PReD-Bench/PRed-Bench huggingface dataset:
Silver(I) metallodrugs of thiosemicarbazones and naproxen: biocompatibility, anti-proliferative activity and interaction studies with EGFR, VEGFR2 and LOX receptors
Authors: Kyobum Kim
Aziz Kalilur Rahiman
Raju Senthil Kumar
Hyo Jeong Choi
Dharmasivam Mahendiran
Sundaram Bharathi
Mani Gajendiran
Journal: Toxicology Research (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: apoptosis; biocompatibility; geometry optimization; in silico studies; naproxen
Affiliations: Department of Chemistry, The New College (Autonomous), University of Madras, Chennai 600 014, India, Molecular Pharmacology and Pathology Program, Department of Pathology, Bosch Institute, University of Sydney, Sydney 2006, Australia, Department of Pharmaceutical Chemistry, Swamy Vivekanandha College of Pharmacy, Elayampalayam, Tiruchengodu 637 205, India, Division of Bioengineering, School of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea, Department of Chemical and Biochemical Engineering, Dongguk University, Seoul 04620, Republic of Korea

Abstract:  Four new heteroleptic silver(I) complexes with the general formula [Ag(L1-4)(nap)] (1-4), where L1-4 = 2-(1-(4-substitutedphenyl)ethylidene)hydrazinecarbothioamide and nap = naproxen, have been synthesized and characterized. The geometric parameters determined from density functional theory and UV-Vis studies indicate distorted tetrahedral geometry around silver(I) ion. Fourier transform infrared (FT IR) spectra evidenced asymmetric bidentate coordination mode of carboxyl oxygen atoms of naproxen with silver(I) ion. The complexes are stable for 72 h and biocompatibility was analysed towards normal human dermal fibroblast cells, which showed non-toxic nature up to 100 ng/ml. In vitro anti-proliferative activity of the complexes by MTT assay was tested against three human cancerous cell lines and one non-tumorigenic human breast epithelial cell line (MCF-10a) in which the complex 4 exhibited enhanced activity. The morphological changes observed by acridine orange/ethidium bromide and Hoechst 33258 staining method reveal apoptosis-inducing ability of the complexes. The molecular docking studies suggest hydrogen bonding, hydrophobic and π-pair interactions with the active site of epidermal growth factor receptor, vascular endothelial growth factor receptor 2 and lipoxygenase receptors. 

Retracted: No

PubPeer comments:
 Could the authors comment on what appear to be several repeated features in Figure 7? ![file] ,
Knockdown of long noncoding RNA DLX6-AS1 inhibits cell proliferation and invasion of cervical cancer cells by downregulating FUS
Authors: Y-R Wang
S-H Jia
Y Tian
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA DLX6-AS1; cervical cancer; FUS; cell proliferation; metastasis
Affiliations: Department of Histology and Embryology, Changzhi Medical College, Changzhi, China. .

Abstract:  Objective: Recently, the vital role of long noncoding RNAs (lncRNAs) in human diseases have got much attention. In this research, lncRNA DLX6-AS1 is studied to verify how it affects the development of cervical cancer (CC). Patients and methods: DLX6-AS1 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both CC cells and tissue samples. Besides, functional experiments including cell counting kit-8 (CCK-8) assay, colony formation assay, and transwell assay were performed. Meanwhile, the underlying mechanism was explored through qRT-PCR and Western blot assay. The function of DLX6-AS1 was also identified in vivo. Results: By comparing with corresponding tissues, the DLX6-AS1 expression level was significantly higher in CC samples. Moreover, cell growth ability and invaded ability of CC cells were inhibited after DLX6-AS1 was knocked down. Furthermore, the expression of FUS was inhibited after knockdown of DLX6-AS1. It was found that the expression level of FUS positively correlated to the expression of DLX6-AS1 in CC tissues. In addition, knockdown of DLX6-AS1 inhibited tumor formation and metastasis of CC in nude mice. Conclusions: These results suggest that DLX6-AS1 could enhance cell proliferation and metastasis of CC by upregulating FUS, which might be a potential therapeutic target in CC. 

Retracted: Yes

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: The point being addressed here is a small one, that I had addressed in several other papers already , and would go on to address elsewhere . This paper is much too long, and contains far too many analyses and supplementary materials. I have laboured this point too many times, out of desperation that science still hasn t learnt basic statistical lessons from the 1880s. The point I was making is correct, but this should either have been a much shorter commentary, or a proper systematic review and meta-analysis. ,
Aurora A is a repressed effector target of the chromatin remodeling protein INI1/hSNF5 required for rhabdoid tumor cell survival
Authors: Ganjam V Kalpana
Nandini Ramachandra
Velasco Cimica
Seungjae Lee
David Zagzag
Journal: Cancer Research (2011)
Discipline: CLINICAL MEDICINE
Keywords: Rhabdoid tumors; INI1/hSNF5; Aurora A; mitotic genes; chromatin remodeling
Affiliations: Department of Genetics, Albert Einstein College of Medicine, New York University, New York, NY, USA.

Abstract:  Rhabdoid tumors (RT) are aggressive pediatric malignancies with poor prognosis. INI1/hSNF5 is a component of the chromatin remodeling SWI/SNF complex and a tumor suppressor deleted in RT. Previous microarray studies indicated that reintroduction of INI1/hSNF5 into RT cells leads to repression of a high degree of mitotic genes including Aurora Kinase A (Aurora A, STK6). Here, we found that INI1/SNF5 represses Aurora A transcription in a cell-type-specific manner. INI1-mediated repression was observed in RT and normal cells but not in non-RT cell lines. Chromatin immunoprecipitation (ChIP) assay indicated that INI1/hSNF5 associates with Aurora A promoter in RT and normal cells but not in non-RT cells. Real-time PCR and immunohistochemical analyses of primary human and mouse RTs harboring mutations in INI1/hSNF5 gene indicated that Aurora A was overexpressed/derepressed in these tumor cells, confirming that INI1/hSNF5 represses Aurora A in vivo. Knockdown of Aurora A impaired cell growth, induced mitotic arrest and aberrant nuclear division leading to decreased survival, and increased cell death and caspase 3/7-mediated apoptosis in RT cells (but not in normal cells). These results indicated that Aurora A is a direct downstream target of INI1/hSNF5-mediated repression in RT cells and that loss of INI1/hSNF5 leads to aberrant overexpression of Aurora A in these tumors, which is required for their survival. We propose that a high degree of Aurora A expression may play a role in aggressive behavior of RTs and that targeting expression or activity of this gene is a novel therapeutic strategy for these tumors. 

Retracted: No

PubPeer comments:
 Figure 1D. Much more similar after 180 degree rotation and vertical stretch than expected. ![file] ,
Insulin inhibits hepatocellular glucose production by utilizing liver-enriched transcriptional inhibitory protein to disrupt the association of CREB-binding protein and RNA polymerase II with the phosphoenolpyruvate carboxykinase gene promoter
Authors: Daryl K Granner
Mary E Waltner-Law
Linda Sealy
David T Duong
Rosalie Sears
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hormones; Glucose homeostasis; Gluconeogenic enzymes; Phosphoenolpyruvate carboxykinase (PEPCK); Insulin
Affiliations: Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Abstract:  Hormones regulate glucose homeostasis, in part, by controlling the expression of gluconeogenic enzymes, such as phosphoenolpyruvate carboxykinase (PEPCK). Insulin and glucocorticoids reciprocally regulate PEPCK expression primarily at the level of gene transcription. We demonstrate here that glucocorticoids promote, whereas insulin disrupts, the association of CREB-binding protein (CBP) and RNA polymerase II with the hepatic PEPCK gene promoter in vivo. We also show that accessory factors, such as CCAAT/enhancer-binding protein beta (C/EBP beta), can recruit CBP to drive transcription. Insulin increases protein levels of liver-enriched transcriptional inhibitory protein (LIP), an inhibitory form of C/EBP beta, in a phosphatidylinositol 3-kinase-dependent manner. LIP concomitantly replaces liver-enriched transcriptional activator protein on the PEPCK gene promoter, which can abrogate the recruitment of CBP and polymerase II, culminating in the repression of PEPCK expression and the attenuation of hepatocellular glucose production. 

Retracted: No

PubPeer comments:
 The input of Western blot in FIG.2D and FIG.2E were similar, just with different exposure time. ![file] ,
Erythrocyte sedimentation rate and fibrinogen concentration of whole blood influences the cellular composition of platelet-rich plasma obtained from centrifugation methods
Authors: Wenjing Yin
Changqing Zhang
Zhengliang Xu
Xuetao Xie
Jiagen Sheng
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: cellular composition; erythrocyte sedimentation rate; fibrinogen concentration; platelet-rich plasma; preparation systems.
Affiliations: Department of Orthopaedic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.

Abstract:  Erythrocyte sedimentation rate (ESR), which reflects the sedimentation rate of platelets, leukocytes and erythrocytes in response to centrifugal force, may influence the cellular composition of platelet-rich plasma (PRP) obtained via centrifugation methods. However, no relevant studies have substantiated this. In the present study, blood was collected from 40 healthy volunteers and used to prepare PRP with two plasma-based preparation systems [YinPRP and Plasma Rich in Growth Factor (PRGF) systems] and two buffy coat-based systems (RegenPRP and WEGOPRP systems) in a single-donor model. Volumes of PRP and platelet-poor plasma (PPP) that were removed in the preparation process were recorded. Analyses of ESR, haematocrit, C-reaction protein, coagulation, serum glucose and serum lipid of the whole blood used for PRP preparation were performed to evaluate the levels of ESR and the factors known to influence it. Whole blood analysis was performed to evaluate the cellular composition of PRP. Results demonstrated that there were marked positive correlations between the ESR of the whole blood used for PRP preparation and PPP removal efficiencies, platelet concentrations, platelet capture efficiencies and platelet enrichment factors of PRP formulations obtained from plasma-based systems, and PRP yield efficiency of RegenPRP and PPP removal efficiency of WEGOPRP. Furthermore, there were marked negative correlations between ESR and concentrations and enrichment factors of platelets, leukocytes and erythrocytes of RegenPRP. Fibrinogen concentration of the whole blood, which had a marked positive correlation with ESR, also influenced the cellular composition of PRP. These findings may increase the understanding of PRP preparation and provide substantial evidence for the individualised optimisation of PRP preparation systems used in clinical practice. 

Retracted: No

PubPeer comments:
 Figures 4D and 4F appear to have some patterns which are repeated. A question for the authors: is this expected? *** ![file] ,
Polycomb group protein ezh2 controls actin polymerization and cell signaling
Authors: Alexander Tarakhovsky
Matthew Oser
Raphael Marqueron
Danny Reinberg
Ephraim Dickinson
Ashwin Basavaraj
I-hsin Su
Christoph Wülfing
Marc-Werner Dobenecker
Agnes Viale
Journal: Cell (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Ezh2; Polycomb group protein; histone methylation; cytosolic; methyltransferase complex
Affiliations: Laboratory of Lymphocyte Signaling, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. 

Abstract:  Polycomb group protein Ezh2, one of the key regulators of development in organisms from flies to mice, exerts its epigenetic function through regulation of histone methylation. Here, we report the existence of the cytosolic Ezh2-containing methyltransferase complex and tie the function of this complex to regulation of actin polymerization in various cell types. Genetic evidence supports the essential role of cytosolic Ezh2 in actin polymerization-dependent processes such as antigen receptor signaling in T cells and PDGF-induced dorsal circular ruffle formation in fibroblasts. Revealed function of Ezh2 points to a broader usage of lysine methylation in regulation of both nuclear and extra-nuclear signaling processes. 

Retracted: No

PubPeer comments:
 Figure 1A. Splice in nuclear Ezh2 panel, bot not in nuclear Lamin B panel. https: imgur.com M64rvLw , 
 Figure 2A. Splice in Ezh2 panel, but no splice in Actin panel. There are random light streaks in the Actin panel, but they are less sharp, and cut the bands (not features of splice marks). https: imgur.com CTDeQ5Z , 
 #1 Figure 1A. Splice in nuclear Ezh2 panel, but not in nuclear Lamin B panel. So that the image appears on this page. ![file] , 
 #2 Figure 2A. Splice in Ezh2 panel, but no splice in Actin panel. There are random light streaks in the Actin panel, but they are less sharp, and cut the bands (not features of splice marks). So that the image appears on this page. ![file] ,
Crosstalk between JNK and SUMO signaling pathways: deSUMOylation is protective against H2O2-induced cell injury
Authors: Andrea Arnaboldi
Alessandra Sclip
Elisa Brambilla
Xanthi Antoniou
Tiziana Borsello
Federica Morelli
Agata Camassa
Marco Feligioni
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Oxidative stress; Neurological disorders; c-Jun N-terminal kinase (JNK); Small ubiquitin-related modifier (SUMO); H(2)O(2)
Affiliations: Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milano, Italy.

Abstract:  Background: Oxidative stress is a key feature in the pathogenesis of several neurological disorders. Following oxidative stress stimuli a wide range of pathways are activated and contribute to cellular death. The mechanism that couples c-Jun N-terminal kinase (JNK) signaling, a key pathway in stress conditions, to the small ubiquitin-related modifier (SUMO), an emerging protein in the field, is largely unknown. Methodology/principal findings: With this study we investigated if SUMOylation participates in the regulation of JNK activation as well as cellular death in a model of H(2)O(2) induced-oxidative stress. Our data show that H(2)O(2) modulates JNK activation and induces cellular death in neuroblastoma SH-SY5Y cells. Inhibition of JNK's action with the D-JNKI1 peptide rescued cells from death. Following H(2)O(2), SUMO-1 over-expression increased phosphorylation of JNK and exacerbated cell death, although only in conditions of mild oxidative stress. Furthermore inhibition of SUMOylation, following transfection with SENP1, interfered with JNK activation and rescued cells from H(2)O(2) induced death. Importantly, in our model, direct interaction between these proteins can occur. Conclusions/significance: Taken together our results show that SUMOylation may significantly contribute to modulation of JNK activation and contribute to cell death in oxidative stress conditions. 

Retracted: No

PubPeer comments:
 The same data is shown for control in Fig. 1, 4 and 5: ![file] ![file] ![file] ,
Correlation between the histological grade of chondrosarcoma and the expression of MMPs, ADAMTSs and TIMPs
Authors: Masahiko Sugitani
Norimichi Nemoto
Makoto Sano
Yukihiro Yoshida
Eiji Osaka
Shunzo Osaka
Junnosuke Ryu
Hideyuki Sugita
Masato Toriyama
Journal: Anticancer research (0)
Discipline: CLINICAL MEDICINE
Keywords: chondrosarcoma; matrix metalloproteinases; ADAMTS; TIMPs; histological grade
Affiliations: Department of Orthopaedic Surgery, Nihon University School of Medicine, Tokyo, Japan. 

Abstract:  Background: The malignant degree of human chondrosarcoma can be difficult to determine using only histological findings. We, therefore, assessed the expression of matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase (ADAM) with thrombospondin motifs (ADAMTSs) and tissue inhibitor of metalloproteinases (TIMPs) in chondrosarcoma and ascertained the relationships to histological degree of malignancy and prognosis. Materials and methods: In 28 chondrosarcoma cases, immunostaining was performed using antibodies against MMP 2, 3, 7, 9, 13, ADAMTS 4, 5 and TIMP 1, 2, 3. Results: The chondrosarcoma were classified into groups of 7, 15 and 6 cases based on histologically malignant grade I, II and III, respectively. All target proteins were expressed in chondrosarcoma. Positive correlations (p &lt; 0.05) existed between immunostaining scores and histological grades for all proteins except MMP 9, with strong correlations (p &lt; 0.01) for MMPs 2, 3 and 13, both ADAMTSs and all 3 TIMPs. No correlation existed between prognosis and immunostaining scores. Conclusion: These target proteins could, thus, indicate the degree of malignancy in human chondrosarcoma. 

Retracted: No

PubPeer comments:
 It is considered that these papers are duplication. ![file] ![file] ![file] ![file] ![file] ![file] ,
Craniosynostosis in transgenic mice overexpressing Nell-1
Authors: Norihiro Kanayama
Ichiro Nishimura
Fei-Ya Hu
Kang Ting
Keisuke Iida
Naoaki Saito
Shun&#x27;ichi Kuroda
Eric Wisner
Steve Beanes
Steve Miao
Rex Moats
Katsuyuki Tanizawa
Michael Longaker
Dale Carpenter
Chia Soo
Heleni Vastardis
Catherine Dang
Xinli Zhang
Journal: Journal of Clinical Investigation (2002)
Discipline: CLINICAL MEDICINE
Keywords: NELL-1; transgenic mice; craniosynostosis; calvarial overgrowth; osteoblast differentiation
Affiliations: Dental and Craniofacial Research Institute, University of California, Los Angeles, California 90095, USA.

Abstract:  Previously, we reported NELL-1 as a novel molecule overexpressed during premature cranial suture closure in patients with craniosynostosis (CS), one of the most common congenital craniofacial deformities. Here we describe the creation and analysis of transgenic mice overexpressing Nell-1. Nell-1 transgenic animals exhibited CS-like phenotypes that ranged from simple to compound synostoses. Histologically, the osteogenic fronts of abnormally closing/closed sutures in these animals revealed calvarial overgrowth and overlap along with increased osteoblast differentiation and reduced cell proliferation. Furthermore, anomalies were restricted to calvarial bone, despite generalized, non-tissue-specific overexpression of Nell-1. In vitro, Nell-1 overexpression accelerated calvarial osteoblast differentiation and mineralization under normal culture conditions. Moreover, Nell-1 overexpression in osteoblasts was sufficient to promote alkaline phosphatase expression and micronodule formation. Conversely, downregulation of Nell-1 inhibited osteoblast differentiation in vitro. In summary, Nell-1 overexpression induced calvarial overgrowth resulting in premature suture closure in a rodent model. Nell-1, therefore, has a novel role in CS development, perhaps as part of a complex chain of events resulting in premature suture closure. On a cellular level, Nell-1 expression may modulate and be both sufficient and required for osteoblast differentiation. 

Retracted: No

PubPeer comments:
 Western blots from Figure 1C were spliced and partially duplicated from blots in Figure 1A. ![file] ,
Inhibition of TNF-α improves the bladder dysfunction that is associated with type 2 diabetes
Authors: Edward Gong
Maryrose P Sullivan
Vivian Cristofaro
Pablo Gomez
Aria F Olumi
Jijun Li
Morris F White
Zongwei Wang
Klemen Strle
Zhiyong Cheng
Rongbin Ge
Xingyuan Xiao
Rosalyn M Adam
Journal: Diabetes (2012)
Discipline: CLINICAL MEDICINE
Keywords: Diabetic bladder dysfunction; mouse model; insulin receptor substrate; detrusor overactivity; detrusor hypoactivity
Affiliations: Department of Urology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Abstract:  Diabetic bladder dysfunction (DBD) is common and affects 80% of diabetic patients. However, the molecular mechanisms underlying DBD remain elusive because of a lack of appropriate animal models. We demonstrate DBD in a mouse model that harbors hepatic-specific insulin receptor substrate 1 and 2 deletions (double knockout [DKO]), which develops type 2 diabetes. Bladders of DKO animals exhibited detrusor overactivity at an early stage: increased frequency of nonvoiding contractions during bladder filling, decreased voided volume, and dispersed urine spot patterns. In contrast, older animals with diabetes exhibited detrusor hypoactivity, findings consistent with clinical features of diabetes in humans. The tumor necrosis factor (TNF) superfamily genes were upregulated in DKO bladders. In particular, TNF-α was upregulated in serum and in bladder smooth muscle tissue. TNF-α augmented the contraction of primary cultured bladder smooth muscle cells through upregulating Rho kinase activity and phosphorylating myosin light chain. Systemic treatment of DKO animals with soluble TNF receptor 1 (TNFRI) prevented upregulation of Rho A signaling and reversed the bladder dysfunction, without affecting hyperglycemia. TNFRI combined with the antidiabetic agent, metformin, improved DBD beyond that achieved with metformin alone, suggesting that therapies targeting TNF-α may have utility in reversing the secondary urologic complications of type 2 diabetes. 

Retracted: No

PubPeer comments:
 Figure 2F and 7F. * Red boxes: The CTR 12W photo in Figure 2F looks very similar to the DKO+TNFRI photo in Figure 7F. ![file] , 
 Thank you for the careful reading of our Diabetes paper u201cInhibition of TNF-a Improves the Bladder Dysfunction That Is Associated With Type 2 Diabetesu201d . DOI: 10.2337 db11-1763. As you have pointed out, the wrong image was used for figure 7F. We plan to correct this and will contact Diabetes directly to make the correction. Please let us know if you have any other questions or suggestions. , 
 Erratum, July 2021: https: diabetesjournals.org diabetes article 70 6 1416 137754 Erratum-Inhibition-of-TNF-Improves-the-Bladder  In the above-cited article, the u201cCTR 12wu201d image in Fig. 2F was inadvertently duplicated in Fig. 7F as the u201cDKO+TNFRIu201d image. The correct u201cDKO+TNFRIu201d image for Fig. 7F is shown below. The online version of the article has been updated with the corrected figure. The authors apologize to the readers for any confusion this may have caused. I thank the authors and the journal for addressing this error. ,
Novel mode for neutrophil protease cathepsin G-mediated signaling: membrane shedding of epidermal growth factor is required for cardiomyocyte anoikis
Authors: Kristoffer Valerie
Susan F Steinberg
Abdelkarim Sabri
Marie Hanscom
Khadija Rafiq
Journal: Circulation Research (2008)
Discipline: CLINICAL MEDICINE
Keywords: Neutrophils; myocardial remodeling; cardiac failure; reactive oxygen species; antimicrobial peptides
Affiliations: Cardiovascular Research Center, Department of Anatomy & Cell Biology, Temple University, 3420 N Broad St, Philadelphia, PA 19140, USA.

Abstract:  Neutrophils are thought to orchestrate myocardial remodeling during the early progression to cardiac failure through the release of reactive oxygen species, antimicrobial peptides, and proteases. Although neutrophil activation may be beneficial at early stages of disease, excessive neutrophil infiltration can induce cardiomyocyte death and tissue damage. The neutrophil-derived serine protease cathepsin G (Cat.G) has been shown to induce neonatal rat cardiomyocyte detachment and apoptosis by anoikis. However, the involved signaling mechanisms for Cat.G are not well understood. This study identifies epidermal growth factor receptor (EGFR) transactivation as a mechanism whereby Cat.G induces signaling in cardiomyocytes. Cat.G induced a rapid and transient increase in EGFR tyrosine phosphorylation, and inhibition of EGFR kinase activity, either with AG1478 or by expression of kinase inactive EGFR mutants (EGFR-CD533), markedly attenuated EGFR downstream signaling and myocyte anoikis induced by Cat.G. Consistent with this effect of EGFR, high level expression of wild-type EGFR was sufficient to promote myocyte apoptosis. We also found that matrix metalloproteinase-dependent membrane shedding of heparin-binding EGF was involved in Cat.G signaling and that membrane type 1 matrix metalloproteinase activation may constitute a potential target that entails matrix metalloproteinase activation induced by Cat.G. The paradoxical proapoptotic effect of EGFR appeared to be dependent on protein tyrosine phosphatase SHP2 (Src homology domain 2-containing tyrosine phosphatase 2) activation and focal adhesion kinase downregulation. These results show that Cat.G-induced cardiomyocyte apoptosis involves an increase in EGFR-dependent activation of SHP2 that promotes focal adhesion kinase dephosphorylation and subsequent cardiomyocyte anoikis. 

Retracted: No

PubPeer comments:
 Figure 5C. Much more similar than expected. https: imgur.com zQHdHKZ , 
 Figure 2B. Much more similar than expected. ![file] , 
 Figures 2A and 2B. Much more similar than expected. ![file] , 
 Figure 3. Much more similar than expected. ![file] ,
Human herpesvirus 8 viral interleukin-6 signaling through gp130 promotes virus replication in primary effusion lymphoma and endothelial cells
Authors: John Nicholas
Emily Cousins
Yang Gao
Gordon Sandford
Journal: Journal of Virology (2014)
Discipline: MICROBIOLOGY
Keywords: HHV-8; viral interleukin-6; vIL-6; gp130 signaling; productive replication
Affiliations: Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA .

Abstract:  The contributions of human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) to virus biology remain unclear. Here we examined the role of vIL-6/gp130 signaling in HHV-8 productive replication in primary effusion lymphoma and endothelial cells. Depletion and depletion-complementation experiments revealed that endoplasmic reticulum-localized vIL-6 activity via gp130 and gp130-activated signal transducer and activator of transcription (STAT) signaling, but not extracellular signal-regulated kinase (ERK) activation, was critical for vIL-6 proreplication activity. Our data significantly extend current understanding of vIL-6 function and associated mechanisms in HHV-8 biology. 

Retracted: No

PubPeer comments:
 November 2017 correction, found here: https: jvi.asm.org content 91 23 e01572-17 It reads: *Volume 88, no. 20, p. 12167u201312172, 2014, https: doi.org 10.1128 JVI.01751-14. Page 12168, Fig. 1D, bottom right: u201c2 days + Doxu201d should read u201c1 day + Dox.u201d Page 12168, legend to Fig. 1C and D, line 5 from bottom: The following should be added before u201c(E)u201d: u201cThe data for panels C and D were from the same experiment, so the NS data sets are the same for both panels.u201d* Here is the original panel of Figure 1E (or 1C 1D; as the labeling is not clear), with the duplication marked in red: ![file] I thank the authors and journal for addressing this issue, which was reported in December 2014. ,
Fam57b (family with sequence similarity 57, member B), a novel peroxisome proliferator-activated receptor γ target gene that regulates adipogenesis through ceramide synthesis
Authors: Yzumi Yamashita-Sugahara
Masahito Matsumoto
Yutaka Nakachi
Yoshimi Tokuzawa
Yasushi Okazaki
Yukiko Kanesaki-Yatsuka
Yosuke Mizuno
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: gene; Fam57b; PPARγ; obesity; adipocyte differentiation
Affiliations: Division of Functional Genomics and Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka City, Saitama 350-1241, Japan.

Abstract:  This report identifies a novel gene encoding Fam57b (family with sequence similarity 57, member B) as a novel peroxisome proliferator-activated receptor γ (PPARγ)-responsive transmembrane gene that is related to obesity. The gene was identified based on an integrated bioinformatics analysis of the following three expression profiling data sets: adipocyte differentiation of mouse stromal cells (ST2 cells), adipose tissues from obesity mice, and siRNA-mediated knockdown of Pparγ using ST2 cells. Fam57b consists of three variants expressed from different promoters and contains a Tram-Lag1-CLN8 domain that is related to ceramide synthase. Reporter and ChIP assays showed that Fam57b variant 2 is a bona fide PPARγ target gene in ST2 cells. Fam57b was up-regulated during adipocyte differentiation, suggesting that FAM57B is involved in this process. Surprisingly, FAM57B overexpression inhibited adipogenesis, and siRNA-mediated knockdown promoted adipocyte differentiation. Analysis of the ceramide content by lipid assay found that ceramides were in fact augmented in FAM57B-overexpressing ST2 cells. We also confirmed that ceramide inhibits adipogenesis. Therefore, the aforementioned results of FAM57B overexpression and siRNA experiments are reconciled by ceramide synthesis. In summary, we present in vitro evidence showing that PPARγ regulates Fam57b transcription during the adipogenesis of ST2 cells. In addition, our results suggest that PPARγ activation contributes to the regulation of ceramide metabolism during adipogenesis via FAM57B. 

Retracted: No

PubPeer comments:
 2020 correction. https: www.jbc.org content 295 15 5176.short In Fig. 6B, the wrong image was used for siFam57b-B. This error has been corrected with the correct image and does not affect any results or conclusions of this wor ,
A simultaneous grafting/vinyl polymerization process generates a polycationic surface for enhanced antibacterial activity of bacterial cellulose
Authors: Shu Chen
Haobo Pan
Xin Zhou
Xiuping Wu
Pengfei Tian
Yang Hu
Haiyan Liu
Yongjun Zhu
Journal: International Journal of Biological Macromolecules (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Antibacterial activity; Bacterial cellulose; Polycationic; Quaternary ammonium salt with vinyl groups.
Affiliations: School and Hospital of Stomatology, Shanxi Medical University, Taiyuan, Shanxi 030001, China; Center for Human Tissue and Organs Degeneration and Shenzhen Key Laboratory of Marine Biomedical Materials, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China., Center for Human Tissue and Organs Degeneration and Shenzhen Key Laboratory of Marine Biomedical Materials, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China; Fiber and Biopolymer Research Institute, Department of Plant and Soil Science, Texas Tech University, Lubbock, TX 79403, USA. Electronic address: ., Center for Human Tissue and Organs Degeneration and Shenzhen Key Laboratory of Marine Biomedical Materials, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China., School and Hospital of Stomatology, Shanxi Medical University, Taiyuan, Shanxi 030001, China. Electronic address: .

Abstract:  Bacterial cellulose (BC) is a biosynthesized carbohydrate polymer with excellent biocompatibility and water holding capability. However, it lacks an inherent antibacterial activity that has limited its in-depth biomedical applications. This study investigated a novel strategy of adopting a simultaneous process to chemically anchor a quaternary ammonium salt (R-N(CH3)+) with a special vinyl group (2-methacryloyloxyethyl trimethylammonium chloride, METAC) onto the BC, and meanwhile, enhance the density of (R-N(CH3)+) via free radical vinyl polymerization. The results have confirmed the transition of BC surface from a negatively-charged surface to a polycationic surface via such a simultaneous reaction. As compared to chitin film (a representative of R-NH3+), the resulting METAC-grafted BC (a representative of high-density R- N(CH3)+) acquired excellent water absorbability (40 times of dry weight of the BC), 99% antibacterial activity against Escherichia coli and Staphylococcus aureus, a satisfactory in-vitro biocompatibility, and a better in-vivo wound healing outcome with an excellent in-vivo antibacterial efficacy. This study has exhibited potential in utilizing a facile method to prepare a bio-safe, adaptive antibacterial surface for various biomedical applications. 

Retracted: No

PubPeer comments:
 In Figure 8a, two images of agar dishes share same background and some bacteria colonies (red solid circles, examples shown). In addition, two other images of agar dishes show similar background (red dashed circles). ![file] ,
Activated carbon preparation from eucalyptus wood chips using continuous carbonization–steam activation process in a batch intermittent rotary kiln
Authors: Nuchjira Dejang
Sumrit Mopoung
Journal: Scientific Reports (2021)
Discipline: Multidisciplinary
Keywords: Activated carbon; Eucalyptus wood chips; Steam activation; Rotary kiln; FTIR
Affiliations: Chemistry Department, Faculty of Science, Naresuan University, Phitsanulok, 65000, Thailand. ., Department of Physics, Faculty of Science, Naresuan University, Phitsanulok, 65000, Thailand.

Abstract:  The production of activated carbon from eucalyptus wood chips by steam activation in a 2000 kg batch intermittent rotary kiln with continuous carbonization-steam activation process conducted at 500 °C to 700 °C was studied. The activated carbon products were characterized by FTIR, SEM-EDS, Raman spectroscopy, and BET analysis. Percent yields, iodine number, and methylene blue number of the produced activated carbon materials were measured as well. It was shown that the percent yields of the activated carbon materials made in the temperature range from 500 to 700 °C are 21.63 ± 1.52%-31.79 ± 0.70% with capacities of 518-737 mg I2/g and 70.11-96.93 mg methylene blue/g. The BET surface area and micropore volume of the activated carbons are 426.8125-870.4732 m2/g and 0.102390-0.215473 cm3/g, respectively. The steam used in the process could create various oxygen containing surface functional groups such as -CO and -COC groups. In addition, it could also increase the amorphous nature of the activated carbon product. These properties of the activated carbon products are increased with increasing steam activation temperature from 500 to 700 °C. As a result, the activated carbon materials produced at activation temperatures of 600 °C and 700 °C exhibit higher adsorption. 

Retracted: No

PubPeer comments:
 Figure 4. XRD patterns of (a) eucalyptus wood chip activated carbon prepared at 500 u00b0C, (b) eucalyptus wood chip activated carbon prepared at 600 u00b0C, and (c) eucalyptus wood chip activated carbon prepared at 700 u00b0C. two identical XRD patterns for different samples ![file] ,
Matrix metalloproteinase 13‐containing exosomes promote nasopharyngeal carcinoma metastasis
Authors: Si Shi
Bo You
Ying Shan
Huijun Yue
Jing Chen
Xingyu Li
Yiwen You
Xiaolei Cao
Journal: Cancer Science (2015)
Discipline: CLINICAL MEDICINE
Keywords: Exosomes; MMP13; metastasis; microenvironment nasopharyngeal carcinoma.
Affiliations: Department of Otorhinolaryngology Affiliated Hospital of Nantong University Nantong China, Department of Otorhinolaryngology Medical School of Nantong University Nantong China, Department of Pathology Medical School of Nantong University Nantong China

Abstract:  Nasopharyngeal cancer (NPC) is an endemic type of head and neck cancer with a high rate of cervical lymph node metastasis. Metastasis is the major cause of death in NPC patients. Increasing evidence indicates that exosomes play a pivotal role in promoting cancer metastasis by enhancing angiogenesis and ECM degradation. Matrix metalloproteinase 13 is an important kind of matrix proteinase that is often overexpressed in various tumors and increases the risk of metastasis. However, little is known about the potential role of MMP13-containing exosomes in NPC. In this study, we found that MMP13 was overexpressed in NPC cells and exosomes purified from conditioned medium (CM) as well as NPC patients' plasma. Transwell analysis revealed that MMP13-containing exosomes facilitated the metastasis of NPC cells. Furthermore, siRNA inhibited the effect of MMP13-containing exosomes on tumor cells metastasis as well as angiogenesis. The current findings provided novel insight into the vital role of MMP13-containing exosomes in NPC progression which might offer unique insights for potential therapeutic strategies for NPC progressions. 

Retracted: No

PubPeer comments:
 Fig. 4a and Fig. 4j. More similar than expected. ![file] ,
Mantle cell lymphoma cells express predominantly cyclin D1a isoform and are highly sensitive to selective inhibition of CDK4 kinase activity
Authors: Peter Nowell
Samuel E Deprimo
Mariusz A Wasik
Monika Kasprzycka
Pawel Wlodarski
Michal Marzec
Stephen Eck
Ewa Tomczak
J Alan Diehl
Andrew B Gladden
Seth Sadis
Stephen J Schuster
Raymond Lai
Journal: Blood (2006)
Discipline: CLINICAL MEDICINE
Keywords: Mantle cell lymphoma; cyclin D1; gene translocation; CDK4; Rb phosphorylation
Affiliations: Department of Pathology and Laboratory Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania Medical Center, 7.106 Founders, Philadelphia, PA 19104, USA.

Abstract:  The prognosis for patients with mantle cell lymphoma (MCL) is poor, and at present there is no truly effective therapy. Gene translocation-mediated constitutive expression of cyclin D1 seems to play the key role in the pathogenesis of MCL. Here we report that although 3 of 4 MCL cell lines expressed the recently identified, highly oncogenic cyclin D1b isoform, as well as the canonical cyclin D1a, 8 MCL patient samples expressed only the cyclin D1a protein despite expressing detectable cyclin D1b mRNA. Cell lines and tissue samples displayed constitutive activation of the cyclin D1 signaling cascade, as evidenced by strong expression of CDK4, Rb phosphorylation, and cyclin D1/CDK4 coassociation. All MCL cell lines and tissues examined displayed nondetectable to diminished expression of the cyclin D1 inhibitor p16. Novel small molecule CDK4/CDK6 inhibitor PD0332991 profoundly suppressed--at low nanomolar concentrations--Rb phosphorylation, proliferation, and cell cycle progression at the G0/G1 phase of MCL cells. These findings provide evidence that MCL should be very sensitive to targeted therapy aimed at functional inhibition of the cyclin D1/CDK4 complex. 

Retracted: No

PubPeer comments:
 Figure 3B. Much more similar than you would expect. https: imgur.com 49s7UUZ ,
Novel role for PDEF in epithelial cell migration and invasion
Authors: Eugene Koh
Carolyn N Wrobel
George Q Daley
Dennis C Sgroi
Joan S Brugge
Ruwanthi N Gunawardane
Journal: Cancer research (2005)
Discipline: CLINICAL MEDICINE
Keywords: Cell migration; invasion; tumorigenesis; retroviral screen; PDEF
Affiliations: Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

Abstract:  Cell migration and invasion are two critical cellular processes that are often deregulated during tumorigenesis. To identify factors that contribute to oncogenic progression by stimulating cell migration, we conducted a powerful retroviral based migration screen using an MCF7 cDNA library and the immortalized human breast epithelial cell line MCF-10A. We identified prostate derived Ets factor (PDEF), an Ets transcription factor that is overexpressed in both prostate and breast carcinoma, as a candidate promigratory gene from this screen. Whereas PDEF induced limited motility of MCF-10A cells, coexpression of PDEF with the receptor tyrosine kinases (RTK) ErbB2 and colony-stimulating factor receptor (CSF-1R)/CSF-1 significantly enhanced MCF-10A motility. Furthermore, cells coexpressing PDEF with either ErbB2 or CSF-1R/CSF-1 induced a dramatic invasive phenotype in three-dimensional cultures. Constitutive activation of the extracellular signal-regulated kinase (ERK) pathway also enhanced PDEF-induced motility and invasion, suggesting that activation of the ERK/mitogen-activated protein kinase by ErbB2 and CSF-1R/CSF-1 can cooperate with PDEF to promote motility and invasion. Furthermore, PDEF promoted anchorage-independent growth of ErbB2 and CSF-1R/CSF-1-expressing cells. Using laser capture microdissection, we also found that PDEF mRNA is overexpressed in breast tumor epithelia throughout tumor progression. Taken together, these findings suggest that the transcription factor PDEF may play an important role in breast tumorigenesis and that PDEF overexpression may be particularly significant in tumors that exhibit activation of oncogenic RTKs such as ErbB2 and CSF-1R. 

Retracted: No

PubPeer comments:
 Figure 5C. Much more similar than you would expect. https: imgur.com 2KxSMrE , 
 I agree and will look into this with the person who ran this experiment. All of our experimental notebooks from this time are archived and inaccessible until after we have access to the lab. , 
 We agree that this is a duplication that was missed in assembling the paper. We were able to locate all of the original digital files and have sent appropriate image for the Control from this figure to Cancer Research. This mistake does not in any way affect the conclusions of the report. ,
Met is the most frequently amplified gene in endometriosis-associated ovarian clear cell adenocarcinoma and correlates with worsened prognosis
Authors: Fumitaka Kikkawa
Shinya Akatsuka
Hiroshi Seko
Hiroaki Kajiyama
Shinya Toyokuni
Kanako Shinjo
Hiroharu Kobayashi
Yasushi Yatabe
Yoriko Yamashita
Takashi Takahashi
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Clear cell adenocarcinoma; ovary; Met gene; AKT2 gene; amplification
Affiliations: Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.

Abstract:  Clear cell adenocarcinoma of the ovary (OCC) is a chemo-resistant tumor with a relatively poor prognosis and is frequently associated with endometriosis. Although it is assumed that oxidative stress plays some role in the malignant transformation of this tumor, the characteristic molecular events leading to carcinogenesis remain unknown. In this study, an array-based comparative genomic hybridization (CGH) analysis revealed Met gene amplification in 4/13 OCC primary tumors and 2/8 OCC cell lines. Amplification of the AKT2 gene, which is a downstream component of the Met/PI3K signaling pathway, was also observed in 5/21 samples by array-based CGH analysis. In one patient, both the Met and AKT2 genes were amplified. These findings were confirmed using fluorescence in situ hybridization, real-time quantitative PCR, immunoblotting, and immunohistochemistry. In total, 73 OCC cases were evaluated using real-time quantitative PCR; 37.0% demonstrated Met gene amplification (&gt;4 copies), and 8.2% had AKT2 amplification. Furthermore, stage 1 and 2 patients with Met gene amplification had significantly worse survival than patients without Met gene amplification (p&lt;0.05). Met knockdown by shRNA resulted in reduced viability of OCC cells with Met amplification due to increased apoptosis and cellular senescence, suggesting that the Met signaling pathway plays an important role in OCC carcinogenesis. Thus, we believe that targeted inhibition of the Met pathway may be a promising treatment for OCC. 

Retracted: No

PubPeer comments:
 https: twitter.com franciscodeasis status 1415367555779289091?s=20 , 
 https: twitter.com scotub status 1415399876213444608?s=20 ,
Histiocytic necrotizing lymphadenitis (Kikuchi’s disease) with aseptic meningitis
Authors: H Kuno
Y Sato
K Oizumi
Journal: Journal of the Neurological Sciences (1999)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Histiocytic necrotizing lymphadenitis; Kikuchi's disease; meningitis; cerebrospinal fluid; lymphocytes

Abstract:  Histiocytic necrotizing lymphadenitis, or Kikuchi's disease (KD), is a self-limited clinicopathologic entity recognized increasingly worldwide. A 27-year-old man with cervical lymphadenopathy and fever who was diagnosed with KD developed mild headache with no nuchal rigidity. The cerebrospinal fluid (CSF) was sterile and contained 78 white blood cells/mm3 with lymphocytes predominating, accompanied by smaller numbers of monocytes and granulocytes. This abnormality normalized spontaneously over 5 weeks. Eleven similar cases have been reported, all but one from Japan. The development of meningitis in KD was observed in four (9.8%) of 41 KD patients we have treated, suggesting that the meningitis was related to KD and not merely coincidental. 

Retracted: No

PubPeer comments:
 On June 14 2020, the publisher informed us that this paper was to be retracted. 9 months later it has not been. Lengthy delays in publishing retraction notices is not in the best interest of readers. , 
 It is now 21 months since Elsevier communicated, via COPE, its undertaking to retract this paper. Recent requests for an update on the retraction to Elsevier, COPE, and the journal did not receive a response. The society associated with the journal, the World Federation of Neurology, responded but was unable to provide any information. ,
miR-129-5p improves cardiac function in rats with chronic heart failure through targeting HMGB1
Authors: Jun Zhang
Na Xiao
Yanfang Wan
Ning Wang
Chao Chen
Jing Yang
Journal: Mammalian Genome (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: miRNAs; cardiovascular diseases; heart failure; miR-129-5p; HMGB1
Affiliations: Department Cardiovascular V, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061000, Hebei, China. ., Department Cardiovascular V, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061000, Hebei, China.

Abstract:  Increasing evidence shows that miRNAs play pivotal roles in cardiovascular diseases, including heart failure (HF). The aim of this study was to investigate the role of miR-129-5p in chronic heart failure and the underlying mechanisms. The levels of miR-129-5p and HMGB1 in chronic heart failure patients (CHF) and normal controls were examined by RT-qPCR and ELISA. Cardiac function, hemodynamics parameters, oxidative stress, and inflammation factors were analyzed in CHF rat model after transfection of miR-129-5p or HMGB1. Dual-luciferase activity reporter assay was conducted to validate the interaction between miR-129-5p and HMGB1. Downregulation of miR-129-5p and upregulation of HMGB1 were observed in the serum of CHF patients, respectively. Transfection of miR-129-5p improved heart function and hemodynamic parameters, as well as attenuated oxidative stress and inflammation factors in CHF rats. We further confirmed that HMGB1 is a direct target of miR-129-5p. Transfection of miR-129-5p also decreased the mRNA and protein levels of HMGB1 in myocardial tissues of CHF rats. Overexpression of HMGB1 diminished the effects of miR-129-5p on ameliorating oxidative stress and inflammatory response in rats with CHF. Our findings suggest that miR-129-5p protects the heart by targeting HMGB1. 

Retracted: No

PubPeer comments:
 Comparing Figs 7(c) and 8(d). Could the authors clarify whether the two marked GAPDH blobs are controlling for conditions  Sham and  CHF , as in 7(c); or CHF + miR-129-5p mimics with without LV-HMBG1, as in 8(d)? ![file] ,