that top-down mechanisms provide an important contribution to the Ponzo illusion. Nonetheless, additional maximum likelihood estimation analyses revealed that linear perspective fulfilled a greater contribution in experiment 2, which is suggestive of a bottom-up mechanism. We conclude that both top-down and bottom-up mechanisms play important roles. However, the former seems to fulfil a more prominent role when both stimuli are presented in the image. 

Retracted: No

PubPeer comments:
  The visual system estimates greater depth when two lines on the retina converge closer together. This is not a defensible statement, for the reasons discussed (and illustrated) in this preprint - https: psyarxiv.com x2bsk ,
miR-141-3p promotes proliferation and metastasis of nasopharyngeal carcinoma by targeting NME1
Authors: Haiping Huang
Manyi Li
Fuwei Cheng
Jisheng Liu
Xiaoqing Hu
Journal: Advances in Medical Sciences (2020)
Discipline: CLINICAL MEDICINE
Keywords: Metastasis; NME1; NPC; Proliferation; miR-141-3p.
Affiliations: Department of Otolaryngology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China., Department of Otolaryngology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China. Electronic address: .

Abstract:  Purpose: This study aimed to investigate the expression and biological function of miR-141-3p in nasopharyngeal carcinoma (NPC) via targeting neoplasm metastasis 1 (NME1). Materials and methods: The expression of miR-141-3p and NME1 in 5-8F, C666-1, CNE-1, CNE-2, 6-10B and NP69 nasopharyngeal epithelial cells were detected using real-time Polymerase Chain Reaction (real-time PCR) and western blot, respectively. Cell proliferation was detected using Cell Counting Kit-8 (CCK-8), and the metastasis was detected using Transwell. The binding of miR-141-3p to NME1 was detected by dual luciferase reporter gene detection system. The effects of miR-141-3p on tumor growth were also determined in vivo. Results: The results showed that the expression of miR-141-3p significantly increased in various tumor cell lines and the expression of NME1 was higher in NP69 cells and lower in 5-8F cells, which had significant negative correlation. Furthermore, the expression of NME1 was significantly reduced after transfection of miR-141-3p and miR-141-3p promoted cell proliferation and metastasis. The double luciferase reporter gene detection system confirmed that NME1 was the target gene of miR-141-3p. Knockout of NME1 promoted the proliferation and metastasis of NP69 or 6-10B cells and the activation of p-Akt, which were abrogated by miR-141-3p. In vivo, the tumor volumes and weights in the miR-141-3p group significantly increased followed by down-regulation of NME1 and activation of p-Akt. Conclusions: We confirmed that miR-141-3p promotes the proliferation and metastasis of NPC by targeting NME1. 

Retracted: No

PubPeer comments:
 Two images in figure 1G appear to be the same, albeit flipped horizontally. *** ![file] , 
 In addition to the issue above, figure 1F appears to have a overlapping image in the migration section, when one image is rotated and recolored slightly. *** ![file] *** Original figure ![file] , 
 #2 Figure 3C has similar issues. I circled common features here for illustration, but the images again have been flipped relative to each other. I will stop flogging now. *** ![file] , 
 #2 #2 We will check all the images.Thank you very much. , 
 #3 Versatile! ![file] ,
Baicalin ameliorates chronic unpredictable mild stress-induced depressive behavior: Involving the inhibition of NLRP3 inflammasome activation in rat prefrontal cortex
Authors: Xiaoxin Liu
Chao Liu
Journal: International Immunopharmacology (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Antidepressant; Baicalin; Chronic unpredictable mild stress; IL-1β; NLRP3 inflammasome.
Affiliations: Department of Physiology, School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 210009, PR China. Electronic address: ., Department of Pharmaceutical, Nanjing First Hospital, China Pharmaceutical University, Nanjing 210000, PR China. Electronic address: .

Abstract:  Abnormal activation of nucleotide-binding domain, leucine-rich repeat, pyrin domain containing protein 3 (NLRP3) inflammasome could induce inflammation in the central nervous system and result in the hyperactivity of HPA axis, which were involved in the pathophysiology of depression. Baicalin, a major polyphenol compound extracts from Scutellaria radix roots, has been previously confirmed to normalize the hyperactivity of HPA axis in rats received chronic mild stress. However, its antidepressant effects and mechanisms are remains unclear in chronic unpredictable mild stress (CUMS) model of depression. In this study, CUMS treated rats showed a notable depressive-like behavior (decreased sucrose intake and locomotor activity, and increased immobility time), and significant increase in the activation of NLRP3 inflammasome and the levels of pro-inflammatory cytokines (IL-1β and IL-6) in rat prefrontal cortex. Treatment with baicalin (20, 40mg/kg) significantly reversed these changes. The present study confirmed that baicalin has antidepressant effect and its mechanisms likely related to the inhibition of NLRP3 inflammasome activation in rat prefrontal cortex. 

Retracted: No

PubPeer comments:
 Despite being framed in such a way, and despite using a shared loading control, the western blots in Figure 4 are clearly not from the same scan. ![file] What is the reason for this weird composition, and do the authors have uncropped scans of the original blots? ,
The efficacy of trans-esophageal echocardiography in treatment of nonvalvular atrial fibrillation with left atrial appendage occlusion
Authors: S-C Qin
X-L Wang
K Chen
R-F Zhang
Z-M Jiang
Y Liuang
X Fu
Y Liu
Y Song
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: trans-esophageal echocardiography; nonvalvular atrial fibrillation; left atrial appendage occlusion; efficacy; treatment
Affiliations: Departments of Ultrasonography, Cardiology and Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China. Zhangruifang999@hotmail.

Abstract:  The article "The efficacy of trans-esophageal echocardiography in treatment of nonvalvular atrial fibrillation with left atrial appendage occlusion" by Y. Song, S.-C. Qin, X. Fu, Z.-M. Jiang, K. Chen, X.-L. Wang, R.-F. Zhang, Y. Liuang, R.-F. Zhang, Y. Liu, published in Eur Rev Med Pharmacol Sci 2018; 22 (16): 5335-5338 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
Effects of microRNA-21 targeting PITX2 on proliferation and apoptosis of pituitary tumor cells
Authors: M Cui
M Zhang
H-F Liu
J-P Wang
Journal: European Review for Medical and Pharmacological Sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: PITX2; miR-21; proliferation; apoptosis; pituitary adenoma
Affiliations: Department of Neurology, The 5th Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. .

Abstract:  Objective: Expression of pituitary homeobox 2 (PITX2) is significantly elevated in pituitary adenoma tissues, which also has lower microRNA (miR)-21 expression, indicating possible tumor-suppression role of miR-21. Bio-informatics analysis revealed targeting onto 3'-UTR of PITX2 by miR-21. This study aims to investigate the role of miR-21/PITX2 expression in proliferation and apoptosis of pituitary adenoma cells and pathogenesis. Patients and methods: A total of 48 pituitary adenoma samples were collected in parallel with 12 normal brain tissues and were recruited in this study. Flow cytometry was employed to test Ki-67 expression and apoptosis. Expressions of miR-21 and PITX2 were compared, along with their targeted relationship by dual-luciferase reporter assay. Cultured HP75 cells were transfected with miR-21 mimic and/or si-PITX2. Caspase-3 activity was further quantified, followed by flow cytometry for apoptosis. MiR-21, cleaved caspase-3 and PITX2 expressions were tested. Results: Invasive pituitary adenoma tissues had significantly higher Ki-67 and PITX2, and lower miR-21 expressions or apoptosis than non-invasive tumors. MiR-21 targeted 3'-UTR of PITX2 gene to inhibit its expression. Elevated miR-21 and/or silencing PITX2 significantly depressed PITX2 expression in HP75 cells, potentiating caspase-3 activity, decreasing cell proliferation and facilitating apoptosis. Conclusions: MiR-21 was down-regulated while PITX2 was up-regulated in pituitary adenoma tissues. MiR-21 can inhibit pituitary adenoma cell HP75 proliferation and facilitate apoptosis via inhibiting PITX2 expression. 

Retracted: Yes

PubPeer comments:
 [Retracted] some time in the last 25 days.  Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, u201cEffects of microRNA-21 targeting PITX2 on proliferation and apoptosis of pituitary tumor cells, by M. Cui, M. Zhang, H.-F. Liu, J.-P. Wang, published in Eur Rev Med Pharmacol Sci 2017; 21 (13): 2995-3004u2013PMID: 28742208u201d has been withdrawn. The Publisher apologizes for any inconvenience this may cause. It was included in a spreadsheet of papers suspected to be the products of a papermill (on the grounds of styled WBs and flow cytometry, as described at https: forbetterscience.com 2020 02 27 dark-satanic-papermills ![file] ,
DNA vaccine protection against SARS-CoV-2 in rhesus macaques
Authors: Makda S Gebre
Meghan Travers
John S Burke
Lori F Maxfield
Shaghayegh Habibi
Ralph S Baric
Shant H Mahrokhian
Stephanie Fischinger
Huahua Wan
Yongfei Cai
Nicole Kordana
Felipe J N Lelis
Caroline Atyeo
David R Martinez
Aaron G Schmidt
Kelvin Blade
Mark G Lewis
Esther A Bondzie
John D Ventura
Yuezhou Chen
Anthony Cook
Abishek Chandrashekar
Laurent Pessaint
Alan Dodson
Gabriel Dagotto
Roland Zahn
Zhenfeng Li
Matthew D Slein
Elyse Teow
Catherine Jacob-Dolan
Dan H Barouch
Carolin Loos
Alex Van Ry
Lauren Peter
Frank Wegmann
Katherine McMahan
Jason Velasco
Felix Nampanya
Renita Brown
Duane R Wesemann
Xuan He
Galit Alter
Bing Chen
Lisa H Tostanoski
Brad Finneyfrock
Jinyan Liu
Noe B Mercado
Hanne Andersen
Zijin Lin
Jingyou Yu
Joseph P Nkolola
Ramya Nityanandam
Marinela Kirilova
Adam Zuiani
Journal: Science (2020)
Discipline: Multidisciplinary
Keywords: COVID-19; SARS-CoV-2; DNA vaccine; spike protein; rhesus macaques
Affiliations: Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA., Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA., Ragon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA., Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA., Bioqual, Rockville, MD 20852, USA., Janssen Vaccines & Prevention BV, Leiden, Netherlands., Children’s Hospital, Boston, MA 02115, USA., Massachusetts Consortium on Pathogen Readiness, Boston, MA 02215, USA.

Abstract:  The global coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has made the development of a vaccine a top biomedical priority. In this study, we developed a series of DNA vaccine candidates expressing different forms of the SARS-CoV-2 spike (S) protein and evaluated them in 35 rhesus macaques. Vaccinated animals developed humoral and cellular immune responses, including neutralizing antibody titers at levels comparable to those found in convalescent humans and macaques infected with SARS-CoV-2. After vaccination, all animals were challenged with SARS-CoV-2, and the vaccine encoding the full-length S protein resulted in &gt;3.1 and &gt;3.7 log10 reductions in median viral loads in bronchoalveolar lavage and nasal mucosa, respectively, as compared with viral loads in sham controls. Vaccine-elicited neutralizing antibody titers correlated with protective efficacy, suggesting an immune correlate of protection. These data demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates. 

Retracted: No

PubPeer comments:
 This Open Journal comes to us from PeerTechz, a publisher characterised memorably by Jeffrey Beall: https: web.archive.org web 20170113050824 https: scholarlyoa.com 2016 07 07 more-rubbish-from-hyderabad-peertechz The four most recent papers in the journal (finishing with this one) share a single co-author, who also edits. Isn t this perhaps excessive? ![file] ,
FANCA knockout in human embryonic stem cells causes a severe growth disadvantage
Authors: Satish Khurana
Nisha Nair
Catherine M Verfaillie
Kim Vanuytsel
Swati Shetty
Joris R Vermeesch
Laura Ordovas
Qing Cai
Journal: Stem Cell Research (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Fanconi anemia; bone marrow failure; pluripotent stem cells; zinc finger nuclease; FANCA knockout
Affiliations: KU Leuven Stem Cell Institute, Department of Development and Regeneration, Cluster Stem Cell Biology and Embryology, Herestraat 49, Onderwijs en Navorsing 4, Box 804, 3000 Leuven, Belgium. Electronic address: ., KU Leuven Stem Cell Institute, Department of Development and Regeneration, Cluster Stem Cell Biology and Embryology, Herestraat 49, Onderwijs en Navorsing 4, Box 804, 3000 Leuven, Belgium., KU Leuven Center for Human Genetics, 3000 Leuven, Belgium.

Abstract:  Fanconi anemia (FA) is an autosomal recessive disorder characterized by progressive bone marrow failure (BMF) during childhood, aside from numerous congenital abnormalities. FA mouse models have been generated; however, they do not fully mimic the hematopoietic phenotype. As there is mounting evidence that the hematopoietic impairment starts already in utero, a human pluripotent stem cell model would constitute a more appropriate system to investigate the mechanisms underlying BMF in FA and its developmental basis. Using zinc finger nuclease (ZFN) technology, we have created a knockout of FANCA in human embryonic stem cells (hESC). We introduced a selection cassette into exon 2 thereby disrupting the FANCA coding sequence and found that whereas mono-allelically targeted cells retain an unaltered proliferation potential, disruption of the second allele causes a severe growth disadvantage. As a result, heterogeneous cultures arise due to the presence of cells still carrying an unaffected FANCA allele, quickly outgrowing the knockout cells. When pure cultures of FANCA knockout hESC are pursued either through selection or single cell cloning, this rapidly results in growth arrest and such cultures cannot be maintained. These data highlight the importance of a functional FA pathway at the pluripotent stem cell stage. 

Retracted: No

PubPeer comments:
 (a) Eq(1) and eq(2) are confusing. The meaning of the term u201cfuzzy model of the vehicle imageu201d is not clear in the context. (b) Eq(3) is confusing because it is not a vector according to the context. (c) Fig 8 is hard to interpret. (d) Many cited papers are irrelevant, for example, ref[12]. ![file] ![file] ![file] ![file] ![file] ![file] ,
An NF-Y-dependent switch of positive and negative histone methyl marks on CCAAT promoters
Authors: Diletta Dolfini
Michele Ceribelli
Giacomo Donati
Roberto Mantovani
Andrea Fossati
Raffaella Gatta
Journal: PLoS ONE (2008)
Discipline: Multidisciplinary
Keywords: Histone tails; post-translational modifications; H3K4me3; H3K79me2; H4K20me3
Affiliations: Dipartimento di Scienze Biomolecolari e Biotecnologie, Università di Milano, Milano, Italy.

Abstract:  Background: Histone tails have a plethora of different post-translational modifications, which are located differently in "open" and "closed" parts of genomes. H3K4me3/H3K79me2 and H4K20me3 are among the histone marks associated with the early establishment of active and inactive chromatin, respectively. One of the most widespread promoter elements is the CCAAT box, bound by the NF-Y trimer. Two of NF-Y subunits have an H2A-H2B-like structure. Principal findings: We established the causal relationship between NF-Y binding and positioning of methyl marks, by ChIP analysis of mouse and human cells infected with a dominant negative NF-YA: a parallel decrease in NF-Y binding, H3K4me3, H3K79me2 and transcription was observed in promoters that are dependent upon NF-Y. On the contrary, changes in the levels of H3K9-14ac were more subtle. Components of the H3K4 methylating MLL complex are not recruited in the absence of NF-Y. As for repressed promoters, NF-Y removal leads to a decrease in the H4K20me3 mark and deposition of H3K4me3. Conclusions: Two relevant findings are reported: (i) NF-Y gains access to its genomic locations independently from the presence of methyl histone marks, either positive or negative; (ii) NF-Y binding has profound positive or negative consequences on the deposition of histone methyl marks. Therefore NF-Y is a fundamental switch at the heart of decision between gene activation and repression in CCAAT regulated genes. 

Retracted: No

PubPeer comments:
null, 
 Here is the correction note https: journals.plos.org plosone article?id=10.1371 journal.pone.0102282 All the duplications reported on Pubpeer were corrected and  [...] there are errors in some of the data for the control experiments displayed in the HCT116 (left) panels of Supplementary Figure 2. These errors do not affect the conclusions reported in the article. While some of the errors may be related to the processing of the files during the production process, the authors consulted the Commission of Scientific Integrity appointed by the Department of Biosciences, University of Milan in relation to the data from this study. The Commission supports the publication of a Correction. The authors apologize for these errors and provide a revised version for each of the figures above with the original, correct panels. The raw blots for each figure are also available via this Correction. I attach the original S. Figure 2 and the new one. I marked the lines that were changed. Original: ![file] New one: ![file] In the raw blots avaliable there are no names, how should the reader know what are the lines to compare? Here some of them: ![file] ,
LAMC2 regulated by microRNA-125a-5p accelerates the progression of ovarian cancer via activating p38 MAPK signalling
Authors: Wei Feng
Hongjun Guo
Haifeng Qiu
Dongya Zhang
Journal: Life Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: LAMC2; Ovarian cancer; miR-125a-5p; p38.
Affiliations: Department of Gynaecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province 450000, China. Electronic address: ., Department of Gynaecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province 450000, China.

Abstract:  Aims: Laminin γ2 (LAMC2) is over-expressed in ovarian cancer, and its high expression facilitates cell invasion. Nevertheless, the effects of LAMC2 on other ovarian cancer cell functions and its underlying mechanism remain largely unclear. Bioinformatics analysis shows that LAMC2 is a predicted target of miR-125a-5p and miR-193a-3p. Therefore, the present study aimed to investigate the effects of LAMC2 in ovarian cancer progression and determine whether LAMC2 expression is under the regulation of miR-125a-5p or miR-193a-3p in ovarian cancer. Materials and methods: Immunohistochemistry staining, western blot and qPCR were used to detect LAMC2 expression profiles. CCK-8, flow cytometry and tumour formation assays were used to assess cell proliferation, apoptosis and tumorigenesis. The interaction between miR-125a-5p/miR-193a-3p and LAMC2 were determined by the luciferase gene reporter assay. Key findings: The results showed that LAMC2 was over-expressed in ovarian cancer tissues and cell lines. Over-expression of LAMC2 significantly promoted cell proliferation and repressed cell apoptosis, as well as increased the expression levels of p38, p-p38, c-myc and CREB, and translocated p38 protein to the nucleus. In addition, the promotion of cell proliferation and repression of cell apoptosis mediated by LAMC2 over-expression were all weakened when p38 was downregulated. Moreover, LAMC2 expression was negatively regulated by miR-125a-5p, which inhibited the nuclear accumulation of p38 protein. Upregulation of LAMC2 significantly abolished the effects of miR-125a-5p on cell proliferation inhibition and cell apoptosis promotion, as well as tumourigenesis repression. Significance: The present study clarified that LAMC2 functioned as an oncogene in ovarian cancer through upregulating p38 under the regulation of miR-125a-5p. 

Retracted: No

PubPeer comments:
 Figure 2E. Some parts of the flow cytometry look similar to parts in other panels. Boxes of the same color draw attention to areas that look similar. ![file] Figure 4I appears to have the same problems, which I will leave for somebody else to color code. ,
Synthesis of stabilized myrrh-capped hydrocolloidal magnetite nanoparticles
Authors: Ayman M Atta
Sami A Al-Hussain
Hamad A Al-Lohedan
Journal: Molecules (2014)
Discipline: CHEMISTRY
Keywords: stabilized; magnetic nanoparticle; colloids; monodisperse; water-soluble
Affiliations: Surfactants research chair, Department of Chemistry, College of Science, King Saud University, Riyadh 11541, Kingdom of Saudi Arabia. .

Abstract:  Herein we report a new method for synthesizing stabilized magnetic nanoparticle (MNP) colloids. A new class of monodisperse water-soluble magnetite nano-particles was prepared by a simple and inexpensive co-precipitation method. Iron ions and iodine were prepared by the reaction between ferric chloride and potassium iodide. The ferrous and ferric ions were hydrolyzed at low temperature at pH 9 in the presence of iodine to produce iron oxide nanoparticles. The natural product myrrh gum was used as capping agent to produce highly dispersed coated magnetite nanoparticles. The structure and morphology of the magnetic nanogel was characterized by Fourier transform infrared spectroscopy (FTIR) and transmission electron microscopy (TEM), and X-ray diffraction (XRD) was used to examine the crystal structure of the produced magnetite nanoparticles. 

Retracted: No

PubPeer comments:
 Figure 1 has some oddities, some of which i have circled in red ![file] there appear to be blue lines under Fig 1A, yellow lines under Fig 1B, magenta lines under Fig 1C Some of the colored lines appear well off of the black curve, e.g. expanded view of 1C ![file] some of the colored lines also show up below the horizontal axes. There are also breaks and offsets in the FTIR curve, e.g. ![file] ![file] ![file] would the authors care to comment on or explain these peculiarities? , 
 Figure 3 also has oddities that look like the DLS curves were created by drawing software rather than graphing software using output from the measuring instrument. The curves have breaks and when the count increases on the lower size side, the curve breaks to a lower particle size and in 3C the horizontal and vertically trending curves cross and in one case, the verticle curve indicates a negative count. It s very odd that there are no tails on the particle size distributions. Figure 4 shows some agglomeration but the DLS shows extraordinarily narrow and well defined distributions ![file] ![file] ![file] ![file] ![file] , 
 The journal required high resolution images and it should be improved by colour change from bright colour to black ,
ROS-mediated iron overload injures the hematopoiesis of bone marrow by damaging hematopoietic stem/progenitor cells in mice
Authors: Juan Mu
Yuchen Zhang
Jishi Wang
Wenyi Lu
Juanxia Meng
Chengcheng Li
Deguan Li
Qing Li
Aimin Meng
Xia Xiao
Mingfeng Zhao
Xiaoli Cao
Xiao Chai
Jie Chen
Journal: Scientific Reports (2015)
Discipline: Multidisciplinary
Keywords: Iron overload; hereditary hemochromatosis; blood transfusions; beta thalassemia; bone marrow failure
Affiliations: 1] Department of Hematology, Tianjin First Central Hospital, Tianjin 300192, China [2] Department of Hematology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China., Tianjin Key Lab of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Academy of Medical Science and Peking Union Medical College, Tianjin 300192, China., Department of Hematology, Tianjin First Central Hospital, Tianjin 300192, China., Department of Hematology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China.

Abstract:  Iron overload, caused by hereditary hemochromatosis or repeated blood transfusions in some diseases, such as beta thalassemia, bone marrow failure and myelodysplastic syndrome, can significantly induce injured bone marrow (BM) function as well as parenchyma organ dysfunctions. However, the effect of iron overload and its mechanism remain elusive. In this study, we investigated the effects of iron overload on the hematopoietic stem and progenitor cells (HSPCs) from a mouse model. Our results showed that iron overload markedly decreased the ratio and clonogenic function of murine HSPCs by the elevation of reactive oxygen species (ROS). This finding is supported by the results of NAC or DFX treatment, which reduced ROS level by inhibiting NOX4 and p38MAPK and improved the long-term and multi-lineage engrafment of iron overload HSCs after transplantation. Therefore, all of these data demonstrate that iron overload injures the hematopoiesis of BM by enhancing ROS through NOX4 and p38MAPK. This will be helpful for the treatment of iron overload in patients with hematopoietic dysfunction. 

Retracted: No

PubPeer comments:
 Images in this paper appear very similar to images in another paper with shared authors. I did not see either paper referenced in the other. Apologies if I missed that. I did not look elsewhere. Other thread: https: pubpeer.com publications CA2A524B1A8A8709D44C10F26458CA *** ![file] ,
Synergistic combination of PEGylated selenium nanoparticles and X-ray-induced radiotherapy for enhanced anticancer effect in human lung carcinoma
Authors: Tianyu Yu
Qingjia Sun
Yanru Hao
Lingling Tong
Hejia Zhang
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Apoptosis; Combination effect; Lung cancer; Nanoparticles; Selenium
Affiliations: Ultrasonic Department, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China., Otorhinolaryngological Department, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China., Department of Gynaecology and Obstetrics, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China., Otorhinolaryngological Department, No. 2 Hospital of Jilin University, Changchun, Jilin, 130000, China., Department of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China. Electronic address: .

Abstract:  In this study, PEGylated selenium nanoparticles (PSNP) was successfully prepared and combined with X-ray for effective anticancer efficacy in lung cancer cells. The particles were nanosized and observed in spherical shape. The combination of PSNP and X-ray effectively killed the cancer cells and decreased the cell viability in a concentration dependent manner. PSNP combined with X-ray showed a significantly higher apoptosis of cancer cells with around 23% of cells in late apoptosis stage. Consistently, Caspase-3 activity was significantly higher when exposed to X-ray than in the absence of X-ray. The caspase-3 activity has been doubled in the presence of X-ray and PSNPs were actively involved in the activation of effector caspase-3 and downstream target. Importantly, treatment with the combination of PSNP and X-ray showed predominant red fluorescence which is indicative of dead cells. The results clearly indicate the cytotoxic potential of PSNP + X-ray combination against lung cancer cells. Overall, novel strategy of combination of PSNP and X-ray could be an alternative and effective chemo-radiotherapy. 

Retracted: No

PubPeer comments:
 Fig. 8.  Qualitative cytotoxic effect: Live dead assay of cancer cells upon treated with PSNP with and without X-ray irradiation. The images were captured from fluorescence microscope. The cancer cells were stained with staining agents corresponding to live and dead cells. **p 0.001 is the statistical difference between PSNP + X-ray and PSNP. Control, PSNP, PSNP+Xray images are successive transformations of a single panel. ![file] ,
Tonin and kallikrein in the brain of transgenic rat line expressing human tissue kallikrein
Authors: Jorge L Pesquero
Ronaldo C Araujo
Joao B Pesquero
Michael Bader
Eliane S L Lomez
Journal: Hypertension (2002)
Discipline: CLINICAL MEDICINE
Keywords: transgenic rat; human tissue kallikrein gene; tonin; kallikrein; brain regions
Affiliations: From the Departments of Physiology and Biophysics, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais (E.S.L.L., J.L.P.), University of Mogi das Cruzes (R.C.A.), and Universidade Federal de Sao Paulo (J.B.P.), Brazil; and Molecular Biology of Peptides Hormones, Max-Delbruck Center for Molecular Medicine (M.B.), Berlin-Buch, Germany.

Abstract:  A transgenic rat line harboring the human tissue kallikrein gene was investigated for expression and activity of tonin and kallikrein in different regions of the brain. The introduction of the transgene into the rat genome produced a significant augmentation of the expression levels and activity of rat tissue kallikrein. The possibility that human kallikrein does not hydrolyze the rat substrate is probably responsible for the augmented expression of the rat enzyme. On the other hand, although expression of tonin was significantly reduced, tonin activity was not altered in most brain structures, except for cerebellum and neurohypophysis. 

Retracted: No

PubPeer comments:
 Beta-actin in Figure 1 to 3 are more similar than expected, although they should represent different samples. Could authors check please? ![file] ,