PReD-Bench/PRed-Bench huggingface dataset:
Structural Diversity of Zinc(II), Manganese(II), and Gadolinium(III) Coordination Polymers Based on Two Isomeric N-Heteroaromatic Polycarboxylate Ligands: Structures and Their Derived Mn2O3 for Lithium Storage Applications
Authors: Jia Lin
Jincheng Liu
R Chenna Krishna Reddy
Hong Deng
Xiaoming Lin
Journal: Inorganic Chemistry (2020)
Discipline: CHEMISTRY
Keywords: coordination polymers; isomeric ligands; structural analysis; network topology; interpenetrated structure
Affiliations: School of Environment and Energy, South China University of Technology, Guangzhou, Guangdong 510006, P.R. China, Key Laboratory of Theoretical Chemistry of Environment, Ministry of Education, School of Chemistry, South China Normal University, Guangzhou, Guangdong 510006, P.R. China, EVE Energy Company Limited, Huizhou, Guangdong 516006, P.R. China

Abstract:  Tuning the coordination sites of two isomeric semirigid ligands, 5-(4-pyridin-3-yl-benzoylamino)isophthalic acid (3-H2PBI) and 5-(4-pyridin-4-yl-benzoylamino)isophthalic acid (4-H2PBI), afforded six new coordination polymers (CPs), [Zn(3-PBI)(H2O)]n (1), {[Mn2(3-PBI)2(H2O)]·DMF·2H2O}n (2), {[Gd2(3-PBI)3(H2O)3]·DMF·3H2O}n (3), {[Zn2(4-PBI)2]·H2O}n (4), {[Mn2(4-PBI)2(H2O)2]·4H2O}n (5), and {(Me2NH2)[Gd(4-PBI)2]·H2O}n (6). Structural analysis shows that 1 consists of 2D honeycomb (6,3) net, three sets of networks interlace mutually, generating an unexpected 2D + 2D + 2D → 3D polycatenating interesting system. 2 exhibits a 3D pcu topology. 3 presents a unique 3D with 3,3,6T13 network topology. 4 possesses 3D 2-fold interpenetrated structure with rutile topology. 5 presents an alluring 2D architecture comprising two distinct topologies (kgd and hcb), stacked arrangement in an unexpected ABBABB mode. 6 displays 2D (4,4)-grid network. A differentiation of these structural features indicate that coordination connectivity of metals, together with binding modes of two ligands are accountable for the fascinating structural contrast. In addition, 2 and 5 were then transformed into Mn2O3 via a simple heat treatment. Electrochemical test results show that both of the obtained Mn2O3 moieties exhibit stable lithium storage properties and excellent rate capabilities. 

Retracted: No

PubPeer comments:
 The Gd complex (compound **3** in the paper) has exactly the same unit-cell parameters as for an Eu complex reported one year earlier in another journal (compound **4** in the *J. Solid State Chem*. paper). Although both complexes are structurally related, such a coincidence is very unlikely to occur for a triclinic cell. Even standard deviations are identical. Original cif files may be downloaded from the CSD database, with deposition codes [CCDC-1961926] (*Inorg. Chem*.) and [CCDC-1859214] (*J. Solid State Chem*.) Please could the authors check where the error lies? ![file] ,
Foot-and-Mouth Disease Virus 3A Protein Causes Upregulation of Autophagy-Related Protein LRRC25 To Inhibit the G3BP1-Mediated RIG-Like Helicase-Signaling Pathway
Authors: Xiangtao Liu
Lulu Li
Jingjing Ren
Yi Ru
Jing Zhang
Wenping Yang
Juncui Bai
Dan Li
Haixue Zheng
Journal: Journal of Virology (2020)
Discipline: MICROBIOLOGY
Keywords: 3A; FMDV; G3BP1; LRRC25; autophagy.
Affiliations: State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China., OIE/National Foot and Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China., State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China .

Abstract:  Foot-and-mouth disease virus (FMDV) is one of the most notorious pathogens in the global livestock industry. To establish an infection, FMDV needs to counteract host antiviral responses. Several studies have shown how FMDV suppresses the type I interferon (IFN) response; however, whether FMDV modulates the integrated autophagy and innate immunity remains largely unknown. Here, the porcine Ras-GAP SH3-binding protein 1 (G3BP1) was shown to promote the retinoic acid-inducible gene I (RIG-I)-like helicase (RLH) signaling by upregulating the expression of RIG-I and melanoma differentiation-associated gene 5 (MDA5). FMDV nonstructural protein 3A interacted with G3BP1 to inhibit G3BP1 expression and G3BP1-mediated RLH signaling by upregulating the expression of autophagy-related protein LRRC25. In addition, 3A proteins of other picornaviruses, including Seneca Valley virus (SVV) 3A, enterovirus 71 (EV71) 3A, and encephalomyocarditis virus (EMCV) 3A, also showed similar actions. Taking the data together, we elucidated, for the first time, a novel mechanism by which FMDV has evolved to inhibit IFN signaling and counteract host innate antiviral responses by autophagy.IMPORTANCE We show that foot-and-mouth disease virus (FMDV) 3A inhibits retinoic acid-inducible gene I (RIG-I)-like helicase signaling by degrading G3BP1 protein. Furthermore, FMDV 3A reduces G3BP1 by upregulating the expression of autophagy-related protein LRRC25. Additionally, other picornavirus 3A proteins, such as Seneca Valley virus (SVV) 3A, enterovirus 71 (EV71) 3A, and encephalomyocarditis virus (EMCV) 3A, also degrade G3BP1 by upregulating LRRC25 expression. This study will help us improve the design of current vaccines and aid the development of novel control strategies to combat FMD. 

Retracted: No

PubPeer comments:
 After viral infection, G3BP1 was cleaved? or why the molecular weight is different? ![file] , 
 Thanks for your interesting in our study. In agreement with your comment, G3BP1was indeed cleaved during FMDV infection. ,
Hypothalamic ERK mediates the anorectic and thermogenic sympathetic effects of leptin
Authors: Kamal Rahmouni
Allyn L Mark
William G Haynes
Curt D Sigmund
Journal: Diabetes (2009)
Discipline: CLINICAL MEDICINE
Keywords: Leptin; ERK; hypothalamus; STAT3; PI 3-kinase
Affiliations: Center on Functional Genomics of Hypertension, Department of Internal Medicine, University of Iowa, Iowa City, Iowa, USA. 

Abstract:  Objective: Leptin is an adipocyte hormone that plays a major role in energy balance. Leptin receptors in the hypothalamus are known to signal via distinct mechanisms, including signal transducer and activator of transcription-3 (STAT3) and phosphoinositol-3 kinase (PI 3-kinase). Here, we tested the hypothesis that extracellular signal-regulated kinase (ERK) is mediating leptin action in the hypothalamus. Research design and methods: Biochemical, pharmacological, and physiological approaches were combined to characterize leptin activation of ERK in the hypothalamus in rats. Results: Leptin activates ERK1/2 in a receptor-mediated manner that involves JAK2. Leptin-induced ERK1/2 activation was restricted to the hypothalamic arcuate nucleus. Pharmacological blockade of hypothalamic ERK1/2 reverses the anorectic and weight-reducing effects of leptin. The pharmacological antagonists of ERK1/2 did not attenuate leptin-induced activation of STAT3 or PI 3-kinase. Blockade of ERK1/2 abolishes leptin-induced increases in sympathetic nerve traffic to thermogenic brown adipose tissue (BAT) but does not alter the stimulatory effects of leptin on sympathetic nerve activity to kidney, hindlimb, or adrenal gland. In contrast, blockade of PI 3-kinase prevents leptin-induced sympathetic activation to kidney but not to BAT, hindlimb, or adrenal gland. Conclusions: Our findings indicate that hypothalamic ERK plays a key role in the control of food intake, body weight, and thermogenic sympathetic outflow by leptin but does not participate in the cardiovascular and renal sympathetic actions of leptin. 

Retracted: No

PubPeer comments:
 Both wild-type ISG15 and mutant ISG15 (LRLRAA) could mediate the degradation of RIG-I (N) by LRRC25 in MAVS KO cells (Fig. 5F), suggesting that non-covalent ISG15 promotes the degradation of RIG-I mediated by LRRC25. But, the interaction between RIG-I (N) and p62 was completely abolished in the absence of ISG15 (Fig.5G). ![file] , 
 The p-IRF is very significant in 16h, the non-p IRF3 can not be similar, there should be some difference. ![file] , 
 The IP protein should be coreelated with lysates. ![file] ,
Xanthoxyletin Inhibits Proliferation of Human Oral Squamous Carcinoma Cells and Induces Apoptosis, Autophagy, and Cell Cycle Arrest by Modulation of the MEK/ERK Signaling Pathway
Authors: Hong Yang
Weiguo Liao
Haiyan Huang
Kai Luo
Qingquan Wen
Journal: Medical Science Monitor (2019)
Discipline: CLINICAL MEDICINE
Keywords: xanthoxyletin; oral squamous cancer cells; apoptosis; autophagy; cell cycle arrest
Affiliations: Department of Head and Neck Oncology Surgery, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, Guangdong, China (mainland)., The Research Institute, Cancer Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China (mainland)., Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, Guangdong, China (mainland).

Abstract:  BACKGROUND This study aimed to investigate the effects of xanthoxyletin, a plant-derived coumarin, on human oral squamous cancer cells in vitro and in mouse xenografts in vivo. MATERIAL AND METHODS The study included SCC-1 human oral cancer cells and EBTr normal embryonic bovine tracheal epithelial cells, which were treated with 0 µM, 5 µM, 10 µM, and 20 µM of xanthoxyletin for 24 hours. The MTT assay assessed cell viability, and autophagy was detected by electron microscopy. Cell apoptosis was investigated using 4',6-diamidino-2-phenylindole (DAPI), annexin V, and propidium iodide (PI) fluorescence flow cytometry, which was also used to investigate the cell cycle. Protein expression was measured by Western blot. Mouse xenografts were used for the in vivo evaluation of the effects of xanthoxyletin. RESULTS Xanthoxyletin significantly inhibited the proliferation of oral cancer cells (IC₅₀, 10-30 µM) with lower cytotoxicity for normal cells. Xanthoxyletin treatment was associated with G2/M arrest of the cell cycle and with increased apoptosis and autophagy of SCC-1 cells. Apoptosis and autophagy induced by xanthoxyletin were also associated with changes in expression of the apoptosis-associated proteins, Bax and Bcl-2, and the autophagy-associated proteins, LC3I, LC3II, Beclin 1, p62, and VSp34. Xanthoxyletin inhibited the expression of components of the signaling cascade of the MEK/ERK pathway in the SCC-1 oral cancer cells. The in vivo effects of xanthoxyletin showed inhibition of growth of mouse xenografts. CONCLUSIONS Xanthoxyletin inhibited the proliferation of human oral squamous carcinoma cells and induced apoptosis, autophagy, and cell cycle arrest by modulation of the MEK/ERK signaling pathway. 

Retracted: Yes

PubPeer comments:
 There appears to be an image duplication of the western blots in figure 3. The actin bands seem to be identical, even though they represent samples from different regions (hippocampus and PFC). The authors may want to go back and double check their blots (and perhaps upload uncropped images). Placement: ![file] Closer look: ![file] ,
Blockade of LINC01605-enriched exosome generation in M2 macrophages impairs M2 macrophage-induced proliferation, migration, and invasion of human dermal fibroblasts
Authors: Liang Peng
Xiongxiang Zhu
Songying Gao
Zhensen Zhu
Bo Chen
Jingdong Guo
Journal: International Journal of Immunopathology and Pharmacology (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: AKT1; LINC01605; exosomes derived from M2 macrophages; hypertrophic scar; miR-493-3p.
Affiliations: Department of Plastic and Burn Surgery, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China

Abstract:  Activated M2 macrophages are involved in hypertrophic scar (HS) formation via manipulating the differentiation of fibroblasts to myofibroblasts having the proliferative capacity and biological function. However, the function of exosomes derived from M2 macrophages in HS formation is unclear. Thus, this study aims to investigate the role of exosomes derived by M2 in the formation of HS. To understand the effect of exosomes derived from M2 macrophages on formation of HS, M2 macrophages were co-cultured with human dermal fibroblast (HDF) cells. Cell Counting Kit-8 assay was performed to evaluate HDF proliferation. To evaluate the migration and invasion of HDFs, wound-healing and transwell invasion assays were performed, respectively. To investigate the interaction between LINC01605 and miR-493-3p, a dual-luciferase reporter gene assay was adopted; consequently, an interaction between miR-493-3p and AKT1 was detected. Our results demonstrated that exosomes derived from M2 macrophages promoted the proliferation, migration, and invasion of HDFs. Additionally, we found that long noncoding RNA LINC01605, enriched in exosomes derived from M2 macrophages, promoted fibrosis of HDFs and that GW4869, an inhibitor of exosomes, could revert this effect. Mechanistically, LINC01605 promoted fibrosis of HDFs by directly inhibiting the secretion of miR-493-3p, and miR-493-3p down-regulated the expression of AKT1. Exosomes derived from M2 macrophages promote the proliferation and migration of HDFs by transmitting LINC01605, which may activate the AKT signaling pathway by sponging miR-493-3p. Our results provide a novel approach and basis for further investigation of the function of M2 macrophages in HS formation. 

Retracted: No

PubPeer comments:
 I am concerned about several overlapping images in this paper. Figure 1: ![file] Figure 3 ![file] Figure 5: ![file] ,
Nature Neuroscience offers open access publishing
Authors: Nat Neurosci
Journal: Nature Neuroscience (2022)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: authors; primary research papers; journal; freely available; publication.

Abstract: The authors of primary research papers accepted by our journal have the opportunity to make their work freely available to all upon publication.

Retracted: No

PubPeer comments:
 https: twitter.com MarcCoutanche status 1350072745409748996 , 
 https: twitter.com AJKowaltowski status 1481217198777643010 , 
 https: twitter.com sTeamTraen status 1481215255128727558 ,
PLGA-based dual targeted nanoparticles enhance miRNA transfection efficiency in hepatic carcinoma
Authors: Yan Zhou
Xianming Kong
Hongmei Liu
Yanan Zhao
Chenlei Cai
Xiaojing Chen
Peifeng Liu
Dejun Liu
Liangliang Wu
Hanbing Zou
Yuexia Xie
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Hepatic carcinoma; gene therapy; microRNA-99a; nanoparticles; targeting properties
Affiliations: Central Laboratory, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China., State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200032, China., Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.

Abstract:  Hepatic carcinoma (HCC) is a lethal disease associated with high morbidity and poor prognosis. Recently years, gene therapies have offered novel modalities to improve the prognosis of HCC patients. MicroRNA-99a (miR-99a) is frequently down-regulated in HCC, where it acts as a tumor suppressor. Therefore, we constructed monomethoxy (polyethylene glycol)-poly(D,L-lactide-co-glycolide)-poly(L-lysine)-lactobionic acid- anti-vascular endothelial growth factor antibody (mPEG-PLGA-PLL-LA/VEGFab or PEAL-LA/VEGFab) nanoparticles (NPs) with highly specific targeting properties as carriers to restore the expression of miR-99a both in vitro and in vivo, to inhibit HCC progression. In vitro, PEAL-LA/VEGFab NPs showed more efficient delivery of miR-99a to HepG2 cells than the conventional transfection reagent LipofectamineTM2000 (Lip2000). The higher delivery efficiency associated with PEAL-LA/VEGFab NPs consequently resulted in down-regulation of target genes and suppression of the proliferation, migration and invasion of HepG2 cells. In vivo, miR-99a-PEAL-LA/VEGFab NPs inhibited tumor xenograft growth in HCC-bearing mice without causing obvious systemic toxicity. Our results demonstrate that PEAL-LA/VEGFab NPs selectively and effectively deliver miR-99a to HCC cells based on the double-targeting character of these nanoparticles, thereby offering potential for translation into effective clinical therapies for HCC. 

Retracted: No

PubPeer comments:
 Figure B appears to include two images that overlap. Roughly indicated with red boxes. *** ![file] , 
 #1 Per an editor at the journal: u201dI am writing to update you that, having seen the original data from for this figure, and corresponded with the author, we shall be publishing a correction to address what seems to have been a genuine error.u201d , 
 Correction published April 20, 2020 ![file] ,
TGFbeta influences Myc, Miz-1 and Smad to control the CDK inhibitor p15INK4b
Authors: J Seoane
M Schader
P Staller
J Massagué
M Eilers
C Pouponnot
Journal: Nature Cell Biology (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Transforming growth factor-beta; TGFbeta; epithelial cell division; c-myc; cyclin-dependent kinase inhibitors
Affiliations: Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA.

Abstract:  Transforming growth factor-beta (TGFbeta) is a cytokine that arrests epithelial cell division by switching off the proto-oncogene c-myc and rapidly switching on cyclin-dependent kinase (CDK) inhibitors such as p15INK4b. Gene responses to TGFbeta involve Smad transcription factors that are directly activated by the TGFbeta receptor. Why downregulation of c-myc expression by TGFbeta is required for rapid activation of p15INK4b has remained unknown. Here we provide evidence that TGFbeta signalling prevents recruitment of Myc to the p15INK4b transcriptional initiator by Myc-interacting zinc-finger protein 1 (Miz-1). This relieves repression and enables transcriptional activation by a TGFbeta-induced Smad protein complex that recognizes an upstream p15INK4b promoter region and contacts Miz-1. Thus, two separate TGFbeta-dependent inputs - Smad-mediated transactivation and relief of repression by Myc - keep tight control over p15INK4b activation. 

Retracted: No

PubPeer comments:
 Figure 7b. https: imgur.com lASrQ61 ,
miR-139 Functions as An Antioncomir to Repress Glioma Progression Through Targeting IGF-1 R, AMY-1, and PGC-1β
Authors: Xi-Tuan Ji
Shi-Wen Guo
Hong Wang
Ping Wang
San-Zhong Li
Xi Yan
Li-Ya Ji
Journal: Technology in Cancer Research & Treatment (2017)
Discipline: CLINICAL MEDICINE
Keywords: AMY-1; IGF-1 R; PGC-1β; glioma; miR-139
Affiliations: 1 Department of Neurosurgery, the First Affiliated Hospital of Xi'an Jiaotong, University College of Medicine, Xi'an, China., 3 Department of Internal Medicine, Xi'an Dongfang Hospital., 4 Department of Neurology, the Affiliated Xi'an Central Hospital of Xi'an Jiaotong, University College of Medicine, Xi'an, China., 5 Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China., 2 Department of Neurosurgery, the Affiliated Xi'an Central Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, China.

Abstract:  Gliomas are the most common primary malignant brain tumor with poor prognosis, characterized by a highly heterogeneous cell population, extensive proliferation, and migration. A lot of molecular mechanisms regulate gliomas development and invasion, including abnormal expression of oncogenes and variation of epigenetic modification. MicroRNAs could affect cell growth and functions. Several reports have demonstrated that miR-139 plays multifunctions in kinds of solid tumors through different pathways. However, the antitumor mechanisms of this miR-139 are not unveiled in detail. In this study, we not only validated the low expression level of miR-139 in glioma tissues and cell lines but also detected the effect of miR-139 on modulating gliomas proliferation and invasion both in vitro and in vivo. We identified insulin-like growth factor 1 receptor, associate of Myc 1, and peroxisome proliferator-activated receptor γ coactivator 1β as direct targets of miR-139 and the levels of them were all inversely correlated with miR-139 in gliomas. Insulin like growth factor 1 receptor promoted gliomas invasion through Akt signaling and increased proliferation in the peroxisome proliferator-activated receptor γ coactivator 1β-dependent way. Associate of Myc 1 also facilitated gliomas progression by activating c-Myc pathway. Overexpression of the target genes could retrieve the antitumor function of miR-139, respectively, in different degrees. The nude mice transplantation tumor experiment displayed that glioma cells stably expressed miR-139 growth much slower in vivo than the negative control cells. Taken together, these findings suggested miR-139 acted as a favorable factor against gliomas progression and uncovered a novel regulatory mechanism, which may provide a new evidenced prognostic marker and therapeutic target for gliomas. 

Retracted: No

PubPeer comments:
 Figure 3 and figure 7 appear to have some duplications ![file] ![file] ,
Expression of Bim, Noxa, and Puma in non-small cell lung cancer
Authors: Hirotoshi Dosaka-Akita
Masaharu Nishimura
Junko Kikuchi
Ichiro Kinoshita
Hidenori Mizugaki
Eiki Kikuchi
Satoshi Oizumi
Jun Sakakibara-Konishi
Journal: BMC Cancer (2012)
Discipline: CLINICAL MEDICINE
Keywords: BH3-only proteins; Bim; Noxa; Puma; apoptosis
Affiliations: First Department of Medicine, Hokkaido University School of Medicine, North 15, West 7, Kita-ku, Sapporo, 060-8638, Japan. 

Abstract:  Background: The BH3-only members of the Bcl-2 protein family have been proposed to play a key role in the control of apoptosis and in the initiation of the apoptotic pathways. In this study, we evaluated the expression of Bim, Noxa, and Puma in non-small cell lung cancer (NSCLC). Methods: A total of 135 surgically resected NSCLCs were immunohistochemically assessed for Bim, Noxa, and Puma expression. The immunoscores were determined, and then its correlation with either the clinicopathological variables or the survival outcomes were analyzed. Results: Immunohistochemical reactivity for Bim, Noxa, and Puma was detected in the cytoplasm of the tumor cells. Bim expression was associated with several clinicopathological factors, including sex (p &lt; 0.001), smoking habit (p = 0.03), pathological histology (p = 0.001), pathological T stage (p = 0.03), pathological disease stage (p = 0.02), and differentiation of tumor (p &lt; 0.001). Multivariate logistic regression analysis showed a significant correlation between low Bim expression and squamous cell carcinoma (p = 0.04), in addition to a correlation between high Bim expression and well differentiated tumors (p = 0.02). Analysis of cellular biological expression demonstrated a link between low Bim expression and high Ki67. While Noxa expression was also shown to be correlated with both smoking habit (p = 0.02) and the pathological histology (p = 0.03), there was no strong association observed between the expression and the clinical features when they were examined by a multivariate logistic regression analysis. No correlations were noted between Puma expression and any of the variables. Our analyses also indicated that the expression levels of the BH3-only proteins were not pertinent to the survival outcome. Conclusions: The current analyses demonstrated that Bim expression in the NSCLCs was associated with both squamous cell carcinoma histology and tumor proliferation. 

Retracted: No

PubPeer comments:
 case 1 and 3 cannot show the same microscopic image ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
MiRNA-96 accelerates the malignant progression of ovarian cancer via targeting FOXO3a
Authors: N Yang
Q Zhang
X-J Bi
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miRNA-96; ovarian cancer; malignant progression; FOXO3a; clinical parameters
Affiliations: Department of Gynecology, The Centre Hospital Weinan, Weinan, China. .

Abstract:  Objective: To clarify the potential function of miRNA-96 in accelerating the malignant progression of ovarian cancer (OC) and its underlying mechanism. Patients and methods: The expression patterns of miRNA-96 in 36 matched OC tissues and adjacent normal tissues were determined by qRT-PCR. We analyzed the correlation between the miRNA-96 level and the clinical parameters of OC patients. Subsequently, the cellular levels of miRNA-96 in OC cell lines were determined as well. To construct miRNA-96 inhibitor and NC, the regulatory effects of miRNA-96 on the proliferative and migratory abilities in OC cells were examined. The target gene of miRNA-96 was verified by Dual-Luciferase Reporter Gene Assay. Finally, the rescue experiments were conducted to clarify the regulatory role of miRNA-96/FOXO3a axis in the malignant progression of OC. Results: MiRNA-96 was upregulated in OC tissues relative to adjacent normal ones. Compared with OC patients presenting high-level of miRNA-96, those with low-level miRNA-96 suffered more advanced tumor staging and a worse overall survival. The transfection of miRNA-96 inhibitor markedly attenuated proliferative and migratory abilities in SKOV3 and CAOV3 cells. In addition, FOXO3a was identified to be the target gene of miRNA-96, which was negatively regulated by miRNA-96. FOXO3a exerted a lower abundance in OC tissues relative to adjacent normal ones. Finally, the rescue experiments revealed that FOXO3a knockdown could abolish the inhibitory role of miRNA-96 knockdown in the proliferative, migratory, and invasive abilities in OC cells. Conclusions: The knockdown of miRNA-96 attenuated the proliferative and migratory abilities in OC cells by targeting FOXO3a. We believed that miRNA-96 accelerates the malignant progression of OC, which could be utilized as a therapeutic target in clinical application. 

Retracted: No

PubPeer comments:
 Fig 1C.  Kaplan-Meier curve introduced based on miR96 level in ovarian cancer patients . ![file] Another manifestation of Hoya s Law for J.BUOn and ERMPS...  When 40 or 50 cases of any given cancer are dichotomised into half-groups of high- or low-expression of any given nc-RNA, survival rate for one half-group or both will drop to 0% at 75 months. Other examples, from left to right: - Fig 1 from [Zang et al (2020)] - Fig 1 from [Li et al (2020)] - Fig 1, and Fig 4D, from [Cui et al (2019)] - Fig 1D from [Gao et al (2019)] . ![file] *[left]* Figure 1C from [Wu et al (2020)] . *[right]* Figs 1D, 3E from [Wu et al (2019)] . ![file] ,
Retracted Article: Spectrin-like domain 2 of DRP2 serves as a novel binding region for the NLS2 and 3 sub-domains of L-periaxin
Authors: Yan Yang
YaWei Shi
Journal: RSC Advances (2015)
Discipline: CHEMISTRY
Keywords: L-periaxin; Schwann cells; PRX gene; DRP2; dystroglycan
Affiliations: Key Laboratory of Chemical Biology and Molecular Engineering of the Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan 030006, China

Abstract: L-periaxin is an important scaffolding protein that is expressed in Schwann cells and lens fiber cells. In Schwann cells, loss or mutation of the PRX gene disrupts compact peripheral myelin and causes severe demyelination neuropathy. DRP2 is the only reported protein to interact with periaxin to form the L-periaxin–DRP2–dystroglycan (PDG) complex, which can provide structural and signaling functions by linking the extracellular matrix to the Schwann cell cytoskeleton. In this report, the interaction between L-periaxin and DRP2 was further investigated by bimolecular fluorescence complementation (BiFC), GST pull-down, CO-IP, and fluorescence spectroscopy. Results demonstrated that spectrin-like domain 2 of DRP2 played a critical role in the complex of DRP2 and L-periaxin. Furthermore, the DRP2 spectrin-like domain 2 only interacted with the NLS2 and NLS3 sub-domains in L-periaxin. These data revealed a previously unknown binding model between DRP2 and L-periaxin.

Retracted: Yes

PubPeer comments:
 Retraction of u2018Spectrin-like domain 2 of DRP2 serves as a novel binding region for the NLS2 and 3 sub-domains of L-periaxinu2019 by Yan Yang et al., RSC Adv., 2015, 5, 84356u201384366, DOI: 10.1039 C5RA12703C. The Royal Society of Chemistry, with the agreement of the authors, hereby wholly retracts this RSC Advances article due to concerns with the reliability of the data in the published article. The authors confirmed that the western blot images in Fig. 1, 2, and 4 had been inappropriately manipulated. Given the significance of the concerns about the validity of the data, the findings presented in this paper are no longer reliable. Signed: Yan Yang and YaWei Shi Date: 8th April 2021 Retraction endorsed by Laura Fisher, Executive Editor, RSC Advances ,
Evaluation of the BH3-only protein Puma as a direct Bak activator
Authors: Scott H Kaufmann
Haiming Dai
Yuan-Ping Pang
Marina Ramirez-Alvarado
Journal: Journal of Biological Chemistry (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apoptosis; Bak; Bcl-2 Family Proteins; Cell Death; Mitochondrial Apoptosis
Affiliations: From the Division of Oncology Research and.

Abstract:  Interactions among Bcl-2 family proteins play critical roles in cellular life and death decisions. Previous studies have established the BH3-only proteins Bim, tBid, and Noxa as "direct activators" that are able to directly initiate the oligomerization and activation of Bak and/or Bax. Earlier studies of Puma have yielded equivocal results, with some concluding that it also acts as a direct activator and other studies suggesting that it acts solely as a sensitizer BH3-only protein. In the present study we examined the interaction of Puma BH3 domain or full-length protein with Bak by surface plasmon resonance, assessed Bak oligomerization status by cross-linking followed by immunoblotting, evaluated the ability of the Puma BH3 domain to induce Bak-mediated permeabilization of liposomes and mitochondria, and determined the effect of wild type and mutant Puma on cell viability in a variety of cellular contexts. Results of this analysis demonstrate high affinity (KD = 26 ± 5 nM) binding of the Puma BH3 domain to purified Bak ex vivo, leading to Bak homo-oligomerization and membrane permeabilization. Mutations in Puma that inhibit (L141E/M144E/L148E) or enhance (M144I/A145G) Puma BH3 binding to Bak also produce corresponding alterations in Bak oligomerization, Bak-mediated membrane permeabilization and, in a cellular context, Bak-mediated killing. Collectively, these results provide strong evidence that Puma, like Bim, Noxa, and tBid, is able to act as a direct Bak activator. 

Retracted: No

PubPeer comments:
 The flow cytometry dot plots in red boxes appear to look similar in Fig 4A and 7F. ![file] ,
Accumulation of Acrolein–Protein Adducts after Traumatic Spinal Cord Injury
Authors: Koji Uchida
Jian Luo
Riyi Shi
Journal: Neurochemical Research (2005)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Reactive oxygen species; lipid peroxidation; acrolein; 4-hydroxynonenal; protein-bound
Affiliations: Department of Basic Medical Sciences, Institute for Applied Neurology, Center for Paralysis Research, Purdue University, West Lafayette, IN 47907, USA.

Abstract:  Reactive oxygen species and resultant lipid peroxidation (LPO) have been associated with central nervous system trauma. Acrolein (2-propenal) and 4-hydroxynonenal (HNE) are the most toxic byproducts of LPO, with detrimental effects in various types of cells. In this study, we used immunoblotting techniques to detect the accumulation of protein-bound acrolein and HNE. We report that protein-bound acrolein and HNE were significantly increased in guinea pig spinal cord following a controlled compression injury. The acrolein and HNE protein-adducts increased in the damaged spinal cord as early as 4 h after injury, reached a peak at 24 h after injury, and remained at a significantly high level up to 7 days after injury. Such increase of protein adducts was also observed in the adjacent segments of the injury site beginning at 24 h post injury. These results suggest that products of lipid peroxidation, especially acrolein, may play a critical role in the secondary neuronal degeneration, which follows mechanical insults. 

Retracted: No

PubPeer comments:
 Figures one and two appear to have a repeated image. The graphs are different. *** ![file] , 
 Dear Actinopolyspora, Thank you for pointing out the problem in our paper. It appears an image duplication mistake. We will try to check the original data and fix the problem if possible. We are sorry for the mistake. Best wishes, Jian ,
Novel Nanosized Chitosan-Betulinic Acid Against Resistant Leishmania Major and First Clinical Observation of such parasite in Kidney
Authors: Mostafa Haji Molla Hoseini
Mehdi Shafiee Ardestani
Amitis Ramezani
Ali Khamesipour
Tahereh Zadeh Mehrizi
Nariman Mosaffa
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: Betulinic acid; nanochitosan; Leishmaniasis; therapeutic effects; side effects
Affiliations: Department of Clinical Research, Pasteur Institute of Iran, Tehran, Iran., Department of Radiopharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran. ., Department of Medical Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran., Center for Research and Training in Skin Diseases and Leprosy, Tehran University of Medical Sciences, Tehran, Iran., Department of Clinical Research, Pasteur Institute of Iran, Tehran, Iran. .

Abstract:  Regarding the antiparasitic effects of Betulinic acid (B) against Leishmaniasis, it was loaded into nanochitosan (K) for the first time in order to improve its therapeutic effects and decrease its side effects for the treatment of Leishmania major-infected Balb/c mice. Improvement the therapeutic efficacy of Bas an anti-leishmania agent through increasing the effective dose was achieved by using a novel solvent and phase separation method for K synthesis. The synthesized K with the size of 102 nm and Betulinic acid-nanochitosan (BK) with the size of 124 nm and drug loading efficiency of 93%, cellular uptake of 97.5% with the slow drug release pattern was prepared. To increase the therapeutic dose, a modified 10% acetic acid solvent was used. The in vitro and in vivo results showed that the nanodrug of BK was non toxic by 100% and BK20 mg/kg could completely performed the wound healing and inhibit the parasite in a large extent (P ˂ 0.001) compared to other groups. Therefore, BK could be considered as an alternative regimen for treatment of L. major. 

Retracted: No

PubPeer comments:
 Some more questionable images by an overlapping group of authors as this: https: pubpeer.com publications 6F91195571CAF273A4DD5D386438A5 *** Figure 16 ![file] *** Figure 4a, false color ![file] *** Figure 4a ![file] ,
An antioxidant exopolysaccharide devoid of pro-oxidant activity produced by the soil bacterium Bordetella sp. B4
Authors: Jinglei Liu
Yibo Hu
Xin Song
Yanliang Lin
Yueran Zhao
Journal: Bioresource Technology (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Exopolysaccharide; Bordetella sp. B4; Antioxidant; Free radical scavenging; NMR spectroscopy
Affiliations: Department of Center Laboratory, Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.

Abstract:  An exopolysaccharide (EPS) with a molecular weight of 230 kDa, was isolated from Bordetella sp. B4. The EPS was identified as linear alpha-1,6-(6-methyl)-glucan with N-acetyl-D-glucosamine branches at alpha-1, 4-linkages by IR and NMR spectroscopy. The free radical scavenging capacities of EPS on 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS(+)), H(2)O(2), -OH and lipid peroxidation were 2-, 86-, 134- and 18-fold higher than that of ascorbic acid, respectively. Compared with ascorbic acid, the EPS was more effective in preventing DNA and protein from free radical damage induced by 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH). More significantly, the EPS did not degrade DNA and protein by the pro-oxidant effect in the presence of copper ions and H(2)O(2). Furthermore, EPS could protect human umbilical vein endothelium cells (HUVECs) from high glucose-mediated damage. The production of EPS reached 10.2 g/L in the fermentation medium containing 3.0 g/L cholesterol, suggesting that Bordetella sp. B4 was a potential producer of antioxidant EPS. 

Retracted: No

PubPeer comments:
 Figure 3B * Red boxes. Lanes  T in both panels look remarkably similar to each other (minus one dot). ![file] , 
 ![file] ![file] The above picture is our raw results,. Althoug they are similar , they are true results. ,
Do multi-ingredient protein supplements augment resistance training-induced gains in skeletal muscle mass and strength? A systematic review and meta-analysis of 35 trials
Authors: Thomas M Doering
Robert W Morton
Stuart M Phillips
Gregory R Cox
Vernon G Coffey
Kerry R O&#x27;Bryan
Journal: British Journal of Sports Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: muscle; protein; strength; supplements.
Affiliations: Faculty of Health Sciences and Medicine, Bond University, Gold Coast, Queensland, Australia., Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.

Abstract:  Objective: To determine the effects of multi-ingredient protein (MIP) supplements on resistance exercise training (RT)-induced gains in muscle mass and strength compared with protein-only (PRO) or placebo supplementation. Data sources: Systematic search of MEDLINE, Embase, CINAHL and SPORTDiscus. Eligibility criteria: Randomised controlled trials with interventions including RT ≥6 weeks in duration and a MIP supplement. Design: Random effects meta-analyses were conducted to determine the effect of supplementation on fat-free mass (FFM), fat mass, one-repetition maximum (1RM) upper body and 1RM lower body muscular strength. Subgroup analyses compared the efficacy of MIP supplementation relative to training status and chronological age. Results: The most common MIP supplements included protein with creatine (n=17) or vitamin D (n=10). Data from 35 trials with 1387 participants showed significant (p&lt;0.05) increases in FFM (0.80 kg (95% CI 0.44 to 1.15)), 1RM lower body (4.22 kg (95% CI 0.79 to 7.64)) and 1RM upper body (2.56 kg (95% CI 0.79 to 4.33)) where a supplement was compared with all non-MIP supplemented conditions (means (95% CI)). Subgroup analyses indicated a greater effect of MIP supplements compared with all non-MIP supplements on FFM in untrained (0.95 kg (95% CI 0.51 to 1.39), p&lt;0.0001) and older participants (0.77 kg (95% CI 0.11 to 1.43), p=0.02); taking MIP supplements was also associated with gains in 1RM upper body (1.56 kg (95% CI 0.80 to 2.33), p=0.01) in older adults. Summary/conclusions: When MIP supplements were combined with resistance exercise training, there were greater gains in FFM and strength in healthy adults than in counterparts who were supplemented with non-MIP. MIP supplements were not superior when directly compared with PRO supplements. The magnitude of effect of MIP supplements was greater (in absolute values) in untrained and elderly individuals undertaking RT than it was in trained individuals and in younger people. Trial registration number: CRD42017081970. 

Retracted: No

PubPeer comments:
 See https: retractionwatch.com 2021 02 12 eleven-papers-corrected-after-nutrition-prof-fails-to-disclose-patent-company-ties for backgrounds about a correction. ,
Assessment of probiotic potential and anticancer activity of newly isolated vaginal bacterium Lactobacillus plantarum 5BL
Authors: Rozita Rosli
Yousef Nami
Dayang Radiah
Norhafizah Abdullah
Ahmad Yari Khosroushahi
Babak Haghshenas
Journal: Microbiology and Immunology (2014)
Discipline: MICROBIOLOGY
Keywords: anticancer; apoptosis; microbial biotherapy.
Affiliations: Institute of Bioscience., Chemical and Environmental Engineering Department; Faculty of Engineering; University Putra Malaysia; 43400 UPM Serdang Selangor Malaysia, Institute of Bioscience, Drug Applied Research Center, Department of Pharmacognosy; Faculty of Pharmacy; Tabriz University of Medical Sciences; Tabriz Iran

Abstract:  Numerous bacteria in and on its external parts protect the human body from harmful threats. This study aimed to investigate the potential beneficial effects of the vaginal ecosystem microbiota. A type of bacteria was isolated from vaginal secretions of adolescent and young adult women, cultured on an appropriate specific culture medium, and then molecularly identified through 16S rDNA gene sequencing. Results of 16S rDNA sequencing revealed that the isolate belongs to the Lactobacillus plantarum species. The isolated strain exhibited probiotic properties such as low pH and high bile salt concentration tolerance, antibiotic susceptibility and antimicrobial activity against some pathogenic bacteria. The anticancer effects of the strain on human cancer cell lines (cervical, HeLa; gastric, AGS; colon, HT-29; breast, MCF-7) and on a human normal cell line (human umbilical vein endothelial cells [HUVEC]) were investigated. Toxic side effects were assessed by studying apoptosis in the treated cells. The strain exhibited desirable probiotic properties and remarkable anticancer activity against the tested human cancer cell lines (P ≤ 0.05) with no significant cytotoxic effects on HUVEC normal cells (P ≤ 0.05). Overall, the isolated strain showed favorable potential as a bioactive therapeutic agent. Therefore, this strain should be subjected to the other required tests to prove its suitability for clinical therapeutic application. 

Retracted: No

PubPeer comments:
 Figure 4. Panels a (without treatment, 24h) and b (without treatment, 48h) appear to share a similar group of dots. Shown with blue boxes. ![file] , 
 Figure 3 of this paper shares similarities with Figure 2 of another paper by the same research group, submitted around the same time, but displaying somewhat different experiments. That other paper is: * Nami et al. - Anaerobe (2014) -  Probiotic potential and biotherapeutic effects of newly isolated vaginal Lactobacillus acidophilus 36YL strain on cancer cells - DOI: 10.1016 j.anaerobe.2014.04.012 - https: pubpeer.com publications 33760A49AA8385B625A4A6823F0F5E Here is a side-by-side comparison of the 2 figures, with boxes of the same color highlighting areas that look similar to each other. ![file] ,
Gelam honey attenuates carrageenan-induced rat paw inflammation via NF-κB pathway
Authors: Suzana Makpol
Saba Zuhair Hussein
Kamaruddin Mohd Yusoff
Yasmin Anum Mohd Yusof
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: NF-κB; Gelam honey; inflammation; rats; paw edema
Affiliations: Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.

Abstract:  The activation of nuclear factor kappa B (NF-κB) plays a major role in the pathogenesis of a number of inflammatory diseases. In this study, we investigated the anti-inflammatory mechanism of Gelam honey in inflammation induced rats via NF-κB signalling pathway. Rats paw edema was induced by subplantar injection of 1% carrageenan into the right hind paw. Rats were pre-treated with Gelam honey at different doses (1 or 2 g/kg, p.o.) and NSAID Indomethacin (10 mg/kg, p.o.), in two time points (1 and 7 days). Our results showed that Gelam honey at both concentrations suppressed the gene expressions of NF-κB (p65 &amp; p50) and IκBα in inflamed rats paw tissues. In addition, Gelam honey inhibited the nuclear translocation and activation of NF-κB and decreased the cytosolic degradation of IκBα dose dependently in inflamed rats paw tissues. The immunohistochemical expressions of pro-inflammatory mediators COX-2 and TNF-α were also decreased in inflamed rats paw tissues when treated with Gelam honey. The results of our findings suggest that Gelam honey exhibits its inhibitory effects by attenuating NF-κB translocation to the nucleus and inhibiting IκBα degradation, with subsequent decrease of inflammatory mediators COX-2 and TNF-α. 

Retracted: No

PubPeer comments:
 Concern about Figure 3, reported to the journal in October 2015. * Red boxes: In the IkBa 7 days panel, lanes 1-3 look remarkably similar to lanes 5-7. ![file] , 
 Concern about Figure 4, also reported to the journal in October 2015. * Green boxes: Panels D and F appear to show an overlap. ![file] ,
Long noncoding RNA GAS5 attenuates cardiac fibroblast proliferation in atrial fibrillation via repressing ALK5
Authors: J Lu
P-L Lin
F-Q Xu
Z Meng
J-J Guo
L-G Hu
D Li
X-H Lu
J Li
Y An
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA GAS5; atrial fibrillation; cell proliferation; ALK5; mechanism
Affiliations: Department of Cardiology, the Affiliated Hospital of Qingdao University, Qingdao, China. .

Abstract:  Objective: Recently, long noncoding RNAs (lncRNAs) have caught more attention for their role in the progression of many diseases. Among them, lncRNA GAS5 (Growth Inhibition Specificity 5) was studied in this research to identify how it affects the progression of atrial fibrillation (AF). Patients and methods: In 40 patients with AF and 30 patients with sinus rhythm (SR), the GAS5 expression of the right atrial appendage (RAA) tissues was detected by the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, the cell proliferation assay was conducted in AC16 cells transfected with GAS5 inhibitor and mimics, respectively. Furthermore, the qRT-PCR was performed to uncover the mechanism. Results: In the research, the expression of GAS5 in RAA tissues was decreased significantly in AF patients than that in SR ones. Moreover, overexpression of GAS5 inhibited cell growth in AC16 cells, while knockdown of GAS5 promoted cell growth in AC16 cells. In addition, further experiments revealed that ALK5 was a target of GAS5 and its expression in AF tissues negatively correlated to GAS5 expression. Conclusions: These results indicate that GAS5 could inhibit cell proliferation of AF via suppressing ALK5, which may offer a new vision for interpreting the mechanism of AF development. 

Retracted: No

PubPeer comments:
 This paper is one of a set of 121 papers that all contain images from the same library of about 100 photos and plots. This is unexpected, because each paper has different authors and different affiliations, with little to no overlap, and describes different cancer types and molecules. It would be very hard to explain how authors from different labs would all obtain the same photo. Therefore, the papers might have all be derived from the same source, such as a paper mill that sells ready-to-be-published papers. This  Stock Photo paper set has been described in more detail on my blog post, https: scienceintegritydigest.com 2020 07 05 the-stock-photo-paper-mill and in a Wall Street Journal article by Eva Xiao (currently behind a paywall): https: www.wsj.com articles chinese-research-papers-raise-doubts-fueling-global-questions-about-scientific-integrity-11593939600 The vast majority (113 121) of the papers were published in the same journal, European Review for Medical and Pharmacological Sciences (ERMPS). A link to the full set of papers can be found here: https: docs.google.com spreadsheets d 172RWS18w1lTNJ9Nnj80fuXXTqTm4fGkoK0sdYyvKE3g edit?usp=sharing All papers have been reported to the journal editors on July 2, 2020. ,