PReD-Bench/PRed-Bench huggingface dataset:
Effects of daily consumption of synbiotic bread on insulin metabolism and serum high-sensitivity C-reactive protein among diabetic patients: a double-blind, randomized, controlled clinical trial
Authors: Fereashteh Bahmani
Maryam Tajadadi-Ebrahimi
Mohammad Hijijafari
Zatollah Asemi
Fatemeh Abedi
Haleh Hadaegh
Hossein Shakeri
Journal: Annals of Nutrition and Metabolism (2014)
Discipline: CLINICAL MEDICINE
Keywords: synbiotic bread; type 2 diabetes mellitus; metabolic status; Lactobacillus sporogenes; inulin
Affiliations: Science Department, Science Faculty, Islamic Azad University, Tehran Central Branch, Tehran, Iran.

Abstract:  Background: This study was conducted to evaluate the effects of daily consumption of synbiotic bread on the metabolic status of patients with type 2 diabetes mellitus. Methods: This randomized, double-blind, controlled clinical trial was performed in 81 diabetic patients. The subjects were randomly assigned to consumption of synbiotic (n = 27), probiotic (n = 27), or control bread (n = 27) for 8 weeks 3 times a day in a 40-gram package. The synbiotic bread contained Lactobacillus sporogenes (1 × 10(8) CFU) and 0.07 g inulin per 1 g. The probiotic bread contained L. sporogenes (1 × 10(8) CFU per 1 g). Fasting blood samples were taken at baseline and after an 8-week intervention for quantification of related factors. Results: Consumption of the synbiotic bread resulted in a significant reduction in serum insulin levels (-3.2 ± 5.4 vs. -0.3 ± 3.4 and 0.6 ± 4.7 µIU/ml, respectively, p = 0.007), homeostatic model assessment for insulin resistance scores (-1.5 ± 2.7 vs. -0.2 ± 1.6 and 0.4 ± 3.5, respectively, p = 0.03), and homeostatic model assessment-β-cell function (-7.2 ± 16.3 vs. -0.7 ± 10.8 and 0.7 ± 8.2, respectively, p = 0.04) compared to the probiotic and control breads. We did not find any significant effect of synbiotic bread consumption on fasting plasma glucose, the quantitative insulin sensitivity check index, or serum hs-CRP levels compared to other breads. Conclusion: Consumption of the synbiotic bread among diabetic patients had beneficial effects on insulin metabolism. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A24 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Increased multi-drug resistance and reduced apoptosis in osteosarcoma side population cells are crucial factors for tumor recurrence
Authors: Yang Wang
Jia-Song Teng
Journal: Experimental and Therapeutic Medicine (2016)
Discipline: CLINICAL MEDICINE
Keywords: ATPase binding cassette transporters; anticancer drugs; drug resistance; metastasis; sarcospheres

Abstract:  The present study investigated the characteristic features of cancer stem cells (CSCs) using an aggressive human osteosarcoma cell line OS-65. Hoechst 33342 dye exclusion was used to distinguish the cancer stem-like side population (SP) cells from OS-65 cells. Furthermore, the SP cells were characterized via chemoresistance and cell death assays, reverse transcription-quantitative polymerase chain reaction and immunofluorescence. The present study identified ~3.3% of cancer stem-like SP cells from OS-65 cells whose prevalence is reduced significantly (0.9%) following treatment with verapamil. It was demonstrated that osteosarcoma SP cells are highly efficient at generating additional sarcospheres as transcriptional regulation of stemness genes, including SOX2, OCT-4 and NANOG, is highly upregulated. Notably, these SP cells demonstrated high resistance against chemotherapeutic drugs and apoptosis via elevated transcriptional regulation of several ATPase binding cassette (ABC) transporter and anti-apoptotic proteins, including ABCG2, ABCB1/MDR1 ABCB5, B cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein, respectively. The results of the present study suggested that CSCs may be a novel therapeutic target for the prevention of tumor relapse. 

Retracted: No

PubPeer comments:
  Figure 1. - Identification and characterization of SP cells from an OS-65 osteosarcoma cell line. (A) Representative images of dot plot analysis by FACS demonstrating the presence of 3.3% SP cells. I am not an expert but I do not feel that FACS plots should fade in and out of focus as if they were assembled from different sections, superimposed with Photoshop smudging at the edges. Nor should they contain large repeating areas. ![file] , 
  Figure 3. - Representative images of immunofluorescence analysis for (A) CD44, (B) Nanog and (C) Oct-3 4A protein expression in human osteosarcoma cell line OS-65 SP cells and (D) non-SP cells. I would hate to see the unrepresentative images. ![file] ,
Synthesis and characterization of polyethylene glycol mediated silver nanoparticles by the green method
Authors: Mansor Bin Ahmad
Parvaneh Shabanzadeh
Kamyar Shameli
Mahnaz Mahdavi
Sajjad Sedaghat
Hossein Jahangirian
Yadollah Abdollahi
Seyed Davoud Jazayeri
Journal: International Journal of Molecular Sciences (2012)
Discipline: CHEMISTRY
Keywords: green chemistry; polyethylene glycol; reaction time effect; silver nanoparticles; transmission electron microscopy.
Affiliations: Department of Chemistry, Faculty of Science, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia; E-Mails:  mansorahmad@gmail.com  (M.B.A.);    (H.J.);    (M.M.).

Abstract:  The roles of green chemistry in nanotechnology and nanoscience fields are very significant in the synthesis of diverse nanomaterials. Herein, we report a green chemistry method for synthesized colloidal silver nanoparticles (Ag NPs) in polymeric media. The colloidal Ag NPs were synthesized in an aqueous solution using silver nitrate, polyethylene glycol (PEG), and β-D-glucose as a silver precursor, stabilizer, and reducing agent, respectively. The properties of synthesized colloidal Ag NPs were studied at different reaction times. The ultraviolet-visible spectra were in excellent agreement with the obtained nanostructure studies performed by transmission electron microscopy (TEM) and their size distributions. The Ag NPs were characterized by utilizing X-ray diffraction (XRD), zeta potential measurements and Fourier transform infrared (FT-IR). The use of green chemistry reagents, such as glucose, provides green and economic features to this work. 

Retracted: No

PubPeer comments:
 Readers should be aware of the potential overlap between this article and another in a different journal, discussed here: https: pubpeer.com publications 832F4971226CDB4170E947215595FC This issue seems similar to another set of overlaps between papers with common authors discussed here: https: pubpeer.com publications 5CB7359F4C9CB2B8BC2AF958688F32 ,
MicroRNA-99a-5p suppresses breast cancer progression and cell-cycle pathway through downregulating CDC25A
Authors: Wenfei Liu
Hongzhen Qin
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CDC25A; breast cancer; cell-cycle pathway; miR-99a-5p.
Affiliations: Department of General Surgery, 305 Hospital of PLA, Beijing, China.

Abstract:  In this study, we aimed to explore the association between miR-99a-5p and CDC25A in breast cancer and the regulatory mechanisms of miR-99a-5p on breast cancer. The expressions of messenger RNA and microRNAs in breast cancer tissues and adjacent tissues were analyzed by the Cancer Genome Atlas microarray analysis. Quantitative real-time polymerase chain reaction was conducted to find out the expression levels of miR-99a-5p and CDC25A. The expression levels of proteins (CDC25A, ki67, cyclin D1, p21, BAX, BCL-2, BCL-XL, MMP2, and MMP9) were determined by Western blot analysis. The relationship between miR-99a-5p and CDC25A was predicted and verified by bioinformatics analysis and dual luciferase assay. After transfection, cell proliferation, invasion, and apoptosis of breast cancer tissues were, respectively, observed by cell counting kit-8 assay, transwell assay, and flow cytometry (FCM). Furthermore, the relationship among miR-99a-5p, CDC25A, and cell-cycle progression was determined by FCM assay. The nude mouse transplantation tumor experiment was performed to verify the influence of miR-99a-5p on breast cancer cell in vivo. The expression of miR-99a-5p in breast cancer tissues and cells was significantly downregulated, whereas CDC25A expression was upregulated. MiR-99a-5p targeted CDC25A and suppressed its expression in breast cancer cells. Overexpression of miR-99a-5p and decreased expression of CDC25A could suppress breast cancer cell proliferation and invasion and facilitate apoptosis. Cell-cycle progression was significantly activated by downregulated miR-99a-5p and upregulated CDC25A. Moreover, miR-99a-5p overexpression repressed the expressions of CDC25A, marker ki67, and Cyclin D1 proteins, whereas it upregulated the expression of p21 protein. MicroRNA-99a-5p suppresses breast cancer progression and cell-cycle pathway through downregulating CDC25A. 

Retracted: No

PubPeer comments:
 Fig 6(c),  Transwell assay (u00d7200, 50 u03bcm) was applied to analyze invasion; the level of invasion decreased in the miRu201099au20105p mimics group, the siu2010CDC25A group, and the miRu201099au20105p+siu2010CDC25A group . Could the authors check the identification of the images? ![file] ,
Inhibition of AKT2 enhances sensitivity to gemcitabine via regulating PUMA and NF-κB signaling pathway in human pancreatic ductal adenocarcinoma
Authors: Kejun Zhang
Xuelong Jiao
Jun Liang
Min Niu
Dianliang Zhang
Dong Chen
Journal: International Journal of Molecular Sciences (2012)
Discipline: CHEMISTRY
Keywords: AKT; NF-κB; PUMA; gemcitabine; pancreatic cancer.
Affiliations: Department of General Surgery, The Affiliated Hospital of Medical College, Qingdao University, Qingdao 266003, China.

Abstract:  Invasion, metastasis and resistance to conventional chemotherapeutic agents are obstacles to successful treatment of pancreatic cancer, and a better understanding of the molecular basis of this malignancy may lead to improved therapeutics. In the present study, we investigated whether AKT2 silencing sensitized pancreatic cancer L3.6pl, BxPC-3, PANC-1 and MIAPaCa-2 cells to gemcitabine via regulating PUMA (p53-upregulated modulator of apoptosis) and nuclear factor (NF)-κB signaling pathway. MTT, TUNEL, EMSA and NF-κB reporter assays were used to detect tumor cell proliferation, apoptosis and NF-κB activity. Western blotting was used to detect different protein levels. Xenograft of established tumors was used to evaluate primary tumor growth and apoptosis after treatment with gemcitabine alone or in combination with AKT2 siRNA. Gemcitabine activated AKT2 and NF-κB in MIAPaCa-2 and L3.6pl cells in vitro or in vivo, and in PANC-1 cells only in vivo. Gemcitabine only activated NF-κB in BxPC-3 cells in vitro. The presence of PUMA was necessary for gemcitabine-induced apoptosis only in BxPC-3 cells in vitro. AKT2 inhibition sensitized gemcitabine-induced apoptosis via PUMA upregulation in MIAPaCa-2 cells in vitro, and via NF-κB activity inhibition in L3.6pl cells in vitro. In PANC-1 and MIAPaCa-2 cells in vivo, AKT2 inhibition sensitized gemcitabine-induced apoptosis and growth inhibition via both PUMA upregulation and NF-κB inhibition. We suggest that AKT2 inhibition abrogates gemcitabine-induced activation of AKT2 and NF-κB, and promotes gemcitabine-induced PUMA upregulation, resulting in chemosensitization of pancreatic tumors to gemcitabine, which is probably an important strategy for the treatment of pancreatic cancer. 

Retracted: No

PubPeer comments:
 Fig.1A at the bottom, for loading controls of MIAPaCa-2 and PANC-1, the latter looked like a vertical flip away from the former, might be with some minor edits of the details: ![file] , 
 #1 This is the original original image, we did retouch it, the background of the original image is too messy, we remove the background.![file] ,
Opposing roles of FoxP1 and Nfat3 in transcriptional control of cardiomyocyte hypertrophy
Authors: Shoumei Bai
Tom K Kerppola
Journal: Molecular and Cellular Biology (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cardiac homeostasis; growth-promoting factors; growth-modulating factors; calcium signaling; cardiac hypertrophy
Affiliations: Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan 48109-0650, USA.

Abstract:  Cardiac homeostasis is maintained by a balance of growth-promoting and growth-modulating factors. Sustained elevation of calcium signaling can induce cardiac hypertrophy through activation of Nfat family transcription factors. FoxP family transcription factors are known to interact with Nfat proteins and to modulate their transcriptional activities in lymphocytes. We investigated FoxP1 interaction with Nfat3 (Nfatc4) and their effects on transcription of hypertrophy-associated genes in neonatal rat cardiomyocytes. FoxP1-Nfat3 complexes were visualized using bimolecular fluorescence complementation (BiFC) analysis. Calcineurin activation induced FoxP1-Nfat3 BiFC complex formation. Amino acid substitutions in the predicted interaction interface inhibited it. FoxP1 repressed hypertrophy-associated genes (Myh7, Rcan1, Cx43, Anf, and Bnp) and counteracted their activation by constitutively nuclear Nfat3 (cnNfat3). In contrast, FoxP1 activated genes that maintain normal heart functions (Myh6 and p57Kip2) and cnNfat3 counteracted their activation by FoxP1. Amino acid substitutions in FoxP1 or cnNfat3 that inhibited their interaction abrogated the activation of hypertrophy-associated gene transcription by cnNfat3 and the repression of these genes by FoxP1. FoxP1 and Nfat3 co-occupied the promoter regions of hypertrophy-associated genes in neonatal and adult heart tissue. FoxP1 counteracted hypertrophic cardiomyocyte growth, and connexin 43 mislocalization caused by cnNfat3 expression. These data suggest that the opposing transcriptional activities of FoxP1 and Nfat3 maintain cardiomyocyte homeostasis. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: mcb.asm.org content 41 1 e00544-20 RETRACTION Volume 31, no. 14, p. 3068u20133080, 2011, https: doi.org 10.1128 MCB.00925-10. I retract this article due to image duplication and manipulation. I apologize to the scientific community and readers of Molecular and Cellular Biology and regret any damage that this has caused. , 
 #1 FOOTNOTES S. Bai did not agree to this retraction. Copyright u00a9 2020 American Society for Microbiology. First author appears to currently be affiliated with University of Pittsburgh, and has the unfortunate distinction of appearing as coauthor of multiple papers with similar image concerns while at different institutions: https: pubpeer.com search?q=Shoumei+Bai ![file] ,
Infection of lymphoid cells by integration-defective human immunodeficiency virus type 1 increases de novo methylation
Authors: F W Ruscetti
C L Petrow-Sadowski
R Bagni
J Y Fang
J A Mikovits
Journal: Journal of virology (2001)
Discipline: MICROBIOLOGY
Keywords: DNA methylation; DNMTs; HIV-1 infection; gene transcription; gamma interferon gene
Affiliations: Basic Research Laboratory, CCR, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA.

Abstract:  DNA methylation, by regulating the transcription of genes, is a major modifier of the eukaryotic genome. DNA methyltransferases (DNMTs) are responsible for both maintenance and de novo methylation. We have reported that human immunodeficiency virus type 1 (HIV-1) infection increases DNMT1 expression and de novo methylation of genes such as the gamma interferon gene in CD4(+) cells. Here, we examined the mechanism(s) by which HIV-1 infection increases the cellular capacity to methylate genes. While the RNAs and proteins of all three DNMTs (1, 3a, and 3b) were detected in Hut 78 lymphoid cells, only the expression of DNMT1 was significantly increased 3 to 5 days postinfection. This increase was observed with either wild-type HIV-1 or an integrase (IN) mutant, which renders HIV replication defective, due to the inability of the provirus to integrate into the host genome. Unintegrated viral DNA is a common feature of many retroviral infections and is thought to play a role in pathogenesis. These results indicate another mechanism by which unintegrated viral DNA affects the host. In addition to the increase in overall genomic methylation, hypermethylation and reduced expression of the p16(INK4A) gene, one of the most commonly altered genes in human cancer, were seen in cells infected with both wild-type and IN-defective HIV-1. Thus, infection of lymphoid cells with integration-defective HIV-1 can increase the methylation of CpG islands in the promoters of genes such as the p16(INK4A) gene, silencing their expression. 

Retracted: No

PubPeer comments:
 Table 1 shows the area under the melting curve as determined by real-time PCRR, shown as the mean + - standard deviation (SD) of two measurements, and the specific melting temperature between parenthesis. Many values appear to be identical to each other. Is there any reason that could explain how the means are all unique but the SDs and melting temperatures are often exactly the same? There could be a perfectly good reason, but I just cannot come up with one. Values that are identical are shown with boxes of the same color. ![file] ,
Electrokinetic potential-stabilization by bile acid-microencapsulating formulation of pancreatic β-cells cultured in high ratio poly-L-ornithine-gel hydrogel colloidal dispersion: applications in cell-biomaterials, tissue engineering and biotechnological applications
Authors: Grant Morahan
Armin Mooranian
Rebecca Negrulj
Ryu Takechi
Hani Al-Salami
Emma Jamieson
Journal: Artificial Cells Nanomedicine and Biotechnology (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Electrokinetic potential; biomaterials; polymers; tissue engineering.
Affiliations: Biotechnology and Drug Development Research Laboratory, School of Pharmacy, Curtin Health Innovation Research Institute, Curtin University, Perth, WA, Australia;, School of Public Health, Curtin Health Innovation Research Institute, Curtin University, Perth, WA, Australia;, Centre for Medical Research, University of Western Australia, Perth, WA, Australia;, Clinical Sciences Division, The Harry Perkins Institute of Medical Research, Perth, WA, Australia

Abstract:  Introduction: Current trials for β-cell transplantation have been hindered by poor cell viability and function post-transplantation. Recently, electric charges of the microencapsulating formulation carrying β-cells have shown significant effects on cell survival and function. Thus, this study aimed at investigating the effects of electric charge, of novel colloidal formulation containing β-cells, on cell viability, biological activity and insulin release. Methods: A new formulation, containing high ratios of poly-L-ornithine, suspending electrical-stimulation hydrogel and polystyrene sulphone (1:1:0.1 ratio), was used to form microcapsules utilizing 800 V and 2000 Hz encapsulating conditions. The bile acid, ursodeoxycholic acid, was added into the microcapsules to measure its effects on electric charges. Results: The electric charge of the microencapsulating formulation was enhanced by bile acid addition, and resulted in better cell viability and function. Conclusion: Ursodeoxycholic acid microencapsulated with poly-L-ornithine, suspending electrical-stimulation hydrogel and polystyrene sulphone at 1:1:0.1 ratio, using 800 V and 2000 Hz microencapsulating conditions, produced enhanced electrokinetic parameters of microcapsules with optimized cell functions. This suggests that electric charge of formulations containing pancreatic β-cell may have significant effects on cell mass and functions, post-transplantation. 

Retracted: No

PubPeer comments:
 Brief commentary: https: reason.com 2020 06 11 policing-the-police-the-impact-of-pattern-or-practice-investigations-on-crime ,
MicroRNA-101 inhibits proliferation, migration and invasion in osteosarcoma cells by targeting ROCK1
Authors: Guangyao Liu
Chao Zhang
Rui Jiang
Rui Gu
Han Wu
Journal: American journal of cancer research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Osteosarcoma; ROCK1; cell apoptosis; cell migration; microRNA-101.
Affiliations: Department of Orthopedics, China-Japan Union Hospital of Jilin University Changchun 130033, China., Department of Ophthalmology, The Second Hospital of Jilin University Changchun 130041, China.

Abstract:  Osteosarcoma is a rare malignant bone tumor in adolescents, with high degree of malignancy, and highly incidence of recurrence and metastasis. Our study aimed to explore the role of miR-101 in osteosarcoma cells by targeting ROCK1. In the present study, reverse transcription-quantitative polymerase chain reaction data revealed that miR-101 was down-regulated in the tissue samples of 20 patients with osteosarcoma compared with their matched adjacent non-tumor tissues (P &lt; 0.01). Furthermore, miR-101 was significantly down-regulated in three common OS cell lines, MG63, U2OS, and OS732 compared with the human osteoblast cell line, hFOB1.19 (P &lt; 0.01). MiR-101 was shown to target the ROCK1 3'-UTR in dual-luciferase reporter assays in MG63 cells. Overexpression of miR-101 significantly suppressed the protein expression levels of ROCK1, while knockdown of miR-101 significantly enhanced the formers' expression levels in MG63 cells (P &lt; 0.05). Overexpression of miR-101 inhibited cell viability, migration, and invasion while promoted apoptosis. Independent inhibition of ROCK1 and knockdown of miR-101 expression levels significantly promoted MG63 cell proliferation, migration and invasion while inhibited apoptosis (P &lt; 0.01). Moreover, knockdown of ROCK1 reversed the promotion effect of miR-101 knockdown on proliferation, migration, and invasion while promoted apoptosis of MG63 cells, suggesting that miR-101 acts as a tumor suppressor in osteosarcoma cells via targeting ROCK1. Furthermore, overexpression of miR-101 inhibited tumor growth and motion by inactivating PI3K/AKT and JAK/STAT signaling pathways via downregulation of ROCK1. To conclude, miR-101/ROCK1 may be a potential therapeutic target for osteosarcoma therapy. 

Retracted: No

PubPeer comments:
 Copied, Pasted and Cropped IMAGE with NO CITATION! Source of origin: [Link] ![file] ,
Synergistic effects of curcumin with emodin against the proliferation and invasion of breast cancer cells through upregulation of miR-34a
Authors: Jiaoli Guo
Peng Liu
Hailin Tang
Wenping Li
Xinhua Xie
Laisheng Li
Xiaoming Xie
Lu Yang
Yanan Kong
Hongliu Shi
Weidong Wei
Jie Gao
Minqing Wu
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Curcumin; Emodin; Breast cancer; Synergy; Proliferation
Affiliations: Department of Breast Oncology, Sun Yat-Sen University Cancer Center, 651 East Dong Feng Road, Guangzhou, 510060, People's Republic of China.

Abstract:  Curcumin, a biphenyl compound derived from rhizome, is a powerful anti-cancer agent. Emodin is an active component isolated from the root and rhizome of Rheum palmatum that has been widely used in traditional Chinese medicine for the treatment of various diseases. Currently, there are no studies examining the effect of curcumin in combination with emodin on tumor cell growth. In this study, we report for the first time that combined curcumin and emodin administration synergistically inhibits proliferation (MTT assay), survival (flow cytometry), and invasion (transwell migration assay) of breast cancer cells. Synergism is determined by the Chou-Talalay method. Moreover, we demonstrate that miR-34a is upregulated by curcumin and emodin. This microRNA helps mediate the anti-tumor effects of curcumin and emodin by downregulating Bcl-2 and Bmi-1. Our results not only provide insight into the mechanism of synergy between curcumin and emodin in breast cancer cells, but also suggest a new and potentially useful approach for breast cancer therapy. 

Retracted: No

PubPeer comments:
 Judging from the scatter plot, the numerous data points of HIF-1u03b1 expression seem to contain only nine values. The expression data in this research somehow look like discrete variable. ![] ,
LincRNA Cox-2 Regulates Lipopolysaccharide-Induced Inflammatory Response of Human Peritoneal Mesothelial Cells via Modulating miR-21/NF-κB Axis
Authors: Lili Yang
Yaoyao Bian
Xi Chen
Wen Li
Shuling Jiang
Bin Zhang
Li Zeng
Sen Wang
Wenlin Li
Journal: Mediators of inflammation (2019)
Discipline: IMMUNOLOGY
Keywords: Postoperative peritoneal adhesion; large intergenic non-coding RNAs (lincRNAs); Cox-2; inflammation reaction; adhesion formation
Affiliations: School of Nursing, Nanjing University of Chinese Medicine, Nanjing, China., School of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, China., Jingwen Library, Nanjing University of Chinese Medicine, Nanjing, China., Digestive Department, Ningbo Hospital of traditional Chinese Medicine, Ningbo, China., School of Preclinical Medicine, Guiyang University of Chinese Medicine, Guiyang, China., Department of Anorectal, Huainan Second People's Hospital, Huainan, China.

Abstract:  Postoperative peritoneal adhesion (PPA) is a common postoperative complication caused by any peritoneal inflammatory process. This study aimed to identify the biological function of large intergenic non-coding RNAs (lincRNAs) Cox-2 in the inflammation reaction of adhesion formation. The Cox-2 expression in peritoneal adhesion tissues and normal tissues was detected. The human peritoneal mesothelium cells (HPMCs) were treated with lipopolysaccharide (LPS) to induce inflammatory injury. The effect of Cox-2 suppression on cell viability, apoptosis and inflammatory factors of LPS induced HPMCs injury were explored. The regulatory correlation between Cox-2 and miR-21, as well as the targeted genes of miR-21 were identified. Meanwhile, the regulatory mechanism of Cox-2/miR-21 axis on NF-κB pathway was explored. It indicated that Cox-2 was highly expressed in peritoneal adhesion tissues compared with that in normal tissues. Suppression of Cox-2 ameliorated LPS induced HMPCs injury as cell viability was promoted, and cell apoptosis and the production of inflammatory factors were inhibited. And suppression of Cox-2 reversed the LPS induced HPMCs injury by regulation of miR-21 negatively. miR-21 was negatively correlated with TLR4, and TLR4 was predicted as target gene of miR-21. Furthermore, the suppression of miR-21 on LPS induced HPMCs injury was reversed by knockdown of TLR4, which could inhibited the activation of NF-κB pathway axis. It suggested that the effect of Cox-2 on LPS induced HPMCs injury was achieved by negatively regulation of miR-21 and targeted TLR4 through NF-κB pathway axis. The findings may provide a new insight into preventing postoperative peritoneal adhesion. 

Retracted: No

PubPeer comments:
 Figure 2e: Gels with possible splice marks![file] , 
 I am Head of Research Integrity at Hindawi, thank you for your query about this image. We asked the authors to provide the underlying image and they sent us the files below and said:  Attached please find the original cleaved caspase-9 blots in the Figure 2E. In addition, the results of repeated tests at that time has also been attached. ![file] ![file] ![file] ,
Gut-licensed IFNγ+ NK cells drive LAMP1+TRAIL+ anti-inflammatory astrocytes
Authors: Douglas L Rosene
Stephanie E J Zandee
Giulia Scalisi
Michael A Wheeler
Cristina Gutiérrez-Vázquez
Federico Giovannoni
Alexandre Prat
Burkhard Becher
Liliana M Sanmarco
Isaac M Chiu
Mathias Linnerbauer
Moneera Alsuwailm
Francisco J Quintana
Felipe A Pinho-Ribeiro
Zhaorong Li
Evelyn S Heck
Carolina Manganeli Polonio
Katelyn V Batterman
Journal: Nature (2021)
Discipline: Multidisciplinary
Keywords: Astrocytes; CNS; homeostatic; anti-inflammatory; LAMP1
Affiliations: Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA., Department of Immunology, Harvard Medical School, Boston, MA, USA., Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA, USA., Neuroimmunology Unit, Centre de Recherche du CHUM, Montréal, Quebec, Canada., Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland., Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. .

Abstract:  Astrocytes are glial cells that are abundant in the central nervous system (CNS) and that have important homeostatic and disease-promoting functions1. However, little is known about the homeostatic anti-inflammatory activities of astrocytes and their regulation. Here, using high-throughput flow cytometry screening, single-cell RNA sequencing and CRISPR-Cas9-based cell-specific in vivo genetic perturbations in mice, we identify a subset of astrocytes that expresses the lysosomal protein LAMP12 and the death receptor ligand TRAIL3. LAMP1+TRAIL+ astrocytes limit inflammation in the CNS by inducing T cell apoptosis through TRAIL-DR5 signalling. In homeostatic conditions, the expression of TRAIL in astrocytes is driven by interferon-γ (IFNγ) produced by meningeal natural killer (NK) cells, in which IFNγ expression is modulated by the gut microbiome. TRAIL expression in astrocytes is repressed by molecules produced by T cells and microglia in the context of inflammation. Altogether, we show that LAMP1+TRAIL+ astrocytes limit CNS inflammation by inducing T cell apoptosis, and that this astrocyte subset is maintained by meningeal IFNγ+ NK cells that are licensed by the microbiome. 

Retracted: No

PubPeer comments:
  Consistent with this, astrocytes deficient in TNF or GM-CSF signalling expressed less Tnfsf10 during EAE (Extended Data Fig. 6d). It seems to be a typo. The paper is trying to show TNF and GM-CSF pathway hinder the TRAIL expression of astrocyte. ![file] ,
TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice
Authors: Ming Yang
Xu-Gang Xia
Cao Huang
Hongxia Zhou
Tian Tian
Jianbin Tong
Journal: International Journal of Biological Sciences (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Parkinson's disease; TDP-43; alpha-synuclein; dopaminergic neuron; frontotemporal lobe degeneration
Affiliations: Department of Pathology, Anatomy & Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Abstract:  TDP-43 and α-synuclein are two disease proteins involved in a wide range of neurodegenerative diseases. While TDP-43 proteinopathy is considered a pathologic hallmark of sporadic amyotrophic lateral sclerosis and frontotemporal lobe degeneration, α-synuclein is a major component of Lewy body characteristic of Parkinson's disease. Intriguingly, TDP-43 proteinopathy also coexists with Lewy body and with synucleinopathy in certain disease conditions. Here we reported the effects of TDP-43 on α-synuclein neurotoxicity in transgenic mice. Overexpression of mutant TDP-43 (M337V substitution) in mice caused early death in transgenic founders, but overexpression of normal TDP-43 only induced a moderate loss of cortical neurons in the transgenic mice at advanced ages. Interestingly, concomitant overexpression of normal TDP-43 and mutant α-synuclein caused a more severe loss of dopaminergic neurons in the double transgenic mice as compared to single-gene transgenic mice. TDP-43 potentiated α-synuclein toxicity to dopaminergic neurons in living animals. Our finding provides in vivo evidence suggesting that disease proteins such as TDP-43 and α-synuclein may play a synergistic role in disease induction in neurodegenerative diseases. 

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. ,
MRG15, a novel chromodomain protein, is present in two distinct multiprotein complexes involved in transcriptional activation
Authors: John C Lucchesi
Patricia S Pardo
James K Leung
Olivia M Pereira-Smith
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MRG15; chromodomain protein; MORF4; senescence; tumor cell lines
Affiliations: Roy M. and Phyllis Gough Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, USA.

Abstract:  MRG15 is a novel chromodomain protein that is a member of a family of genes related to MORF4. MORF4 (mortality factor on chromosome 4) induces senescence in a subset of human tumor cell lines. Our previous results indicated that MRG15 (MORF-related gene on chromosome 15) could derepress the B-myb promoter by association with Rb. In this study, sucrose gradient analysis demonstrated that MRG15 was present in two distinct nuclear protein complexes, MAF1 (MRG15-associated factor 1) and MAF2. Rb was associated with MRG15 and PAM14 (a novel coil-coil protein) in MAF1, and a histone acetyl transferase, hMOF, was an MRG15 partner in MAF2. Analysis of deletion mutants of MRG15 indicated that the leucine zipper at the C-terminal region of MRG15 was important for the protein associations in MAF1 and that the N-terminal chromodomain was required for the assembly of the MAF2 protein complex. Consistent with these data was the fact that a histone acetyltransferase activity associated with MRG15 was lost when the chromodomain was deleted and that both mutant MRG15 proteins failed to activate the B-myb promoter. The various mechanisms by which MRG15 could activate gene transcription are discussed. 

Retracted: No

PubPeer comments:
 The Immunoblot results of Rb (red boxes) and MRG15-HA (blue boxes) were similar in Fig. 1A and Fig. 4B. ![file] ,
A novel highly active and reusable carbon based platinum-ruthenium nanocatalyst for dimethylamine-borane dehydrogenation in water at room conditions
Authors: Fatih Sen
Yasar Karatas
Hilal Acidereli
Mehmet Gulcan
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Platinum; Ruthenium; Nanoparticles; Vulcan carbon; Nanocatalyst
Affiliations: Department of Chemistry, Faculty of Science, University of Van Yuzuncu Yıl, 65080, Tusba, Van, Turkey., Department of Biochemistry, Dumlupınar University, 43100, Kutahya, Turkey., Department of Chemistry, Faculty of Science, University of Van Yuzuncu Yıl, 65080, Tusba, Van, Turkey. ., Department of Biochemistry, Dumlupınar University, 43100, Kutahya, Turkey. .

Abstract:  In this paper, we present platinum/ruthenium nanoparticles supported on Vulcan carbon (PtRu@VC) as a nanocatalyst for the dehydrogenation of dimethylamine-borane (DMAB) in aqueous solution under mild conditions. PtRu@VC nanocatalyst was fabricated using the alcohol-reduction techniques which is a facile and effective method. The prepared PtRu@VC nanocatalyst exhibited a good stabilization and an effective catalytic activity for hydrogen evolution from the DMAB dehydrogenation in water at room temperature. The composition of PtRu@VC nanocatalyst was investigated using different analytical techniques inductively coupled plasma optical emission spectroscopy (ICP-OES), transmission electron microscopy (TEM), high-resolution transmission electron microscopy (HR-TEM), powder X-ray diffraction (P-XRD) and X-ray photoelectron spectroscopy (XPS). A monodispersedPt/Ru metals distributions on VC (as supporting material) were revealed by TEM and HR-TEM analyses. The mean particle size of PtRu@VC nanocatalyst was found to be 3.15 ± 0.76 nm. XPS analysis for PtRu@VC nanocatalyst showed that almost Pt-Ru metals were found to be the metallic state. Catalytic experimental results showed that PtRu@VC nanocatalyst has a high catalytic activity with an excellent turn-over frequency (TOFinitial) value of 14926.2 h-1 (248.77 min-1) in the dehydrogenation of DMAB in water at room temperature. Additionally, in the paper, we report some different kinetic data obtained from different experimental parameters of temperature, catalyst and substrate concentrations conducted for DMAB dehydrogenation in water catalyzed with PtRu@VC nanocatalyst. 

Retracted: No

PubPeer comments:
 Figure 4C appears to have two images which overlap. *** ![file] ,
ASPP2 inhibits APP-BP1-mediated NEDD8 conjugation to cullin-1 and decreases APP-BP1-induced cell proliferation and neuronal apoptosis
Authors: Louie Naumovski
Yuzhi Chen
Rachael L Neve
Wenyun Liu
Journal: Journal of Neurochemistry (2003)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: APP-BP1; ASPP2; NEDD8; apoptosis; neurons
Affiliations: Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, Massachusetts, USA. 

Abstract:  APP-BP1, first identified as a protein that interacts with the carboxyl (C) terminus of the amyloid precursor protein (APP), is one-half of the bipartite activating enzyme for the ubiquitin-like protein NEDD8. We report here that APP-BP1 also specifically interacts with apoptosis stimulating protein of p53 ASPP2 in non-transfected cells through the functional predominant N-terminal domain ASPP2(332-483). ASPP2 inhibits the ability of APP-BP1 to rescue the ts41 cell cycle mutation and inhibits APP-BP1 induced apoptosis in primary neurons. ASPP2 reduces the ability of NEDD8 to conjugate to Cullin-1, inhibits APP-BP1-dependent ts41 cell proliferation, and blocks the ability of APP-BP1 to cause apoptosis and to cause DNA synthesis in neurons. We also show that ASPP2 activates nuclear factor-kappaB (NF-kappaB) transcriptional activity, which seems to be inhibited by the neddylation pathway since the dominant negative NEDD8 activating enzyme causes enhanced NF-kappaB activity. Our data provide the first in vivo evidence that ASPP2 is a negative regulator of the neddylation pathway through specific interaction with APP-BP1 and suggest that dysfunction of the APP-BP1 interaction with APP may be one cause of Alzheimer's disease. 

Retracted: No

PubPeer comments:
 Two images in figure 2F appear to overlap. Roughly indicated in red boxes. *** ![file] , 
 ![file] , 
 ![file] #1 The reviewer is correct. We had so many similar photos of the cell cultures, particularly, fNT, f1,f2,f3 and f4. After double checking the image, we found that f3 was a different photo of f2 sample . And we were able to find the correct image of f3 as shown above. At the same time we will send the correct image to the publisher as an erratum. Thanks for review our work after publication. ,
LncRNA625 modulates prostate cancer cells proliferation and apoptosis through regulating the Wnt/β-catenin pathway by targeting miR-432
Authors: B-P Zhang
Y-H Zhang
W-K Bai
F Liu
J-B Li
L-J Yu
W Cheng
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Prostate cancer; lncRNA625; miR-432; cell proliferation; apoptosis
Affiliations: Department of Ultrasound, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang Province, China. .

Abstract:  Objective: Prostate cancer (PCa) is the second leading contributor to male malignancy-associated death in developed countries. The study aimed to evaluate the effects of lncRNA625/miR-432 on the prostate cancer cells and the underlying molecular mechanism. Patients and methods: The cell proliferation was detected using the MTT and colony formation, and cells apoptosis and cell cycle were analyzed with the ﬂow cytometry. Luciferase reporter assay was carried out to detect the correlation between miR-432 and TRIM29 and PYGO2. Besides, reverse transcription-PCR and Western blot were performed to detect the mRNA and protein levels in prostate tissues and PC3 cells. Results: lncRNA625 and miR-432 levels were consistently reduced in the PCa tissues compared with the healthy control and lncRNA625 levels significantly affect the miR-432 expression in PC3 cells, indicating that miR-432 is a direct target of lncRNA625. Besides, lncRNA625 overexpression could inhibit the cancer cells growth, arresting cell cycle progression at the G1/S phase, and significantly induce apoptosis of PC3 cells, but reversed by the miR-432 inhibitor. Most importantly, we further found that miR-432 could deactivate Wnt/β-catenin pathway via suppressing TRIM29 and PYGO2 directly. Conclusions: lncRNA625 could functionally inhibit PC3 cells proliferation and promote cells apoptosis through regulating the Wnt/β-catenin pathway by targeting miR-432. 

Retracted: No

PubPeer comments:
 Fig 5 A-D.  LncRNA625 overexpression induces PC3 cells apoptosis. Flow cytometric analysis of apoptosis in the PC3 cells after transfections with lncRNA625 or treated along with miR-432 inhibitor. A, NC; B, Mock; C, LncRNA625; D, LncRNA625+miR-432 inhibitor . B and D are almost identical. ![file] ,
Nafamostat mesylate attenuates the pathophysiologic sequelae of neurovascular ischemia
Authors: Michael George Zaki Ghali
George Zaki Ghali
Journal: Neural Regeneration Research (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: apoptosis; cerebrovascular; excitotoxicity; infarction; ischemia
Affiliations: United States Environmental Protection Agency, Arlington, VA; Department of Toxicology, Purdue University, West Lafayette, IN, USA., Department of Neurological Surgery, University of California San Francisco, San Francisco, CA; Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA, USA.

Abstract:  Nafamostat mesylate, an apparent soi-disant panacea of sorts, is widely used to anticoagulate patients undergoing hemodialysis or cardiopulmonary bypass, mitigate the inflammatory response in patients diagnosed with acute pancreatitis, and reverse the coagulopathy of patients experiencing the commonly preterminal disseminated intravascular coagulation in the Far East. The serine protease inhibitor nafamostat mesylate exhibits significant neuroprotective effects in the setting of neurovascular ischemia. Nafamostat mesylate generates neuroprotective effects by attenuating the enzymatic activity of serine proteases, neuroinflammatory signaling cascades, and the endoplasmic reticulum stress responses, downregulating excitotoxic transient receptor membrane channel subfamily 7 cationic currents, modulating the activity of intracellular signal transduction pathways, and supporting neuronal survival (brain-derived neurotrophic factor/TrkB/ERK1/2/CREB, nuclear factor kappa B. The effects collectively reduce neuronal necrosis and apoptosis and prevent ischemia mediated disruption of blood-brain barrier microarchitecture. Investigational clinical applications of these compounds may mitigate ischemic reperfusion injury in patients undergoing cardiac, hepatic, renal, or intestinal transplant, preventing allograft rejection, and treating solid organ malignancies. Neuroprotective effects mediated by nafamostat mesylate support the wise conduct of randomized prospective controlled trials in Western countries to evaluate the clinical utility of this compound. 

Retracted: Yes

PubPeer comments:
 Retraction [May 2022] . Background [here] . -------------------- The Editors of NRR have retracted the following article entitled u201cNafamostat mesylate attenuates the pathophysiologic sequelae of neurovascular ischemiau201d (2020;15:2217-2234. doi: 10.4103 1673-5374.284981). An investigation by Drexel University and University of California San Francisco has determined that the study was found using fraudulent affiliations. The author, Michael George Zaki Ghali, cannot provide valid evidence to prove the authenticity of his affiliation. As accurately stating the authorship, affiliated institution, ethics approval and the source of funding is core to the integrity of published work, we are therefore retracting the article. The corresponding author listed in this publication has been informed. The authors did not agree with the decision to retract the article. ,
MiR-195 alleviates ulcerative colitis in rats via MAPK signaling pathway
Authors: G Bai
L-D Tang
Y Huan
H Wang
X-S Bai
Y Li
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-195; ulcerative colitis; inflammatory response; regulatory mechanism; TNBS/ethanol assay
Affiliations: Department of Gastroenterology, Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, China. .

Abstract:  Objective: To study the effect of micro ribonucleic acid (miR)-195 on the inflammatory response of ulcerative colitis (UC) model rats and to explore its regulatory mechanism, thus providing a new scheme for the clinical treatment of UC. Materials and methods: A rat model of UC was prepared by 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)/ethanol assay, and the rats were randomly divided into Control group, Model group, and miR-195 mimic (miR-195 agomir) group. The disease activity index (DAI) in each group was observed. Hematoxylin and eosin (H&amp;E) staining was utilized to detect the pathological changes in the rat colon tissues in each group. The levels of interleukin-6 (IL-6) and IL-1β in the colon tissues of the rats in each group were detected by enzyme-linked immunosorbent assay (ELISA). In addition, the messenger RNA (mRNA) and protein levels of p38 mitogen-activated protein kinase (p38 MAPK) and tumor necrosis factor-alpha (TNF-α) in the colon tissues of each group of rats were examined via Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting, respectively. Results: Compared with those in Control group, the rats in Model group had an increased DAI score, severely pathologically damaged colon tissues, raised levels of IL-6 and IL-1β in the colon tissues and significantly elevated mRNA and protein levels of p38 MAPK and TNF-α. In comparison with those in Model group, the DAI score was decreased, the pathological damage to the rat colon tissues was improved, the levels of IL-6 and IL-1β in the rat colon tissues were reduced, and the mRNA and protein levels of p38 MAPK and TNF-α were notably lowered in miR-195 agomir group. Conclusions: MiR-195 mimics can alleviate the pathological damage to the colon and inflammatory responses in UC model rats, and its mechanism may be related to the inhibition on the p38 MAPK signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 2 shows three panels, but they all appear to be showing the same sample. All three can be matched to each other. * Red boxes: Overlap between Control and Model * Blue boxes: Overlap between Model and miR-195 agomir Of particular note, the area in the top right of the red boxes differs a bit between panels  Control and  Model , with more red visible in the latter. ![file] Confirmation by Sherloq: ![file] ,