PReD-Bench/PRed-Bench huggingface dataset:
p53 regulates cellular resistance to complement lysis through enhanced expression of CD59
Authors: Baalasubramanian Sivasankar
B Paul Morgan
Rossen M Donev
Timothy R Hughes
Duncan S Cole
Journal: Cancer Research (2006)
Discipline: CLINICAL MEDICINE
Keywords: CD59 gene; p53-responsive elements; complement system; inflammation; regulation
Affiliations: Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff, United Kingdom.

Abstract:  It has been recently hypothesized that the CD59 gene has two putative p53-responsive elements that may be involved in defense of host cells from damage by the complement system in inflammation. Here we have examined the roles of these putative p53-binding sequences within the CD59 gene in regulation of CD59 expression. We have shown that both of these potential responsive elements bind p53 in vitro. Knocking down expression of p53 using small interfering RNA led to a 6-fold decrease in CD59 protein expression in HeLa cells. We have previously observed a decrease of CD59 in camptothecin-induced apoptotic IMR32 cells, whereas expression was increased in the surviving fraction compared with untreated cells. Here, we have shown that these changes are associated with altered expression levels and acetylation status of p53. We have also shown that acetylation status of p53 regulates CD59 expression on cells exposed to inflammatory cytokines to model inflammation. Our data suggest that p53 and in vivo positive/negative regulators of p53 could be used to modulate susceptibility of tumor cells to complement lysis in chemotherapy. 

Retracted: Yes

PubPeer comments:
 Some irrelevant references are identified in this paper, which are associated with Shaofei Wu. ![file] ![file] ![file] ![file] ,
Nicotine smoking concentrations modulate GABAergic synaptic transmission in murine medial prefrontal cortex by activation of α7* and β2* nicotinic receptors
Authors: Marco Atzori
Roberto Salgado-Delgado
Marcela Miranda-Morales
Carlos Barajas-Lόpez
Nadia Saderi
Eric Esquivel-Rendon
Jorge Vargas-Mireles
Hugo R Arias
Roberto Cuevas-Olguin
Journal: European Journal of Neuroscience (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: central nervous system; gamma-aminobutyric acid; pair pulse; patch clamp.
Affiliations: Faculty of Science Universidad Autónoma de San Luis Potosí San Luis potosí México, División de Biología Molecular Instituto de Investigación Científica y Tecnológica San Luis Potosí México, Department of Pharmacology and Physiology College of Osteopathic Medicine Oklahoma State University Center for Health Sciences Tahlequah OK USA

Abstract:  Nicotine is the major addictive component of cigarettes, reaching a brain concentration of ~300 nM during smoking of a single cigarette. The prefrontal cortex (PFC) mechanisms underlying temporary changes of working memory during smoking are incompletely understood. Here, we investigated whether 300 nM nicotine modulates γ-aminobutyric acid (GABA) ergic synaptic transmission from pyramidal neurons of the output layer (V) of the murine medial PFC. We used patch clamp in vitro recording from C57BL/6 mice in the whole-cell configuration to investigate the effect of nicotine on pharmacologically isolated GABAergic postsynaptic currents (IPSCs) in the absence or presence of methyllycaconitine (MLA) or dihydro-β-erythroidine (DHβE), selective antagonists of α7- and β2-containing (α7* and β2*) nicotinic acetylcholine receptors (AChRs), respectively. Our results indicated that nicotine, alone or in the presence of MLA, decreases electrically evoked IPSC (eIPSC) amplitude, whereas in the presence of DHβE, nicotine elicited either an eIPSCs amplitude increase or a decrease. In the presence of DHβE, nicotine increased membrane conductance leaving the paired pulse ratio unchanged in all conditions, suggesting a non-β2* mediated effect. In the presence of MLA, nicotine decreased the mean spontaneous IPSC (sIPSC) frequency but increased their rise time, suggesting a non-α7* AChR-mediated synaptic modulation. Also, in the presence of DHβE, nicotine decreased both eIPSC rise and decay times. No receptors other than α7* and β2* appear to be involved in the nicotine effect. Our results indicate that nicotine smoking concentrations modulate GABAergic synaptic currents through mixed pre- and post-synaptic mechanisms by activation of α7* and β2* AChRs. 

Retracted: No

PubPeer comments:
 The open peer review reports are not available on the article s website. Moreover, the claimed open peer review reports have a faulty URL, which, once corrected, leads to a Publons page with no open peer review:  Edited by Prof. Paul Bolam. The peer review history for this article is available at http: publo ns.com publo n 10.1111 EJN.14595u201d The correct URL is: https: publons.com publon 10.1111 EJN.14595 ,
The mitochondrial C16069T polymorphism, not mitochondrial D310 (D-loop) mononucleotide sequence variations, is associated with bladder cancer
Authors: Nasser Shakhssalim
Mohammad Hossein Sanati
Sepideh Dadgar
Rozita Rosli
Massoud Houshmand
Reza Sarhangnejad
Abolfazl Faraji
Maryam Mobaraki
Behnam Kamalidehghan
Journal: Cancer Cell International (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bladder cancer; Mitochondrial displacement loop (D-loop); Deletions; Sequence variations; Tumoral tissues
Affiliations: National Institute for Genetic Engineering and Biotechnology, Tehran, Iran. .

Abstract:  Background: Bladder cancer is a relatively common and potentially life-threatening neoplasm that ranks ninth in terms of worldwide cancer incidence. The aim of this study was to determine deletions and sequence variations in the mitochondrial displacement loop (D-loop) region from the blood specimens and tumoral tissues of patients with bladder cancer, compared to adjacent non-tumoral tissues. Methods: The DNA from blood, tumoral tissues and adjacent non-tumoral tissues of twenty-six patients with bladder cancer and DNA from blood of 504 healthy controls from different ethnicities were investigated to determine sequence variation in the mitochondrial D-loop region using multiplex polymerase chain reaction (PCR), DNA sequencing and southern blotting analysis. Results: From a total of 110 variations, 48 were reported as new mutations. No deletions were detected in tumoral tissues, adjacent non-tumoral tissues and blood samples from patients. Although the polymorphisms at loci 16189, 16261 and 16311 were not significantly correlated with bladder cancer, the C16069T variation was significantly present in patient samples compared to control samples (p &lt; 0.05). Interestingly, there was no significant difference (p &gt; 0.05) of C variations, including C7TC6, C8TC6, C9TC6 and C10TC6, in D310 mitochondrial DNA between patients and control samples. Conclusion: Our study suggests that 16069 mitochondrial DNA D-Loop mutations may play a significant role in the etiology of bladder cancer and facilitate the definition of carcinogenesis-related mutations in human cancer. 

Retracted: No

PubPeer comments:
 Figure 3 was brought to my attention by Roger Galligan. Here is the full figure first: ![file] Here is the photo itself, with contrast enhanced to bring out details. Some areas appear to be visible multiple times. ![file] ,
MiRNA-101 inhibits oral squamous-cell carcinoma growth and metastasis by targeting zinc finger E-box binding homeobox 1
Authors: Sen Jia
Xinjie Yang
Lei Wang
Delin Lei
Chun Shan
Chenping Zhang
Zihui Yang
Baolei Wu
Bin Lu
Xi Yang
Journal: American journal of cancer research (2016)
Discipline: CLINICAL MEDICINE
Keywords: metastasis; microRNA-101; oral squamous-cell carcinoma; proliferation; zinc finger E-box binding homeobox 1.
Affiliations: State Key Laboratory of Military Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University No. 145 Changle West Road, Xi'an, Shaanxi 710032, PR China., Shanghai Key Laboratory of Stomatology, Department of Oral & Maxillofacial-Head & Neck Oncology, Ninth People's Hospital, School of Stomatology, Shanghai Jiao Tong University School of Medicine No. 639 Zhizaoju Road, Shanghai 200011, PR China.

Abstract:  MicroRNAs (miRNAs) are implicated in the pathogenesis of oral squamous-cell carcinoma (OSCC). miR-101 is involved in the development and progression of OSCC, but the biological functions and underlying molecular mechanisms of this miRNA remain largely unknown. In this study, we showed that miR-101 was underexpressed in OSCC tissues and cell lines. miR-101 downregulation was inversely correlated with zinc finger E-box binding homeobox 1 (ZEB1) expression, lymph-node metastasis, and poor prognosis in OSCC patients. Enhanced expression of miR-101 significantly inhibited OSCC cell proliferation, apoptosis resistance, migration and invasion in vitro, and suppressed tumor growth and lung metastasis in vivo. Bioinformatics analyses showed that miR-101 directly targeted ZEB1, as confirmed by a dual-luciferase reporter assay. The inhibitory effects of miR-101 on OSCC growth and metastasis were attenuated and phenocopied by ZEB1 overexpression and knockdown, respectively. Overall, our findings indicated that miRNA-101 reduced OSCC growth and metastasis by targeting ZEB1 and provided new evidence of miR-101 as a potential therapeutic target for OSCC patients. 

Retracted: No

PubPeer comments:
 *[right]* Fig 1E.  Spearmanu2019s correlation analysis between miR-101 and ZEB1 in OSCC specimens analyzed by qPCR assay . *[left]* Fig 1H from [Han et al (2018)] .  Correlation of the ZEB1 level and miR-101 expression in NSCLC cells. ![file] Surprisingly many data points in common. , 
 *[right]* Fig 1B.  Kaplan-Meier survival curves of 40 patients with OSCCs divided by miR-101 expression. Log-rank test was used for survival analysis . *[left]* Fig 1B from [Han et al (2018)] .  Kaplan-Meier survival curves showed lower five-year overall survival rate of NSCLC patients with low miR-101 levels (n = 73) compared with individuals with high miR-101 expression (n = 87). Unexpectedly similar. ![file] ,
Two-dimensional (2D), three-dimensional static (3D) and real-time (4D) contrast enhanced voiding urosonography (ceVUS) versus voiding cystourethrography (VCUG) in children with vesicoureteral reflux
Authors: Halina Borzęcka
Magdalena Maria Woźniak
Andrzej Paweł Wieczorek
Agata Pawelec
Maria Małgorzata Zajączkowska
Agnieszka Brodzisz
Paweł Nachulewicz
Journal: European Journal of Radiology (2016)
Discipline: CLINICAL MEDICINE
Keywords: 3D/4D ultrasound; Children; Contrast enhanced voiding urosonography; SonoVue(®); Vesicoureteral reflux.
Affiliations: Department of Pediatric Radiology, Medical University of Lublin, Al. Racławickie 1, Lublin 20-059, Poland. Electronic address: ., Department of Pediatric Radiology, Medical University of Lublin, Al. Racławickie 1, Lublin 20-059, Poland., Department of Pediatric Nephrology, Medical University of Lublin, Al. Racławickie 1, Lublin 20-059, Poland., Department of Pediatric Surgery and Traumatology, Medical University of Lublin, Al. Racławickie 1, Lublin 20-059, Poland.

Abstract:  Background: Two-dimensional (2DUS) contrast enhanced voiding urosonography has been used in the diagnosis and treatment monitoring of the vesicoureteral reflux in children for over 15 years. The opportunity of performing this examination with the use of three-dimensional static (3DUS) and real-time (4DUS) techniques opens up new diagnostic horizons. Objective: To analyze if 3DUS/4DUS bring additional information leading to an increased detection rate or change in the grading of reflux compared to 2DUS and voiding cystouretrography. Material and methods: We evaluated 69 patients (mean 4.1 years) who underwent 2DUS/3DUS/4DUS contrast enhanced voiding urosonography (ceVUS) and voiding cystourethrography (VCUG) for the diagnosis and grading of vesicoureteral reflux. Results: 2DUS and 3DUS/4DUS urosonography diagnosed 10 more refluxes (7.25%) than cystourethrography and in 3 refluxes (2.17%) detected a higher grade. In 9 refluxes (6.52%) 3DUS/4DUS urosonography and cystourethrography diagnosed a higher grade than 2DUS. There was a statistically significant difference between cystourethrography and 3DUS/4DUS urosonography when the number of detected refluxes and differences in grading were compared. 4DUS enabled a better visualization of reflux than 3DUS. Conclusions: 3DUS/4DUS techniques bring additional information leading to a change in reflux grading compared to 2DUS and a detect higher number of refluxes compared to cystourethrography. 

Retracted: No

PubPeer comments:
 It says in the results section,  The difference was statistically significant (p 0.005). As with all p-values given by the authors in the results, they have confused the direction of the inequality sign! Otherwise, what they report is  not statistically significant, whatever that means... ,
miR-25 promotes metastasis via targeting FBXW7 in esophageal squamous cell carcinoma
Authors: Yuting Su
Ye Hua
Kai Zhao
Gang Tao
Chunhua Dai
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: miR-25; esophageal squamous cell carcinoma; oncogene; tumor invasion; tumor stage
Affiliations: Institute of Oncology, Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China., Department of Gastroenterology, Changzhou Jintan People's Hospital, Changzhou, Jiangsu 213200, P.R. China., Department of Gastroenterology, Zhenjiang Hospital of Traditional Chinese and Western Medicine, Zhenjiang, Jiangsu 212001, P.R. China.

Abstract:  Increasing evidence suggests that miR-25 can function as an oncogene in different types of human malignancies, whereas little is known concerning the role of miR-25 in esophageal squamous cell carcinoma (ESCC). The aim of the present study was to investigate the role of miR-25 in ESCC and to determine the molecular mechanisms underlying its function. The expression level of miR-25 was detected in primary ESCC tissues and cell lines by real-time quantitative PCR. We also assessed whether knockdown of miR-25 influences in vitro cell invasion and migration. Western blot analysis was used to detect the influence of miR-25 on a target gene, and Pearson analysis was used to calculate the correlation between the expression of a target gene and miR-25 in ESCC tissues. The results revealed that the relative level of miR-25 expression was significantly upregulated in ESCC tissues and cell lines. Expression of miR-25 in ESCC tissues was positively associated with depth of tumor invasion and tumor stage. Moreover, high miR-25 expression conferred poorer overall survival (OS), and a multivariate analysis revealed that miR-25 was an independent risk factor for OS. In addition, knockdown of miR-25 in ESCC cells significantly suppressed cell migration and invasion. Furthermore, we identified F-box and WD repeat domain-containing 7 (FBXW7) protein as a direct functional target of miR-25 in ESCC. In conclusion, the present study supports the potential of miR-25 as a prognostic predictor with its high expression in cancer tissues and its association with tumor progression by targeting FBXW7 in ESCC. 

Retracted: No

PubPeer comments:
 Figure 3C and 5. * Some panels appear to show overlapping areas, as shown here with boxes of the same color. ![file] , 
 #1 A few more colored rectangles... ![file] ... to accommodate the overlaps with Fig 3F from  The lncRNA HNF1A-AS1 is a negative prognostic factor and promotes tumorigenesis in osteosarcoma ([Cai et al 2017] ). ![file] , 
 Fig 4B. The splice in the substantive band, and the absence of a splice in the GADPH loading control, suggests that they came from different gels. Contrary to the point of having a loading control. ![file] ,
The autophagic inhibitor 3-methyladenine potently stimulates PKA-dependent lipolysis in adipocytes
Authors: Bradlee L Heckmann
Jun Liu
Xiaodong Zhang
Xingyuan Yang
Journal: British journal of pharmacology (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: PI3K inhibitor; 3-methyladenine; autophagy; lipid turnover; adipocyte lipolysis
Affiliations: Department of Biochemistry & Molecular Biology, Mayo Clinic, Scottsdale, AZ, USA.

Abstract:  BACKGROUND AND PURPOSE The class III PI3K inhibitor, 3-methyladenine (3-MA), is commonly used to selectively block autophagy. Recent findings suggest a strong relationship between autophagy and lipid turnover. Here, we explore the effect of 3-MA on adipocyte lipolysis. EXPERIMENTAL APPROACH Assays were performed in 3T3-L1 cells. Cells were treated with 3-MA and wortmannin, a pan PI3K and autophagy inhibitor. Pharmacological and genetic manipulation of endogenous autophagic and lipolytic pathways was used to ascertain the contribution of 3-MA to the observed effects on lipolysis. KEY RESULTS 3T3-L1 cells that were exposed to 3-MA showed a consistent increase in lipolysis, approximately 50% over basal levels. The effect of 3-MA was not secondary to autophagic inhibition as treatment of 3T3-L1 cells with wortmannin yielded no such changes. Dosing and time course experiments showed that 3-MA's ability to activate lipolysis was more sensitive than its inhibitory effect on autophagy. Knockdown of adipose triglyceride lipase (ATGL) negated the stimulatory effect of 3-MA by &gt;90%, indicating that 3-MA enhanced ATGL-dependent hydrolysis of triacylglycerols. Additionally, the lipolytic effect of 3-MA was dependent on the activation of PKA and 3-MA induced a rapid and potent elevation of intracellular cAMP levels in adipocytes. CONCLUSIONS AND IMPLICATIONS Cumulatively, we show that 3-MA potently modulated a cellular mechanism and its underlying signalling pathways not associated with autophagy. Furthermore, we describe a novel stimulatory effect on a major signalling pathway. Our findings provide valuable information to studies employing 3-MA as a specific inhibitor for PI3K and autophagy. 

Retracted: No

PubPeer comments:
 Apparent re-use of actin loading control westerns in figure 2 and figure 4. Note that these are from 2 different knockdown experiments so should have independent loading control westerns. https: i.imgur.com en4tujS.jpg https: imgur.com en4tujS ,
Ceiling effects in the Movement Assessment Battery for Children-2 (MABC-2) suggest that non-parametric scoring methods are required
Authors: Nicole J Sycamore
Blandine French
Caroline C V Blanchard
Hannah L McGlashan
Nicholas P Holmes
Journal: PLoS ONE (2018)
Discipline: Multidisciplinary
Keywords: Movement Assessment Battery for Children-2 (MABC-2); children; movement impairments; parametric methods; ceiling effects
Affiliations: School of Psychology, University of Nottingham, Nottingham, United Kingdom.

Abstract:  Initially designed to identify children's movement impairments in clinical settings, the Movement Assessment Battery for Children-2 (MABC-2) is also widely used to evaluate children's movement in research. Standardised scores on the test are calculated using parametric methods under the assumption of normally-distributed data. In a pilot study with thirty five 8-10 year old children (i.e., in Age Band 2 of the MABC-2), we found that maximal performance was often reached. These 'ceiling effects' created distributions of scores that may violate parametric assumptions. Tests of normality, skew, and goodness-of-fit revealed this violation, most clearly on three of the eight sub-tests. A strong deviation from normality was again observed in a sample of 161 children (8-10 years, Experiment 1), however ceiling effects were reduced by modifying the scoring methods, and administering items designed for older children when maximal performance was reached. Experiment 2 (n = 81, 7-10 years) further refined the administration and scoring methods, and again improved the distributions of scores. Despite reducing ceiling effects, scores remained non-parametrically distributed, justifying non-parametric analytic approaches. By randomly and repeatedly resampling from the raw data, we generated non-parametric reference distributions for assigning percentiles to each child's performance, and compared the results with the standardised scores. Distributions of scores obtained with both parametric and non-parametric methods were skewed, and the methods resulted in different rankings of the same data. Overall, we demonstrate that some MABC-2 item scores are not normally-distributed, and violate parametric assumptions. Changes in administering and scoring may partially address these issues. We propose that resampling or other non-parametric methods are required to create new reference distributions to which an individual child's performance can be referred. The modifications we propose are preliminary, but the implication is that a new standardisation is required to deal with the non-parametric data acquired with the MABC-2 performance test. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: After doing this critique of the MABC2 test, we heard that the MABC3 was in production. I hope our work still influences how the MABC3 is done and standardized, but we could should have tried to collaborate more earlier with the MABC guys - I fear that it is too late for us to influence and improve this important project. ,
Tumor-induced oxidative stress perturbs nuclear factor-kappaB activity-augmenting tumor necrosis factor-alpha-mediated T-cell death: protection by curcumin
Authors: Gouri Sankar Sen
Lakshmishri Lahiry
Gaurisankar Sa
Debaprasad Mandal
Suman Pal
Charles S Tannenbaum
Tanya Das
James H Finke
Shuvomoy Banerjee
Sankar Bhattacharyya
Journal: Cancer Research (2007)
Discipline: CLINICAL MEDICINE
Keywords: Cancer patients; cell-mediated immunity; effector T-cell population; thymus; T-cell maturation
Affiliations: Animal Physiology Section, Bose Institute, Calcutta, India.

Abstract:  Cancer patients often exhibit loss of proper cell-mediated immunity and reduced effector T-cell population in the circulation. Thymus is a major site of T-cell maturation, and tumors induce thymic atrophy to evade cellular immune response. Here, we report severe thymic hypocellularity along with decreased thymic integrity in tumor bearer. In an effort to delineate the mechanisms behind such thymic atrophy, we observed that tumor-induced oxidative stress played a critical role, as it perturbed nuclear factor-kappaB (NF-kappaB) activity. Tumor-induced oxidative stress increased cytosolic IkappaBalpha retention and inhibited NF-kappaB nuclear translocation in thymic T cells. These NF-kappaB-perturbed cells became vulnerable to tumor-secreted tumor necrosis factor (TNF)-alpha (TNF-alpha)-mediated apoptosis through the activation of TNF receptor-associated protein death domain-associated Fas-associated protein death domain and caspase-8. Interestingly, TNF-alpha-depleted tumor supernatants, either by antibody neutralization or by TNF-alpha-small interfering RNA transfection of tumor cells, were unable to kill T cell effectively. When T cells were overexpressed with NF-kappaB, the cells became resistant to tumor-induced apoptosis. In contrast, when degradation-defective IkappaBalpha (IkappaBalpha super-repressor) was introduced into T cells, the cells became more vulnerable, indicating that inhibition of NF-kappaB is the reason behind such tumor/TNF-alpha-mediated apoptosis. Curcumin could prevent tumor-induced thymic atrophy by restoring the activity of NF-kappaB. Further investigations suggest that neutralization of tumor-induced oxidative stress and restoration of NF-kappaB activity along with the reeducation of the TNF-alpha signaling pathway can be the mechanism behind curcumin-mediated thymic protection. Thus, our results suggest that unlike many other anticancer agents, curcumin is not only devoid of immunosuppressive effects but also acts as immunorestorer in tumor-bearing host. 

Retracted: No

PubPeer comments:
 Fig 5 ![file] Fig 5B: Lane and 6 from all proteins tested in the WB (Curcumin and TNF alpha treated samples) apparently came from different blot as showed by distinct splice mark raised, but not the a-Actin, raised concerns about integrity of the data. The marking is prominent on p50-NFkB and pro-caspase 8 blots. Could authors clarify by posting their original data? ,
Extracellular acidosis promotes neutrophil transdifferentiation to MHC class II-expressing cells
Authors: Alexander B Sumarokov
Lyudmila I Buriachkovskaia
Boris K Pliyev
Mikhail Menshikov
Journal: Cellular immunology (2011)
Discipline: IMMUNOLOGY
Keywords: Inflammation; Acidosis; Neutrophils; GM-CSF; IFN-γ

Abstract:  Inflammation in peripheral tissues is usually associated with local acidosis. In the present study, we demonstrate that extracellular acidification enhances GM-CSF- and IFN-γ-induced expression of HLA-DR, CD80 and CD86 in human neutrophils (neutrophil transdifferentiation), and potentiates antigen-capturing capacities (both endocytosis and phagocytosis) of the transdifferentiated cells. Furthermore, in acidic conditions the transdifferentiated neutrophils have stronger antigen-presenting capacity, inducing more intense proliferation of autologous T lymphocytes in the presence of staphylococcal enterotoxin A. Thus, extracellular acidosis can represent a factor that promotes neutrophil transdifferentiation and potentiates the functional abilities of the transdifferentiated cells in inflammatory foci in vivo. 

Retracted: No

PubPeer comments:
 Figure 3. Two of the flow cytometry panels appear to share some unexpected similarities. ![file] ,
Detection of bacterial pathogens including potential new species in human head lice from Mali
Authors: Ogobara K Doumbo
Nadia Amanzougaghene
Didier Raoult
Abdoul Karim Sangaré
Mahamadou S Sissoko
Oleg Mediannikov
Florence Fenollar
Journal: PLoS ONE (2017)
Discipline: Multidisciplinary
Keywords: African countries; emerging pathogens; head lice; Pediculus humanus capitis; xenodiagnosis
Affiliations: Aix Marseille Univ, CNRS, IRD, INSERM, AP-HM, URMITE, IHU - Méditerranée Infection, Marseille, France., University of Bamako, Epidemiology Department of Parasitic Diseases, Faculty of Medicine and Odonto-Stomatology, Faculty of Pharmacy (MRTC/DEAP/FMOS-FAPH), Bamako, Mali., Campus International UCAD-IRD, Dakar, Senegal.

Abstract:  In poor African countries, where no medical and biological facilities are available, the identification of potential emerging pathogens of concern at an early stage is challenging. Head lice, Pediculus humanus capitis, have a short life, feed only on human blood and do not transmit pathogens to their progeny. They are, therefore, a perfect tool for the xenodiagnosis of current or recent human infection. This study assessed the occurrence of bacterial pathogens from head lice collected in two rural villages from Mali, where a high frequency of head lice infestation had previously been reported, using molecular methods. Results show that all 600 head lice, collected from 117 individuals, belonged to clade E, specific to West Africa. Bartonella quintana, the causative agent of trench fever, was identified in three of the 600 (0.5%) head lice studied. Our study also shows, for the first time, the presence of the DNA of two pathogenic bacteria, namely Coxiella burnetii (5.1%) and Rickettsia aeschlimannii (0.6%), detected in human head lice, as well as the DNA of potential new species from the Anaplasma and Ehrlichia genera of unknown pathogenicity. The finding of several Malian head lice infected with B. quintana, C. burnetii, R. aeschlimannii, Anaplasma and Ehrlichia is alarming and highlights the need for active survey programs to define the public health consequences of the detection of these emerging bacterial pathogens in human head lice. 

Retracted: No

PubPeer comments:
 The scope of this paper is the Detection of bacterial pathogens including potential new species in human head lice. The authors declared no competing interests. However, according to a poster from the Institut Hospitalo-Universitaire de Marseille (see below), 1 of the author is mentioned as one of the founder of a pharmaceutical company called Arthrobac Pharma in 2014. This pharmaceutical company is dedicated to the treatment of lice using ivermectin in combination with other products. Being a founder of a pharmaceutical company dedicated to the treatment of lice may be considered as a competing interest when the article address a topic covering the head lice. Can the author explain why this competing interest was not mentioned ? ![Image](http: backup.mediterranee-infection.com arkotheque client ihumed _depot_arko articles 579 poster_img.jpg) ,
MeCP2 binds to nucleosome free (linker DNA) regions and to H3K9/H3K27 methylated nucleosomes in the brain
Authors: Frank Lutz
Juan Ausió
Christoph H Borchers
Marlee K Ng
Ryan Mackie
Philippe T Georgel
Jason J Serpa
Begonia Silva-Moreno
J Adam Hall
Evgeniy V Petrotchenko
Anita A Thambirajah
Michael Hendzel
Andra Li
Lindsay J Frehlick
Brent E Gowen
Kristal K Missiaen
Journal: Nucleic Acids Research (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MeCP2; chromatin-binding protein; transcriptional regulation; brain; DNA methylation
Affiliations: Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, Canada V8W 3P6.

Abstract:  Methyl-CpG-binding protein 2 (MeCP2) is a chromatin-binding protein that mediates transcriptional regulation, and is highly abundant in brain. The nature of its binding to reconstituted templates has been well characterized in vitro. However, its interactions with native chromatin are less understood. Here we show that MeCP2 displays a distinct distribution within fractionated chromatin from various tissues and cell types. Artificially induced global changes in DNA methylation by 3-aminobenzamide or 5-aza-2'-deoxycytidine, do not significantly affect the distribution or amount of MeCP2 in HeLa S3 or 3T3 cells. Most MeCP2 in brain is chromatin-bound and localized within highly nuclease-accessible regions. We also show that, while in most tissues and cell lines, MeCP2 forms stable complexes with nucleosome, in brain, a fraction of it is loosely bound to chromatin, likely to nucleosome-depleted regions. Finally, we provide evidence for novel associations of MeCP2 with mononucleosomes containing histone H2A.X, H3K9me(2) and H3K27me(3) in different chromatin fractions from brain cortex and in vitro. We postulate that the functional compartmentalization and tissue-specific distribution of MeCP2 within different chromatin types may be directed by its association with nucleosomes containing specific histone variants, and post-translational modifications. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
 22 March 2022 correction. https: academic.oup.com nar advance-article doi 10.1093 nar gkac204 6552053 Figures 1 and 2 show multiple signs of splicing. Different lanes of gels were brought together to make final figures. The splicing was done for cosmetic reason, without intent to deceive, and is visible to the naked eye. New figures are provided below. These corrections do not affect the interpretation of the results and conclusions of the article. ,
Brand Suicide? Memory and Liking of Negative Brand Names
Authors: Zachary Estes
David Mazursky
Duncan Guest
Michael Gibbert
Journal: PLoS ONE (2016)
Discipline: Multidisciplinary
Keywords: Negative brand names; consumer behavior; brand name memory; liking; valence
Affiliations: Psychology Division, Nottingham Trent University, Nottingham, United Kingdom., Department of Marketing, Bocconi University, Milan, Italy., Institute of Marketing and Communication, University of Lugano, Lugano, Switzerland., The Jerusalem School of Business Administration, The Hebrew University Of Jerusalem, Jerusalem, Israel., The Centre for Academic Studies, Or Yehuda, Israel.

Abstract:  Negative brand names are surprisingly common in the marketplace (e.g., Poison perfume; Hell pizza, and Monster energy drink), yet their effects on consumer behavior are currently unknown. Three studies investigated the effects of negative brand name valence on brand name memory and liking of a branded product. Study 1 demonstrates that relative to non-negative brand names, negative brand names and their associated logos are better recognised. Studies 2 and 3 demonstrate that negative valence of a brand name tends to have a detrimental influence on product evaluation with evaluations worsening as negative valence increases. However, evaluation is also dependent on brand name arousal, with high arousal brand names resulting in more positive evaluations, such that moderately negative brand names are equally as attractive as some non-negative brand names. Study 3 shows evidence for affective habituation, whereby the effects of negative valence reduce with repeated exposures to some classes of negative brand name. 

Retracted: No

PubPeer comments:
 Why did the authors not test valence and arousal in a set of brand items that did not have  negative brand names ? It would seem intuitive that some brand names might actually have high arousal values. ,
Macrophage-Derived Slit3 Controls Cell Migration and Axon Pathfinding in the Peripheral Nerve Bridge
Authors: Thomas Mindos
Lauren Carr
David B Parkinson
Riordan W Barry
Sheridan L Roberts
Xin-Peng Dun
Alison C Lloyd
Louisa K Drake
Patricia K Woodley
Journal: Cell Reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Robo1; Schwann cell; Slit3; Sox2; fibroblast
Affiliations: Faculty of Medicine and Dentistry, Plymouth University, Plymouth, Devon, UK; School of Pharmacy, Hubei University of Science and Technology, Xian-Ning City, Hubei, China; The Co-innovation Center of Neuroregeneration, Nantong University, Jiangsu Province, China. Electronic address: ., Faculty of Medicine and Dentistry, Plymouth University, Plymouth, Devon, UK., University of Bath, Bath, UK., MRC Laboratory for Molecular Cell Biology, University College London, London, UK.

Abstract:  Slit-Robo signaling has been characterized as a repulsive signal for precise axon pathfinding and cell migration during embryonic development. Here, we describe a role for Sox2 in the regulation of Robo1 in Schwann cells and for Slit3-Robo1 signaling in controlling axon guidance within the newly formed nerve bridge following peripheral nerve transection injury. In particular, we show that macrophages form the outermost layer of the nerve bridge and secrete high levels of Slit3, while migratory Schwann cells and fibroblasts inside the nerve bridge express the Robo1 receptor. In line with this pattern of Slit3 and Robo1 expression, we observed multiple axon regeneration and cell migration defects in the nerve bridge of Sox2-, Slit3-, and Robo1-mutant mice. Our findings have revealed important functions for macrophages in the peripheral nervous system, utilizing Slit3-Robo1 signaling to control correct peripheral nerve bridge formation and precise axon targeting to the distal nerve stump following injury. 

Retracted: No

PubPeer comments:
 ![file] Figure 2O. The Slit1 DRG band is the same as the Slit3 Bridge band. , 
 ![file] Re-use of a band from an earlier publication in a different context. Apparent re-use of the adjacent empty lane (resolution very low in 2019 image). , 
 #1 ![file] , 
 We are grateful for bringing this to our attention. An investigation was carried out and action has been taken by the University against the individual concerned. The data in Figure 2O was however reproduced by another researcher and demonstrated the same pattern of expression. After a lengthy consultation with the journal, the decision to retract the paper has been made and will be done shortly with all authors agreement. ,
miR-196a Is Able to Restore the Aggressive Phenotype of Annexin A1 Knock-Out in Pancreatic Cancer Cells by CRISPR/Cas9 Genome Editing
Authors: Antonello Petrella
Luca Parente
Valentina Bizzarro
Domenico Memoli
Alessandro Weisz
Raffaella Belvedere
Francesca Rizzo
Emanuela Pessolano
Pasquale Saggese
Journal: International Journal of Molecular Sciences (2018)
Discipline: CHEMISTRY
Keywords: EMT; annexin A1; biomarkers; miR-196a-5p; pancreatic cancer.
Affiliations: Department of Pharmacy, University of Salerno, via Giovanni Paolo II 132, 84084 Fisciano (SA), Italy. ., Laboratory of Molecular Medicine and Genomics, Department of Medicine, Surgery and Dentistry 'Scuola Medica Salernitana', University of Salerno, via S. Allende, 1, 84081 Baronissi (SA), Italy. .

Abstract:  Annexin A1 (ANXA1) is a Ca2+-binding protein that is involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. Our previous studies showed that ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process appeared affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells finding that the modification in miRNA expression suggests the significant involvement of ANXA1 in PC development. In this study, we focused on miR-196a which appeared down modulated in absence of ANXA1. This miRNA is a well known oncogenic factor in several tumour models and it is able to trigger the agents of the epithelial to mesenchymal transition (EMT), like ANXA1. Our results show that the reintroduction in ANXA1 KO cells of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate cytoskeletal dynamics and other protein functions promoting PC cell migration and invasion. This work describes the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a. These results could lead to further information on ANXA1 intracellular role in PC, explaining other aspects that are apart from its tumorigenic behaviour. 

Retracted: No

PubPeer comments:
 Could the authors examine Figure 4B? When viewed in inverse one or two areas of contrast appear, possibly suggesting undisclosed splicing. The band between the red and blue arrows appears different than adjacent bands. Providing original scans here may address these concerns. *** Inverted ![file] *** Original ![file] ,
Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism
Authors: Monica A Maldonado
Antonella Caccamo
Salvatore Oddo
Andrea Magrí
Smita Majumder
David X Medina
Walter Holbein
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: mTOR; Alzheimer disease; protein homeostasis; neurodegenerative disorders; mutant amyloid precursor protein (APP)
Affiliations: Department of Physiology, University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA.

Abstract:  Reducing the mammalian target of rapamycin (mTOR) activity increases lifespan and health span in a variety of organisms. Alterations in protein homeostasis and mTOR activity and signaling have been reported in several neurodegenerative disorders, including Alzheimer disease (AD); however, the causes of such deregulations remain elusive. Here, we show that mTOR activity and signaling are increased in cell lines stably transfected with mutant amyloid precursor protein (APP) and in brains of 3xTg-AD mice, an animal model of AD. In addition, we show that in the 3xTg-AD mice, mTOR activity can be reduced to wild type levels by genetically preventing Aβ accumulation. Similarly, intrahippocampal injections of an anti-Aβ antibody reduced Aβ levels and normalized mTOR activity, indicating that high Aβ levels are necessary for mTOR hyperactivity in 3xTg-AD mice. We also show that the intrahippocampal injection of naturally secreted Aβ is sufficient to increase mTOR signaling in the brains of wild type mice. The mechanism behind the Aβ-induced mTOR hyperactivity is mediated by the proline-rich Akt substrate 40 (PRAS40) as we show that the activation of PRAS40 plays a key role in the Aβ-induced mTOR hyperactivity. Taken together, our data show that Aβ accumulation, which has been suggested to be the culprit of AD pathogenesis, causes mTOR hyperactivity by regulating PRAS40 phosphorylation. These data further indicate that the mTOR pathway is one of the pathways by which Aβ exerts its toxicity and further support the idea that reducing mTOR signaling in AD may be a valid therapeutic approach. 

Retracted: No

PubPeer comments:
 Figures 1D G u2013 4EBP1 (pSer65) bands are more similar than expected ![file] Zoom: ![file] , 
 It is actually more worrisome than that, because these 4E-BP1 (pSer65) blot of this paper, which is duplicated at the 6 and 12 months conditions, has been used and labeled as B-Actin in another previous, Pubpeer flagged, paper of the same group: https: pubpeer.com publications CB3EA933EE92E9A5898679D4CB401B. ![file] Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism Journal of Biological Chemistry (2011) - 1 Comment pubmed: 21266573 doi: 10.1074 jbc.m110.180638 issn: 0021-9258 issn: 1083-351x ![file] Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments Journal of Biological Chemistry (2010) - 1 Comment pubmed: 20178983 doi: 10.1074 jbc.m110.100420 issn: 0021-9258 issn: 1083-351x ,
Intracellular activated Notch1 is critical for proliferation of Kaposi's sarcoma-associated herpesvirus-associated B-lymphoma cell lines in vitro
Authors: Ke Lan
Daniel A Kuppers
Masanao Murakami
Erle S Robertson
Tathagata Choudhuri
Journal: Journal of virology (2006)
Discipline: MICROBIOLOGY
Keywords: Kaposi's sarcoma-associated herpesvirus; KSHV; Notch signaling; oncogenesis; ICN
Affiliations: Department of Microbiology, and Tumor Virology Program of Abramson Comprehensive Cancer Center, University of Pennsylvania Medical School, 201E Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104, USA., Department of Microbiology and Tumor Virology Program of Abramson Comprehensive Cancer Center, University of Pennsylvania Medical School, Philadelphia, Pennsylvania 19104

Abstract:  Kaposi's sarcoma-associated herpesvirus (KSHV) is a human tumor virus expressing latent antigens critical for pathogenesis. The mechanism by which KSHV mediates oncogenesis has not been fully elucidated. Notch signaling is an evolutionarily conserved pathway controlling diverse events related to development, proliferation, and tissue homeostasis. Deregulation of Notch signaling has also been shown to be highly correlated with oncogenesis. Here we show that the activated intracellular domain of Notch1 (ICN) is aberrantly accumulated in latently KSHV-infected pleural effusion lymphoma cells and results in increased proliferation. Specifically, growth of the infected cells was dramatically inhibited at the G(1) phase by treatment with a gamma-secretase inhibitor which specifically blocks the production of ICN. Increased ICN also up-regulated the cyclin D1 cell cycle regulator. Taken together, these studies define an important mechanism directly linking latent KSHV infection to induction of oncogenesis through dysregulation of the conserved Notch signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 6B. Much more similar than you would expect. https: imgur.com 35lLgw5 , 
 Last author appears to be on this journalu2019s editorial board: https: jvi.asm.org content board-editors ,
Grhl2 reduces invasion and migration through inhibition of TGFβ-induced EMT in gastric cancer
Authors: J Xiang
Z Wang
W Ran
X Fu
Journal: Oncogenesis (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Metastasis; Epithelial-mesenchymal transition (EMT); Grainyhead-like 2 (Grhl2); Invasion; Migration
Affiliations: Department of Gastrointestinal Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China., Department of General Surgery, Chongqing General Hospital, Chongqing, People's Republic of China., Department of General Surgery, Qianjiang Central Hospital of Chongqing, Chongqing, People's Republic of China.

Abstract:  Metastasis is one of the typical features of malignancy that significantly increases cancer-related mortality. Recent studies have shown that epithelial-mesenchymal transition (EMT) is closely related to the invasion and migration of cancer cells. Grainyhead-like 2 (Grhl2), a transcription factor, has been reported to be associated with several tumor processes including EMT. In the previous study, we have reported that Grhl2 functioned as a tumor suppressor in proliferation and apoptosis of gastric cancer. Here we aim to explore the effects of Grhl2 on invasion and migration of gastric cancer and further clarify its possible underlying mechanisms. As a result, in both SGC7901 and MKN45 cells, Grhl2 overexpression significantly inhibited the ability of invasion and migration. In addition, preliminary experiments showed that Grhl2 reduces the protein expression of matrix metalloproteinase-2, -7 and -9 (MMP-2, MMP-7 and MMP-9). Most importantly, Grhl2 antagonizes transforming growth factor-β (TGFβ)-induced EMT, and inhibition of TGFβ signaling pathways can restore Grhl2 expression. Finally, the results of subcutaneous xenograft model indicated that Grhl2 suppresses the growth of gastric cancer and reverses EMT process in vivo. Meanwhile, the metastatic tumor model further confirmed the inhibition of Grhl2 on metastasis of gastric cancer. Taken together, our findings proved that Grhl2, functioned as a tumor suppressor, reduces the invasion and migration through inhibition of TGFβ-induced EMT in gastric cancer. 

Retracted: No

PubPeer comments:
 In Figure 5c, a micrograph has been duplicated and presented as something else (7901-Grhl2-E-cadherin vs 7901-NC-Tgfb21). In addition, the tumors presented in Figure 5b do not correspond with the graphical illustration of the turmor size (Figure 5a). ![file] ,
Lidamycin induces marked G2 cell cycle arrest in human colon carcinoma HT-29 cells through activation of p38 MAPK pathway
Authors: Kaihuan Ren
Haixia Jin
Baowei Li
Xia Liu
Rong-Guang Shao
Chunjing Bian
Journal: Oncology Reports (2007)
Discipline: CLINICAL MEDICINE
Keywords: Lidamycin; enediyne antibiotic; cell cycle arrest; mechanisms; clinical cancer therapy
Affiliations: Institute of Medicinal Biotechnology, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100050, P.R. China.

Abstract:  Lidamycin (LDM), a member of the enediyne antibiotic family, is presently undergoing phase I clinical trials in P.R. China. In this study, we investigated the mechanisms of LDM-induced cell cycle arrest in order to support its use in clinical cancer therapy. Using human colon carcinoma HT-29 cells, we observed that LDM induced G2 cell cycle arrest in a time- and dose-dependent manner. LDM-induced G2 arrest was associated with increasing phosphorylation of Chk1, Chk2, Cdc25C, Cdc2 and expression of Cdc2 and cyclin B1. In addition, cytoplasmic localization of cyclin B1 was also involved in LDM-induced G2 arrest. Moreover, we found that p38 MAPK pathway contributed to LDM-induced G2 arrest. Inhibition of p38 MAPK by its inhibitor SB203580 not only attenuated LDM-induced G2 arrest but also potentiated LDM-induced apoptosis, which was accompanied by decreasing phosphorylation of Cdc2 and increasing expression of FasL and phosphorylation of JNK. Finally, we demonstrated that cells at G1 phase were more sensitive to LDM. Together, our findings suggest that p38 MAPK signaling pathway is involved in LDM-induced G2 arrest, at least partly, and a combination of LDM with p38 MAPK inhibitor may represent a new strategy for human colon cancer therapy. 

Retracted: No

PubPeer comments:
 There appears to be a repeated image in Figure 7B and Figure 4C. with different Sub-G1 values. ![file] ,