PReD-Bench/PRed-Bench huggingface dataset:
Activated platelet-rich plasma improves adipose-derived stem cell transplantation efficiency in injured articular cartilage
Authors: Dung Minh Le
Khanh Hong-Thien Bui
Dat Quoc Ngo
Nhung Hai Truong
Triet Dinh Duong
Nhan Lu-Chinh Phan
Phuc Van Pham
Ngoc Kim Phan
Ngoc Bich Vu
Vien Tuong Le
Thanh Duc Nguyen
Journal: Stem Cell Research & Therapy (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Adipose-derived stem cells; Platelet-rich plasma; Articular cartilage; Treatment efficiency; Proliferation

Abstract:  Introduction: Adipose-derived stem cells (ADSCs) have been isolated, expanded, and applied in the treatment of many diseases. ADSCs have also been used to treat injured articular cartilage. However, there is controversy regarding the treatment efficiency. We considered that ADSC transplantation with activated platelet-rich plasma (PRP) may improve injured articular cartilage compared with that of ADSC transplantation alone. In this study, we determined the role of PRP in ADSC transplantation to improve the treatment efficiency. Methods: ADSCs were isolated and expanded from human adipose tissue. PRP was collected and activated from human peripheral blood. The effects of PRP were evaluated in vitro and in ADSC transplantation in vivo. In vitro, the effects of PRP on ADSC proliferation, differentiation into chondrogenic cells, and inhibition of angiogenic factors were investigated at three concentrations of PRP (10%, 15% and 20%). In vivo, ADSCs pretreated with or without PRP were transplanted into murine models of injured articular cartilage. Results: PRP promoted ADSC proliferation and differentiation into chondrogenic cells that strongly expressed collagen II, Sox9 and aggrecan. Moreover, PRP inhibited expression of the angiogenic factor vascular endothelial growth factor. As a result, PRP-pretreated ADSCs improved healing of injured articular cartilage in murine models compared with that of untreated ADSCs. Conclusion: Pretreatment of ADSCs with PRP is a simple method to efficiently apply ADSCs in cartilage regeneration. This study provides an important step toward the use of autologous ADSCs in the treatment of injured articular cartilage. 

Retracted: No

PubPeer comments:
 Images B and C in the Figure 2 are identical to each other (see the RED box for details). Could authors explain why ? ![file] ,
IL-33 attenuates EAE by suppressing IL-17 and IFN-γ production and inducing alternatively activated macrophages
Authors: Anne-Galle Besnard
Jose C Alves-Filho
Marija Milovanović
Debbie Allan
Hui-Rong Jiang
Dieudonnée Togbe
Damo Xu
Wanda Niedbala
Sandra Y Fukada
Foo Y Liew
Carl S Goodyear
Christopher Linington
Miodrag L Lukic
Journal: European Journal of Immunology (2012)
Discipline: IMMUNOLOGY
Keywords: IL-33; autoimmune CNS diseases; experimental autoimmune encephalomyelitis (EAE); ST2; IL-33Rα
Affiliations: Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, UK. , Center for Molecular Medicine Faculty of Medicine; University of Kragujevac; Serbia, Strathclyde Institute of Pharmacy and Biomedical Sciences; University of Strathclyde; Glasgow; UK, Institute of Infection; Immunology and Inflammation; University of Glasgow; UK, University of Orléans; Molecular Immunology and Embryology; CNRS UMR6218; Orleans; France

Abstract:  Interleukin (IL)-33, a member of the IL-1 cytokine family, is an important modulator of the immune system associated with several immune-mediated disorders. High levels of IL-33 are expressed by the central nervous system (CNS) suggesting a potential role of IL-33 in autoimmune CNS diseases. We have investigated the expression and function of IL-33 in the development of experimental autoimmune encephalomyelitis (EAE) in mice. We report here that IL-33 and its receptor ST2 (IL-33Rα) are highly expressed in spinal cord tissue, and ST2 expression is markedly increased in the spinal cords of mice with EAE. Furthermore, ST2-deficient (ST2(-/-) ) mice developed exacerbated EAE compared with wild-type (WT) mice while WT, but not ST2(-/-) EAE mice treated with IL-33 developed significantly attenuated disease. IL-33-treated mice had reduced levels of IL-17 and IFN-γ but produced increased amounts of IL-5 and IL-13. Lymph node and splenic macrophages of IL-33-treated mice showed polarization toward an alternatively activated macrophage (M2) phenotype with significantly increased frequency of MR(+) PD-L2(+) cells. Importantly, adoptive transfer of these IL-33-treated macrophages attenuated EAE development. Our data therefore demonstrate that IL-33 plays a therapeutic role in autoimmune CNS disease by switching a predominantly pathogenic Th17/Th1 response to Th2 activity, and by polarization of anti-inflammatory M2 macrophages. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] ,
Prediction of Tubulin Resonant Frequencies Using the Resonant Recognition Model (RRM)
Authors: Drasko Cosic
Katarina Lazar
Irena Cosic
Journal: IEEE Transactions on NanoBioscience (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Tubulin proteins; Resonant Recognition Model; electromagnetic resonances; charge transfer; frequencies

Abstract:  Tubulin proteins were analyzed using the Resonant Recognition Model to predict possible electromagnetic resonances in tubulin and microtubules. We propose that these electromagnetic resonances are caused by charge transfer through the protein molecule. The frequencies of these electromagnetic resonances depend on charge velocity. Using different velocities of charge transfer, we predicted resonant frequencies in different frequency ranges from KHz to THz. These resonant frequencies could be relevant for taxol binding as well as a possible role of microtubules as a macromolecular computer. 

Retracted: No

PubPeer comments:
 I am confused by the data information summarized in Table 2. For example, there is a row termed u201cUber rider total tripsu201d. I believe that it is safe to assume that the value of this term is positive (or at least nonnegative). If this is the case, it is very unlikely that a naturally observed sample has **mean 115.28, median 55 and at the same time standard deviation 169.97.** Could the authors kindly provide a histogram or more detailed information on this sample? ![file] ,
MicroRNA‑21‑5p targeting PDCD4 suppresses apoptosis via regulating the PI3K/AKT/FOXO1 signaling pathway in tongue squamous cell carcinoma
Authors: Luming Tian
Zhou Tong
Zengxi Xin
Zhiying Wang
Changfu Liu
Jingyu Tan
Journal: Experimental and Therapeutic Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: apoptosis; microRNA-21-5p; phosphoinositide 3-kinase pathway; programmed cell death 4; tongue squamous cell carcinoma.
Affiliations: Department of Oral and Maxillofacial Surgery, The Second Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China., Department of Stomatology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China., Department of Prosthodontics, The Second Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China., Department of Dental Implants, The Second Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China.

Abstract:  The aim of the present study was to analyze the role of microRNA (miRNA)-21-5p in tongue squamous cell carcinoma (TSCC), predict the target gene of miR-21-5p and provide novel strategies for gene therapy in TSCC treatment. The expression levels of miRNA-21-5p in TSCC tissues were analyzed using reverse transcription quantitative polymerase chain reaction, and the effects of miRNA-21-5p on cell proliferation, invasion and apoptosis and the expression levels of target protein PDCD4 in the Cal 27 and SCC9 cell lines were determined. PI3K/AKT/Forkhead Box O1 (FOXO1) pathway-associated protein expression levels were evaluated by western blot analysis. miRNA-21-5p was consistently upregulated in TSCC tissues compared with normal tissues. Inhibition of miR-21-5p inhibited cell proliferation and invasion, and promoted cell apoptosis. A luciferase reporter assay confirmed that PDCD4 was the target of miR-21-5p. Inhibition of miRNA21-5p suppressed the PI3K/Akt/FOXO1 signaling pathway. The results from the present study indicated that miR-21-5p-targeting PDCD4 suppresses apoptosis in human TSCC cell lines. This anti-apoptotic effect was achieved by regulating the PI3K/Akt/FOXO1 signaling pathway. These data represent the basis for a promising novel strategy for the treatment of TSCC. 

Retracted: No

PubPeer comments:
 Figure 2 micrograph s appear to have an overlap ![file] ,
Hummingbird-sized dinosaur from the Cretaceous period of Myanmar
Authors: Lida Xing
Gang Li
Qiru Yi
Jingmai K O&#x27;Connor
Lars Schmitz
Ryan C McKellar
Luis M Chiappe
Journal: Nature (2020)
Discipline: Multidisciplinary
Keywords: Amber deposits; Oculudentavis khaungraae; skeletal anatomy; enantiornithine birds; Mesozoic era
Affiliations: State Key Laboratory of Biogeology and Environmental Geology, China University of Geosciences, Beijing, China., School of the Earth Sciences and Resources, China University of Geosciences, Beijing, China., Key Laboratory of Vertebrate Evolution and Human Origins of the Chinese Academy of Sciences, Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, China. ., Center for Excellence in Life and Paleoenvironment, Chinese Academy of Sciences, Beijing, China. ., Dinosaur Institute, Natural History Museum of Los Angeles County, Los Angeles, CA, USA., W. M. Keck Science Department, Claremont McKenna, Scripps and Pitzer Colleges, Claremont, CA, USA., Royal Saskatchewan Museum, Regina, Saskatchewan, Canada., Biology Department, University of Regina, Regina, Saskatchewan, Canada., Beijing Advanced Sciences and Innovation Center, Chinese Academy of Sciences, Beijing, China., Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, China.

Abstract:  Skeletal inclusions in approximately 99-million-year-old amber from northern Myanmar provide unprecedented insights into the soft tissue and skeletal anatomy of minute fauna, which are not typically preserved in other depositional environments1-3. Among a diversity of vertebrates, seven specimens that preserve the skeletal remains of enantiornithine birds have previously been described1,4-8, all of which (including at least one seemingly mature specimen) are smaller than specimens recovered from lithic materials. Here we describe an exceptionally well-preserved and diminutive bird-like skull that documents a new species, which we name Oculudentavis khaungraae gen. et sp. nov. The find appears to represent the smallest known dinosaur of the Mesozoic era, rivalling the bee hummingbird (Mellisuga helenae)-the smallest living bird-in size. The O. khaungraae specimen preserves features that hint at miniaturization constraints, including a unique pattern of cranial fusion and an autapomorphic ocular morphology9 that resembles the eyes of lizards. The conically arranged scleral ossicles define a small pupil, indicative of diurnal activity. Miniaturization most commonly arises in isolated environments, and the diminutive size of Oculudentavis is therefore consistent with previous suggestions that this amber formed on an island within the Trans-Tethyan arc10. The size and morphology of this species suggest a previously unknown bauplan, and a previously undetected ecology. This discovery highlights the potential of amber deposits to reveal the lowest limits of vertebrate body size. 

Retracted: Yes

PubPeer comments:
 Retracted, see https: retractionwatch.com 2020 07 22 a-big-nature-study-on-a-tiny-dinosaur-is-being-retracted ,
N6-methyldeoxyadenine and histone methylation mediate transgenerational survival advantages induced by hormetic heat stress
Authors: Xiao Meng
Wenyu Dai
Jing Yang
Qinghua Zhou
Xiaodie Fu
Qunshan Ye
Chongyang Wang
Qin-Li Wan
Zhenhuan Luo
Journal: Science Advances (2021)
Discipline: Multidisciplinary
Keywords: Environmental stress; survival advantages; evolutionarily advantageous adaptation; nematode worm; Caenorhabditis elegans
Affiliations: Zhuhai Precision Medical Center, Zhuhai People’s Hospital (Zhuhai Hospital Affiliated with Jinan University), Jinan University, Guangzhou, Guangdong 510632, China., Biomedical Translational Research Institute, Jinan University, Guangzhou, Guangdong 510632, China., The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510632, China.

Abstract:  Environmental stress can induce survival advantages that are passed down to multiple generations, representing an evolutionarily advantageous adaptation at the species level. Using the nematode worm Caenorhabditis elegans as a model, we found that heat shock experienced in either parent could increase the longevity of themselves and up to the fifth generation of descendants. Mechanistic analyses revealed that transcription factor DAF-16/FOXO, heat shock factor HSF-1, and nuclear receptor DAF-12/FXR functioned transgenerationally to implement the hormetic stress response. Histone H3K9me3 methyltransferases SET-25 and SET-32 and DNA N6-methyl methyltransferase DAMT-1 participated in transmitting high-temperature memory across generations. H3K9me3 and N6-methyladenine could mark heat stress response genes and promote their transcription in progeny to extend life span. We dissected the mechanisms responsible for implementing and transmitting environmental memories in descendants from heat-shocked parents and demonstrated that hormetic stress caused survival benefits could be transmitted to multiple generations through H3K9me3 and N6-mA modifications. 

Retracted: No

PubPeer comments:
 Readers should become aware that the methodology used by this paper to measure N6-methyldeoxyadenine could be interpreted as an artifact https: www.nature.com articles s41589-020-0504-2 https: bmcgenomics.biomedcentral.com articles 10.1186 s12864-019-5754-6 , 
 This paper cites a previous paper which showed the presence of N6-methyldeoxyadenine in C. elegans. . The same authors later published another paper concluding that their previous work was likely an artefact following extensive mass spectrometry analysis . Current paper by Wan et al., uses a much less sensitive method which is very likely to show artefact. It would have been more suitable if they cited the above papers and discussed these problems. ,
Persistent and stable gene expression by a cytoplasmic RNA replicon based on a noncytopathic variant Sendai virus
Authors: Ken Nishimura
Kunitada Shimotono
Takemasa Sakaguchi
Tetsuya Yoshida
Toru Imamura
Takahiro Goto
Yoshihiro Ohmiya
Akinori Masago
Mariko Morishita
Hitoshi Takahashi
Hiroaki Segawa
Mahito Nakanishi
Masahiro Asada
Kozo Takayama
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: foreign genes; mammalian cells; gene expression; RNA replicon; Sendai virus
Affiliations: Biotherapeutic Research Laboratory, National Institute of Advanced Industrial Science and Technology, 1-1-1 Higashi, Tsukuba, Ibaraki 305-8562, Japan.

Abstract:  Persistent and stable expression of foreign genes has been achieved in mammalian cells by integrating the genes into the host chromosomes. However, this approach has several shortcomings in practical applications. For example, large scale production of protein pharmaceutics frequently requires laborious amplification of the inserted genes to optimize the gene expression. The random chromosomal insertion of exogenous DNA also results occasionally in malignant transformation of normal tissue cells, raising safety concerns in medical applications. Here we report a novel cytoplasmic RNA replicon capable of expressing installed genes stably without chromosome insertion. This system is based on the RNA genome of a noncytopathic variant Sendai virus strain, Cl.151. We found that this variant virus establishes stable symbiosis with host cells by escaping from retinoic acid-inducible gene I-interferon regulatory factor 3-mediated antiviral machinery. Using a cloned genome cDNA of Sendai virus Cl.151, we developed a recombinant RNA installed with exogenous marker genes that was maintained stably in the cytoplasm as a high copy replicon (about 4 x 10(4) copies/cell) without interfering with normal cellular function. Strong expression of the marker genes persisted for more than 6 months in various types of cultured cells and for at least two months in rat colonic mucosa without any apparent side effects. This stable RNA replicon is a potentially valuable genetic platform for various biological applications. 

Retracted: No

PubPeer comments:
 The Morphology of cells in N C C group is the same as in N C N group in Fig2B. ![file] ,
The Snf1 protein kinase and Sit4 protein phosphatase have opposing functions in regulating TATA-binding protein association with the Saccharomyces cerevisiae INO1 promoter
Authors: Diane E Alexander
Margaret K Shirra
Karen M Arndt
Sarah E Rogers
Journal: Genetics (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: mechanisms; signaling pathways; gene expression; S. cerevisiae; INO1
Affiliations: Department of Biological Sciences, University of Pittsburgh, Pennsylvania 15260, USA.

Abstract:  To identify the mechanisms by which multiple signaling pathways coordinately affect gene expression, we investigated regulation of the S. cerevisiae INO1 gene. Full activation of INO1 transcription occurs in the absence of inositol and requires the Snf1 protein kinase in addition to other signaling molecules and transcription factors. Here, we present evidence that the Sit4 protein phosphatase negatively regulates INO1 transcription. A mutation in SIT4 was uncovered as a suppressor of the inositol auxotrophy of snf1Delta strains. We found that sit4 mutant strains exhibit an Spt(-) phenotype, suggesting a more general role for Sit4 in transcription. In fact, like the gene-specific regulators of INO1 transcription, Opi1, Ino2, and Ino4, both Snf1 and Sit4 regulate binding of TBP to the INO1 promoter, as determined by chromatin immunoprecipitation analysis. Experiments involving double-mutant strains indicate that the negative effect of Sit4 on INO1 transcription is unlikely to occur through dephosphorylation of histone H3 or Opi1. Sit4 is a known component of the target of rapamycin (TOR) signaling pathway, and treatment of cells with rapamycin reduces INO1 activation. However, analysis of rapamycin-treated cells suggests that Sit4 represses INO1 transcription through multiple mechanisms, only one of which may involve inhibition of TOR signaling. 

Retracted: No

PubPeer comments:
 Figure 5A should represent strains growing in different plates (with or without inositol). However, itu2019s very surprising to me the similarity of the pattern of colonies between the plates (in red), suggesting that this could be the same plate just photographed on different days. Could the authors check this, please? Beforehand, thanks to the author s attention. ![file] , 
 #1 It is not a mystery. Rather, it is expected. The patterns are the same because the left and right plates were replica-plated from a prior plate. So they are each copies of the same original template plate, transferred to 2 different types of growth media. This was explained in the Figure Legend: * (A) Strains grown on 5-FOA medium were replica plated to synthetic medium lacking inositol or containing 200 u03bcm inositol and allowed to grow for 1 day (SNF1 SIT4) or 2 days (snf1u0394 sit4-731) at 30u00b0. * ,
Synergistic effect of Co–Ni co-bridging with MoS2 nanosheets for enhanced electrocatalytic hydrogen evolution reactions
Authors: Ammar Bin Yousaf
Muhammad Imran
Muhammad Farooq
Peter Kasak
Journal: RSC Advances (2018)
Discipline: CHEMISTRY
Keywords: renewable energy resources; electrocatalytic hydrogen evolution; Co-Ni/MoS2 nanocomposite; HRTEM; elemental mapping
Affiliations: Center for Advanced Materials, Qatar University, Doha 2713, Qatar, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, PR China, Department of Chemistry, University of Management and Technology, Lahore, Pakistan

Abstract:  The depletion of fossil fuels and associated environmental problems have drawn our attention to renewable energy resources in order to meet the global energy demand. Electrocatalytic hydrogen evolution has been considered a potential energy solution due of its high energy density and environment friendly technology. Herein, we have successfully synthesized a noble-metal-free Co-Ni/MoS2 nanocomposite for enhanced electrocatalytic hydrogen evolution. The nanocomposite has been well characterized using HRTEM, elemental mapping, XRD, and XPS analysis. The as-synthesized nanocomposite exhibits a much smaller onset potential and better current density than those of Co-MoS2, Ni-MoS2 and MoS2, with a Tafel value of 49 mV dec-1, which is comparable to that of a commercial Pt/C catalyst. The synergistic effect and interfacial interaction of Co-Ni bimetallic nanoparticles enhances the intrinsic modulation in the electronic structure resulting in an improved HER performance. Moreover, the electrochemical impedance spectroscopic results suggest smaller resistance values for the Co-Ni/MoS2 nanocomposite, compared to those for the charge transfer of bare nanosheets, which increase the faradaic process and in turn enhance the HER kinetics for a better performance. Our as-synthesized Co-Ni/MoS2 nanocomposite holds great potential for the future synthesis of noble-metal-free catalysts. 

Retracted: No

PubPeer comments:
 Fig 2E,F.  The apoptotic behavior were detected by flow cytometry after staining with Annexin-V and PI in the different groups of cells, and the sum of early and late apoptotic cells were calculated as the apoptotic cells. ![file] These peculiar alopecia-stricken images all appear to derive from a single flow-cytometry plot, though the red box marks two that are relatively similar, and the eight in blue boxes are also relatively similar. Some of the original FC plot image (the small dots) remain visible behind the blotches, white patches and smears of the present versions. ![file] I can only suppose that the Editors and peer reviewers of JCB were so impressed by the **realism** of these images that they didn t notice the similarities. ,
Identification and immunogold localization of a novel bromegrass (Bromus inermis Leyss) peroxisome channel protein induced by ABA, cold and drought stresses, and late embryogenesis
Authors: Albert J Robertson
Xunjia Liu
Guohai Wu
Ping Zheng
Lawrence V Gusta
Journal: Gene (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: cDNA; Bromegrass; Peroxisome; Channel protein; ABA
Affiliations: Bioriginal Food and Science Corporation, 110 Gymnasium Place, Saskatoon, Saskatchewan, Canada S7N 0W9.

Abstract:  A cDNA (BG-15) was isolated through differential screening of a cDNA library made from an ABA-treated bromegrass (Bromus inermis Leyss) suspension cell culture. The 819 bp pair cDNA encoded a 174 amino acid polypeptide with a calculated molecular mass of 18.08 kD and isolectric point of 7.50. The deduced amino acid sequences for the cDNA were 29.5% and 32.6% homologous to the known amino acid-selective channel proteins of the chloroplastic outer membrane in pea and barley, but were highly homologous (55.6% to 83.2%) to the putative membrane channel proteins from rice and Arabidopsis. Immunogold localization demonstrated that the channel protein encoded by this cDNA was present on the peroxisome membrane. High stringency southern analysis revealed that 1 to 2 copies of the peroxisomal channel protein (PCP) genes were present in the bromegrass genome. Northern and Western blots revealed that the PCP gene was responsive to both cold and drought stresses, and was rapidly induced by ABA (75 microM). The transcript of the PCP gene also accumulated during late embryogenesis, but declined rapidly during germination. Data taken together, responsiveness of the PCP to cold and drought stresses, and accumulation during late embryogenesis suggest this novel peroxisomal channel protein is associated with sugar and fatty acid metabolism through fatty acid import or succinate export from peroxisome during desiccation tolerance and energy metabolism. 

Retracted: No

PubPeer comments:
 Figure 3B: Differential accumulation of a bromegrass peroxisomal channel protein (BG-15) in embryogenesis and germination. Boxes of the same colors highlight bands that appear to be duplicated. Could the authors please comment? ![file] , 
 Figure 1A may also have issues. The area in the green boxes appears repeated, and the smears in the yellow may share the same source. Could the authors please post the original uncropped scans? *** ![file] , 
 Figure 3A: Differential accumulation of a bromegrass peroxisomal channel protein (BG-15) in **ABA treated** suspension cell cultures. Same control 18S rRNA (red box) was reused from another paper published a year before by the same group ([Wu et al. 2014](http: pubpeer.com publications AADA5B550C5461B92F01DC751F710E#1), red boxes), although vertical dimention is slightly different. Importantly, in [Wu et al. 2014](http: pubpeer.com publications AADA5B550C5461B92F01DC751F710E#1) this loading control is used for a different experiment, where differential induction of the bromegrass LTP gene (BG-14) **by anisomycin and sphingosine** was monitored in suspension cell cultures. Could the authors please comment? ![file] ,
Knocking down miR-384 promotes growth and metastasis of osteosarcoma MG63 cells by targeting SLBP
Authors: Yang Wang
Yi Li
Hong Huang
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MEK/ERK pathway; Osteosarcoma; PI3K/AKT pathway; SLBP; miRNA-384.
Affiliations: Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun, China;, Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun, China

Abstract:  Osteosarcoma is a common malignant bone tumour in adolescents and old people, with highly invasive and metastatic features and poor prognosis. This study aimed to explore the role of miR-384 in osteosarcoma MG63 cells by targeting SLBP. Cell viability, migration and invasion, apoptosis, as well as apoptosis-related factors were evaluated by CCK-8 assay, Transwell assay, flow cytometer and Western blotting, respectively. Dual-luciferase reporter assay was used to determine the target of miR-384. SLBP level was analyzed using qRT-PCR and Western blotting. Important factors of MEK/ERK and PI3K/AKT signalling pathways were analyzed using Western blotting. We found that miR-384 was down-regulated in osteosarcoma tissue samples and cell lines (MG63, U2OS and OS732). miR-384 overexpression inhibited viability, migration and invasion, but promoted apoptosis of MG63 cells; whereas, miR-384 silence exhibited the contrary effects on MG63 cells. SLBP was a target of miR-384. Knockdown of SLBP reversed the promoting effect of miR-384 silence on cells, indicating that miR-384 silence promoted growth and metastasis of MG63 cells by up-regulating SLBP. In conclusion, knocking down miR-384 promoted the growth and metastasis of osteosarcoma MG63 cells by up-regulating SLBP. To conclude, miR-384-SLBP may be a potential therapeutic target for osteosarcoma therapy. 

Retracted: No

PubPeer comments:
 Figure 7. * Red boxes: In the P. aeruginosa column, three panels appear to look similar to each other. ![file] ,
Sublingual immunotherapy provides long-term relief in allergic rhinitis and reduces the risk of asthma: A retrospective, real-world database analysis
Authors: H Richter
P Devillier
J Heinrich
U Wahn
S Zielen
Journal: Allergy (2018)
Discipline: IMMUNOLOGY
Keywords: allergic rhinitis; asthma; database analysis; grass pollen; sublingual immunotherapy.
Affiliations: Division of Allergology, Pulmonology and Cystic Fibrosis, Department for Children and Adolescents, Goethe University Hospital, Frankfurt, Germany., UPRES EA 220, Hospital Foch, University Versailles Saint Quentin, Suresnes, France., Helmholtz Zentrum Munich, German Research Centre for Environmental Health GmbH, Institute of Epidemiology, Neuherberg, Germany., QuintilesIMS GmbH & Co. oHG, Frankfurt am Main, Germany., Department for Paediatric Pneumology and Immunology, Charité Medical University, Berlin, Germany.

Abstract:  Background: Allergy immunotherapy (AIT) is the only treatment for allergic rhinitis (AR) and/or allergic asthma (AA) with long-term efficacy. However, there are few real-life data on the progression of AR and/or AA in patients receiving AIT. Objectives: To assess the real-world, long-term efficacy of grass pollen sublingual immunotherapy (SLIT) tablets in AR and their impact on asthma onset and progression. Methods: In a retrospective analysis of a German longitudinal prescription database, AR patients treated with grass pollen SLIT tablets were compared with a control group not having received AIT. Multiple regression analysis was used to compare changes over time in rescue symptomatic AR medication use after treatment cessation, asthma medication use, and the time to asthma onset in the two groups. Results: After applying all selection criteria, 2851 SLIT and 71 275 control patients were selected for the study. After treatment cessation, AR medication use was 18.8 percentage points lower (after adjustment for covariates, and relative to the pretreatment period) in SLIT tablet group than in the non-AIT group (P&lt;.001). Asthma onset was less frequent in SLIT tablet group than in non-AIT group (odds ratio: 0.696, P=.002), and time to asthma was significantly longer (hazard ratio: 0.523; P=.003). After SLIT cessation, asthma medication use fell by an additional 16.7 percentage points (relative to the pretreatment period) in the SLIT tablet group vs the non-AIT group (P=.004). Conclusions: Real-world treatment of AR patients with grass pollen SLIT tablets was associated with slower AR progression, less frequent asthma onset, and slower asthma progression. 

Retracted: No

PubPeer comments:
 1. Present study is not pre-registered, high COI of all authors (2 retired with misleading addresses), industry funded. 2. Biased data source that does neither include private insurance nor frequent OTC medication. 3. Poor data quality: 99% missing dates, 27% missing sex, 0% physician diagnosis. 4. Unclear why 50% of therapies ended prematurely. Excluding these therapy failures leads to a massive over estimate of effect. 5. Control group is using steroids by definition, leading to a further overestimate of effect in therapy group making all conclusions obsolete. ,
The effects of omalizumab on IgE-induced cytokine synthesis by asthmatic airway smooth muscle cells
Authors: Michael Roth
Michael Tamm
Journal: Annals of Allergy Asthma & Immunology (2010)
Discipline: IMMUNOLOGY
Keywords: Airway smooth muscle cells; IgE receptors; Omalizumab; Cytokine secretion; mRNA synthesis
Affiliations: Division of Pulmonary Cell Research, Department of Research, University Hospital Basel, Basel, Switzerland. 

Abstract:  Background: Human airway smooth muscle cells (ASMCs) express high- and low-affinity IgE receptors and respond to IgE, thereby contributing to airway inflammation. Objective: To determine whether anti-IgE antibodies (omalizumab) block the response of ASMCs to IgE in patients with asthma. Methods: Airway smooth muscle cells, isolated from the biopsy specimens of patients with asthma, patients with chronic obstructive pulmonary disease, and control participants (6 in each group), were stimulated with IgE with and without omalizumab treatment, and cytokine secretion was determined by enzyme-linked immunosorbent assay, and messenger RNA (mRNA) secretion by real-time polymerase chain reaction, over 24 hours. IgE receptor expression was determined by immunoblotting. Results: IgE-stimulated mRNA synthesis encoded for interleukin (IL) 6, IL-8, and tumor necrosis factor a in ASMCs via mitogen-activated protein kinases, extracellular signal-regulated kinase 1/2, or p38. The secretion of the respective cytokines increased significantly: IL-6, IL-8, and tumor necrosis factor a at 6 hours and IL-4 at 24 hours. Cytokine mRNA synthesis and protein secretion were inhibited by omalizumab in a dose-dependent manner. The expression of low- and high-affinity IgE receptors was not altered by omalizumab in ASMCs. Conclusions: Omalizumab reduced IgE-stimulated synthesis and secretion of proinflammatory cytokines by human ASMCs. These findings imply a beneficial action of omalizumab in asthma therapy. This effect is not restricted to inflammatory cells; it also includes tissue-forming cells. 

Retracted: No

PubPeer comments:
 Figure 5A and 5B appear to include some repeated bands. There may be more than the 2 sets marked. *** ![file] *** ![file] ,
Long noncoding RNA SLC30A10 promotes colorectal tumor proliferation and migration via miR-21c/APC axis
Authors: P Liu
L Hou
T Zhu
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Colorectal cancer; Long non-coding RNAs; lncRNA; SLC30A10; Tumor progression
Affiliations: Department of Gastrointestinal Surgery, Affiliated Hospital of Chengde Medical College, Chengde, China. .

Abstract:  Objective: Colorectal cancer is a common malignancy and a common cause of tumor-related death. Long non-coding RNAs (lncRNAs) have become an important regulatory factor and tissue specific biomarker for a variety of cancers, including colorectal cancer. Recent evidence indicates that the novel lncRNA SLC30A10 plays an important role in tumor progression and metastasis. However, its role and molecular mechanisms in colorectal cancer are unclear. Patients and methods: SLC30A10 expression was detected in 12 colorectal cancer and adjacent normal tissues by quantitative reverse transcription PCR. Insights into the underlying mechanisms of competitive endogenous RNAs (ceRNAs) were determined by transwell assay, CCK8 assay, and luciferase assay. Results: SLC30A10 was down-regulated in colorectal cancer tissues and cell lines, and its low expression was positively correlated with colorectal cancer progression and metastasis. Functionally, SLC30A10 depletion promotes cell proliferation and migration in colorectal cancer cells, while SLC30A10 overexpression has the opposite effect. Bioinformatics prediction and luciferase assay indicated that miR-21c is a direct target of SLC30A10, which plays the role of ceRNA in regulating colorectal cancer metastasis. In addition, miR-21c specifically targets APC gene. Conclusions: Our findings suggest that reduced expression of SLC30A10 is associated with aggressive tumor phenotypes and poor patient outcomes in colorectal cancer. SLC30A10 inhibits colorectal cancer progression and metastasis by acting as a ceRNA for miR-21c to regulate APC expression, suggesting that SLC30A10 may serve as a potential prognostic biomarker and anti-metastatic therapeutic target for colorectal cancer. 

Retracted: No

PubPeer comments:
 I found authors research regarding SLC30A10 very interesting. However, I was surprised that the authors only referred to SLC30A10 as a noncoding RNA. Since it is established that the Slc30a10 gene codes for the ZNT10 metal transporters, I was hoping the paper would discuss this relationship, or at least mention it. I am hoping the authors, or someone else on here, can clarify how a transcript can be both coding and non-coding? , 
 Primer sequences do not appear to correspond to either Slc30a10 or Gapdh. Could the authors please check their primer sequences? ,
Enhancement of susceptibility to Fas-mediated apoptosis in oral squamous cell carcinoma cells by phosphatidylinositol 3-kinase inhibitor
Authors: Masaru Ohashi
Masao Nagumo
Masayasu Iwase
Gen Kondo
Hitoshi Watanabe
Makiko Uchida
Sayaka Takaoka
Journal: Oral Oncology (2006)
Discipline: CLINICAL MEDICINE
Keywords: oral squamous cell carcinoma; Fas-mediated apoptosis; PI 3-K/Akt; inhibitors; caspase-3
Affiliations: Department of Oral and Maxillofacial Surgery, Showa University School of Dentistry, 2-1-1, Kitasenzoku, Ota-ku, Tokyo 145-8515, Japan.

Abstract:  In general, oral squamous cell carcinoma (OSCC) cells are relatively resistant to Fas-mediated apoptosis during in vitro culture. Here, we studied the role of survival/apoptosis associated phosphatidylinositol 3-kinase (PI 3-K)/Akt in this process. We found that both PI 3-K inhibitors, wortmannin and LY294002, markedly suppressed the phosphorylation of Akt and accelerated Fas-mediated apoptosis in OSCC cells. It was found that caspase-3 and -8 inhibitors reduced the accelerative effect of PI 3-K inhibitor on Fas-mediated apoptosis in OSCC cells, but not caspase-9 inhibitor. Although PI 3-K inhibitors did not affect the Fas expression of OSCC cells, cellular FLICE-inhibitory protein (c-FLIP) levels were markedly reduced by PI 3-K inhibitor treatment. Moreover, antisense oligonucleotide to c-FLIP confirmed that the down-regulation of c-FLIP enhanced the sensitization to Fas-mediated apoptosis in OSCC cells. These results suggest that PI 3-K/Akt signaling pathway may, in part, regulate Fas-mediated apoptosis in OSCC cells through c-FLIP expression. 

Retracted: No

PubPeer comments:
 **Figure 6A**: both cFLIP and actin control panels obtained from **HSC-4 cells** (left side) appear to be much more similar than expected to cFLIP and actin control panels of **Figure 6B** from another paper, published by the same group three years before [Iwase_et_al_2003](http: pubpeer.com publications D801E78C0D311B1B9A7B6B56C4DA39#2) (right side), where another cell type (**NA cells**) was used. In turn, Figure 6B from [Iwase_et_al_2003](http: pubpeer.com publications D801E78C0D311B1B9A7B6B56C4DA39#2) has duplicated actin panels itself. Could the authors please comment? ![file] **** , 
 Could the authors please comment? , 
 #2 Dear Aneurus Inconstans Thank you for your series of valuable suggestions. We will sincerely verify the matters pointed out. Therefore, we will report again after a while for verification. , 
 Dear Aneurus Inconstans Thank you for your series of valuable suggestions. We will sincerely verify the matters pointed out. Therefore, we will report again after a while for verification. , 
 #1 Dear Aneurus Inconstans Thank you for your series of valuable suggestions. We will sincerely verify the matters pointed out. I m sorry, many collaborators have already resigned from academia. Therefore, we will report again after a while for verification. ,
Gene expression modulation in TGF ‐β3‐mediated rabbit bone marrow stem cells using electrospun scaffolds of various stiffness
Authors: Caihong Zhu
Qianping Guo
Bin Li
Huilin Yang
Jun Li
Chen Liu
Journal: Journal of Cellular and Molecular Medicine (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TGF-β3 treatment; annulus fibrosus-derived stem cells; bone marrow stem cells; electrospun scaffolds; gene expression
Affiliations: Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China., Orthopedic Institute, Soochow University, Suzhou, Jiangsu, China.

Abstract:  Tissue engineering has recently evolved into a promising approach for annulus fibrosus (AF) regeneration. However, selection of an ideal cell source, which can be readily differentiated into AF cells of various regions, remains challenging because of the heterogeneity of AF tissue. In this study, we set out to explore the feasibility of using transforming growth factor-β3-mediated bone marrow stem cells (tBMSCs) for AF tissue engineering. Since the differentiation of stem cells significantly relies on the stiffness of substrate, we fabricated nanofibrous scaffolds from a series of biodegradable poly(ether carbonate urethane)-urea (PECUU) materials whose elastic modulus approximated that of native AF tissue. We cultured tBMSCs on PECUU scaffolds and compared their gene expression profile to AF-derived stem cells (AFSCs), the newly identified AF tissue-specific stem cells. As predicted, the expression of collagen-I in both tBMSCs and AFSCs increased with scaffold stiffness, whereas the expression of collagen-II and aggrecan genes showed an opposite trend. Interestingly, the expression of collagen-I, collagen-II and aggrecan genes in tBMSCs on PECUU scaffolds were consistently higher than those in AFSCs regardless of scaffold stiffness. In addition, the cell traction forces (CTFs) of both tBMSCs and AFSCs gradually decreased with scaffold stiffness, which is similar to the CTF change of cells from inner to outer regions of native AF tissue. Together, findings from this study indicate that tBMSCs had strong tendency to differentiate into various types of AF cells and presented gene expression profiles similar to AFSCs, thereby establishing a rationale for the use of tBMSCs in AF tissue engineering. 

Retracted: No

PubPeer comments:
 Figure 1 appears to have some areas in the images which overlap. The magenta boxes may be a situation where a figured number was changed and someone cut and pasted from another area for cosmetic reasons. *** ![file] , 
 Similar issue in Figure 3. *** ![file] , 
 Two images in Figure 5 seem to overlap, after rotation. *** ![file] *** Acknowledgements. The authors greatly acknowledge the financial support from National Natural Science Foundation of China (81171479, 51303120, 81471790), Natural Science Foundation of Jiangsu Province (BK2011291), the Innovation Project of Graduate Education of Jiangsu Province (CXLX13-832), Jiangsu Provincial Special Program of Medical Science (BL2012004), and China Postdoctoral Science Foundation (2012M521121). ,
The Preparation of Hollow Mesoporous Bioglass Nanoparticles With Excellent Drug Delivery Capacity for Bone Tissue Regeneration
Authors: Xiaofeng Chen
Haobo Pan
Yudong Wang
Journal: Frontiers in Chemistry (2019)
Discipline: CHEMISTRY
Keywords: bioglass; bone repair; drug delivery; hollow structure; nanoparticles.
Affiliations: Research Center for Human Tissue and Organs Degeneration, Institute Biomedical and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China., School of Materials Science and Engineering, South China University of Technology, Guangzhou, China., National Engineering Research Center for Tissue Restoration and Reconstruction, Guangzhou, China.

Abstract:  In this work, hollow mesoporous bioglass (HMBG) nanoparticles were prepared in a hexadecyl trimethyl ammonium bromide (CTAB)-cyclonexane-ethanol-water (O/W) emulsion system. The HMBG nanoparticles possessed higher drug storage ability and stable drug release behavior which resulted from HMBG's unique mesoporous structure. The mesoporous structure could be modulated by adjusting the concentration of CTAB. The specific surface area and drug loading efficiency was as high as 749.619 m2g-1 and 55.1%. Besides, in vivo experiments demonstrated that the HMBG nanoparticles could promote the bone tissue regeneration and the drug-loading HMBG nanoparticles possessed better repair capability. The unique structure and properties might make the HMBG nanoparticles good candidates as drug carriers and repair materials for bone tissue regeneration. 

Retracted: No

PubPeer comments:
 Images in Figure 4 from this paper seem very similar to images in Figure 3 of 10.1016 j.matlet.2016.12.004 Materials Letters (2017). While the 2017 paper is included as a reference, I did not see a mention that the images had been reused. I may have missed this. Could the authors please check? *** ![file] ,
Galangin ameliorates cardiac remodeling via the MEK1/2–ERK1/2 and PI3K–AKT pathways
Authors: Qi-Zhu Tang
Hai-Han Liao
Si-Hui Huang
Chun-Xia Wan
Di Fan
Jian Yang
Hui-Bo Wang
Jun Yang
Ming-Xin Liu
Man Xu
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: AKT; ERK1/2; GATA4; cardiac remodeling; fibrosis
Affiliations: Department of Cardiology, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China., Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University, Institute of Cardiovascular Diseases, Yichang, People's Republic of China.

Abstract:  Cardiac remodeling is associated with inflammation and apoptosis. Galangin, as a natural flavonol, has the potent function of regulating inflammation and apoptosis, which are factors related to cardiac remodeling. Beginning 3 days after aortic banding (AB) or Sham surgery, mice were treated with galangin for 4 weeks. Cardiac remodeling was assessed according to echocardiographic parameters, histological analyses, and hypertrophy and fibrosis markers. Our results showed that galangin administration attenuated cardiac hypertrophy, dysfunction, and fibrosis response in AB mice and angiotensin II-treated H9c2 cells. The inhibitory action of galangin in cardiac remodeling was mediated by MEK1/2-extracellular-regulated protein kinases 1/2 (ERK1/2)-GATA4 and phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT)-glycogen synthase kinase 3β (GSK3β) activation. Furthermore, we found that galangin inhibited inflammatory response and apoptosis. Our findings suggest that galangin protects against cardiac remodeling through decreasing inflammatory responses and apoptosis, which are associated with inhibition of the MEK1/2-ERK1/2-GATA4 and PI3K-AKT-GSK3β signals. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,