PReD-Bench/PRed-Bench huggingface dataset:
<p>CIRP regulates BEV-induced cell migration in gliomas</p>
Authors: Yu-Xiao Liu
Xiang-Pin Fu
Ke-Hui Liu
Jun-Nian Zhou
Qin-Hong Zhang
Wen Yue
Zhi-Wen Zhang
Journal: Cancer Management and Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: CXCL12; RNA binding; proteomics; therapeutic resistance.
Affiliations: Department of Neurosurgery, The Fourth Medical Centre of Chinese PLA General Hospital, Beijing 100048, China, ., Stem Cell and Regenerative Medicine Lab, Institute of Health Service and Transfusion Medicine, Beijing 100850, China, ., Experimental Hematology and Biochemistry Lab, Beijing Institute of Radiation Medicine, Beijing 100850, China., South China Research Center for Stem Cell & Regenerative Medicine, SCIB, Guangzhou 510005, China., State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.

Abstract:  Purpose: A better understanding of the underlying molecular mechanisms in treatment failure of bevacizumab (BEV) for malignant glioma would contribute to overcome therapeutic resistance. Methods: Here, we used a quantitative proteomic method to identify molecular signatures of glioblastoma cell after BEV treatment by two-dimensional liquid chromatography-tandem mass spectrometry analysis and 6-plex iTRAQ quantification. Next, the function of cold-inducible RNA-binding protein (CIRP), one of the most significantly affected proteins by drug treatment, was evaluated in drug resistance of glioma cells by invasion assays and animal xenograft assays. Target molecules bound by CIRP were determined using RNA-binding protein immunoprecipitation and microarray analysis. Then, these mRNAs were identified by quantitative real-time PCR. Results: Eighty-seven proteins were identified with significant fold changes. The biological functional analysis indicated that most of the proteins were involved in the process of cellular signal transduction, cell adhesion, and protein transport. The expression of CIRP greatly decreased after BEV treatment, and ectopic expression of CIRP abolished cell migration in BEV-treated glioma cells. In addition, CIRP could bind mRNA of CXCL12 and inhibit BEV-induced increase of CXCL12 in glioma cells. Conclusion: These data suggested that CIRP may take part in BEV-induced migration of gliomas by binding of migration-relative RNAs. 

Retracted: No

PubPeer comments:
 Figure 4B appears to have 2 images which overlap. *** Closeup ![file] *** Full figure and location of above in green ![file] , 
 we are very sorry to make mistakes in this pictures, and we will correct it , 
 we are very sorry to make errors in save pictures. a pictures of u87 were saved in a wrong place .we will contact with the editor soon and corrected it as soon as possible , 
 ![file] ![file] ,
PAX6, a novel target of microRNA-7, promotes cellular proliferation and invasion in human colorectal cancer cells
Authors: Yanhong Liu
Pingli Xie
Guancheng Li
Yanwen Li
Feng Li
Yuehui Li
Journal: Digestive Diseases and Sciences (2014)
Discipline: CLINICAL MEDICINE
Keywords: PAX6; miR-7; colorectal cancer; tumorigenesis; molecular mechanisms
Affiliations: Tumor Immunobiology Laboratory of Cancer Research Institute, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Ministry of Health, Central South University, 110 Xiangya Road, Changsha, 410078, Hunan, China.

Abstract:  Background: Paired box 6 (PAX6), a highly conserved transcriptional factor, has been implicated in tumorigenesis. Aim: We aimed to explore the roles and molecular mechanisms of PAX6 and microRNA (miR-7) in colorectal cancer cells. Methods: Tissue microarray immunohistochemistry and Western blot were applied to examine the PAX6 expression. Real-time RT-PCR and Western blot were performed to determine the expression of miR-7 and PAX6. Luciferase reporter assay was used to determine whether PAX6 was a target of miR-7. Effects of miR-7 and PAX6 on colorectal cell proliferation, cell cycle progression, colony formation and invasion were then investigated. Western blot was used to determine the activities of the ERK and PI3K signal pathways, as well as the protein expression of MMP2 and MMP9. Results: The protein levels of PAX6 were gradually increased, while the expression of miR-7 was gradually reduced with malignancy of colorectal cancer. PAX6 was further identified as a target of miR-7, and its protein expression was negatively regulated by miR-7 in human colorectal cancer cells. Overexpression of PAX6 in Caco-2 and SW480 cells enhanced cellular proliferation, cell cycle progression, colony formation, and invasion, while miR-7 upregulation repressed these biological processes. Furthermore, the activities of ERK and PI3K signal pathways, as well as the protein levels of MMP2 and MMP9, were upregulated in PAX6-overexpressed Caco-2 and SW480 cells but deregulated in miR-7-overexpressed Caco-2 and SW480 cells. Conclusions: Our study suggests that as a novel target of miR-7, PAX6 may serve as a promising therapeutic target for colorectal cancer. 

Retracted: No

PubPeer comments:
 Fig 6A B: ![file] Figs 3E, 4E from [Huang et al (2013)] : ![file] Figs 2C, 2F, 4E, 4F from [Su et al (2017)] : ![file] Figs 2D, 5C from [Liang et al (2017)] . ![file] Shared panels are marked. UPDATE: Another sighting! Fig 2A from [Liu et al (2017)] . ![] ,
Cellular prion protein modulates age-related behavioral and neurochemical alterations in mice
Authors: C P Figueiredo
F S Duarte
J C Xikota
R D S Prediger
R Walz
A E Schmitz
A L Dafré
D Rial
Journal: Neuroscience (2009)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Prion protein; PrP(C); age-related alterations; behavioral tasks; cognitive processes
Affiliations: Departamento de Farmacologia, UFSC, Florianópolis, SC, Brazil.

Abstract:  The cellular prion protein (PrP(C)) is a neuronal-anchored glycoprotein that has been associated with various functions in the CNS such as synaptic plasticity, cognitive processes and neuroprotection. Here we investigated age-related behavioral and neurochemical alterations in wild-type (Prnp(+/+)), PrP(C) knockout (Prnp(0/0)) and the PrP(C) overexpressing Tg-20 mice. Three- or 11 month-old animals were submitted to a battery of behavioral tasks including open field, activity cages, elevated plus-maze, social recognition and inhibitory avoidance tasks. The 11 month-old Prnp(+/+) and Prnp(0/0) mice exhibited significant impairments in their locomotor activity and social recognition memory and increased anxiety-related responses. Remarkably, Tg-20 mice did not present these age-related impairments. The i.c.v. infusion of STI1 peptide 230-245, which includes the PrP(C) binding site, improved the age-related social recognition deficits in Prnp(+/+). In comparison with the two other age-matched genotypes, the 11 month-old Tg-20 mice also exhibited reduced activity of seric acetylcholinesterase, increased expression of the protein synaptophysin and decreased caspase-3 positive-cells in the hippocampus. The present findings obtained with genetic and pharmacological approaches provide convincing evidence that PrP(C) exerts a critical role in the age-related behavioral deficits in mice probably through adaptive mechanisms including apoptotic pathways and synaptic plasticity. 

Retracted: No

PubPeer comments:
 Fig 3.  Estimation of the percentage of SKOV3 human ovarian carcinoma cells undergoing apoptosis shown by Annexin-V and propidium iodide (PI) staining. ![file] For comparison, *[left]* Fig 4 from [Zeng et al (2019)] .  Annexin V PI staining showing apoptotic CH157-MN cell percentage at indicated concentrations of chrysophanol. *[right]* Figure 1B from [Zhang et al (2018)] .  Metformin induces apoptosis in ovarian cancer cells. ... (B) Apoptosis assay for OVCAR-3 cells treated with metformin as determined by Annexin V PI double staining. ![file] For added comparison, [left] Fig 5B from [Bi et al (2018)] .  Effect of indicated doses of genistein on apoptosis (A) DAPI staining (B) Estimation of apoptotic Mia-PaCa2 cell populations a indicated doses by annexin V PI using flow cytometry . *[right]* Figure 6 from [Zhang et al (2018b)] .  Annexin V PI showing apoptotic cell populations. .. The Figure shows that safranal triggered apoptosis at IC50 (20u03bcu039c). ![] , 
 Retracted [25 January 2021] .  This paper is retracted at the authoru2019s request. , 
 #2 Well, color me skeptical, but could the authors explain what happened here? ,
LncRNA SNHG3 promotes cell proliferation and invasion through the miR-384/hepatoma-derived growth factor axis in breast cancer
Authors: Liang Li
Libo Chen
Xiaona Lin
Wei Hu
Qiuhong Ma
Xiangqin Qi
Journal: Human Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Breast cancer; Invasion; LncRNA SNHG3; Proliferation; miR-384.
Affiliations: Department of Clinical Laboratory, Zibo Central Hospital, Zibo, 255000, China., Department of Ultrasonography, Zibo Central Hospital, Zibo, 255000, China., Department of Breast and Thyroid Surgery, Zibo Central Hospital, Zibo, 255000, China., Zibo City Key Laboratory of Individualized Diagnosis and Transformation of Breast Cancer, Zibo Central Hospital, Zibo, 255000, China., Department of Surgery, Zibo Linzi Traditional Chinese Medicine Hospital, Zibo, 255000, China., Department of Breast and Thyroid Surgery, Zibo Central Hospital, Zibo, 255000, China. ., Zibo City Key Laboratory of Individualized Diagnosis and Transformation of Breast Cancer, Zibo Central Hospital, Zibo, 255000, China. .

Abstract:  Long noncoding RNAs (lncRNAs) have been found to be abnormally expressed in cancer, and lncRNA small nucleolar RNA host genes (SNHGs) play critical roles in tumour progression. SNHG3 has been identified as an oncogene in multiple tumour types. However, the role of SNHG3 in breast cancer has not been reported. In this study, we found that SNHG3 was upregulated and associated with tumour malignancy in patients with breast cancer. SNHG3 knockdown inhibited the growth and metastatic capabilities of breast cancer cells in vitro and vivo. We used bioinformatics prediction and functional assay validation to determine that SNHG3 upregulation inhibited miR-384 activity and led to hepatoma-derived growth factor (HDGF) overexpression in breast cancer cells. The findings of this study show that SNHG3 functions as an oncogene in breast cancer and promotes breast cancer cell proliferation and invasion by regulating the miR-384/HDGF axis. The present study might provide a new target for the treatment of breast cancer. 

Retracted: No

PubPeer comments:
 In Figure 1b and c, the presented data points are very similar. If you flip the illustration in Figure 1b (LM) the distribution of data points at the top is identical with the illustration in Figure 1c (TNM II+III). ![file] ,
Synthesis and characterization of nanoscale dendritic RGD clusters for potential applications in tissue engineering and drug delivery
Authors: Hu Yang
Weiyuan John Kao
Journal: International Journal of Nanomedicine (2007)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Spatial control; RGD peptides; nanoscale clustering; integrins; dendrimers
Affiliations: Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA. 

Abstract:  Spatial control over the distribution and the aggregation of arginine-glycine-aspartate (RGD) peptides at the nanoscale significantly affects cell responses. For example, nanoscale clustering of RGD peptides can induce integrins to cluster, thus triggering complete cell signaling. Dendrimers have a unique, highly branched, nearly spherical and symmetrical structure with low polydispersity, nanoscale size, and high functionality. Therefore, dendrimers are a class of ideal scaffold for construction of nanoscale dendritic RGD clusters in which RGD loading degree and cluster size can be finely adjusted. This new type of nanoscale dendritic RGD cluster will aid us to better understand the impact of spatial arrangement of RGD on cellular responses and to engineer RGD to trigger more favorable cellular responses. In this study, nanoscale dendritic RGD clusters were synthesized based on Starburst anionic G3.5 and cationic G4.0 polyamidoamine (PAMAM) dendrimers. The multiple terminal functional groups on the outermost layer of the dendrimer were coupled with RGD tripeptides. Biofunctionalized dendrimer structures were found to be highly dependent on the generation and the extent of peptide modification (ie, number of peptides per PAMAM dendrimer). Fluorescein isothiocyanate (FITC)-conjugated PAMAM dendrimers were utilized to monitor cellular internalization of dendrimers by adherent fibroblasts. Anionic G3.5-based dendritic RGD clusters have been shown to have no negative effect on fibroblast viability and a concentration-dependent effect on lowering cell adhesion on tissue culture polystyrene (TCPS) as that of free RGD. A similar concentration-dependent effect in cell viability and adhesion was also observed for cationic G4.0-based dendritic RGD clusters at lower but not at high concentrations. The results imply that the synthesized nanoscale dendritic RGD clusters have great potential for tissue engineering and drug delivery applications. 

Retracted: No

PubPeer comments:
 In this study, Ca and boron was used to reduce shoot tip necrosis, using concentration ranges very similar to those already tested 2 years earlier by Abousalim and Mantell (1994), but the 1994 study was not cited. The main u201cfindingsu201d of the 1996 study are thus not u201coriginalu201d. Reference Abousalim A, Mantell SH (1994) A practical method for alleviating shoot-tip necrosis symptoms in in vitro shoot cultures of Pistacia vera cv. Mateur. Journal of Horticultural Science 69:357u2013365. doi: 10.1080 14620316.1994.11516465 ,
SIRT inhibitors induce cell death and p53 acetylation through targeting both SIRT1 and SIRT2
Authors: Paolo Di Fruscia
Chwan-Deng Hsiao
Barrie Peck
Stephen S Myatt
Chun-Yuan Chen
R Charles Coombes
Matthew J Fuchter
Eric W-F Lam
Ka-Kei Ho
Journal: Molecular Cancer Therapeutics (2010)
Discipline: CLINICAL MEDICINE
Keywords: SIRT proteins; tumor cells; drug resistance; chemotherapy; SIRT inhibitors
Affiliations: Cancer Research-UK Laboratory, Department of Surgery and Cancer, MRC Cyclotron Building, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK.

Abstract:  SIRT proteins play an important role in the survival and drug resistance of tumor cells, especially during chemotherapy. In this study, we investigated the potency, specificity, and cellular targets of three SIRT inhibitors, Sirtinol, Salermide, and EX527. Cell proliferative and cell cycle analyses showed that Sirtinol and Salermide, but not EX527, were effective in inducing cell death at concentrations of 50 micromol/L or over in MCF-7 cells. Instead, EX527 caused cell cycle arrest at G(1) at comparable concentrations. In vitro SIRT assays using a p53 peptide substrate showed that all three compounds are potent SIRT1/2 inhibitors, with EX527 having the highest inhibitory activity for SIRT1. Computational docking analysis showed that Sirtinol and Salermide have high degrees of selectivity for SIRT1/2, whereas EX527 has high specificity for SIRT1 but not SIRT2. Consistently, Sirtinol and Salermide, but not EX527, treatment resulted in the in vivo acetylation of the SIRT1/2 target p53 and SIRT2 target tubulin in MCF-7 cells, suggesting that EX527 is ineffective in inhibiting SIRT2 and that p53 mediates the cytotoxic function of Sirtinol and Salermide. Studies using breast carcinoma cell lines and p53-deficient mouse fibroblasts confirmed that p53 is essential for the Sirtinol and Salermide-induced apoptosis. Further, we showed using small interfering RNA that silencing both SIRTs, but not SIRT1 and SIRT2 individually, can induce cell death in MCF-7 cells. Together, our results identify the specificity and cellular targets of these novel inhibitors and suggest that SIRT inhibitors require combined targeting of both SIRT1 and SIRT2 to induce p53 acetylation and cell death. Mol Cancer Ther; 9(4); 844-55. (c)2010 AACR. 

Retracted: No

PubPeer comments:
 Figure 4B. Left SIRT2 and left Tubulin panels look very similar, yet right SIRT2 and right Tubulin panels look quite different. Ac-Tubulin and Tubulin panels do not look like they come from the same blot. Modified and unmodified proteins bands should be superimposable. ![file] ,
Monodispersed palladium–cobalt alloy nanoparticles assembled on poly(N-vinyl-pyrrolidone) (PVP) as a highly effective catalyst for dimethylamine borane (DMAB) dehydrocoupling
Authors: Betül Çelik
Yunus Yıldız
Hakan Sert
Esma Erken
Yagmur Koşkun
Fatih Şen
Journal: RSC Advances (2016)
Discipline: CHEMISTRY
Keywords: fabrication; poly(N-vinyl-2-pyrrolidone); palladium-cobalt nanomaterials; catalysts; dimethylamine-borane dehydrogenation
Affiliations: Sen Research Group, Department of Biochemistry, Faculty of Arts and Science, Dumlupınar University, 43100 Kütahya

Abstract: Herein we report the fabrication of monodispersed poly(N-vinyl-2-pyrrolidone) supported palladium–cobalt nanomaterials (3.45 ± 0.36 nm) and their outstanding efficiency as catalysts in dimethylamine-borane dehydrogenation. By the use of an ultrasonic double reduction method, palladium and cobalt cations were co-reduced in PVP solution and then the prepared nanocatalysts were characterized by UV-Vis, XRD, XPS and HR-TEM-EDX analyses. The nanocatalysts could be easily reused, and at extremely low concentrations and temperature they showed record catalytic activity, giving the best catalytic performance yet with a very high turnover frequency (330.94 h\u22121) and a low Ea value of 50.78 ± 2 kJ mol\u22121 for DMAB dehydrocoupling.

Retracted: Yes

PubPeer comments:
 Fig. 2 XRD of Pd@PVP, Co@PVP and Pdu2013Co@PVP NPs. Low angle part of XRD patterns is identical, the rest is not. Blue pattern has repetition of noise fragments. ![file] , 
 Retraction, October 2021: https: pubs.rsc.org en content articlelanding 2021 ra d1ra90154k  The Royal Society of Chemistry hereby wholly retracts this RSC Advances article due to concerns with the reliability of the data in the published article. The low angle portions of the three XRD spectra in Fig. 2, representing three different materials: Pd@PVP, Co@PVP and Pdu2013Co@PVP NPs, are the same. The blue spectrum representing Co@PVP also has repeating fragments at higher angles. An expert reviewed the authorsu2019 responses but concluded that they did not satisfactorily address the concerns, and that the replacement data provided by the authors did not fully support the conclusions. Given the significance of the concerns about the validity of the data, the findings presented in this paper are no longer reliable. Fatih Sen, Betu00fcl u00c7elik and Hakan Sert oppose this retraction. Esma Erken, Yunus Yu0131ldu0131z and Yagmur Koskun were contacted but did not respond. Signed: Laura Fisher, Executive Editor, RSC Advances Date: 23rd September 2021 ,
JMJD3 regulates CD4 T cell trafficking by targeting actin cytoskeleton regulatory gene Pdlim4
Authors: Mei Luo
Chuntang Fu
Jia Zou
Bingnan Yin
Xin Liu
Changsheng Xing
Junjun Chu
Jiaming Yu
Helen Y Wang
Qingtian Li
Rong-Fu Wang
Journal: Journal of Clinical Investigation (2019)
Discipline: CLINICAL MEDICINE
Keywords: Autoimmunity; Cancer immunotherapy; Cell Biology; Cell migration/adhesion; Cytoskeleton
Affiliations: Institute of Bioscience and Technology, Texas A&M University Health Science Center, Houston, Texas, USA., Center for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, Texas, USA., Xiangya Hospital, Central South University, Changsha, China.

Abstract:  Histone H3K27 demethylase, JMJD3 plays a critical role in gene expression and T-cell differentiation. However, the role and mechanisms of JMJD3 in T cell trafficking remain poorly understood. Here we show that JMJD3 deficiency in CD4+ T cells resulted in an accumulation of T cells in the thymus, and reduction of T cell number in the secondary lymphoid organs. We identified PDLIM4 as a significantly down-regulated target gene in JMJD3-deficient CD4+ T cells by gene profiling and ChIP-seq analyses. We further showed that PDLIM4 functioned as an adaptor protein to interact with S1P1 and filamentous actin (F-actin), thus serving as a key regulator of T cell trafficking. Mechanistically, JMJD3 bound to the promoter and gene body regions of Pdlim4 gene and regulated its expression by interacting with zinc finger transcription factor KLF2. Our findings have identified Pdlim4 as a JMJD3 target gene that affects T-cell trafficking by cooperating with S1P1, and provided insights into the molecular mechanisms by which JMJD3 regulates genes involved in T cell trafficking. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] ,
Targeted proteomics of right heart adaptation to pulmonary arterial hypertension
Authors: Myriam Amsallem
Edda Spiekerkoetter
Julien Guihaire
Maria Rosa Ghigna
Mélanie Lambert
Yuqiang Mao
Jennifer Arthur Ataam
Md Khadem Ali
Vinicio de Jesus Perez
Roham T Zamanian
Florence Lecerf
Marlene Rabinovitch
Elie Fadel
Francois Haddad
Andrew J Sweatt
Olaf Mercier
Journal: European Respiratory Journal (2021)
Discipline: CLINICAL MEDICINE
Keywords: proteomic profiling; right ventricle; pulmonary arterial hypertension; right heart maladaptive phenotype; RHMP
Affiliations: Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA., Vera Moulton Wall Center at Stanford, Stanford University School of Medicine, Stanford, CA, USA., Research and Innovation Laboratory, INSERM U999, Marie Lannelongue Hospital, Paris Sud Saclay University, Le Plessis Robinson, France., Division of Pathology, Marie Lannelongue Hospital, Le Plessis Robinson, France.

Abstract:  No prior proteomic screening study has centred on the right ventricle (RV) in pulmonary arterial hypertension (PAH). This study investigates the circulating proteomic profile associated with right heart maladaptive phenotype (RHMP) in PAH.Plasma proteomic profiling was performed using multiplex immunoassay in 121 (discovery cohort) and 76 (validation cohort) PAH patients. The association between proteomic markers and RHMP, defined by the Mayo right heart score (combining RV strain, New York Heart Association (NYHA) class and N-terminal pro-brain natriuretic peptide (NT-proBNP)) and Stanford score (RV end-systolic remodelling index, NYHA class and NT-proBNP), was assessed by partial least squares regression. Biomarker expression was measured in RV samples from PAH patients and controls, and pulmonary artery banding (PAB) mice.High levels of hepatocyte growth factor (HGF), stem cell growth factor-β, nerve growth factor and stromal derived factor-1 were associated with worse Mayo and Stanford scores independently from pulmonary resistance or pressure in both cohorts (the validation cohort had more severe disease features: lower cardiac index and higher NT-proBNP). In both cohorts, HGF added value to the REVEAL score in the prediction of death, transplant or hospitalisation at 3 years. RV expression levels of HGF and its receptor c-Met were higher in end-stage PAH patients than controls, and in PAB mice than shams.High plasma HGF levels are associated with RHMP and predictive of 3-year clinical worsening. Both HGF and c-Met RV expression levels are increased in PAH. Assessing plasma HGF levels might identify patients at risk of heart failure who warrant closer follow-up and intensified therapy. 

Retracted: No

PubPeer comments:
 Dear authors, Could you please check Fig.4, the WesternBlot images for HGF and TrkA seem more similar than expected, further GAPDH controls of HGF, TrkA and Met seem identical. ![file] ,
Ameliorating effect of eugenol on hyperglycemia by attenuating the key enzymes of glucose metabolism in streptozotocin-induced diabetic rats
Authors: Subramani Srinivasan
Gajendren Sathish
Udaiyar Muruganathan
Jayachandran Muthukumaran
Vinayagam Ramachandran
Mahadevan Jayanthi
Journal: Molecular and Cellular Biochemistry (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: diabetes mellitus; eugenol; antihyperglycemic potential; streptozotocin; key enzymes

Abstract:  Epidemiological studies have demonstrated that diabetes mellitus is a serious health burden for both governments and healthcare providers. This study was hypothesized to evaluate the antihyperglycemic potential of eugenol by determine the activities of key enzymes of glucose metabolism in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced into male albino Wistar rats by intraperitoneal administration of STZ (40 mg/kg body weight (b.w.)). Eugenol was administered to diabetic rats intragastrically at 2.5, 5, and 10 mg/kg b.w. for 30 days. The dose 10 mg/kg b.w. significantly reduced the levels of blood glucose and glycosylated hemoglobin (HbA1c) and increased plasma insulin level. The altered activities of the key enzymes of carbohydrate metabolism such as hexokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, fructose-1,6-bisphosphatase, and liver marker enzymes (AST, ALT, and ALP), creatine kinase and blood urea nitrogen in serum and blood of diabetic rats were significantly reverted to near normal levels by the administration of eugenol. Further, eugenol administration to diabetic rats improved body weight and hepatic glycogen content demonstrated the antihyperglycemic potential of eugenol in diabetic rats. The present findings suggest that eugenol can potentially ameliorate key enzymes of glucose metabolism in experimental diabetes, and it is sensible to broaden the scale of use of eugenol in a trial to alleviate the adverse effects of diabetes. 

Retracted: No

PubPeer comments:
 This paper is one of several from this research group at the Department of Biochemistry and Biotechnology of Annamalai University that report measurements with an unexpectedly narrow range of standard deviations (SDs). Together, these cast serious doubts over the existence of real, replicate measurements in studies by this group. Tables 1 through 5 in this paper together show 92 measurements with SDs. Here, for example, is a screenshot of Table 1. ![file] All SDs are between 7 and 8% of their measurement; with almost all of them between 7.6 and 7.7%. Here is a histogram of the SD percentages, showing an unexpected narrow range of values. ![file] This is a very unusual distribution of SDs in biological measurements. Could the authors please explain? Update: For comparison, here is a collage of 12 papers from other research groups to show the expected range of SDs. All of these use groups of 6 to 8 rats, and do similar measurements. I graphed their SDs in the same way as the graph above, but with the X axis up to 100%. Each of these graphs show a much wider and more even spread of SDs than the graph above. ![file] ,
Hsp27 negatively regulates cell death by interacting with cytochrome c
Authors: C Garrido
L Ravagnan
C Ducasse
C Diaz-Latoud
E Solary
J M Bruey
S A Susin
P Bonniaud
G Kroemer
A P Arrigo
S Gurbuxani
Journal: Nature Cell Biology (2000)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mammalian cells; stress response; heat-shock proteins; Hsp27; apoptosis
Affiliations: INSERM U-517, Faculty of Medicine and Pharmacy, 7 Boulevard Jeanne d'Arc, 21033 Dijon, France.

Abstract:  Mammalian cells respond to stress by accumulating or activating a set of highly conserved proteins known as heat-shock proteins (HSPs). Several of these proteins interfere negatively with apoptosis. We show that the small HSP known as Hsp27 inhibits cytochrome-c-mediated activation of caspases in the cytosol. Hsp27 does not interfere with granzyme-B-induced activation of caspases, nor with apoptosis-inducing factor-mediated, caspase-independent, nuclear changes. Hsp27 binds to cytochrome c released from the mitochondria to the cytosol and prevents cytochrome-c-mediated interaction of Apaf-1 with procaspase-9. Thus, Hsp27 interferes specifically with the mitochondrial pathway of caspase-dependent cell death. 

Retracted: No

PubPeer comments:
 The authors state, in fig. 6, that no differences were found in the tumor in regard to NK and NKT cell percentages, BUT the text gives the opposite story and states that no differences were found in the spleen:  we did not find any changes in the population of the population of CD3u2212 NK1.1+ and CD3+NK1.1+ cells in the spleen of the PSC cotransplanted group (P 0.05) (Figs. 6C and D).  However, our results did not find any changes in the population of NKT cells and NK cells in orthotopic spleen of the mice derived from coinjection of Panc02 cells plus PSCs. The question: what is wrong? the text (results+discussion) or the figure 6 (images+didascaly)? , 
 Thank you for pointing out the mistake. The fig.6 is wrong. We examined our article carefully and found that there was a discrepancy between the image of fig.6 and the description (results+discussion). We made a mistake about the labels on fig.6. As described in the results, fig.6A B represent the population of CD3u2212 NK1.1+ and CD3+NK1.1+ cells in the tumor tissue of tumor-bearing mice and fig.6C D represent the population of CD3u2212 NK1.1+ and CD3+NK1.1+ cells in the spleen. Therefore, the labels of the fig.6 is wrong. We will contact the magazine to correct this mistake as soon as possible. ,
Hypomorphic mutation of PGC-1beta causes mitochondrial dysfunction and liver insulin resistance
Authors: Bruce M Spiegelman
Roberto Coppari
Cheol Soo Choi
Iphigenia Tzameli
Saverio Cinti
Young-Bum Kim
Jiandie Lin
Giorgio Barbatelli
Claudia R Vianna
Bradford B Lowell
Michael Huntgeburth
Gerald I Shulman
Stefan Krauss
Journal: Cell Metabolism (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PGC-1beta; mitochondrial biogenesis; respiration; transcriptional coactivator; ERRalpha
Affiliations: Department of Medicine, Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.

Abstract:  PGC-1beta is a transcriptional coactivator that potently stimulates mitochondrial biogenesis and respiration of cells. Here, we have generated mice lacking exons 3 to 4 of the Pgc-1beta gene (Pgc-1beta(E3,4-/E3,4-) mice). These mice express a mutant protein that has reduced coactivation activity on a subset of transcription factors, including ERRalpha, a major target of PGC-1beta in the induction of mitochondrial gene expression. The mutant mice have reduced expression of OXPHOS genes and mitochondrial dysfunction in liver and skeletal muscle as well as elevated liver triglycerides. Euglycemic-hyperinsulinemic clamp and insulin signaling studies show that PGC-1beta mutant mice have normal skeletal muscle response to insulin but have hepatic insulin resistance. These results demonstrate that PGC-1beta is required for normal expression of OXPHOS genes and mitochondrial function in liver and skeletal muscle. Importantly, these abnormalities do not cause insulin resistance in skeletal muscle but cause substantially reduced insulin action in the liver. 

Retracted: No

PubPeer comments:
 Same blots? ![file] , 
 They are not the same blots. ![file] , 
 Also note that neither clamp insulin levels are reported nor clamp Rd . Striking since there is no difference in glucose infusion rate. Furthermore, the ITTs don t support the clamp data. ![file] , 
 #3 In the context of an euglycemic-hyperinsulinemic clamp the glucose infusion rate indicates whole-body insulin sensitivity. The ITT is also a measure of whole-body insulin sensitivity. In this paper, data shown in Fig. 5B (clamp data) and results shown in Figs. 6A and 6B (ITT data) indicate that the mutant mice have normal whole-body insulin sensitivity. Hence, the ITT data do support the clamp data (or vice versa). , 
 #2 I agree that bands 3 and 5 appear unexpectedly similar. 2 and 4 have been more difficult for me to compare as the contrast has been too difficult for me to equalize. Could the authors please provide the original uncropped scans? *** False color illustration ![file] , 
 Could the authors clarify if gastrocnemius glucose uptake is meant to indicate whole body glucose uptake in the experiments? Figure 5c, shown above by another poster. Thanks. ,
Anti-hyperuricemic and anti-inflammatory actions of vaticaffinol isolated from Dipterocarpus alatus in hyperuricemic mice
Authors: Hui-Ming Ge
Chao-Jun Chen
Yu-Sheng Chen
Ling-Dong Kong
Wei Yan
Journal: Chinese Journal of Natural Medicines (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Anti-hyperuricemic effect; Dipterocarpus alatus; Kidney inflammation; Kidney organic ion transporters; Vaticaffinol.
Affiliations: Institute of Functional Biomolecules, State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210023, China., Institute of Functional Biomolecules, State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210023, China. Electronic address: .

Abstract:  The present study was designed to examine the anti-hyperuricemic and anti-inflammatory effects and possible mechanisms of vaticaffinol, a resveratrol tetramer isolated from ethanol extracts of Dipterocarpus alatus, in oxonate-induced hyperuricemic mice. At 1 h after 250 mg·kg-1 potassium oxonate was given, vaticaffinol at 20, 40, and 60 mg·kg-1 was intragastrically administered to hyperuricemic mice once daily for seven consecutive days. Vaticaffinol significantly decreased serum uric acid levels and improved kidney function in hyperuricemic mice. It inhibited hepatic activity of xanthine dehydrogenase (XDH) and xanthine oxidase (XOD), regulated renal mRNA and protein levels of urate transporter 1 (URAT1), glucose transporter 9 (GLUT9), organic anion transporter 1 (OAT1), organic cation transporter 1 (OCT1), OCT2, organic cation/carnitine transporter 1 (OCTN1), and OCTN2 in hyperuricemic mice. Moreover, vaticaffinol markedly down-regulated renal protein levels of NOD-like receptor 3 (NLRP3), apoptosis-associated speck-like (ASC), and Caspase-1, resulting in the reduction of interleukin (IL)-1β, IL-18, IL-6 and tumor necrosis factor-α (TNF-α) levels in this animal model. Additionally, HPLC and LC-MS analyses clearly testified the presence of vaticaffinol in the crude extract. These results suggest that vaticaffinol may be useful for the prevention and treatment of hyperuricemia with kidney inflammation. 

Retracted: No

PubPeer comments:
 2020 retraction. https: www.sciencedirect.com science article pii S0344033818305351?via%3Dihub This article has been retracted at the request of the Executive Editor (Chairman) as panels from Figures 3A,B and 4D are similar to panels from Figures 4A,B and 5E of the article published by Mingjun Bi, Hongmei Yu, Bin Huang and Cuiyan Tang in Gene 626 (2017) 337u2013343 http: dx.doi.org 10.1016 j.gene.2017.05.049. Also, Figures 3C and 4A are similar to Figures 4C and 5A of the Gene article. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. As such this article represents an abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process. ,
Assessment of the biological pathways targeted by isocyanate using N-succinimidyl N-methylcarbamate in budding yeast Saccharomyces cerevisiae
Authors: Vikash Singh
Raghuvir S Tomar
Gajendra Kumar Azad
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Isocyanates; N-succinimidyl N-methylcarbamate; budding yeast; Saccharomyces cerevisiae; chromatin
Affiliations: Laboratory of Chromatin Biology, Department of Biological Sciences, Indian Institute of Science Education and Research, Bhopal, India.

Abstract:  Isocyanates, a group of low molecular weight aromatic and aliphatic compounds possesses the functional isocyanate group. They are highly toxic in nature hence; we used N-succinimidyl N-methylcarbamate (NSNM), a surrogate chemical containing a functional isocyanate group to understand the mode of action of this class of compounds. We employed budding yeast Saccharomyces cerevisiae as a model organism to study the pathways targeted by NSNM. Our screening with yeast mutants revealed that it affects chromatin, DNA damage response, protein-ubiquitylation and chaperones, oxidative stress, TOR pathway and DNA repair processes. We also show that NSNM acts as an epigenetic modifier as its treatment causes reduction in global histone acetylation and formation of histone adducts. Cells treated with NSNM exhibited increase in mitochondrial membrane potential as well as intracellular ROS levels and the effects were rescued by addition of reduced glutathione to the medium. We also report that deletion of SOD1 and SOD2, the superoxide dismutase in Saccharomyces cerevisiae displayed hypersensitivity to NSNM. Furthermore, NSNM treatment causes rapid depletion of total glutathione and reduced glutathione. We also demonstrated that NSNM induces degradation of Sml1, a ribonucleotide reductase inhibitor involved in regulating dNTPs production. In summary, we define the various biological pathways targeted by isocyanates. 

Retracted: No

PubPeer comments:
 Figure 2E and 2F. Some panels appear to show an overlap. Boxes of the same color draw attention to areas that look quite similar. ![file] , 
 Figure 4E and 4F. Two panels appear to show an overlap. Boxes of the same color draw attention to areas that look quite similar. ![file] , 
 An additional finding for Figure 2E, marked in brown. This might imply that the four panels marked in Figure 2E could all have been derived from the same sample. ![file] Simon White created this video to illustrate the possible original arrangement of the four panels shown in Figure 2E. https: twitter.com simoninthelakes status 1226894194616229890 Screenshot from the video, to which I added green arrows. ![file] ,
Expression analyses of 27 DNA repair genes in astrocytoma by TaqMan low-density array
Authors: Yuquan Jiang
Wei Zhou
Jin Hu
Daru Lu
Zheng Jiang
Xingang Li
Journal: Neuroscience Letters (2006)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: DNA repair systems; mRNA expressions; astrocytoma; TaqMan low-density array; clinical characteristics
Affiliations: Laboratory of Neurosurgery, Qilu Hospital of Shandong University, Jinan 250012, China.

Abstract:  DNA repair systems act to maintain genome integrity in the face of replication errors, environmental insults, and the cumulative effects of age. The mRNA expressions of 27 genes of the DNA repair system as well as their correlation with the clinical characteristics were studied in human astrocytoma. We applied TaqMan low-density array to investigate the mRNA expressions of 27 DNA repair genes in 40 astrocytoma tissues (10 of grade II, 10 of grade III, and 20 of grade IV, according to the WHO Grading System). And the normal brain tissues from 10 non-astrocytoma patients were collected as the control. In addition, correlation of their mRNA levels with clinical characteristics was also analyzed. We found that the expression of the 13 genes were significantly (P&lt;0.01) down-regulated in grade II, III, IV of astrocytoma compared to normal brain tissues, including ERCC1, ERCC2, ERCC3, ERCC4, MGMT, MLH1, MLH3, NTHL1, OGG1, RAD50, SMUG1, XRCC4 and XRCC5. Meanwhile, we found that the expression of MSH2, MSH6, NUDT1 and XRCC3 were only significantly lower in grade II and III of astrocytoma, and the expression of MRE11A and MUS81 were only significantly lower in grade III and IV. But the expression of MPG, MSH3, MUTHY and RAD51 were not changed in any grade of astrocytoma. Furthermore, we found that the decrease expression of eight genes was significantly (P&lt;0.05) associated with a poor prognosis, including ERCC3, ERCC4, MLH3, MRE11A, NTHL1, RAD50, XRCC4 and XRCC5. We suggest that TaqMan low-density array is an effective multivariate technique to examine the expression of DNA repair genes in astrocytomas, which can be applied to identify tumor-specific genes. We also suggest that the down-regulation of some DNA repair genes may be associated with pathogenesis and poor prognosis of astrocytoma. 

Retracted: No

PubPeer comments:
 Figure 3 has a duplication between D and E. ![file] ,
MicroRNA-26b suppresses autophagy in breast cancer cells by targeting DRAM1 mRNA, and is downregulated by irradiation
Authors: Cuida Meng
Zhicheng Wang
Shuchun Liu
Xiaodong Liu
Hongyang Liu
Yang Liu
Lili Jia
Yannan Shen
Qingsheng Ye
Journal: Oncology Letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: DNA damage-regulated autophagy modulator 1; autophagy; breast cancer; microRNA-26b.
Affiliations: Key Laboratory of Radiobiology (Ministry of Health), School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China., Department of Otolaryngology Head and Neck Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China., Medical Ultrasonic Engineering Department, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences, Tianjin 300192, P.R. China.

Abstract:  MicroRNAs (miRs) are small RNAs that do not code for proteins, but instead decrease the stability and suppress the translation of target mRNAs by binding with complementary sequences in their 3'-untranslated regions (3'-UTRs). In the present study, it is reported that breast cancer tumor tissue, as well as irradiated MCF7 breast cancer cells, exhibit decreased levels of miR-26b expression compared with normal breast tissue and MCF7 cells without exposure to radiation. Additionally, a luciferase reporter assay was used to demonstrate that miR-26b directly targetsDNA damage-regulated autophagy modulator 1 (DRAM1). MCF7 cells that were transfected with an miR-26b mimicexhibited the downregulated expression of DRAM1 protein and a reduced level of irradiation-induced autophagy. Inhibiting miR-26b resulted in the upregulation of DRAM1 and increased levels of irradiation-induced autophagy in MCF7 cells. These results suggest that therapeutic strategies to target miR-26b may increase the efficacy of certain types of cancer therapy. 

Retracted: No

PubPeer comments:
 These two image were similar. ![file] , 
 Corrigendum: [12 January 2021] . ----------------------------------------------- Subsequently to the publication of this paper, an interested reader drew to the authorsu2019 attention that a pair of data panels featured in Fig. 2B (specifically, those showing the data from the u2018mimic miR-26b + 4 Gyu2019 and u2018inhibitor miT-26b + 0 Gyu2019 experiments) appeared to be strikingly similar. The authors have re-examined their data, and realized that Fig. 2B was assembled incorrectly (the panel showing the data for the u2018mimic miR-26b + 4 Gyu2019 experiment had been accidentally duplicated in the figure). The revised version of Fig. 2, containing the correct data for the u2018inhibitor miT-26b + 0 Gyu2019 experiment in Fig. 2B, is shown opposite. The authors regret the error that was made in the preparation of the published figure, and confirm that this error did not seriously affect the conclusions reported in the paper. The authors are grateful to the editor of Oncology Letters for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. ![] ,
A TLR9 agonist promotes IL-22-dependent pancreatic islet allograft survival in type 1 diabetic mice
Authors: Padmaja Paidipally
Amy R Tvinnereim
Ramakrishna Vankayalapati
Deepak Tripathi
Satyanarayana S Cheekatla
Elwyn Welch
Sambasivan Venkatasubramanian
Journal: Nature Communications (2016)
Discipline: Multidisciplinary
Keywords: Pancreatic islet transplantation; type 1 diabetes; liver NK1.1+ cells; allograft tolerance; IL-22 production
Affiliations: Department of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health Science Center at Tyler, Tyler, Texas 75708, USA.

Abstract:  Pancreatic islet transplantation is a promising potential cure for type 1 diabetes (T1D). Islet allografts can survive long term in the liver parenchyma. Here we show that liver NK1.1+ cells induce allograft tolerance in a T1D mouse model. The tolerogenic effects of NK1.1+ cells are mediated through IL-22 production, which enhances allograft survival and increases insulin secretion. Increased expression of NKG2A by liver NK1.1+ cells in islet allograft-transplanted mice is involved in the production of IL-22 and in the reduced inflammatory response to allografts. Vaccination of T1D mice with a CpG oligonucleotide TLR9 agonist (ODN 1585) enhances expansion of IL-22-producing CD3-NK1.1+ cells in the liver and prolongs allograft survival. Our study identifies a role for liver NK1.1+ cells, IL-22 and CpG oligonucleotides in the induction of tolerance to islet allografts in the liver parenchyma. 

Retracted: No

PubPeer comments:
 Figure 2B. * Rounded boxes of the same color: Two panels appear to share some data points. ![file]  This work was supported by grants from the National Institutes of Health (AI088201 to R.V., CRDF Global, the Cain Foundation for Infectious Disease Research) and the Department of Pulmonary Immunology. , 
 Thank you very much for your comment. We will investigate this and respond. , 
 In Fig. 2b, the flow cytometry image file from the control group was inadvertently assigned as diabetic and equivalent representative image appeared in control. A correction was sent to the journal. , 
 Thank you, Theope, for sending in the correction. But how to explain the extra dot in the  Control panel (in the bottom left corner of the blue box)? That dot is present in one, but not in the other graph, so this does not seem to be a simple duplication type of error. There appear to be some differences in the lower part of the plots as well. Can you please clarify how these differences can be explained? ,
FVM method based on K − ε model to simulate the turbulent convection of nanofluid through the heat exchanger porous media
Authors: Abu-Hamdeh, Nidal H.
Almitani, Khalid H.
Gari, Abdullatif A.
Alimoradi, Ashkan
Sun, Chuan
Journal: Journal of thermal analysis and calorimetry (2021)
Discipline: CHEMISTRY
Keywords: magnetic field; nanoparticle distribution; heat transfer rate; natural convection; turbulent flow

Abstract: The current study investigates the effect of the magnetic field on nanoparticle distribution and heat transfer rate. The natural convection of turbulent flow is simulated inside two half-cylinders heat exchanger. The cylinders are considered porous, and the boundary conditions are contemplated as constant flux and constant temperature. The simulation follows the k\u2212\u025b turbulent model while utilizes the finite volume method for solving the governing equations. The effects of porous Rayleigh number (Rap), porosity number (η), magnetic number (Mn), and nanoparticle volume fraction (φ) on isothermal counters, nanoparticle distributions, and average Nusselt number are studied. The results outlined that adding nanoparticles declined the heat transfer rate in the absence of a magnetic field. At low Rayleigh numbers, the Nusselt number has a direct relation with Mn number and η, while at higher Ra numbers, although Nu number has a direct connection with η, it has a diverse relation with Mn number. Overall, the results highlighted that the heat transfer rate enhances in the presence of a magnetic field by adding nanoparticles.

Retracted: No

PubPeer comments:
 No REFERENCE for  Equation 6 and  Table 1 ! ![file] ![file] ,