PReD-Bench/PRed-Bench huggingface dataset:
Let-7 regulates cell cycle dynamics in the developing cerebral cortex and retina
Authors: Anna La Torre
Keiko Hino
Simranjeet K Cheema
Sergi Sim√≥
Corinne L A Fairchild
Joanna Wong
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: neural progenitors; cell proliferation; cell cycle; let-7; miRNA
Affiliations: Department of Cell Biology and Human Anatomy, University of California - Davis, Davis, CA, USA., Department of Cell Biology and Human Anatomy, University of California - Davis, Davis, CA, USA. .

Abstract:  In the neural progenitors of the developing central nervous system (CNS), cell proliferation is tightly controlled and coordinated with cell fate decisions. Progenitors divide rapidly during early development and their cell cycle lengthens progressively as development advances to eventually give rise to a tissue of the correct size and cellular composition. However, our understanding of the molecules linking cell cycle progression to developmental time is incomplete. Here, we show that the microRNA (miRNA) let-7 accumulates in neural progenitors over time throughout the developing CNS. Intriguingly, we find that the level and activity of let-7 oscillate as neural progenitors progress through the cell cycle by in situ hybridization and fluorescent miRNA sensor analyses. We also show that let-7 mediates cell cycle dynamics: increasing the level of let-7 promotes cell cycle exit and lengthens the S/G2 phase of the cell cycle, while let-7 knock down shortens the cell cycle in neural progenitors. Together, our findings suggest that let-7 may link cell proliferation to developmental time and regulate the progressive cell cycle lengthening that occurs during development. 

Retracted: No

PubPeer comments:
 In Figure 5A, a flowcytometry dot plot has been duplicated and presented as something else. The values are also different.  , 
 Thank you for noticing this! The values are correct. We made a mistake attaching the plots when building the figure. The corrected figures will be submitted asap. , 
 After looking into the issue, we realized that a copy and paste error was made while generating figure 5, resulting in an accidental duplication of G2 M phase data of Let-7s in the place of S-phase for Let-7s (the middle upper panel in Fig. 5A). The representative images shown in Fig. 5A were obtained after quantifying the data shown in Fig. 5B, thus the change does not affect quantification or overall outcome interpretation of the data. An erratum has been submitted. We apologize for the inconvenience that this may have caused.  ,
Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and Reperfusion via FoxO1 Nuclear Translocation in H9c2 Cells
Authors: Dandan Zhou
Dandan Zhao
Zejian Wang
Hongyu Zhang
Ming Yin
Yihui Wang
Jinqiang Zhuang
Lidong Zhao
Jinjun Pu
Shun Zhu
Jiang Hong
Journal: Frontiers in Physiology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DNA damage; FoxO1; ROS; oxygen glucose deprivation and reperfusion; propofol.
Affiliations: Department of Internal and Emergency Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China., School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China., Department of Emergency Medicine, Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China., Department of Biomedicine, KG Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway.

Abstract:  Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac myocytes. Many studies have revealed that propofol alleviates the important organelle-mediated injury from oxidative stress in vitro. However, it remains unclear whether propofol prevents I/R-induced DNA damage in cardiomyocytes. In our study, we established an oxygen glucose deprivation/reoxygenation (OGD/R) model in H9c2 cells and found that propofol decreased reactive oxygen species (ROS) levels and suppressed cell apoptosis induced by OGD/R in H9c2 cells. In addition, propofol significantly reduced the molecular marker of DNA damage and inhibited double-strand breaks of DNA damage induced by OGD/R in H9c2 cells in a dose-dependent manner. Furthermore, we investigated the molecular mechanisms and demonstrated that propofol inhibited forkhead box O 1 (FoxO1) phosphorylation and increased FoxO1 nuclear translocation through inhibition of protein kinase B (Akt) and adenosine 5'-monophosphate-activated protein kinase (AMPK) pathways. The protective effects of propofol against oxidative stress-induced DNA damage were reversed by silencing FoxO1. Taken together, our results suggest that oxidative stress aggravates DNA damage and apoptosis in H9C2 cells, which can be reversed by propofol via FoxO1 nuclear translocation. 

Retracted: No

PubPeer comments:
 This paper has previously been corrected due to duplication of Western immunoblots in Figure 6. In Figure 2, two of the flow cytometry dot plots have areas which are idential.  ,
MiRNA-1297 inhibits myocardial fibrosis by targeting ULK1
Authors: Y Wang
C-L Qv
B Jiang
Y-M Ma
Y-Y Song
W-X Hu
Y-J Zhang
R-N Li
Y-J Chen
M-L Li
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miRNA-1297; myocardial fibrosis; ULK1; Angiotensin II; fibrosis-related genes
Affiliations: Department of Cardiovascular Surgery, General Hospital of Ningxia Medical University, Yinchuan, China. .

Abstract:  Objective: The aim of this study was to explore the potential effect of miRNA-1297 on myocardial fibrosis (MF) and its underlying mechanism. Materials and methods: MF model was established by cardiac perfusion of Angiotensin II (Ang-II) in mice. The primary myocardial fibroblasts were extracted from MF mice (Ang-II infusion group) and controls (sham group), respectively. The relative levels of miRNA-1297 and ULK1 in the in vivo and in vitro MF models were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Meanwhile, the protein expressions of fibrosis-related genes in MF mice and primary myocardial fibroblasts were determined by Western Blot. Subsequently, the Dual-Luciferase Reporter Gene Assay was applied to verify the downstream gene of miRNA-1297. In addition, a series of rescue experiments were conducted to elucidate the role of miRNA-1297/ULK1 in regulating MF. Results: Masson staining showed plenty of micro-vessels around myocardial tissues and significantly increased contents of intercellular collagen in Ang-II infusion group when compared with those in the sham group. Western blot results revealed that the protein expressions of Col1a1 and Œ±-SMA were significantly upregulated in myocardial tissues of MF mice. QRT-PCR data illustrated that miRNA-1297 was remarkably downregulated in MF model. ULK1 was verified as the target gene of miRNA-1297, which was upregulated in the MF model. The overexpression of miRNA-1297 or the knockdown of ULK1 could downregulate the protein levels of Col1a1 and Œ±-SMA in primary myocardial fibroblasts extracted from MF mice. Notably, ULK1 overexpression could reverse the regulatory effect of miRNA-1297 on MF. Conclusions: MiRNA-1297 suppresses myocardial fibrosis via down-regulating ULK1. 

Retracted: No

PubPeer comments:
    ,
Activation of p53 by spermine mediates induction of autophagy in HT1080 cells
Authors: Moon-Moo Kim
Yong-Byung Chae
Journal: International Journal of Biological Macromolecules (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Acetyl-p53; Autopagy; HAT; SIRT1; Spermine.
Affiliations: Department of Chemistry, Dong-Eui University, Busan 614-714, Republic of Korea., Department of Chemistry, Dong-Eui University, Busan 614-714, Republic of Korea. Electronic address: .

Abstract:  The recent evidences indicate that autophagy is associated with a number of pathological processes including cancer, muscular disorder and neurodegeneration in addition to longevity. The efficacy of spermine was investigated on induction of autophagy through histone deacetylation and p53 activation in human fibrosarcoma cell line, HT1080. In this study, it was discovered that spermine increases the activity of HAT and autophagy. It was also identified that the transcriptional activation of p53 and the activation of p21 promoter by spermine are related to the induction of autophagy in reporter gene assay. Furthermore, western blot analyses demonstrated that spermine modulates the expression of proteins related to autophagy and apoptosis. The expression levels of Ac-histone H3, HDAC1, HAT1, p300 and SIRT1 were increased in HT1080 cells treated with spermine. In addition, the expression levels of protein such as acetyl-p53, p-p53, Bcl-2 and caspase-9 inducing apoptosis were increased in the presence of spermine. Moreover, the levels of Mdm2 and caspase-3 expression were reduced in the cells exposed to spermine compared to blank group. These results suggest that activation of HAT in the presence of spermine promotes the induction of autophagy in HT1080 cells through the enhanced activity of p-p53 and acetyl p53. 

Retracted: No

PubPeer comments:
 Readers should become aware of a recent paper published in JBC showing that autophagy induction by exogenous polyamines (including spermidine and spermine) is an artifact of BSA oxidase activity in culture serum. https: www.jbc.org content early 2020 05 19 jbc.RA120.013867.abstract From the article:  Consequently, considerable caution must be used when interpreting much of the published mechanistic data produced in in vitro cell culture systems as any observed autophagy included in such systems is likely the result of the toxic metabolites formed by BSAO following polyamines addition to the serum-containing medium and not a function of the polyamines themselves ,
Cinnamaldehyde Ameliorates High-Glucose‚ÄìInduced Oxidative Stress and Cardiomyocyte Injury Through Transient Receptor Potential Ankyrin 1
Authors: Jindong Wan
Jixin Hou
Peng Zhou
Dan Wang
Yi Yang
Peijian Wang
Sen Liu
Journal: Journal of cardiovascular pharmacology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Oxidative stress; Diabetic cardiomyopathy; TRPA1; Cinnamaldehyde; High-glucose-induced injury
Affiliations: Department of Cardiology, The First Affiliated Hospital, Chengdu Medical College, Chengdu, Sichuan, China., Key Laboratory of Aging and Vascular Homeostasis of Sichuan Higher Education Institutes, Chengdu, Sichuan, China.

Abstract:  Oxidative stress plays a critical role in diabetic cardiomyopathy. Transient receptor potential ankyrin subtype 1 (TRPA1) has antioxidative property. In this study, we tested whether activation of TRPA1 with cinnamaldehyde protects against high-glucose-induced cardiomyocyte injury. Cinnamaldehyde remarkably decreased high-glucose-induced mitochondrial superoxide overproduction, upregulation of nitrotyrosine, P22, and P47, and apoptosis in cultured H9C2 cardiomyocytes (P &lt; 0.01), which were abolished by a TRPA1 antagonist HC030031 (P &lt; 0.01). Nrf2 and its induced genes heme oxygenase-1 (HO-1), glutathione peroxidase-1 (GPx-1), and quinone oxidoreductase-1 (NQO-1) were slightly increased by high glucose (P &lt; 0.01) and further upregulated by cinnamaldehyde (P &lt; 0.05 or P &lt; 0.01). Feeding with cinnamaldehyde (0.02%)-containing diet for 12 weeks significantly decreased cardiac nitrotyrosine levels (P &lt; 0.01), fibrosis, and cardiomyocyte hypertrophy (P &lt; 0.05), while increased expression of antioxidative enzymes (HO-1, GPx-1, NQO-1, and catalase) (P &lt; 0.01) in the myocardial tissue of db/db diabetic mice. These results suggest that cinnamaldehyde protects against high-glucose-induced oxidative damage of cardiomyocytes likely through the TRPA1/Nrf2 pathway. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: pubmed.ncbi.nlm.nih.gov 32898016 ,
Vitamin D receptor expression in human bone tissue and dose-dependent activation in resorbing osteoclasts
Authors: Allahdad Zarei
Kassim Javaid
Alireza Morovat
Cameron P Brown
Journal: Bone research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Vitamin D; osteoblast; osteoclast; 25-hydroxy vitamin D3; 1,25-dihydroxy vitamin D3
Affiliations: Botnar Research Centre, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Science, University of Oxford , Oxford, UK., Clinical Biochemistry, Oxford University Hospitals NHS Trust , Oxford, UK.

Abstract:  The effects of vitamin D on osteoblast mineralization are well documented. Reports of the effects of vitamin D on osteoclasts, however, are conflicting, showing both inhibition and stimulation. Finding that resorbing osteoclasts in human bone express vitamin D receptor (VDR), we examined their response to different concentrations of 25-hydroxy vitamin D3 [25(OH)D3] (100 or 500 nmol¬∑L-1) and 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] (0.1 or 0.5 nmol¬∑L-1) metabolites in cell cultures. Specifically, CD14+ monocytes were cultured in charcoal-stripped serum in the presence of receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). Tartrate-resistant acid phosphatase (TRAP) histochemical staining assays and dentine resorption analysis were used to identify the size and number of osteoclast cells, number of nuclei per cell and resorption activity. The expression of VDR was detected in human bone tissue (ex vivo) by immunohistochemistry and in vitro cell cultures by western blotting. Quantitative reverse transcription-PCR (qRT-PCR) was used to determine the level of expression of vitamin D-related genes in response to vitamin D metabolites. VDR-related genes during osteoclastogenesis, shown by qRT-PCR, was stimulated in response to 500 nmol¬∑L-1 of 25(OH)D3 and 0.1-0.5 nmol¬∑L-1 of 1,25(OH)2D3, upregulating cytochrome P450 family 27 subfamily B member 1 (CYP27B1) and cytochrome P450 family 24 subfamily A member 1 (CYP24A1). Osteoclast fusion transcripts transmembrane 7 subfamily member 4 (tm7sf4) and nuclear factor of activated T-cell cytoplasmic 1 (nfatc1) where downregulated in response to vitamin D metabolites. Osteoclast number and resorption activity were also increased. Both 25(OH)D3 and 1,25(OH)2D3 reduced osteoclast size and number when co-treated with RANKL and M-CSF. The evidence for VDR expression in resorbing osteoclasts in vivo and low-dose effects of 1,25(OH)2D3 on osteoclasts in vitro may therefore provide insight into the effects of clinical vitamin D treatments, further providing a counterpoint to the high-dose effects reported from in vitro experiments. 

Retracted: No

PubPeer comments:
 Figure 1 may have some errors. The caption, visible below, seems to refer to H E staining as appearing in the right column, but the figure appears to show those in the left column. Additionally, there appears to be a repeated image; although the caption refers to serial sections, I cannot discern any differences. Apologies if I have misunderstood something. ***  ,
Farnesyltransferase inhibitor R115777 inhibits cell growth and induces apoptosis in mantle cell lymphoma
Authors: Vincent Ribrag
Delphine Rolland
Catherine Thieblemont
Aur√©lie Barbarat
Val√©rie Camara-Clayette
Gilles Salles
Bertrand Coiffier
Journal: Cancer Chemotherapy and Pharmacology (2008)
Discipline: CLINICAL MEDICINE
Keywords: farnesyltransferase inhibitor; mantle cell lymphoma; cytotoxic activity; cell lines; apoptosis
Affiliations: Universit√© Joseph Fourier, INSERM U836 (√©quipe 7), Grenoble, France.

Abstract:  Introduction: The cytotoxic activity of the farnesyltranseferase inhibitor R115777 was evaluated in cell lines representative of mantle cell lymphoma (MCL). Methods: Cell growth, proliferation, and apoptosis were analyzed in four human MCL cell lines (Granta, NCEB, REC, and UPN1) in presence of R115777, alone or in combination with vincristin, doxorubicin, bortezomib, cisplatin and cytarabine. Inhibition of farnesylation was determined by the appearance of prelamin A. The antitumor activity of R115777, administered p.o. at 100, 250 and 500 mg/kg, was determined in vivo in nude mice xenografted with UPN1 cells. Results: R115777 inhibited the growth of MCL cell lines in vitro with inhibitory concentrations ranging between 2 and 15 nM. A fifty percent decrease of cell viability was observed at concentrations comprised between 0.08 and 17 microM. Apoptosis, evaluated by annexin V and activated caspase 3 staining, was induced in all cell lines, in 40 to 71% of the cells depending on the cell lines. In addition, R115777 significantly increased the cytotoxic effect of vincristine, doxorubicin, bortezomib, cisplatin and cytarabine (p=0.001, p=0.016, p=0.006, p=0.014 and p=0.007 respectively). Exposure of MCL cell lines to R115777 during 72 hours resulted in inhibition of protein farnesylation. R115777 administered p.o. twice daily for 8 consecutive days to mice bearing established s.c. UPN1 xenograft displayed cytostatic activity at the 500 mg/kg dosage. Conclusion: We have demonstrated that inhibition of farnesyltransferase by R115777 was associated with growth inhibition and apoptosis of MCL cell lines in vitro and tumor xenograft stability in vivo. 

Retracted: No

PubPeer comments:
 Figure 2. * Orange boxes: the left 4 lanes look remarkably similar to the right 4 lanes. Reported to the journal together with 28 other papers in the summer of 2015, with a friendly reminder in April 2017, but no answer. With the exception of one paper, the journal did not correct or retract a single paper from this set.  ,
GH-releasing peptide-2 increases fat mass in mice lacking NPY: indication for a crucial mediating role of hypothalamic agouti-related protein
Authors: Mark L Heiman
Michael A Statnick
Todd M Suter
Matthias Tsch√∂p
Journal: Endocrinology (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Ghrelin; GHRP-2; adiposity; NPY neurons; body composition
Affiliations: Endocrine Research, Lilly Research Laboratories, Eli Lilly & Co., Indianapolis, Indiana 46285, USA. , Endocrine Research, Lilly Research Laboratories Eli Lilly \|[amp ]\| Co., Indianapolis, Indiana 46285

Abstract:  Ghrelin, an endogenous GH secretagogue, is capable of stimulating adiposity in rodents. Because such adiposity was thought to be mediated by hypothalamic NPY neurons, we investigated by which mechanism a synthetic ghrelin receptor agonist, GHRP-2, would generate a positive energy balance in NPY-deficient [Npy(-/-) mice] and wild-type controls. A dose-dependent increase in body weight and food intake was observed during daily sc injections with GHRP-2. Pre- and posttreatment analysis of body composition indicated increased fat mass and bone mass but not lean mass. Respiratory quotient was increased in GHRP-2-treated mice, indicating preservation of fat. Hypothalamic mRNA levels of agouti- related protein (AGRP), an orexigenic melanocortin receptor antagonist, increased after GHRP-2 treatment. Competitive blockade of AGRP action by melanocortin-receptor agonist MT-II prevented GHRP-induced weight gain in Npy(-/-) mice. In conclusion, chronic peripheral treatment with a ghrelin receptor agonist induced a positive energy balance leading to fat gain in the absence of NPY. These effects could be mediated in part by AGRP. To date, there are few therapeutics that can produce a positive energy balance. Ghrelin receptor agonists offer a treatment option for syndromes like anorexia nervosa, cancer cachexia, or AIDS wasting. 

Retracted: No

PubPeer comments:
 I admit that only 9 mice in Fig 3 were measured by DXA (out of 14 in Fig 1) but I still wonder how you these could get 4.41g extra fat while their body weight increased only 3.50g?  ,
Repression of Smad4 by miR‚Ä?05 moderates TGF-Œ≤-induced epithelial-mesenchymal transition in A549 cell lines
Authors: Dan Shen
Yuanyuan Zeng
Hualong Qin
Jianjie Zhu
Wei Li
Zeyi Liu
Jian-An Huang
Zhe Lei
Journal: International Journal of Oncology (2016)
Discipline: CLINICAL MEDICINE
Keywords: TGF-Œ≤/Smad signaling pathway; cancer cell proliferation; apoptosis; differentiation; angiogenesis
Affiliations: Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China., Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China., Suzhou Key Laboratory for Molecular Cancer Genetics, Suzhou, P.R. China., Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China.

Abstract:  The TGF-Œ≤/Smad signaling pathway plays important roles in cancer cell proliferation, apoptosis, differentiation, angiogenesis and epithelial-mesenchymal transition (EMT), which is the key event in the early stages of cancer metastasis and enhances the capability of cell migration and invasion. Smad4 acts as the only Co-Smad of TGF/Smad signaling pathway and plays the key role in TGF-Œ≤-mediated EMT. Nevertheless, the mRNA regulation mechanisms of Smad4 in human non-small cell lung cancer (NSCLC) remains largely unclear. Computational algorithms predicted that the 3'-UTR of Smad4 is a target of miR‚Ä?05. Here, we validated that miR‚Ä?05 could directly bind to 3'-UTR of Smad4 by luciferase assays. Moreover, we investigated the functional roles of miR‚Ä?05 and its molecular link to Smad4 in lung cancer cells. In this study, we confirmed that overexpression of miR‚Ä?05 suppressed the expression of Smad4, in turn, weakened the TGF-Œ≤/Smad signaling pathway and inhibited TGF-Œ≤/Smad4-induced EMT, invasion and migration ultimately. Furthermore, this study shows that miR‚Ä?05 can serve as a promising therapeutic target of highly aggressive NSCLC. 

Retracted: No

PubPeer comments:
 Figure 6 contains several overlapping images:  ,
miR-182-5p affects human bladder cancer cell proliferation, migration and invasion through regulating Cofilin 1
Authors: Liangju Su
Jiye Zhang
Jianbing Xu
Fengrong He
Defan Luo
Zhanping Xu
Jianxiang Chen
Dinglan Wu
Fei Wang
Xiaojuan Li
Weifu Wang
Shiliang Chen
Shufang Zhang
Journal: Cancer Cell International (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bladder cancer; Cofilin 1; Invasion; Migration; Proliferation
Affiliations: 1Department of Urology, Hainan General Hospital, Haikou, China., 2Shenzhen Key Laboratory of Viral Oncology, The Clinical Innovation & Research Centre, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong Province China., 3Department of Urology, Foshan Hospital of TCM, Foshan, Guangdong Province China., Department of Urology, Affiliated Hospital of Xiangnan College, Chenzhou, China., 5Central Laboratory, Hainan General Hospital, Haikou, China., 6Department of Pathology, Hainan General Hospital, Haikou, China., Central Laboratory, Affiliated Haikou Hospital Xiangya School of Medicine Central South University (HaiKou Municipal People Hospital), Haikou, Hainan China.

Abstract:  Background: Human bladder cancer is one of the common malignant tumors, and it mainly occurs in men. miR-182-5p, a member of miR-183 family, acts as tumor suppressor or oncogene in various kinds of tumors. In this study, we first investigate that the absence of miR-182-5p in human bladder cancer promotes tumor growth by regulating the expression of Cofilin 1, an actin modulating-protein. Methods: Human bladder tumor tissue specimens were collected to detect the expression of miR-182-5p and Cofilin 1 by qRT-PCR. Luciferase activity assay was performed to demonstrate the regulation of Cofilin 1 mRNA 3'UTR by miR-182-5p. Then, cell experiments were performed to analysis the effect of miR-182-5p/Cofilin 1 pathway on tumor cell proliferation, migration, invasion and colony forming efficiency. Finally, xenograft tumor models were established to evaluate the role of miR-182-5p in tumorigenesis abilities in vivo. Results: qRT-PCR and Western blotting analysis showed that Cofilin 1 expression was up-regulated in both bladder cancer tissues and cell lines compared with normal. Luciferase activity assay showed that miR-182-5p specifically targets Cofilin 1 mRNA 3'UTR and represses the expression of Cofilin 1. Also, miR-182-5p inhibited bladder tumor cell proliferation, migration, invasion and colony forming efficiency. Furthermore, xenograft tumor model assay showed that miR-182-5p plays a negative role in bladder cancer tumorigenesis abilities in vivo. Conclusion: Present results suggest that miR-182-5p could inhibit human bladder tumor growth by repressing Cofilin 1 expression. Our findings may provide a new horizon for exploring therapeutic target of bladder cancer. 

Retracted: No

PubPeer comments:
 Figure 7 and 8 appear to show several overlapping panels, as shown with boxes to the same color. Reported to the journal in October 2015 (I found one additional overlap today), with a friendly reminder in 2017, but no response as of today.  ,
Novel and Unique Diagnostic Biomarkers for Bacillus anthracis Infection
Authors: Theodor Chitlaru
Orit Gat
Haim Grosfeld
Ofer Cohen
Avigdor Shafferman
Sagit Sela-Abramovich
Journal: Applied and Environmental Microbiology (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bacterium-specific biomarkers; Bacillus anthracis; DNA vaccination; highly immunogenic bacterial antigens; genomic/proteomic/serologic screen
Affiliations: Life Science Research Israel Ltd., Ness-Ziona 74100, Israel, Department of Biochemistry and Molecular Genetics, Israel Institute for Biological Research

Abstract:  A search for bacterium-specific biomarkers in peripheral blood following infection with Bacillus anthracis was carried out with rabbits, using a battery of specific antibodies generated by DNA vaccination against 10 preselected highly immunogenic bacterial antigens which were identified previously by a genomic/proteomic/serologic screen of the B. anthracis secretome. Detection of infection biomarkers in the circulation of infected rabbits could be achieved only after removal of highly abundant serum proteins by chromatography using a random-ligand affinity column. Besides the toxin component protective antigen, the following three secreted proteins were detected in the circulation of infected animals: the chaperone and protease HtrA (BA3660), an NlpC/P60 endopeptidase (BA1952), and a protein of unknown function harboring two SH3 (Src homology 3) domains (BA0796). The three proteins could be detected in plasma samples from infected animals exhibiting 10(3) to 10(5) CFU/ml blood and also in standard blood cultures at 3 to 6 h post-bacterial inoculation at a bacteremic level as low as 10(3) CFU/ml. Furthermore, the three biomarkers appear to be present only in the secretome of B. anthracis, not in those of the related pathogens B. thuringiensis and B. cereus. To the best of our knowledge, this is the first report of direct detection of B. anthracis-specific proteins, other than the toxin components, in the circulation of infected animals. 

Retracted: No

PubPeer comments:
 Figure 2A, made darker, In the  Western panels on the right, unexpected sharp vertical and horizontal transitions are visible around some of the bands - shown here with red arrows. The  N lanes show no background at all. In the  Total protein photos on the left, sharp horizontal transitions are visible between the two lanes in the top and middle panels - shown with blue arrows. In addition, the bottom halves of the lanes in the top and bottom panels look similar to each other, and do not appear to match well with the top halves. Shown with pink boxes.  , 
 Figure 2D. Unexpected vertical and horizontal sharp transitions between lanes or bands. Shown with red arrows.  ,
Strengthening the Medical Error ‚ÄúMeme Pool‚Ä?1
Authors: Chadi Nabhan
Benjamin L Mazer
Journal: Journal of general internal medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: media; medical error; patient safety; quality improvement.

Abstract:  The exact number of patients in the USA who die from preventable medical errors each year is highly debated. Despite uncertainty in the underlying science, two very large estimates have spread rapidly through both the academic and popular media. We utilize Richard Dawkins' concept of the "meme" to explore why these imprecise estimates remain so compelling, and examine what potential harms can occur from their dissemination. We conclude by suggesting that instead of simply providing more precise estimates, physicians should encourage nuance in public medical error discussions, and strive to provide narrative context about the reality of the complex biological and social systems in which we practice medicine. 

Retracted: No

PubPeer comments:
 See https: statmodeling.stat.columbia.edu 2020 02 18 how-many-patients-do-doctors-kill-by-accident for some comments on this article. ,
LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
Authors: Jinghao Liu
Xin Li
Xingyu Liu
Sen Wei
Journal: BMC pulmonary medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: Bach-1; MIR17HG; Non-small cell lung cancer; miR-142-3p.
Affiliations: Department of Lung Cancer Surgery, General Hospital of Tianjin Medical University, No. 154 An'shan Road, Tianjin, 300052, China. ., Department of Lung Cancer Surgery, General Hospital of Tianjin Medical University, No. 154 An'shan Road, Tianjin, 300052, China.

Abstract:  Background: This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). Methods: Differential expression of MIR17HG in NSCLC was first detected by exploring the TCGA dataset. Expression levels of miR-142-3p in both NSCLC and non-tumor tissues were determined by qPCR. The effects of overexpressing MIR17HG on the methylation of miR-142 were assessed by MSP. The effects of overexpressing MIR17HG, miR-142-3p and Bach-1 on the invasion and migration of NSCLC cells were assessed by Trasnwell invasion or migration assay. Results: Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC. This downregulation was further confirmed by measuring the expression levels of MIR17HG in NSCLC and non-tumor tissues from NSCLC patients. MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. Conclusion: MIR17HG inhibits NSCLC by upregulating miR-142-3p to downregulate Bach-1. Trial registration: TJ-MU-2012-0148594, registered January 2, 2012. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: the images representing the invasion and migration assays appear to look identical.  In addition, the word  Transwell is misspelled several times as  Trasnwell . ,
Control of Development, Secondary Metabolism and Light-Dependent Carotenoid Biosynthesis by the Velvet Complex of
Authors: Eva M Luque
Nicola M Moloney
Luis M Corrochano
Eric U Selker
David C√°novas
David A Fitzpatrick
Jamie McGowan
Alejandro Miralles-Dur√°n
√ñzlem Sarikaya Bayram
Tereza Ormsby
Sara Cea-S√°nchez
√ñzg√ºr Bayram
Anne Dettmann
Betim Karahoda
Guilherme T P Brancini
Stephan Seiler
Sean Doyle
Journal: Genetics (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Aspergillus nidulans; Neurospora crassa; light control; secondary metabolism; velvet complex.
Affiliations: Department of Biology, Maynooth University, Co. Kildare, W23 F2H6, Ireland., Institute for Biology II, Molecular Plant Physiology, Albert-Ludwigs-University 79104 Freiburg, Germany., Institute of Molecular Biology, University of Oregon, Eugene, 97403 Oregon., Departmento de Gen√©tica, Facultad de Biologia, Universidad de Sevilla, 41012 Sevilla, Spain., Institute for Biology II, Molecular Plant Physiology, Albert-Ludwigs-University 79104 Freiburg, Germany  ., Department of Biology, Maynooth University, Co. Kildare, W23 F2H6, Ireland  ., Human Health Research Institute, Maynooth University, Co. Kildare, W23 F2H6, Ireland.

Abstract:  Neurospora crassa is an established reference organism to investigate carotene biosynthesis and light regulation. However, there is little evidence of its capacity to produce secondary metabolites. Here, we report the role of the fungal-specific regulatory velvet complexes in development and secondary metabolism (SM) in N. crassa Three velvet proteins VE-1, VE-2, VOS-1, and a putative methyltransferase LAE-1 show light-independent nucleocytoplasmic localization. Two distinct velvet complexes, a heterotrimeric VE-1/VE-2/LAE-1 and a heterodimeric VE-2/VOS-1 are found in vivo The heterotrimer-complex, which positively regulates sexual development and represses asexual sporulation, suppresses siderophore coprogen production under iron starvation conditions. The VE-1/VE-2 heterodimer controls carotene production. VE-1 regulates the expression of &gt;15% of the whole genome, comprising mainly regulatory and developmental features. We also studied intergenera functions of the velvet complex through complementation of Aspergillus nidulans veA, velB, laeA, vosA mutants with their N. crassa orthologs ve-1, ve-2, lae-1, and vos-1, respectively. Expression of VE-1 and VE-2 in A. nidulans successfully substitutes the developmental and SM functions of VeA and VelB by forming two functional chimeric velvet complexes in vivo, VelB/VE-1/LaeA and VE-2/VeA/LaeA, respectively. Reciprocally, expression of veA restores the phenotypes of the N. crassa ve-1 mutant. All N. crassa velvet proteins heterologously expressed in A. nidulans are localized to the nuclear fraction independent of light. These data highlight the conservation of the complex formation in N. crassa and A. nidulans However, they also underline the intergenera similarities and differences of velvet roles according to different life styles, niches and ontogenetic processes. 

Retracted: No

PubPeer comments:
 Potential image duplication in Fig. 1B  ,
Aloe vera induced biomimetic assemblage of nucleobase into nanosized particles
Authors: Asif Sherwani
Arun Chauhan
Mohammad Owais
Swaleha Zubair
Journal: PLoS ONE (2012)
Discipline: Multidisciplinary
Keywords: Biomimetic nano-assembly; organic molecules; anticancer agent; Aloe vera leaf extract; nano-particles
Affiliations: Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, Uttar Pradesh, India.

Abstract:  Aim: Biomimetic nano-assembly formation offers a convenient and bio friendly approach to fabricate complex structures from simple components with sub-nanometer precision. Recently, biomimetic (employing microorganism/plants) synthesis of metal and inorganic materials nano-particles has emerged as a simple and viable strategy. In the present study, we have extended biological synthesis of nano-particles to organic molecules, namely the anticancer agent 5-fluorouracil (5-FU), using Aloe vera leaf extract. Methodology: The 5-FU nano- particles synthesized by using Aloe vera leaf extract were characterized by UV, FT-IR and fluorescence spectroscopic techniques. The size and shape of the synthesized nanoparticles were determined by TEM, while crystalline nature of 5-FU particles was established by X-ray diffraction study. The cytotoxic effects of 5-FU nanoparticles were assessed against HT-29 and Caco-2 (human adenocarcinoma colorectal) cell lines. Results: Transmission electron microscopy and atomic force microscopic techniques confirmed nano-size of the synthesized particles. Importantly, the nano-assembled 5-FU retained its anticancer action against various cancerous cell lines. Conclusion: In the present study, we have explored the potential of biomimetic synthesis of nanoparticles employing organic molecules with the hope that such developments will be helpful to introduce novel nano-particle formulations that will not only be more effective but would also be devoid of nano-particle associated putative toxicity constraints. 

Retracted: No

PubPeer comments:
 Figure 4 seems to have two sets of images that overlap. In one case, the image has been resized. *** Enhanced brightness  *** Original  ,
Vaspin protects rats against myocardial ischemia/reperfusion injury (MIRI) through the TLR4/NF-Œ∫B signaling pathway
Authors: Gu Gong
Lu Lin
Libang Yuan
Daming Sui
Xuemei Dai
Lin Yang
Xiaowu Wang
Peng Zha
Haiyu Fu
Journal: European Journal of Pharmacology (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Myocardial ischemia/reperfusion injury; Protects; TLR4/NF-Œ∫B; Vaspin.
Affiliations: Department of Anesthesiology, General Hospital of Chengdu Military Region of PLA, 270 Rongdu Road, Chengdu 610083, China., Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 111 Liuhua Road, Guangzhou, Guangdong 510010, China. Electronic address: ., Department of Anesthesiology, General Hospital of Chengdu Military Region of PLA, 270 Rongdu Road, Chengdu 610083, China. Electronic address: .

Abstract:  The purpose of our study was to investigate the effect of vaspin on myocardial ischemia reperfusion injury (MIRI) and explore the underlying mechanism. The MIRI model was induced with 30 min of left anterior descending (LAD) occlusion followed by 24 h of reperfusion. In vivo, the rats were randomly divided into five groups: (1) Sham, (2) MIRI, (3) MIRI + vaspin (10 mg/kg), (4) MIRI + vaspin (20 mg/kg) and (5) MIRI + vaspin (40 mg/kg). In vitro, H9C2 cells were assigned to five groups: (1) control, (2) hypoxia-re-oxygenation (H/R), (3) H/R + vaspin (1 Œºg/ml), (4) H/R + vaspin (2 Œºg/ml) and (5) H/R + vaspin (4 Œºg/ml). As a result, vaspin ameliorated MIRI and H/R in a dose-dependent manner, as evidenced by triphenyl tetrazolium chloride (TTC) staining, TUNEL Assay and MTT assay, respectively, meanwhile vaspin decreased the levels of creatine phosphokinase-isoenzyme (CK-MB) and lactate dehydrogenase (LDH) in rat serum, moreover, vaspin could reduce the contents of interleukin-1Œ≤ (IL-1Œ≤), IL-18 and tumor necrosis factor alpha (TNF-Œ±) in serum of rats and supernatant of H9C2 cells. Furthermore, vaspin down-regulated the expression of toll-like receptor 4 (TLR4) and the phosphorylation of nuclear factor Œ∫B (NF-Œ∫B) in MIRI rats and H/R-induced H9C2 cells. In addition, patients with acute myocardial infarction (AMI) had lower levels of vaspin than patients without. In conclusion, vaspin might be a useful predictive biomarker in patients with AMI; furthermore, vaspin exhibits cardioprotective effects on MIRI which might act through inhibiting TLR4/NF-Œ∫B signaling pathway in vivo and in vitro. 

Retracted: No

PubPeer comments:
 At left, Fig. 1.  The suppression of vaspin in myocardial infarct size and cardiomyocyte apoptosis induced by MIRI. (A) Representative photos of myocardial infarct size. Myocardial infarction area was identified by TTC staining . At right, Fig. 1 from [Zhang et al (2017)] .  Lut decreased infarct size in I R rats. Infarct size of each rat was assessed by the TTC assay. Red stainu2013viable area; White stain-infarct region.  Images appear to be reused. ,
Nervous and Neuroendocrine regulation of the pathophysiology of cholestasis and of biliary carcinogenesis
Authors: Marco Marzioni
Giammarco Fava
Antonio Benedetti
Journal: World journal of gastroenterology (2006)
Discipline: CLINICAL MEDICINE
Keywords: Cholangiocytes; liver diseases; cholangiopathies; cholangiocarcinoma; hormones

Abstract:  Cholangiocytes, the epithelial cells lining the biliary ducts, are the target cells in several liver diseases. Cholangiopathies and cholangiocarcinoma generate interest in many scientists since the genesis. The developing mechanisms, and the therapeutic tools of these diseases are still undefined. Several studies demonstrate that many hormones, neuropeptides and neurotransmitters regulate malignant and non-malignant cholangiocyte pathophysiology in the course of chronic biliary diseases. The aim of this review is to present the findings of several studies published in the recent years that contributed to clarifying the role of nervous and neuroendocrine regulation of the pathophysiologic events associated with cholestasis and cholangiocarcinoma development. This manuscript is organized into two parts. The first part offers an overview of the innervation of the liver and the origin of neuroendocrine hormones, neurotransmitters and neuropeptides affecting cholangiocyte function and metabolism. The first section also reviews the effects played by several neuroendocrine hormones and nervous system on cholangiocyte growth, survival and functional activity in the course of cholestasis. In the second section, we summarize the results of some studies describing the role of nervous system and neuroendocrine hormones in the regulation of malignant cholangiocyte growth. 

Retracted: No

PubPeer comments:
 This review features 35 self citations over 110 references. A large partion of the self cited papers are mentioned in PubPeer. See: https: pubpeer.com search?q=benedetti Additionally this review is reproduced verbatim in: Control of cholangiocyte adaptive responses by visceral hormones and neuropeptides. Clinical Reviews in Allergy Immunology (2009). doi: 10.1007 s12016-008-8090-1 issn: 1080-0549 issn: 1559-0267 pubmed: 18548352. See the two abstract below.  ,
Smad6 inhibits BMP/Smad1 signaling by specifically competing with the Smad4 tumor suppressor
Authors: J Massagu√©
A Hemmati-Brivanlou
A Hata
G Lagna
Journal: Genes & Development (1998)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bone morphogenetic protein (BMP); receptors; Smad1; Smad4; inhibitor
Affiliations: Cell Biology Program, Howard Hughes Medical Institute and The Sloan-Kettering Division of the Cornell University Graduate School of Medical Sciences, Memorial Sloan-Kettering Cancer Center, The Rockefeller University, New York, NY 10021, USA.

Abstract:  Bone morphogenetic protein (BMP) receptors signal by phosphorylating Smad1, which then associates with Smad4; this complex moves into the nucleus and activates transcription. Here we report the existence of a natural inhibitor of this process, Smad6, a longer version of the previously reported JV15-1. In Xenopus embryos and in mammalian cells, Smad6 specifically blocks signaling by the BMP/Smad1 pathway. Smad6 inhibits BMP/Smad1 signaling without interfering with receptor-mediated phosphorylation of Smad1. Smad6 specifically competes with Smad4 for binding to receptor-activated Smad1, yielding an apparently inactive Smad1-Smad6 complex. Therefore, Smad6 selectively antagonizes BMP-activated Smad1 by acting as a Smad4 decoy. 

Retracted: No

PubPeer comments:
  , 
 I am sure the authors will get to work on this urgent matter of correcting an undisclosed splice in a 22 year old paper. ,
Long noncoding RNA NNT-AS1 promotes gastric cancer proliferation and invasion by regulating microRNA-363 expression
Authors: Yarui Li
Dan Guo
Junbi Hu
Xin Wang
Guifang Lu
Mudan Ren
Wenhui Ma
Xinlan Lu
Shuixiang He
Journal: Journal of cellular biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: long noncoding RNAs; miR-363; nicotinamide nucleotide transhydrogenase-antisense RNA1.
Affiliations: Department of Gastroenterology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Abstract:  Increasing studies showed that long noncoding RNAs (lncRNAs) had crucial regulatory roles in various tumors, including gastric cancer (GC). Recent studies demonstrated that lncRNA nicotinamide nucleotide transhydrogenase-antisense RNA1 (NNT-AS1) played an important role in several tumors. However, the role and expression of NNT-AS1 in GC progression remain unknown. In our study, we indicated that NNT-AS1 expression was upregulated in GC samples compared with the nontumor tissues. We also showed that NNT-AS1 expression was upregulated in the GC cell lines. Ectopic expression of NNT-AS1 promoted GC cell line HGC-27 cell proliferation, cell cycle progression, and invasion. In addition, we showed that NNT-AS1 acted as a sponge competing endogenous RNA for microRNA-363 (miR-363), which was downregulated in the GC samples and cell lines. miR-363 expression was negatively related with NNT-AS1 expression in GC samples. Upregulated expression of miR-363 suppressed GC cell growth, cycle, and invasion. Furthermore, we reported that elevated expression of NNT-AS1 promoted GC cell proliferation, cycle, and invasion partly by suppressing miR-363 expression. These results indicated that lncRNA NNT-AS1 acted as an oncogene in the development of GC partly by inhibiting miR-363 expression. 

Retracted: No

PubPeer comments:
 Figure 2D. Some groups of cells appear to be visible multiple times. Boxes of the same color highlight some areas that look more similar than expected.  , 
 Figure 5C. Some groups of cells appear to be visible multiple times. Boxes of the same color highlight some areas that look more similar than expected.  , 
 Figure 6C. Some groups of cells appear to be visible multiple times. Boxes of the same color highlight some areas that look more similar than expected.  ,
Dual Delivery of BMP-2 and bFGF from a New Nano-Composite Scaffold, Loaded with Vascular Stents for Large-Size Mandibular Defect Regeneration
Authors: Hang Zhao
Jun Sun
Jiansheng Su
Xue Gong
Hongzhen Xu
Journal: International Journal of Molecular Sciences (2013)
Discipline: CHEMISTRY
Keywords: bone morphogenetic protein-2 (BMP-2); basic fibroblast growth factor (bFGF); nano-composite scaffolds; large bone defect regeneration; rabbit mandibles
Affiliations: Institute of Prosthodontics, School of Stomatology, Tongji University, 399 Yanchang Road, Shanghai 200092, China. .

Abstract:  The aim of this study was to investigate the feasibility and advantages of the dual delivery of bone morphogenetic protein-2 (BMP-2) and basic fibroblast growth factor (bFGF) from nano-composite scaffolds (PLGA/PCL/nHA) loaded with vascular stents (PLCL/Col/nHA) for large bone defect regeneration in rabbit mandibles. Thirty-six large bone defects were repaired in rabbits using engineering bone composed of allogeneic bone marrow mesenchymal stem cells (BMSCs), bFGF, BMP-2 and scaffolds composed of PLGA/PCL/nHA loaded with PLCL/Col/nHA. The experiments were divided into six groups: BMSCs/bFGF/BMP-2/scaffold, BMSCs/BMP-2/scaffold, BMSCs/bFGF/scaffold, BMSCs/scaffold, scaffold alone and no treatment. Sodium alginate hydrogel was used as the carrier for BMP-2 and bFGF and its features, including gelling, degradation and controlled release properties, was detected by the determination of gelation and degradation time coupled with a controlled release study of bovine serum albumin (BSA). AlamarBlue assay and alkaline phosphatase (ALP) activity were used to evaluate the proliferation and osteogenic differentiation of BMSCs in different groups. X-ray and histological examinations of the samples were performed after 4 and 12 weeks post-implantation to clarify new bone formation in the mandible defects. The results verified that the use of sodium alginate hydrogel as a controlled release carrier has good sustained release ability, and the combined application of bFGF and BMP-2 could significantly promote the proliferation and osteogenic differentiation of BMSCs (p &lt; 0.05 or p &lt; 0.01). In addition, X-ray and histological examinations of the samples exhibited that the dual release group had significantly higher bone formation than the other groups. The above results indicate that the delivery of both growth factors could enhance new bone formation and vascularization compared with delivery of BMP-2 or bFGF alone, and may supply a promising way of repairing large bone defects in bone tissue engineering. 

Retracted: No

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