PReD-Bench/PRed-Bench huggingface dataset:
Fluorescent labelling in living dental pulp stem cells by graphene oxide quantum dots
Authors: Xincong Li
Yijun Yu
Shuangshuang Ren
Haowei Guo
Ruirui Fan
He Zhang
Chao Liu
Leiying Miao
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cellular labelling; biocompatibility; graphene oxide quantum dot; photoluminescence.
Affiliations: Department of Cariology and Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, People’s Republic of China;, Department of Breast and Thyroid Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, People’s Republic of China;, Department of Periodontology, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, People’s Republic of China;, Department of Orthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, People’s Republic of China

Abstract:  Cellular labelling is possible to offer significant information after transplantation for the purpose of determining stem cell therapy's efficacy. According to the research, it has been reported that graphene oxide quantum dots (GOQDs) are a kind of healthy biological labelling agent for stem cells which show little cytotoxicity. GOQDs' interactions have been examined on the dental pulp stem cells (hDPSCs) of human beings for the purpose of investigating GOQD's biocompatibility and uptake and explored GOQDs' effects on hDPSCs' metabolic activity and the proliferation. According to the outcomes, GDQDs have been accepted by hDPSCs in a time-dependent and concentration-dependent behaviour. Moreover, no important changes have been discovered within hDOPSCs' proliferation, viability as well as metabolic activity after treatment with GOQDs. Therefore, such resources have shown that GOQDs can be multifunctional agents for cell therapy, drug delivery as well as cell imaging and also as outstanding candidates for labelling stem cells. 

Retracted: Yes

PubPeer comments:
 https: retractionwatch.com 2020 03 31 a-tale-of-one-exceedingly-clear-retraction-notice-and-two-nonexistent-ones #more-119186 Retraction notice: https: www.liebertpub.com doi 10.1089 ten.tea.2013.0260.retract ,
Tinea profunda of the genital area. Successful treatment of a rare skin disease
Authors: Anastasiya Chokoeva
Ilko Bakardzhiev
Torello Lotti
Uwe Wollina
Georgi Tchernev
Journal: Dermatologic Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: Majocchi granuloma; Trichophyton mentagrophytes; pubis; tinea genitalis profunda.
Affiliations: Medical College, Medical University of Varna; 84 Tzar Osvoboditel str. Varna 9000 Bulgaria, “Onkoderma”-Policlinic for Dermatology and Dermatologic Surgery; General Skobelev 26 blvd. Sofia Bulgaria, Medical Faculty, Policlinic for Dermatology and Venereology; Saint Kliment Ohridski University, University Hospital Lozenetz; Koziak street 1 Sofia 1407 Bulgaria, Department of Dermatology and Allergology; Academic Teaching Hospital Dresden-Friedrichstadt; Dresden Germany, University of Rome “G. Marconi”; Rome Italy, Department of Biotechnology; Delft University of Technology; 2628 BC Delft The Netherlands

Abstract:  We present a rare case of 36-year-old female patient, who developed a severe Majocchi granuloma in the pubis after waxing, with isolated causative agent Trichophyton mentagrophytes. The condition was initially misdiagnosed as a bacterial folliculitis and treated unsuccessfully with topical corticosteroids and antibiotics. After the adequate diagnose was confirmed by mycological examination, followed by histopathological verification, complete remission of the symptoms was achieved at the 4th week after initiating 6 weeks course of antifungal therapy with Terbinafine 250 mg/daily dose, while good therapeutic response was observed even in the 10th day. The etiopathogenesis of the disease, as well as its current treatment options are considered, in respect to the rare occurrence of this condition in the pubic area and its frequent misdiagnosis. 

Retracted: No

PubPeer comments:
 As far as I know, TISIDB and TIMER are both based on TCGA data. Can the results obtained by these two methods be used as mutual validation results? When the data sources are the same, can the results obtain be representative? , 
 #1 Dear Miconia livida, Thanks for your comments. The TISIDB and TIMER were used in this article. There are differences in data sources and methods of operation for these two web-based analysis tools. TISIDB integrates multiple types of data resources in oncoimmunology, including literature mining results from the **PubMed database and TCGA**. While, TIMER includes 10,897 samples across 32 cancer types from **TCGA** to estimate the abundance of six TIIC subsets (B cells, CD4 T cells, CD8 T cells, macrophages, neutrophils, and dendritic cells). We verified the correlation between CD38 and immune-related genes and immune cells by using the complementarity between the two databases in data and result parameters. ,
Differential regulation of HIC1 target genes by CtBP and NuRD, via an acetylation/SUMOylation switch, in quiescent versus proliferating cells
Authors: Sébastien Pinte
Cateline Guérardel
Capucine Van Rechem
Gaylor Boulay
Nicolas Stankovic-Valentin
Dominique Leprince
Journal: Molecular and Cellular Biology (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: tumor suppressor gene; HIC1; transcriptional repressor; P53-dependent; E2F1-dependent
Affiliations: CNRS UMR 8161, Institut de Biologie de Lille, Université Lille Nord de France, Institut Pasteur de Lille, IFR 142, 1 Rue Calmette, 59017 Lille Cedex, France.

Abstract:  The tumor suppressor gene HIC1 encodes a transcriptional repressor involved in regulatory loops modulating P53-dependent and E2F1-dependent cell survival, growth control, and stress responses. Despite its importance, few HIC1 corepressors and target genes have been characterized thus far. Using a yeast two-hybrid approach, we identify MTA1, a subunit of the NuRD complex, as a new HIC1 corepressor. This interaction is regulated by two competitive posttranslational modifications of HIC1 at lysine 314, promotion by SUMOylation, and inhibition by acetylation. Consistent with the role of HIC1 in growth control, we demonstrate that HIC1/MTA1 complexes bind on two new target genes, Cyclin D1 and p57KIP2 in quiescent but not in growing WI38 cells. In addition, HIC1/MTA1 and HIC1/CtBP complexes differentially bind on two mutually exclusive HIC1 binding sites (HiRE) on the SIRT1 promoter. SIRT1 transcriptional activation induced by short-term serum starvation coincides with loss of occupancy of the distal sites by HIC1/MTA1 and HIC1/CtBP. Upon longer starvation, both complexes are found but on a newly identified proximal HiRE that is evolutionarily conserved and specifically enriched with repressive histone marks. Our results decipher a mechanistic link between two competitive posttranslational modifications of HIC1 and corepressor recruitment to specific genes, leading to growth control. 

Retracted: No

PubPeer comments:
 ![file] , 
 Multiple instances of what appears to be western blot and DNA gel splicing in this paper https: i.imgur.com JodFTko.jpg https: i.imgur.com SP3gNGg.jpg https: i.imgur.com 9UY1tXB.jpg ,
Fluorescent, Magnetic Multifunctional Carbon Dots for Selective Separation, Identification, and Eradication of Drug-Resistant Superbugs
Authors: Stacy Jones
Carrie Sweet
Vikram Ruppa-Kasani
Avijit Pramanik
Aruna Vangara
Mariah S Williams
Paresh Chandra Ray
Sean Edward Risher
Francisco Pedraza
Dhiraj Sardar
Journal: ACS Omega (2017)
Discipline: CHEMISTRY
Keywords: drug-resistant superbugs; sepsis; blood infections; fluorescent carbon dot; magnetic nanoparticle
Affiliations: Department of Chemistry and Biochemistry, Jackson State University , 1400 J. R. Lynch Street, P.O. Box 17910, Jackson, Mississippi 39217-0510, United States., Department of Physics and Astronomy, University of Texas at San Antonio , One UTSA Circle, San Antonio, Texas 78249-0697, United States.

Abstract:  The emergence of drug-resistant superbugs remains a major burden to society. As the mortality rate caused by sepsis due to superbugs is more than 40%, accurate identification of blood infections during the early stage will have a huge significance in the clinical setting. Here, we report the synthesis of red/blue fluorescent carbon dot (CD)-attached magnetic nanoparticle-based multicolor multifunctional CD-based nanosystems, which can be used for selective separation and identification of superbugs from infected blood samples. The reported data show that multifunctional fluorescent magneto-CD nanoparticles are capable of isolating Methicillin-resistant Staphylococcus aureus (MRSA) and Salmonella DT104 superbug from whole blood samples, followed by accurate identification via multicolor fluorescence imaging. As multidrug-resistant (MDR) superbugs are resistant to antibiotics available in the market, this article also reports the design of antimicrobial peptide-conjugated multicolor fluorescent magneto-CDs for effective separation, accurate identification, and complete disinfection of MDR superbugs from infected blood. The reported data demonstrate that by combining pardaxin antimicrobial peptides, magnetic nanoparticles, and multicolor fluorescent CDs into a single system, multifunctional CDs represent a novel material for efficient separation, differentiation, and eradication of superbugs. This material shows great promise for use in clinical settings. 

Retracted: No

PubPeer comments:
 The images in this article are overly saturated...could the authors provide originals so that we can determine the signal to noise in the data? ![file] ,
Synthesis of Multi-Functional Carbon Quantum Dots for Targeted Antitumor Therapy
Authors: Shuting Lu
Ting Wang
Rongyao Lv
Genrong Li
Journal: Journal of Fluorescence (2021)
Discipline: CHEMISTRY
Keywords: Carbon dots; Fluorescence labeling and targeted antitumor; Multi-functions.
Affiliations: College of Chemistry, Chemical Engineering and Resource Utilization, Northeast Forestry University, Harbin, 150040, Heilongjiang, People's Republic of China., Chongqing Academy of Metrology and Quality Inspection, Chongqing, 401123, People's Republic of China., College of Chemistry, Chemical Engineering and Resource Utilization, Northeast Forestry University, Harbin, 150040, Heilongjiang, People's Republic of China. .

Abstract:  Carbon dots are nano-sized photoluminescence materials which have good biocompatibility and low cytotoxicity, while the previously synthesized carbon dots lack tumor targeting capability and therapy function so that it cannot achieve the purpose of diagnosis and treatment. Herein, a new kind of multi-functional carbon dots (GFCDs) is promising to be applied in tumor cells imaging and clinical targeted therapy. Gallic acid (GA) was used as the carbon resource and antitumor active molecule, folic acid (FA) was used as the nitrogen resource and tumor targeting molecule, and citric acid monohydrate (CA) was used as the auxiliary carbon source. Multi-functional GACDs were synthesized by a simple one-step microwave-assisted procedure and analyzed with UV - vis spectrophotometer, fourier transform infrared spectrometer, transmission electron microscopy and X-ray photoelectron spectrometer. Results show that the diameter of GFCDs is about 3 nm. And GFCDs are pale-yellow under natural light which turn blue under 360 nm UV lamp. Besides ester bond is the connecting mode between functional molecules. In addition, the results of in vitro cell imaging experiments and in vivo antitumor experiments demonstrate the targeting imaging and antitumor abilities towards Hela cells. The synthesis route and properties of GFCDs. 

Retracted: No

PubPeer comments:
 **Introduction** Tumor is a major human health problem with high recurring and death rates [28]. References 28. Zhang M, Wang W, Cui Y, Zhou N, Shen J (2018) Magnetofluorescent carbon quantum dot decorated multiwalled carbon nanotubes for dual-modal targeted imaging in chemo-photothermal synergistic therapy. ACS Biomater Sci Eng 4:151u2013162. https: doi.org 10.1021 acsbiomaterials.7b00531 Could the authors explain the relevance of Reference 28? ,
MiRNA-506 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targetting TLR4
Authors: Gaojian Hu
Gang Wang
Dan Li
Qingchen Zhou
Journal: Bioscience Reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Rheumatoid arthritis; TLR4; fibroblast-like synoviocytes; miR-506.
Affiliations: Department of Radiology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Orthopedics, The Third Hospital of Jilin University, Changchun, Jilin 130033, P.R. China., Department of Orthopedics, The Third Hospital of Jilin University, Changchun, Jilin 130033, P.R. China .

Abstract:  Fibroblast-like synoviocytes (FLSs) play a crucial role in rheumatoid arthritis (RA) pathogenesis. While miRNA (miR)-506 has been implicated in the progression of multiple diseases, its role in RA remains to be explored. The present study evaluated the function of miR-506 in the regulation of RA-FLSs. FLSs were prepared from RA and healthy synovial tissues. The expression of miR-506 was measured by quantitative real time PCR (qRT-PCR). The effects of miR-506 on RA-FLSs proliferation and apoptosis were detected by cell counting Kit-8 and flow cytometry assays, respectively. The determination of TNF-α, IL-6, and IL-1β concentrations in RA-FLSs supernatant were done by ELISA. The levels of miR-506 were detected to be significantly lower in the synovial tissues and FLSs of RA than in the synovial tissues and FLSs of healthy controls. The miR-506 up-regulation in RA-FLSs significantly inhibited the proliferation and promoted cell cycle arrest at the G0/G1 phase. The overexpression of miR-506 induced apoptosis, along with an increase in activities of caspase-3 and -8. A target gene Toll-like receptor 4 (TLR4) under the direct regulation of miR-506 was identified through the luciferase assay, qRT-PCR and western blot analysis. Forced overexpression of TLR4 in the rescue experiments showed that TLR4 effectively reversed the effect on proliferation and apoptosis in miR-506-overexpressing RA-FLSs. Thus, miR-506 may be a potential target for RA prevention and therapy of RA. 

Retracted: Yes

PubPeer comments:
 Figure 6D. * Red boxes: Two panels appear to show an overlap. ![file] ,
Characterisation of ATP-dependent Mur ligases involved in the biogenesis of cell wall peptidoglycan in Mycobacterium tuberculosis
Authors: Dimitrios Evangelopoulos
Simon Gibbons
Tulika Munshi
Sanjib Bhakta
Juan David Guzman
Antima Gupta
Nicholas H Keep
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Mur ligases; cell wall peptidoglycan; antibacterial drug discovery; dcw operon; Mur synthetases
Affiliations: Department of Biological Sciences, Institute of Structural and Molecular Biology, Birkbeck, University of London, London, United Kingdom.

Abstract:  ATP-dependent Mur ligases (Mur synthetases) play essential roles in the biosynthesis of cell wall peptidoglycan (PG) as they catalyze the ligation of key amino acid residues to the stem peptide at the expense of ATP hydrolysis, thus representing potential targets for antibacterial drug discovery. In this study we characterized the division/cell wall (dcw) operon and identified a promoter driving the co-transcription of mur synthetases along with key cell division genes such as ftsQ and ftsW. Furthermore, we have extended our previous investigations of MurE to MurC, MurD and MurF synthetases from Mycobacterium tuberculosis. Functional analyses of the pure recombinant enzymes revealed that the presence of divalent cations is an absolute requirement for their activities. We also observed that higher concentrations of ATP and UDP-sugar substrates were inhibitory for the activities of all Mur synthetases suggesting stringent control of the cytoplasmic steps of the peptidoglycan biosynthetic pathway. In line with the previous findings on the regulation of mycobacterial MurD and corynebacterial MurC synthetases via phosphorylation, we found that all of the Mur synthetases interacted with the Ser/Thr protein kinases, PknA and PknB. In addition, we critically analyzed the interaction network of all of the Mur synthetases with proteins involved in cell division and cell wall PG biosynthesis to re-evaluate the importance of these key enzymes as novel therapeutic targets in anti-tubercular drug discovery. 

Retracted: No

PubPeer comments:
 Figure 5A * Green arrow: A text box appears to be visible in the MurC-Rv2147c panel * Red boxes: The MurE-Wag31 and MurF-Wag31 panels appear to look very similar. Reported in 2014 to the journal, with a friendly reminder in 2016, but no action yet. ![file] ,
Innovative Microcapsules for Pancreatic β-Cells Harvested from Mature Double-Transgenic Mice: Cell Imaging, Viability, Induced Glucose-Stimulated Insulin Measurements and Proinflammatory Cytokines Analysis
Authors: Grant Morahan
Ryu Tackechi
Armin Mooranian
Hani Al-Salami
Emma Jamieson
Journal: Pharmaceutical Research (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cytokines; Microencapsulation; Microscopy; RIP-DsRED pancreatic β-cells; Ursodeoxycholic acid.
Affiliations: Biotechnology and Drug Development Research Laboratory, School of Pharmacy, Curtin Health Innovation Research Institute (CHIRI), Curtin University, Perth, WA, Australia., School of Public Health, Curtin Health Innovation Research Institute, Curtin University, Perth, WA, Australia., Harry Perkins Institute of Medical Research, Centre for Diabetes Research, Perth, WA, Australia., Biotechnology and Drug Development Research Laboratory, School of Pharmacy, Curtin Health Innovation Research Institute (CHIRI), Curtin University, Perth, WA, Australia. .

Abstract:  Purpose: Recently we demonstrated that microencapsulation of a murine pancreatic β-cell line using an alginate-ursodeoxycholic acid (UDCA) matrix produced microcapsules with good stability and cell viability. In this study, we investigated if translation of this formulation to microencapsulation of primary β-cells harvested from mature double-transgenic healthy mice would also generate stable microcapsules with good cell viability. Methods: Islets of Langerhans were isolated from Ngn3-GFP/RIP-DsRED mice by intraductal collagenase P digestion and density gradient centrifugation, dissociated into single cells and the β-cell population purified by Fluorescence Activated Cell Sorting. β-cells were microencapsulated using either alginate-poly-l-ornithine (F1; control) or alginate-poly-l-ornithine-UDCA (F2; test) formulations. Microcapsules were microscopically examined and microencapsulated cells were analyzed for viability, insulin and cytokine release, 2 days post-microencapsulation. Results: Microcapsules showed good uniformity and morphological characteristics and even cell distribution within microcapsules with or without UDCA. Two days post microencapsulation cell viability, mitochondrial ATP and insulin production were shown to be optimized in the presence of UDCA whilst production of the proinflammatory cytokine IL-1β was reduced. Contradictory to our previous studies, UDCA did not reduce production of any other pro-inflammatory biomarkers. Conclusions: These results suggest that UDCA incorporation improves microcapsules' physical and morphological characteristics and improves the viability and function of encapsulated mature primary pancreatic β-cells. 

Retracted: No

PubPeer comments:
 The article appears to contain duplicate images. Figure 2t and Figure 2v seem the same. ![file] ,
Circular RNA circMAN2B2 promotes growth and migration of gastric cancer cells by down-regulation of miR-145
Authors: Yue Lun
Haiyuan Sun
Xinhong Wang
Qunying Wang
Dongfang Dong
Bo Sun
Jingzi Quan
Journal: Journal of clinical laboratory analysis (2020)
Discipline: CLINICAL MEDICINE
Keywords: AGS cell; JNK pathway; PI3K/AKT pathway; SNU-16 cell; apoptosis.
Affiliations: Department of Gastroenterology The Chinese People's Liberation Army Navy 971 Hospital Qingdao China

Abstract:  Background: CircMAN2B2 is a newly discovered circRNA that has been found to be an oncogene in lung cancer and glioma. The present study was designed to reveal the role of circMAN2B2 in gastric carcinoma (GC). Methods: qRT-PCR method was utilized to examine circMAN2B2 expression in GC tissues and paracancerous tissues. Next, circMAN2B2 expression in SNU-16 and AGS cells was silenced by transfection. CCK-8 assay, colony formation assay, flow cytometer, Transwell assay, and Western blot were conducted for testing cell phenotype changes. Further, the downstream genes and signaling were uncovered by qRT-PCR and Western blot. Results: As relative to paracancerous tissues, circMAN2B2 was high-expressed in GC tissues. Silence of circMAN2B2 clearly declined SNU-16 and AGS cells viability, survival, migration but enhanced apoptosis. Meanwhile, silence of circMAN2B2 induced the cleavage of caspases (-3 and -9), down-regulation of MMPs (-2 and -9), and up-regulation of miR-145. The impacts of circMAN2B2 silence toward SNU-16 and AGS cells were attenuated by miR-145 silence. Moreover, circMAN2B2 silence deactivated PI3K, AKT while activated JNK through regulating miR-145. Conclusion: This work presented the oncogenic function of circMAN2B2 in GC cells growth and migration. CircMAN2B2 exerted its function possibly through regulating miR-145 as well as PI3K/AKT and JNK pathways. 

Retracted: No

PubPeer comments:
 Figure 6A, image duplication (red boxes). Could the authors please check? ![file] ,
Exosomal microRNA-16-5p from human urine-derived stem cells ameliorates diabetic nephropathy through protection of podocyte
Authors: Jun Shi
Yu-Rui Duan
Fang Chen
Su-Xia Yang
Yang Li
Ya-Li Ma
Chao-Yang Zhu
Bao-Ping Chen
Journal: Journal of Cellular and Molecular Medicine (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: diabetic nephropathy; exosomes; human urine-derived stem cells; microRNA-16-5p; podocyte
Affiliations: Department of Nephrology, Huaihe Hospital of Henan University, Kaifeng, China., Department of Urology, Huaihe Hospital of Henan University, Kaifeng, China.

Abstract:  Diabetic nephropathy (DN) remains one of the severe complications associated with diabetes mellitus. It is worthwhile to uncover the underlying mechanisms of clinical benefits of human urine-derived stem cells (hUSCs) in the treatment of DN. At present, the clinical benefits associated with hUSCs in the treatment of DN remains unclear. Hence, our study aims to investigate protective effect of hUSC exosome along with microRNA-16-5p (miR-16-5p) on podocytes in DN via vascular endothelial growth factor A (VEGFA). Initially, miR-16-5p was predicated to target VEGFA based on data retrieved from several bioinformatics databases. Notably, dual-luciferase report gene assay provided further verification confirming the prediction. Moreover, our results demonstrated that high glucose (HG) stimulation could inhibit miR-16-5p and promote VEGFA in human podocytes (HPDCs). miR-16-5p in hUSCs was transferred through the exosome pathway to HG-treated HPDCs. The viability and apoptosis rate of podocytes after HG treatment together with expression of the related factors were subsequently determined. The results indicated that miR-16-5p secreted by hUSCs could improve podocyte injury induced by HG. In addition, VEGA silencing could also ameliorate HG-induced podocyte injury. Finally, hUSC exosomes containing overexpressed miR-16-5p were injected into diabetic rats via tail vein, followed by qualification of miR-16-5p and observation on the changes of podocytes, which revealed that overexpressed miR-16-5p in hUSCs conferred protective effects on HPDCs in diabetic rats. Taken together, the present study revealed that overexpressed miR-16-5p in hUSC exosomes could protect HPDCs induced by HG and suppress VEGFA expression and podocytic apoptosis, providing fresh insights for novel treatment of DN. 

Retracted: No

PubPeer comments:
 Could the authors comment on the appearance of the plots in figure 3B? Some appear to trend back to the left, which doesnu2019t seem possible, and the plot extends beyond the axis in some cases. Perhaps this is just a byproduct of the software settings. *** ![file] ![file] , 
 The middle image of Figure 3A seems to have some unexpectedly similar, possibly duplicated, regions. *** ![file] ,
Novel Molecular Hybrids of N-Benzylpiperidine and 1,3,4-Oxadiazole as Multitargeted Therapeutics to Treat Alzheimer’s Disease
Authors: Surya Pratap Singh
Sushant Kumar Shrivastava
Avanish Tripathi
Prabhash Nath Tripathi
Saumitra Sen Singh
Piyoosh Sharma
Journal: ACS Chemical Neuroscience (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer’s disease; Multitargeted hybrids; acetylcholinesterase (AChE); butyrylcholinesterase (BChE); β-secretase-1 (BACE-1).
Affiliations: Department of Pharmaceutical Engineering & Technology , Indian Institute of Technology (Banaras Hindu University) , Varanasi 221 005 , India., Department of Biochemistry, Faculty of Science , Banaras Hindu University , Varanasi 221 005 , India.

Abstract:  Multitargeted hybrids of N-benzylpiperidine and substituted 5-phenyl-1,3,4-oxadiazoles were designed, synthesized, and evaluated against Alzheimer's disease (AD). Tested compounds exhibited moderate to excellent inhibition against human acetylcholinesterase (hAChE), butyrylcholinesterase (hBChE), and beta-secretase-1 (hBACE-1). The potential leads 6g and 10f exhibited balanced inhibitory profiles against all the targets, with a substantial displacement of propidium iodide from the peripheral anionic site of hAChE. Hybrids 6g and 10f also elicited favorable permeation across the blood-brain barrier and were devoid of neurotoxic liability toward SH-SY5Y neuroblastoma cells. Both leads remarkably disassembled Aβ aggregation in thioflavin T-based self- and AChE-induced experiments. Compounds 6g and 10f ameliorated scopolamine-induced cognitive dysfunctions in the Y-maze test. The ex vivo studies of rat brain homogenates established the reduced AChE levels and antioxidant activity of both compounds. Compound 6g also elicited noteworthy improvement in Aβ-induced cognitive dysfunctions in the Morris water maze test with downregulation in the expression of Aβ and BACE-1 proteins corroborated by Western blot and immunohistochemical analysis. The pharmacokinetic study showed excellent oral absorption characteristics of compound 6g. The in silico molecular docking and dynamics simulation studies of lead compounds affirmed their consensual binding interactions with PAS-AChE and aspartate dyad of BACE-1. 

Retracted: No

PubPeer comments:
 Potential recycling of image between two journals as shown below. Background and color modifications appear to have been done. Authors are requested to post unedited source images for these two images. ![file] , 
 @Festuca Contracta The panel presented in both the papers are different and do not bear any resemblance whatsoever with each other except being both belong to aggregates of amyloid beta. The images are the outcomes of different raw data and are not duplication by altering magnification. I therefore do not accept your opinion on the same. Sushant ,
Disruption of the Blood–Brain Barrier and Neuronal Cell Death in Cingulate Cortex, Dentate Gyrus, Thalamus, and Hypothalamus in a Rat Model of Gulf-War Syndrome
Authors: Ali Abdel-Rahman
Mohamed B Abou-Donia
Ashok K Shetty
Journal: Neurobiology of Disease (2002)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Gulf-War syndrome; stress; chemicals; pyridostigmine bromide; DEET
Affiliations: Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Caroloina 277109, USA.

Abstract:  We investigated the effects of a combined exposure to restraint stress and low doses of chemicals pyridostigmine bromide (PB), N, N-diethyl-m-toluamide (DEET), and permethrin in adult male rats, a model of Gulf-War syndrome. Animals were exposed daily to one of the following for 28 days: (i) a combination of stress and chemicals (PB, 1.3 mg/kg/day; DEET, 40 mg/kg/day; and permethrin, 0.13 mg/kg/day); (ii) stress and vehicle; (iii) chemicals alone; and (iv) vehicle alone. All animals were evaluated for: (i) the disruption of the blood-brain barrier (BBB) using intravenous horseradish peroxidase (HRP) injections and endothelial barrier antigen (EBA) immunostaining; (ii) neuronal cell death using H&amp;E staining, silver staining, and glial fibrillary acidic protein (GFAP) immunostaining; and (iii) acetylcholinesterase (AChE) activity and m2-muscarinic acetylcholine receptors (m2-AChR). Animals subjected to stress and chemicals exhibited both disruption of the BBB and neuronal cell death in the cingulate cortex, the dentate gyrus, the thalamus, and the hypothalamus. Other regions of the brain, although they demonstrated some neuronal cell death, did not exhibit disruption of the BBB. The neuropathological changes in the above four brain regions were highly conspicuous and revealed by a large number of HRP-positive neurons (21-40% of total neurons), a decreased EBA immunostaining (42-51% reduction), a decreased number of surviving neurons (27-40% reduction), the presence of dying neurons (4-10% of total neurons), and an increased GFAP immunostaining (45-51% increase). These changes were also associated with decreased forebrain AChE activity and m2-AchR (19-25% reduction). In contrast, in animals exposed to stress and vehicle or chemicals alone, the above indices were mostly comparable to that of animals exposed to vehicle alone. Thus, a combined exposure to stress and low doses of PB, DEET, and permethrin leads to significant brain injury. The various neurological symptoms reported by Gulf-War veterans could be linked to this kind of brain injury incurred during the war. 

Retracted: No

PubPeer comments:
 Could the authors please check? In Figure 2, panel B2, some elements in the top right corner appear to be visible two times. Marked with boxes of the same color. ![file] ,
Mechanisms of enhanced radiation response following epidermal growth factor receptor signaling inhibition by erlotinib (Tarceva)
Authors: Geetha Vallabhaneni
Sooryanarayana Varambally
Paul M Harari
Arul M Chinnaiyan
Shyhmin Huang
Eric Armstrong
Scott A Tomlins
Prakash Chinnaiyan
Journal: Cancer Research (2005)
Discipline: CLINICAL MEDICINE
Keywords: Erlotinib; radiation response; EGFR; apoptosis; cell cycle kinetics
Affiliations: Department of Human Oncology, University of Wisconsin, 600 Highland Avenue, Madison, WI 53792, USA.

Abstract:  Erlotinib (Tarceva) is an orally available HER1 (epidermal growth factor receptor, EGFR) tyrosine kinase inhibitor advancing through clinical trials for the treatment of a range of human malignancies. In this study, we examine the capacity of erlotinib to modulate radiation response and investigate specific mechanisms underlying these interactions in human tumor cell lines and xenografts. The impact of erlotinib on cell cycle kinetics was analyzed using flow cytometry, and the impact on apoptosis was evaluated via fluorescein-labeled pan-caspase inhibition and poly(ADP-ribose) polymerase cleavage. Radiation-induced EGFR autophosphorylation and Rad51 expression were examined by Western blot analysis. Radiation survival was analyzed using a clonogenic assay and assessment of in vivo tumor growth was done using a mouse xenograft model system. Microarray studies were carried out using 20 K human cDNA microarray and select genes were validated using quantitative reverse transcription-PCR (RT-PCR). Independently, erlotinib and radiation induce accumulation of tumor cells in G(1) and G(2)-M phase, respectively, with a reduction of cells in S phase. When combined with radiation, erlotinib promotes a further reduction in S-phase fraction. Erlotinib enhances the induction of apoptosis, inhibits EGFR autophosphorylation and Rad51 expression following radiation exposure, and promotes an increase in radiosensitivity. Tumor xenograft studies confirm that systemic administration of erlotinib results in profound tumor growth inhibition when combined with radiation. cDNA microarray analysis assessing genes differentially regulated by erlotinib following radiation exposure identifies a diverse set of genes deriving from several functional classes. Validation is confirmed for several specific genes that may influence radiosensitization by erlotinib including Egr-1, CXCL1, and IL-1beta. These results identify the capacity of erlotinib to enhance radiation response at several levels, including cell cycle arrest, apoptosis induction, accelerated cellular repopulation, and DNA damage repair. Preliminary microarray data suggests additional mechanisms underlying the complex interaction between EGFR signaling and radiation response. These data suggest that the erlotinib/radiation combination represents a strategy worthy of further examination in clinical trials. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than expected. ![file] ,
Th1/Th2 PB balance and CD200 expression of patients with active severe alopecia areata
Authors: Xinhua Ma
Yu Gao
Wanwan Jin
Shisheng Chen
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: CD200; RT-PCR; Th1/Th2; enzyme-linked immunosorbent assay; flow cytometry
Affiliations: Department of Dermatology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China.

Abstract:  Th1/Th2 peripheral blood balance and CD200 expression in patients with severe alopecia areata (SAA) in the active stage were investigated. Fifty patients with active SAA, 50 patients with stable SAA and 50 healthy controls were continuously selected and expression of Th1/Th2 of peripheral T lymphocytes, and peripheral B lymphocytes was detected by flow cytometry; RT-PCR was used to detect the expression of the PBMC CD200 mRNA and the expression of CD200 in hair follicles of alopecia area was detected by immunohistochemically staining; ELISA was used to detect expression levels of serum LFN-γ and serum interleukin (IL)-10. The expression of CD200 in patients with alopecia areata in active phase on CD3+ T lymphocytes and CD19+ B lymphocytes was significantly lower (P&lt;0.05) than those in stable phase and of the control group. CD200 expression in patients with alopecia areata in stable phase on T lymphocytes was greatly lower than that of the control group (P&lt;0.05). However, the comparison of expression of CD200 in patients with alopecia areata in stable phase on B lymphocytes with the control group were statistically non-significant. The level of the expression of CD200 mRNA in active phase was obviously lower than those of the other two groups and the difference was statistically significant (P&lt;0.05); the moderate positive and strong positive percentage of CD200 in the active phase was significantly lower than those of the other two groups. Positive expression rate of CK15 among the three groups were compared with each other; the differences had no statistical significance. The level of LFN-γ in the active phase had obviously increased while the IL-10 level decreased significantly (P&lt;0.05). In conclusion, the level of expression of CD200 on peripheral blood and hair follicle outer root sheath of patients with SAA was decreased. This may be associated with the imbalance of the Th1/Th2 equilibrium. 

Retracted: No

PubPeer comments:
  Figure 3. Results of immunohistochemical staining. The upper row CD200 and the bottom row CK15. The left is in active phase, the middle in stable phase, the right is the control group. Stable and Control images of the upper row appear to be the same (with minor changes in the lower-left corners). ![file] Stable and Control images of the lower row appear to be the same (with a duplicated area in the latter). H t to an anonymous colleague on social media. ,
The pestivirus N terminal protease N(pro) redistributes to mitochondria and peroxisomes suggesting new sites for regulation of IRF3 by N(pro.)
Authors: Irina Mohorianu
Matthew Jefferson
Matthew Whelband
Penny P Powell
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: N(pro); IRF3; apoptosis; Bax activation; mitochondrial pathway
Affiliations: Biomedical Research Centre, Norwich Medical School and Biological Sciences, University of East Anglia, Norwich, United Kingdom.

Abstract:  The N-terminal protease of pestiviruses, N(pro) is a unique viral protein, both because it is a distinct autoprotease that cleaves itself from the following polyprotein chain, and also because it binds and inactivates IRF3, a central regulator of interferon production. An important question remains the role of N(pro) in the inhibition of apoptosis. In this study, apoptotic signals induced by staurosporine, interferon, double stranded RNA, sodium arsenate and hydrogen peroxide were inhibited by expression of wild type N(pro), but not by mutant protein N(pro) C112R, which we show is less efficient at promoting degradation of IRF3, and led to the conclusion that N(pro) inhibits the stress-induced intrinsic mitochondrial pathway through inhibition of IRF3-dependent Bax activation. Both expression of N(pro) and infection with Bovine Viral Diarrhea Virus (BVDV) prevented Bax redistribution and mitochondrial fragmentation. Given the role played by signaling platforms during IRF3 activation, we have studied the subcellular distribution of N(pro) and we show that, in common with many other viral proteins, N(pro) targets mitochondria to inhibit apoptosis in response to cell stress. N(pro) itself not only relocated to mitochondria but in addition, both N(pro) and IRF3 associated with peroxisomes, with over 85% of N(pro) puncta co-distributing with PMP70, a marker for peroxisomes. In addition, peroxisomes containing N(pro) and IRF3 associated with ubiquitin. IRF3 was degraded, whereas N(pro) accumulated in response to cell stress. These results implicate mitochondria and peroxisomes as new sites for IRF3 regulation by N(pro), and highlight the role of these organelles in the anti-viral pathway. 

Retracted: No

PubPeer comments:
 Figures 1A and 5B: * Red boxes: four lanes in the Actin panels appear to look unexpectedly similar * Blue boxes: lanes in the IRF3 panels appear to look similar; from the labeling it appears these were different experiments (with or without NaA) * Green arrows: sharp vertical transitions appear to be visible Reported to the journal in October 2015. ![file] ,
miR-192-5p suppresses the progression of lung cancer bone metastasis by targeting TRIM44
Authors: Yongchao Yang
Jijun Liu
Menghai Zhu
Xinhui Cui
Xiaoming Zhang
Peng Zou
Chong Lian
Jiaqiang Wang
Xinfeng Chen
Hexuan Wang
Qi Wen
Ji Yi
Zhiquan Chen
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: Lung cancer; bone metastasis; miRNAs; miR-192-5p; TRIM44
Affiliations: Department of orthopedics, Zhengzhou Seventh People's Hospital, Zhengzhou, China. ., The First Affiliated Hospital of Sun Yat-sen University, GuangZhou, China., Laboratory of Immunotherapy, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, China., Department of orthopedics, Zhengzhou Seventh People's Hospital, Zhengzhou, China., Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou, China.

Abstract:  Lung cancer is the leading cause of cancer-related deaths worldwide, with 50-70% of patients suffering from bone metastasis. Accumulating evidence has demonstrated that miRNAs are involved in cell proliferation, migration, and invasion in malignancy, such as lung cancer bone metastasis. In the present study, we demonstrated that reduced miR-192-5p and increased TRIM44 levels were associated with the proliferation, migration and invasion of lung cancer. Furthermore, the potential functions of miR-192-5p were explored in A549 and NCI-H1299 cells. We found that miR-192-5p upregulation suppressed tumour behaviours in lung cancer cells. To further investigate whether miR-192-5p is associated with TRIM44, we used TargetScan software to predict the binding site between miR-192-5p and TRIM44. Luciferase activity assays were performed to verify this prediction. In addition, the significant role of miR-192-5p in negatively regulating TRIM44 expression was manifested by our research group. our results suggest that miR-192-5p inhibited the proliferation, migration and invasion of lung cancer through TRIM44. 

Retracted: No

PubPeer comments:
 Two images in figure 3A appear to overlap. *** ![file] , 
 Figure 5D appears to have some images which overlap. Marked with red and green boxes. *** ![file] , 
 Figure 3 reanalysis. *** ![file] ,
Allergic manifestation 15 years after early intervention with hydrolyzed formulas – the GINI Study
Authors: C Flexeder
C Zeller
K Werkstetter
M Sußmann
C P Bauer
A von Berg
M Schnappinger
M Standl
B Filipiak-Pittroff
I Brüske
D Berdel
E Thiering
D Sugiri
U Krämer
J Heinrich
U Hoffmann
S Koletzko
C Klümper
E Link
C-P Bauer
H Schulz
B Hoffmann
C Tiesler
GINIplus study group
Journal: Allergy (2016)
Discipline: IMMUNOLOGY
Keywords: 15-year follow-up from birth; allergy prevention; double-blind; hydrolyzed infant formulas; nutritional intervention
Affiliations: Department of Pediatrics Marien‐Hospital Wesel, Research Institute Wesel Germany, Institute of Epidemiology I Helmholtz Zentrum Munich German Research Center for Environmental Health (GmbH) Neuherberg Germany, Comprehensive Pneumology Center Munich (CPC‐M) Munich Germany, Department of Pediatrics Technical University of Munich Munich Germany, IUF – Leibniz Research Institute for Environmental Medicine at the Heinrich‐Heine‐University Düsseldorf Germany, Medical Faculty Deanery of Medicine Heinrich‐Heine University Düsseldorf Germany, LVA Oberbayern Munich Germany, Dr von Hauner Children's Hospital Ludwig‐Maximilians‐University University of Munich Medical Center Munich Germany

Abstract:  Background: Data on the long-term impact of hydrolyzed formulas on allergies are scarce. Objective: To assess the association between early intervention with hydrolyzed formulas in high-risk children and allergic outcomes in adolescence. Methods: GINI trial participants (n = 2252) received one of four formulas in the first four months of life as breastmilk substitute if necessary: partial or extensive whey hydrolyzate (pHF-W, eHF-W), extensive casein hydrolyzate (eHF-C) or standard cow's milk formula (CMF) as reference. Associations between these formulas and the cumulative incidence and prevalence of parent-reported physician-diagnosed asthma, allergic rhinitis (AR) and eczema, as well as spirometric indices and sensitization, were examined using generalized linear models. Results: Between 11 and 15 years, the prevalence of asthma was reduced in the eHF-C group compared to CMF (odds ratio (OR) 0.49, 95% confidence interval (CI) 0.26-0.89), which is consistent with the spirometric results. The cumulative incidence of AR was lower in eHF-C (risk ratio (RR) 0.77, 95% CI 0.59-0.99]) and the AR prevalence in pHF-W (OR 0.67, 95% CI 0.47-0.95) and eHF-C (OR 0.59, 95% CI 0.41-0.84). The cumulative incidence of eczema was reduced in pHF-W (RR 0.75, 95% CI 0.59-0.96) and eHF-C (RR 0.60, 95% CI 0.46-0.77), as was the eczema prevalence between 11 and 15 years in eHF-C (OR 0.42, 95% CI 0.23-0.79). No significant effects were found in the eHF-W group on any manifestation,nor was there an effect on sensitization with any formula. Conclusion: In high-risk children, early intervention using different hydrolyzed formulas has variable preventative effects on asthma, allergic rhinitis and eczema up to adolescence. 

Retracted: No

PubPeer comments:
 frequently cited by industry but shady data with impossible transitions between surveys ![file] , 
 how can dropped out individuals appear in later surveys? ![file] ,
Ribonuclease/angiogenin inhibitor 1 regulates stress-induced subcellular localization of angiogenin to control growth and survival
Authors: Carmen Sarcinelli
Sabato Fusco
Paolo Netti
Fabio Formiggini
Elio Pizzo
Giuseppe D&#x27;Alessio
Guo-Fu Hu
Jinghao Sheng
Wenhao Yu
Journal: Journal of Cell Science (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Angiogenin; RNH1; Stress granules.
Affiliations: Department of Biology, University of Naples Federico II, Complesso Universitario di Monte S. Angelo, via Cintia, Naples 80126, Italy.

Abstract:  Angiogenin (ANG) promotes cell growth and survival. Under growth conditions, ANG undergoes nuclear translocation and accumulates in the nucleolus where it stimulates rRNA transcription. When cells are stressed, ANG mediates the production of tRNA-derived stress-induced small RNA (tiRNA), which reprograms protein translation into a survival mechanism. The ribonucleolytic activity of ANG is essential for both processes but how this activity is regulated is unknown. We report here that ribonuclease/angiogenin inhibitor 1 (RNH1) controls both the localization and activity of ANG. Under growth conditions, ANG is located in the nucleus and is not associated with RNH1 so that the ribonucleolytic activity is retained to ensure rRNA transcription. Cytoplasmic ANG is associated with and inhibited by RNH1 so that random cleavage of cellular RNA is prevented. Under stress conditions, ANG is localized to the cytoplasm and is concentrated in stress granules where it is not associated with RNH1 and thus remains enzymatically active for tiRNA production. By contrast, nuclear ANG is associated with RNH1 in stressed cells to ensure that the enzymatic activity is inhibited and no unnecessary rRNA is produced to save anabolic energy. Knockdown of RNH1 abolished stress-induced relocalization of ANG and decreased cell growth and survival. 

Retracted: No

PubPeer comments:
 In this publication, several u00a0discrepancies were found in the fig no. 2. The descriptionu00a0in the text for this fig. does not match withu00a0the data in the fig. 1) In the fig. 2A, PCNA is shown as a cytoplasm purity marker while in 2B it is shown as a nuclear extract purity marker. PCNA is actually a nuclear marker. A similar mistake can be seen for the b-tubulin. 2) Authors claim in the text,  RNH1 was precipitated by ANG monoclonal antibody (mAb) (Fig. 2A, lane 3). but I don t see any band of RNH1 in lane 3. Also ANG IP should also show ANG band but it is absent in lane 3. 3) Then authors say,  Under these conditions, no ANG and RNH1 could be co-immunoprecipitated in the nuclear extracts (Fig. 2A, lanes 5 to 8). but I clearly see the band of ANG in RNH1 IP lane 8. 4) Next,  When cells were stressed with SA treatment, no association between ANG and RNH1 was detected by co-IP in the cytoplasmic extracts (Fig. 2B, lanes 1 to 4) but was apparent in the nuclear extracts (Fig. 2B, lanes 5 to 8). However with ANG pull down I don t see any RNH1 band in 2B lane 7. 5) control IgG should not pull down ANG in lane 2 and 6 of fig 2A. These discrepancies make the authors claim (about the mechanism of RNH1 mediated ANG localisation) false . ![file] ,