PReD-Bench/PRed-Bench huggingface dataset:
One-step Solution Processing of Ag, Au and Pd@MXene Hybrids for SERS
Authors: Hayk Minassian
Masahiro Yoshimura
Elumalai Satheeshkumar
Yury Gogotsi
Taron Makaryan
Armen Melikyan
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: hybridization; nanoparticles; MXene; surface-enhanced Raman spectroscopy (SERS); surface plasmon resonance (SPR)
Affiliations: Promotion Center for Global Materials Research (PCGMR), Department of Material Science and Engineering, National Cheng Kung University, Tainan, Taiwan R.O.C., Department of Materials Science and Engineering, and A.J. Drexel Nanomaterials Institute, Drexel University, Philadelphia, PA 19104, USA., Russian-Armenian (Slavonic) State University, 0051, Yerevan, Armenia., A. Alikhanian National Science Laboratory, 0036, Yerevan, Armenia.

Abstract:  We report on one-step hybridization of silver, gold and palladium nanoparticles from solution onto exfoliated two-dimensional (2D) Ti3C2 titanium carbide (MXene) nanosheets. The produced hybrid materials can be used as substrates for surface-enhanced Raman spectroscopy (SERS). An approximate analytical approach is also developed for the calculation of the surface plasmon resonance (SPR) frequency of nanoparticles immersed in a medium, near the interface of two dielectric media with different dielectric constants. We obtained a good match with the experimental data for SPR wavelengths, 440 nm and 558 nm, respectively for silver and gold nanoparticles. In the case of palladium, our calculated SPR wavelength for the planar geometry was 160 nm, demonstrating that non-spherical palladium nanoparticles coupled with 2D MXene yield a broad, significanlty red-shifted SPR band with a peak at 230 nm. We propose a possible mechanism of the plasmonic hybridization of nanoparticles with MXene. The as-prepared noble metal nanoparticles on MXene show a highly sensitive SERS detection of methylene blue (MB) with calculated enhancement factors on the order of 10(5). These findings open a pathway for extending visible-range SERS applications of novel 2D hybrid materials in sensors, catalysis, and biomedical applications. 

Retracted: No

PubPeer comments:
 XRD patterns at low angle part 10 degrees: unexpected similarities of noise. ![file] , 
 I ll ask the first author for original Raman spectra. We synthesized and provided MXene samples for this study. , 
 After discussion with the first author who produced the figure, it appeared that some XRD patterns were recorded from 10 degree and he attached a section of background to make them look like they were all recorded from 5 degree. XRD is simply supplementary characterization for this Raman study and there are no peaks in that part of the pattern, so this violation does not affect any conclusions from the work. Still, I ve asked Elumalai Satheeshkumar to produce a corrected figure and ask the journal to publish an erratum. I did not find any problems in other figures. , 
 #3 Thank you for reply. The first author admitted intentional fraud which does not affect conclusions. I am looking forward to see the corrected figure. ,
Suppression of endoplasmic reticulum stress-induced invasion and migration of breast cancer cells through the downregulation of heparanase
Authors: Hao Liu
Zhi Wen Jiang
Ying Ying Huang
Chen Chen Jiang
Long Jian Pu
Yang Li
Xu Dong Zhang
Journal: International Journal of Molecular Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: Tumor metastasis; Basement membrane; Extracellular matrix; Heparanase; Heparan sulfate
Affiliations: Faculty of Pharmacy, Bengbu Medical College, Bengbu, Anhui 233000, P.R. China.

Abstract:  Tumor metastasis is the ultimate stage of cancer, and the primary cause of mortality in patients. Tumor cells breaking through the natural barrier consisting of the basement membrane (BM) and extracellular matrix (ECM) is the a crucial step in tumor invasion and metastasis. Thus, protecting this barrier is the key to reducing mortality. Heparanase is a mammalian endo-β-glucuronidase which has been found to promote the cleavage of heparan sulfate (HS), and plays a significant role in tumor cell invasion and metastasis. Although chemotherapeutic reagents have a strong antitumor activity, they may promote the invasion and migration of cancer cells, as has been observed during clinical treatment. Chemotherapeutic reagents can induce endoplasmic reticulum (ER) stress; in this study, we used adriamycin (ADM) and a classical ER stress inducer, tunicamycin (TM). We report that the activation of ER stress is involved in the enhanced invasion and migration ability of breast cancer cells and we hypothesized that this effect is associated with the activation of heparanase. In support of this, we used the heparanase inhibitor, OGT2115, and low molecular weight heparin (LMWH) to inhibit the expression and activity of heparanase, and we found that the invasion and migration ability of the cells was suppressed. Our findings demonstrate that heparanase inhibitors suppress breast cancer cell invasion and migration induced by ER stress, and provide a strong rationale for the development of heparanase-based therapeutics for the prevention of metastasis induced by chemotherapeutic reagents. 

Retracted: Yes

PubPeer comments:
 *[right]* Fig 3C. *[left]* Fig 3C from [Ye, Liu Qian (2016)] . ![file] ,
Ammonia synthesis. Ammonia synthesis by N₂ and steam electrolysis in molten hydroxide suspensions of nanoscale Fe₂O₃
Authors: Shuzhi Liu
Baochen Cui
Stuart Licht
Fang-Fang Li
Jason Lau
Baohui Wang
Journal: Science (2014)
Discipline: Multidisciplinary
Keywords: Haber-Bosch process; ammonia production; electrochemical pathway; electrolysis; nano-Fe2O3
Affiliations: Department of Chemistry, George Washington University, Washington, DC 20052, USA. ., Department of Chemistry, George Washington University, Washington, DC 20052, USA.

Abstract:  The Haber-Bosch process to produce ammonia for fertilizer currently relies on carbon-intensive steam reforming of methane as a hydrogen source. We present an electrochemical pathway in which ammonia is produced by electrolysis of air and steam in a molten hydroxide suspension of nano-Fe2O3. At 200°C in an electrolyte with a molar ratio of 0.5 NaOH/0.5 KOH, ammonia is produced at 1.2 volts (V) under 2 milliamperes per centimeter squared (mA cm(-2)) of applied current at coulombic efficiency of 35% (35% of the applied current results in the six-electron conversion of N2 and water to ammonia, and excess H2 is cogenerated with the ammonia). At 250°C and 25 bar of steam pressure, the electrolysis voltage necessary for 2 mA cm(-2) current density decreased to 1.0 V. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: pubmed.ncbi.nlm.nih.gov 32792388 ,
The miR-24-3p/p130Cas: a novel axis regulating the migration and invasion of cancer cells
Authors: Sojin Ahn
Yun Hyun Huh
Wook Kim
Eun Kyung Lee
Chongtae Kim
Heejin Lee
Hyosun Tak
Eunbyul Ji
A-Ri Shin
Hyun-Il Cho
Woo Keun Song
Hoin Kang
Jun Gi Rho
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: MicroRNAs; miR-24-3p; metastatic cancer; gene expression; translation
Affiliations: Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, South Korea., Department of Molecular Science and Technology, Ajou University, Suwon, South Korea., Catholic Cancer Research Institute, College of Medicine, The Catholic University of Korea, South Korea., Department of Life Science, Bio Imaging and Cell Dynamics Research Center, Gwangju Institute of Science and Technology, Gwangju, South Korea.

Abstract:  MicroRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression by suppressing translation or facilitating mRNA decay. Differential expression of miRNAs is involved in the pathogenesis of several diseases including cancer. Here, we investigated the role of-miR-24-3p as a downregulated miRNA in metastatic cancer. miR-24-3p was decreased in metastatic cancer and lower expression of miR-24-3p was related to poor survival of cancer patients. Consistently, ectopic expression of miR-24-3p suppressed the cell migration, invasion, and proliferation of MCF7, Hep3B, B16F10, SK-Hep1, and PC-3 cells by directly targeting p130Cas. Stable expression of p130Cas restored miR-24-3p-mediated inhibition of cell migration and invasion. These results suggest that miR-24-3p functions as a tumor suppressor and the miR-24-3p/p130Cas axis is a novel factor of cancer progression by regulating cell migration and invasion. 

Retracted: No

PubPeer comments:
 ![](http: ) ![file] , 
 We apologize for the delay in responding to your comment. After evaluating the results, we noticed that the error was made while arranging the data. Weu2019ll contact the Editorial office to correct it and post the decision made as soon as possible. Thank you for your comments. , 
 Three images (each for red, yellow and blue circle) at Fig. 2D are identical to another three images (each for red, yellow and blue circle) at Fig. 2B in the Cell Death and Differentiation manuscript. ![file] ,
Investigating the Heteronjunction between ZnO/Fe2O3 and g-C3N4 for an Enhanced Photocatalytic H2 production under visible-light irradiation
Authors: Na Mao
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: ZnO; Fe2O3; g-C3N4; photocatalysts; impregnation
Affiliations: Shaanxi Key Laboratory for Advanced Energy Devices, Key Laboratory for Macromolecular Science of Shaanxi Province, School of Materials Science and Engineering, Shaanxi Normal University, Xi'an, Shaanxi, 710062, P.R. China. ., College of Chemistry and Materials, Weinan Normal University, Weinan, Shaanxi, 714099, P.R. China. .

Abstract:  A series of ZnO/Fe2O3/g-C3N4 photocatalysts were synthetized by impregnation of g-C3N4 with Zn(NO3)2·6H2O, and Fe(NO3)2·9H2O followed by calcination. The morphology, chemical composition, and structure of the resulted materials were carefully analyzed by various characterization techniques. The photocatalytic performance of ZnO/Fe2O3/g-C3N4 composites was evaluated based on the H2 evolution from water splitting reaction. The results showed that the ZnO/Fe2O3/g-C3N4 composite can effectively produce more H2 than pure g-C3N4 when irradiated under visible-light. H2 production rate over 3-ZnO/Fe2O3/g-C3N4 composite was of 25 μmol·h-1, which is 4 times higher than that obtained in the presence of pure g-C3N4, clearly showing a significant improvement of the photocatalytic activity of the prepared nanocomposite. This result was attributed to the formation of a heterojunction between g-C3N4 and ZnO/Fe2O3, which delayed the recombination of holes-electrons pairs and resulted in a remarkable increase in photocatalytic performance. 

Retracted: No

PubPeer comments:
 Figure 2a. Four identical XRD patterns ![file] ,
Oncolytic Newcastle disease virus expressing the co-stimulator OX40L as immunopotentiator for colorectal cancer therapy
Authors: Han Su
Deshan Li
Zhenzhong Wang
Guiping Ren
Yukai Cao
Kai Kang
Limin Tian
Tianyan Liu
Shan Jiang
Wei Xiao
Journal: Gene Therapy (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NDV; oncolytic immunotherapy; OX40 ligand; anti-tumor immunity; CD4+ T cells
Affiliations: College of Life Science, Northeast Agricultural University, Harbin, China., Jiangsu Kanion Pharmaceutical CO. LTD, State Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Lianyungang, Jiangsu, China., Jiangsu Kanion Pharmaceutical CO. LTD, State Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Lianyungang, Jiangsu, China. ., College of Life Science, Northeast Agricultural University, Harbin, China. .

Abstract:  NDV as an attractive candidate for oncolytic immunotherapy selectively lyses tumor cells but shows limited anti-tumor immunity. Immune co-stimulator OX40 ligand (OX40L) boosts anti-tumor immunity response by delivering a potent costimulatory signal to CD4+ and CD8+ T cells. To improve the anti-tumor immunity of NDV, the recombinant NDV expressing the murine OX40L (rNDV-mOX40L) was engineered. The viral growth kinetics was examined in CT26 cell lines. The ability of rNDV-mOX40L to express mOX40L was detected in the infected tumor cells and tumor tissues. The anti-tumor activity of rNDV-mOX40L was studied in the CT26 animal model. Tumor-specific CD4+, CD8+ and OX40+ T cells were examined by immunohistochemistry staining. The virus growth curve showed that the insertion of the mOX40L gene did not affect the growth kinetics of NDV. rNDV-mOX40L expresses mOX40L and effectively inhibits the growth of CT26 colorectal cancer in vivo. The tumor inhibition rate of the rNDV-mOX40L-treated group was increased by 15.8% compared to that of NDV-treated group in the CT26 model. Furthermore, immunohistochemistry staining of tumor tissues removed from the CT26 model revealed that intense infiltration of tumor-specific CD4+, CD8+ T cells, especially OX40+ T cells were found in the rNDV-mOX40L-treated group. FACS showed that rNDV-mOX40L significantly enhanced the number of CD4+ and CD8+ T cells in spleen. Moreover, compared to the NDV-treated group, the level of mouse IFN-γ protein in the tumor site increased significantly in the rNDV-mOX40L-treated group. Taken together, rNDV-mOX40L exhibited superior anti-tumor immunity by stimulating tumor-specific T cells and may be a promising agent for cancer immunotherapy. 

Retracted: No

PubPeer comments:
 Figure 2E: There is an overlap, I ve added the magenta boxes to show where I mean. Obviously, these are supposed to be an image of the same cells, but I would expect at least some change in 24 hours. Would the authors please comment? ![file] ,
Intermittent Hypoxia Induces Autophagy to Protect Cardiomyocytes From Endoplasmic Reticulum Stress and Apoptosis
Authors: Jui-Chih Chang
Jian-Hong Lin
Kun-Ta Yang
Huai-Ren Chang
Pei-Ching Ting
Wen-Sen Lee
Wei-Fen Hu
Kun-Ruey Shieh
Tsung-I Chen
Journal: Frontiers in Physiology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: apoptosis; autophagy; cell death; endoplasmic reticulum; intermittent hypoxia
Affiliations: Department of Surgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan., School of Medicine, Tzu Chi University, Hualien, Taiwan., Master Program in Medical Physiology, School of Medicine, Tzu Chi University, Hualien, Taiwan., Graduate Institute of Medical Sciences, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan., PhD Program in Pharmacology and Toxicology, School of Medicine, Tzu Chi University, Hualien, Taiwan., Division of Cardiology, Department of Internal Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan., Department of Physiology, School of Medicine, Tzu Chi University, Hualien, Taiwan., Center for Physical Education, College of Education and Communication, Tzu Chi University, Hualien, Taiwan., Institute of Education, College of Education and Communication, Tzu Chi University, Hualien, Taiwan.

Abstract:  Intermittent hypoxia (IH), characterized as cyclic episodes of short-period hypoxia followed by normoxia, occurs in many physiological and pathophysiological conditions such as pregnancy, athlete, obstructive sleep apnea, and asthma. Hypoxia can induce autophagy, which is activated in response to protein aggregates, in the proteotoxic forms of cardiac diseases. Previous studies suggested that autophagy can protect cells by avoiding accumulation of misfolded proteins, which can be generated in response to ischemia/reperfusion (I/R) injury. The objective of the present study was to determine whether IH-induced autophagy can attenuate endoplasmic reticulum (ER) stress and cell death. In this study, H9c2 cell line, rat primary cultured cardiomyocytes, and C57BL/6 male mice underwent IH with an oscillating O2 concentration between 4 and 20% every 30 min for 1-4 days in an incubator. The levels of LC3, an autophagy indicator protein and CHOP and GRP78 (ER stress-related proteins) were measured by Western blotting analyses. Our data demonstrated that the autophagy-related proteins were upregulated in days 1-3, while the ER stress-related proteins were downregulated on the second day after IH. Treatment with H2O2 (100 μM) for 24 h caused ER stress and increased the level of ER stress-related proteins, and these effects were abolished by pre-treatment with IH condition. In response to the autophagy inhibitor, the level of ER stress-related proteins was upregulated again. Taken together, our data suggested that IH could increase myocardial autophagy as an adaptive response to prevent the ER stress and apoptosis. 

Retracted: No

PubPeer comments:
 Too many repeated GAPDH in Western blots. ![file] ,
Neuroprotective Effects of the Sonic Hedgehog Signaling Pathway in Ischemic Injury through Promotion of Synaptic and Neuronal Health
Authors: Tingting Li
Min Han
Xili Chu
Wenqiang Chen
Danqing Xin
Hongfei Ke
Sen Yin
Zhen Wang
Xuemei Bai
Xingang Li
Journal: Neural Plasticity (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Cerebral ischemia; neuronal apoptosis; sonic hedgehog (Shh) signaling pathway; oxygen-glucose deprivation (OGD); Ptch
Affiliations: Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China., Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.

Abstract:  Cerebral ischemia is a common cerebrovascular condition which often induces neuronal apoptosis, leading to brain damage. The sonic hedgehog (Shh) signaling pathway has been reported to be involved in ischemic stroke, but the underlying mechanisms have not been fully elucidated. In the present study, we demonstrated that expressions of Shh, Ptch, and Gli-1 were significantly downregulated at 24 h following oxygen-glucose deprivation (OGD) injury in neurons in vitro, effects which were associated with increasing numbers of apoptotic cells and reactive oxygen species generation. In addition, expressions of synaptic proteins (neuroligin and neurexin) were significantly downregulated at 8 h following OGD, also associated with concomitant neuronal apoptosis. Treatment with purmorphamine, a Shh agonist, increased Gli-1 in the nucleus of neurons and protected against OGD injury, whereas the Shh inhibitor, cyclopamine, produced the opposite effects. Activation of Shh signals promoted CREB and Akt phosphorylation; upregulated the expressions of BDNF, neuroligin, and neurexin; and decreased NF-κB phosphorylation following OGD. Notably, this activation of Shh signals was accompanied by improved neurobehavioral responses along with attenuations in edema and apoptosis at 48 h postischemic insult in rats. Taken together, these results demonstrate that activation of the Shh signaling pathway played a neuroprotective role in response to ischemic exposure via promotion of synaptic and neuronal health. 

Retracted: No

PubPeer comments:
 In Figure 4c, a figure has been duplicated, but the R2 values are different. ![file] ,
Effect of ascophyllan from brown algae Padina tetrastromatica on inflammation and oxidative stress in carrageenan-induced rats
Authors: R Mahadevan
G Muraleedhara Kurup
Sulaiman Mohsin
Journal: Inflammation (2013)
Discipline: IMMUNOLOGY
Keywords: Sulfated polysaccharide; ascophyllan; anti-inflammatory effect; carrageenan-induced paw edema; rats
Affiliations: Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, 695 581, India.

Abstract:  Sulfated polysaccharide ascophyllan was isolated from the brown algae Padina tetrastromatica and purified by ion-exchange chromatography. Anti-inflammatory effect of ascophyllan fraction against carrageenan-induced paw edema in rats was studied. Paw edema in rats was induced by injecting 0.1 ml, 1 % carrageenan suspension in 0.9 % NaCl solution into the sub-plantar tissue of the right hind paw. Carrageenan caused a significant increase in the activity of inflammatory marker enzymes like lipoxygenases and cyclooxygenase in peripheral blood mononuclear cells and paw tissue and also increased the concentration of prostaglandin E2 (PGE2) and myeloperoxidase (MPO) in paw tissue. When compared to the reference drug diclofenac, ascophyllan fraction-3 (AF3) treatment significantly reduced the activities of anti-inflammatory enzymes, concentration of PGE2 and MPO. AF3 treatment decreased the mRNA level expression of TNF-α and IL-6. Concentration of thiobarbituric acid reactive substances was decreased. Activities of antioxidant enzymes and reduced glutathione level were increased on treatment with AF3. Histopathology of paw tissue showed decreased edema formation and cellular infiltration on supplementation with AF3. Thus the results demonstrated the potential beneficiary effect of ascophyllan fraction on carrageenan-treated rats. 

Retracted: No

PubPeer comments:
 Could the authors clarify the duplication of the same images in two publications? ![file] ,
Escheriosome mediated cytosolic delivery of Candida albicans cytosolic proteins induces enhanced cytotoxic T lymphocyte response and protective immunity
Authors: Z Swaleha
A Chauhan
A Vasco
M Farazuddin
Owais Mohammad
N Ahmad
M Abida
Journal: Vaccine (2011)
Discipline: IMMUNOLOGY
Keywords: intracellular fungal infections; humoral immune responses; cell mediated immune responses; antigen delivery vehicles; Escherichia coli membrane lipid vesicles
Affiliations: Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh-202002, India.

Abstract:  Protection against intracellular fungal infections, in a manner similar to viral challenges necessitates activation of both humoral and cell mediated immune responses in unison. Most of the presently available antigen delivery vehicles including egg phosphatidyl-choline (egg-PC) liposomes, can evoke mainly humoral immune responses in the immunized animals. Keeping this fact into consideration, we earlier developed Escherichia coli membrane lipid vesicles (escheriosomes) and demonstrated that escheriosomes successfully fuse with the plasma membrane of macrophages ensuing in effective cytoplasmic delivery of entrapped antigen, a pre-requisite for inducing CD8(+) T cell response against antigens. In the present study, we report the ability of escheriosomes encapsulated Candida albicans (C. albicans) cytosolic antigens (cAg), to generate protective immunity against systemic C. albicans infection in BALB/c mice. The immunization schedule using escheriosome encapsulated cAg induced strong antigen-specific CD8(+) T-cell responses, which were markedly higher than that observed in mice immunized with IFA-antigen emulsion, or antigen encapsulated in egg PC liposomes. Interestingly, immunization with cAg delivered in escheriosomes was also successful in complete elimination of C. albicans infection in Balb/c mice. The study suggests that escheriosomes may function as a novel immunoadjuvants and emerge as an effective tool for generating protective immunity against C. albicans infection. 

Retracted: No

PubPeer comments:
 Figure 5. * Purple boxes: CD4+ panel b and CD8+ panel d appear to look very similar. * Blue boxes: CD8+ panels b and c appear to look very similar. ![file] ,
Efficient gene correction of an aberrant splice site in β-thalassaemia iPSCs by CRISPR/Cas9 and single-strand oligodeoxynucleotides
Authors: Ding Wang
Dian Lu
Bing Song
Diyu Chen
Yingjun Xie
Yi Yang
Xiaofang Sun
Yanting Xue
Shouheng Lin
Zeyu Xiong
Lina He
Yinghong Yang
Journal: Journal of Cellular and Molecular Medicine (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CRISPR/Cas9; HBB gene; gene correction; induced pluripotent stem cells; secondary cleavage
Affiliations: Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.

Abstract:  β-thalassaemia is a prevalent hereditary haematological disease caused by mutations in the human haemoglobin β (HBB) gene. Among them, the HBB IVS2-654 (C &gt; T) mutation, which is in the intron, creates an aberrant splicing site. Bone marrow transplantation for curing β-thalassaemia is limited due to the lack of matched donors. The clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9), as a widely used tool for gene editing, is able to target specific sequence and create double-strand break (DSB), which can be combined with the single-stranded oligodeoxynucleotide (ssODN) to correct mutations. In this study, according to two different strategies, the HBB IVS2-654 mutation was seamlessly corrected in iPSCs by CRISPR/Cas9 system and ssODN. To reduce the occurrence of secondary cleavage, a more efficient strategy was adopted. The corrected iPSCs kept pluripotency and genome stability. Moreover, they could differentiate normally. Through CRISPR/Cas9 system and ssODN, our study provides improved strategies for gene correction of β-Thalassaemia, and the expression of the HBB gene can be restored, which can be used for gene therapy in the future. 

Retracted: No

PubPeer comments:
 there are problems in this paper that are detailed in the PubPeer entry for Thermal-sensitive hydrogel as adjuvant-free vaccine delivery system for H5N1 intranasal immunization Biomaterials (2012) doi: 10.1016 j.biomaterials.2011.11.068 ,
Naringenin enhances insulin-stimulated tyrosine phosphorylation and improves the cellular actions of insulin in a dietary model of metabolic syndrome
Authors: Carani Venkatraman Anuradha
Sriramajayam Kannappan
Journal: European journal of nutrition (2010)
Discipline: CLINICAL MEDICINE
Keywords: insulin sensitizer; naringenin; high fructose-induced model; insulin resistance; Wistar rats
Affiliations: Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar, Tamil Nadu, India.

Abstract:  Background: There is a growing interest in identifying putative insulin sensitizers from the herbal sources. Aim of the study: The present study explores the effects of naringenin, a bioflavonoid, in the high fructose-induced model of insulin resistance. Methods: Adult male Wistar rats were divided into two groups and were fed either a starch-based control diet or a high fructose diet (60 g/100 g) for 60 days. From the 16th day, rats in each group were divided into two, one of which was administered naringenin (50 mg/kg b.w.) and the other was untreated for the next 45 days. Oral glucose tolerance test (OGTT) was done on day 59. On day 60, the levels of glucose, insulin, triglycerides (TG), free fatty acids (FFA) in blood, and the activities of insulin-inducible and suppressible enzymes in the cytosolic and mitochondrial fractions of liver and skeletal muscle were assayed. The extent of protein tyrosine phosphorylation in response to insulin was determined by assaying protein tyrosine kinase (PTK) and protein tyrosine phosphatase (PTP) in liver. Liver histology with periodic acid-Schiff (PAS) staining was done to detect glycogen. Results: Fructose administration increased the plasma levels of glucose, insulin, TG, and FFA as compared to control rats. Insulin resistance was indicated by alterations in insulin sensitivity indices. Alterations in enzyme activities and reduced glycogen content were observed in fructose-fed rats. PTP activity was higher, while PTK activity was lower suggesting reduced tyrosine phosphorylation status. Administration of naringenin improved insulin sensitivity and enhanced tyrosine phosphorylation in fructose-fed animals, while it did not affect the parameters in control diet-fed rats. Conclusions: Naringenin improves insulin signaling and sensitivity and thereby promotes the cellular actions of insulin in this model. 

Retracted: No

PubPeer comments:
 Concern about Figure 3. *Panels  CON and  CON+NAR appear to show many groups of cells in common, but differ in one other region. * Panel CON, FRU+NAR, and CON+NAR appear to show the same groups of cells within the same photo. Could the authors please explain what happened here? These repetitions are not expected in biological tissues. ![file] ,
miR-504 promotes tumour growth and metastasis in human osteosarcoma by targeting TP53INP1
Authors: Junlong Wu
Sixiang Zeng
Qingchun Cai
Xing Dai
Wei Ma
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: microRNAs; osteosarcoma; miR-504; TP53INP1; tumour growth
Affiliations: Department of Orthopaedics, First Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.

Abstract:  An increasing number of studies have demonstrated that microRNAs participate in the development of osteosarcoma by acting as tumour suppressor or tumour-promoting genes. We investigated the role of miR-504 in the growth and metastasis of osteosarcoma. The expression of miR-504 in clinical osteosarcoma samples was higher than that in the adjacent normal tissue and correlated with tumour size and clinical stage. Tumour protein p53-inducible nuclear protein 1 (TP53INP1) was downregulated in the clinical osteosarcoma samples compared with the adjacent normal tissues and was consistently correlated with the clinical stage. The results of dual-luciferase reporter assay and western blot analysis demonstrated that the TP53INP1 gene is a direct target of miR-504. Altogether, the Cell Counting Kit-8 (CCK-8), the colony formation, the flow cytometry and the Transwell assay results demonstrated that miR-504 promoted osteosarcoma cell growth and metastasis in vitro. P73, P21, Bax, cleaved-caspase-3 and secreted protein acidic and rich in cysteine (SPARC) were associated with the suppressive role of miR-504/TP53INP1. The overexpression of miR-504 in osteosarcoma xenografts enhanced the tumour growth and increased the metastatic burden. Collectively, these results revealed that TP53INP1 is a target gene of miR-504 and that miR-504 enhances osteosarcoma growth and promotes distant metastases by targeting TP53INP1. Thus, miR-504/TP53INP1 may be associated with osteosarcoma size and clinical stage. 

Retracted: No

PubPeer comments:
 Figure 2F. * Red boxes: Two panels appear to show an overlap. ![file] ,
Isoniazid-induced apoptosis in HepG2 cells: generation of oxidative stress and Bcl-2 down-regulation
Authors: Ranjana Kanchan
Anurag Srivastava
Sharad Sharma
Rajeev Mishra
Chakrapani Tripathi
Ashutosh Tiwari
Smrati Bhadauria
Journal: Toxicology mechanisms and methods (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Isoniazid; hepatotoxicity; apoptosis; HepG2 cells; oxidative stress
Affiliations: Division of Toxicology, Central Drug Research Institute, Lucknow 262 001, (CSIR) India. 

Abstract:  Isoniazid (INH) is a first-line antibiotic used in the treatment of infections caused by Mycobacterium tuberculosis. However it has a serious limitation of being hepatotoxic. Delineating the mechanism underlying INH-induced hepatotoxicity may be beneficial in devising ways to counteract its toxic manifestations. Studies in human hepatoma HepG2 cells have indicated that INH exposure causes induction of apoptosis. This study was aimed at identifying the key components/pathways of the INH-induced apoptotic pathway using HepG2 cells. HepG2 cells were exposed to increasing concentrations of INH (6.5, 13, 26, and 52 mM). Hydrogen peroxide (0.3 mM) served as positive control. After incubating for specific time intervals cells were harvested and evidences of cytotoxicity, oxidative stress, and apoptosis were sought. The findings indicated that INH exposure causes increased ROS generation along with alteration in levels of enzymatic antioxidants such as Superoxide dismutase, Catalase, and Glucose-6-Phosphate dehydrogenase. Altered Bcl-2/Bax content, cytochrome-c translocation, caspase activation, and DNA fragmentation emphasized involvement of apoptosis. 

Retracted: No

PubPeer comments:
 ![file] , 
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 ![](http: ) ![file] , 
 ![](http: ) ![file] ,
Targets of Vitamin C With Therapeutic Potential for Cardiovascular Disease and Underlying Mechanisms: A Study of Network Pharmacology
Authors: Bingwu Huang
Ning Zhu
Wenbing Jiang
Journal: Frontiers in Pharmacology (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: cardiovascular disease; inflammation; jak-stat; network pharmacology; vitamin C.
Affiliations: Department of Cardiology, The Third Affiliated Hospital of Shanghai University, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China., Department of Anesthesiology, The Third Affiliated Hospital of Shanghai University, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.

Abstract:  Vitamin C (ascorbic acid) is a nutrient used to treat cardiovascular disease (CVD). However, the pharmacological targets of vitamin C and the mechanisms underlying the therapeutic effects of vitamin C on CVD remain to be elucidated. In this study, we used network pharmacology approach to investigate the pharmacological mechanisms of vitamin C for the treatment of CVD. The core targets, major hubs, enriched biological processes, and key signaling pathways were identified. A protein-protein interaction network and an interaction diagram of core target-related pathways were constructed. Three core targets were identified, including phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform, signal transducer and activator of transcription-3 (STAT3), and prothrombin. The GO and KEGG analyses identified top 20 enriched biological processes and signaling pathways involved in the therapeutic effects of vitamin C on CVD. The JAK-STAT, STAT, PD1, EGFR, FoxO, and chemokines signaling pathways may be highly involved in the protective effects of vitamin C against CVD. In conclusion, our bioinformatics analyses provided evidence on the possible therapeutic mechanisms of vitamin C in CVD treatment, which may contribute to the development of novel drugs for CVD. 

Retracted: No

PubPeer comments:
 Zhu et al. write that they obtained * a total of 339 known target genes of vitamin C * [1]. However, the effects of vitamin C on the genome seem to be much more extensive. Young et al. wrote that  studies have shown that ascorbate has the capacity to modify the status of DNA methylation in mammalian cells. For instance, ascorbate causes the widespread DNA demethylation of nearly 2,000 genes in embryonic stem cells (11) [2]. Furthermore, vitamin C is an important water soluble antioxidant and it seems highly unlikely that the effects on the genome can cover the effects of this vitamin. Criticism of an analogous paper has been published [3]. 1. https: doi.org 10.3389 fphar.2020.591337 2. https: doi.org 10.1146 annurev-nutr-071714-034228 3. https: doi.org 10.1039 d0fo02189j ,
Identification of proteins involved in transcription/translation (eEF 1A1) as an inhibitor of Bax induced apoptosis
Authors: Damilare D Akintade
Bhabatosh Chaudhuri
Journal: Molecular Biology Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Anti-Apoptosis; Bcl-2A1 and yeast; Human eEF-1A1; Yeast apoptosis; eEF-1A1 and yeast.
Affiliations: School of Life Sciences, Medical School, University of Nottingham, Nottingham, NG7 2UH, UK. ., Leicester School of Pharmacy, De Montfort University, Leicester, LE1 9BH, UK. ., Leicester School of Pharmacy, De Montfort University, Leicester, LE1 9BH, UK.

Abstract:  Eukaryotic elongation factor 1A1 (eEF1A1) is central to translational activity. It is involved in complexes that form signal transduction with protein kinase C, as well as being a signal transducer and activator of transcription 3. eEF1A1 and eEF1A2 are isoforms of the alpha subunit of elongating factor 1 complex. It has been reported that eEF1A1 is expressed in most human tissues but the brain, skeletal muscle and heart. eEF1A1 has been linked to both apoptosis and anti-apoptotic activities. In this study, eEF1A1 was co-expressed with Bax, a proapoptotic protein via heterologous expression of recombinant DNA in yeast cells. Assays were carried out to monitor the fate and state of yeast cells when eEF1A1 was co-expressed with Bax. The yeast strain (bearing an integrated copy of the Bax gene) was transformed with an episomal 2-micron plasmid that encodes HA-tagged eEF1A1 gene. The resultant strain would allow co-expression of Bax and eEF1A1 in yeast cells, Bax being under the control of the GAL1 promoter, while the PGK1 promoter drives eEF1A1 expression. Bcl 2A1, a known anti-apoptotic protein, was also co-expressed with Bax in yeast cells as a positive control, to study the anti-apoptotic characteristic of eEF-1A1. The part eEF1A1 plays in apoptosis has been contentious, amidst the pro and anti-apoptotic properties of eEF1A1, it was shown clearly, in this study that eEF1A1 portrays only anti-apoptotic property in the presence of pro-apoptotic protein, Bax. 

Retracted: No

PubPeer comments:
 Figure 3G appears to have a repeated band, after resizing. Difficult to understand how this could occur by accident. *** ![file] ,
DNA methylation of heparanase promoter influences its expression and associated with the progression of human breast cancer
Authors: Juan Wang
Shi-Yu Bai
Zhong-Hai Yan
Ying Ma
Xin Wang
Fei Jiao
Yuan Yu
Zhen Yue
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Heparanase; breast cancer; DNA methylation; gene expression; tumor invasion
Affiliations: Department of Biochemistry and Molecular Biology, Binzhou Medical College, Yantai, Shandong Province, People's Republic of China., Department of Clinical Laboratory, Tai'an City Central Hospital, Tai'an, Shandong Province, People's Republic of China., Department of Medicine, Columbia University, New York, New York, United States of America., Department of Clinical Laboratory, the PLA 107th Hospital Affiliated to Binzhou Medical College Yantai, Shandong Province, Jinan Military Area Command, People's Republic of China., Department of Biotechnology, Binzhou Medical College, Yantai, Shandong Province, People's Republic of China.

Abstract:  Heparanase promotes tumor invasion and metastasis in several malignancies including breast cancer. However, the roles and regulation mechanisms of heparanase during breast cancer progression are still not fully understood. The aim of this study is to determine the differential regulation of heparanase gene expression in specific stages of breast cancer by DNA methylation. We detected levels of heparanase expression and DNA methylation patterns of its promoter in breast cancer cell lines (MCF-7 and MDA-MB-435) and clinical tissues, respectively. It has been observed that heparanase is highly expressed in the invasive MDA-MB-435 cells with low methylation modification in the heparanase promoter. In contrast, lower expression of heparanase in MCF-7 cells is accompanied by higher methylation in the promoter. Treatment of MCF-7 cells with 5-aza-2'-deoxycytidine (5-aza-dC), a potent demethylating agent, results in induction of heparanase expression and higher invasion potential in vitro and leads to an advantage of tumor formation in vivo. In 54 tissue samples, cancer samples at late stages (stage IV) showed the highest heparanase expression accomplished by little DNA methylation. On the contrary, methylation prevalence is highest in normal tissue and inversely correlated with heparanase expression. A significant correlation between DNA methylation and clinical stage was demonstrated (p = 0.012). Collectively, these results demonstrate that DNA methylation play the regulation role in heparanase gene in different stages of breast cancer and present a direct effect on tumor progression. 

Retracted: No

PubPeer comments:
 Figure 2 and 5. * Red boxes: The marker and first five lanes in Figure 2D look very similar to the marker and first five lanes in Figure 5A. albeit stretched differently. Note the position of some white specks, marked by me with colored arrows. Reported to the journal in October 2015, but no action taken as of today. ![file] ,
MicroRNA signatures of TRAIL resistance in human non-small cell lung cancer
Authors: C G Liu
G Romano
M Garofalo
C Zanca
G Di Leva
C M Croce
C Quintavalle
C Taccioli
G Condorelli
Journal: Oncogene (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TRAIL; miR-221; miR-222; apoptosis; NSCLC
Affiliations: Department of Cellular and Molecular Biology and Pathology, University of Naples Federico II, Naples, Italy.

Abstract:  To define novel pathways that regulate susceptibility to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in non-small cell lung cancer (NSCLC), we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant NSCLC cells, levels of different miRs are increased, and in particular, miR-221 and -222. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. Indeed, transfection with anti-miR-221 and -222 rendered CALU-1-resistant cells sensitive to TRAIL. Conversely, H460-sensitive cells treated with -221 and -222 pre-miRs become resistant to TRAIL. miR-221 and -222 target the 3'-UTR of Kit and p27(kip1) mRNAs, but interfere with TRAIL signaling mainly through p27(kip1). In conclusion, we show that high expression levels of miR-221 and -222 are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets or diagnostic tool for TRAIL resistance in NSCLC. 

Retracted: No

PubPeer comments:
null, 
null, 
 #3 I think they are. The same actin blot for samples from different cell lines is problematic. , 
null, 
 Figure 3B. Please compare the U6 blot in this figure to the U6 blot in Figure 4C of PNAS (2008), doi: 10.1073 pnas.08001351 with shared authorship. The blots appear to show different experiments. ![file] , 
 Correction to: Oncogene https: doi.org 10.1038 onc.2008.6 Following the publication of this article the authors noted that the control b-actin bands included in Figs. 4c and 7a were incorrect. The authors have provided the corrected figures below. These changes have no impact on the results presented in this paper. Fig. 4 ![file] Fig. 7 ![file] Published 04 January 2021 , 
 2021 correction. https: www.nature.com articles s41388-020-01608-1 Following the publication of this article the authors noted that the control b-actin bands included in Figs. 4c and 7a were incorrect. The authors have provided the corrected figures below. These changes have no impact on the results presented in this paper. , 
 That leaves only the loading-control duplication between the present Fig 3B and Fig 4C in the companion paper, PNAS (2008) 10.1073 pnas.0800135105. https: pubpeer.com publications A249426718B43A94364F9ACF017D38 ![] ,
Silence of lncRNA CHRF protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating microRNA-221
Authors: Li Wang
Yuefeng Qi
Enyu Guo
Lijuan Zhang
Journal: Experimental and molecular pathology (2019)
Discipline: CLINICAL MEDICINE
Keywords: H9c2 cell; Lipopolysaccharide (LPS); LncRNA CHRF; Myocarditis; miR-221.
Affiliations: Department of Pediatrics, Jining No.1 People's Hospital, Jining 272011, China., Department of Pediatrics, Jining No.1 People's Hospital, Jining 272011, China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. Given the comments of Dr Elisabeth Bik regarding this article “… the Western blot bands in all 400+ papers are all very regularly spaced and have a smooth appearance in the shape of a dumbbell or tadpole, without any of the usual smudges or stains. All bands are placed on similar looking backgrounds, suggesting they were copy/pasted from other sources, or computer generated”, the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article. 

Retracted: Yes

PubPeer comments:
 Figure 1b, it seems two lanes have been duplicated (red boxes). This hypothesis is also supported by evident splice (arrow). Could the authors please comment? ![file] ,
Bicomponent polymeric micelles for pH-controlled delivery of doxorubicin
Authors: Yanan Zhang
Peilan Qi
Chunyun Wang
Qianli Sheng
Tianshun Wang
Shiyong Song
Lei Liu
Rui Wang
Yan Lu
Mengying Zhang
Journal: Drug Delivery (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Drug delivery; boronate ester; cancer; micelle; pH-responsive.
Affiliations: Institute of Pharmacy, School of Pharmacy, Henan University, Kaifeng, China.

Abstract:  Stimuli-responsive drug delivery systems (DDSs) are expected to realize site-specific drug release and kill cancer cells selectively. In this study, a pH-responsive micelle was designed utilizing the pH-sensitivity of borate bonds formed between dopamine and boronic acid. First, methyl (polyethylene glycol)-block-polycaprolactone (mPEG-PCL) was conjugated with 4-cyano-4-(thiobenzoylthio)pentanoic acid (CTP) to obtain a macroinitiator. Two different segments poly(dopamine methacrylamide) (PDMA) and poly(vinylphenylboronic acid) (PVBA) were then grafted to the end of mPEG-PCL. Two triblock copolymers, mPEG-PCL-PDMA and mPEG-PCL-PVBA, were then obtained by reversible addition-fragmentation transfer (RAFT) polymerization. These copolymers and their mixture self-assembled in aqueous solution to form micelles that were able to load hydrophobic anticancer drug doxorubicin (DOX). These two-component micelles were found to be pH-sensitive, in contrast to the one-component micelles. Furthermore, MTT studies showed that the micelles were almost nontoxic. The DOX-loaded micelles showed cytotoxicity equivalent to that of DOX at high concentration. In vivo antitumor experiments showed that this pH-sensitive polymeric micellar system had an enhanced therapeutic effect on tumors. These two-component boronate-based pH micelles are universally applicable to the delivery of anticancer drugs, showing great potential for cancer therapy. 

Retracted: No

PubPeer comments:
 Figure 9 appears to have 2 images which overlap. *** Closeup ![file] *** Full figure showing location ![file] ,