PReD-Bench/PRed-Bench huggingface dataset:
Hepatocellular carcinoma xenograft supports HCV replication: a mouse model for evaluating antivirals
Authors: Partha K Chandra
Luis A Balart
Henry J Hefler
Feyza Gunduz
Bret Poat
Tara Ooms
Tong Wu
Sidhartha Hazari
Srikanta Dash
Journal: World Journal of Gastroenterology (2011)
Discipline: CLINICAL MEDICINE
Keywords: Antiviral agent; Hepatitis C virus; Hepatocellular carcinoma; Interferon-α; SCID mouse
Affiliations: Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.

Abstract:  Aim: To develop a hepatocellular carcinoma (HCC) xenograft model for studying hepatitis C virus (HCV) replication in a mice, and antiviral treatment. Methods: We developed a stable S3-green fluorescence protein (GFP) cell line that replicated the GFP-tagged HCV sub-genomic RNA derived from a highly efficient JFH1 virus. S3-GFP replicon cell line was injected subcutaneously into γ-irradiated SCID mice. We showed that the S3-GFP replicon cell line formed human HCC xenografts in SCID mice. Cells were isolated from subcutaneous tumors and then serially passaged multiple times in SCID mice by culturing in growth medium supplemented with G-418. The mouse-adapted S3-GFP replicon cells were implanted subcutaneously and also into the liver of SCID mice via intrasplenic infusion to study the replication of HCV in the HCC xenografts. The tumor model was validated for antiviral testing after intraperitoneal injection of interferon-α (IFN-α). Results: A highly tumorigenic S3-GFP replicon cell line was developed that formed subcutaneous tumors within 2 wk and diffuse liver metastasis within 4 wk in SCID mice. Replication of HCV in the subcutaneous and liver tumors was confirmed by cell colony assay, detection of the viral RNA by ribonuclease protection assay and real-time quantitative reverse transcription polymerase chain reaction. High-level replication of HCV sub-genomic RNA in the tumor could be visualized by GFP expression using fluorescence microscopy. IFN-α cleared HCV RNA replication in the subcutaneous tumors within 2 wk and 4 wk in the liver tumor model. Conclusion: A non-infectious mouse model allows us to study replication of HCV in subcutaneous and metastatic liver tumors. Clearance of HCV by IFN-α supports use of this model to test other anti-HCV drugs. 

Retracted: No

PubPeer comments:
 Figure 9. * Red boxes: Two panels representing differently treated mice appear to look similar, but shown in a different color * Blue boxes: Two panels representing differently treated mice appear to look similar, but shown in a different color ![file] ,
α-Galactosylceramide Promotes Killing of Listeria monocytogenes within the Macrophage Phagosome through Invariant NKT-Cell Activation
Authors: Masashi Emoto
Stefan H E Kaufmann
Robert Hurwitz
Ikuo Kawamura
Yoshiko Emoto
Masao Mitsuyama
Tomomi Yoshida
Toshio Fukuda
Eiji Kita
Journal: Infection and Immunity (2010)
Discipline: IMMUNOLOGY
Keywords: alpha-Galactosylceramide; iNKT-cell; macrophages; microbial infections; listeriosis
Affiliations: Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Maebashi, Gunma 371-8511, Japan. , Laboratory of Pathology and Diagnostic Cytology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Gunma 371-8511, Japan, Department of Microbiology, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan, Department of Bacteriology, Nara Medical University, Nara 634-8521, Japan, Core Facilities Biochemistry, Max Planck Institute for Infection Biology, Berlin 10117, Germany, Department of Immunology, Max Planck Institute for Infection Biology, Berlin 10117, Germany, Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Gunma 371-8511, Japan

Abstract:  alpha-Galactosylceramide (alpha-GalCer) has been exploited for the treatment of microbial infections. Although amelioration of infection by alpha-GalCer involves invariant natural killer T (iNKT)-cell activation, it remains to be determined whether macrophages (Mphi) participate in the control of microbial pathogens. In the present study, we examined the participation of Mphi in immune intervention in infection by alpha-GalCer using a murine model of listeriosis. Phagocytic and bactericidal activities of peritoneal Mphi from C57BL/6 mice, but not iNKT cell-deficient mice, were enhanced after intraperitoneal injection of alpha-GalCer despite the absence of iNKT cells in the peritoneal cavity. High levels of gamma interferon (IFN-gamma) and nitric oxide (NO) were detected in the peritoneal cavities of mice treated with alpha-GalCer and in culture supernatants of peritoneal Mphi from mice treated with alpha-GalCer, respectively. Although enhanced bactericidal activity of peritoneal Mphi by alpha-GalCer was abrogated by endogenous IFN-gamma neutralization, this was only marginally affected by NO inhibition. Similar results were obtained by using a listeriolysin O-deficient strain of Listeria monocytogenes. Moreover, respiratory burst in Mphi was increased after alpha-GalCer treatment. Our results suggest that amelioration of listeriosis by alpha-GalCer is, in part, caused by enhanced killing of L. monocytogenes within phagosomes of Mphi activated by IFN-gamma from iNKT cells residing in an organ(s) other than the peritoneal cavity. 

Retracted: No

PubPeer comments:
 ![file] See also an investigation carried out by Gunma University (http: www.gunma-u.ac.jp wp-content uploads 2017 10 chosakekka29.pdf). ,
Serum peptidome based biomarkers searching for monitoring minimal residual disease in adult acute lymphocytic leukemia
Authors: Yun Yang
Chen Huang
Pengyu Zhang
Juan Yang
Yang Zhang
Fuling Zhou
Ju Bai
Jianli Wang
Aili He
Wanggang Zhang
Journal: Proteome science (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Adult acute lymphocytic leukemia; Biomarker; Minimal residual disease; Serum peptidome.
Affiliations: Department of Hematology, Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004 Shaanxi Province China., Department of Genetics and Molecular Biology, Medical school of Xi'an Jiaotong University/Key Laboratory of Environment and Disease-Related Gene, Ministry of Education, Xi'an, 710061 Shaanxi China.

Abstract:  Background: The persistence of minimal residual disease (MRD) during therapy is the strongest adverse prognostic factor in acute lymphocytic leukemia (ALL). This study was to identify serum candidate peptides for monitoring MRD in adult ALL. Results: A total of 33 peptides in the molecular weight range of 1000-10000 Da were detected using ClinProt system and statistically different between adult patients with ALL and healthy controls. Quick classifier (QC) algorithm was used to obtain a diagnostic model consisting of five peptides that could discriminate patients with ALL from controls with a high sensitivity (100%) and specificity (96.67%). The peptides in the QC model were identified as fibrinogen alpha chain (FGA), glutathione S-transferase P1 (GSTP1), isoform 1 of fibrinogen alpha chain precursor, platelet factor 4 (PF4) by high pressure/performance liquid chromatography mass spectrometry/mass spectrometry. Relative intensities of the five peptides were compared among ALL different groups for the potential importance of MRD evaluation in ALL. The peptides with increased relative intensities in newly diagnosed (ND) ALL patients were found to be decreased in their relative intensities after complete remission (CR) of adult ALL. When ALL patients were refractory &amp; relapsed (RR), relative intensities of the peptides were elevated again. Peptides with decreased relative intensities in ND and RR ALL patients were found to be increased in their relative intensities when ALL patients achieved CR. The findings were validated by ELISA and western blot. Further linear regression analyses were performed to eliminate the influence of platelet and white blood cell counts on serum protein contents and indicated that there were no correlations between the contents of all four proteins (PF4, connective tissue active peptide III, FGA and GSTP1) and white blood cell or platelet counts in ALL different groups and healthy control. Conclusions: We speculate the five peptides, FGA, isoform 1 of fibrinogen alpha chain precursor, GSTP1, PF4 and connective tissue active peptide III would be potential biomarkers for forecasting relapse, monitoring MRD and evaluating therapeutic response in adult ALL. 

Retracted: No

PubPeer comments:
 Supplemental Fig. 3C: Contrast enhanced. It looks like a differential splicing in the ELF4 lanes. Could authors check or provide an explanation please? ![file] ,
Mutant p53 in MDA-MB-231 breast cancer cells is stabilized by elevated phospholipase D activity and contributes to survival signals generated by phospholipase D
Authors: Y Zheng
Y Yan
L Hui
D A Foster
J Bargonetti
Journal: Oncogene (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p53; mutant; cancer; tumor suppressor; gain-of-function
Affiliations: Department of Biological Sciences, Hunter College of the City University of New York, New York, NY 10021, USA.

Abstract:  p53 is the most commonly mutated gene in human cancer. Although the loss of tumor suppressor functions for p53 in tumorigenesis is well characterized, gain-of-function p53 mutations observed in most cancers are not as widely appreciated. The human breast cancer cell line MDA-MB-231, which has high levels of a mutant p53, has high levels of phospholipase D (PLD) activity, which provides a survival signal in these cells when deprived of serum growth factors. We report here that the mutant p53 in MDA-MB-231 cells is stabilized by the elevated PLD activity in these cells. Surprisingly, the survival of MDA-MB-231 cells deprived of serum was dependent on the mutant p53. These data indicate that a mutant p53, stabilized by elevated PLD activity, can contribute to the suppression of apoptosis in a human breast cancer cell line and suggest a rationale for the selection of p53 mutations early in tumorigenesis to suppress apoptosis in an emerging tumor. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than expected. ![file] , 
 Figure 4. Much more similar than expected. ![file] ,
Cognitive dysfunction in diabetic rats is prevented by pyridoxamine treatment. A multidisciplinary investigation
Authors: Sarah Kassab
Cleo Chevalier-Riffard
Paul Begley
Andrew W Dowsey
Stephanie J Church
Garth J S Cooper
Leo A H Zeef
Alexander M Phillips
Joanna C Neill
Sanziana M Rotariu
Ben Grayson
Natalie J Gardiner
Richard D Unwin
Journal: Molecular Metabolism (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cognitive decline; Diabetes; Metabolomics; Proteomics; Pyridoxamine
Affiliations: Faculty of Biology, Medicine and Health, University of Manchester, UK., Department of Population Health Sciences and Bristol Veterinary School, Faculty of Health Sciences, University of Bristol, Bristol, BS8 2BN, UK., Department of Electrical Engineering and Electronics, University of Liverpool, UK., Faculty of Biology, Medicine and Health, University of Manchester, UK; School of Biological Sciences, University of Auckland, New Zealand., Faculty of Biology, Medicine and Health, University of Manchester, UK. Electronic address: .

Abstract:  Objective: The impact of diabetes mellitus on the central nervous system is less widely studied than in the peripheral nervous system, but there is increasing evidence that it elevates the risk of developing cognitive deficits. The aim of this study was to characterize the impact of experimental diabetes on the proteome and metabolome of the hippocampus. We tested the hypothesis that the vitamin B6 isoform pyridoxamine is protective against functional and molecular changes in diabetes. Methods: We tested recognition memory using the novel object recognition (NOR) test in streptozotocin (STZ)-induced diabetic, age-matched control, and pyridoxamine- or insulin-treated diabetic male Wistar rats. Comprehensive untargeted metabolomic and proteomic analyses, using gas chromatography-mass spectrometry and iTRAQ-enabled protein quantitation respectively, were utilized to characterize the molecular changes in the hippocampus in diabetes. Results: We demonstrated diabetes-specific, long-term (but not short-term) recognition memory impairment and that this deficit was prevented by insulin or pyridoxamine treatment. Metabolomic analysis showed diabetes-associated changes in 13/82 identified metabolites including polyol pathway intermediates glucose (9.2-fold), fructose (4.9-fold) and sorbitol (5.2-fold). We identified and quantified 4807 hippocampal proteins; 806 were significantly altered in diabetes. Pathway analysis revealed significant alterations in cytoskeletal components associated with synaptic plasticity, glutamatergic signaling, oxidative stress, DNA damage and FXR/RXR activation pathways in the diabetic rat hippocampus. Conclusions: Our data indicate a protective effect of pyridoxamine against diabetes-induced cognitive deficits, and our comprehensive 'omics datasets provide insight into the pathogenesis of cognitive dysfunction enabling development of further mechanistic and therapeutic studies. 

Retracted: No

PubPeer comments:
 There are a number of problems with this paper. The first is with the output of Fig. 5B, which is meaningless, as currently represented. ,
Immunological effect of Moringa Oleifera leaf extract on vaccinated and non-vaccinated Hubbard chickens experimentally infected with Newcastle virus
Authors: Hend A Elakkad
Gamelat Kotb Farag
Hala M N Tolba
Azza Abo Elmaaty
Doaa A Mansou
Journal: Saudi Journal of Biological Sciences (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Broilers; Immunity; Moringa Oleifera; Phagocytic activity; Velogenic Newcastle disease.
Affiliations: Department of Avian and Rabbit Medicine, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt., Department of Pharmacology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt., Department of Virology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt., Department of Biochemistry and Chemistry of Nutrition, Faculty of Veterinary Medicine University of Sadat City, Egypt., Biochemistry Department, Faculty of Agriculture, Zagazig University, Zagazig 44511, Egypt.

Abstract:  In veterinary medicine plant based medicine is achieving a huge importance worldwide. This research was subjected to rectify the hydrophilic Moringa Oleifera alcoholic leaves extract could improve the immune system in vaccinated and non-vaccinated broiler Hubbard chickens experimentally exposed to Newcastle disease (ND) virus. Seventy five chicks with age one day old were splitted randomly into five groups equally in distribution with fifteen chick in each group. Group I was untreated unvaccinated (control negative group) while group IV was infected group with NDV (control positive group). The experimental Groups II and V were given daily oral treatment of hydrophilic alcoholic leaves extract of M. oleifera at 200 mg/kg body weight until day 21 of age while groups III and V were ND vaccinated with La Sota strain of ND vaccines. The four groups (II, III, IV, V) were infected with ND virus velogenic strain (VNDV) on day 21. Following to infection, Monitoring of birds were done daily for clinical signs, postmortem examination, morbidity and mortality. Cellular, humeral immune response and phagocytic activity were evaluated and the data were statistically analyzed using (SPSS). Total and differential cell numbers as well as Haemagglutination inhibition (HI) titre increased in the extract treated and vaccinated group which give total protection against NDV much more than treated and unvaccinated group. As a result it could be recommended to use M. Olifera extract from the first day of rearing in Hubbard chicken with ND vaccination program as a prophylactic treatment in protection of birds against ND infection. 

Retracted: No

PubPeer comments:
 https: twitter.com tinyicybubbles status 1362743531438227457 , 
 https: twitter.com johnhawks status 1362877702122913799 ,
Blockade of Pan-Fibroblast Growth Factor Receptors Mediates Bidirectional Effects in Lung Fibrosis
Authors: Yajuan Chen
Haruka Nishimura
Hisatsugu Goto
Hiroshi Kawano
Yuko Toyoda
Shun Morizumi
Hiroyasu Okazaki
Yasuhiko Nishioka
Hisanori Uehara
Kozo Kagawa
Kazuya Koyama
Hirohisa Ogawa
Seidai Sato
Journal: American Journal of Respiratory Cell and Molecular Biology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: epithelial recovery; fibroblast growth factor; pulmonary fibrosis.
Affiliations: Department of Respiratory Medicine and Rheumatology, and., Department of Pathology and Laboratory Medicine, Graduate School of Biomedical Sciences, Tokushima University, Tokushima, Japan; and., Division of Pathology, Tokushima University Hospital, Tokushima, Japan.

Abstract:  FGFs (fibroblast growth factors) are major factors associated with the pathogenesis of pulmonary fibrosis. On the one hand, nintedanib, a tyrosine kinase inhibitor targeting several growth factor receptors, including the FGF receptor (FGFR), has been approved for the treatment of idiopathic pulmonary fibrosis. On the other hand, recent reports suggest that FGFs are required for epithelial recovery. In this study, we focused on FGF signaling to both fibroblasts and alveolar epithelial cells (AECs), and we examined the effect of a pan-FGFR blocker on experimental pulmonary fibrosis in mice. The effects of BGJ398, a pan-FGFR inhibitor, on the migration and proliferation of fibroblasts and AECs were assessed using Transwell migration or [3H]thymidine incorporation assays. The expression of FGFR was analyzed using IB or flow cytometry. We also investigated the effect of BGJ398 on pulmonary fibrosis induced by bleomycin in mice. Both lung fibroblasts and AECs expressed FGFRs. BGJ398 significantly inhibited the proliferation and migration of lung fibroblasts stimulated with FGF2. BGJ398 also reduced the proliferation of AECs in response to FGF2. Although the administration of BGJ398 ameliorated pulmonary fibrosis in bleomycin-treated mice, it increased mortality resulting from alveolar injury and inhibition of AEC regeneration. These data suggest that the total inhibition of FGFR signaling can suppress lung fibrosis by inhibiting fibroblast activities, although alveolar injury is simultaneously caused. 

Retracted: No

PubPeer comments:
 I don t get the point why duplicating all FIG4 images in the supplement if there are 6 more animals that could be shown for comparison? ![file] ,
Low-Dose Total Body Irradiation Can Enhance Systemic Immune Related Response Induced by Hypo-Fractionated Radiation
Authors: Yue Chen
Peng Wu
Juan Yang
Sheng Lin
ChuanFei Hu
Dong Li
YongXia Cui
Ping Chen
Jie Zhou
Min Wu
Jing Liu
JingBo Wu
ShaoZhi Fu
Journal: Frontiers in Immunology (2019)
Discipline: IMMUNOLOGY
Keywords: hypo-fractionated radiation therapy; immune enhancement; immunosuppressive microenvironment; low-dose total body irradiation; systemic immune related response.
Affiliations: Department of Oncology, The Affiliated Hospital of Southwest Medical University, Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, Luzhou, China., Department of Radiation Oncology, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China., Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, Department of Nuclear Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, China.

Abstract:  A systemic immune related response (SIME) of radiotherapy has been occasionally observed on metastatic tumors, but the clinical outcomes remain poor. Novel treatment approaches are therefore needed to improve SIME ratio. We used a combination of hypo-fractionated radiation therapy (H-RT) with low-dose total body irradiation (L-TBI) in a syngeneic mouse model of breast and colon carcinoma. The combination therapy of H-RT and L-TBI potentially enhanced SIME by infiltration of CD8+ T cell and altering the immunosuppressive microenvironment in non-irradiated subcutaneous tumor lesions. The frequency of IFN-γ, as a tumor-specific CD8+ T cells producing, significantly inhibited the secondary tumor growth of breast and colon. Our findings suggest that L-TBI could serve as a potential therapeutic agent for metastatic breast and colon cancer and, together with H-RT, their therapeutic potential is enhanced significantly. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: I was a long-distance advisor on this project (I ve never met my co-authors, unfortunately!). I can t really critique the clinical parts, but I think there are too many behavioural tasks being used as a battery here. The experimental questions need more focus. ,
MicroRNA-29a inhibits cell migration and invasion by targeting Roundabout 1 in breast cancer cells
Authors: Hui Li
Bin Xu
Kaijun Luo
Juan Hou
Jiashun Luo
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: Epithelial ovarian cancer; miRNAs; miR-137; diagnostic; treatment regimens
Affiliations: Department of Microbiology and Immunology, Medical School of Jishou University, Jishou, Hunan 416000, P.R. China., Institute of Medical Research, Medical School of Jishou University, Jishou, Hunan 416000, P.R. China.

Abstract:  Epithelial ovarian cancer (EOC) remains a major gynecological problem, with a poor 5-year-survival rate due to distant metastases. The identification of microRNAs (miRNAs) may provide a novel avenue for diagnostic and treatment regimens for EOC. Several miRNAs have been reported to be involved in the progression of EOC, among which miRNA (miR)-137 has been observed to be downregulated in the ovarian tissues of patients with EOC. However, the functions of miR-137 in EOC cell apoptosis, migration and invasion remain to be elucidated. In the present study, the expression of miR-137 was measured in clinical ovarian cancer specimens and cell lines using reverse transcription-quantitative polymerase chain reaction. The role of miR-137 in the growth and survival of the SKOV3 human ovarian cancer cell line was determined using several in vitro approaches and in nude mouse models. The results demonstrated that the expression of miR-137 was downregulated in the ovarian cancer specimens and cell lines. It was also observed that enforced expression of miR-137 in the EOC cell lines decreased cell proliferation, clonogenicity, migration and invasion, and induced G1 arrest and cell apoptosis in vitro. Notably, the enforced expression of miR-137 suppressed tumor growth in the nude mice models. These findings suggested that miR-137 may act as a tumor suppressor and be used as a potential therapeutic agent for the treatment of EOC. 

Retracted: No

PubPeer comments:
  **Statistical Analysis** ... 57 PC patients completed follow-up and they were divided into high (n=26) and low (n=31) DGCR5 groups using DGCR5 expression data in PC tissues according to Youdenu2019s index. K-M method and **log-rank t-test** were used to plot and compare survival curves, respectively.  **Low DGCR5 Level in PC Tissues Was Correlated with Poor Survival** ... In this study, 57 PC patients completed follow-up and they were divided into high (n=26) and low (n=31) DGCR5 groups using DGCR5 expression data in PC tissues according to Youdenu2019s index. K-M method and **log-rank t-test** were used to plot and compare survival curves, respectively. It was observed that patients in low DGCR5 groups had a significantly lower 5-year overall survival rate (Figure 2B). The  log rank t test for comparing K-M survival curves is perhaps a garbled form of the  log rank test . ,
Macrophages activating chemokine (C-X-C motif) ligand 8/miR-17 cluster modulate hepatocellular carcinoma cell growth and metastasis
Authors: Zi Yin
Dezhi Li
Zhongshi Wu
Zhixiang Jian
Tingting Ma
Baohua Hou
Jianyu Huang
Journal: American journal of translational research (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CXCL8; hepatocellular carcinoma; macrophages; miR-17 cluster.
Affiliations: Department of General Surgery, Guangdong General Hospital, Guangdong Academy of Medical SciencesGuangzhou, China., Department of Gynaecology and Obstetrics, Sun Yat-sen Memorial Hospital, Sun Yat-sen UniversityGuangzhou, China.

Abstract:  Macrophages are a major component of tumor stroma and the infiltrated macrophages in malignant tumor tissues (as called tumor associated macrophages, TAM) play a pivotal role in hepatocellular carcinoma (HCC) progression. However, the molecular mechanisms of macrophages promoting HCC metastasis are poorly understood. The study was to investigate the effects of macrophages on liver cancer cell proliferation and metastasis through chemokine (C-X-C Motif) Ligand 8 (CXCL8). We found that macrophages activated by co-cultured liver cancer cells produced higher levels of CXCL8, which accelerated cell growth and metastasis. The expression of miR-18a and miR-19a (belonging to miR-17 cluster) increased in HCC cells by CXCL8 simulation and led to the enhancement of HCC cell proliferation and metastasis. In a conclusion, HCC cells and macrophages interaction promoted cancer cell proliferation and metastasis through the up-regulation of CXCL8/miR-17 cluster. 

Retracted: No

PubPeer comments:
 Figure 5E and 5F The survival plots of Fig. 5E 5F are ridiculous. They don t look like normal survival curves.u000b Red boxes: The survival rates were re-elevated? It is impossible for survival curves of overall survival rates.u000b Black box: Double-lines existed in a survival curve. The author claimed that the survival curves were plotted by the Kaplan-Meier method, but how could double-lines appear in a curve for one group of patient ?u000b Brown box: Smear mark. ![file] , 
 Thank you very much for your concern and help. After receiving your comments, we quickly re- investigated all the original data. We found that it was due to the negligence of a graduate student who was responsible for this part of data statistics at that time. Because the previous statistical method of survival analysis was wrong, it simply connected the survival time curve of patients, and did not use Kaplan Meier plot to show, resulting in the survival plot in the original paper turned into a curve, rather than a broken line that should be presented. Therefore, in the process of this correction, we conducted survival statistics again. A Kaplan-Meier plot is used to analyze the survival curves and a log-rank test is used to compare the survival curves, at this time. At present, image correction is in progress for the Journal. We guarantee that the results of the Corrigendum are consistent with those in the original paper and will not affect the overall conclusion of the paper. ,
Nanostructured metal coatings on polymers increase osteoblast attachment
Authors: Chang Yao
Dan Storey
Thomas J Webster
Journal: International Journal of Nanomedicine (2007)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Bioactive coatings; osteoblast adhesion; orthopedic polymeric materials; Ionic Plasma Deposition; nanostructure
Affiliations: Division of Engineering, Brown University, 184 Hope Street, Providence, RI 02912, USA.

Abstract:  Bioactive coatings are in high demand to increase the functions of cells for numerous medical devices. The objective of this in vitro study was to characterize osteoblast (bone-forming cell) adhesion on several potential orthopedic polymeric materials (specifically, polyetheretherketone, ultra-high molecular weight polyethylene, and polytetrafluoroethylene) coated with either titanium or gold using a novel Ionic Plasma Deposition process which creates a surface-engineered nanostructure (with features below 100 nm). Results demonstrated that compared to currently-used titanium and uncoated polymers, polymers coated with either titanium or gold using Ionic Plasma Deposition significantly increased osteoblast adhesion. Qualitative cell morphology results supported quantitative adhesion results as increased osteoblast cell spreading was observed on coated polymers compared to uncoated polymers. In this manner, this in vitro study strongly suggests that Ionic Plasma Deposition should be further studied for creating nanometer surface features on a wide variety of materials to enhance osteoblast functions necessary for orthopedic applications. 

Retracted: No

PubPeer comments:
 Could the authors comment on what appear to be some repeated features? ![file] , 
 Fig. 7. Gel electrophoresis pattern showing cleavage of pBR322 supercoiled DNA (10 u03bcM) in the presence of AH2 (100 u03bcM). Lane 1: DNA control (10 u03bcM); lane 2: CuCl2 (100 u03bcM); lane 3: CoCl2 (100 u03bcM); lane 4: DNA+ [L1] (50 u03bcM) + AH2; lane 5: DNA + [L2] (50 u03bcM) + AH2; lane 6: DNA + 1 (50 u03bcM) + AH2; lane 7: DNA + 2 (50 u03bcM) + AH2; lane 8: DNA + 5 (50 u03bcM) + AH2; lane 9: DNA + 6 (50 u03bcM) + AH2. ![file] All the Form-III letterboxes seem to be vertically-compressed versions of the corresponding Form-II letterboxes. Is this normal? ,
Examining the effect of gene reduction in miR-95 and enhanced radiosensitivity in non-small cell lung cancer
Authors: X-d Li
W Ma
Y-j Zhang
C-n Ma
Journal: Cancer gene therapy (0)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; lung cancer treatment; non-small cell lung cancer; miRNA profiling; radiosensitivity
Affiliations: Department of Respiratory, Huaihe Hospital of Henan University, Kaifeng, China.

Abstract:  MicroRNAs (miRNAs) represent a group of novel therapeutic small molecules involved in the management of lung cancer treatment. Our study aims to investigate the potential role of miRNAs in the treatment of non-small cell lung cancer (NSCLC). Human miRNA microarray was performed in 60 recurrent NSCLC patient tissue samples following radiotherapy and their adjacent normal tissues. miRNA profiling results were validated using quantitative real-time PCR. Inner cell radiosensitivity and endogenous miRNA expression was determined by colony-formation assay and RT-PCR. We determined the effect of miRNA on cell proliferation, survival and metastasis; tumor xenografts were taken to identify the presence of miRNA in vivo. miRNA panel results indicated that a total of 14 miRNAs were differentially expressed in the recurrent NSCLC samples. In our study, miRNA-95 was highly overexpressed in recurrent NSCLC cells. Knockdown of miRNA-95 expression increased the radiosensitivity of NSCLC, promoted tumor cell apoptosis and decreased cellular proliferation. In vivo assays demonstrated reduced tumor growth and resistance to radiation in tumor xenografts by downregulating miRNA-95. Our study demonstrated a potential therapeutic measure of miRNA-95 as a radiosensitive marker for the treatment of non-small lung cancer. 

Retracted: No

PubPeer comments:
 The falsification in Figure 4b must be characterized as rather foolish, but apparently not foolish enough for peer-reviewer and editors at Cancer Gene Therapy. ![file] , 
 More than two years since reporting: no response from the authors. To embarrassing to address? ,
Antidepressant-like effects of the saponins extracted from Chaihu-jia-longgu-muli-tang in a rat unpredictable chronic mild stress model
Authors: Chang-Liang Xu
Jie Yang
Xiu-Min Li
Jie Lu
Lu-Fan Li
Shi-Ping Ma
Rong Qu
Journal: Fitoterapia (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Chaihu-jia-longgu-muli-tang; Saponins; Antidepressant-like effect; Chronic mild stress; Behavior tests
Affiliations: Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, 210009, PR China.

Abstract:  Chaihu-jia-longgu-muli-tang (CLM) has been used for treating depressive disorders for thousands of years in China. In the present study, we investigated the antidepressant-like effect of the saponins extracted from CLM (SCLM) in rats subjected to unpredictable chronic mild stress (UCMS). The ameliorative effect of SCLM on symptom of depression through behavior tests including: sucrose preference test, open-field test and forced-swimming test was investigated. In addition, high performance liquid chromatography with electrochemical detection (HPLC-ECD), immunohistochemical staining analysis and RT-PCR were applied to explore the mechanisms underlying the antidepressant-like effects of SCLM. It was observed that administration of SCLM (70, 140 mg/kg) reversed the depressive-like behaviors, restored the reduction in the levels of monoamine neurotransmitters and up-regulated the expression of brain-derived neurotrophic factor (BDNF) in UCMS-treated rats. These findings confirmed the antidepressant-like effects of SCLM in UCMS model of rats. 

Retracted: No

PubPeer comments:
 Figure 15a,b,c appear to have images which overlap. *** ![file] *** Full figure ![file] ,
Autoantibodies against muscarinic receptors in breast cancer: their role in tumor angiogenesis
Authors: María Pía Negroni
María Eugenia Azar
Gabriel L Fiszman
María Ester Castro
Carlos Cresta Morgado
María Elena Sales
María Gabriela Lombardi
Laura Tatiana Pelegrina
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: autoantibodies; breast cancer; muscarinic acetylcholine receptors; IgG; T1N0Mx stage
Affiliations: Laboratorio de Inmunofarmacología Tumoral, Centro de Estudios Farmacológicos y Botánicos (CEFYBO)-CONICET, UBA, Buenos Aires, Argentina.

Abstract:  The presence of autoantibodies in cancer has become relevant in recent years. We demonstrated that autoantibodies purified from the sera of breast cancer patients activate muscarinic acetylcholine receptors in tumor cells. Immunoglobulin G (IgG) from breast cancer patients in T1N0Mx stage (tumor size≤2 cm, without lymph node metastasis) mimics the action of the muscarinic agonist carbachol stimulating MCF-7 cell proliferation, migration and invasion. Angiogenesis is a central step in tumor progression because it promotes tumor invasion and metastatic spread. Vascular endothelial growth factor-A (VEGF-A) is the main angiogenic mediator, and its levels have been correlated with poor prognosis in cancer. The aim of the present work was to investigate the effect of T1N0Mx-IgG on the expression of VEGF-A, and the in vivo neovascular response triggered by MCF-7 cells, via muscarinic receptor activation. We demonstrated that T1N0Mx-IgG (10(-8) M) and carbachol (10(-9) M) increased the constitutive expression of VEGF-A in tumor cells, effect that was reverted by the muscarinic antagonist atropine. We also observed that T1N0Mx-IgG and carbachol enhanced the neovascular response produced by MCF-7 cells in the skin of NUDE mice. The action of IgG or carbachol was reduced in the presence of atropine. In conclusion, T1N0Mx-IgG and carbachol may promote VEGF-A production and neovascularization induced by breast tumor cells via muscarinic receptors activation. These effects may be accelerating breast tumor progression. 

Retracted: No

PubPeer comments:
 Figure 1 and 2. * Blue arrows: Sharp vertical background transitions * Red boxes: A GAPDH panel in Figure 1A (supernatant MCF-7 cells) looks similar to a GAPDH panel in Figure 2A (lysate MCF-7 cells) * Blue boxes: A GAPDH panel in Figure 1B (lysate MCF-10A cells) looks similar to a GAPDH panel in Figure 2A (lysate MCF-7 cells + T1N0Mx-IgG) * Green boxes: A VEGF-A panel in Figure 1A (supernatant MCF-7 cells) looks similar to a VEGF-A panel in Figure 2A (lysate MCF-7 cells) ![file] ,
Ebola Virus Neutralizing Antibodies in Dogs from Sierra Leone, 2017
Authors: Bashiru Koroma
Thomas Strecker
Juliet Jabaty
Roland Suluku
Kerstin Fischer
Sarah Katharina Fehling
Sandra Diederich
Martin H Groschup
Journal: Emerging Infectious Diseases (2020)
Discipline: IMMUNOLOGY
Keywords: Ebola virus; Sierra Leone; dogs; neutralizing antibodies; serology

Abstract:  Ebola virus (EBOV) is a highly pathogenic zoonotic virus for which the reservoir host has not been identified. To study the role of dogs as potential hosts, we screened 300 serum samples from dogs in Sierra Leone and found EBOV neutralizing antibodies in 12, suggesting their susceptibility to natural infection. 

Retracted: No

PubPeer comments:
 These serological studies for EBOV desperately need control groups. It s just too easy to have unexplained cross-reaction or cross-neutralization. Past studies have found no filovirus RNA and have found antibodies in dogs in locations with no identified human cases. In this study some of the dogs weren t even alive during the EBOV epidemic yet they tested positive. It s possible this reflects cryptic transmission, but the more likely explanation, which needs much more work to rule out, is cross-reaction. ,
LncRNA CYTOR attenuates sepsis‐induced myocardial injury via regulating miR‐24/XIAP
Authors: Chongyang Ye
Chunyan Zhu
Ting Chen
Journal: Cell Biochemistry and Function (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CYTOR; XIAP; cardiac injury; miR-24; sepsis.
Affiliations: Intensive Care Unit, The Second People's Hospital of Heifei Hefei China, Intensive Care Unit, Anhui Provincial Hospitalthe First Affiliated Hospital of University of Science and Technology of China, Heifei China

Abstract:  This work aims to investigate the function and mechanism of long non-coding RNA (lncRNA) cytoskeleton regulator RNA (CYTOR) in myocardial injury induced by sepsis. The sepsis-induced myocardial injury model in mice was established by intraperitoneal injection of LPS (10 mg/kg) in vivo, and cardiomyocyte H9c2 was treated with LPS to mimic sepsis in vitro. CYTOR expression and miR-24 expression were detected by qRT-PCR. After up-regulation or down-regulation of CYTOR and miR-24 expression in the H9c2 cells, and the viability of the cells was detected via MTT assay, and cell apoptosis was detected by TUNEL assay. Western blot was applied to determine the expression level of caspase 3, Bax and X-chromosome-linked inhibitor of apoptosis (XIAP). Interaction between CYTOR and miR-24 was determined by bioinformatics analysis, RT-PCR and dual luciferase reporter assay. Interaction between miR-24 and XIAP was determined through bioinformatics analysis, RT-PCR, western blot and dual luciferase reporter assay. CYTOR was markedly down-regulated. CYTOR interacted with miR-24, and negatively regulated its expression level. Over-expression of CYTOR or transfection of miR-24 inhibitors significantly promoted viability and inhibited apoptosis of H9c2 cells, while the knockdown of CYTOR and transfection of miR-24 mimics had opposite effects. CYTOR suppressed the expression level of apoptosis-related proteins, but miR-24 increased them. miR-24 directly targeted the 3'UTR of XIAP, and suppressed it, and XIAP was modulated indirectly by CYTOR. Down-regulation of CYTOR aggravates sepsis-induced cardiac injury via regulating miR-24 and XIAP. 

Retracted: No

PubPeer comments:
 The authors state in the **Materials and Methods section**: ![file] I refer the authors to a H9c2 [description ] ![file] https: www.lgcstandards-atcc.org products all CRL-1446.aspx?geo_country=gr Could the authors explain this discrepancy? A correction to proceed with is the logical route to take. ,
MALAT1 recruited the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation and participated in trophoblast migration and invasion
Authors: Xiaofang Yi
Qian Liu
Cuifang Fan
Biheng Cheng
Lianzhi Wu
Journal: Journal of Cellular Physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CRY2; FBXW7; MALAT1; recurrent spontaneous abortion; trophoblast.
Affiliations: Department of Obstetrics, Renmin Hospital of Wuhan University, Wuhan, Hubei, China., Reproductive Medical CenterRenmin Hospital of Wuhan UniversityWuhan Hubei China, Department of ObstetricsRenmin Hospital of Wuhan UniversityWuhan Hubei China, Department of Reproductive MedicineRenmin Hospital of Wuhan UniversityWuhan Hubei China

Abstract:  This study aimed to investigate the mechanism by which MALAT1 regulates CRY2 expression and participates in trophoblast migration and invasion. Three patients with unexplained recurrent spontaneous abortion, four patients with missed abortion, and four women who underwent artificial miscarriages were enrolled in this study. Quantitative reverse-transcription polymerase chain reaction and western blot analysis were used to detect RNA and protein expression, respectively. Trophoblast migration and invasion were detected by wound-healing and transwell invasion assays. RNA pull-down and Co-IP assays were used to indicate the interaction between MALAT1 and FBXW7 or the interaction between FBXW7 and CRY2. The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens. MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. MALAT1 recruited FBXW7 to impair CRY2 protein stability. In conclusion, MALAT1 downregulation in trophoblasts might be related to miscarriage. MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation and participate in trophoblast migration and invasion. 

Retracted: No

PubPeer comments:
 Figure 1C. * Red boxes: The Bmi-1 and TRIM-14 panels appear to show a large area of overlap. ![file] ,
Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line
Authors: I Levi
B Schwartz
D Benharroch
M Barshishat
Journal: British Journal of Cancer (2002)
Discipline: CLINICAL MEDICINE
Keywords: CD44; metastasis; butyrate; transcription; epidermal growth factor
Affiliations: Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100 Israel.

Abstract:  Over-expression of the adhesion molecule CD44 and its splice variants, especially CD44v6, is associated with poor prognosis and metastasis. We aimed at regulating the expression of CD44 in the highly metastatic human colon cancer cell line HM7 and thereby affecting its metastatic ability. HM7 cells show constitutive expression of CD44 standard and variants isoforms, which were significantly down-regulated by treatment with butyrate. Butyrate significantly inhibited transcription of the CD44 gene and abolished epidermal growth factor-mediated up-regulation of the reporter gene luciferase subcloned upstream to the CD44 promoter (-1.1 kb) and transfected to HM7 cells. Nuclear proteins from butyrate-treated cells bound to an epidermal growth factor receptor element motif present in the CD44 promoter. Epidermal growth factor receptor element-site directed mutations eliminated the inducibility of the luciferase reporter gene and did not allowed binding of nuclear proteins harvested from butyrate-treated cells. Butyrate induced CD44 gene repression by specifically interacting with an epidermal growth factor receptor element nuclear transcriptional factor. This interaction affects CD44 transcriptional activity vis-à-vis in vivo metastatic ability of HM7 cells. These results provide additional insight into the anticarcinogenic properties of butyrate. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: The bottom parts of four lanes in panels D and E look similar to each other, minus a black dot. Image made a bit darker to show more details. ![file] ,
Acupuncture protected cerebral multi-infarction rats from memory impairment by regulating the expression of apoptosis related genes Bcl-2 and Bax in hippocampus
Authors: Jing-Xian Han
Jian-Chun Yu
Cun-Zhi Liu
Wen Jiang
Tong Wang
Journal: Physiology & behavior (2009)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Vascular dementia; acupuncture; memory impairment; apoptosis; Bcl-2
Affiliations: Molecular Biology Laboratory, Acupuncture and Moxibustion Research Institute, the First Hospital affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.

Abstract:  Vascular dementia (VaD) is the second most common cause of dementia in the world today. In this paper, we observed the effect of acupuncture on memory impairment, apoptosis and expression of Bcl-2 and Bax in hippocampus of cerebral multi-infarction rats. The results indicated that acupuncture significantly improved memory impairment induced by cerebral multi-infarction, as evaluated by shortened escape latency and increased swimming time in the target quadrant. Meanwhile, based on the observation in hippocampal CA1 region through methods of the terminal deoxynucleotidyl transferase nick end labeling (TUNEL), immunohistochemistry and in situ hybridization, acupuncture decreased the number of apoptotic cells and expression of the proapoptotic Bax gene, on the contrary, it increased expression of the antiapoptotic gene Bcl-2. The result of the research suggested that acupuncture can exert antiapoptotic effect through counter-regulating Bcl-2 and Bax gene expression. 

Retracted: No

PubPeer comments:
 Figure 6. * Blue boxes: The impaired group panel appears to show an overlap with the placebo-acup group panel. ![file] ,
ATR affecting cell radiosensitivity is dependent on homologous recombination repair but independent of nonhomologous end joining
Authors: Y Wang
George Iliakis
Ya Wang
Huichen Wang
Hongyan Wang
Simon N Powell
Journal: Cancer research (2004)
Discipline: CLINICAL MEDICINE
Keywords: ATR; DNA damage; ionizing radiation; DNA double-strand breaks; homologous recombination repair
Affiliations: Department of Radiation Oncology, Kimmel Cancer Center of Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

Abstract:  ATR is one of the most important checkpoint proteins in mammalian cells responding to DNA damage. Cells defective in normal ATR activity are sensitive to ionizing radiation (IR). The mechanism by which ATR protects the cells from IR-induced killing remains unclear. DNA double-strand breaks (DSBs) induced by IR are critical lesions for cell survival. Two major DNA DSB repair pathways exist in mammalian cells: homologous recombination repair (HRR) and nonhomologous end joining (NHEJ). We show that the doxycycline (dox)-induced ATR kinase dead (ATRkd) cells have the similar inductions and rejoining rates of DNA DSBs compared with cells without dox induction, although the dox-induced ATRkd cells are more sensitive to IR and have the deficient S and G(2) checkpoints. We also show that the dox-induced ATRkd cells have a lower HRR efficiency compared with the cells without dox induction. These results indicate that the effects of ATR on cell radiosensitivity are independent of NHEJ but are linked to HRR that may be affected by the deficient S and G(2) checkpoints. 

Retracted: No

PubPeer comments:
 Article retracted. http: retractionwatch.com 2019 10 08 materials-scientist-will-soon-be-up-to-30-retractions ,