PReD-Bench/PRed-Bench huggingface dataset:
Development and characterization of nanolipobeads-based dual drug delivery system for H. pylori targeting
Authors: Ashish Kumar Jain
Sunil Kumar Jain
Journal: Journal of drug targeting (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: nanolipobeads; drug targeting; H. Pylori; gastric ulcer; polyvinyl alcohol nanoparticles
Affiliations: Adina Institute of Pharmaceutical Sciences, Sagar, Madhya Pradesh, India. 

Abstract:  The objective of the present investigation was to prepare and evaluate nanolipobeads which permit the targeting of drugs to H. Pylori and potentially used for the treatment of gastric ulcer. For this polyvinyl alcohol nanoparticles were prepared by freeze thaw cyclizing method and surface acylation was done by treating with (1M) palmitoyl chloride in hexane followed by addition of 0.1 N NaOH to induce acylation by adjusting pH below 6.5. Finally, nanolipobeads synthesis was carried out by combining equal parts of suspension of acylated poly vinyl alcohol nanoparticles (PVA-NPs) and AMOX encapsulated PE liposomes suspension. The uniformity of supported PE lipid layer on acylated PVA-NPs was examined using fluorescence and confocal laser scanning electron microscopy. The optimized nanolipobeads formulation demonstrated 773.3 ± 4.3 nm average age size and 84.7 ± 2.9% of AMOX and 67.5 ± 2.8% of RBC release up to 72 h, respectively. Furthermore, binding specificity and targeting propensity toward H. pylori (SKP-56) was confirmed by agglutination and in situ adherence assay. Reduction of the absolute alcohol induced ulcerogenic index from 3.01 ± 0.25 to 0.31 ± 0.09 and 100% H. pylori clearance rate was observed. These results suggested that nanolipobeads are potential vector for development of dual drug delivery for effective treatment of H. pylori associated peptic ulcer. 

Retracted: No

PubPeer comments:
 Fig 7: Image duplication after background alteration shown in red boxes (segment of similarity). ![file] , 
 Image recycled from their 2009 paper. ![file] , 
 Fig 2(B),  fluorescence photomicrograph of rhodamine-123 labeled nanolipobeads formulation . ![file] Is there any reason why the central image has triplicated itself at the right? UPDATE: Here is an earlier version of the same image, without the righthand triplication. Fig 4 from [Jain, Agrawal Agrawal (2011)] . ![file] ,
The UPF1 RNA surveillance gene is commonly mutated in pancreatic adenosquamous carcinoma
Authors: Fang Su
Mark A Valasek
YiFan Zhao
GuoTong Xu
YingQi Zhou
MingXin Zuo
Gang Li
LiXia Lu
YanJun Lu
MeiYi Song
JingPing Zhu
ChongRen Wang
Yuan Ji
Milind Javle
Chen Liu
Wai Chin Foo
Miles F Wilkinson
YiRan Wang
Rachid Karam
Journal: Nature Medicine (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Pancreatic adenosquamous carcinoma; UPF1 gene mutations; Nonsense-mediated RNA decay pathway; Tumor-specific mutations; RNA splicing
Affiliations: 1] Clinical and Translational Cancer Research Center, The Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. [2] Tongji University School of Life Science and Technology, Shanghai, China. [3]., 1] Department of Reproductive Medicine, School of Medicine, University of California San Diego, La Jolla, California, USA. [2]., 1] The Third General Surgery Department, Changhai Hospital, Second Military Medical University, Shanghai, China. [2]., 1] Clinical and Translational Cancer Research Center, The Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. [2]., 1] Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China. [2]., The Third General Surgery Department, Changhai Hospital, Second Military Medical University, Shanghai, China., Clinical and Translational Cancer Research Center, The Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China., Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA., Department of Gastrointestinal Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA., Division of Anatomic Pathology, Department of Pathology, University of California San Diego, San Diego, California, USA., 1] Department of Reproductive Medicine, School of Medicine, University of California San Diego, La Jolla, California, USA. [2] Institute for Genomic Medicine, University of California San Diego, La Jolla, California, USA.

Abstract:  Pancreatic adenosquamous carcinoma (ASC) is an enigmatic and aggressive tumor that has a worse prognosis and higher metastatic potential than its adenocarcinoma counterpart. Here we report that ASC tumors frequently harbor somatically acquired mutations in the UPF1 gene, which encodes the core component of the nonsense-mediated RNA decay (NMD) pathway. These tumor-specific mutations alter UPF1 RNA splicing and perturb NMD, leading to upregulated levels of NMD substrate mRNAs. UPF1 mutations are, to our knowledge, the first known unique molecular signatures of pancreatic ASC. 

Retracted: No

PubPeer comments:
 https: twitter.com bradleybio status 1348680325254139904 ,
Seedless preparation of Au nanorods by hydroquinone assistant and red blood cell membrane camouflage
Authors: Xue Zhang
Jinlan Jiang
Xiuying Li
Hua Yao
Wenjing Wang
Xupeng Mu
Zhenhong Wei
Jing Li
Hao Zhang
Journal: RSC Advances (2018)
Discipline: CHEMISTRY
Keywords: Au nanorods; photothermal effects; preparation methods; seedless method; hydroquinone
Affiliations: The Scientific Research Center, China-Japan Union Hospital, Jilin University, Changchun 130033, P. R. China, State Key Laboratory of Supramolecular Structure and Materials, College of Chemistry, Changchun 130012, College of Resources and Environment, Jilin Agricultural University, Changchun 130118, China

Abstract:  Au nanorods (AuNRs) have attracted extensive attention in diagnosis and therapy, because of their excellent photothermal effects. Although many of attempts have been employed to prepare AuNRs with a good-size monodispersity, facile and feasible preparation methods are still welcomed in consideration of theranostics-related photothermal applications. In this work, AuNRs are prepared through a seedless method using hydroquinone as the reductant. The longitudinal located surface plasmon resonance peak of the as-prepared AuNRs can be tuned from 650 to 840 nm and the AuNRs indicate a good photothermal conversion efficiency. To lower the toxicity, natural red blood cell membranes are employed to coat the AuNRs. In the primary experiment in vitro, red blood cell membrane-coated AuNRs exhibit good biocompatibility and photothermal treatment effect. 

Retracted: No

PubPeer comments:
 Figure 2 * Red boxes: The b-actin panel representing Scramble in Figure 2C looks similar to the b-actin panel representing Mock in Figure 2D. ![file] , 
 Figure 7A, top part. The same two groups of cells appear to be visible in two different panels, with a different spacing. ![file] , 
 Figure 7A, bottom part. Some groups of dots appear to be visible in multiple panels. Boxes of the same color focus attention to some of these groups. ![file] , 
 Figure 7B, bottom part. Some groups of dots appear to be visible in multiple panels. Boxes of the same color focus attention to some of these groups. ![file] , 
 Figure 7E appears to show the same group of dots in two panels. ![file] , 
 Figure 8A. * Pink boxes: Lanes 2-4 in the left b-actin panel look similar to lanes 1-3 in the right b-actin panel * In the right p53 panel, some areas appear to be visible multiple times ![file] ,
A designer self-assembled supramolecule amplifies macrophage immune responses against aggressive cancer
Authors: Jayashree Nirgud
Shiladitya Sengupta
Anujan Ramesh
Prithvi Pandey
Harshangda Bhatnagar
Amrendra Kumar Ajay
Siva Kumar Natarajan
Driti Ashok
Ashish Kulkarni
Vineethkrishna Chandrasekar
Journal: Nature Biomedical Engineering (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: macrophages; cancer cells; colony stimulating factor; CD47; SIRPα
Affiliations: Division of Engineering in Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. ., Department of Chemical Engineering, University of Massachusetts, Amherst, MA, USA. ., Center for Bioactive Delivery, Institute for Applied Life Sciences, University of Massachusetts, Amherst, MA, USA. ., Division of Engineering in Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA., Department of Chemical Engineering, University of Massachusetts, Amherst, MA, USA., India Innovation Research Center, Invictus Oncology, New Delhi, India., Dana Farber Cancer Institute, Boston, MA, USA. ., Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA, USA. .

Abstract:  Effectively activating macrophages that can 'eat' cancer cells is challenging. In particular, cancer cells secrete macrophage colony stimulating factor (MCSF), which polarizes tumour-associated macrophages from an antitumour M1 phenotype to a pro-tumourigenic M2 phenotype. Also, cancer cells can express CD47, an 'eat me not' signal that ligates with the signal regulatory protein alpha (SIRPα) receptor on macrophages to prevent phagocytosis. Here, we show that a supramolecular assembly consisting of amphiphiles inhibiting the colony stimulating factor 1 receptor (CSF-1R) and displaying SIRPα-blocking antibodies with a drug-to-antibody ratio of 17,000 can disable both mechanisms. The supramolecule homes onto SIRPα on macrophages, blocking the CD47-SIRPα signalling axis while sustainedly inhibiting CSF-1R. The supramolecule enhances the M2-to-M1 repolarization within the tumour microenvironment, and significantly improves antitumour and antimetastatic efficacies in two aggressive animal models of melanoma and breast cancer, with respect to clinically available small-molecule and biologic inhibitors of CSF-1R signalling. Simultaneously blocking the CD47-SIRPα and MCSF-CSF-1R signalling axes may constitute a promising immunotherapy. 

Retracted: No

PubPeer comments:
 BLZ-945 targeting CSF-1R. How does it reverse the effect of IL-4 induced M2 macrophage in Raw 264.7 cells? Does IL-4 binding to CSF-1R? Or Is there any cross-talk in signaling pathway? , 
 Thanks for the question. We have thought about that. We wanted to check whether cells pushed towards a M2 lineage can switch back to M1, and if an inherent CSF1R block can have an inhibitory effect on that, i.e. does macrophages exists in a state of plasticity. We don t have any data to believe that IL4 binds to CSF1R or that the drug antagonizes IL4 signaling, nor have we looked at any cross talks, but the latter could be possible. We don t know what controls macrophage plasticity. ,
Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143
Authors: H-Y Zhang
K-M Ren
J-G Zhao
F-S Zheng
J-Z Zhao
T Jun
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lung cancer; UCA1; therapeutic targets; lncRNA; miR-143
Affiliations: Department of The First Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China. .

Abstract:  Objective: Accounting for 25% of all the cancers and 20% of the cancer-related mortality, lung cancer is one of the devastating types of cancers. Due to an increase in the incidence of lung cancer and limited treatment options, there is a pressing need to look for novel drug options and to identify potential therapeutic targets. Long non-coding RNAs (LncRNAs) have been considered to be important therapeutic targets due to their plethora of cellular roles. Herein, we investigated the therapeutic potential of UCA1 in lung cancer and also attempted to examine the underlying mechanism through UCA1 exerts its growth inhibitory effects on cancer cells. Materials and methods: The quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) was used to perform the expression analysis. The CCK-8 assay was used to monitor the growth of the cells. The AO/EB assay was used to check apoptosis and flow cytometry was used for cell cycle distribution. The wound heal and transwell assays were used to monitor the cell migration and invasion. Results: It was found that the lncRNA UCA was significantly (p &lt; 0.05) upregulated in the lung cancer cells and silencing of UCA1 could inhibit the proliferation of the SK-MES-1 lung cancer cells via induction of G2/M cell cycle arrest and apoptosis. Moreover, UCA1 silencing could also suppress the migration and invasion of the SK-MES-1 cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation. Conclusions: UCA1, as well as miR-143, may be essential therapeutic targets for the management of lung cancer and warrant further investigations. 

Retracted: No

PubPeer comments:
 *[left]* Fig 2B.  Transwell assay showing the invasion of NC or SiUCA1 transfected SK-MES-1 lung cancer cells . *[right]* Fig 8 from [Ye et al (2020)] .  Transwell assay showing that limonene induced dose-dependent inhibition of invasion in T24 human bladder cells . ![file] ,
Sophoridine inhibits lung cancer cell growth and enhances cisplatin sensitivity through activation of the p53 and Hippo signaling pathways
Authors: Lingling Zhu
Yangyang Yao
Xiaojun Xiang
Li Li
Jianping Xiong
Shanshan Huang
Junhe Li
Jun Chen
Jun Deng
Hui Guo
Journal: Gene (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cisplatin sensitivity; Hippo; Lung cancer; Sophoridine; p53.
Affiliations: Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province 330006, China; Lung Cancer Center, West China Hospital of Sichuan University, Chengdu, China., Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province 330006, China., Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province 330006, China. Electronic address: .

Abstract:  Background: Sophoridine, a quinolizidine alkaloid extracted from the Chinese herb Sophora alopecuroides L., has been reported to exert antitumor effects against multiple human cancers. However, few studies have evaluated its tumor-suppressing effects and associated mechanism with respect to lung cancer, in addition to its potential to be used for clinical lung cancer treatment. Methods: Different types of lung cancer cells were used to investigate the antitumor effects of sophoridine using cell viability, colony formation, and cell invasion, and migration assays. To determine the signaling pathways involved, western blot analysis, quantitative real-time polymerase chain reaction, an in vivo ubiquitination assay, and immunohistochemistry were used in cellular assays and with a subcutaneous xenograft model in BALB/c mice. Results: Sophoridine significantly suppressed the proliferation of and colony formation by lung cancer cells in vitro. Transwell assays demonstrated that sophoridine also inhibited invasion and migration in lung cancer cells. In addition, sophoridine enhanced the effects of cisplatin on lung cancer cells. A mechanistic study revealed that sophoridine significantly activated the Hippo and p53 signaling pathways, and mouse xenograft experiments further confirmed in vitro findings in lung cancer cells. Conclusions: Taken together, these results suggest that sophoridine can inhibit lung cancer progression and enhance the effects of the anticancer drug cisplatin against lung cancer cells. The mechanism of action of sophoridine might involve the Hippo and p53 signaling pathways. 

Retracted: No

PubPeer comments:
 image duplication ![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. ,
Tool-Use: Capturing Multisensory Spatial Attention or Extending Multisensory Peripersonal Space?
Authors: Gemma A Calvert
Daniel Sanabria
Charles Spence
Nicholas P Holmes
Journal: Cortex (2007)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: tool-use; peripersonal space; visual-tactile interactions; attention; spatial allocation

Abstract:  The active and skilful use of tools has been claimed to lead to the "extension" of the visual receptive fields of single neurons representing peripersonal space--the visual space immediately surrounding one's body parts. While this hypothesis provides an attractive and potentially powerful explanation for one neural basis of tool-use behaviours in human and nonhuman primates, a number of competing hypotheses for the reported behavioural effects of tool-use have not yet been subjected to empirical test. Here, we report five behavioural experiments in healthy human participants (n=120) involving the effects of tool-use on visual-tactile interactions in peripersonal space. Specifically, we address the possibility that the use of only a single tool, which is typical of many neuropsychological studies of tool-use, induces a spatial allocation of attention towards the side where the tool is held. Participants' tactile discrimination responses were more strongly affected by visual stimuli presented on the right side when they held a single tool on the right, compared to visual stimuli presented on the left. When [corrected] two tools were held, one in each hand, this spatial effect disappeared. Our results are incompatible with the hypothesis that tool-use extends peripersonal space, and suggest instead that the use and/or manipulation of [corrected] tools results in an automatic multisensory shift of spatial attention to the side of space where the tip of the tool is actively held. These results have implications for many of the cognitive neuroscientific studies of tool-use published to date. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: At 15,000 words, this egregiously-long paper was my attempt to show that tool use affects multisensory spatial attention. In part, this paper was a data-dump of a number of experiments with small effect-sizes, and the very long discussion was me shouting into the abyss, wondering why no-one else seemed to see the problems that I did. I should have respected the reader s time a lot more and taken half the space. ,
Activation of Dinitrogen as A Dipolarophile in 1,3-Dipolar Cycloadditions: A Theoretical Study Using Nitrile Imines as "Octet" 1,3-Dipoles
Authors: Ibon Alkorta
José Elguero
M Merced Montero-Campillo
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Theoretical calculations; G4MP2 level of theory; dinitrogen activation; dipolar cycloadditions; neutral beryllium derivatives
Affiliations: Instituto de Química Médica, CSIC, Juan de la Cierva, 3, E-28006, Madrid, Spain., Instituto de Química Médica, CSIC, Juan de la Cierva, 3, E-28006, Madrid, Spain. .

Abstract:  Theoretical calculations at the G4MP2 level of theory demonstrate that it is possible to activate dinitrogen to make it react in dipolar cycloadditions using neutral beryllium derivatives and other neutral metallic compounds. For the particular case of beryllium, the barrier decreases more than 40 kJ·mol-1 with respect to the non-catalysed reaction. The activation achieved is lower than using diazonium salts (models of protonated N2), but still in a range that can be experimentally attainable. 

Retracted: No

PubPeer comments:
 Figure 3D appears to have a repeated image, after rotation, but they are described differently. *** ![file] ,
FT-IR and GC-MS analyses of potential bioactive compounds of cow urine and its antibacterial activity
Authors: Vipin Nautiyal
R C Dubey
Journal: Saudi Journal of Biological Sciences (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Antibacterial activity; Badri cow urine; FT-IR; GC-MS; ICP-MS

Abstract:  The main emphasis of this study was to identify the bioactive compounds responsible for antibacterial activity of Badri cow urine isolated by thin layer chromatography. The most effective bioactive fraction was analysed by FT-IR and GC-MS analyses. Among the four major fractions (EW1, EW2, CA1 and CA2) obtained by TLC profiling, EW1 was found most active against bacterial strains viz., Listeria monocytogenes (MTCC657), Staphylococcus aureus (MTCC7443), Pseudomonas aeruginosa (MTCC424), Klebsiella pneumoniae (MTCC432) and Salmonella typhi (MTCC733). However, Escherichia coli (MTCC118), was found resistant to all the fractions. In FT-IR spectroscopy, functional groups like alcohol, amide, alkene, alkyl halide, polysulfide and phosphate ions were identified. The GC-MS analysis of EW1 fraction exhibited the presence of 12 compounds, of which 1-heneicosanol was found as the major compound. These compounds might be responsible synergistically or individually for antibacterial activity of cow urine. Nine elements namely sodium (Na), calcium (Ca), chromium (Cr), iron (Fe), magnesium (Mg), aluminium (Al), potassium (K) and zinc (Zn), Gold (Au) were measured by ICP-MS analysis. 

Retracted: No

PubPeer comments:
 There appears to be a massive amount of organosilicon contamination in the cow urine samples used: ![file] ,
Differential activation of signaling pathways by UVA and UVB radiation in normal human epidermal keratinocytes
Authors: Deeba N Syed
Farrukh Afaq
Hasan Mukhtar
Journal: Photochemistry and photobiology (0)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: UV radiation; cutaneous pathologies; cell signaling pathways; UVA; UVB
Affiliations: Department of Dermatology, University of Wisconsin, Madison, WI, USA.

Abstract:  Ultraviolet (UV) radiation from the solar spectrum is a major etiological factor for many cutaneous pathologies including cancer. By understanding changes in cell signaling pathways induced by UVA and UVB, novel strategies for prevention and treatment of UV-related pathologies could be developed. However, much of the information in the literature from various laboratories cannot cross talk because of difficulties associated with the use of ill-defined light sources and physiologically irrelevant light dosimetry. Herein, we have assessed the effect of exposure of normal human epidermal keratinocytes (NHEK) to UVA (2 and 4 J cm(-2)) or UVB (20 and 40 mJ cm(-2)) radiation. Employing western blot analysis, we found that exposure of NHEK to UVB, but not UVA, phosphorylates JNK1/2 at Th(183)/Tyr(185), STAT3 at Ser(727) , AKT at Ser(473) and increases c-Fos expression, whereas exposure to UVA, but not UVB, phosphorylates AKT at Thr(308). UVB as well as UVA exposure leads to increased phosphorylation of (1) ERK1/2 at Th(202)/Tyr(204); (2) p38 at Th(180)/Tyr(204); (3) STAT3 at Tyr(705); (4) mTOR at Thr(2448); and (v) p70S6k at Thr(421) /Ser(424); enhanced expression of PI3K (p85) and c-jun; and nuclear translocation of NFκB proteins. These findings could be considered as a beginning for understanding the differential effects of UVA and UVB in the human skin and may have implications both with respect to risk assessment from exposure to solar UV radiation, and to target interventions against signaling events mediated by UVA and UVB. 

Retracted: No

PubPeer comments:
 ![file] There are undeclared cut and splice sites (indicated with boxes and arrowheads) in the immunoblots in Figure 1E, 2A and 7A. Could authors show the original gel data at here? , 
 ![file] ![file] There are undeclared cut and splice sites (indicated with boxes and arrowheads) in the immunoblots in Figure 1E, 2A and 7A. Could authors show the original gel data at here? ,
Proliferation and invasion of colon cancer cells are suppressed by knockdown of TOP2A
Authors: Rui Zhang
Jian Zhao
Jian Xu
Jing H Bai
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TOP2A; colon cancer cells; invasion; proliferation.
Affiliations: Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Insititute, Shenyang, Liaoning Province, P.R. China., Department of Internal Medicine, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Insititute, Shenyang, Liaoning Province, P.R. China.

Abstract:  Recent research has shown that TOP2A plays an important role in the tumorigenesis of many malignancies, such as breast cancer, ovarian cancer, and prostate cancer. However, few studies have been conducted on TOP2A expression and functions in colon cancer. In the present study, we found that TOP2A expression was obviously elevated in colon cancer tissues compared to adjacent non-cancerous tissues. Depletion of TOP2A in HCT116 and SW480 colon cancer cells by transfection of specific small interfering RNA significantly suppressed proliferation and inhibited invasion of cells, even induced apoptosis as indicated by both MTT assay, Annexin V/propidium iodide staining, and Transwell assay. Furthermore, we explored the underlying mechanisms. Knockdown of TOP2A not only affects the expression of cell apoptosis-related (Bcl-2 and Bax) and invasion-related proteins (MMP-2 and MMP-9), but also reduced the phosphorylation levels of ERK and AKT. In conclusion, we showed that TOP2A was upregulated in colon cancer tissue samples and that TOP2A may serve as an oncogene in colon cancer. 

Retracted: No

PubPeer comments:
  FIGURE 4 Suppressing TOP2A expression induces colon cancer cell apoptosis. A, HCT116 and (B) SW480 cells were transfected with indicated siRNA. After 48 h of culture, cells were collected, stained with Annexin V PI and analyzed by flow cytometry . ![file] Teal box marks a panel with very similar panels in Figs 1F of [Yu Chai (2017)] and 3A of [Long et al (2017)] . ![] ![] Peach box marks a panel with a match in Fig 3A of [Li et al (2019)] . The match is not perfect and the similarities are greater in the left-hand quadrants. ![file] UPDATE: Dark grey rectangle matches the 2nd panel of Fig 2A from [Tang, Yang Zhang (2017)] .  Vitexin suppresses apoptosis of H9c2 cells in MI R injury. H9c2 cells were divided into control group, MI R model group and MI R + vitexin treated group (50 u03bcM, 100 u03bcM and 200 u03bcM respectively) . ![file] ,
Dual targeted polymeric nanoparticles based on tumor endothelium and tumor cells for enhanced antitumor drug delivery
Authors: Govind Prasad Agrawal
Suresh Prasad Vyas
Gousia Chashoo
Madhu Gupta
Parduman Raj Sharma
Ajit Kumar Saxena
Prem Narayan Gupta
Journal: Molecular pharmaceutics (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: CD13 receptor; cyclic NGR; docetaxel; nanoparticles; solid tumor.
Affiliations: Drug Delivery Research Laboratory, Department of Pharmaceutical Sciences, Dr. H. S. Gour Vishwavidyalaya , Sagar-470003, M.P., India.

Abstract:  Some specific types of tumor cells and tumor endothelial cells represented CD13 proteins and act as receptors for Asn-Gly-Arg (NGR) motifs containing peptide. These CD13 receptors can be specifically recognized and bind through the specific sequence of cyclic NGR (cNGR) peptide and presented more affinity and specificity toward them. The cNGR peptide was conjugated to the poly(ethylene glycol) (PEG) terminal end in the poly(lactic-co-glycolic) acid PLGA-PEG block copolymer. Then, the ligand conjugated nanoparticles (cNGR-DNB-NPs) encapsulating docetaxel (DTX) were synthesized from preformed block copolymer by the emulsion/solvent evaporation method and characterized for different parameters. The various studies such as in vitro cytotoxicity, cell apoptosis, and cell cycle analysis presented the enhanced therapeutic potential of cNGR-DNB-NPs. The higher cellular uptake was also found in cNGR peptide anchored NPs into HUVEC and HT-1080 cells. However, free cNGR could inhibit receptor mediated intracellular uptake of NPs into both types of cells at 37 and 4 °C temperatures, revealing the involvement of receptor-mediated endocytosis. The in vivo biodistribution and antitumor efficacy studies indicated that targeted NPs have a higher therapeutic efficacy through targeting the tumor-specific site. Therefore, the study exhibited that cNGR-functionalized PEG-PLGA-NPs could be a promising approach for therapeutic applications to efficient antitumor drug delivery. 

Retracted: No

PubPeer comments:
  Figure 2. (a) SEM photograph of cNGR-DNB-NP ![file] Lots of unexpectedly identical particles environs. I have marked a few pairs and triplets. , 
 #1 Fig 2(a) had previously appeared (with fewer duplicated NPs) as 1B of [Gupta Vyas (2012)] . ![] ,
Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome
Authors: A G Coran
E Yakirevich
L Siplovich
E Sabo
M Krausz
A Kramer
I Sukhotnik
E Shiloni
Journal: Pediatric Surgery International (2002)
Discipline: CLINICAL MEDICINE
Keywords: Sepsis; Short-bowel syndrome; Lipopolysaccharide; Endotoxemia; Enterocyte proliferation
Affiliations: Rappoport Faculty of Medicine, Technion, Israel. 

Abstract:  Sepsis is frequently associated with or complicates short-bowel syndrome (SBS). To investigate the effects of lipopolysaccharide (LPS) endotoxemia on enterocyte proliferation and death via apoptosis in a rat model of SBS, adult male Sprague-Dawley rats were divided into three experimental groups: sham rats underwent bowel transection and reanastomosis; SBS rats underwent 75% small-bowel resection; and SBS-LPS rats underwent 75% bowel resection and were given intraperitoneal injections of LPS 10 mg/kg. Parameters of intestinal adaptation (bowel and mucosal weights, mucosal DNA and protein, villus height, and crypt depth), enterocyte proliferation, and death via apoptosis were determined on day 15 after the operation. Statistical analysis was determined by Student's and ANOVA tests with a P less than 0.05 considered significant. SBS-LPS animals demonstrated a significant decrease (vs SBS rats) in duodenal (20%), jejunal (30%), and ileal (15%) overall weight, duodenal (20%), jejunal (27%), and ileal (18%) mucosal weight, jejunal (20%) and ileal (30%) mucosal DNA, jejunal (29%) and ileal (31%) villus height, and jejunal (14%) and ileal (29%) crypt depth. LPS endotoxemia led to reduced cell proliferation and enterocyte apoptosis compared to untreated SBS animals. Thus, in a rat model of SBS, LPS endotoxemia inhibits intestinal adaptation. A possible mechanism may be decreased cell proliferation. Decreased enterocyte loss via apoptosis may reflect a reduced number of enterocytes. Other mechanisms (necrosis) may be mainly responsible for cell death following LPS injection. 

Retracted: No

PubPeer comments:
 This paper appears to be part of a set of at least 3 papers that appear to share immunohistochemistry images. All papers list Igor Sukhotnik as the first author. Boxes of the same color highlight areas in microscopy panels that look similar. The images do not always represent the same experiments, in particular the region marked with an orange box. * Sukhotnik I et al., Digestive Diseases and Sciences (2002), DOI: 10.1023 a:1019641416671 * Sukhotnik I et al., Journal of Surgical Research (2002), DOI: 10.1006 jsre.2002.6556 * Sukhotnik I et al., Pediatr Surg Int (2002) 18: 615u2013619, DOI: 10.1007 s00383-002-0862-8 ![file] ,
Regulation of sprouty stability by Mnk1-dependent phosphorylation
Authors: John DaSilva
Dafna Bar-Sagi
Lizhong Xu
W Todd Miller
Hong Joo Kim
Journal: Molecular and Cellular Biology (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Sprouty proteins; receptor tyrosine kinase pathways; serine phosphorylation; mitogen-activated protein kinase-interacting kinase 1; degradation
Affiliations: Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA., Department of Molecular Genetics and Microbiology, Graduate Program in Molecular and Cellular Biology, Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, New York 11794

Abstract:  Sprouty (Spry) proteins are negative feedback modulators of receptor tyrosine kinase pathways in Drosophila melanogaster and mammals. Mammalian Spry proteins have been shown to undergo tyrosine and serine phosphorylation in response to growth factor stimulation. While several studies have addressed the function of tyrosine phosphorylation of Spry, little is known about the significance of Spry serine phosphorylation. Here we identify mitogen-activated protein kinase-interacting kinase 1 (Mnk1) as the kinase that phosphorylates human Spry2 (hSpry2) on serines 112 and 121. Mutation of these serine residues to alanine or inhibition of Mnk1 activity increases the rate of ligand-induced degradation of hSpry2. Conversely, enhancement of serine phosphorylation achieved through either the inhibition of cellular phosphatases or the expression of active Mnk1 results in the stabilization of hSpry2. Previous studies have shown that growth factor stimulation induces the proteolytic degradation of hSpry2 by stimulating tyrosine phosphorylation on hSpry2, which in turn promotes c-Cbl binding and polyubiquitination. A mutant of hSpry2 that is deficient in serine phosphorylation displays enhanced tyrosine phosphorylation and c-Cbl binding, indicating that serine phosphorylation stabilizes hSpry2 by exerting an antagonistic effect on tyrosine phosphorylation. Moreover, loss of serine phosphorylation and the resulting enhanced degradation of hSpry2 impair its capacity to antagonize fibroblast growth factor-induced extracellular signal-regulated kinase activation. Our results imply that Mnk1-mediated serine phosphorylation of hSpry2 constitutes a regulatory mechanism to extend the temporal range of Spry activity. 

Retracted: No

PubPeer comments:
 Figure 2 and 3D. Much more similar than you would expect. ![file] ,
MicroRNA-449b-5p Suppresses Proliferation, Migration, and Invasion of Osteosarcoma by Targeting c-Met
Authors: Qian Li
Jingye Wang
Changliang Lu
Wei Gao
Min Gao
Journal: Medical Science Monitor (2019)
Discipline: CLINICAL MEDICINE
Keywords: microRNA-449b-5p; osteosarcoma; biological function; progression; mechanism
Affiliations: Department of Laboratory Medicine, Weifang Medical University, Weifang, Shandong, China (mainland)., School of Clinical Medicine, Weifang Medical University, Weifang, Shandong, China (mainland)., Department of Pathology, Weifang Maternal and Child Health Care Hospital, Weifang, Shandong, China (mainland)., Department of Otolaryngology, Weifang People's Hospital, Weifang, Shandong, China (mainland).

Abstract:  BACKGROUND The aim of this study was to clarify the biological function of microRNA-449b-5p in the progression of osteosarcoma (OS) and to define the underlying mechanism. MATERIAL AND METHODS Relative levels of microRNA-449b-5p in OS tissues and cell lines was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The correlation between microRNA-449b-5p level and pathological characteristics of OS patients was analyzed by chi-square test. Kaplan-Meier analysis was used for survival analysis of OS patients based on their expression level of microRNA-449b-5p. Regulatory effects of microRNA-449b-5p on cellular behaviors of OS cells were evaluated by cell counting kit-8 (CCK-8) and Transwell assay. The binding relationship between microRNA-449b-5p and c-Met was verified through dual-luciferase reporter gene assay, and their interaction in OS progression was further examined through a series of rescue experiments. RESULTS MicroRNA-449b-5p was expressed at low levels in OS. Lower levels of microRNA-449b-5p were seen in OS tissues with worse tumor grade or histological differentiation. OS patients with low levels of microRNA-449b-5p had worse overall survival relative to those with high level of microRNA-449b-5p. Overexpression of microRNA-449b-5p markedly attenuated proliferative, migratory, and invasive abilities of OS cells. C-Met is the downstream target of microRNA-449b-5p, and its level was inhibited in OS cells overexpressing microRNA-449b-5p. Importantly, c-Met partially rescued the inhibitory effects of microRNA-449b-5p on behavior of OS cells. CONCLUSIONS MicroRNA-449b-5p is downregulated in OS, which alleviates the malignant progression of OS by targeting c-Met. 

Retracted: No

PubPeer comments:
 From the Methods:  Tumor tissues and paracancerous tissues were surgically resected from 60 OS patients treated in Weifang Peopleu2019s Hospital from December 2016 to February 2018. This paper was published in August 2019. Yet, the survival curve in Figure 1D appears to show that the patients were followed for more than 50 months, almost for 5 years. Can the authors explain how they managed to do this? ![file] ,
Procyanidin A2, an anti-diabetic condensed tannin extracted from Wendlandia glabrata, reduces elevated G-6-Pase and mRNA levels in diabetic mice and increases glucose uptake in CC1 hepatocytes and C1C12 myoblast cells
Authors: Prasenjit Manna
Asamanja Chattoraj
Dibakar Chandra Deka
Gopinath Mondal
Narayan Chandra Talukdar
Yunush Sheikh
Maibam Beebina Chanu
Jagat Chandra Borah
Journal: RSC Advances (2019)
Discipline: CHEMISTRY
Keywords: diabetes; functional foods; herbal remedies; Wendlandia glabrata; procyanidin A2
Affiliations: Institute of Buioresources and Sustainable Development, Imphal-795001, India, CSIR-North East Institute of Science and Technology, Jorhat-785006, Department of Chemistry, Gauhati University, Guwahati-781014, Laboratory of Natural Medicinal Chemistry, Life Sciences Division, Institute of Advanced Study in Science & Technology, Guwahati-781035

Abstract:  To reduce the global burden of diabetes in an affordable way great attention has been paid to the search for functional foods and herbal remedies. One of the most popularly used functional foods in the North Eastern region of India is tender shoots of Wendlandia glabrata DC. In the current study identification of active anti-diabetic constituent of the tender shoots of W. glabrata was guided through α-glucosidase inhibition and procyanidin A2 was identified with IC50 0.27 ± 0.01 μg mL-1 making it potential source for postprandial management of DM type 2. The study has also demonstrated procyanidin A2 as a potent anti-diabetic agent that exhibits significant glucose-6-phosphatase inhibitory activities and downregulated mRNA level in diabetic mice as well as increases glucose uptake in hepatocytes and myoblast cells. This study revealed that easily available tender shoots of W. glabrata could be used to make specific dietary recommendations for consumption for affordable management of diabetes. 

Retracted: No

PubPeer comments:
 https: imgur.com a nrTjGxy , 
 Last author is currently the Founding Editor in Charge of this journal. ,
In vitro and in vivo studies of the inhibitory effects of emodin isolated from Polygonum cuspidatum on Coxsakievirus B₄
Authors: Zhao Liu
Liang-Jun Chen
Zhan-Qiu Yang
Hong Xiao
Wei Hou
Fei Wei
Yuan-Yuan Liu
Fan Luo
Hai-Rong Xiong
Journal: Molecules (2013)
Discipline: CHEMISTRY
Keywords: Coxsackievirus B₄; Emodin; Antiviral; Hep-2 cells; In vitro
Affiliations: State Key Laboratory of Virology, Institute of Medical Virology, School of Medicine, Wuhan 430071, China. .

Abstract:  The lack of effective therapeutics for Coxsackievirus B₄ (CVB₄) infection underscores the importance of finding novel antiviral compounds. Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is one of the natural anthraquinone derivatives obtained from the root and rhizome of Polygonum cuspidatum. In the present study, the possibility of using emodin as a potential antiviral to treat CVB₄ infection was explored in vitro and in mice. Emodin reduced CVB₄ entry and replication on Hep-2 cells in a concentration- and time-dependent manner, with a 50% effective concentration (EC₅₀) of 12.06 μM and selectivity index (SI) of 5.08, respectively. The inhibitory effect of emodin for CVB₄ entry and replication was further confirmed by a quantitative real time PCR (qPCR) assay. The results further showed that the mice orally treated with different dosages of emodin displayed a dose dependent increase of survival rate, body weight and prolonged mean time of death (MTD), accompanied by significantly decreased myocardial virus titers and pathologic scores/lesions. Moreover, emodin could inhibit CVB₄-induced apoptosis in vitro and in vivo. Our results indicated that emodin could be used as potential antiviral in the post-exposure prophylaxis for CVB₄ infection. 

Retracted: No

PubPeer comments:
 Could the authors comment on the relevance of References [4] and [12]?  The phenomenon of fluid flow plays a vital role in various industrial and engineering applications [1u201317]. - [4]. Zhao C, Qiao X, Cao Y, Shao Q. **Application of hydrogen peroxide presoaking prior to ammonia fiber expansion pretreatment of energy crops**. Fuel. 2017;205:184u201391. - [12]. Qiao X, Zhao C, Shao Q, Hassan M. Structural characterization of corn stover lignin after hydrogen peroxide presoaking prior to ammonia fiber expansion pretreatment. Energy Fuels. 2018;32:6022u201330. Other references seem unrepresentative of the entire literature. One cannot help wondering who edited this paper, and who reviewed it. ![file] ---------- For comparison - a citations payload from [Tian et al (2020)] : ![] ,
RETRACTED: Kinase inhibitors and airway inflammation
Authors: Gaetano Caramori
Ian M Adcock
K Fan Chung
Kazuhiro Ito
Journal: European Journal of Pharmacology (2006)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Kinases; Inflammatory mediators; Airway; T-cell function; Airway remodelling
Affiliations: Cell and Molecular Biology Group, Airways Disease Section, National Heart and Lung Institute, Imperial College London, Dovehouse Street, London, SW3, 6LY, United Kingdom. 

Abstract:  Kinases are believed to play a crucial role in the expression and activation of inflammatory mediators in the airway, in T-cell function and airway remodelling. Important kinases such as Inhibitor of kappaB kinase (IKK)2, mitogen activated protein (MAP) kinases and phsopho-inositol (PI)3 kinase regulate inflammation either through activation of pro-inflammatory transcription factors such as activating protein-1 (AP-1) and nuclear factor kappaB (NF-kappaB), which are activated in airway disease, or through regulation of mRNA half-life. Selective kinase inhibitors have been developed which reduce inflammation and some characteristics of disease in animal models. Targeting specific kinases that are overexpressed or over active in disease should allow for selective treatment of respiratory diseases. Interest in this area has intensified due to the success of the specific Abelson murine leukaemia viral oncogene (Abl) kinase inhibitor imatinib mesylate (Gleevec) in the treatment of chronic myelogenous leukaemia. Encouraging data from animal models and primary cells and early Phase I and II studies in other diseases suggest that inhibitors of p38 MAP kinase and IKK2 may prove to be useful novel therapies in the treatment of severe asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis and other inflammatory airway diseases. 

Retracted: Yes

PubPeer comments:
null, 
 Reason: This article has been retracted: please see Elsevier Policy on Article Withdrawal (http: www.elsevier.com locate withdrawalpolicy). This article has been retracted because of significant textual overlap (self-plagiarism) with Ian M. Adcock Gaetano Caramori Kinase Targets and Inhibitors for the Treatment of Airway Inflammatory Diseases Biodrugs 2004; 18 (3): 167u2013180 doi:10.2165 00063030-200418030-00003 Apologies are offered to readers of the journal that this was not detected during the submission process. , 
 and the point of this is? , 
 #3 I was perusing the other dozen or so papers with image concerns here on PubPeer and had to look up the reason for this retraction. I thought I would save others the time by posting the text here. , 
 #3 As pointed out, many correction and retraction notices get copied to PubPeer. It s a convenience, because journals are really bad at making the information visible and easy to find. ,
LncRNA SNHG4 promotes tumour growth by sponging miR-224-3p and predicts poor survival and recurrence in human osteosarcoma
Authors: Fan Feng
Lifeng Lao
Ruida Xu
Zude Liu
Xiaosheng Yu
Journal: Cell Proliferation (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: lncRNA; SNHG4; osteosarcoma; tumour growth; miR-224-3p
Affiliations: Department of Orthopaedic Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Abstract:  Objective: Accumulating data show that dysregulation of long noncoding RNAs (lncRNAs) acts a critical role in a variety of malignancies. Among these lncRNAs, small nucleolar RNA host genes (SNHGs) are associated with tumour growth and progression. But, the molecular mechanisms by which SNHG4 contributes to osteosarcoma remain undocumented. Methods: The association between lncRNA SNHG4 expression and clinicopathologic characteristics and prognosis in patients with osteosarcoma was analysed by TCGA RNA-sequencing data. Cell viability and colony formation abilities were respectively assessed by MTT and colony formation assays. LncRNA SNHG4-specific binding with miR-224-3p was verified by bioinformatic analysis, luciferase gene report, and RNA immunoprecipitation assays. Regulation relationship between SNHG4 and miR-224-3p expression was further evaluated by the rescue experiments. Results: The expression level of lncRNA SNHG4 was significantly elevated in osteosarcoma samples and cell lines as compared with the adjacent normal tissues, and SNHG4 high expression was associated with tumour size (TS) and poor prognosis in patients with osteosarcoma. Knockdown of SNHG4 suppressed cell viability and invasive potential, whereas ectopic SNHG4 expression displayed the opposite effects. Moreover, we found that lncRNA SNHG4 acted as a sponge of miR-224-3p, and miR-224-3p mimic reversed SNHG4 induced tumour-promoting effects in osteosarcoma cells. The expression of miR-224-3p depicted a negative correlation with SNHG4 in osteosarcoma samples and miR-224-3p low expression was associated with TS and poor survival in patients with osteosarcoma. Conclusion: Our findings demonstrated that LncRNA SNHG4 promoted tumour growth by sponging miR-224-3p and represented a poor prognostic factor in patients with osteosarcoma. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have overlapping images for different cell lines. ![file] , 
 Figures 2 and 5 appear to have the same problem. Also it appears that there is an overlap between images in 2 and 5 (light blue oval) ![file] ![file] ,