PReD-Bench/PRed-Bench huggingface dataset:
Delivery of miR-375 and doxorubicin hydrochloride by lipid-coated hollow mesoporous silica nanoparticles to overcome multiple drug resistance in hepatocellular carcinoma
Authors: Chuanrui Xu
Xingxing He
Robert J Lee
Tan Yang
Weigang Yuan
Zhaoyang Yu
Huiying Xue
Lei Li
Jia You
Yong Liu
Journal: International Journal of Nanomedicine (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: AEG-1; doxorubicin; hepatocel-lular carcinoma; hollow mesoporous silica nanoparticle; miR-375
Affiliations: School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology., Institute of Liver Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China., Division of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, The Ohio State University, Columbus, Ohio, USA.

Abstract:  Multidrug resistance (MDR) due to overexpression of P-glycoprotein (P-gp) is a major obstacle that hinders the treatment of hepatocellular carcinoma (HCC). It has been shown that miR-375 inhibits P-gp expression via inhibition of astrocyte elevated gene-1 (AEG-1) expression in HCC, and induces apoptosis in HCC cells by targeting AEG-1 and YAP1. In this study, we prepared lipid-coated hollow mesoporous silica nanoparticles (LH) containing doxorubicin hydrochloride (DOX) and miR-375 (LHD/miR-375) to deliver the two agents into MDR HCC cells in vitro and in vivo. We found that LHD/miR-375 overcame drug efflux and delivered miR-375 and DOX into MDR HepG2/ADR cells or HCC tissues. MiR-375 delivered by LHD/miR-375 was taken up through phagocytosis and clathrin- and caveolae-mediated endocytosis. Following release from late endosomes, it repressed the expression of P-gp in HepG2/ADR cells. The synergistic effects of miR-375 and hollow mesoporous silica nanoparticles (HMSN) resulted in a profound increase in the uptake of DOX by the HCC cells and prevented HCC cell growth. Enhanced antitumor effects of LHD/miR-375 were also validated in HCC xenografts and primary tumors; however, no significant toxicity was observed. Mechanistic studies also revealed that miR-375 and DOX exerted a synergistic antitumor effect by promoting apoptosis. Our study illustrates that delivery of miR-375 using HMSN is a feasible approach to circumvent MDR in the management of HCC. It, therefore, merits further development for potential clinical application. 

Retracted: No

PubPeer comments:
 Figure 8E appears to include a repeated image. *** ![file] , 
 Corrected ![file] , 
 Two images in Figure 4B may overlap (green boxes). *** Brightness enhanced ![file] ,
Associations of polymorphisms in CTLA-4 and IL-18 with liver diseases: evidence from a meta-analysis
Authors: Shenglong Zhang
Wentao Wang
Xianwei Yang
Journal: Bioscience reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cytotoxic T-lymphocyte-associated antigen 4; Interleukin-18; Liver diseases; Meta-analysis.
Affiliations: West China Hospital of Sichuan University, Chengdu, China.

Abstract:  Background: Associations between polymorphisms in cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) / interleukin-18 (IL-18) and susceptibility to liver diseases were already reported by many publications. The aim of this meta-analysis was to clarify associations between polymorphisms in CTLA-4/IL-18 and liver diseases by combing the results of all relevant publications. Methods: Eligible publications were searched from Pubmed, Embase, WOS and CNKI. The latest literature searching update was performed on 2nd October, 2019. We used Review Manager to combine the results of individual studies. Results: Sixty-seven studies were included in this study. Combined results revealed that CTLA-4 rs231775 (dominant comparison: OR 0.83, 95 % CI 0.79-0.88; recessive comparison: OR 1.33, 95 % CI 1.23-1.43; allele comparison: OR 0.84, 95 % CI 0.78-0.90), IL-18 rs1946518 (dominant comparison: OR 0.85, 95 % CI 0.78-0.92; recessive comparison: OR 1.29, 95 % CI 1.13-1.48; allele comparison: OR 0.79, 95 % CI 0.71-0.88) and IL-18 rs187238 (dominant comparison: OR 1.28, 95 % CI 1.07-1.53; over-dominant comparison: OR 0.81, 95 % CI 0.68-0.97; allele comparison: OR 1.22, 95 % CI 1.07-1.39) polymorphisms were all significantly associated with liver diseases in the general population. We also obtained similar significant associations for CTLA-4 rs231775, CTLA-4 rs5742909, CTLA-4 rs3087243, IL-18 rs1946518 and IL-18 rs187238 polymorphisms in subgroup analyses. Conclusions: Collectively, this meta-analysis proved that CTLA-4 rs231775, CTLA-4 rs5742909, CTLA-4 rs3087243, IL-18 rs1946518 and IL-18 rs187238 polymorphisms may confer susceptibility to various types of liver diseases. 

Retracted: No

PubPeer comments:
 WITHDRAWN ARTICLE WITHDRAWN: Associations of polymorphisms in CTLA-4 and IL-18 with liver diseases: evidence from a meta-analysis Shenglong Zhang, Xianwei Yang, Wentao Wang Bioscience Reports (2020) BSR20193518; DOI: 10.1042 BSR20193518 The Accepted Manuscript version of this article (published on 23 December 2019) was withdrawn on 7 July 2020 due to concerns over data validity. ,
Polyadenylate polymerase modulations in human epithelioid cervix and breast cancer cell lines, treated with etoposide or cordycepin, follow cell cycle rather than apoptosis induction
Authors: Hellinida Thomadaki
Andreas Scorilas
Chris M Tsiapalis
Journal: Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cancer; Cell cycle; Apoptosis; Anticancer drugs; Polyadenylation trans-acting factors
Affiliations: Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Athens, Panepistimiopolis, GR-15701 Athens, Greece.

Abstract:  Cancer results from an imbalance between cell cycle progression and apoptosis. Therefore, most anticancer drugs exert their antiproliferative and cytotoxic activity via cell cycle arrest and induction of apoptosis, a controlled form of cell death that is dysregulated in cancer. Many polyadenylation trans-acting factors, including polyadenylate polymerase (PAP), are increasingly found to be involved in cell cycle, apoptosis and cancer prognosis. The objective of the present study was to identify PAP modulations in the response of two epithelial cancer cell lines (HeLa and MCF-7) to apoptosis induction by the anticancer drugs etoposide and cordycepin. Cells were assessed for PAP activity and isoforms by the highly sensitive PAP activity assay and Western blotting, respectively. Induction of apoptosis was determined by endonucleosomal DNA cleavage, 4'6-diamidino-2-phenylindol (DAPI) staining and caspase-6 activity assay, whereas cytotoxicity and cell cycle status were assessed by trypan blue staining, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Our results indicate that PAP changes very early in response to either etoposide or cordycepin treatment, even prior to the hallmarks of apoptosis (chromatin condensation and cleavage), in both cell lines tested, but in a different mode. Our results suggest, for the first time, that in the epithelial cancer cell lines used, PAP modulations follow cell cycle progression rather than the course of apoptosis. 

Retracted: No

PubPeer comments:
 Figure 6 and 7. * Red boxes: Unexpected similarities between the blots in the two figures * Blue boxes: Unexpected similarities between lanes representing different experiments ![file] ,
Postprandial hepatic lipid metabolism requires signaling through Akt2 independent of the transcription factors FoxA2, FoxO1, and SREBP1c
Authors: Danish Saleh
Klaus H Kaestner
Min Wan
Morris J Birnbaum
Karla F Leavens
David A Guertin
Timothy R Peterson
David M Sabatini
Rachael M Easton
Journal: Cell Metabolism (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: obesity; insulin resistance; Akt/PKB; lipid accumulation; liver
Affiliations: The Institute of Diabetes, Obesity, and Metabolism, University of Pennsylvania, Philadelphia, PA 19104, USA.

Abstract:  Under conditions of obesity and insulin resistance, the serine/threonine protein kinase Akt/PKB is required for lipid accumulation in liver. Two forkhead transcription factors, FoxA2 and FoxO1, have been suggested to function downstream of and to be negatively regulated by Akt and are proposed as key determinants of hepatic triglyceride content. In this study, we utilize genetic loss of function experiments to show that constitutive activation of neither FoxA2 nor FoxO1 can account for the protection from steatosis afforded by deletion of Akt2 in liver. Rather, another downstream target positively regulated by Akt, the mTORC1 complex, is required in vivo for de novo lipogenesis and Srebp1c expression. Nonetheless, activation of mTORC1 and SREBP1c is not sufficient to drive postprandial lipogenesis in the absence of Akt2. These data show that insulin signaling through Akt2 promotes anabolic lipid metabolism independent of Foxa2 or FoxO1 and through pathways additional to the mTORC1-dependent activation of SREBP1c. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
 I found some possible issues with the primers used in this article. I humbly ask the authors to check this. i) The Real-time PCR primers sequences provided for the TSC1 gene seems to match **only** introns of this gene http: www.ensembl.org Mus_musculus Gene Sequence?db=core;g=ENSMUSG00000026812;r=2:28641228-28691167 **Forward primer** in orange, exons in red ![file] **Reverse primer** ![file] ii) Same pair of primers were used for Acl and Gpat? ![file] iii) The authors chose two FORWARD primers to measure Srebpc1? http: www.ensembl.org Mus_musculus Gene Sequence?db=core;g=ENSMUSG00000020538;r=11:60199089-60222581 **u201cForwardu201d** ![file] **u201cReverseu201d (?)** ![file] iv) Sestrin1 forward primer is not a specific primer for this gene. A blast of this sequence with the M. musculus transcriptome look like this ![file] ,
MiR-145-5p alleviates hypoxia/reoxygenation- induced cardiac microvascular endothelial cell injury in coronary heart disease by inhibiting Smad4 expression
Authors: L-L Li
A-G Xue
G-P Wang
N Wang
C-D Mao
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-145-5p; hypoxia/reoxygenation; cardiac microvascular endothelial cell; coronary heart disease; Smad4
Affiliations: Department of Inspection, Jiaozhou Central Hospital Of Qingdao, Shandong Province, Qingdao, P.R. China. .

Abstract:  Objective: To investigate the effects and mechanism of miR-145-5p on hypoxia/reoxygenation (H/R)-induced cardiac microvascular endothelial cell (CMEC) injury in coronary heart disease (CHD). Patients and methods: Patients with CHD (n=96) and healthy volunteers (n=96) were enrolled, and H/R injury model of CMECs was established. The expression of miR-145-5p and mothers against decapentaplegic homolog 4 (Smad4) mRNA in cells was quantified with reverse transcription polymerase chain reaction (RT-PCR). Then, miR-145-5p mimics and Smad4 inhibitor were transfected into CMECs. Cell counting kit-8 (CCK-8) was employed for proliferation detection, flow cytometry for apoptosis detection, and Western Blot for measuring the expression of apoptosis-related proteins and Smad4 protein. Results: The expression of serum miR-145-5p in patients with CHD was significantly lower than that in healthy individuals. The area under the curve (AUC) of miR-145-5p in diagnosing CHD was 0.894, and the expression of miR-145-5p was negatively correlated with that of Smad4 (p&lt;0.05). Over-expression of miR-145-5p promoted the proliferation, inhibited the apoptosis, and reduced inflammatory responses and oxidative stress in H/R-injured CMECs. Moreover, miR-145-5p might negatively regulate the expression of Smad4 in CMECs. Dual-Luciferase reporter assay determined the targeting relation between miR-145-5p and Smad4. Conclusions: MiR-145-5p is lowly expressed in patients with CHD, and its over-expression effectively alleviates H/R-induced CMEC injury by inhibiting Smad4. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 #2 Figures 2 and 3, now with increased contrast to accentuate the mottled background: ![file] An interesting feature of the mottled pattern is the way it repeats periodically. Some kind of defect in a scanner? But as Channa Pleurophthalma pointed out in #1, the same periodic mottles are also visible in Figures of [Zhou et al (2020)] - different authors at a different institution. In that other thread, Elisabeth Bik has provided contrast-enhanced versions: ![] They remind me of Philippe Starck anti-ergonomic door-handles. ![] , 
 Fig 2C and 3C are FAflow-cytometry plots illustrating  apoptotic rate of injured CMECs . ![file] Note the similarity to the corresponding plots in Zhou et al (2020), despite the differences between cardiomyocytes and CMECs. ![] ,
A self-amplifying loop of YAP and SHH drives formation and expansion of heterotopic ossification
Authors: Qian Cong
Bo Gao
Ruoshi Xu
Meijun Yan
Zhiheng Liao
Hye Soo Chung
Geoffrey A Bocobo
Hyeon Ju Song
Paul B Yu
Yaxing Zhou
Yingzi Yang
Peiqiang Su
Yuchen Liu
Taylor A Covington
Caiqi Cheng
Hang Zhou
Taifeng Zhou
Journal: Science Translational Medicine (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Heterotopic ossification; Yes-associated protein (YAP); Sonic hedgehog (SHH); mouse models; progressive osseous heteroplasia (POH)
Affiliations: Department of Developmental Biology, Harvard School of Dental Medicine, Harvard Stem Cell Institute, 188 Longwood Ave., Boston, MA 02115, USA., Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA., Department of Orthopaedic Surgery, Guangdong Provincial Key Laboratory of Orthopedics and Traumatology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.

Abstract:  Heterotopic ossification (HO) occurs as a common complication after injury or in genetic disorders. The mechanisms underlying HO remain incompletely understood, and there are no approved prophylactic or secondary treatments available. Here, we identify a self-amplifying, self-propagating loop of Yes-associated protein (YAP)-Sonic hedgehog (SHH) as a core molecular mechanism underlying diverse forms of HO. In mouse models of progressive osseous heteroplasia (POH), a disease caused by null mutations in GNAS, we found that Gnas-/- mesenchymal cells secreted SHH, which induced osteoblast differentiation of the surrounding wild-type cells. We further showed that loss of Gnas led to activation of YAP transcription activity, which directly drove Shh expression. Secreted SHH further induced YAP activation, Shh expression, and osteoblast differentiation in surrounding wild-type cells. This self-propagating positive feedback loop was both necessary and sufficient for HO expansion and could act independently of Gnas in fibrodysplasia ossificans progressiva (FOP), another genetic HO, and nonhereditary HO mouse models. Genetic or pharmacological inhibition of YAP or SHH abolished HO in POH and FOP and acquired HO mouse models without affecting normal bone homeostasis, providing a previously unrecognized therapeutic rationale to prevent, reduce, and shrink HO. 

Retracted: No

PubPeer comments:
 Please check for duplication in the areas represented by same colored boxes and share the source data. ![file] , 
 The two controls are not duplicates, although they look similar. I have included the source data of the original Western blotting here, with long and short exposures. ![file] ,
Ubiquitination increases parkin activity to promote autophagic α-synuclein clearance
Authors: Michaeline L Hebron
Charbel E-H Moussa
Irina Lonskaya
Nicole M Desforges
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Parkinson's disease; movement disorder; genetic; age related; autosomal recessive
Affiliations: Department of Neuroscience, Laboratory for Dementia and Parkinsonism, Georgetown University Medical Center, Washington, DC, United States of America.

Abstract:  Parkinson's disease (PD) is a movement disorder associated with genetic and age related causes. Although autosomal recessive early onset PD linked to parkin mutations does not exhibit α-Synuclein accumulation, while autosomal dominant and sporadic PD manifest with α-Synuclein inclusions, loss of dopaminergic substantia nigra neurons is a common denominator in PD. Here we show that decreased parkin ubiquitination and loss of parkin stability impair interaction with Beclin-1 and alter α-Synuclein degradation, leading to death of dopaminergic neurons. Tyrosine kinase inhibition increases parkin ubiquitination and interaction with Beclin-1, promoting autophagic α-Synuclein clearance and nigral neuron survival. However, loss of parkin via deletion increases α-Synuclein in the blood compared to the brain, suggesting that functional parkin prevents α-Synuclein release into the blood. These studies demonstrate that parkin ubiquitination affects its protein stability and E3 ligase activity, possibly leading to α-Synuclein sequestration and subsequent clearance. 

Retracted: No

PubPeer comments:
 Concern about Figure 4. * Red blue boxes: Three panels appear to overlap with each other. ![file] , 
 I agree with concerns posted above and have also found additional concerning images from Figures 2 and 4. ![file] , 
 further overlap with other papers from the same group ![file] , 
 There also appears to be overlap with another paper in IHC images. The two papers claim the images are of different proteins. Additionally by analyzing the overlaps it appears that the independent panels within each paper are also simply cross of single larger image despite claiming to represent different conditions. ![image] ,
Perceptual organization and the judgment of brightness
Authors: E H Adelson
Journal: Science (1993)
Discipline: Multidisciplinary
Keywords: brightness illusions; perceived brightness; gray patch; surrounding context; perceptual organization
Affiliations: Media Laboratory, Massachusetts Institute of Technology, Cambridge 02139.

Abstract:  The perceived brightness of a gray patch depends on the surrounding context. For example, a medium-gray patch appears darker when placed on a bright background and brighter when placed on a dark background. Models to explain these effects are usually based on simple low-level mechanisms. A new set of brightness illusions cannot be explained by such models. In these illusions, the brightness percept is strongly influenced by the perceptual organization of the stimuli. Simple modifications of the stimuli that should have little effect on low-level mechanisms greatly alter the strength of the illusion. These effects may be ascribed to more complex mechanisms occurring later in the visual system. 

Retracted: No

PubPeer comments:
  All of the phenomena discussed above lead to the same conclusion: Brightness judgments cannot be simply explained with low-level mechanisms. Geometrical changes that should be inconsequential for low-level mechanisms can cause dramatic changes in the brightness report. This was not news in 1993. That the structure of an image determines the perceived lightness brightness of an area of the image was known at least since the construction of the Benary cross (on a suggestion by Wertheimer), in the 1920 s, precisely for the purpose of falsifying proposed  lateral inhibition mechanisms. Transparency effects, similarly incompatible with local inhibition, have also been studied for decades, famously by F. Metelli. Adelson seems to believe that, despite these falsifying demonstrations, so -called  low level mechanisms explain certain perceptual experiences. As Teller (1984) has pointed out, such a view leaves open the question of how the responses of  low-level neurons are preserved all the way up to consciousness - dubious, she referred to this view as the  nothing mucks it up hypothesis. Oddly enough, Adelson does cite Metelli (citation  7 ), albeit somewhat opaquely:  Figure 2A is seen as a wall of cubical blocks viewed through light and dark horizontal strips, as if there were light and dark transparent filters interposed between the observer and the blocks. The luminance may be perceptually divided between the strips and the blocks (7), so that a diamond of a given luminance can be seen either as a dark diamond behind a light strip or a light diamond behind a dark strip. The perceptual inferences apparently influence the brightness judgments.  If we read the passage as indicating that Metelli had already demonstrated (as he had) that certain configurations radically affect the relative perceived lightness brightness of surfaces, then the claim of novelty becomes even more puzzling. ,
MicroRNA-148a suppresses epithelial-mesenchymal transition and invasion of pancreatic cancer cells by targeting Wnt10b and inhibiting the Wnt/β-catenin signaling pathway
Authors: Zhen Wan
Yong Li
Long Peng
Zhanying Liu
Yi Tu
Jian Xiao
Haiwei Xiong
Weidong Xiao
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Epithelial-mesenchymal transition (EMT); Wnt/β-catenin signaling pathway; microRNAs (miRNAs); pancreatic cancer; miR-148a
Affiliations: Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China., Department of Pathology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Abstract:  Epithelial-mesenchymal transition (EMT) plays a critical role in the process of cancer invasion and metastasis. The Wnt/β-catenin signaling pathway is known as a stimulative factor, which may trigger EMT and metastasis of cancer cells. In addition, several microRNAs (miRNAs) have been proven to regulate the EMT process. Recent research revealed that miR‑148a is downregulated in pancreatic cancer. However, the definite role of miR-148a in EMT and invasion of pancreatic cancer is still unknown. The present study attempted to demonstrate the underlying mechanism of miR-148a in the regulation of EMT and invasion of pancreatic cancer cells. Our data revealed that the expression of miR-148a was markedly downregulated in human pancreatic ductal adenocarcinoma (PDAC) cell lines and tissues. In addition, the downregulation of miR-148a was associated with poor prognosis and EMT phenotype. Furthermore, restoration of miR-148a expression inhibited the EMT process, as well as the migration and invasion of BxPC-3 pancreatic cancer cells. Wnt10b, a promoting molecule of the Wnt/β-catenin signaling pathway, was demonstrated by dual‑luciferase reporter assay to be a direct target of miR‑148a. Subsequently, we found that miR‑148a negatively regulated the protein expression of β-catenin, cyclin D1 and MMP-9, which were important components of the Wnt/β-catenin signaling pathway. In conclusion, these findings revealed that miR-148a suppresses EMT and invasion of pancreatic cancer cells by targeting Wnt10b and inhibiting the Wnt/β-catenin signaling pathway, and thus, miR-148a may serve as a novel therapeutic target for pancreatic cancer. 

Retracted: No

PubPeer comments:
 Figure 2 and 4 have numerous unexpectedly similar (or the same) cells recurring in different images. (The dark green box is the same Blank image, but that is fine) ![file] ![file] ,
PAG1 stimulates proliferation and metastasis of nasopharyngeal carcinoma through downregulating PTEN
Authors: H-B Sha
X-J Ge
J-J Fan
J-J Lin
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: PAG1; nasopharyngeal carcinoma; PTEN; proliferation; migration
Affiliations: Department of Clinical Laboratory, The Second Children & Women's Healthcare of Jinan City, Jinan, China. .

Abstract:  Objective: We aim to uncover the expression pattern and biological functions of PAG1 in the progression of nasopharyngeal carcinoma (NPC). Patients and methods: PAG1 levels in 28 paired NPC tissues and paracancerous tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Then, the potential influences of PAG1 on proliferative, migratory and invasive abilities of SUNE2 and CNE2 cells were assessed by cell counting kit-8 (CCK-8) and transwell assay, respectively. Next, the interaction between PAG1 and its direct target gene of phosphate and tension homology deleted on chromosome ten (PTEN) was verified by Dual-Luciferase reporter gene assay. At last, rescue experiments were conducted to uncover the role of PAG1/PTEN axis in the malignant progression of NPC. Results: PAG1 was highly expressed in NPC tissues and cell lines. Knockdown of PAG1 blocked NPC cells to proliferate, migrate, and invade. Dual-Luciferase reporter gene assay indicated the binding relationship between PAG1 and PTEN. In addition, both mRNA and protein levels of PTEN were negatively regulated by PAG1 in NPC cells. Notably, PTEN was responsible for PAG1-regulated malignant progression of NPC. Conclusions: PAG1 is upregulated in NPC tissues and cells and stimulates the proliferative and metastatic abilities in NPC by targeting PTEN, thus aggravating the malignant progression of NPC. 

Retracted: No

PubPeer comments:
 Table 1. The column headings promise to convert the numbers of each patient subgroup into percentages, but the body of the table reneges on the promise. ![file] In itself this would be a minor error, but table 1s of this form are one characteristic feature of a  Comb papermill . Another recurring feature is pairs of Kaplan-Meier plots, crenellated along the survival curves so that they resemble combs or walls made of Lego, with survival nose-diving precipitously as time approaches 75 months. Here, Figs 1C, 3E. ![file] Suffice to say that the two figures are incompatible (with **everyone** dead after 75 months when subgrouped by PAG1, but not by PTEN), and that the number of steps deaths in each curve is unrelated to the number of patients in the subgroups. ,
Metallic glass coating for improving diamond dicing performance
Authors: Bo-Zhang Lai
Pakman Yiu
Yu-Lin Shen
Chia-Wei Chang
Jinn P Chu
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: diamond dicing blades; metallic glass coating; chipping reduction; coefficient-of-friction; Zr-based
Affiliations: Department of Materials Science and Engineering, National Taiwan University of Science and Technology, Taipei, 10607, Taiwan. ., Applied Research Center for Thin-Film Metallic Glass, National Taiwan University of Science and Technology, Taipei, 10607, Taiwan. ., Department of Materials Science and Engineering, National Taiwan University of Science and Technology, Taipei, 10607, Taiwan., Applied Research Center for Thin-Film Metallic Glass, National Taiwan University of Science and Technology, Taipei, 10607, Taiwan., Department of Mechanical Engineering, University of New Mexico, Albuquerque, NM, 87131, USA.

Abstract:  This is the first report on the coating of diamond dicing blades with metallic glass (MG) coating to reduce chipping when used to cut Si, SiC, sapphire, and patterned sapphire substrates (PSS). The low coefficient-of-friction (CoF) of Zr-based MG-coated dicing blades was shown to reduce the number and size of chips, regardless of the target substrate. Overall, SiC, sapphire and PSS were most affected by chipping, due to the fact that higher cutting forces were needed for the higher hardness of SiC, sapphire and PSS. Compared to the bare blade, the MG coating provided the following reductions in chipping area: Si (~ 23%), SiC (~ 36%), sapphire (~ 45%), and PSS (~ 33%). The proposed coating proved particularly effective in reducing chips of larger size (&gt; 41 µm in chipping width), as indicated by an ~ 80% reduction when cutting sapphire. Small variations in kerf angle and depth demonstrate the durability of the coated blades, which would no doubt enhance consistency in dicing performance and extend the blade lifespan. Finite-element modeling revealed significant reductions in tensile stress and elastic-plastic deformation during dicing, thanks to a lower CoF. 

Retracted: No

PubPeer comments:
 Figure 4 Two identical XRD patterns presented as different samples. ![file] , 
 #1 Thank you for pointing out this error. The XRD pattern for  Bare Blade in orange was mistakenly placed. As seen in the attached XRD patterns below from B.C. Lai s MS thesis, the pattern for Bare blade is different from other coated blades. We will write an errata to the journal to correct this error. Again, thank you for this. Regards, Jinn P. Chu ![file] ,
The role of heme oxygenase 1 in rapamycin-induced renal dysfunction after ischemia and reperfusion injury
Authors: V P Antunes Teixeira
N O S Câmara
A Pacheco-Silva
C Q Feitoza
M A Cenedeze
P M H Wang
H S Pinheiro
M A dos Reis
A P F Bertocchi
G M Gonçalves
M J Damião
Journal: Kidney International (2006)
Discipline: CLINICAL MEDICINE
Keywords: Ischemia; reperfusion injury; acute renal failure; immunosuppressive drugs; rapamycin
Affiliations: Laboratório de Imunologia Clínica e Experimental, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil.

Abstract:  Ischemia and reperfusion injury (IRI) is the main etiology of acute renal failure in native and transplanted kidneys. In the transplantation field, immunosuppressive drugs may play an additional role in acute graft dysfunction. Rapamycin may impair renal regeneration post IRI. Heme oxygenase 1 (HO-1) is a protective gene with anti-inflammatory and anti-apoptotic actions. We investigated whether HO-1 played a role in rapamycin-induced renal dysfunction in an established model of IRI. Rapamycin (3 mg/kg) was administered to mice before being subjected to 45 min of ischemia. Animals subjected to IRI presented with impaired renal function that peaked at 24 h (2.05+/-0.23 mg/dl), decreasing thereafter. Treatment with rapamycin caused even more renal dysfunctions (2.30+/-0.33 mg/dl), sustained up to 120 h after reperfusion (1.54+/-0.4 mg/dl), when compared to the control (0.63+/-0.09 mg/dl, P&lt;0.05). Rapamycin delayed tubular regeneration that was normally higher in the control group at day 5 (68.53+/-2.30 vs 43.63+/-3.11%, P&lt;0.05). HO-1 was markedly upregulated after IRI and its expression was even enhanced by rapamycin (1.32-fold). However, prior induction of HO-1 by cobalt protoporphyrin improved the renal dysfunction imposed by rapamycin, mostly at later time points. These results demonstrated that rapamycin used in ischemic-injured organs could also negatively affect post-transplantation recovery. Modulation of HO-1 expression may represent a feasible approach to limit rapamycin acute toxicity. 

Retracted: No

PubPeer comments:
 The abstract of this paper, including the key results, is almost identical to that of another paper (PMID 17219692). https: pubpeer.com publications 1ECCDE4BEF713276A18158499AF5C0 ,
Targeted delivery of doxorubicin-utilizing chitosan nanoparticles surface-functionalized with anti-Her2 trastuzumab
Authors: Fatemeh Atyabi
Ali-Akbar Mousavi Movahedi
Ebrahim Vasheghani-Farahani
Rassoul Dinarvand
Parisa Yousefpour
Journal: International journal of nanomedicine (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: active targeting; chitosan; doxorubicin; self-assembled nanoparticles; trastuzumab.

Abstract:  Background: Targeting drugs to their sites of action to overcome the systemic side effects associated with most antineoplastic agents is still a major challenge in pharmaceutical research. In this study, the monoclonal antibody, trastuzumab, was used as a targeting agent in nanoparticles carrying the antitumor drug, doxorubicin, specifically to its site of action. Methods: Chitosan-doxorubicin conjugation was carried out using succinic anhydride as a crosslinker. Trastuzumab was conjugated to self-assembled chitosan-doxorubin conjugate (CS-DOX) nanoparticles (particle size, 200 nm) via thiolation of lysine residues and subsequent linking of the resulted thiols to chitosan. Conjugation was confirmed by gel permeation chromatography, differential scanning calorimetry, Fourier transform infrared spectroscopy, and (1)H nuclear magnetic resonance spectroscopy studies. Dynamic light scattering, transmission electron microscopy, and zeta potential determination were used to characterize the nanoparticles. Results: CS-DOX conjugated nanoparticles had a spherical shape and smooth surface with a narrow size distribution and core-shell structure. Increasing the ratio of doxorubicin to chitosan in the conjugation reaction gave rise to a higher doxorubicin content but lower conjugation efficiency. Trastuzumab-decorated nanoparticles (CS-DOX-mAb) contained 47 μg/mg doxorubicin and 33.5 μg/mg trastuzumab. Binding of trastuzumab to the nanoparticles was further probed thermodynamically by isothermal titration calorimetry. Fluorescence microscopy demonstrated enhanced and selective uptake of CS-DOX-mAb by Her2+ cancer cells compared with nontargeted CS-DOX nanoparticles and free drug. Conclusion: Antibody-conjugated nanoparticles were shown to discriminate between Her2+ and Her2⁻ cells, and thus have the potential to be used in active targeted drug delivery, with reduction of drug side effects in Her2+ breast and ovarian cancers. 

Retracted: No

PubPeer comments:
 Panels in Figure 9B and 9D are repeated: original image ![file] contrast enhanced image ![file] , 
 To whom it may concern , This is Ramin Sakhtianchi and I am writing to complain about the author s name of this article in your site. Although I was not in this article you mentioned me as the first author! [Moderator: The metadata are sourced from public databases like Crossref, so it seems the article information is or was incorrect in one of those sources. It is the responsibility of the journal to populate the databases correctly. Corrected information should feed through eventually.] ,
Apocrine Carcinoma of the Groin Possibly Associated with Extramammary Paget's Disease
Authors: Sang-Hee Seo
Dong-Hoon Shin
Hyun-Woo Sung
Journal: Annals of dermatology (2011)
Discipline: CLINICAL MEDICINE
Keywords: Carcinoma; Extramammary Paget's disease; Groin.
Affiliations: Department of Dermatology and Medical Research Institute, Pusan National University School of Medicine, Yangsan, Korea., Department of Pathology, Pusan National University Yangsan Hospital, Yangsan, Korea., Department of Orthopedics, Dong-A University School of Medicine, Busan, Korea.

Abstract:  Apocrine carcinoma is a rare malignancy with invasive potential. It presents as painless, slow-growing, firm or cystic, red nodules with focal ulcerations. The tumor is capable of hematogenous dissemination to the liver, lungs, and bone as well as lymphatic spread. In addition, apocrine carcinomas cause intra-epidemial pagetoid spread. We report a case of an apocrine carcinoma related with extensive extramammary Paget's disease (EMPD). The relationship between apocrine carcinoma and EMPD remains to be understood. Co-existing cases with apocrine carcinoma and EMPD are discussed to better understand the relationship between these two malignant apocrine tumors. 

Retracted: No

PubPeer comments:
 In Figure 3A, a micrograph has been duplicated and presented as something else. ![file] , 
 Thank you very much for pointing out our mistake. This is because the mirograph of CD11C in Ogr1- - group were incorrectly used during the overall picture layout. We are extremely sorry for such mistake. We have again checked all the raw data carefully, there was no difference for CD11c and B220 between WT and ogr1- - groups, which will not change the conclusion. We will contact the editor to make correction for this. Again, we appreciate your comment. ,
Shelf Life Evaluation of Clinical Grade Chondrogenic Induced Aged Adult Stem Cells for Cartilage Regeneration
Authors: B S Aminuddin
C C Ude
B H I Ruszymah
W T Seet
S Sharen Aini
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: BMSCs; ADSCs; proliferation; chondrogenic induction; shelf life
Affiliations: Tissue Engineering Centre, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, Cheras, 56000, K. L, Malaysia., Bioartificial Organ and Regenerative Medicine Unit, National Defence University of Malaysia, Sungai Besi, Camp, 57000, K. L, Malaysia., ENT Consultant Clinic, Ampang Putri Specialist Hospital, 68000, Ampang, Malaysia., Department of Physiology, Medical Faculty Universiti Kebangsaan Malaysia, Jalan Yaacob Latif, Bandar Tun Razak, Cheras, 56000, K. L, Malaysia. .

Abstract:  The study objectives include, enhancing the proliferations of aged bone marrow stem cells (BMSCs) and adipose stem cells (ADSCs); and evaluating the shelf lives of clinical grade chondrogenically induced cells from both samples. ADSCs and BMSCs from 56 patients (76 ± 8 yrs) were proliferated using basal medium (FD) and at (5, 10, 15, 20 and 25) ng/ml of basal fibroblast growth factor (bFGF). They were induced to chondrogenic lineage and stored for more than 120 hrs in FD, serum, Dulbecco's phosphate buffered saline (DPBS) and saline at 4 °C. In FD, cells stagnated and BMSCs' population doubling time (PDT) was 137 ± 30 hrs, while ADSCs' was 129.7 ± 40 hrs. bFGF caused PDT's decrease to 24.5 ± 5.8 hrs in BMSCs and 22.0 ± 6.5 hrs in ADSCs (p = 0.0001). Both cells were positive to stem cell markers before inductions and thereafter, expressed significantly high chondrogenic genes (p = 0.0001). On shelf life, both cells maintained viabilities and counts above 70% in FD and serum after 120 hrs. BMSCs' viabilities in DPBS fell below 70% after 96 hrs and saline after 72 hrs. ADSCs' viability fell below 70% in DPBS after 24 hrs and saline within 24 hrs. Concentrations between 20 ng/ml bFGF is ideal for aged adult cells' proliferation and delivery time of induced BMSCs and ADSCs can be 120 hrs in 4 °C serum. 

Retracted: No

PubPeer comments:
 Could the authors examine Figure 5b; days 3 and 5 appear to share unexpected similarities. May be the same with slightly different magnification. Marked with red boxes below. *** ![file] ,
MicroRNA-199 inhibits proliferation and promotes apoptosis in children with acute myeloid leukemia by mediating caspase-3
Authors: L-J Zhou
F Xu
Y Zhu
S-C Wang
F Xue
F Han
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-199; acute myeloid leukemia; proliferation; apoptosis; caspase-3
Affiliations: Department of Pediatrics, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China. .

Abstract:  Objective: The aim of this study was to detect the expression level of microRNA-199 in acute myeloid leukemia (AML). Meanwhile, we also investigated whether microRNA-199 could inhibit the proliferation and promote apoptosis of AML cells by regulating caspase-3. Patients and methods: The expression level of microRNA-199 in peripheral blood samples of AML patients and healthy controls was determined using Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Similarly, microRNA-199 expression was also detected in AML cells and human medullary cells. The overexpression plasmid of microRNA-199 was constructed and transfected into cells. Subsequently, the regulatory effects of microRNA-199 on the proliferation, cell cycle, apoptosis, invasion and migration were accessed. The relationship between microRNA-199 and caspase-3 expression was further elucidated by Western blot and RT-qPCR. Results: MicroRNA-199 was lowly expressed in peripheral blood of AML patients and AML cell lines than normal controls. The overexpression of microRNA-199 significantly decreased proliferative, invasive and migratory capacities of AML cells, whereas markedly increased apoptotic rate. Western blot results showed that microRNA-199 increased caspase-3 expression in AML cells. Rescue experiments demonstrated that microRNA-199 inhibited malignant progression of AML by targeting caspase-3. Conclusions: MicroRNA-199 is lowly expressed in AML patients. Furthermore, it inhibits the malignant progression of AML by targeting caspase-3. 

Retracted: Yes

PubPeer comments:
 Concern about Figure 3A. Some groups of cells appear to be visible multiple times within the same panel or across different panels, as highlighted here with boxes of the same color. ![file] , 
 Withdrawn. https: www.europeanreview.org article 23165 *Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, u201cMicroRNA-199 inhibits proliferation and promotes apoptosis in children with acute myeloid leukemia by mediating caspase-3, by F. Xue, Y. Zhu, F. Xu, L.-J. Zhou, F. Han, S.-C. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (9): 3584-3593u2013DOI: 10.26355 eurrev_201905_17780u2013PMID: 31114982u201d has been withdrawn.* *The Publisher apologizes for any inconvenience this may cause.* ,
Synergistic antitumor activities of docetaxel and octreotide associated with apoptotic-upregulation in castration-resistant prostate cancer
Authors: Sanqiang Li
Sha Zhu
Ying Du
Judith Apondi Oremo
Minghui Zhen
Yue Tang
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Androgen deprivation therapy; metastatic prostate cancer; castrate resistance disease; somatostatin analogue octreotide; docetaxel
Affiliations: Department of Microbiology and Immunology, College of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China., Department of Biochemistry and Molecular Biology, Medical College, Henan University of Science and Technology, Luoyang, P. R. China.

Abstract:  Androgen deprivation therapy has become the fist-line treatment of metastatic prostate cancer; however, progression to castrate resistance disease occurs in the majority of patients. Thus, there is an urgent need for improvements in therapy for castration-resistant prostate cancer. The aims of the present study were to determine the efficacy somatostatin analogue octreotide (OCT) combined with a low dose of docetaxel (DTX) using castration resistant prostate cancer cells and to investigate the involved molecular mechanisms in vitro. The anti-proliferative and synergism potential effects were determined by MTT assay. Induction of apoptosis was analyzed employing annexing V and propidium iodide staining and flow cytometry. VEGFA, CASP9, CASP3 and ABCB1 gene expression was evaluated by RT-PCR and Q-RT-PCR analysis. OCT in combination with DTX treatments on DU145 cell migration was also evaluated. Investigation revealed that combined administration of DTX and OCT had significant, synergistically greater cytotoxicity than DTX or OCT treatment alone. The combination of the two drugs caused a more marked increase in apoptosis and resulted in greater suppression of invasive potential than either individual agent. There was obvious increase in caspase 3 expression in the OCT alone and two-drug combined treatment groups, however, VEGFA expression was markedly suppressed in them. These results support the conclusion that somatostatin analogues combined with docetaxel may enhance the chemotherapy efficacies through multiple mechanisms in castration-resistant PCa cell line. This work provides a preclinical rationale for the therapeutic strategies to improve the treatment in castrate resistance disease. 

Retracted: No

PubPeer comments:
 Iu2019m confused by Figure 4. The ft ft control samples appear to be the same, but the group plots appear different. Could there be an accidentally duplicated image? Apologies if Iu2019m misunderstanding. *** ![file] , 
 Thank you for bringing this concern to my attention I have contacted Dr Miller as these images were generated in his laboratory He will be contacting the journal editor to correct the error and will drop a note to Pubpeer , 
 Thank you for pointing out this error and representative images were accidentally duplicated in panels A and E. The numerical data on the graphs in B and F are correct. We are working with the journal to correct the error. , 
 #3 Thank you for addressing this. ,
Electrospun chitosan membranes containing bioactive and therapeutic agents for enhanced wound healing
Authors: Rashid Ahmed
Anwarul Hasan
Robin Augustine
Mojtaba Falahati
Alap Ali Zahid
Syed Raza Ur Rehman
Majid Sharifi
Journal: International journal of biological macromolecules (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Chitosan; Electrospinning; Skin substitutes; Tissue regeneration; Wound healing.
Affiliations: Department of Mechanical and Industrial Engineering, College of Engineering, Qatar University, Doha 2713, Qatar; Biomedical Research Centre, Qatar University, Doha 2713, Qatar., Department of Nanotechnology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran., Department of Mechanical and Industrial Engineering, College of Engineering, Qatar University, Doha 2713, Qatar; Biomedical Research Centre, Qatar University, Doha 2713, Qatar. Electronic address: .

Abstract:  Electrospinning is one of the most promising techniques for generating porous, nonwoven, and submicron fiber-based membranes for various applications such as catalysis, sensing, tissue engineering and wound healing. Wide range of biopolymers including chitosan can be used to generate submicron fibrous membranes. Owing to the extra cellular matrix (ECM) mimicking property, exudate uptake capacity, biocompatibility, antibacterial activity and biodegradability, electrospun membranes based on chitosan loaded with biologically active agents can play important role in wound healing applications. In order to improve the mechanical stability, degradation, antimicrobial property, vascularization potential and wound healing capacity, various active components such as other polymers, therapeutic agents, nanoparticles and biomolecules were introduced. Approaches such as coaxial electrospinning with other polymers have also been tried to improve the properties of chitosan membranes. To improve the mechanical stability under in vivo conditions, various crosslinking strategies ranging from physical, chemical and biological approaches were also tried by researchers. Electrospun chitosan meshes have also been designed in a highly specialized manner with specific functionalities to deal with the challenging wound environment of diabetic and burn wounds. This review provides a detailed overview of electrospun chitosan-based membranes containing various bioactive and therapeutic agents in the perspective of wound healing and skin regeneration. 

Retracted: No

PubPeer comments:
 All the Western immunoblots in this article have the similar unusual pattern, with a  shadow around the bands seen when enhancing the contrast. E.g. from Figure 5E and H. A quick look at the text gives you an impression that this article is written by someone who doesn t know the basics in biomedical science and doesn t care. It is full of serious errors and misunderstandings. ![file] ,