PReD-Bench/PRed-Bench huggingface dataset:
Establishment of an Acanthamoeba keratitis mouse model confirmed by amoebic DNA amplification
Authors: Jong-Hyun Kim
Jeong-Heon Lee
Kyongmin Kim
Ho-Joon Shin
Hongseok Yang
A-Young Park
A-Jeong Ham
Heekyoung Kang
Suk-Yul Jung
Sun Park
Yong-Joon Chwae
Young-Hwan Oh
Hae-Jin Sohn
Journal: Scientific Reports (2021)
Discipline: Multidisciplinary
Keywords: Acanthamoeba castellanii; Acanthamoeba keratitis; in vivo model; BALB/c mice; contact lens
Affiliations: Department of Microbiology, Ajou University School of Medicine, Suwon, 16499, Republic of Korea., Department of Biomedical Science, Graduate School of Ajou University, Suwon, 16499, Republic of Korea., Department of Tropical Medicine and Parasitology, Institute of Endemic Diseases, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea., Yonsei Eye Clinic, Yeongtong-gu Bongyeong-ro 1606, Suwon, 16704, Republic of Korea., Department of Biomedical Laboratory Science, Molecular Diagnostics Research Institute, School of Health and Medicine, Namseoul University, Cheonan, 31020, Republic of Korea., Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea. ., Department of Microbiology, Ajou University School of Medicine, Suwon, 16499, Republic of Korea. ., Department of Biomedical Science, Graduate School of Ajou University, Suwon, 16499, Republic of Korea. .

Abstract:  Acanthamoeba castellanii, the causative agent of Acanthamoeba keratitis (AK), occurs mainly in contact lens users with poor eye hygiene. The findings of many in vitro studies of AK, as well as the testing of therapeutic drugs, need validation in in vivo experiments. BALB/c mice were used in this study to establish in vivo AK model. A. castellanii cell suspensions (equal mixtures of trophozoites and cysts) were loaded onto 2-mm contact lens pieces and inserted into mouse eyes that were scratched using an ophthalmic surgical blade under anesthesia and the eyelids of the mice were sutured. The AK signs were grossly observed and PCR was performed using P-FLA primers to amplify the Acanthamoeba 18S-rRNA gene from mouse ocular tissue. The experimental AK mouse model was characterized by typical hazy blurring and melting of the mouse cornea established on day 1 post-inoculation. AK was induced with at least 0.3 × 105 A. castellanii cells (optimal number, 5 × 104), and the infection persisted for two months. The PCR products amplified from the extracted mouse eye DNA confirmed the development of Acanthamoeba-induced keratitis during the infection periods. In conclusion, the present AK mouse model may serve as an important in vivo model for the development of various therapeutic drugs against AK. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have a repeated image (green boxes). Some differences in cropping and color brightness. TAM. *** ![file] ,
Studies on HOXB4 expression during differentiation of human cytomegalovirus-infected hematopoietic stem cells into lymphocyte and erythrocyte progenitor cells
Authors: Chen Hong-ying
Zou Yan
Huang Mei-Xian
Guo qu-lian
Liu Wen-jun
Journal: Cell Biochemistry and Biophysics (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: HOXB4; mRNA; protein; human cytomegalovirus; HCMV
Affiliations: Department of Pediatrics, Affiliated Hospital of Luzhou Medical College, Luzhou 646000, Sichuan Province, China. 

Abstract:  We investigated the role of homeobox B4 (HOXB4) mRNA/protein expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) in proliferation and committed differentiation of human cord blood hematopoietic stem cells (HSCs) into colony-forming-units of T-lymphocyte (CFU-TL) and erythroid (CFU-E) progenitors in vitro. Twelve cord blood samples were collected from the fetal placenta umbilical vein and cultured in vitro. The proliferation and differentiation of cord blood HSCs into CFU-TL and CFU-E were continuously disrupted with HCMV-AD169 and/or 6 × 10(-8) mol/l of ATRA. HOXB4 mRNA/protein expression in CFU-TL and CFU-E was detected in control, ATRA, HCMV and ATRA + HCMV groups on days 3, 7, and 12 of culture by fluorescent qRT-PCR/western blot. We found that HOXB4 mRNA/protein expression was detectable on day 3, increased on day 7 and was highest on day 12. HOXB4 mRNA/protein expression in HCMV group was downregulated compared with control group (P &lt; 0.05). However, the levels were significantly upregulated in HCMV + ATRA group compared with HCMV group (P &lt; 0.05). We concluded that the abnormal HOXB4 mRNA/protein expression induced by HCMV could play a role in hematopoietic damage. ATRA, at the concentration used, significantly up-regulated HOXB4 mRNA/protein expression in normal lymphocyte and erythrocyte progenitor cells as well as in HCMV-infected cells. 

Retracted: No

PubPeer comments:
 Figure 2 appears to have a repeated image. *** ![file] ,
Omethoate induces pharyngeal cancer cell proliferation and G1/S cell cycle progression by activation of Akt/GSK-3β/cyclin D1 signaling pathway
Authors: Liting Lv
Ranyao Yang
Shulong Jiang
Zhenjie Qin
Yan Feng
Dongdong Huo
Yuanye Li
Journal: Toxicology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cyclin D1; FaDu cells; Glycogen synthase kinase-3β (GSK-3β); Omethoate; Proliferation
Affiliations: Department of Otolaryngology Head and Neck Surgery, Jining NO.1 People's Hospital, Jining, 272000, Shandong, China., Clinical Medical Laboratory Center, Jining NO.1 People's Hospital, Jining Medical University, Jining, 272000, Shandong, China., Department of Stomatology, People's Hospital of Zoucheng, Zoucheng, 273500, Shandong, China., Department of Infection Management, Jining NO.1 People's Hospital, Jining, 272000, Shandong, China., Department of Clinical Pharmacy, Jining NO.1 People's Hospital, Jining Medical University, Jining, 272000, Shandong, China., Department of Oncology, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China. Electronic address: ., Department of Infection Management, Jining NO.1 People's Hospital, Jining, 272000, Shandong, China. Electronic address: .

Abstract:  Omethoate is a broad category of organophosphorous pesticides (OPs) and has toxic effects on human health under long-term, low-dose exposure. However, the role of omethoate in cancer development remains elusive. The incidence of global head and neck squamous cell carcinomas (HNSCC) has markedly increased in recent years. Thus, we examined whether omethoate induced the proliferation of FaDu cells (a cell line of HNSCC) and if so, what the underlying mechanism was. The study revealed that omethoate induced FaDu cell growth in a dose- and time-dependent manner. Omethoate stimulated FaDu cell proliferation was mainly due to enhancing the G1 to S phase transition by flow cytometry analysis. We also found that omethoate up-regulated cyclin D1, a key gene controlling the G1-S transition. Furthermore, we showed that omethoate was capable of activating the Akt/GSK-3β signaling pathway. Blockage of Akt by siRNA or small molecule inhibitor significantly suppressed omethoate-induced cyclin D1 expression and cell proliferation. Collectively, these findings demonstrated for the first time that omethoate could induce the pharyngeal cancer cell proliferation by activation of the Akt/GSK-3β/cyclin D1 signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 4C. The  Control and  Akt inhibitor + Omethoate panels look more similar than expected. Boxes of the same color focus attention to groups of cells that look very similar. ![file] ,
Combustion heat of nitrogen-doped graphene nanoflakes studied by differential scanning calorimetry
Authors: Arkhipova, Ekaterina A.
Ivanov, Anton S.
Strokova, Natalia E.
Maslakov, Konstantin I.
Chernyak, Sergei A.
Savilov, Serguei V.
Journal: Journal of Thermal Analysis and Calorimetry (2021)
Discipline: CHEMISTRY
Keywords: Nitrogen-doped graphene nanoflakes; chemical vapor deposition; combustion heats; nitrogen content; transmission electron microscopy

Abstract: Nitrogen-doped graphene nanoflakes (NGNFs) with variable N-doping level of 5.0–10.7&nbsp;at.% were produced by chemical vapor deposition from different CH3CN/C6H6 mixtures. NGNFs were characterized by transmission electron microscopy, low-temperature nitrogen physisorption, X-ray photoelectron and Raman spectroscopies. Their combustion heats were measured by differential scanning calorimetry in the temperature range of 303–1273&nbsp;K and showed a bell-shaped dependence on the nitrogen content with a maximum of 30.1\u2009±\u20091.0&nbsp;kJ&nbsp;g\u22121 at a nitrogen level of 7.8&nbsp;at.%. The contributions of the π–π stacking, resonance and surface/edge energies to the combustion heat were discussed. The approach for estimation of the combustion heat of NGNFs assuming the contributions from pyridinic, pyrrolic and graphitic nitrogen species was proposed for the first time.

Retracted: No

PubPeer comments:
 Image (b) is not a magnified spot of image (a)! ![file] ,
Upregulation of C Terminus of Hsc70-Interacting Protein Attenuates Apoptosis and Procoagulant Activity and Facilitates Brain Repair After Traumatic Brain Injury
Authors: Yao Jing
Dianxu Yang
Zhiming Xu
Shiming Ju
Hao Chen
Hengli Tian
Lixia Xue
Yan Guo
Journal: Frontiers in Neuroscience (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: C terminus of Hsc70-interacting protein; apoptosis; coagulopathy; phosphatase and tensin homolog deleted on chromosome 10; procoagulant activity
Affiliations: Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China., Department of Neurology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Abstract:  Traumatic brain injury (TBI) could highly induce coagulopathy through breaking the dynamic balance between coagulation and fibrinolysis systems, which may be a major contributor to the progressive secondary injury cascade that occurs after TBI. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibition is reported to exert neuroprotection in TBI, making it a potential regulatory target involved in TBI-induced coagulation disorder. PTEN level is controlled in a major way by E3 ligase-mediated degradation through the ubiquitin-proteasome system. The C terminus of Hsc70-interacting protein (CHIP) has been shown to regulate proteasomal degradation and ubiquitination level of PTEN. In the present study, CHIP was overexpressed and knocked down in mouse brain microvascular endothelial cells (bEnd.3) and tissues during the early phase of TBI. In vitro cell proliferation, cell apoptosis, migration capacity, and invasion capacity were determined. The changes of procoagulant and apoptosis molecules after TBI were also detected as well as the micrangium density and blood-brain barrier permeability after in vivo TBI. In vitro results demonstrated that CHIP overexpression facilitated bEnd.3 cell proliferation, migration, and invasion and downregulated cell apoptosis and the expressions of procoagulant molecules through promoting PTEN ubiquitination in a simulated TBI model with stretch-induced injury treatment. In vivo experiments also demonstrated that CHIP overexpression suppressed post-TBI apoptosis and procoagulant protein expressions, as well as increased microvessel density, reduced hemorrhagic injury, and blood-brain barrier permeability. These findings suggested that the upregulation of CHIP may attenuate apoptosis and procoagulant activity, facilitate brain repair, and thus exerts neuroprotective effects in TBI. 

Retracted: No

PubPeer comments:
 Figure 7E appears to have some images which overlap. *** ![file] ,
iRhom2 is essential for innate immunity to DNA viruses by mediating trafficking and stability of the adaptor STING
Authors: Chen Li
Shu Li
Qing Yang
Huan Lian
Bo Zhong
Wei-Wei Luo
Hong-Bing Shu
Journal: Nature Immunology (2016)
Discipline: IMMUNOLOGY
Keywords: STING; iRhom2; DNA viruses; type I interferons; signaling
Affiliations: College of Life Sciences, Wuhan University, Wuhan, China., Medical Research Institute, Collaborative Innovation Center for Viral Immunology, School of Medicine, Wuhan University, Wuhan, China.

Abstract:  STING is a central adaptor in the innate immune response to DNA viruses. However, the manner in which STING activity is regulated remains unclear. We identified iRhom2 ('inactive rhomboid protein 2') as a positive regulator of DNA-virus-triggered induction of type I interferons. iRhom2 deficiency markedly impaired DNA-virus- and intracellular-DNA-induced signaling in cells, and iRhom2-deficient mice were more susceptible to lethal herpes simplex virus type 1 (HSV-1) infection. iRhom2 was constitutively associated with STING and acted in two distinct processes to regulate STING activity. iRhom2 recruited the translocon-associated protein TRAPβ to the STING complex to facilitate trafficking of STING from the endoplasmic reticulum to perinuclear microsomes. iRhom2 also recruited the deubiquitination enzyme EIF3S5 to maintain the stability of STING through removal of its K48-linked polyubiquitin chains. These results suggest that iRhom2 is essential for STING activity, as it regulates TRAPβ-mediated translocation and EIF3S5-mediated deubiquitination of STING. 

Retracted: No

PubPeer comments:
 The qPCR primers for IFNA4 is not specific. According to In-Silico PCR, IFNA15 and IFNA6 sequence would also be amplified. ![file] , 
 Fig.3a: According to figure legend of Fig.3a, the mice number is 7 in each group. I measured the survivorship curve and found a contradiction of iRhom2+ + data. As it showed in the black box, if 1 mouse died at day4 (red line), we can derive that 2 mice died at day8 (purple line). The dead mice number should be 1 but 2. If 1 mouse died at day5 or day6 (green or blue line), we can derive that less than 1 mice died at day4 (red line) and dead mice number at day8 should be 1 but 2. Both conclusions are against common sense. Could authors explain how to get this survivorship curve? ![file] , 
 #2 I am Wei-Wei Luo, the first author of this paper. Thank you for pointing this out for us. For figure 3A, we incorrectly set parameters u201c0u201d when using Graphpad Prism to analyze the data. This mistake caused the Y-axis (survival rate for iRhom2- - mice) to be displayed abnormally. We analyze the original data by the correct statistical method and the conclusion of this figure is not affected. ![file] #1  Ifna4 primers should be pan qPCR primers for Ifna4 and other Ifna subtypes, and this didn t affect our conclusion. ,
Hepatitis C virus (HCV) constitutively activates STAT-3 via oxidative stress: role of STAT-3 in HCV replication
Authors: Aleem Siddiqui
James Turkson
Tarek Hassanein
Gulam Waris
Journal: Journal of Virology (2005)
Discipline: MICROBIOLOGY
Keywords: hepatitis C virus; HCV; chronic hepatitis; liver cirrhosis; hepatocellular carcinoma
Affiliations: Department of Microbiology and Program in Molecular Biology, University of Colorado HSC, 4200 East Ninth Ave., Denver, CO 80262, USA., Molecular Oncology Program, Moffitt Cancer Center, Tampa, Florida, Department of Clinical Medicine and Surgery, School of Medicine, University of California, San Diego, California, Department of Microbiology and Program in Molecular Biology, University of Colorado Health Sciences Center, Denver, Colorado

Abstract:  The hepatitis C virus (HCV) causes chronic hepatitis, which often results in liver cirrhosis and hepatocellular carcinoma. We have previously shown that HCV nonstructural proteins induce activation of STAT-3 via oxidative stress and Ca2+ signaling (G. Gong, G. Waris, R. Tanveer, and A. Siddiqui, Proc. Natl. Acad. Sci. USA 98:9599-9604, 2001). In this study, we focus on the signaling pathway leading to STAT-3 activation in response to oxidative stress induced by HCV translation and replication activities. Here, we demonstrate the constitutive activation of STAT-3 in HCV replicon-expressing cells. The HCV-induced STAT-3 activation was inhibited in the presence of antioxidant (pyrrolidine dithiocarbamate) and Ca2+ chelators (BAPTA-AM and TMB-8). Previous studies have shown that maximum STAT-3 transactivation requires Ser727 phosphorylation in addition to tyrosine phosphorylation. Using a series of inhibitors and dominant negative mutants, we show that HCV-induced activation of STAT-3 is mediated by oxidative stress and influenced by the activation of cellular kinases, including p38 mitogen-activated protein kinase, JNK, JAK-2, and Src. Our results also suggest a potential role of STAT-3 in HCV RNA replication. We also observed the constitutive activation of STAT-3 in the liver biopsy of an HCV-infected patient. These studies provide an insight into the mechanisms by which HCV induces intracellular events relevant to liver pathogenesis associated with the viral infection. 

Retracted: Yes

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 2020 retraction. https: jvi.asm.org content 94 19 e01358-20 Volume 79, no. 3, p. 1569u20131580, 2005, https: doi.org 10.1128 JVI.79.3.1569-1580.2005 It has been called to our attention that the bands highlighted in Fig. 2A and 3D in Journal of Biological Chemistry 278:40778u201340787, 2003, https: doi.org 10.1074 jbc.M303248200 (article retracted), were reused in Fig. 1E and 4A. Unfortunately, the laboratory no longer has the original data nor the corresponding lab notes. We cannot therefore say with certainty that the data were wrongly duplicated or manipulated. Given the circumstances, we retract this paper. ,
ERK and p38 MAPK Activities Determine Sensitivity to PI3K/mTOR Inhibition via Regulation of MYC and YAP
Authors: Laura M Selfors
Seong A Kang
Gordon B Mills
Taru Muranen
Lisa L Gallegos
Jonathan L Coloff
Julie Hwang
Joan S Brugge
David M Sabatini
Carson C Thoreen
Journal: Cancer research (2016)
Discipline: CLINICAL MEDICINE
Keywords: PI3K/mTOR pathway; resistance; tumor growth; proto-oncogene; c-MYC
Affiliations: Department of Cell Biology and Ludwig Center at Harvard, Harvard Medical School, Boston, Massachusetts., Department of Biology, Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology, Cambridge, Massachusetts., Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts., Koch Institute for Integrative Cancer Research, Cambridge, Massachusetts., Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts., Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas., Department of Cell Biology and Ludwig Center at Harvard, Harvard Medical School, Boston, Massachusetts. .

Abstract:  Aberrant activation of the PI3K/mTOR pathway is a common feature of many cancers and an attractive target for therapy, but resistance inevitably evolves as is the case for any cancer cell-targeted therapy. In animal tumor models, chronic inhibition of PI3K/mTOR initially inhibits tumor growth, but over time, tumor cells escape inhibition. In this study, we identified a context-dependent mechanism of escape whereby tumor cells upregulated the proto-oncogene transcriptional regulators c-MYC and YAP1. This mechanism was dependent on both constitutive ERK activity as well as inhibition of the stress kinase p38. Inhibition of p38 relieved proliferation arrest and allowed upregulation of MYC and YAP through stabilization of CREB. These data provide new insights into cellular signaling mechanisms that influence resistance to PI3K/mTOR inhibitors. Furthermore, they suggest that therapies that inactivate YAP or MYC or augment p38 activity could enhance the efficacy of PI3K/mTOR inhibitors. Cancer Res; 76(24); 7168-80. ©2016 AACR. 

Retracted: No

PubPeer comments:
 ![file] ,
Dephosphorylation-dependent sorting of SR splicing factors during mRNP maturation
Authors: Xiangdong Xu
Peiqing Sun
Shengrong Lin
Xiang-Dong Fu
Ran Xiao
Journal: Molecular Cell (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SR proteins; RNA binding proteins; pre-mRNA splicing; mRNA transport; mRNA stability
Affiliations: Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, California 92093, USA.

Abstract:  SR proteins are a family of sequence-specific RNA binding proteins originally discovered as essential factors for pre-mRNA splicing and recently implicated in mRNA transport, stability, and translation. Here, we used a genetic complementation system derived from conditional knockout mice to address the function and regulation of SR proteins in vivo. We demonstrate that ASF/SF2 and SC35 are each required for cell viability, but, surprisingly, the effector RS domain of ASF/SF2 is dispensable for cell survival in MEFs. Although shuttling SR proteins have been implicated in mRNA export, prevention of ASF/SF2 from shuttling had little impact on mRNA export. We found that shuttling and nonshuttling SR proteins are segregated in an orderly fashion during mRNP maturation, indicating distinct recycling pathways for different SR proteins. We further showed that this process is regulated by differential dephosphorylation of the RS domain, thus revealing a sorting mechanism for mRNP transition from splicing to export. 

Retracted: No

PubPeer comments:
 Figure 5C showed distinct exposure intensity for the gel of aHA and aA1 for ASF SF2(RD). Could the authors please clarify? ![file] ,
Displacement of SATB1-bound histone deacetylase 1 corepressor by the human immunodeficiency virus type 1 transactivator induces expression of interleukin-2 and its receptor in T cells
Authors: Sanjeev Galande
Dyavar S Ravi
Prabhat Kumar Purbey
Debashis Mitra
P Pavan Kumar
Journal: Molecular and Cellular Biology (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HIV-1; cytokine gene expression; T cells; SATB1; IL-2
Affiliations: National Centre for Cell Science, NCCS Complex, Ganeshkhind, Pune 411007, India.

Abstract:  One hallmark of human immunodeficiency virus type 1 (HIV-1) infection is the dysregulation of cytokine gene expression in T cells. Transfection of T cells with human T-cell leukemia type 1 or 2 transactivator results in the induction of the T-cell-restricted cytokine interleukin-2 (IL-2) and its receptor (IL-2Ralpha). However, no T-cell-specific factor(s) has been directly linked with the regulation of IL-2 and IL-2Ralpha transcription by influencing the promoter activity. Thymocytes from SATB1 (special AT-rich sequence binding protein 1) knockout mice have been shown to ectopically express IL-2Ralpha, suggesting involvement of SATB1 in its negative regulation. Here we show that SATB1, a T-cell-specific global gene regulator, binds to the promoters of human IL-2 and IL-2Ralpha and recruits histone deacetylase 1 (HDAC1) in vivo. SATB1 also interacts with Tat in HIV-1-infected T cells. The functional interaction between HIV-1 Tat and SATB1 requires its PDZ-like domain, and the binding of the HDAC1 corepressor occurs through the same. Furthermore, Tat competitively displaces HDAC1 that is bound to SATB1, leading to increased acetylation of the promoters in vivo. Transduction with SATB1 interaction-deficient soluble Tat (Tat 40-72) and reporter assays using a transactivation-negative mutant (C22G) of Tat unequivocally demonstrated that the displacement of HDAC1 itself is sufficient for derepression of these promoters in vivo. These results suggest a novel mechanism by which HIV-1 Tat might overcome SATB1-mediated repression in T cells. 

Retracted: No

PubPeer comments:
 I donu2019t see any information about approval from the local ethics committee What about the lack of approval from the ethics committee? Is it possible to publish a clinical document without approval? This paper deals with surgical procedures and no surgeon is among the authors. ,
Retracted : Effects and mechanism of puerarin on the human retinoblastoma cells
Authors: Shuxia Fan
Xiaohui Fan
Chao Yang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: invasion; migration; proliferation; puerarin; retinoblastoma.
Affiliations: Department of Ophthalmology, Binzhou People's Hospital, Binzhou, China., Department of Nursing, Binzhou People's Hospital, Binzhou, China.

Abstract:  Puerarin is an isoflavonoid that is extracted from Kudzu root and is considered to have an anti-tumor effect. In the present study, the effects of puerarin on human retinoblastoma (RB) cells and the related pathways was determined. The retinoblastoma RB cell lines were used in this study. Cell viability and colony formation capacity were measured by MTT and colony formation assays. Cell cycle was determined by flow cytometry. Cell migration and invasion were examined by Transwell assay. The expression of cell cycle, EMT, and MAPK/ERK signal pathway-related proteins were detected by western blot following puerarin treatment. The results revealed that cell viability and proliferation of RB cells treated with puerarin were significantly lower in RB cells compared to the control group. Puerarin significantly decreased the proportion of cells during S phase which was accompanied with increase in cells at G0/1 and G2 phases. Moreover, puerarin suppressed cell migration, invasion and up-regulated E-Cadherin expression as well as down-regulated Vimentin and α-SMA expression. Furthermore, puerarin treatment suppressed the expression of p-MEK and p-ERK in RB cells. Our findings suggest that puerarin contributes to in the treatment of RB and other malignant tumors. 

Retracted: Yes

PubPeer comments:
 the cultured cells in this paper don t look like typical sensory neurons, but nonneuronal cells ![file] A good example of what cultured sensory neurons look like can be found here: PMID: 30237325 ,
Identifying predictors of high sodium excretion in patients with heart failure: a mixed effect analysis of longitudinal data
Authors: Maxim Topaz
Houry Puzantian
Terry A Lennie
Ruth Masterson Creber
Christopher S Lee
Barbara Riegel
Journal: European Journal of Cardiovascular Nursing (2014)
Discipline: CLINICAL MEDICINE
Keywords: Heart failure; diet; diet therapy; sodium-restricted; urine sodium.
Affiliations: School of Nursing, University of Pennsylvania USA ., School of Nursing, University of Pennsylvania USA., College of Nursing, University of Kentucky, USA., Oregon Health & Science University, Portland, USA., Department of Biobehavioral Health Science, University of Illinois at Chicago, USA.

Abstract:  Background: A low-sodium diet is a core component of heart failure self-care but patients have difficulty following the diet. Aim: The aim of this study was to identify predictors of higher than recommended sodium excretion among patients with heart failure. Methods: The World Health Organization Five Dimensions of Adherence model was used to guide analysis of existing data collected from a prospective, longitudinal study of 280 community-dwelling adults with previously or currently symptomatic heart failure. Sodium excretion was measured objectively using 24-hour urine sodium measured at three time points over six months. A mixed effect logistic model identified predictors of higher than recommended sodium excretion. Results: The adjusted odds of higher sodium excretion were 2.90, (95% confidence interval (CI): 1.15-4.25, p&lt;0.001) for patients who were obese; 2.80 (95% CI: 1.33-5.89, p=0.007) for patients with diabetes; and 2.22 (95% CI: 1.09-4.53, p=0.028) for patients who were cognitively intact. Conclusion: Three factors were associated with excess sodium excretion and two factors, obesity and diabetes, are modifiable by changing dietary food patterns. 

Retracted: No

PubPeer comments:
 Creber et al cite and extensively discuss findings from a 2008 paper by Paterna et al published in Clinical Science that has been found to contain data duplicated in a later study from the same author group published in the Journal of Cardiac Failure (Parinnello 2009). Data from both these studies were contained in a 2012 systematic review published in BMJ Heart journal that was later retracted (Aug 21, 2012) due to the inability of the study group to provide the original data to verify the duplicate data issues due to a u201ccomputer failureu201d. u2028Additional PubPeer posts for the specific papers are available: https: pubpeer.com publications E03BB72DBAA939C61082F4608D558B https: pubpeer.com publications B24491C479E0C003418D1F1CBECE07 A complete blog of the story leading to retraction of the BMJ Heart systematic review is available here: https: www.cebm.net 2019 02 salt-reduction-in-heart-failure-where-has-the-uncertainty-come-from ,
Snus use, smoking and survival among prostate cancer patients
Authors: Hans-Olov Adami
Olof Nyrén
Lorelei A Mucci
Caroline Nordenvall
Fang Fang
Kathryn M Wilson
Sarah C Markt
Jennifer R Rider
Weimin Ye
Pär Stattin
Journal: International Journal of Cancer (2016)
Discipline: CLINICAL MEDICINE
Keywords: cancer survival; prostate cancer; smoking; snus; tobacco use.
Affiliations: Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA USA., Channing Division of Network Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA USA., Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden., Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden., Department of Epidemiology, Boston University School of Public Health, Boston, MA USA.

Abstract:  Smoking is associated with prostate cancer mortality. The Scandinavian smokeless tobacco product snus is a source of nicotine but not the combustion products of smoke and has not been studied with respect to prostate cancer survival. The study is nested among 9,582 men with incident prostate cancer within a prospective cohort of 336,381 Swedish construction workers. Information on tobacco use was collected at study entry between 1971 and 1992, and categorized into (i) never users of any tobacco, (ii) exclusive snus: ever users of snus only, (iii) exclusive smokers: ever smokers (cigarette, cigar and/or pipe) only and (iv) ever users of both snus and smoking. Hazard ratios for prostate cancer-specific and total mortality for smoking and snus use based on Cox proportional hazards models adjusted for age, calendar period at diagnosis and body mass index at baseline. During 36 years of follow-up, 4,758 patients died-2,489 due to prostate cancer. Compared to never users of tobacco, exclusive smokers were at increased risk of prostate cancer mortality (HR 1.15, 95% CI: 1.05-1.27) and total mortality (HR 1.17, 95% CI: 1.09-1.26). Exclusive snus users also had increased risks for prostate cancer mortality (HR 1.24, 95% CI: 1.03-1.49) and total mortality (HR 1.19, 95% CI: 1.04-1.37). Among men diagnosed with nonmetastatic disease, the HR for prostate cancer death among exclusive snus users was 3.17 (95% CI: 1.66-6.06). The study is limited by a single assessment of tobacco use prior to diagnosis. Snus use was associated with increased risks of prostate cancer and total mortality among prostate cancer patients. This suggests that tobacco-related components such as nicotine or tobacco-specific carcinogens may promote cancer progression independent of tobacco's combustion products. 

Retracted: No

PubPeer comments:
null, 
 Can the authors provide the dose-response data? ,
Non‐coding RNA MFI2‐AS1 promotes colorectal cancer cell proliferation, migration and invasion through miR‐574‐5p/MYCBP axis
Authors: Lunqiang Zhang
Qian Pei
Zhongyi Zhou
Chenglong Li
Haiping Pei
Fengbo Tan
Yuan Zhou
Dan Wang
Journal: Cell Proliferation (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LncRNA MFI2-AS1; MYC binding protein; colorectal cancer; miR-574-5p.
Affiliations: Department of Gastrointestinal Surgery, Xiangya Hospital Central South University Changsha China

Abstract:  Objective: Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play essential roles in the tumour progression. LncRNAs mostly act as competing endogenous RNAs (ceRNAs) by sponging miRNAs. This study aimed to study the association of a novel lncRNA MFI2-AS1 with miR-574-5p/MYCBP axis in the development of colorectal cancer (CRC). Methods: Ninety-four CRC tissues and paired adjacent non-tumour tissues were included in our study. The relative expression level of MFI2-AS1 was detected, and its relationship with clinico-pathological factors was analysed. Then, the CRC cells lines (LoVo and RKO) were transfected with MFI2-AS1 siRNA, miR-574-5p mimics and inhibitors. Cell proliferation, migration, invasion, cell cycle distribution and DNA damage in response to different transfection conditions were examined. Dual-luciferase reporter assay was performed to identify the target interactions between MFI2-AS1 and miR-574-5p, miR-574-5p and MYCBP. Results: LncRNA MFI2-AS1 and MYCBP were up-regulated in CRC tissues when compared with adjacent non-tumour tissues. The expression levels of MFI2-AS1 were significantly associated with tumour histological grade, lymph and distant metastasis, TNM stage and vascular invasion. Both MFI2-AS1 siRNA and miR-574-5p mimics inhibited proliferation, migration and invasion in LoVo and RKO cells. The transfection of miR-574-5p inhibitor showed MFI2-AS1 siRNA-induced changes in CRC cells. Dual-luciferase reporter assay revealed target interactions between MFI2-AS1 and miR-574-5p, miR-574-5p and MYCBP. Conclusions: These findings suggested that lncRNA MFI2-AS1 and MYCBP have promoting effects in CRC tissues. LncRNA MFI2-AS1 promoted CRC cell proliferation, migration and invasion through activating MYCBP and by sponging miR-574-5p. 

Retracted: No

PubPeer comments:
 ![file] ,
Inhibitory effects of C-type natriuretic peptide on the differentiation of cardiac fibroblasts, and secretion of monocyte chemoattractant protein-1 and plasminogen activator inhibitor-1
Authors: Yang Liu
Bin Li
Xiao-Feng Li
Gang Li
Ying-Long Liu
Ai-Jun Liu
Zhi-Qiang Li
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: C-type natriuretic peptide (CNP); cardiac fibroblasts (CFs); myofibroblast marker proteins; extracellular signal-regulated kinase 1/2 (ERK1/2); morphological changes
Affiliations: Department of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, P.R. China.

Abstract:  The present study aimed to investigate the effect of C-type natriuretic peptide (CNP) on the function of cardiac fibroblasts (CFs). Western blotting was used to investigate the expression of myofibroblast marker proteins: α-smooth muscle actin (α-SMA), extra domain-A fibronectin, collagen I and collagen III, and the activity of extracellular signal-regulated kinase 1/2 (ERK1/2). Immunofluorescence was used to examine the morphological changes; a transwell assay was used to analyze migration, and reverse transcription-quantitative polymerase chain reaction and ELISA were employed to determine the mRNA expression and protein secretion of monocyte chemoattractant protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1). The results demonstrated that CNP significantly reduced the protein expression of α-SMA, fibronectin, collagen I and collagen III, and suppressed the migratory ability of CFs. Additionally, the mRNA and protein expression of MCP-1 and PAI-1 was inhibited under the CNP treatment; and this effect was mediated by the inhibition of the ERK1/2 activity. In conclusion, CNP inhibited cardiac fibroblast differentiation and migration, and reduced the secretion of MCP-1 and PAI-1, which demonstrates novel mechanisms to explain the antifibrotic effect of CNP. 

Retracted: No

PubPeer comments:
 Figures 3A and 3C appear to have an area of overlap, roughly shown in red. *** ![file] ,
Whole transcriptome approach to evaluate the effect of aluminium hydroxide in ovine encephalon
Authors: Lluís Luján
Marta Pérez
Martin Bilbao-Arribas
Javier Asín
Endika Varela-Martínez
Begoña M Jugo
Damián de Andrés
Naiara Abendaño
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Aluminium hydroxide adjuvants; central nervous system; vaccines; lambs; RNA-seq
Affiliations: Department of Genetics, Physical Anthropology and Animal Physiology, Faculty of Science and Technology, University of the Basque Country (UPV/EHU), Leioa, Spain., Department of Animal Pathology, University of Zaragoza, Zaragoza, Spain., Institute of Agrobiotechnology (CSIC-UPNA-Gov. Navarra), Navarra, Spain., Department of Genetics, Physical Anthropology and Animal Physiology, Faculty of Science and Technology, University of the Basque Country (UPV/EHU), Leioa, Spain. .

Abstract:  Aluminium hydroxide adjuvants are crucial for livestock and human vaccines. Few studies have analysed their effect on the central nervous system in vivo. In this work, lambs received three different treatments of parallel subcutaneous inoculations during 16 months with aluminium-containing commercial vaccines, an equivalent dose of aluminium hydroxide or mock injections. Brain samples were sequenced by RNA-seq and miRNA-seq for the expression analysis of mRNAs, long non-coding RNAs and microRNAs and three expression comparisons were made. Although few differentially expressed genes were identified, some dysregulated genes by aluminium hydroxide alone were linked to neurological functions, the lncRNA TUNA among them, or were enriched in mitochondrial energy metabolism related functions. In the same way, the miRNA expression was mainly disrupted by the adjuvant alone treatment. Some differentially expressed miRNAs had been previously linked to neurological diseases, oxidative stress and apoptosis. In brief, in this study aluminium hydroxide alone altered the transcriptome of the encephalon to a higher degree than commercial vaccines that present a milder effect. The expression changes in the animals inoculated with aluminium hydroxide suggest mitochondrial disfunction. Further research is needed to elucidate to which extent these changes could have pathological consequences. 

Retracted: No

PubPeer comments:
 I have a problem for interpreting the data of this paper. ![file] So, if I understand correctly these data, adjuvant alone is more potent to induce changes than adjuvants associated with vaccines. How is it possible in term of biology? Does it mean that vaccines contain a component that protect against aluminium? ,
Shugoshin 1 is dislocated by KSHV-encoded LANA inducing aneuploidy
Authors: Hem Chandra Jha
Yonggang Pei
Zhiguo Sun
Rajnish Kumar Singh
Erle S Robertson
Fengchao Lang
Journal: PLoS Pathogens (2018)
Discipline: MICROBIOLOGY
Keywords: Shugoshin-1; H2A phosphorylation; Bub1; chromosome segregation; chromosomal instability (CIN)
Affiliations: Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, the Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, United States of America.

Abstract:  Shugoshin-1 (Sgo1) protects the integrity of the centromeres, and H2A phosphorylation is critical for this process. The mitotic checkpoint kinase Bub1, phosphorylates H2A and ensures fidelity of chromosome segregation and chromosome number. Oncogenic KSHV induces genetic alterations through chromosomal instability (CIN), and its essential antigen LANA regulates Bub1. We show that LANA inhibits Bub1 phosphorylation of H2A and Cdc20, important for chromosome segregation and mitotic signaling. Inhibition of H2A phosphorylation at residue T120 by LANA resulted in dislocation of Sgo1, and cohesin from the centromeres. Arrest of Cdc20 phosphorylation also rescued degradation of Securin and Cyclin B1 at mitotic exit, and interaction of H2A, and Cdc20 with Bub1 was inhibited by LANA. The N-terminal nuclear localization sequence domain of LANA was essential for LANA and Bub1 interaction, reversed LANA inhibited phosphorylation of H2A and Cdc20, and attenuated LANA-induced aneuploidy and cell proliferation. This molecular mechanism whereby KSHV-induced CIN, demonstrated that the NNLS of LANA is a promising target for development of anti-viral therapies targeting KSHV associated cancers. 

Retracted: No

PubPeer comments:
 Figure 5C and D: granulocytes MPs : graphs looks similar ![file] , 
 Thanks for this comment. Indeed, those are the the same figures. In fact, the data of L-sel-positive GMPs were incorrectly plotted in the total GMP chart (right panel 5C). We did not catch this problem during the reviewing process. Fortunately, this error doesn t impact the other results We just wrote to the editor of STM and provided the new figure Best regards Patrick blanco and Christophe Richez ,
STAT3 induces muscle stem cell differentiation by interaction with myoD
Authors: Guozi Yang
Kewei Ma
Ying Xu
Yanqiu Song
Wei Li
Xue Han
Zhonghua Du
Yanping Yang
Guanjun Wang
Luguo Sun
Journal: Cytokine (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: STAT proteins; cytokines; hormones; STAT3; myogenesis
Affiliations: Department of Hematology and Oncology, The First Hospital, Jilin University, 71 Xinmin Street, Changchun 130021, China.

Abstract:  Signal transducers and activators of transcription (STAT) family proteins transduce pivotal biological effects of various cytokines and hormones. STAT3 proteins are known to play a central role in the regulation of growth, differentiation, and survival of many types of cells. However, the function of STAT3 in myogenesis still remains largely unknown. We now provided direct evidence that STAT3 could induce myogenic differentiation and this effect might be mediated by interaction with MyoD--the essential transcription factor during myogenic differentiation. Furthermore, leukemia inhibitory factor (LIF) might be the upstream factor which activated JAK2/STAT3 pathway to stimulate muscle cell differentiation. Taken together, these results provide a molecular basis for further understanding of the muscle regeneration mechanism. 

Retracted: No

PubPeer comments:
 Figures 1 2 3: * Blue boxes: An actin band in Figure 1A looks similar to an actin band in Figure 2. * Red boxes: Two MHC bands in Figure 1B look similar to two MHC bands in Figure 3 ![file] ,
Deletion of Lactate Dehydrogenase-A in Myeloid Cells Triggers Antitumor Immunity
Authors: Barbara Wegiel
Han Xie
Andreas Hedblom
Eva Csizmadia
Maria Serena Longhi
Marta Vuerich
Mailin Li
Pankaj Seth
Journal: Cancer Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Immunometabolism; cancer pathophysiology; macrophage; lactate dehydrogenase-A (LDH-A); tumor formation
Affiliations: Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts.  ., Division of Interdisciplinary Medicine and Biotechnology, Boston, Massachusetts., BIDMC Cancer Research Institute, Boston, Massachusetts., Department of Surgery, Transplant Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts., Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts., BIDMC Cancer Research Institute, Boston, Massachusetts.  .

Abstract:  Immunometabolism is emerging as a critical determinant of cancer pathophysiology. In this study, we explored the contributions of macrophage-expressed lactate dehydrogenase-A (LDH-A) to tumor formation in a K-Ras murine model of lung carcinoma. Myeloid-specific deletion of LDH-A promoted accumulation of macrophages with a CD86high and MCP-1high M1-like phenotype that suppressed tumor growth. This phenotypic effect was accompanied by reduced VEGF expression and angiogenesis, diminished numbers of PD-L1+ cancer cells, increased numbers of CD3+ T cells, and activation status of CD8+ T cells. Furthermore, it was associated with more pronounced antitumor T-cell immunity via induction of IL17 and IFNγ-producing CD8+ T (Tc17 and Tc1) cells, likely via suppression of lactate-driven PD-L1 expression. Our results suggest that expressions of LDH-A and lactate by macrophage in the tumor microenvironment are major drivers of T-cell immunosuppression, strongly supporting the concept of targeting stromal LDH-A as an effective strategy to blunt tumoral immune escape. Cancer Res; 77(13); 3632-43. ©2017 AACR. 

Retracted: No

PubPeer comments:
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The cytoskeleton actin binding protein filamin A impairs both IGF2 mitogenic effects and the efficacy of IGF1R inhibitors in adrenocortical cancer cells
Authors: A Spada
M Luconi
A L Serban
E Giardino
F Mangili
M Arosio
F M Elli
M Mannelli
E Peverelli
D Treppiedi
R Catalano
G Mantovani
V Morelli
Journal: Cancer Letters (2021)
Discipline: CLINICAL MEDICINE
Keywords: Adrenocortical carcinoma; Cytoskeleton; Growth factors; Linsitinib; NVP-ADW742.
Affiliations: Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy; PhD Program in Endocrinological Sciences, Sapienza University of Rome, Rome, Italy., Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy., Endocrinology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy., PhD Program in Endocrinological Sciences, Sapienza University of Rome, Rome, Italy; Endocrinology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy., Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy., Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy; Endocrinology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy., Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy; Endocrinology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy. Electronic address: .

Abstract:  Adrenocortical carcinomas (ACCs) overexpress insulin-like growth factor 2 (IGF2), that drives a proliferative autocrine loop by binding to IGF1R and IR, but IGF1R/IR-targeted therapies failed in ACC patients. The cytoskeleton actin-binding protein filamin A (FLNA) impairs IR signalling in melanoma cells. Aims of this study were to test FLNA involvement in regulating IGF1R and IR responsiveness to both IGF2 and inhibitors in ACC. In ACC cells H295R and SW13 and primary cultures (1ACC, 4 adenomas) we found that IGF1R and IR interacted with FLNA, and FLNA silencing increased IGF1R and reduced IR expression, with a downstream effect of increased cell proliferation and ERK phosphorylation. In addition, FLNA knockdown potentiated antiproliferative effects of IGF1R/IR inhibitor Linsitinib and IGF1R inhibitor NVP-ADW742 in H295R. Finally, Western blot showed lower FLNA expression in ACCs (n = 10) than in ACAs (n = 10) and an inverse correlation of FLNA/IGF1R ratio with ERK phosphorylation in ACCs only. In conclusion, we demonstrated that low FLNA levels enhance both IGF2 proliferative effects and IGF1R/IR inhibitors efficacy in ACC cells, suggesting FLNA as a new factor influencing tumor clinical behavior and the response to the therapy with IGF1R/IR-targeted drugs. 

Retracted: No

PubPeer comments:
 Figure 2 * Red arrows: The right GAPDH band in Figure 2F appears to look similar to the left GAPDH band in Figure 2G ![file] ,