PReD-Bench/PRed-Bench huggingface dataset:
Floralozone Ameliorated Atherosclerosis in Experimental Atherosclerotic Rats Involved with Sphingosine 1-Phosphate 1 Enhancement
Authors: Yu-Ping Yang
He-Yun Zhang
Ping Song
Jian Xu
Ya-Ling Yin
Peng Li
Mo-Li Zhu
Journal: Pharmacology (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Atherosclerosis; Experimental atherosclerotic rat; Fingolimod; Floralozone; Sphingosine 1-phosphate receptor.
Affiliations: College of Pharmacy, Xinxiang Medical University, Xinxiang, China., School of Basic Medical Science, Xinxiang Medical University, Xinxiang, China, .

Abstract:  Atherosclerosis (AS) is a chronical pathological process of the arterial narrows due to the AS plaque formation. The aim of this study was to explore the therapeutic effect and the underlying mechanism of Floralozone on experimental atherosclerotic model rats. Experimental atherosclerotic model rats were induced by the right carotid artery balloon injury and intraperitoneal injection of vitamin D3 in rats after 4 weeks high-fat diet. The results exhibited that Floralozone could ameliorate vascular injury and vasorelaxation of descending aortas and increase the superoxide dismutase activity and the expression of sphingosine 1-phosphate (S1P) 1 and reduce the intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, interleukin (IL)-1, IL-6 level, and the malondialdehyde activity in experimental atherosclerotic rats. However, Fingolimod, an S1P1 inhibitor, could reverse these Floralozone effects in experimental atherosclerotic rats. Our results indicated that Floralozone could inhibit the atherosclerotic plaque formation and improves arterial stenosis and reduces endothelial dysfunction in experimental atherosclerotic rats, which might be involved with S1P1 enhancement. 

Retracted: No

PubPeer comments:
 Figure 4 B. S1P1 receptor images in b and c look like identical ![file] ,
Guanidinium-grafted polyethylenimine: an efficient transfecting agent for mammalian cells
Authors: Ramesh Chandra
Surendra Nimesh
Journal: European Journal of Pharmaceutics and Biopharmaceutics (2008)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Polyethylenimine; gene delivery; guanidinium; cytotoxicity; efficiency
Affiliations: Dr. BR Ambedkar Center for Biomedical Research, University of Delhi, Delhi, India.

Abstract:  Polyethylenimine (PEI) is one of the most efficient polycationic non-viral gene delivery vectors. Its efficiency and cytotoxicity depends on molecular weight, with the 25-kDa PEI being most efficient but accompanied with cytotoxicity. In the present study, enhancement in gene delivery efficiency along with reduction in cytotoxicity by attachment of guanidinium side group was explored. The hypothesis was that the guanidination would lead to the delocalization of charge present on primary amines of the polymer thereby leading to enhancement in gene delivery efficiency along with reduction in cytotoxicity. The polymer was guanidinated using O-methylisourea hemisulfate and the chemical linkage characterized by FTIR spectroscopy. The hydrodynamic diameter of guanidinated PEI-DNA complexes was determined using DLS. Subsequently, these complexes were used for DNA binding assay and zeta-potential measurements, taking native PEI as reference. Further, guanidinated PEI-DNA complexes were investigated for their gene delivery efficacy on HEK 293 cells. The hydrodynamic diameter of guanidinated PEI-DNA complexes was found to be in the range of 176-548 nm. As expected, the zeta potential values increased, on increasing the N/P ratios. It was found that guanidinated PEI had higher transfection efficiency at the majority of the N/P ratios tested as compared to commercially available transfecting agent lipofectin and native PEI itself. The toxicity of guanidinated PEI-DNA complexes was also reduced considerably in comparison to PEI polymer, as determined by MTT colorimetric assay. Out of the various derivatives prepared, gPEI 56% was found to be the most efficient in in vitro transfection. 

Retracted: No

PubPeer comments:
 Unexpected noise repetition. Unusual shape of 2639 cm-1 peak. ![file] ,
B7 costimulation and intracellular indoleamine-2,3-dioxygenase (IDO) expression in peripheral blood of healthy pregnant and non-pregnant women
Authors: Anna Bajnok
Tivadar Tulassay
László Berta
Gábor Veres
János Rigó Jr
László Vécsei
István Ilisz
Gergely Toldi
Enikő Grozdics
Péter Klivényi
Journal: BMC Pregnancy and Childbirth (2014)
Discipline: CLINICAL MEDICINE
Keywords: B7 costimulatory molecules; maternal immune tolerance; indoleamine-2,3-dioxygenase (IDO); tryptophane (TRP); kynurenine (KYN)
Affiliations: First Department of Pediatrics, Semmelweis University, Bókay u, 53-54, Budapest H-1083, Hungary. .

Abstract:  Background: B7 costimulatory molecules are expressed on antigen presenting cells (APCs) and are important regulators of T cell activation. We investigated the role of the B7 family of costimulatory molecules in the development of the systemic maternal immune tolerance during healthy pregnancy (HP). We also aimed to investigate the intracellular expression of indoleamine-2,3-dioxygenase (IDO) and plasma levels of tryptophane (TRP), kynurenine (KYN) and kynurenic acid (KYNA), important molecules with immunoregulatory properties, in order to describe their potential contribution to the pregnancy-specific maternal immune tolerance. Methods: We determined the frequency of activated (CD11b+) monocytes expressing B7-1, B7-2, B7-H1, and B7-H2, and that of T cells and CD4+ T helper cells expressing CD28, CTLA-4, PD-1, and ICOS in peripheral blood samples of healthy pregnant (HP) and non-pregnant (NP) women using flow cytometry. We also examined the intracellular expression of IDO applying flow cytometry and plasma levels of TRP, KYN and KYNA using high-performance liquid chromatography. Results: A significant increase in the prevalence of CD28+ T cells was observed in HP compared to NP women. At the same time a decrease was shown in the expression of CTLA-4 on these cells. The frequency of CD80+ monocytes was lower in HP women. The prevalence of IDO-expressing T cells and monocytes was higher in HP compared to NP women. Plasma KYN, KYNA and TRP levels were lower, while at the same time, the KYN/TRP ratio was higher in HP than in NP women. Conclusions: Costimulation via CD28 may not contribute to the immunosuppressive environment, at least in the third trimester of pregnancy. The development of the pregnancy-specific immune tolerance in the mechanism of B7 costimulation may be more related to the altered expression of B7 proteins on APCs rather than that of their receptors on T cells. The elevated intracellular IDO expression in monocytes and T cells, as well as higher plasma enzymatic IDO activity are likely to contribute to the systemic immunosuppressive environment in the third trimester characteristic for healthy gestation. 

Retracted: No

PubPeer comments:
 BBMT Fig. 1 vs BMCPC Fig. 2 Neither paper cites the other. https: imgur.com a NZVBSyd , 
 #1 The two papers were submitted and reviewed simultaneously. ,
miR-26b modulates OA induced BMSC osteogenesis through regulating GSK3β/β-catenin pathway
Authors: Caiyun Liu
Peiguang Zhang
Zhehai Li
Chuanlong Zhao
Hao Xue
He Hu
Yulian Jiang
Enquan Wu
Yalong Liu
Journal: Experimental and Molecular Pathology (2019)
Discipline: CLINICAL MEDICINE
Keywords: BMSC; DEX; GSK3-β; OA; Osteogenesis
Affiliations: Department of Orthopedics, The Inner Mongolia People's Hospital, Hohhot 010017, Inner Mongolia, PR.China., Department of Orthopedics, Ordos Central Hospital, Ordos 017000, Inner Mongolia, PR.China., Department of Orthopedics, The Third Affiliated Hospital, Inner Mongolia Medical University, Baotou, 014010, Inner Mongolia, PR.China., Department of Orthopedics, Yangling, Demonstration Zone hospital District Hospital Xianyang 712100, Xian, PR.China., Hunan Youcheng Biotechnology Co. Ltd, Changsha, 410000, China., Department of Orthopedics, Beijing Northern Hospital, China North Industries, Beijing 100089, PR.China.; Inner Mongolia Medical University, Hohhot 014010, Inner Mongolia, PR.China.. Electronic address: .

Abstract:  Backgrounds: Osteoactivin (OA) is a key regulator promoting bone marrow stromal cells osteogenesis progress, while Dexamethasone (Dex) could inhibit OA induced osteogenesis and lead to osteoporosis. miR-26b increased during BMSC osteogenesis but whether it participates in this progress is enigma. Osteogenesis is under regulation of canonical Wnt signaling pathway which could serve as potential target for miR-26b. It bears therapeutic potential if miR-26b could regulate osteogenesis and antagonize Dex induced Osteoporosis (OP). Methods: BMSC were isolated from bone marrow of rats and induced for osteogenesis by OA administration. We detected miR-26b mRNA level together with osteogenesis related genes or Wnt signal pathway related genes by qRT-PCR. BMSC cells with miR-26b inhibitor or mimics revealed the effect of miR-26b on osteogenesis. The osteogenesis efficiency was detected by Alizarin Red staining and ALP activity. Protein level of canonical Wnt signal pathway and other proteins were detected by Western blot. The interaction between miR-26b and GSK3β was detected by dual luciferase reporter assay. Results: We found that miR-26b was increased during OA induced BMSC osteogenesis. Inhibiting miR-26b could lead to osteogenesis inhibition while miR-26b mimics could promote this progress. The key regulator of Wnt signal pathway GSK3β is down-regulated when miR-26b was overexpressed, resulting in β-catenin activation. Since Dex could promote GSK3β expression and inhibit Wnt signal, miR-26b could also alleviate Dex induced osteogenesis inhibition. Conclusion: Our findings indicate that miR-26b promoted BMSC osteogenesis by directly targeting GSK3β and activating canonical Wnt signal pathway, suggesting miR-26b might be serve as potential therapeutic candidate of osteoporosis. 

Retracted: No

PubPeer comments:
 Figure 8A appears to have two tumors which are the same but described differently. Of concern: one appears to have been resized and re-colored, and shows one area of difference (cyan). *** ![file] ,
Differentiation Induces Dramatic Changes in miRNA Profile, Where Loss of Dicer Diverts Differentiating SH-SY5Y Cells Toward Senescence
Authors: Aditya Bhushan Pant
Nishant Singh
Devendra Parmar
Parul Singh
Sanjay Yadav
Ankur Kumar Srivastava
Ankita Pandey
Abhishek Jauhari
Tanisha Singh
Journal: Molecular Neurobiology (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Dicer; MicroRNAs; Neuronal differentiation; P53; SH-SY5Y
Affiliations: Developmental Toxicology Laboratory, Systems Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (IITR), Vishvigyan Bhawan, 31 Mahatma Gandhi Marg, Lucknow, UP, 226001, India., Academy of Scientific and Innovative Research (AcSIR), IITR Campus, Lucknow, India., Department of Biochemistry, School of Dental Sciences, Babu Banarasi Das University, Lucknow, India., Developmental Toxicology Laboratory, Systems Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (IITR), Vishvigyan Bhawan, 31 Mahatma Gandhi Marg, Lucknow, UP, 226001, India. .

Abstract:  MicroRNAs (miRNAs) are generated by endonuclease activity of Dicer, which also helps in loading of miRNAs to their target sequences. SH-SY5Y, a human neuroblastoma and a cellular model of neurodevelopment, consistently expresses genes related to neurodegenerative disorders at different biological levels (DNA, RNA, and proteins). Using SH-SY5Y cells, we have studied the role of Dicer and miRNAs in neuronal differentiation and explored involvement of P53, a master regulator of gene expression in differentiation-induced induction of miRNAs. Knocking down Dicer gene induced senescence in differentiating SH-SY5Y cells, which indicate the essential role of Dicer in brain development. Differentiation of SH-SY5Y cells by retinoic acid (RA) or RA + brain-derived neurotrophic factor (BDNF) induced dramatic changes in global miRNA expression. Fully differentiated SH-SY5Y cells (5-day RA followed by 3-day BDNF) significantly (p &lt; 0.05 and atleast &gt;3-fold change) upregulated and downregulated the expression of 77 and 17 miRNAs, respectively. Maximum increase was observed in the expression of miR-193-5p, miR-199a-5p, miR-192, miR-145, miR-28-5p, miR-29b, and miR-222 after RA exposure and miR-193-5p, miR-146a, miR-21, miR-199a-5p, miR-153, miR-29b, and miR-222 after RA + BDNF exposure in SH-SY5Y cells. Exploring the role of P53 in differentiating SH-SY5Y cells, we have observed that induction of miR-222, miR-192, and miR-145 is P53 dependent and expression of miR-193a-5p, miR-199a-5p, miR-146a, miR-21, miR-153, and miR-29b is P53 independent. In conclusion, decreased Dicer level enforces differentiating cells to senescence, and differentiating SH-SY5Y cells needs increased expression of P53 to cope up with changes in protein levels of mature neurons. 

Retracted: No

PubPeer comments:
 ![file] Fig 1b. Different orientation of Nestin band relative to actin and other proteins. , 
 ![file] Fig 5c. P53 band too looks like rotated to show the desired expression. , 
 ![file] ,
Noncanonical autophagy is required for type I interferon secretion in response to DNA-immune complexes
Authors: Miwa Sasai
Akiko Iwasaki
Jill Henault
Anthony J Coyle
Douglas R Green
Eicke Latz
Jane Tian
Roland Kolbeck
Payal Mehta
Miguel A Sanjuan
Melanie M Brinkmann
Jennifer Martinez
Jeffrey M Riggs
Lorraine Clarke
Journal: Immunity (2012)
Discipline: IMMUNOLOGY
Keywords: Toll-like receptor-9; self; pathogenic DNA; autoantibodies; type I interferons
Affiliations: Respiratory, Inflammation and Autoimmunity Research Department, Gaithersburg, MD 20878, USA., Department Immunology, St. Jude Children's Research Institute, Memphis, TN 38105, USA., Department of Antibody Discovery and Protein Engineering MedImmune, Gaithersburg, MD 20878, USA., Department of Immunology, Yale University School of Medicine, New Haven, CT 06520, USA., Institute of Innate Immunity, Biomedical Center, 1G008, University Hospitals, University of Bonn, Sigmund-Freud-Str. 25, 53127 Bonn, Germany., Helmholtz Centre for Infection Research, Inhoffenstrasse 7, 38124 Braunschweig, Germany.

Abstract:  Toll-like receptor-9 (TLR9) is largely responsible for discriminating self from pathogenic DNA. However, association of host DNA with autoantibodies activates TLR9, inducing the pathogenic secretion of type I interferons (IFNs) from plasmacytoid dendritic cells (pDCs). Here, we found that in response to DNA-containing immune complexes (DNA-IC), but not to soluble ligands, IFN-α production depended upon the convergence of the phagocytic and autophagic pathways, a process called microtubule-associated protein 1A/1B-light chain 3 (LC3)-associated phagocytosis (LAP). LAP was required for TLR9 trafficking into a specialized interferon signaling compartment by a mechanism that involved autophagy-related proteins, but not the conventional autophagic preinitiation complex, or adaptor protein-3 (AP-3). Our findings unveil a new role for nonconventional autophagy in inflammation and provide one mechanism by which anti-DNA autoantibodies, such as those found in several autoimmune disorders, bypass the controls that normally restrict the apportionment of pathogenic DNA and TLR9 to the interferon signaling compartment. 

Retracted: No

PubPeer comments:
 Figure 7A: More similar than expected. Could authors check please? ![file] , 
 #1 While similarity level is high, I think that there is no any mistake here. Please see below the cropped image with overexaggerated contrast. ![file] , 
 Perhaps the authors can provide the uncropped original scans to dismiss this concern. ,
Invasive ability of human renal cell carcinoma cell line Caki-2 is accelerated by gamma-aminobutyric acid, via sustained activation of ERK1/2 inducible matrix metalloproteinases
Authors: Yoji Katsuoka
Teruo Inamoto
Takeshi Sakamoto
Haruhito Azuma
Satoshi Kiyama
Yatsugu Kotake
Masahito Watanabe
Takanobu Ubai
Journal: Cancer Investigation (2007)
Discipline: CLINICAL MEDICINE
Keywords: Gamma-aminobutyric acid (GABA); inhibitory neurotransmitter; central nervous system (CNS); cell division; cell differentiation
Affiliations: Department of Urology, Osaka Medical College, Osaka, Japan.

Abstract:  Gamma-aminobutyric acid (GABA) was first discovered as an inhibitory neurotransmitter in the central nervous system (CNS) and has been reported to have a variety of functions, including regulation of cell division, cell differentiation and maturation, and to be involved in the development of certain cancers outside the CNS. In the present study, using the human renal cell carcinoma cell line Caki-2, we demonstrated that GABA stimulation significantly increased the expression of MMP-2 and -9 and subsequently increased the invasive activity of the cancer cells. Because MAPK signaling is one of the key regulators of MMP expression, we further evaluated MAPK signaling after stimulation with GABA. It was found that GABA stimulation promoted the phosphorylation of MAPKs, including ERK1/2, JNK, and p38. ERK1/2 phosphorylation was sustained for up to 12 h, while phosphorylation of JNK and p38 returned to the endogenous level by 30 min. It was noteworthy that the ras/raf/MEK/ERK pathway inhibitor PD98059 attenuated GABA-induced MMP-9 expression and that both PD98059 and MMP inhibitors attenuated the GABA-induced invasive activity of Caki-2 cells. Moreover, data obtained by depletion of the MEK/ERK pathway using interfering RNA transfection of Caki-2 cells clearly corroborated the above results, as both MMP-9 expression and GABA-induced invasive ability were decreased significantly. We also demonstrated that the GABA-induced increase in invasive ability via ERK1/2 up-regulation was mediated mainly through the GABA-B receptor. These results indicate that GABA stimulation promotes cancer cell invasion and that the effect is partly due to ERK1/2-dependent up-regulation of MMPs. 

Retracted: No

PubPeer comments:
 Concerns about Figure 2, reported to the journal in 2015. * Pink boxes: lanes in the p38-P panels appear to look similar * Blue boxes: lanes in the JNK-P panels appear to look similar, albeit 180 degrees rotated * Yellow boxes: two adjacent lanes in the MMP9 panels in Figure 2C appear to look very similar ![file] ,
Glial-derived neurotrophic factor modulates enteric neuronal survival and proliferation through neuropeptide Y
Authors: Mallappa Anitha
Shanthi V Sitaraman
Bindu Chandrasekharan
Eric Grouzmann
Simon Mwangi
Shanthi Srinivasan
Joana R Salgado
Journal: Gastroenterology (2006)
Discipline: CLINICAL MEDICINE
Keywords: GDNF; NPY; enteric neurons; proliferation; survival
Affiliations: Division of Digestive Diseases, Emory University, Whitehead Research Building, 615 Michael Street, Atlanta, GA 30322, USA.

Abstract:  Background &amp; aims: Glial-derived neurotrophic factor (GDNF) promotes the survival and proliferation of enteric neurons. Neuropeptide Y (NPY) is an important peptide regulating gastrointestinal motility. The role of NPY on the survival and proliferation of enteric neurons is not known. We examined the effects of GDNF on the expression and release of NPY from enteric neurons and the role of NPY in promoting enteric neuronal proliferation and survival. Methods: Studies were performed in primary enteric neuronal cultures and NPY knockout mice (NPY(-/-)). GDNF-induced expression of NPY was assessed by reverse-transcription polymerase chain reaction (RT-PCR), immunocytochemistry, and enzyme-linked immunosorbent assay. Using NPY-siRNA and NPY-Y1 receptor antagonist, we examined the role of NPY in mediating the survival and proliferation effects of GDNF. Gastrointestinal motility was assessed by measuring gastric emptying, intestinal transit, and isometric muscle recording from intestinal muscle strips. Results: GDNF induced a significant increase in NPY messenger RNA and protein expression in primary enteric neurons and the release of NPY into the culture medium. NPY (1 mumol/L) significantly increased proliferation of neurons and reduced apoptosis. In the presence of NPY-siRNA and NPY-Y1 receptor antagonist or in enteric neurons cultured from NPY(-/-) mice, GDNF-mediated neuronal proliferation and survival was reduced. NPY increased the phosphorylation of Akt, a downstream target of the PI-3-kinase pathway. In NPY(-/-) mice, there were significantly fewer nNOS-containing enteric neurons compared with wild-type (WT) mice. NPY(-/-) mice had accelerated gastric emptying and delayed intestinal transit compared with WT mice. Conclusions: We demonstrate that NPY acts as an autocrine neurotrophic factor for enteric neurons. 

Retracted: No

PubPeer comments:
 more similar than expected (after horizontal stretch). ![file] , 
 Even thought the paper is almost 15 y o but the high resolution images in the paper are sufficient enough to address this concern. Upon adjusting the contrast and brightness and after zooming and rescaling the two plots there appear to be few differences between the two plots in question. Pl see the attached figure below. The areas marked in red boxes appear to be different in the two plots when compared pixel-to-pixel. It appears that the readings for these two plots might be somewhat identical (in a similar range) but not exactly similar. ![file] ,
Anti-gastric cancer activity in three-dimensional tumor spheroids of bufadienolides
Authors: Lai Wei
Xiuli Zhang
Lala Qu
Liying Shi
Xiaolong Li
Tao Hou
Lijuan Zou
Jixia Wang
Xinmiao Liang
Yun Zhang
Yanfang Liu
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: Multicellular spheroids; cancer cells; anti-tumor compounds; bufadienolides; gastric cancer
Affiliations: Key Lab of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China., Co-innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China., Department of Radiation Oncology, Second Affiliated Hospital of Dalian Medical University, Dalian 116027, China.

Abstract:  Multicellular spheroids of cancer cells have been increasingly used to screen anti-tumor compounds, owing to their in vivo like microenvironment and structure as well as compatibility to high-throughput/high-content screening. Here we report the potency and efficacy of a family of bufadienolides to inhibit the growth of gastric cancer cell line HGC-27 in three-dimensional (3D) spheroidal models. Examining the morphological and growth patterns of several cell lines in round-bottomed ultra-low attachment microplate suggested that HGC-27 cells formed reproducibly multicellular spheroidal structures. Profiling of 15 natural bufadienolides isolated from toad skin indicated that 8 14-hydroxy bufadienolides displayed inhibitory activity of the growth of HGC-27 spheroids in a dose-dependent manner. Notably, compared to clinical drugs taxol and epirubicin, active bufadienolides were found to penetrate more effectively into the HGC-27 spheroids, but with a narrower effective concentration range and a shorter lasting inhibitory effect. Furthermore, compared to two-dimensional (2D) cell monolayer assays, active bufadienolides exhibited weaker efficacy and different potency in 3D spheroid model, demonstrating the great potential of 3D multicellular cell spheroid models in anti-cancer drug discovery and development. 

Retracted: No

PubPeer comments:
 Figure 5C appears to have at least one repeated image. *** Closeup ![file] *** Full figure showing location ![file] ,
Replication of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E is inhibited by the drug FK506
Authors: Javier Carbajo-Lozoya
Christian Drosten
Albrecht von Brunn
Volker Thiel
Stephan Kallies
Marcel A Müller
Journal: Virus Research (2012)
Discipline: MICROBIOLOGY
Keywords: Coronavirus replication; FK506; immunophilin pathways; SARS-CoV; HCoV-NL63
Affiliations: Max-von-Pettenkofer Institute, Ludwig-Maximilians-University (LMU) Munich, Pettenkoferstrasse 9a, 80336 München, Germany.

Abstract:  Recent research has shown that Coronavirus (CoV) replication depends on active immunophilin pathways. Here we demonstrate that the drug FK506 (Tacrolimus) inhibited strongly the growth of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E at low, non-cytotoxic concentrations in cell culture. As shown by plaque titration, qPCR, Luciferase- and green fluorescent protein (GFP) reporter gene expression, replication was diminished by several orders of magnitude. Knockdown of the cellular FK506-binding proteins FKBP1A and FKBP1B in CaCo2 cells prevented replication of HCoV-NL63, suggesting the requirement of these members of the immunophilin family for virus growth. 

Retracted: No

PubPeer comments:
 are these image duplications? ![file] ,
MiRNA-339-5p suppresses the malignant development of gastric cancer via targeting ALKBH1
Authors: Jieyun Zhang
Yakai Huang
Chenchen Wang
Yantian Fang
Journal: Experimental and Molecular Pathology (2020)
Discipline: CLINICAL MEDICINE
Keywords: ALKBH1; Gastric cancer; Malignant development; MiRNA-339-5p.
Affiliations: Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China., Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China; Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China., Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China; Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China. Electronic address: .

Abstract:  Objective: To uncover the role of microRNA-339-5p (miRNA-339-5p) in the development of gastric cancer (GC) and its possible molecular mechanism. Methods: Differential expressions of miRNA-339-5p in GC and adjacent normal tissues were detected. The relationship between miRNA-339-5p level and clinical features in GC patients was analyzed. Proliferative and migratory changes in BGC-823 and SGC-7901 cells overexpressing miRNA-339-5p were examined. Finally, luciferase assay and rescue experiments were conducted to explore the regulatory mechanism of miRNA-339-5p in its downstream gene ALKBH1, and their interaction in the development of GC. Results: MiRNA-339-5p was downregulated in GC tissues. Lowly expressed miRNA-339-5p was unfavorable to prognosis in GC because of high rates of lymphatic metastasis and distant metastasis. Overexpression of miRNA-339-5p markedly reduced proliferative and migratory abilities in GC cells. ALKBH1 was identified to be the downstream gene of miRNA-339-5p. In GC tissues, ALKBH1 was upregulated and negatively correlated to miRNA-339-5p level. Overexpression of ALKBH1 was able to reverse the inhibitory effects of overexpressed miRNA-339-5p on proliferative and migratory abilities in GC. Conclusions: Lowly expressed miRNA-339-5p is closely related to metastasis and poor prognosis in GC patients. MiRNA-339-5p suppresses the malignant development of GC by negatively regulating ALKBH1. 

Retracted: No

PubPeer comments:
 Fig 1C.  Overall survival in GC patients with a high or low level of miRNA-339-5p . ![file] Pairs of Kaplan-Keier plots like this, resembling combs or walls of Lego, are one characteristic feature of a  comb papermill . Products from the papermill are tabulated in a Google spreadsheet: https: docs.google.com spreadsheets d 1_762PbYYTCJhek5PdBuiDuN1q48UDgMa-rT6gi_jA8c edit?usp=sharing Another recurring feature is a Table 1 in which the column heads promise to convert the numbers within each patient subgroup into percentages, but do not deliver. ![file] ,
Iguratimod ameliorates bleomycin‐induced alveolar inflammation and pulmonary fibrosis in mice by suppressing expression of matrix metalloproteinase‐9
Authors: Rongwei Zhou
Like Zhao
Yongjing Cheng
Cibo Huang
Bingyao Mu
Journal: International Journal of Rheumatic Diseases (2019)
Discipline: CLINICAL MEDICINE
Keywords: iguratimod; inflammation MMP-9; pulmonary fibrosis.
Affiliations: Department of Rheumatology, Beijing Hospital, National Center of Gerontology, Beijing, China., Department of Nephrology, Miyun Teaching Hospital of Capital Medical University, Beijing, China., Department of Rheumatology, Shanghai Sixth People's Hospital, Shanghai Jiaotong University, Shanghai, China.

Abstract:  Aim: To investigate the potential therapeutic efficacy of iguratimod (IGU) on bleomycin (BLM)-induced pulmonary fibrosis in mice. Methods: A total of 75 C57BL/6 mice were randomly and evenly divided into control group, BLM (5 mg/kg) group, BLM + IGU (90 mg/kg) group, BLM + methylprednisolone (MP, 10 mg/kg) group and BLM + pirfenidone (PF, 100 mg/kg) group. The mice were sacrificed on day 7, 14 and 28. The lung tissue was examined by hematoxylin and eosin staining and Masson staining to evaluate the degree of alveolitis and fibrosis, and serum cytokines were measured. Results: Histopathological results showed that IGU attenuated BLM-induced alveolar inflammation and decreased collagen deposition in lung tissue from day 7 till day 28. Both the pathological alveolitis and fibrosis scores in the drug-treated groups (IGU group, MP group and PF group) were decreased dramatically compared with the BLM group on day 7, 14 and 28 (P &lt; 0.05). There were no statistical significances among these three groups. Cytokine profile showed that IGU decreased the level of tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-6 and matrix metalloproteinase (MMP)-9 which were up-regulated by BLM on day 7, 14 and 28 (P &lt; 0.05). Furthermore, there is a strong correlation between the severity of pulmonary fibrosis and serum MMP-9 levels. Conclusion: IGU can decrease BLM-induced pulmonary fibrosis, and the anti-fibrotic effect of IGU is mediated partly via inhibition of MMP-9, which suggests that IGU could potentially be an effective therapeutic strategy for pulmonary fibrosis. 

Retracted: No

PubPeer comments:
 Figure 1. Some panels appear to look similar to each other or to overlap. Shown with blue and red boxes. ![file] , 
 An additional finding with the help from a person on Twitter: ![file] ,
Ultrasound and ionic-liquid-assisted synthesis and characterization of polyaniline/Y2O3 nanocomposite with controlled conductivity
Authors: E Kowsari
G Faraghi
Journal: Ultrasonics sonochemistry (2010)
Discipline: CHEMISTRY
Keywords: Sonochemical method; Polyaniline-Y(2)O(3) nanocomposite; Ionic liquid; Polymerization; Nanofibers
Affiliations: Department of Chemistry, Amirkabir University of Technology, No 424, Hafez Avenue, 1591634311 Tehran, Iran. 

Abstract:  A sonochemical method has been employed to prepare polyaniline-Y(2)O(3) nanocomposite with controlled conductivity with the assistance of an ionic liquid (IL). Ultrasound energy and the IL replace conventional oxidants and metal complexes in promoting the polymerization of aniline monomer for the first time. Structural characterization has revealed that the resulting nanocomposite consists of microspheres of average diameter 3-5 microm. The products were found to consist of regular solid microspheres covered with some 40 nm nanoparticles. Under certain polymerization conditions, polyaniline nanofibers and nanosheet were obtained. The method may open a new pathway for the preparation of nanoscale conducting polymer nanocomposites with the aid of ILs. The conductivity of the product varies with the mass ratio of aniline monomer to Y(2)O(3) and IL. TG curves of the products suggest that the thermal degradation process of the PANI/Y(2)O(3) composites proceeds in two steps and that the composites are more thermally stable than pure PANI. The reaction conditions have been optimized by varying parameters such as the aniline/Y(2)O(3) ratio and the type and amount of IL used. The effect of the ultrasonic irritation time and frequency on the morphology, conductivity and yield were discussed. 

Retracted: No

PubPeer comments:
 ![file] Three identical patterns for different samples. ,
Long non-coding RNA LINC01314 represses cell migration, invasion, and angiogenesis in gastric cancer via the Wnt/β-catenin signaling pathway by down-regulating KLK4
Authors: Qiang Li
Min Gong
Ping Wen
Lin Tang
Xing Li
Jian-Bo Wen
Journal: Cancer Cell International (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Angiogenesis; Gastric cancer; Kallikrein 4; Long non-coding RNA LINC01314; Wnt/β-catenin signaling pathway.
Affiliations: Department of Gastroenterology, Jiangxi Pingxiang People's Hospital, No. 8, Wugongshan Middle Road, Pingxiang, 337000 Jiangxi People's Republic of China.

Abstract:  Background: In recent years, gastric cancer (GC) has become a major cause of mortality among various malignancies worldwide with high incidence rates. Long non-coding RNA (lncRNAs) may serve as oncogenes and tumor suppressors in cancers. Therefore, we investigated the effect of LINC01314 on the development of GC cells in relation to the Wnt/β-catenin signaling pathway. Methods: Microarray data analysis was conducted to screen GC-related differentially expressed lncRNAs, followed by determination of the binding interaction between LINC01314 and kallikrein 4 (KLK4). Human GC cell line SGC-7901 was treated with over-expressed or silenced LINC01314 or KLK4 to investigate the mechanism LINC01314 affecting GC cellular activities. The levels of KLK4, Wnt-1, β-catenin, cyclin D1, N-cadherin and E-cadherin were measured, and cell invasion and migration were evaluated. Next, the tumor weight, micro-vessel density (MVD) and the expression of VEGF-C and VEGFR-3 in transplanted tumors were measured. Results: LINC01314 was poorly expressed in GC cells and KLK4 was revealed to be a direct target gene of LINC01314. Overexpressed LINC01314 or silencing of KLK4 led to inhibited GC cell migration and invasion, corresponding to decreased Wnt-1, β-catenin, cyclin D1 and N-cadherin while increased E-cadherin. Also, in response to over-expression of LINC01314 or silencing of KLK4, tumor weight and the MVD of transplanted tumors were reduced and angiogenesis was suppressed, which was indicated by down-regulated positive expression of VEGF-C and VEGFR-3. Conclusion: The findings indicated that over-expression of LINC01314 down-regulated KLK4 to inhibit the activation of the Wnt/β-catenin signaling pathway, thus suppressing migration, invasion, and angiogenesis in GC cells, which provides new insight for the treatment of GC. 

Retracted: No

PubPeer comments:
 Fig 3b,  the grey value of KLK4, Wnt-1, u03b2-catenin, cyclin D1, N-cadherin, E-cadherin, and GAPDH determined by Western blot analysis . ![file] I am intrigued by the absence of background on this WB, and the way the bands remain perfectly linear and retain the shape of the protein blobs as they move up the gel. Is it possible for the authors to upload a scan of the original gel? Numerous other papers have Figures which display the same qualities, hence my curiosity. I compiled a montage: ![] ,
Alternol inhibits proliferation and induces apoptosis in mouse lymphocyte leukemia (L1210) cells
Authors: Jin Zhu
Zhao-Zhe Liu
Shuo Geng
Xia Liu
Chang-Ling Li
Shu Liu
Bo Sun
Journal: Molecular and Cellular Biochemistry (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Alternol; apoptosis; L1210 cells; proliferation; chromatin condensation
Affiliations: Department of Pharmacology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100083, PR China.

Abstract:  Alternol is a novel compound purified from the fermenting products by microorganisms named as Alternaria alternata var. monosporus from the bark of Yew. In this study, we tested its effect on mouse lymphocyte leukemia L1210 cells. Alternol was found to inhibit the proliferation and induce apoptosis in L1210 cells. When the cells were treated with Alternol, chromatin condensation and phosphatidylserine externalization were observed with the down-regulation of the pro-survival gene Bcl-2 and the activation of caspase-3, caspase-9, but not caspase-8. Moreover, exposure of cells to Alternol resulted in a significant increase in reactive oxygen species (ROS) and mitochondrial transmembrane potential (DeltaPsim) depolarization. Taken together, these results demonstrate that Alternol is a potent agent in inducing L1210 cells to apoptosis, which involve caspase activation and ROS generation. 

Retracted: No

PubPeer comments:
 Figure 4. * Red and blue boxes: the Control panels in A and B share similarities Reported to the journal in October 2015, but no response as of today. ![file] ,
PRAS40 is an integral regulatory component of erythropoietin mTOR signaling and cytoprotection
Authors: Yan Chen Shang
Kenneth Maiese
Zhao Zhong Chong
Shaohui Wang
Journal: PLoS ONE (2012)
Discipline: Multidisciplinary
Keywords: mTOR signaling; neurodegenerative disorders; erythropoietin (EPO); SH-SY5Y cell injury; oxidative stress
Affiliations: Laboratory of Cellular and Molecular Signaling, Newark, NJ, USA.

Abstract:  Emerging strategies that center upon the mammalian target of rapamycin (mTOR) signaling for neurodegenerative disorders may bring effective treatment for a number of difficult disease entities. Here we show that erythropoietin (EPO), a novel agent for nervous system disorders, prevents apoptotic SH-SY5Y cell injury in an oxidative stress model of oxygen-glucose deprivation through phosphatidylinositol-3-kinase (PI 3-K)/protein kinase B (Akt) dependent activation of mTOR signaling and phosphorylation of the downstream pathways of p70 ribosomal S6 kinase (p70S6K), eukaryotic initiation factor 4E-binding protein 1 (4EBP1), and proline rich Akt substrate 40 kDa (PRAS40). PRAS40 is an important regulatory component either alone or in conjunction with EPO signal transduction that can determine cell survival through apoptotic caspase 3 activation. EPO and the PI 3-K/Akt pathways control cell survival and mTOR activity through the inhibitory post-translational phosphorylation of PRAS40 that leads to subcellular binding of PRAS40 to the cytoplasmic docking protein 14-3-3. However, modulation and phosphorylation of PRAS40 is independent of other protective pathways of EPO that involve extracellular signal related kinase (ERK 1/2) and signal transducer and activator of transcription (STAT5). Our studies highlight EPO and PRAS40 signaling in the mTOR pathway as potential therapeutic strategies for development against degenerative disorders that lead to cell demise. 

Retracted: No

PubPeer comments:
 Two images in Figure 1A appear to overlap. *** ![file] ,
Apoptotic efficacy and antiproliferative potential of silver nanoparticles synthesised from aqueous extract of sumac ( Rhus coriaria L.)
Authors: Ehsan Karimi
Mozhgan Soltani
Farideh Namvar
Parisa Ghorbani
Masoud Homayouni-Tabrizi
Parichehreh Yaghmaei
Journal: IET Nanobiotechnology (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: nanotechnology; nanoparticles; silver NPs; AgNPs; sumac
Affiliations: Department of BiologyScience and Research branch, Islamic Azad UniversityTehranIran, Institute of Tropical Forestry and Forest Products, University Putra MalaysiaSelangorMalaysia, Mashhad BranchIslamic Azad UniversityMashhadIran, Department of BiologyMashhad BranchIslamic Azad UniversityMashhadIran

Abstract:  Currently, nanotechnology and nanoparticles (NPs) are recognised due to their extensive applications in medicine and the treatment of certain diseases, including cancer. Silver NPs (AgNPs) synthesised by environmentally friendly method exhibit a high medical potential. This study was conducted to determine the cytotoxic and apoptotic effects of AgNPs synthesised from sumac (Anacardiaceae family) fruit aqueous extract (AgSu/NPs) on human breast cancer cells (MCF-7). The anti-proliferative effect of AgSu/NPs was determined by MTT assay. The apoptotic properties of AgSu/NPs were assessed by morphological analysis and acridine orange/propidium iodide (AO/PI) and DAPI staining. The mechanism of apoptosis induction in treated cells was investigated using molecular analysis. Overall results of morphological examination and cytotoxic assay revealed that AgSu/NPs exert a concentration-dependent inhibitory effect on the viability of MCF-7 cells (IC50 of ∼10 µmol/48 h). AO/PI staining confirmed the occurrence of apoptosis in cells treated with AgSu/NPs. In addition, molecular analysis demonstrated that the apoptosis in MCF-7 cells exposed to AgSu/NPs was induced via up-regulation of Bax and down-regulation of Bcl-2. These findings suggested the potential use of AgSu/NP as cytotoxic and pro-apoptotic efficacy and its possible application in modern medicine for treating certain disorders, such as cancer. 

Retracted: No

PubPeer comments:
 Two images in Figure 2b appear to overlap, but are described differently. The scale appears to be different. *** ![file] ,
miR-218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin
Authors: Lei Hou
Xing-Rong Song
Yu-Mei Xiong
Jun-Xiang Huang
Ying-Jun She
Hang Tian
Xiao-Bao Bi
Journal: Oncology Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: microRNA-218; tumor suppressor; tumor progression; development; metastasis
Affiliations: Department of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China., Department of Anesthesiology, Shanxi Cancer Hospital, Taiyuan, Shanxi 030013, P.R. China., Department of Pediatric Emergency, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.

Abstract:  A growing body of evidence suggests that microRNA-218 (miR-218) acts as a tumor suppressor and is involved in tumor progression, development and metastasis and confers sensitivity to certain chemotherapeutic drugs in several types of cancer. However, our knowledge concerning the exact roles played by miR-218 in esophageal squamous cell carcinoma (ESCC) and the underlying molecular mechanisms remain relatively unclear. Thus, the aims of this study were to detect the expression of miR-218 in human ESCC tissues and explore its effects on the biological features and chemosensitivity to cisplatin (CDDP) in an ESCC cell line (Eca109), so as to provide new insights for ESCC treatment. Here, we found increased expression of miR-218 in the ESCC tissues compared with that in the matched non-tumor tissues, and its expression level was correlated with key pathological characteristics including clinical stage, tumor depth and metastasis. We also found that enforced expression of miR-218 significantly decreased cell proliferation, colony formation, migration and invasion, induced cell apoptosis and arrested the cell cycle in the G0/G1 phase, as well as suppressed tumor growth in a nude mouse model. In addition, our results showed that miR-218 mimics increased the sensitivity to the antitumor effect of CDDP in the human Eca109 cells. Importantly, this study also showed that miR-218 regulated the expression of phosphorylated PI3K, AKT and mTOR, which may contribute to suppressed tumor growth of ESCC and enhanced sensitivity of ESCC cells. These findings suggest that miR-218 is a potential therapeutic agent for the treatment of ESCC. 

Retracted: Yes

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A53 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Long non‐coding RNA ZEB1‐AS1 promotes colon adenocarcinoma malignant progression via miR‐455‐3p/PAK2 axis
Authors: Yuting Ding
Wenkang Luan
Xin Ni
Haitao Yuan
Jinmin Shao
Min Xu
Rouyu Guo
Yan Yan
Journal: Cell Proliferation (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: COAD; PAK2; ZEB1-AS1; growth and metastasis; miR-455-3p.
Affiliations: Department of Gastroenterology Affiliated Hospital of Jiangsu University Zhenjiang China, Department of Rehabilitation Changshu No. 2 People's Hospital (The 5th Clinical Medical College of Yangzhou University) Changshu China, Department of General Surgery Affiliated People's Hospital of Jiangsu University Zhenjiang China, Department of Liver Disease Zhenjiang Third People's Hospital Zhenjiang China, Department of Plastic Surgery Affiliated People's Hospital of Jiangsu University Zhenjiang China

Abstract:  Objective: The long non-coding RNA zinc finger E-box-binding homeobox 1 antisense 1 (ZEB1-AS1) acts as an oncogenic regulator in many human tumours. In the present study, we identify the role and potential molecular biological mechanisms of ZEB1-AS1 in colon adenocarcinoma (COAD). Methods: QRT-PCR was used to detect the expression of ZEB1-AS1, miR-455-3p and p21-activated kinases 2 (PAK2) in COAD tissues. CCK8 assay, EdU assay, transwell assay and scratch wound assay were used to explore the biological function of ZEB1-AS1 in COAD cells. Bioinformatics, luciferase reporter assays and an RNA pull-down assay were used to demonstrate the mechanism of ZEB1-AS1. We further explore the role of ZEB1-AS1 in vivo though xenograft tumour assay. Results: We found that ZEB1-AS1 expression was significantly up-regulated in COAD tissues, and high ZEB1-AS1 level was correlated with the poor prognosis of COAD patients. MiR-455-3p plays an anti-cancer role in COAD by targeting PAK2. We confirmed that ZEB1-AS1 promotes PAK2 expression by sponging miR-455-3p, thus facilitating COAD cell growth and metastasis. Conclusions: To sum up, this result illustrates the novel molecular mechanism of ZEB1-AS1 in COAD and provides a new target for the diagnosis and treatment of COAD patients. 

Retracted: No

PubPeer comments:
 Lower right here is the SW480 component of Fig 2(D). Blue boxes show overlap with two panels from Fig 5B of [Luan et al. (2019)] (red and green boxes at top) when they are juxtaposed, suggesting that all three panels are enlarged details of a single transwell image. ![] , 
 #1 This unavoidably busy diagram is an attempt to show similarities between (middle left) Figs 2D, 5C of this paper, and (top left) Fig 5B of [Luan et al. (2019)] ; (bottom left) Figs 4D, 4E of [Luan et al. (2018)] ; (right) Figs 2, 5, 6 of [Luan et al. (2017)] . ![] For simplicity I haven t included overlaps that are unique to the latter three. ,