PReD-Bench/PRed-Bench huggingface dataset:
New therapy targeting differential androgen receptor signaling in prostate cancer stem/progenitor vs. non-stem/progenitor cells
Authors: Liang Liang
Zhifang Ma
Tzu-Hua Lin
Jie Luo
Chawnshang Chang
Jing Tian
Kuo-Pao Lai
Yuanjie Niu
Chiung-Kuei Huang
Shinichi Yamashita
Chiuan-Ren Yeh
Lei Li
Shuyuan Yeh
Soo Ok Lee
Qi Jiang
Journal: Journal of molecular cell biology (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Androgen deprivation therapy; Prostate cancer; Stem cells; Progenitor cells; Androgen receptor
Affiliations: George Whipple Lab for Cancer Research, Department of Pathology, University of Rochester Medical Center, Rochester, NY 14642,  USA.

Abstract:  The androgen deprivation therapy (ADT) to systematically suppress/reduce androgens binding to the androgen receptor (AR) has been the standard therapy for prostate cancer (PCa); yet, most of ADT eventually fails leading to the recurrence of castration resistant PCa. Here, we found that the PCa patients who received ADT had increased PCa stem/progenitor cell population. The addition of the anti-androgen, Casodex, or AR-siRNA in various PCa cells led to increased stem/progenitor cells, whereas, in contrast, the addition of functional AR led to decreased stem/progenitor cell population but increased non-stem/progenitor cell population, suggesting that AR functions differentially in PCa stem/progenitor vs. non-stem/progenitor cells. Therefore, the current ADT might result in an undesired expansion of PCa stem/progenitor cell population, which explains why this therapy fails. Using various human PCa cell lines and three different mouse models, we concluded that targeting PCa non-stem/progenitor cells with AR degradation enhancer ASC-J9 and targeting PCa stem/progenitor cells with 5-azathioprine and Œ≥-tocotrienol resulted in a significant suppression of the tumors at the castration resistant stage. This suggests that a combinational therapy that simultaneously targets both stem/progenitor and non-stem/progenitor cells will lead to better therapeutic efficacy and may become a new therapy to battle the PCa before and after castration resistant stages. 

Retracted: No

PubPeer comments:
 Figure 2Ab appears to show an image of the same cell with 2 different solution concentrations  , 
 #1 correction, that should be Figure 3Ab , 
 Figure 5D appears to show the same dishes with different concentration labels.  , 
  correction, that should be Figure 3Ab . See, everyone can make mistakes ,
PKC-eta mediates glioblastoma cell proliferation through the Akt and mTOR signaling pathways
Authors: Jae-Won Soh
Patrick M Martin
Isa M Hussaini
Sean E Aeder
Journal: Oncogene (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: protein kinase C-eta; PMA; glioblastoma; Akt; mTOR
Affiliations: Department of Pathology and Neurology, University of Virginia, Charlottesville, VA 22908, USA. 

Abstract:  We previously demonstrated that protein kinase C-eta (PKC-eta) mediates a phorbol 12-myristate-13-acetate (PMA)-induced proliferative response in human glioblastoma (GBM) cells. In this report, we show that PMA-stimulated activation of PKC-eta in U-251 GBM cells resulted in activation of both Akt and the mammalian target of rapamycin (mTOR) signaling pathways and an increase in cell proliferation. Expression of a kinase dead PKC-eta (PKC-etaKR) construct reduced the basal and PMA-evoked proliferation of PKC-eta-expressing U-251 GBM cells, as well as abrogated the PMA-induced activation of Akt, mTOR, and the mTOR targets 4E-BP1 and STAT-3. Treatment of cells with the PI-3 kinase inhibitor LY294002 (10 muM) or the mTOR inhibitor rapamycin (10 nM) also reduced PMA-induced proliferation and cell-cycle progression. Expression of a constitutively active PKC-eta (PKC-etaDeltaNPS) construct in a GBM cell line with no endogenous PKC-eta (U-1242) also provided evidence that PKC-eta targets the Akt and mTOR signaling pathways. Moreover, activation of 4E-BP1 and STAT-3 in both PMA-treated U-251 and PKC-etaDeltaNPS-expressing U-1242 GBM cells was inhibited by rapamycin. However, activation of Akt, but not mTOR was inhibited by the PI-3 kinase inhibitor LY294002. This study identifies Akt and mTOR as downstream targets of PKC-eta that are involved in GBM cell proliferation. 

Retracted: No

PubPeer comments:
 Figures 3 and 4 seem to share the same tubulin bands for different conditions. Could authors provide an explanation?  ,
A deep sleep stage in Drosophila with a functional role in waste clearance
Authors: Evan R Semenza
Bart van Alphen
Melvyn Yap
Ravi Allada
Bruno van Swinderen
Journal: Science Advances (2021)
Discipline: Multidisciplinary
Keywords: Sleep; proboscis extension sleep; Drosophila; deep sleep stage; arousal thresholds
Affiliations: The Department of Neurobiology, Northwestern University, 2205 Tech Drive, Hogan 2-160, Evanston, Illinois 60208, USA.  ., The Department of Neurobiology, Northwestern University, 2205 Tech Drive, Hogan 2-160, Evanston, Illinois 60208, USA., The Queensland Brain Institute, QBI Building, 79, The University of Queensland, St. Lucia QLD 4072, Australia.

Abstract:  Sleep is a highly conserved state, suggesting that sleep's benefits outweigh the increased vulnerability it brings. Yet, little is known about how sleep fulfills its functions. Here, we used video tracking in tethered flies to identify a discrete deep sleep stage in Drosophila, termed proboscis extension sleep, that is defined by repeated stereotyped proboscis extensions and retractions. Proboscis extension sleep is accompanied by highly elevated arousal thresholds and decreased brain activity, indicative of a deep sleep state. Preventing proboscis extensions increases injury-related mortality and reduces waste clearance. Sleep deprivation reduces waste clearance and during subsequent rebound sleep, sleep, proboscis extensions, and waste clearance are increased. Together, these results provide evidence of a discrete deep sleep stage that is linked to a specific function and suggest that waste clearance is a core and ancient function of deep sleep. 

Retracted: No

PubPeer comments:
 This article was reviewed on the error bar podcast episode 2: https: theerrorbar.com ?e=2. The review was done in the light of newspaper headlines about the article. The slightly-edited transcript is copied here: headline: SLEEP CLEARS TOXIC THOUGHT FROM THE MIND tweet: deep sleep can help to detoxify your brain, so long as it is accompanied by repeated back-and-forth movements of your nose every 3 seconds. and you need to be a fruit fly. description: the Daily Mail informs us that a good night s sleep helps to clear your mind from toxic proteins. they helpfully point out that the NHS recommends 6 to 9 hours sleep a night. the study found that deep sleep is associated with decreased brain activity, high arousal, rhythmic movement and the removal of toxic waste. the study authors from northwestern university, illinois proposed that waste clearance is an ancient function of deep sleep evaluation: the only problem with this story - that it s about fruit flies, and the way they clear their brain of toxins is by repeatedly pumping their proboscis back and forth every 3 seconds, which moves the waste along their guts and out onto the bedsheets. just like humans, the flies were harder to wake up during their deep sleep, and they could be drugged into getting to sleep quicker, but that s where the similarities end. conclusion: sleep is good for your brain, but we recommend against repeated snout-pumping and waste clearance as that may adversely affect your bed partner s sleep quality. ,
Copper induces cell death by targeting lipoylated TCA cycle proteins
Authors: Boryana Petrova
Steven M Corsello
Naama Kanarek
Todd R Golub
Mai Abdusamad
Svetlana Lutsenko
Mustafa Kocak
Sandro Santagata
Peter Tsvetkov
John K Eaton
Shannon Coy
Margaret Dreishpoon
Lena Joesch-Cohen
Ryan D Spangler
Jordan Rossen
Ranad Humeidi
Ana Verma
Evgeni Frenkel
Journal: Science (2022)
Discipline: Multidisciplinary
Keywords: Copper; cell death; mitochondrial respiration; lipoylated components; tricarboxylic acid cycle
Affiliations: Broad Institute of Harvard and MIT, Cambridge, MA, USA., Laboratory of Systems Pharmacology, Department of Systems Biology, Boston, MA, USA., Harvard Medical School, Boston, MA, USA., Whitehead Institute and Massachusetts Institute of Technology, Cambridge, MA, USA., Department of Physiology, Johns Hopkins Medical Institutes, Baltimore, MD, USA.

Abstract:  Copper is an essential cofactor for all organisms, and yet it becomes toxic if concentrations exceed a threshold maintained by evolutionarily conserved homeostatic mechanisms. How excess copper induces cell death, however, is unknown. Here, we show in human cells that copper-dependent, regulated cell death is distinct from known death mechanisms and is dependent on mitochondrial respiration. We show that copper-dependent death occurs by means of direct binding of copper to lipoylated components of the tricarboxylic acid (TCA) cycle. This results in lipoylated protein aggregation and subsequent iron-sulfur cluster protein loss, which leads to proteotoxic stress and ultimately cell death. These findings may explain the need for ancient copper homeostatic mechanisms. 

Retracted: No

PubPeer comments:
 Fig.4C Group Low figures look the same.  , 
 #1 There appears to be an April 21, 2022 correction, but it is behind a paywall. https: www.science.org doi full 10.1126 science.abq4855 , 
 Correction to Tsvetkov et al., Science 375, 1254 (2022) In the Research Article u201cCopper induces cell death by targeting lipoylated TCA cycle proteins,u201d the photomicrograph showing a representative image of a tumor with low expression of FDX1 in Fig. 4C was incorrect. The image has now been corrected. The quantitative measures of FDX1 expression in Fig. 4B remain correct. Table S2 should have contained the underlying data for the genetic modifier screens using both native disulfiram and its active, copper-loaded form, cupric-DDC. The table has therefore been updated to include the complete dataset. In addition, a printer error has been corrected in the text. In the sentence u201cThe source of copper in cell culture medium is serum (fig. S1Q), and accordingly, cells grown in the absence of serum were resistant to elesclomol,u201d the callout to fig. S1Q has been corrected to fig. S1D. ,
The Antiosteoporosis Effects of Yishen Bugu Ye Based on Its Regulation on the Differentiation of Osteoblast and Osteoclast
Authors: Min Hu
Yangyang Li
Yongfeng Zhang
Tao Huang
Yutong Li
Di Wang
Weiqi Meng
Journal: BioMed Research International (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Yishen Bugu Ye; traditional Chinese medicine; bone strength; antiosteoporotic effects; C57BL/6 mice
Affiliations: Department of Orthodontics, School and Hospital of Stomatology, Jilin University, Changchun 130021, China, School of Life Sciences, Jilin University, Changchun 130012, China, Changchun University of Chinese Medicine, Changchun 130117, China

Abstract:  Yishen Bugu Ye (YSBGY), a traditional Chinese medicine comprising 12 types of medicinal herbs, is often prescribed in China to increase bone strength. In this study, the antiosteoporotic effects of YSBGY were investigated in C57BL/6 mice afflicted with dexamethasone- (Dex-) induced osteoporosis (OP). The results showed that YSBGY reduced the interstitial edema in the liver and kidney of mice with Dex-induced OP. It also increased the number of trabecular bone elements and chondrocytes in the femur, promoted cortical bone thickness and trabecular bone density, and modulated the OP-related indexes in the femur and tibia of OP mice. It also increased the serum concentrations of type I collagen, osteocalcin, osteopontin, bone morphogenetic protein-2, bone morphogenetic protein receptor type 2, C-terminal telopeptide of type I collagen, and runt-related transcription factor-2 and reduced those of tartrate-resistant acid phosphatase 5 and nuclear factor of activated T cells in these mice, suggesting that it improved osteoblast differentiation and suppressed osteoclast differentiation. The anti-inflammatory effect of YSBGY was confirmed by the increase in the serum concentrations of interleukin- (IL-) 33 and the decrease in concentrations of IL-1, IL-7, and tumor necrosis factor-Œ± in OP mice. Furthermore, YSBGY enhanced the serum concentrations of superoxide dismutase and catalase in these mice, indicating that it also exerted antioxidative effects. This is the first study to confirm the antiosteoporotic effects of YSBGY in mice with Dex-induced OP, and it showed that these effects may be related to the YSBGY-induced modulation of the osteoblast/osteoclast balance and serum concentrations of inflammatory factors. These results provide experimental evidence supporting the use of YSBGY for supporting bone formation in the clinical setting. 

Retracted: No

PubPeer comments:
 Figure 1 appears they have two images which overlap but seem to be at different scales. ***  *** Closeup  , 
 Really thank you very much for pointing out the mistake of Fig.1. We have carefully checked our records, and confirmed that the H E staining of liver is inaccurate used in the paper. However, this mistake does not affect the experimental conclusions that Yishen Bugu Ye possesses the antisteoporosis effects due to its regulation on the differentiation of osteoblast and osteoclast. Again, sorry for the mistake. We have connected the Journal to make the corrigendum. The correct Fig.1 can be found as follows.   ,
Role of the Phosphatidylinositol-3-Kinase and Extracellular Regulated Kinase Pathways in the Induction of Hypoxia-Inducible Factor (HIF)-1 Activity and the HIF-1 Target Vascular Endothelial Growth Factor in Ovarian Granulosa Cells in Response to Follicle-Stimulating Hormone
Authors: Margaret Ashcroft
Jennifer Weck
Mary Hunzicker-Dunn
Evelyn Maizels
Hena Alam
Eun Jig Lee
Youngkyu Park
Journal: Endocrinology (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: FSH stimulation; granulosa cells; HIF-1alpha protein; PI-3-kinase/AKT pathway; mammalian target of rapamycin
Affiliations: Department of Cell and Molecular Biology (H.A., E.M., Y.P., M.H.-D.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, The School of Molecular Biosciences (J.W.), Washington State University, Pullman, Washington 83843, Department of Medicine (E.J.L.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, Division of Medicine (M.A.), University College, London WC1 E6JJ, United Kingdom

Abstract:  FSH stimulation of granulosa cells (GCs) results in increased hypoxia-inducible factor (HIF)-1alpha protein levels and HIF-1 activity that is necessary for up-regulation of certain FSH target genes including vascular endothelial growth factor. We report that the role of the phosphatidylinositol (PI)-3-kinase/AKT pathway in increasing HIF-1alpha protein in FSH-stimulated GCs extends beyond an increase in mammalian target of rapamycin-stimulated translation. FSH increases phosphorylation of the AKT target mouse double-minute 2 (MDM2); a phosphomimetic mutation of MDM2 is sufficient to induce HIF-1 activity. The PI3-kinase/AKT target forkhead box-containing protein O subfamily 1 (FOXO1) also effects the accumulation of HIF-1alpha as evidenced by the ability of a constitutively active FOXO1 mutant to inhibit the induction by FSH of HIF-1alpha protein and HIF-1 activity. Activation of the PI3-kinase/AKT pathway in GCs by IGF-I is sufficient to induce HIF-1alpha protein but surprisingly not HIF-1 activity. HIF-1 activity also appears to require a PD98059-sensitive protein (kinase) activity stimulated by FSH that is both distinct from mitogen-activated ERK kinase1/2 or 5 and independent of the PI3-kinase/AKT pathway. These results indicate that FSH-stimulated HIF-1 activation leading to up-regulation of targets such as vascular endothelial growth factor requires not only PI3-kinase/AKT-mediated activation of mammalian target of rapamycin as well as phosphorylation of FOXO1 and possibly MDM2 but also a protein (kinase) activity that is inhibited by the classic ERK kinase inhibitor PD98059 but not ERK1/2 or 5. Thus, regulation of HIF-1 activity in GCs by FSH under normoxic conditions is complex and requires input from multiple signaling pathways. 

Retracted: No

PubPeer comments:
 Figure 6B. Multiple splicing. Not obvious that all 3 panels are spliced in the same places. Akt panel. Ends of bands oddly similar.  ,
The role of human and mouse Y chromosome genes in male infertility
Authors: M J Mitchell
N A Affara
Journal: Journal of endocrinological investigation (2000)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Ronald Fisher; genes; Y chromosome; spermatogenesis; male germ cell differentiation

Abstract:  It was suggested by Ronald Fisher in 1931 that genes involved in benefit to the male (including spermatogenesis genes) would accumulate on the Y chromosome. The analysis of mouse Y chromosome deletions and the discovery of microdeletions of the human Y chromosome associated with diverse defective spermatogenic phenotypes has revealed the presence of intervals containing one or more genes controlling male germ cell differentiation. These intervals have been mapped, cloned and examined in detail for functional genes. This review discusses the genes mapping to critical spermatogenesis intervals and the evidence indicating which are the most likely candidates underlying Y-linked male infertility. 

Retracted: No

PubPeer comments:
 Verbatim repetition of text. https: imgur.com 3OmRk68 ,
MiR-587 acts as an oncogene in non-small-cell lung carcinoma via reducing CYLD expression
Authors: P Gao
X-J Li
Y-J Jia
L-W Chen
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-587; CYLD; NSCLC; cancer-associated functions; molecular mechanism
Affiliations: Department of Oncology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China. .

Abstract:  Objective: This study aims to explore the cancer-associated functions of microRNA-587 (miR-587) in the development of non-small-cell lung carcinoma (NSCLC) and the molecular mechanism. Patients and methods: Relative expression levels of miR-587 and CYLD in NSCLC samples were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Proliferative and migratory abilities in A549 and H1299 cells with overexpressed miR-587 were examined by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. The regulatory interaction between miR-587 and CYLD was determined by Dual-Luciferase reporter assay and Pearson correlation test. At last, the co-regulation of miR-587 and CYLD on NSCLC cell functions was assessed by rescue experiments. Results: MiR-587 was upregulated in NSCLC samples and closely linked to tumor staging, whereas CYLD was downregulated and negatively correlated to that of miR-587. Survival analysis suggested that miR-587 was an unfavorable factor to the prognosis of NSCLC. Overexpression of miR-587 stimulated proliferative and migratory abilities in A549 and H1299 cells. CYLD was the downstream gene binding miR-587. Overexpression of CYLD could partially abolish the regulatory effects of overexpressed miR-587 on promoting proliferative and migratory abilities in NSCLC cells. Conclusions: MiR-587 stimulates proliferative and migratory abilities in NSCLC by downregulating CYLD, thus aggravating the progression of NSCLC. 

Retracted: No

PubPeer comments:
 2018 retraction. http: www.jbc.org content 293 33 12948 This article has been withdrawn by the authors. The Journal questioned Figs. 1B and 6B. The authors state they were able to locate original data for Figs. 1B and 6B, which they believe support the published results. The authors stand by the reproducibility of the experimental data and the conclusions of the paper. The paper, with confirmatory data supporting the results, can be obtained by contacting the authors. , 
null, 
null, 
null, 
 Fourth 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  ,
Childhood trauma and adulthood inflammation: a meta-analysis of peripheral C-reactive protein, interleukin-6 and tumour necrosis factor-Œ±
Authors: S Ciufolini
C M Pariante
R Akhtar
D Baumeister
V Mondelli
Journal: Molecular psychiatry (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Childhood trauma; adulthood physical illness; mental illness; immune system dysregulation; meta-analysis
Affiliations: King's College London, Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, London, UK., King's College London, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience, London, UK., Department of Psychology, University College London, London, UK., King's College London, Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, London, UK., National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre, South London and Maudsley, NHS Foundation Trust and King's College London, London, UK.

Abstract:  Childhood trauma confers higher risk of adulthood physical and mental illness; however, the biological mechanism mediating this association remains largely unknown. Recent research has suggested dysregulation of the immune system as a possible biological mediator. The present paper conducted a meta-analysis to establish whether early-life adversity contributes to potentially pathogenic pro-inflammatory phenotypes in adult individuals. A systematic search of Pubmed, PsycINFO, EMBASE, Scopus and Medline identified 25 articles for the meta-analysis, including 18 studies encompassing a sample of 16 870 individuals for C-reactive protein (CRP), 15 studies including 3751 individuals for interleukin-6 (IL-6) and 10 studies including 881 individuals for tumour necrosis factor-Œ± (TNF-Œ±). Random-effects meta-analysis showed that individuals exposed to childhood trauma had significantly elevated baseline peripheral levels of CRP (Fisher's z=0.10, 95% confidence interval (CI)=0.05-0.14), IL-6 (z=0.08, 95% CI=0.03-0.14) and TNF-Œ± (z=0.23, 95% CI=0.14-0.32). Subgroup analyses for specific types of trauma (sexual, physical or emotional abuse) revealed that these impact differentially the single inflammatory markers. Moreover, meta-regression revealed greater effect sizes in clinical samples for the association between childhood trauma and CRP but not for IL-6 or TNF-Œ±. Age, body mass index (BMI) and gender had no moderating effects. The analysis demonstrates that childhood trauma contributes to a pro-inflammatory state in adulthood, with specific inflammatory profiles depending on the specific type of trauma. 

Retracted: No

PubPeer comments:
 1.tAlthough the contrast was adjusted, the images in Fig. 5A and Fig. 8A were duplicated and presented as different groups (shown in red boxes).  2.tThe p62 lane in Fig. 3A was overlapped with Sirt1 lane in Fig. 6G after a 180-degree rotation. A similar concern was shown in LC3 bands, the first lane in these two panels appear to be unexpectedly similar after a horizontal flip. Could the authors please post the original uncropped scans?  ,
Influence of Dy3+ Ions on the Microstructures and Magnetic, Electrical, and Microwave Properties of [Ni0.4Cu0.2Zn0.4](Fe2‚ÄìxDyx)O4 (0.00 ‚â?x ‚â?0.04) Spinel Ferrites
Authors: Yassine Slimani
Fatimah Alahmari
Alex Trukhanov
Tatiana Zubar
Abdulhadi Baykal
Hakan G√ºng√ºne≈ü
Sergei Trukhanov
Munirah Abdullah Almessiere
Ayse Demir Korkmaz
Ayyar Manikandan
Journal: ACS Omega (2021)
Discipline: CHEMISTRY
Keywords: Nanoparticles; Dy3+ concentration; Structural parameters; Magnetic properties; Electrical properties
Affiliations: Department of Biophysics, Institute for Research and Medical Consultations (IRMC), Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia, Department of Physics, Hitit University, √áevre Yolu Bulvarƒ±-√áorum 19030, Turkey, Department of Chemistry, Istanbul Medeniyet University, Dumlupƒ±nar D100 Karayolu No: 98, Uskudar-Istanbul 34700, Turkey, Laboratory of Magnetic Films Physics, Scientific-Practical Materials Research Centre of National Academy of Sciences of Belarus, Brovki 19, Minsk 220072, Belarus, Laboratory of Single Crystal Growth, South Ural State University, Lenina Avenue 76, Chelyabinsk 454080, Russia, Department of Chemistry, Bharath Institute of Higher Education and Research (BIHER), Bharath University, 173, Agaram Main Road, Selaiyur, Chennai 600073, India, Department of Nanomedicine, Institute for Research and Medical Consultations (IRMC), Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia

Abstract:  [Ni0.4Cu0.2Zn0.4](Fe2-x Dy x )O4 spinel ferrite nanoparticles with different Dy3+ concentrations (0.00 ‚â?x ‚â?0.04) were prepared by a citrate sol-gel auto-combustion technique. A strong correlation among Dy concentration, structural parameters, and magnetic, electrical, and microwave properties was established. An increase in the Dy3+ concentration is the reason for a rise in the crystal structure parameters (due to different ionic radii of Fe and Dy ions) and a slight increase in the average particle size with a minor reduction in the specific surface area. It was observed that Dy3+ ions prefer to occupy the octahedral B site due to their large ionic radius (0.91 √Ö). The explanation of the electrical and magnetic properties was given in terms of the features of Dy3+-O2--Fe3+ dysprosium-oxygen-iron indirect exchange. The occurrence of the intensive changes in amplitude-frequency characteristics was observed from 1.6 to 2.7 GHz. The explanation of electromagnetic absorption was given in terms of the peculiarities of the microstructure (resonance of domain boundaries). The results open perspectives in the utilization of [Ni0.4Cu0.2Zn0.4](Fe2-x Dy x )O4 spinel ferrite nanoparticles as functional materials for targeted drug delivery and hyperthermia applications. 

Retracted: No

PubPeer comments:
 There s an issue with the EDS detection of Dysprosium. The peak shape looks unnatural and its at the wrong energy - L-alpha should be at 6.49 keV  ,
MiR-25 protects PC-12 cells from H2O2 mediated oxidative damage via WNT/Œ≤-catenin pathway
Authors: Shizhen Niu
Yi Guo
Journal: Journal of Spinal Cord Medicine (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: H2O2; Nrf2; PC-12 cells; PI3‚ÄÖK/AKT/ERK signaling; Spinal cord injury (SCI)
Affiliations: a Department of Spine Surgery , Jining No.1 People's Hospital , Jining , China.

Abstract:  Objective: Spinal cord injury (SCI) is associated with modulation of different microRNAs (miRs). This study aims to explore the role of miR-25 in PC-12 cells to reveal the potential of miR-25 in SCI treatment. Methods: SCI model was established in C57BL/6 mice, then miR-expression in the injured spinal cords were detected by qRT-PCR. PC-12 cells were exposed to H2O2 conditions to establish an in vitro model of SCI. PC-12 cells were transfected with expressing vector or antisense oligonucleotides (ASO) of miR-25. The effects of miR-25 expression on H2O2-induced oxidative damage was evaluated by detection of cell viability, apoptosis, ROS activity, HIF-Œ± and Œ≥H2A expression, and the level of inflammatory mediators. The expression of Nrf2 in cells was silenced by transfection with Nrf2 siRNA, and the effects of Nrf2 silence on miR-25-mediated PC-12 cells were detected. Besides, the expression of main proteins in Wnt/Œ≤-catenin and PI3 K/AKT/ERK signaling were assessed. Results: miR-25 was low expressed in injured spinal cords. miR-25 protected PC-12 cells against H2O2-induced oxidative damage, as evidenced by significant suppression in cell apoptosis, increase in cell viability, decrease in the level of ROS, HIF-Œ± and Œ≥H2A, and decrease in inflammatory mediators (IL-1Œ≤, TNF-Œ±, IL-6, and MCP-1). However, Nrf2 silence abolished the protective functions of miR-25 on H2O2-induced damage. Furthermore, we found that Wnt/Œ≤-catenin and PI3 K/AKT/ERK signaling were activated by miR-25. Conclusions: miR-25 protects PC-12 cells against H2O2-induced oxidative damage though regulation of Nrf2 and activation of Wnt/Œ≤-catenin and PI3 K/AKT/ERK signaling. 

Retracted: No

PubPeer comments:
  Extended Figure 1D. Representative Western blot shows full groups (n=5 group) corresponding to the graph underneath. But the data points on the graph have very little variability... while the representative Western blot clearly has more variability. Also, it seems that the phospho and total would be exceedingly difficult to accurately isolate from that image. ,
MicroRNA-27b inhibits Spry2 expression and promotes cell invasion in glioma U251 cells
Authors: Jian Fu
Qiming Lin
Chenghui Liu
Shenghui Xiao
Xu Chen
Yi Wu
Shixing Liang
Journal: Oncology Letters (2015)
Discipline: CLINICAL MEDICINE
Keywords: glioma; invasion; microRNA-27b; sprouty homolog 2.
Affiliations: Department of Neurosurgery, Nanhai Hospital of Southern Medical University, Foshan, Guangdong 528200, P.R. China.

Abstract:  MicroRNA (miR)-27b has been reported to participate in glioma. However, a detailed role of miR-27b and the underlying mechanism remain largely unknown. The present study found that the expression of miR-27b was significantly increased in glioma tissues compared with normal adjacent tissues. In addition, miR-27b was also upregulated in the U87, U251 and SHG44 glioma cell lines compared with normal human astrocytes. Sprouty homolog 2 (Spry2), which has been reported to be associated with invasive glioma, was identified as a novel target of miR-27b in U251 glioma cells, and the protein expression of Spry2 was negatively regulated by miR-27b in U251 cells. Additionally, inhibition of miR-27b and upregulation of Spry2 suppressed glioma cell invasion, while downregulation of Spry2 reversed the suppressive effect of miR-27b inhibition on glioma cell invasion. These data suggest that miR-27b may promote glioma cell invasion through direct inhibition of Spry2 expression. The data also suggest that miR-27b may become a promising molecular target for inhibiting the invasion and metastasis of glioma. 

Retracted: No

PubPeer comments:
 Fig 4.  The invasion capacity was determined using Transwell assay in U251 cells transfected with the miR-27b inhibitor, Spry2 plasmid, or co-transfected with miR-27b inhibitor and Spry2 siRNA. I set up a spreadsheet to include the various papers using this versatile suite of Transwell images to represent all possible combinations of cell-lines and treatments. This is the 33rd manifestation. For comparison: Fig 3 C D from [Zhang et al (2016)] .  Transwell assay were performed to examine the migratory and invasive capacities of Saos-2 and U2OS cells transfected with miR-205 mimic or miR-negative control (NC) mimic , and Fig 7C D,  Transwell assay were performed to examine cell migration and invasion of MG63 or U2OS cells transfected with miR-205 mimic, or co-transfected with miR-205 mimic and RUNX2 plasmid .  Figs 4D, 6D from [Xia et al (2016)] .  ,
Gene expression profiling of nasopharyngeal carcinoma reveals the abnormally regulated Wnt signaling pathway
Authors: Shou-Rong Shen
Chen Huang
Yi-Xin Yang
Xiao-Ling Li
Yan-Hong Zhou
Song-Qing Fan
Gui-Yuan Li
Ke Tang
Jun Qian
Zhao-Yang Zeng
Wei Xiong
Xiao-Min Luo
Wen-Ling Zhang
Li Cao
Ming-Hua Wu
Journal: Human Pathology (2007)
Discipline: CLINICAL MEDICINE
Keywords: Nasopharyngeal carcinoma; gene expression profiling; Wnt signaling pathway; transforming growth factor-beta; mitogen-activated protein kinase
Affiliations: Cancer Research Institute, Xiang-Ya School of Medicine, Central South University, Changsha, Hunan 410078, China.

Abstract:  Nasopharyngeal carcinoma (NPC) is a particularly common malignant disease in areas of south China and Southeast Asia. To characterize the gene expression profiling of NPC, we detected the gene expression profiles in 22 NPC and 10 nontumor nasopharyngeal epithelial tissues by complementary DNA microarray. We identified 503 genes that were significantly (P &lt; .001) differentially regulated between NPC and nontumor nasopharyngeal epithelial tissues. The differentially expressed genes are involved in many signaling pathways, such as the Wnt, transforming growth factor-beta, and mitogen-activated protein kinase signaling pathways. The aberrant expression of the Wnt signaling pathway components, such as wingless-type MMTV integration site family, member 5A, Frizzled homolog 7, casein kinase IIbeta, beta-catenin, CREB-binding protein, and Dishevelled-associated activator of morphogenesis 2 was validated on the NPC tissue microarrays. The data suggest that the Wnt signaling pathway may be abnormally regulated in NPC, which provides insight into the molecular mechanisms of NPC. 

Retracted: No

PubPeer comments:
 There seems to be overlap between this paper and [another paper] with some common authors. Figure 1 and a portion of Table 1 are shown as examples. Could the authors please comment? ***  ***  ,
Mutations in COMP cause familial carpal tunnel syndrome
Authors: Zhuo Zhao
Bo Gao
Nga Ting Choi
Yufa Wang
Danny Chan
Yueshu Wang
Gene Elliott
Shusen Cui
Jin Wang
Alejandro A Sch√§ffer
Cheng Wang
Peiqiang Su
Yingzi Yang
Lisa Garrett
Xilin Liu
Chunyu Li
Ni Wang
Journal: Nature Communications (2020)
Discipline: Multidisciplinary
Keywords: Carpal tunnel syndrome; genetic susceptibility; cartilage oligomeric matrix protein (COMP); mutations; tenocytes
Affiliations: Department of Hand Surgery, China-Japan Union Hospital of Jilin University, Changchun, China., School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China., National Center for Biotechnology Information and National Cancer Institute, National Institutes of Health, Bethesda, MD, US., National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, US., Department of Orthopaedic Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China., Department of Hand Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. ., National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, US. ., Department of Developmental Biology, Harvard School of Dental Medicine, Harvard Stem Cell Institute, Harvard University, Boston, MA, US. ., School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. .

Abstract:  Carpal tunnel syndrome (CTS) is the most common peripheral nerve entrapment syndrome, affecting a large proportion of the general population. Genetic susceptibility has been implicated in CTS, but the causative genes remain elusive. Here, we report the identification of two mutations in cartilage oligomeric matrix protein (COMP) that segregate with CTS in two large families with or without multiple epiphyseal dysplasia (MED). Both mutations impair the secretion of COMP by tenocytes, but the mutation associated with MED also perturbs its secretion in chondrocytes. Further functional characterization of the CTS-specific mutation reveals similar histological and molecular changes of tendons/ligaments in patients' biopsies and the mouse models. The mutant COMP fails to oligomerize properly and is trapped in the ER, resulting in ER stress-induced unfolded protein response and cell death, leading to inflammation, progressive fibrosis and cell composition change in tendons/ligaments. The extracellular matrix (ECM) organization is also altered. Our studies uncover a previously unrecognized mechanism in CTS pathogenesis. 

Retracted: No

PubPeer comments:
 Full-length western blot source data is missing from the supplementary information, though in figure legends it was clearly stated that Source data are provided as a Source Data file . Could authors please post full length blot data that were utilized to generate figures 4 and 5. , 
 Thanks for pointing out this. You should find the source data of western blot of Figure 4 and 5 at the end of  Supplementary Information , which was moved from the  Source Data file as requested by the journal publication team. ,
LncRNA MT1JP functions as a tumor suppressor via regulating miR‚Ä?14‚Ä?p expression in bladder cancer
Authors: Haifeng Yu
Dapang Rao
Shuaibin Wang
Haibo Zhu
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MT1JP; bladder cancer; miR-214-3p.
Affiliations: Departments of Urology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Abstract:  Growing evidence suggested that the long noncoding RNAs (lncRNAs) regulate several pathophysiological processes in tumorigenesis and may be new biomarkers for tumor therapy. In this study, we studied the expression and role of lncRNA MT1JP in the development of bladder cancer. We demonstrated that the expression of MT1JP was downregulated in bladder tumor samples and cell lines. Ectopic expression of MT1JP suppressed cell proliferation, cycle, and invasion in bladder cancer. In addition, our result suggested that miR-214-3p overexpression decreased the luciferase activity of wild-type MT1JP but not mutated-type MT1JP and elevated expression of MT1JP decreased miR-214-3p expression in the bladder cancer cell. Furthermore, we indicated that the expression of miR-214-3p was upregulated in bladder tumor samples and cell lines. Ectopic expression of miR-214-3p promoted cell proliferation, cycle, and invasion in bladder cancer. MT1JP suppressed cell proliferation, cycle, and invasion via negative modulation of miR-214-3p in bladder cancer. These data suggested that lncRNA MT1JP acts a tumor suppressor gene in bladder cancer progression, considering MT1JP as a new therapeutic target in bladder cancer. 

Retracted: Yes

PubPeer comments:
 There are serious images duplication in this paper.   , 
 Retracted [16 March 2022] . ----------------------- The above article, published online on 20 February 2019 in Wiley Online Library https: onlinelibrary.wiley.com doi full 10.1002 jcp.28274), has been retracted by agreement between the authors, the journal s Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed after the authors stated that unintentional errors occurred during the research process, and the experimental results cannot be verified. Thus, the conclusions are considered to be invalid. ,
Boundary layer halogens in coastal Antarctica
Authors: Anoop S Mahajan
Anna E Jones
John M C Plane
Stephane J-B Bauguitte
Rhian A Salmon
Howard K Roscoe
Alfonso Saiz-Lopez
Journal: Science (2007)
Discipline: Multidisciplinary
Keywords: Halogens; oxidizing capacity; Earth's troposphere; iodine oxides; ultrafine aerosols
Affiliations: School of Chemistry, University of Leeds, Leeds, LS2 9JT, UK.

Abstract:  Halogens influence the oxidizing capacity of Earth's troposphere, and iodine oxides form ultrafine aerosols, which may have an impact on climate. We report year-round measurements of boundary layer iodine oxide and bromine oxide at the near-coastal site of Halley Station, Antarctica. Surprisingly, both species are present throughout the sunlit period and exhibit similar seasonal cycles and concentrations. The springtime peak of iodine oxide (20 parts per trillion) is the highest concentration recorded anywhere in the atmosphere. These levels of halogens cause substantial ozone depletion, as well as the rapid oxidation of dimethyl sulfide and mercury in the Antarctic boundary layer. 

Retracted: No

PubPeer comments:
 This paper considered the interval version of hesitant fuzzy sets and proposed some aggregation operations. An interval version of hesitant fuzzy prioritized operator is presented in Definition 24. The original version of hesitant fuzzy prioritized operator has been defined in a 2012 paper (doi: 10.1016 j.knosys.2012.03.011). However, according to the comment for the 2012 paper on https: pubpeer.com publications EBD7C0703EC4893A826FDD44A934EC where a concrete counterexample is presented, Theorem 2 (the interval version of idempotency) in this 2013 paper is invalid.  , 
 An unusual citation pattern is identified which is frequently associated with GW Wei, the first author of this paper.     , 
  ,
Slow transit constipation: a functional disorder becomes an enteric neuropathy
Authors: Gabrio Bassotti
Vincenzo Villanacci
Journal: World journal of gastroenterology (2006)
Discipline: CLINICAL MEDICINE
Keywords: Slow transit constipation; functional disorder; neuropathic type; motility alterations; enteric nervous system

Abstract:  Slow transit constipation has been traditionally considered and classified as a functional disorder. However, clinical and manometric evidence has been accumulating that suggests how most of the motility alterations in STC might be considered of neuropathic type. In addition, further investigations showed that subtle alterations of the enteric nervous system, not evident to conventional histological examination, may be present in these patients. In the present article we will discuss these evidences, and will try to put them in relation with the abnormal motor function of the large bowel documented in this pathological condition. 

Retracted: No

PubPeer comments:
 This paper shares a duplicated histopathology image with Figure 3 in Neurogastroenterology and Motility -2008 -https: doi.org 10.1111 j.1365-2982.2008.01146.x  , 
 The same image has been resued in several papers.   , 
   , 
    , 
  ,
FZD8, a target of p53, promotes bone metastasis in prostate cancer by activating canonical Wnt/Œ≤-catenin signaling
Authors: Wei Guo
Yingrong Lai
Xin Zhang
Shuai Huang
Jun Li
Chuyong Lin
Qiji Li
Min Wang
Xinsheng Peng
Libing Song
Hong Du
Liping Ye
Journal: Cancer Letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: Bone metastasis; Canonical Wnt/Œ≤-catenin; FZD8; Prostate cancer; p53.
Affiliations: Department of Orthopaedic Surgery, The First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, Guangdong Province, China., Department of Experimental Research, State Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 510060, Guangzhou, Guangdong Province, China., Department of Pathology, The First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, Guangdong Province, China., Department of Pathology, The First People's Hospital of Guangzhou City, 510180, Guangzhou, Guangdong Province, China., Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, 510060, Guangzhou, Guangdong Province, China., Department of Orthopaedic Surgery, The First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, Guangdong Province, China. Electronic address: .

Abstract:  Prostate cancer (PCa) is the second most frequently diagnosed cancer among men and exhibits a high propensity to metastasize to bone. Currently, bone metastasis remains incurable, and therapies are limited. A better understanding of the molecular mechanisms involved in PCa bone metastasis is needed to develop more effective therapeutics for this disease. Herein, we reported that among the FZD family, FZD8 was robustly upregulated in bone-metastastic PCa cell lines and tissues. High levels of FZD8 expression were significantly positively associated with clinical tumor progression and bone metastasis. Furthermore, we found that overexpressing FZD8 promoted, whereas silencing FZD8 suppressed, PCa cell migration, invasion and stem cell-like phenotypes in vitro, through the activation of canonical Wnt/Œ≤-catenin signaling. Importantly, downregulation of FZD8 greatly suppressed the incidence of PCa bone metastasis in vivo. Moreover, wild-type p53 transcriptionally repressed FZD8 by directly interacting with the FZD8 promoter. Taken together, these findings uncover a novel mechanism for PCa bone metastasis, and indicate that FZD8 might represent a potential therapeutic target for PCa bone metastasis. 

Retracted: No

PubPeer comments:
 Fig. S3A contains two images which appear to overlap.  ,
Moringa oleifera prevents selenite-induced cataractogenesis in rat pups
Authors: B N Rooban
S G Siva Priya
Annie Abraham
V Sahasranamam
V Sasikala
Journal: Journal of Ocular Pharmacology and Therapeutics (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: flavonoid fraction; Moringa oleifera leaves; selenite cataract; in vivo; rat pups
Affiliations: Department of Biochemistry, University of Kerala , Thiruvananthapuram, India., Department of Biochemistry, University of Kerala, Thiruvananthapuram, India., Regional Institute of Ophthalmology, Thiruvananthapuram, India.

Abstract:  Purpose: The aim of this study was to investigate the protective effects of the flavonoid fraction of Moringa oleifera leaves (FMO) on selenite cataract in vivo. Methods: Rat pups of Sprague-Dawley strain initially weighing 10‚Ä?2 g on day 8 were used for the study and grouped as control (G I), selenite induced (G II), and FMO treated (G III). The rat pups in G II and G III received a single subcutaneous injection of sodium selenite (4 ¬µg/g body weight) on day 10 and G III was administered with FMO (2.5 ¬µg/g body weight) from day 8 to 15. Cataract was visualized from day 16. The development of cataract was assessed and rat lenses were analyzed for the activities of antioxidant enzymes (superoxide dismutase and catalase), generation of reactive oxygen species, reduced glutathione, protein oxidation, and lipid peroxidation. FMO was subjected to in vitro antioxidant assays (2,2-diphenyl-picrylhydrazyl and superoxide scavenging assays). Results: The total phenolic content of FMO was 4.4 mg of catechin equivalent/g dried plant material. The extract showed remarkable activity on 2,2-diphenyl-picrylhydrazyl (IC50 36 ¬µg/mL) and in superoxide radical (IC50 33.81¬µg/mL) scavenging assays. FMO effectively prevented the morphological changes and oxidative damage in lens. FMO maintained the activities of antioxidant enzymes and sulfhydryl content and prevented reactive oxygen species generation and lipid peroxidation. Conclusions: FMO was effective in preventing cataractogenesis in selenite model by enhancing the activities of antioxidant enzyme, reducing the intensity of lipid peroxidation, and inhibiting free radical generation. 

Retracted: No

PubPeer comments:
 Figure 2A. One of the photos, representing the eye of a rat induced with selenite and treated with Moringa oleifera leaves (Group III), looks remarkably similar to a photo in another paper by this group (BN Rooban et al., DOI: 10.1007 s12011-010-8633-1 - https: pubpeer.com publications A8BC99B695BF12038EE9D90613AD6B) where it represents the eye of a rat induced with selenite and treated with Vitex negundo.  ,